\\n\\n
Dr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\\n\\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\\n\\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\\n\\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\\n\\nThank you all for being part of the journey. 5,000 times thank you!
\\n\\nNow with 5,000 titles available Open Access, which one will you read next?
\\n\\nRead, share and download for free: https://www.intechopen.com/books
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Preparation of Space Experiments edited by international leading expert Dr. Vladimir Pletser, Director of Space Training Operations at Blue Abyss is the 5,000th Open Access book published by IntechOpen and our milestone publication!
\n\n"This book presents some of the current trends in space microgravity research. The eleven chapters introduce various facets of space research in physical sciences, human physiology and technology developed using the microgravity environment not only to improve our fundamental understanding in these domains but also to adapt this new knowledge for application on earth." says the editor. Listen what else Dr. Pletser has to say...
\n\n\n\nDr. Pletser’s experience includes 30 years of working with the European Space Agency as a Senior Physicist/Engineer and coordinating their parabolic flight campaigns, and he is the Guinness World Record holder for the most number of aircraft flown (12) in parabolas, personally logging more than 7,300 parabolas.
\n\nSeeing the 5,000th book published makes us at the same time proud, happy, humble, and grateful. This is a great opportunity to stop and celebrate what we have done so far, but is also an opportunity to engage even more, grow, and succeed. It wouldn't be possible to get here without the synergy of team members’ hard work and authors and editors who devote time and their expertise into Open Access book publishing with us.
\n\nOver these years, we have gone from pioneering the scientific Open Access book publishing field to being the world’s largest Open Access book publisher. Nonetheless, our vision has remained the same: to meet the challenges of making relevant knowledge available to the worldwide community under the Open Access model.
\n\nWe are excited about the present, and we look forward to sharing many more successes in the future.
\n\nThank you all for being part of the journey. 5,000 times thank you!
\n\nNow with 5,000 titles available Open Access, which one will you read next?
\n\nRead, share and download for free: https://www.intechopen.com/books
\n\n\n\n
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"7360",leadTitle:null,fullTitle:"Fillers - Synthesis, Characterization and Industrial Application",title:"Fillers",subtitle:"Synthesis, Characterization and Industrial Application",reviewType:"peer-reviewed",abstract:"Fillers - Synthesis, Characterization and Industrial Application comprises a set of chapters that brings an interdisciplinary perspective to accomplish a more detailed understanding of filler materials for the synthesis and characterization of different industrial applications. 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Downy mildew caused by Peronospora belbahrii Thines is one of the most destructive diseases of sweet basil (Ocimum basilicum) of the family Lamiaceae Lindl. (alternatively Labiaceae Dulac) which except field farming is also grown as a specialty crop in greenhouses. Downy mildew of basil was first reported in 1932 from Uganda, Africa as Peronospora spp. and again in 1937 as P. lamii from where it is assumed to have originated on sweet basil [1, 2].
First report from Europe was in 2001 from Switzerland where it was observed in greenhouses [3]. After that, the disease was detected in Italy in 2003 on sweet basil in several greenhouses located in Liguria region (Northern Italy). In 2004, it was found in France on some basil crops near Saint Tropez (Southern France) [4]. In the same year, it was found in Belgium, but there are no data about the first detection.
After those first European reports, the pathogen was rapidly spread through Europe. In summer 2009, it was detected in United Kingdom in Agastache (hyssop) plants (Agastache mexicana and Agastache sp.) at Wisley gardens (Surrey) and on the summer of 2010 in protected basil plants in south-east England [5, 6]. In 2010, a significant incidence of downy mildew was reported in Hungary at two plant stands at Budapest-Soroksár and Tordasal though a similar disease had been observed in 2003 in a greenhouse at Albertirsa [7]. It was reported from Czech Republic in 2012 as well as from Cyprus [8]. In 2014, it was found again in United Kingdom but in several plants of coleus (Solenostemon scutellarioides cv. ‘Chocolate Mint’) but in 2016 has been shown that the pathogen causing coleus downy mildew is P. belbahrii sensu lato [9]. In 2016, it has been reported from Spain on basil collected from the island of Tenerife (Islas Canarias) and afterwards was also noted that has been causing severe symptoms and economic losses in Almería, Andalucía [10].
In the United States, downy mildew of basil is considered as relatively new disease but the pathogen has been detected in October 2007 in South Florida [11]. Since its first detection in the United States, it has been observed on basil in at least 42 states [11, 12]. Interesting is founding in 2008 on basil plants produced in various nurseries in Sebastopol, Sonoma County because trace-back investigation revealed that the seeds had originated from Italy. This disease was also reported in Argentina in February 2008 [13] and Canada in 2011 [14]. In 2011, it was reported in Hawaii for the first time and in Mexico in 2015 [15].
First report in Asia was in Iran, where a severe outbreak of downy mildew was observed in sweet basil fields in 2006 [16]. A year later, in April 2007, it has been found in Japan on coleus plants cultivated in a greenhouse in Chiba Prefecture (Honshu) [17]. In the spring of 2009, it has been found in Taiwan in the field of Nantu and Yunlin [18]. In Israel, it was firstly found in December 2011 near Bet She’an, and in 2012 the disease has been spread throughout the country to all basil-growing areas [19]. Recently, it has been found in China in July 2014 on basil on the island of Hainan in Sanya City and in 2016 in the Shunyi and Daxing districts of Beijing which is concerned as first report in mainland China [20, 21]. Last Asian report is from Korea, where it has been first observed in November 2015 on sweet basil plants growing in plastic greenhouses in Gwangmyeong [22].
Until 2017, the disease was considered exotic to Australia, when it has been reported from South-east Queensland. Within 6 months, the disease was present along the eastern seaboard from north Queensland to Victoria, South Australia and the Northern Territory. In the scientific literature, Australia has been listed as a host country as early as 2015; however, no records of detections could be traced [23].
Finally, the first report of P. belbahrii sensu lato detection on coleus (Plectranthus spp.) in Brazil was reported in 2019 [24].
The first official report for Croatia was done in 2015 by Croatian Agency for Agriculture and Food based on symptoms and morphological characteristic not confirmed by molecular diagnostic [25]. In October 2015, as part of regular reporting reviews conducted by the Advisory Service, infected plants were found in greenhouses in the Varaždin County. The disease was spread soon after that founding on areas of four more counties (Krapina-Zagorje, Međimurje, Split-Dalmatian and Zagreb). Interestingly, in Dubrovnik-Neretva County, the disease was found on pot-plants imported from Italy. Up to date in Croatia, downy mildew is recorded only in production of basil in greenhouses. This chapter authors are currently investigating the occurrence on basil in the greenhouse ‘Green friends’ of eco-grower of culinary herbs and spices, situated in Rakovica in the Zagreb County. We confirmed determination of the P. belbahrii by molecular diagnostic (PCR sequence comparison of the ITS rDNA sequences and Cox2 region) (unpublished).
The first symptoms can be spotted on lower leaves, where infection starts and progresses upwards. The most noticeable symptom is yellowing (slightly chlorotic) of the leaves with the veins remaining green. The initial yellowing can be misinterpreted as a nutritional deficiency and so disease can go unrecognised. With time on upper surface of leaves, large chlorotic lesions with soft margins are developing. Chlorosis often involved the entire leaf surface. Since the pathogen is a biotroph, it causes dying of cells from which it absorbed nutrients and therefore necrotisation occur after chlorosis and the central portion of a chlorotic lesion become necrotic. This can lead to slight curvature of leaves. Necrotic spots are variable in size and of irregular shape as they are limited by the main veins. In some cases, entire area of the leaf surface is affected. In humid conditions, necrotic regions can become dark brown to black in colour. On abaxial leaf surfaces, both in chlorotic and necrotic regions, a typical greyish to brown, furry or downy moulds could be observed giving the leaves a dirty appearance (Figure 1). Parasitisation results in shrinkage of leaf and premature leaf fall.
Disease can go asymptomatic under cool and dry conditions [26] and sometimes plants not showing symptoms at harvest can develop symptoms during transport [27]. In report from Taiwan, it was noted that the pathogen caused chlorosis and leaf shrinkage on basil in the field, but did not cause any symptom on coleus, Pai-tsai Chinese cabbage (Brassica rapa), leaf lettuce (Lactuca sativa) and melon (Cucumis melo) [18].
Brown growth of Peronospora belbahrii on abaxial side of basil leaf.
Sweet basil is the natural host of P. belbahrii and the majority of P. belbahrii findings have been on sweet basil. In 2009, Thines et al. concluded that coleus is also the natural host of this pathogen [28]. They also investigated the downy mildew of sage, but were unable to confirm that it is caused by P. belbahrii so did not considered sage as natural host. Coleus has been confirmed as host of P. belbahrii in Japan, United States, United Kingdom and Germany [29]. Species concept has been refined recently and pathogen causal of coleus downy mildew was specified as P. belbahrii sensu lato [9]. Moreover, an unidentified species of Peronospora sp. infects coleus in Israel [30]. Interestingly, Israeli isolates of P. belbahrii from sweet basil do not infect coleus although infects other Lamiaceae species: rosemary (Rosmarinus officinalis) Nepeta (Nepeta curviflora), Clinopodium (Micromeria fruticosa) and two species of sage (Salvia pinnata and S. fruticosa) [30]. Further, the conidia from mentioned species failed to infect sweet basil and therefore the role of these species in the epidemiology of basil downy mildew in Israel is unknown [30]. The Peronospora sp. on coleus was reported in 2005 Louisiana, New York and Florida in U.S. [31, 32]. In 2015, Peronospora sp. on coleus was reported in Tennessee, and the morphological and molecular characteristics were consistent with Thines description of P. belbahrii sensu lato [9, 28]. So, Rivera et al. concluded that P. belbahrii can be described as complex of species likely defined by plant host [9]. Recently, coleus downy mildew causal pathogen is confirmed as P. belbahrii sensu lato host based on pathogenicity test in Brazil, and this is the first such report for the South America [24].
In 2009, the Agastache species (Lamiaceae) was also named as the new P. belbahrii host by Henricot et al. [6]. The host range is today broadened and as alternative hosts are considered culinary and ornamental varieties related to basil and coleus from Lamiaceae family and here are mint (Mentha spp.) and sage (Salvia spp.). All cultivars of sweet basil are hosts and as highly susceptible ones are cv. Genovese Nufar, Italian Large Leaf, Queenette, Superbo, Poppy Joe’s and Milita [27]. Some of the exotic, spice and ornamental basils cultivars such as red types (O. basilicum purpurescens cv. Red Rubin, Red leaf), lemon basil (O. citridiorum cv. Lemon std., Mrs. Burn’s Lemon, Lemona & Lime) and lime basil (O. americanum cv. Blue Spice, Spice & Blue Spice F1) have been found less susceptible or even resistant to downy mildew [9, 28, 33]. This chapter’s authors detected downy mildew on spice cultivars of basil, and P. belbahrii was confirmed as causal pathogen by molecular analysis (unpublished).
The causal pathogen of basil’s downy mildew is pseudofungus Peronospora belbahrii Thines and has been formally introduced under name P. belbahrii by Thines et al. in 2009 as dedication to Lassaard Belbahrii who first suggested that the pathogen on basil might be a distinct undescribed species and distinguished it from a different closely related species that parasitizes sage (Salvia officinalis) [28]. It is assumed that P. belbahrii is of African origin, as its host basil is native to this continent [28]. As oomycete it is classified in Chromysta, Oomycota, Oomycetes, Peronosporales and Peronosporaceae. The pathogen was molecularly determined in 2005 by Belbahri et al. [3] and showed through ITS sequencing that it is a newly occurring species on basil that differs from P. lamii, the only previously reported downy mildew on sweet basil and also differs from Peronospora species that is affecting lamiaceous hosts worldwide [1, 2]. Perhaps, previous findings of Peronospora sp. on sweet basil and coleus may be P. belbahrii but have been misidentified as P. lamii before sequence identification was carried out and before it was first described as a new species P. belbahrii. Confusion between species is likely to occur without sequence data; therefore, samples must be submitted to a competent testing laboratory for identification. Using morphological comparison and molecular phylogenetic reconstructions, Thines et al. also confirmed that P. belbahrii is not identical to P. swingleii on Salvia reflexa [28]. P. belbahrii on basil and coleus seems to be closely related yet; it has been shown that they are morphologically and genetically different [28]. Limited potential to infect basil has been reported for the isolates from coleus, as it was described earlier [30]. The significance of differences between causal pathogen of downy mildew on basil and coleus needs to be investigated further; but for now, the pathogen on coleus is determined as P. belbahrii sensu lato.
The growths on the underside of the symptomatic leaves in a form of a brown downy mould are asexual organs, sporangia bearing sporangiophores which emerge from leaf stomata. Microscopic observations will show that they are consistent with the characteristics of a genus Peronospora. The first descriptions of sporangia and sporangiophores on basil and coleus that were confirmed by molecular determination were provided by Thines et al. in 2009 [28]. The sporangia of genus Peronosporaare spore-like structures and they act as conidia and germinate into a germ-tube when they are near a leaf stoma. Therefore, the use of synonym conidia, or simply spore, has become commonplace for sporangia.
Conidia are dark brown to olive in colour and pedicel is absent. They are rounded and egg-shaped with a length 24–29–30.8–33–36 μm on basil and 26–29–31.3–33–37 μm on coleus. They width are 20–23–24–26–29 μm on basil and 20–23–24.5–26–29 μm on coleus. Ratio of length and width is 1.1–1.2–1.29–1.4–1.5 on basil and 1.1–1.2–1.28–1.4–1.5 on coleus [28].
Sporangiophores are colourless (hyaline) with a long, straight trunk and monopodially with a length 270–300–400–520–680 μm on basil and 330–380–466–570–650 μm on coleus [28]. Numbers of ramifications were 3–4–4.9–5–7 per sporophore on basil and 4–5–5.2–6–7 μm on coleus. Ultimate branchlets were in pairs, curved, longer one in length 13–18–20.6–26–31 μm on basil and 12–13–18–22–31 μm on coleus while the shorter one in length 3.8–7.7–9.80–10–15 μm on basil and 5.1–7.7–10.7–13–17 μm on coleus. Ratio of longer to shorter branches is 1.3–1.8–2.25–2.7–4 on basil and 1.1–1.6–1.71–1.9–2.5 on coleus. Ultimate branches end dichotomically and tips (sterigmata) are acute to subacute on both, basil and coleus. Tips are bearing single sporangia.
The shortest sporangiophores were reported in Iran and were 130–290 μm (avg. 194 μm) long and branched two to five times [16]. The longest sporangiophores were recorded in Hungary, and they were in length of 416–784 μm (avg. 572 μm) and monopodially branched five to seven times [7].
There are two oospore detections published up to date, both from Israel, found in leaves of susceptible sweet basil cultivar ‘Peri’. In 2013, Cohen et al. identified and described oospores as thick-walled, brown in colour, measuring of 46.2 ± 2.8 μm in diameter [34]. Oospores never occurred on the infected leaf surface, but inside the mesophyll [30]. In 2016, in walk-in tunnel experiments that simulated commercial production conditions, oospores were observed attached to the leaf surface, to older parts of the infection area, and also found to water washes of the leaf surface by Elad et al. [35]. Discovery of oospores suggests the potential for sexual reproduction, but little is known on P. belbahrii oospore formation or is it homothallic or heterothallic. Currently, only one mating type has been found [22], although it is already presumed that it is heterothallic [26, 36, 37]. The pathogenicity of oospores is investigated, but without positive infections [30, 38], and their role in the basil downy mildew epidemiology is not known.
The P. belbahrii thrives in warm, humid conditions and produce conidia that can infect in temperatures as low as 15°C (59°F) [26]. For example, downy mildew is present in Israeli basil-cropping regions where in the cooler season temperatures may reach minimum of 5–10°C at night and a maximum of 10–25°C during the day [35]. This corroborates with our observations. Pathogen can tolerate cold weather (10–15°C) but, like its host basil, cannot survive freezing winter temperatures at continental climate. Conidia cannot survive harsh winters and as pathogen is biotroph it needs living host. Therefore, in climates with harsh winters and with just one mating type of the P. belbahrii it can survive only on living plants in greenhouse production operations that produce basil year round. In mild winters and in warm, temperate regions where the host, basil will not freeze, the second overwintering inoculum are mycelium and conidia in infected plant buds, plant stems, leaf tissue and shoots. Congruently, the most devastating damage is often seen in warm and humid conditions, late summer and in greenhouses.
Most of Peronospora species can reside in soil as soil-borne oospores that are formed in leaf tissue and may overwinter in leaf litter or may be released into the soil as leaves decay and considered as soil-borne inoculum. Any movement of soil particles with soil-borne oospores inoculum can spread it from infected plants to non-infected ones. Although Peronospora species are biotrophs, they can survive without host as oil-borne oospores because they are in dormancy and can be viable for few years depending on species. Until now, there are no reports about P. belbahrii soil-borne oospores even in cases when oospores were detected inside the mesophyll of the leaves [30, 35]. Large-scale experiments were conducted to elucidate the pathogenicity of oospores to basil plants. Soil was infested with oospores (10 oospores/5 g of soil/well) and three to four basil seeds were planted in each well. Plants were grown until the four-leaf stage, but none of the 2000 plants that developed showed symptoms of downy mildew or sporulation of P. belbahrii [30]. Also, the experiments conducted in the Israeli walk-in tunnels lead to a conclusion that oospores are minimally affected by high temperature, and therefore the high temperature presumably did not affect pathogen survival [35].
The life cycle of P. belbahrii is initiated as abundantly produced air-borne conidia which can readily be spread by moist wind [37]. The conidia can be carried by rain drops, by wind, and can be splashed by rain to wet leaves near the ground. It does not need a vector for dispersal. Survivability of conidia, contrary to oospores, are strongly affected by temperature and duration of exposure so, a longer exposure period and higher temperature weakened the infection capacity of the conidia. Wetted-dried conidia lost their activity after 55 h at 25°C, 20 h at 30°C and 9 h at 40°C [30]. Therefore, conidia are short lived and viable just for few days so, they will endanger only susceptible host within the conidia dispersal area. McGrath conducted an experiment with field-grown basil at the Long Island Horticultural Research and Extension Center (LIHREC) in Riverhead, NY and considered the primary source of initial inoculum in this area to be long-distance wind dispersed conidia from affected plants [39] although the distance is not specified. The possibility to use frozen conidia as inoculum was also tested and those collected from infected leaves frozen for 3 months at −20°C or 2 years at −80°C retain high germination capability [30]. In other trial, frozen conidia germinated at 25% in contrast to nearly 90% germination rate of freshly harvested conidia [40]. Their germination was favoured between 5 and 15°C on water agar in vitro. Inoculation of basil plants with frozen or fresh conidia (3 × 104 mL−1) resulted in high disease severity 14 days post inoculation [40].
Sporulation occurs in moisture saturated atmosphere at an appropriate temperature and often during the night, in the dark and in chlorotic lesions 5–15 days old [41]. In controlled greenhouse experiments, sporulation occurs 6–7 days post inoculations [37]. The sporulation starts when pathogen biomass in the leaf mesophyll reached a certain threshold and complete within 8–12 h from onset of darkness in optimal conditions (saturated atmosphere at 18°C). During the first 6 h, hyaline sporophores are formed and as they emerge from stomata gradually become dichotomously. In the subsequent 5 h, dark spores are produced on the tips of the sporophore branchlets (sterigmata) [41]. The light strongly inhibits spore formation, but not sporophore development and emergence through leaf stomata. Yet, sporophores formed under the light are abnormal and unable to form spores. Cohen et al. in 2013 discovered that lightning during the second half of the night inhibits spore formation, and narrow band led illumination showed that red light (λmax 625 nm) was most inhibitory to spore formation comparing to blue light (λmax 440 nm) while in other oomycetes is quite the opposite [41]. They speculate that probably P. belbahrii has a different photoreceptor sensitive to red light. The sporulation is greater when the portion of carbohydrates in the leaf is higher [41]. The carbohydrates accumulating during the day are hydrolysed to hexoses during the first half of the night which pathogen uses for formation of conidia during the rest of the night [41]. Therefore, the greater the accumulation of carbohydrates in infected leaves during the daytime contributes to the greater sporulation in the following dark, wet period of the night. This all suggests that the sporulation terminates with necrosis of leaf which obstructs assimilation as plant cells die because of pathogen absorbed all nutrients from it.
Conidia germinate in 3–5 days into one or two germ tubes and infect plant tissues via a germ-tube which penetrates through leaf stomata [28, 36] and it takes 3 h [35]. Germ tubes rarely form an appressoria-like structures prior infection. Developing hypha grows into intercellular spaces within the leaf mesophyll, proliferate and eventually invaginate the host cell plant cells through special globuse structures called haustoria (a hallmark oomycete structure) for nutrient acquisition [37]. Further branching and spreading of this initial hypha lead to forming of a cushion of intercellular mycelia just below the stomata. From this cushion, sporangiophores arise and emerge through stomata on sterigmata bearing sporangia. Conidia are produced simultaneously and are carried by wind and rain to new infection sites of the same or different plant. Leaf wetness of at least 6 h is required for conidial infection [42, 43]. Under favourable conditions, sporulation progresses in the polycyclic disease cycle leading to an epidemic of downy mildew disease.
P. belbahrii is also a seed-borne pathogen. Detection of P. belbahrii in several commercially produced basil seed batches confirmed that the pathogen is seed-borne [3, 28, 44]. It is considered that infected seed act as primary inoculum source in basil production, and is so far considered to be the most important way of this pathogen spreading as it can explain the rapid global spread of P. belbahrii. Great example for the spreading of P. belbahrii with seed transport and seed-marketing to long distances is that the biotype that was detected for the first time in US in 2007 was genetically identical to the one reported in Switzerland in 2001 [27]. Also, the disease occurrence in US Sonoma County in 2008 was connected with the origin of the used seed that was introduced from Italy. Investigation conducted by Farahani-Kofoet and Römer detected P. belbahrii on 80–90% of randomly selected commercial seed stocks [45] and assumed that P. belbahrii can be spread by transport and marketing of seed stocks.
On contaminated seeds, P. belbahrii has been found in form of conidia and oospore [38, 45]. Until now, P. belbahrii was not reported inside the basil seed or embryo. Based on their observations, Farahani-Kofoet and Römer concluded that P. belbahrii is able to survive for several years on seeds [45]. Generally, oospores of Peronospora species can also be formed on seeds and infect the emerging seedling. Their oospores germinate in a way similar to that described for conidia and the infection process is similar. Investigation of P. belbahrii oospore infection of basil seeds was conducted, but plants developed from seeds planted in soil infested with oospores were symptomless and sporulation characteristic for P. belbahrii did not occur [30].
It has not yet been clarified whether the pathogen infects the seed deeply and systematically or is just a contaminant. In some European investigations, systemic infections in seeds and in different plant parts (leaves, stems) even in a symptomless plant have been detected [44, 45]. Novel investigation of seed transmission conducted in Israel showed that P. belbahrii is seed-borne but not seed-transmitted, as seeds produced by infected plants in the field can be externally contaminated with conidia that were embedded in the surface, but not entirely [46]. Further, plants grown in growth chambers until 5–6 leaf stage from contaminated seeds did not show any symptom of downy mildew and did not carry latent infection. Also, systemic infections were rarely seen in the field. They confirmed systemic spread of mycelium in the basil plants which corroborated with previous finding [45]. Systemically infected plants remained stunt and produced no seeds. Therefore, the Israeli investigators postulated that seed infections and seed transmission may occur in Europe, as it was reported [44, 45], and other locations with wetter summers, especially under prolonged wetness periods at the flowering and seed production.
Both investigations, European and Israeli, confirmed that contaminated seeds can be harvested from symptomless, latently infected plants and also, that contaminated seeds can give symptomless, latently infected plants [44, 45, 46].
Peronospora belbahrii can also be spread through vegetative materials like contaminated plant cuttings, transplants and fresh leaves. Novel Israeli investigation showed that P. belbahrii is spread systematically in basil plants [46]. Mycelium has been found to grow acropetally to the stem apex and basipetally to the cotyledons and hypocotyl and laterally to the axillar buds but, mycelium has never reached the roots. Especially in young basil plants, this pathogen systemically runs through tissue and causes plant stunt and fail to produce seeds.
The control methods of the downy mildew pathogen today involve fungicides, seed treatment and breeding for resistance. In the greenhouses, they can be augmented with physical measures: nocturnal illumination, ventilation and daytime solar heating. The last one is also suitable for net-houses [47].
Current control measures rely mainly on fungicide application. In conventionally produced basil, it can be controlled in a preventive program with conventional foliar fungicides. The efficient once are based on mefenoxam, azoxystrobin, cyazofamid, mandipropamid, fluopicolide and fenamidone [11, 12, 26, 34, 38]. There are also phosphorous acid fungicides which are in most cases labelled and allowed in greenhouses. The best control of 98% was achieved with preventive fungicide application, before symptoms occurred, on a weekly schedule [38].
The P. belbahrii developed mefenoxam-resistance within 1 year of use in Israel and was reported in 2013 [34]. It was also detected in Italy were mefenoxam (metalaxyl-M) plus copper has been the most widely used and effective product against P. belbahrii, since its registration on basil in Italy in 2004 [48]. As the systemic fungicides are prone to the resistance development, ingredients with different modes of action are needed [32]. The novel fungicides with extremely high efficacy against oomycete including P. belbahrii are oxathiapiprolin [30] and valifenalate [49]. Oxathiapiprolin acts at multiple stages of the pathogen’s asexual life cycle at extremely low concentrations and due to translaminar and acropetally systemic movement, it protects treated leaves and new leaves as they emerge and grow. In P. belbahrii, it inhibits sporangia germination and curatively, it stops mycelial growth within the host plant before visible lesions occur and inhibits further lesion expansion, offering protection at 1 and 2 days post-infection [50]. It was found to be effective against mefenoxam-resistant biotypes as well [30]. But, as it is a single-site inhibitor and its target is the oxysterol binding protein, the resistance to oxathiapiprolin assume to be medium to high and resistance management is required [51]. The soil application of mixture of oxathiapiprolin and benthiavalicarb or their single application against P. belbahrii was tested. Application to the root of 1 mg active ingredient per plant in the field experiment provided durable protection of up to 4 weeks against P. belbahrii [52]. The mixture performed better than single applications of those two compounds suggesting a synergistic interaction between them. The valifenalate is also a single-site inhibitor and acts as the inhibitor of cellulose synthesis in the Oomycete plant pathogens [49]. The resistance to valifenalate is assumed to be low to medium risk [51].
In organic farming, conventional fungicides are not allowed, so neem oil, potassium bicarbonate and hydrogen dioxide can be used for protection only, but they do not give satisfied protection [38]. Organic fungicides are contacts and do not go into plant tissue where is the pathogen and they are not able to translocate to abaxial side of leaves where sporulation occur. Therefore, their performance is not commercially acceptable and as they provide limited to no control, including when applied twice weekly on a preventive schedule to a moderately resistant variety [12, 38, 39]. As alternative, there are some bio-products based on Bacillus amyloliquefaciens, Streptomyces lydicus and the extract of Reynoutria sachalinensis [38]. Organic production should be in protected conditions and better transplanting then seeding as pathogen-free seed is not available. In greenhouse, it is important to prevent favourable conditions for disease development.
Certain cultural practices which create less optimal conditions for the pathogen can be helpful in reducing the amount of infection. Such practices include providing good soil drainage and good air circulation among plants. Increasing plant spacing in the field or greenhouse prevents the creation of high-humidity conditions on plant surfaces and can inhibit infection as P. belbahrii requires humidity for sporulation as well as free leaf moisture for infection. The humidity should be keeping below 85% and this is crucial. In the greenhouse, the use of plastic mulch and drip irrigation is recommended instead of bare ground and overhead irrigation. Effective measure for reducing ambient relative humidity and avoids vapour deposition of leaves surface is ventilation [47]. In some experiments, combining daytime solar heating with nocturnal illumination without fungicide applications showed to be an effective control in organic farming [30, 47]. High temperature is detrimental to the P. belbahrii and exposure of infected plant of 35–45°C for 6–9 h suppressed survival of conidia and mycelia [47]. Subsequently, solar heating has been used to cure plants. In Israel, solar energy was captured by closing greenhouse windows or covering the house with a transparent IR polyethylene sheet during sunny hours of the days: best is to use three consecutive daily exposures of 3–4 h starting at 8 am [47]. Solar heating should be conducted cautiously to avoid plant heat damage [47]. Ensuring light during the night, especially red light should prevent sporulation. The protective effect of nocturnal illumination was determined in laboratory and greenhouse trials; but in Israel, field trials (net-houses) also demonstrated that light can be successfully used to supress downy mildew in field-grown basil [41]. The inhibitory effect of incandescent or CW fluorescent light of 3.5 or 6 μmoles.m2.s−1 on sporulation was 100% on lower leaf surface even when only the upper leaf surface was exposed to light [41].
The rapid global spread of the downy mildew may be related to transmission of P. belbahrii by infected seeds and/or trade of basil cuttings and plants with latent infection [3, 38, 45, 46]. Infested seeds are a great risk for spreading the pathogen by transport and seed-marketing to long distances. Implementation of seed-certification schemes to exclude seed batches infested with P. belbahrii from marketing would be of great value for both seed-producing companies and growers [45]. Therefore, improving seed production; developing and implementing seed testing, certification protocols, and standards for the basil seed industry and strict following of import restriction may have halted P. belbahrii [38, 45]. To limit the spread of the pathogen by seed shipments, it is crucial for breeders and growers to draw on an early, fast and specific detecting test [45].
Seed should be tested on the presence of P. belbahrii and for that purpose real-time PCR have been designed [3]. Belbahri et al. have designed a specific primer pair (Bas-F/Bas-R) based on sequences within the unique genomic ribosomal DNA (ITS1) and the primer pair generates a single fragment of approximately 134 base pairs [3]. The PCR method proved to be very sensitive for direct detection of P. belbahrii on seeds and plant samples [45]. The PCR detection limit of P. belbahrii in artificially infested seeds corresponded to the DNA amount of a single spore per seed (3.4 pg of P. belbahrii genomic DNA extracted from a pure spore suspension at a density of 103 spores ml−1 using 1 μl as a template) [45]. Further, with this PCR protocol, P. belbahrii can be detected with high sensitivity in leaves and stems as well and not only at seeds, even if symptoms are not evident. Finding that latent systemic infection can result in the contamination of basil seed and vice versa supported the necessity to implement PCR-based detection in a seed-certification scheme [45]. Pathogen-free seed is most important for greenhouse crops plantings not expected to be exposed to wind dispersed spores [53]. It should be emphasised that the presence of pathogen DNA in seeds does not implicate spontaneous disease outbreaks because the PCR test cannot assess the viability of spores as specific fragments can also be generated from DNA material of dead spores. Moreover, the disease inception and development depends on host-pathogen interaction and existing environmental conditions. Yet, PCR test allows the testing of high numbers of samples within a short time and rapidly gives accurate information on P. belbahrii presence. Considering all, it is recommendable to be admitted in seed-certification schemes for routine testing of seed materials in order to inhibit marketing of infested seeds. As the PCR test can be used for detection in different plant parts, it can also be used for evaluation of procedures to control the downy mildew pathogen.
Seed treatments and at-seedling fungicides may have the potential for the good start of basil production [38]. There are no fungicides labelled for use on seed, but the at-seedling fungicides are available although not labelled for use on basil seed. Mefenoxam can be applied at seedling into the soil in field growing basil [38]. In novel trails, the root treatment of mixture of oxathiapiprolin and benthiavalicarb given to the young seedlings, growing in the multi-cell trays in the nursery, may be effective basil downy mildew measure [52]. The only organic fungicide labelled for ground application is based on the extract of Reynoutria sachalinensis [38].
Novel, non-chemical basil seed treatment is steam-air treatment and USA seed companies start to implement it [53]. Steam-air treatment of basil seeds against seed-borne fungi was tested in 1997 in Australia [54]. Steam-air treatment at 54–58°C for 30 min was successful in two-cylinder configuration in the steam-air machine. They noticed that this configuration against sixth-cylinders configuration provides extra steam velocity that prevents basil seed clumping which happened because when wet basil seed easily stick together as they have very thick gelatinous coat. Therefore, basil seeds are not amenable to hot-water treatment as the seed clumping makes the seed challenging to handle [53, 54].
The cultivation of resistant sweet basil cultivars also can be efficient control strategy. Highly resistant cultivars will be especially welcome in organic farming. Earlier, some cultivars of red types, lemon and lime basil have been found less susceptible [9, 30, 31, 33, 39]. New resistant basil varieties started to be marketed in USA in 2018 [53]. The first commercially available resistant variety is Eleonora. The Rutgers University basil breeding program released Devotion, Obsession, Passion, and Thunderstruck. They are marketed by VDF Specialty Seeds. Organically produced seed is available and marketed like Prosperais (Johnny’s Selected Seeds), Emma and Everleaf (aka Basil Pesto Party and M4828Z) [53].
That accurate monitoring can be of great importance in field growing as well as in protected conditions as instrumentation for optimization of plant protection measures was shown by USA monitoring programme. It started in 2009 by McGrath and augmented knowledge of basil downy mildew [38]. It is an online spreadsheet program set-up in Google Docs accessible by anyone. Until 2019, each year a spreadsheet page was set up for anyone to log and view occurrence reports [53]. In 2019, a new website was launched with a mapping program that mapped reports by county plus information about basil downy mildew. The growers need to be educated to accurately based on first symptoms recognise the diseases on time. In greenhouses, monitoring should be on daily basis as downy mildew can develop very quickly [38, 41].
‘One touch of nature makes the whole world kin’ Shakespeare wrote and this is so valid for the pandemic downy mildew agent like P. belbahrii from sweet basil. The only way to deal with this pathogen is knowledge. To fill the existing knowledge gaps research into various aspects of the pathogen will be needed. The dual identification according to the morphology and ITS sequence analysis is recognised and implemented. It would be of the most value to investigate P. belbahrii sexual reproduction and to identify mating types and mechanisms of their compatibility if it is heterothallic. Further, valuable will be to obtain knowledge of the P. belbahrii natural distribution range because its present distribution is due to human activity and trades. More research into aspects of P. belbahrii physiology, asymptomatic infections and oospore role in epidemiology. The seed transmission still needs to be elucidated and the question of whether the pathogen penetrates into the seed should be answered. Because it has been already spread worldwide, the P. belbahrii is not on the quarantine lists; although, it will be beneficial to follow the quarantine guideline, in the context of global trade with seeds.
Cardiovascular disease (CVD) remains the leading cause of death, premature mortality, and disability worldwide. The mortality rate from CVD has been declining since the early 1990s as a result of significant changes in lifestyle and improved health care. This growing prevalence is due to improved survival of people with myocardial infarction and patients with heart failure and a high burden of heart risk factors for people such as hypertension, obesity, diabetes, and smoking. While physical activity and regular exercise are emphasized for the development of general cardiovascular health, modern guidelines for heart failure inadequately emphasized the importance and recommendations for physical activity as a means of preventing a condition [1, 2, 3].
\nNevertheless, there are certain regions with significantly higher total and mortality from cardiovascular diseases, despite relatively good access to medical care and invasive cardiology procedures. Previous reports conducted among residents of these regions showed adverse lifestyles with a very low prevalence of people who follow current recommendations for the prevention of cardiovascular diseases. This poor adherence to recommended recommendations may be a function of a lack of awareness of the methods of preventing CVD. Several studies have indicated that improving awareness of the risk factors for cardiovascular disease and prevention can be a prerequisite for adopting of a healthy lifestyle [2, 3, 4, 5].
\nTo determine the most effective ways to solve the problem of heart failure in different parts of the world, an international approach is needed, as well as the inclusion of necessary measures in everyday practice. Political initiatives at the local, national, and international levels can reduce mortality due to heart failure and improve the quality of life of patients.
\nIn recent years, the survival rates of patients with heart failure have improved in many parts of the world, in parallel with the introduction of modern evidence-based methods and patient management systems. Nevertheless, about 2–17% of those admitted to the hospital with heart failure die in the hospital. Survival rates are better for those who are treated in outpatient clinics, which usually have less pronounced symptoms than those who are treated in the hospital. However, even the newest therapies can only alleviate the symptoms in many patients without slowing the progression of their disease or prolonging life. This is due to the fact that heart failure can arise due to a number of different underlying problems with the structure or function of the heart, some of which are more difficult to treat than others [3, 4].
\nHF may seriously damage developing countries by creating loss of productivity of cardiac patients. It often severely limits a person’s ability to work. Loss of productivity hurts not only the individual but affects the family’s income and the country itself by extension. Also, the weakened cardiac patients often need caregivers; consequently, a caregiver often is a family member, and he or she has to stop working in order to nurse a cardiac patient at home. To treat HF and maintain good health in cardiac patients, it is necessary to prescribe several medicines that can be difficult to afford for some people [5, 6, 7].
\nUnfortunately, globalization creates unforeseen problems for most low- and middle-income countries. Adaptation of the western way of life and malnutrition of developed countries are spreading around the world. Limited financial resources and the weak structure of health systems in developing countries pose a barrier to managing the impending global epidemic of chronic diseases. The need to adapt evidence-based treatment plans and model approaches to public health from successful experiences of other countries should become urgent priorities for low- and middle-income countries [8].
\nInfections remain a common cause of heart failure in many parts of the world and can affect any age. Heart failure is not a disease of the elderly in sub-Saharan Africa, where half of the patients hospitalized with this disease are 55 years or younger. Patients in the Asia-Pacific region are also usually younger than in the western regions. Rheumatic fever due to preventable bacterial infections is an important cause of heart failure in Africa, Asia, Australia, and Latin America. HIV infection is also a major source of cardiovascular disease worldwide. In areas of Latin America where Chagas disease is prevalent, almost half of all cases of heart failure are the direct result of this preventable parasitic infection [9, 10, 11].
\nHeart failure is a widely researched disease because of its burden. There are many studies in which the incidence of heart failure is positively associated with several risk factors. The very first study that addressed the etiology of this disease was a cohort study that followed people for 20 years, a study of the heart of Framingham in the 1970s. According to the Framingham Heart Study, heart failure had several major risk factors. It was found that the highest risk factor for heart failure among the population is hypertension, which accounts for 39% of heart failure in men and 59% in women. The second most significant risk factor was myocardial infarction, which accounts for 34% of heart failure in men and 13% in women. Other important risk factors were diabetes mellitus, left ventricular hypertrophy, and heart valve disease. This was the first scientific evidence of heart failure associated with behavioral factors [12, 13, 14].
\nIt has been proven that reducing risk factors will eventually reduce the likelihood of developing heart failure. Most cases of heart failure (90%) are explained by risk factors, such as diabetes, obesity, smoking, blood pressure, and high cholesterol. By reducing BMI, stopping smoking, keeping low cholesterol and blood pressure, and avoiding the other mentioned risk factors, people can potentially be protected from heart failure, cardiovascular diseases, and other chronic diseases. Knowledge of risk factors is very important for the prevention of HF, but they can also be used to combat heart failure and cardiovascular diseases [11, 13, 14, 15].
\nHeart failure significantly affects the quality of life of patients. Fear, anxiety, and depression are common, and work, travel, and everyday social and leisure activities are difficult for people with shortness of breath and extreme fatigue. Emotional, physical, and financial costs are also high for those who care for family members with heart failure. Heart failure leads to a large number of deaths and a widespread disease and requires huge economic and social costs, and the problem worsens. It is time for coordinated awareness programs about heart failure and strategic and policy initiatives to improve patient care.
\nPrevention of heart failure is of paramount importance. After an establishment the deterioration of a status of the heart can be often treated, but as a rule, it is impossible to cancel. Policymakers should emphasize the need for health professionals in all clinical disciplines to identify patients with diseases that increase the risk of heart failure and prescribe preventive drugs. Ensuring access to preventive drugs should be provided to those who are at greatest risk for developing heart failure, regardless of age, sex, or income. Policymakers should also give priority to the elimination of certain infectious diseases in some parts of the world where they continue to cause heart failure [4, 8, 10].
\nRisk factors for heart failure vary from lifestyle factors to concomitant diseases, medications, laboratory, and visual characteristics for new biomarkers and genomic markers. The risk of heart failure increases with age, and the male sex is associated with a higher risk. Higher physical activity, increased salt intake, and lower socioeconomic status were associated with increased risk. Hypertension, diabetes, obesity, and coronary disease all increase the risk. More than half of patients hospitalized with heart failure, regardless of the ejection fraction, have coronary artery disease. Hypertension and coronary artery disease are the most common and most powerful risk factors, which bring an increased risk of two to three times. Valvular heart disease increases the risk due to hemodynamic changes.
\nObesity, due to a variety of mechanisms, predisposes to heart failure. The excessive use of alcohol increases blood pressure and is a direct myocardial toxin; however, light consumption is moderately associated with risk, especially in men. Smoking contributes to several cardiovascular risk factors associated with heart failure. Dyslipidemia and renal dysfunction predispose to heart failure. Other comorbidities that increase the risk include anemia, sleep breathing disorder, increased heart rate, lung dysfunction, and microalbuminuria. The levels of homocysteine and natriuretic peptide are associated with an increased risk. Serum resistance, lipoproteins associated with phospholipase A2, and myeloperoxidase are also associated with an increased risk [9, 10, 11, 12].
\nMost patients are fragile and elderly with concomitant diseases (e.g., concomitant respiratory diseases and renal dysfunction) that can limit and/or complicate treatment. Although formal classification systems have been developed, the most practical indicator of an increased risk of premature morbidity and mortality or reentering the hospital is the presence of two or more of the following:
Age ≥ 65 years
NYHA class III or class IV symptoms
Charlson Index of Comorbidity Score of 2 or more
Left ventricular ejection fraction (LVEF) ≤ 30%
Living alone or remote from specialist cardiac services
Depression
Language barrier (e.g., non-English speaking)
Lower socioeconomic status (due to poorer compliance, reduced understanding of reasons for medicines, fewer visits to medical practitioners, high-salt diet in “take-away foods,” reduced ability to afford medicines, higher rates of cigarette smoking, etc.)
Significant renal dysfunction (glomerular filtration rate < 60 mL/min/1.73 m)
Several chemotherapeutic agents, for example, doxorubicin, cyclophosphamide, trastuzumab, and 5-fluorouracil, are associated with heart failure. Inhibitors of cyclooxygenase-2 may increase the risk of myocardial infarction. Thiazolidinediones were associated with edema and heart failure. Several cardiac anatomical and physiological measures are associated with a higher risk, including enlargement of the chamber with an increase in terminal diastolic or terminal systolic dimensions, an increase in left ventricular mass, worsening diastolic filling of the left ventricle, an increase in the left atrium, and asymptomatic systolic dysfunction. There is growing interest in genomic predictors of heart failure.
\nWhile patients at high risk benefit greatly from proper and consistent treatment, unfortunately, they often undergo suboptimal management. Their inability to tolerate even minor fluctuations in cardiac and renal function makes them vulnerable to frequent and recurring episodes of acute heart failure.
\nIt is now recognized that up to two-thirds of hospitalizations associated with CHF can be prevented. The following variables are most often associated with poor health outcomes, especially in high-risk patients:
Inadequate/inappropriate medical or surgical treatment
Adverse effects of prescribed therapy
Inadequate knowledge of the underlying illness and prescribed therapy
Inadequate response to, or recognition of, acute episodes of clinical deterioration
Nonadherence to prescribed pharmacological treatment
Lack of motivation/inability to adhere to a non-pharmacological therapy
Problems with caregivers or extended care facilities
Inadequate social support
This is especially important for groups at high risk of developing this condition. Many people have diseases that put them at risk of heart failure. Health-care professionals who treat such patients should adopt a broad approach that includes encouraging positive lifestyle changes that reduce the risk of heart failure and prescribe preventive therapy as needed. Medications that control blood pressure, heart rate, and cholesterol levels are effective in preventing heart failure in a large number of people who have conditions such as high blood pressure, coronary heart disease, kidney disease, and diabetes. Pacemakers and the replacement of heart valves can also prevent heart failure in a small number of people who have a particular heart rate or valve disorders. The range of diseases that predispose patients to heart failure is extremely wide. Health-care professionals in all clinical disciplines should receive education to identify patients with diseases that increase the risk of heart failure and prescribe preventive medications. This ensures that as many people as possible get access to therapy [5, 7, 8].
\nPatients receiving long-term preventive therapy should be evaluated regularly at the expense of health-care providers. In addition, patients with chronic diseases, such as coronary artery disease or Chagas disease, should periodically evaluate and monitor heart changes. Patients with breast cancer are another group that will benefit from such monitoring. Several existing and new methods of treating cancer are toxic to the heart, and it is important for health professionals to be aware of the need to evaluate and manage the risks involved.
\nBacterial infections that cause heart disease are largely eliminated in economically developed countries due to the use of antibiotics. In other regions, bacteria and tropical parasites cause a significant proportion of heart failure, many of which can be prevented by appropriate treatment methods. Therefore, the potential benefits of policy initiatives aimed at eliminating infectious diseases extend to preventing heart failure in many parts of the world. In particular, to continue global efforts, it is necessary to eradicate Chagas disease, based on the progress made in Latin America over the past two decades [1, 2].
\nPreventive treatment could be started earlier, identifying people with early signs of abnormal cardiac muscle remodeling. Unfortunately, large-scale screening programs, such as those that allowed earlier treatment of bowel cancer, cervical cancer, and breast cancer, are unfortunately not possible, because there is no simple diagnostic test for heart failure. Early changes in the structure or function of the heart can be detected using medical imaging technology; however, it is inadvisable to perform these complex procedures in a large number of people with diseases that lead to heart failure and, of course, not for the general population. In the future, extended genetic tests and statistical modeling of risk groups that take into account the myriad potential causes of heart failure may be available, and this can allow individuals to be identified for in-depth screening.
\nTargeting preventive drugs to people with the highest risk of heart failure can increase profitability, allowing more people to take advantage. Further research in these areas continues and should continue to be supported by public and private funds. In addition, information programs should be directed at everyone who has medical conditions that predispose to heart failure. They should include education about the symptoms of heart failure and the benefits of positive lifestyle changes. The same messages are important for public information programs [3, 4, 5, 6].
\nPreventing heart failure in the elderly is becoming a more urgent health priority, as the age of the population. Heart failure is the most common cause of hospitalization in people older than 65 years in economically developed regions. Elderly patients hospitalized with heart failure mostly are women. Although a number of studies of patients with heart failure have shown that survival rates are better in women than in men, recent studies have shown that long-term prospects for women are not as good as previously thought. Therefore, initiatives aimed at improving the prevention of heart failure should include strategies to reach older people, especially older women [14, 15, 16].
\nIn economically developed countries, heart failure is more common and most likely the cause of death in people with low socioeconomic status than the rest of the population. This is still the case after adjusting for age differences, the use of drugs, and the proportion of people with other cardiac diseases. The view was expressed that the role of housing can be played by housing stability, social support, substance abuse, language skills, and distance to the hospital.
\nSeveral studies have reported a reduction in the risk of heart failure with a healthy lifestyle. It has been shown that healthy weight, avoidance of smoking, exercise, and healthy eating reduce the risk factors for heart failure, including ischemic disease, diabetes, and hypertension. Recently, researchers in the health research of doctors reported that habits of a healthy lifestyle, that is, normal body weight, rather than smoking, regular exercise, moderate alcohol consumption, consumption of breakfast cereals, and consumption of fruits and vegetables, were associated with a lower risk of heart disease with the most high risk of 21.3% in men who do not observe any of these habits and the lowest risk of 10.1% in men who adhere to 4 or more of them.
\nAlthough many heart failure risk factors have been described, determining their role in predicting a future event is still difficult. Despite a strong etiological relationship to the disease, the risk factor may be limited in its prognostic role. Although individual risk factors for heart failure, such as hypertension, are well described, how do we clearly identify individual risk in patients with different combinations of risk factors? For coronary events, schemes for predicting multiple risks have been developed, for example, the Framingham risk score. However, heart failure syndrome is a spectrum from ischemic to nonischemic etiology and from normal to depressed ejection fraction. Older patients may develop heart failure due to age-related cardiovascular changes in the absence of traditional risk factors. Thus, high-risk subjects cannot be detected using coronary risk regimes [15].
\nSeveral unique problems make the assessment of the risk of heart failure difficult. First, heart failure is a clinical diagnosis, and this leads to a variety of opinions and diagnostic uncertainties in a number of cases. The most common clinical criteria used to diagnose heart failure are the Framingham criteria, which require at least two basic or one basic and two lower criteria. The main criteria include paroxysmal nocturnal dyspnea, a dilated vein in the throat, rales, radiographic cardiomegaly, acute pulmonary edema, gallop S3, increased venous pressure > 16 cm H2O, circulation time ≥ 25 seconds, hepatojugular reflux or pulmonary edema, or visceral cluster or cardiomegaly at the autopsy. Minor criteria included bilateral ankle edema, night cough, shortness of breath with normal tension, hepatomegaly, pleural effusion, a decrease in vital capacity by one-third of the maximum, and heart rate ≥ 120 beats per minute. Researchers from the cardiovascular study have developed alternative criteria that included the use of drugs and imaging techniques. When both sets of criteria were compared, only half of the patients were considered to have heart failure by both criteria, while the other half were labeled either one or the other, but not both. A similar discrepancy was shown between diagnoses of administrative categories compared to a detailed overview of the diagram [2, 13, 14, 15, 16].
\nSocial changes can affect the CVD epidemic in different ways. It may be influenced by globalization, migration, socioeconomic changes, and unemployment. Over the years, differences in the incidence of CVD among countries, regions, and areas have increased; these inequalities can be explained by the components of human behavior, such as diet, exercise, smoking, and work-related functions, as well as overcrowding, unemployment, and other deprivation indicators. The expected life expectancy is constantly increasing with income.
\nSmoking is a strong predictor of heart failure in men and women; 45% and 88% have an increased risk. The harmful effect of tobacco, apparently, does not depend on the form of use. An increased risk of cardiovascular disease is reported when tobacco is used by non-smokers. There is no “safe” level of smoking; a single cigarette can strengthen the left ventricle, and only one to four cigarettes a day double the risk of myocardial infarction. Mechanisms leading to heart failure in smokers include (i) indirect effects, that is, causing or exacerbating associated diseases associated with heart failure, and (ii) direct exposure to the myocardium.
\nTobacco smoking remains one of the most important preventable causes of premature mortality, and quitting is the most cost-effective strategy for the prevention of cardiovascular disease. Improvements have been made with regard to tobacco smoking, in some countries more than in others, with large differences in accordance with the socioeconomic class. Governmental constraints and rules were successful; high taxes on tobacco products are the most effective policy measure to reduce smoking among young people. However, this needs to be complemented by continuing campaigns in the field of health education, especially those targeting young people and other subgroups of society. There must be restrictions on advertising, promotion, and sponsorship by the industry [12, 16].
\nAll smokers should be advised to quit. Patients should be referred to formal programs to discontinue therapy, and pharmacological therapy should be offered to increase success. Current recommended strategies include the following: (a) Medicines. Several drugs are available for tobacco dependence. Seven first-line drugs significantly increase long-term rates of abstinence from smoking, including bupropion SR, nicotinic gum or inhaler or cake or nasal spray, or patch and varenicline. (b) Counseling and psychosocial support. Individual, group, and telephone practical consultations and social support are effective, and their effectiveness increases with the intensity of treatment. (c) Combination. However, the combination of counseling and medication is more effective than one, so clinicians should encourage all people who attempt to stop using both counseling and medication.
\nSmokers who want to quit smoking should get professional help if needed. Short interventions with recommendations for cessation of smoking, together with pharmacological support and follow-up visits, are effective and safe, but not enough, even for smokers with established ischemic heart disease. If the smoker is ready to stop, a termination plan should be prepared, including the release date, information for friends and families asking for support, and removing all tobacco and smoking-related items from the immediate environment and, finally, ideally within a month and every month after that for 4 months. On a subsequent visit, a person should be congratulated if he/she has stopped smoking. In case of relapse, a more intensive approach should be considered, for example, referral of a specialist or center for cessation of smoking. Avoidance of secondhand smoke is another important recommendation for CVD prevention.
\nIf the recommendations, stimulation, and motivation are likely to be insufficient, drug therapy should be considered at an early stage, including nicotine replacement therapy (NRT), bupropion, or varenicline. Pharmacotherapy for smoking cessation can double or triple throw rates, and a combination of pharmacotherapy and counseling improves throw rates.
\nThe success of cessation of smoking with varenicline is higher than with bupropion; varenicline doubles the chances of stopping smoking compared to placebo. Varenicline reduces cravings for cigarettes and withdrawal symptoms; it should be run 1 to 2 weeks before the release date. Hypersensitivity is the only contraindication. Nausea is the most common side effect, especially at the beginning of therapy and if taken with food. In some cases, a dose titration may be required.
\nElectronic cigarettes, or e-cigarettes, can deliver high concentrations of nicotine as a vapor and have been recommended as a measure to help stop smoking conventional cigarettes. The results of studies of the cardiovascular effect of electronic cigarettes are inconsistent, but in some cases, an increased risk is documented.
\nAs for the dietary habits of the population, the changes occurred in different areas. For example, consumption of salt and saturated fats has been reduced in most societies. The food industry has reduced the presence of trans-fatty acids in different foods. This was promoted by regulatory initiatives in some communities. Nevertheless, the potential for preventing cardiovascular disease through dietary adaptations is still poorly implemented. Compliance with a balanced diet is usually limited. Control of high blood pressure, dyslipidemia, and dysglycemia can be significantly improved due to lifestyle changes. Achieving better adherence to dietary recommendations requires an understanding of the determinants of poor compliance. At the population level, structural measures, such as product information and user-friendly food labeling, can improve health-friendly options. Energy-intensive products with nutrient deficiencies are usually highly available and inexpensive; marketing of such products may be limited and taxed.
\nIn the diet “Dietary Approaches to Stopping Hypertension” (DASH), people are encouraged to consume more (i) fruits and vegetables; (ii) grains and cereals; (iii) lean meat, fish, and poultry; (iv) low-fat or low-fat dairy products; and (v) nuts, seeds, and pulses and reduce consumption of red meat, fat, and sugar while maintaining low-sodium intake. Initially it was elevated for hypertension; however, recent data confirm a reduction in the risk of heart failure with an observed decrease of 37% in women who adhere to the DASH diet. The DASH diet can help prevent heart failure by lowering blood pressure and coronary heart disease. Daily consumption of whole grain breakfast cereals was associated with a 30% reduction in heart failure, egg consumption more than twice a day was associated with an increase of 64%, fish consumption was associated with a 20–31% lower heart failure rate depending on consumption, and consumption of 100 mmol or more of sodium was associated with a 26% rate; only the consumption of nuts was not associated with heart failure. Whole grains can protect against the risk of heart failure as a result of exposure to weight, hypertension, myocardial infarction, and diabetes mellitus.
\nFish consumption has a beneficial effect on the risk of heart failure with about 20% less risk associated with consumption one to two times a week and about 30% less risk when consumed ≥3 times a week, compared with consumption less than one time per week/month. The estimated consumption of marine n-3 fatty acids was associated with a 37% reduction in the risk of heart failure in the highest quintile of consumption compared to the lowest. Short-term tests of fish oil supplementation of 3–5 g per day can reduce the risk, while dietary doses of about 0.5 g per day can lead to more modest effects, which over time can reduce the risk of heart failure. It has been reported that the consumption of fried fish or baked fish is inversely related to systolic blood pressure, C-reactive protein level, and carotid intimal medial thickness, while consumption of fried fish is positively associated with them, indicating that the type of preparation can influence the effects.
\nAt the clinical level, general practitioners have the opportunity to provide advice on a diet for treating risk factors for coronary diseases. However, obstacles related to time constraints, knowledge, and perceived effectiveness were reported. The degree to which doctors are familiar with a healthy dietary pattern (i.e., DASH, the Mediterranean diet) and with the translation of this information into practical recommendations may be limited. A multidisciplinary approach, including dieticians and nutritionists, can help but needs to improve coverage of reimbursement.
\nAt the individual level, new strategies can help improve patient self-control and lead to a sustained behavior change. Many applications and devices are available that provide data that can be useful for lifestyle changes and patient self-care.
\nPhysical inactivity is an important risk factor for cardiovascular disease, including heart failure. Regular physical activity has important and broad benefits, such as reducing the risk of cardiovascular disease, hypertension, and diabetes. Physical activity is a key to good health and an important component of weight loss and weight maintenance, improving the profile of lipoproteins and reducing the risk of hypertension, diabetes, and coronary artery disease. These favorable effects on the profile of cardiovascular risks, in turn, reduce the likelihood of heart failure [14, 15, 16].
\nPromotion of physical exercises is a crucial and central issue in all strategies for the prevention of cardiovascular diseases. At the individual level, physical activity should be recommended at different times; he must become part of ordinary life from childhood. Children and adolescents should be encouraged to spend from 30 to 45 minutes of exercise at school or in their free time every day. This should be maintained as long as possible, through adolescence to adulthood.
\nPhysical activity can also reduce left ventricular hypertrophy and improve endothelial function. Chronic physical activity reduces the production of cytokines by fat tissue, skeletal muscles, and endothelial and blood mononuclear cells and regulates antioxidant enzymes. These modifying effects on risk factors for heart failure or the intermediate pathways leading to heart failure can reduce heart failure. Integration of physical activity into everyday life of the population proved to be a difficult task.
\nHealthy adults in all age groups are encouraged to choose pleasant physical exercises that fit into everyday life on most days of the week. It is recommended to perform at least 150 minutes per week of moderate aerobic physical activity (30 minutes for 5 days a week) or 75 minutes per week of intense aerobic physical activity (15 minutes for 5 days a week) or a combination thereof. At the individual level, the purpose of the exercise should be more personalized. Therefore, a brief history of the individual’s physical level is needed (how many minutes per day is spent on average with activity at moderate or strong intensity).
\nCurrently, the recommendations of the American College of Sports Medicine and the American Heart Association for regular physical activity in healthy adults 18–65 years include the following: (a) Aerobic activity. Aerobic physical activity with moderate intensity for at least 30 minutes for 5 days a week or intense aerobic activity for a minimum of 20 minutes for 3 days a week. (b) Strengthening of muscles. It is recommended that 8–10 exercises are performed for 2 or several days without Monday to a week using the main muscle groups. To maximize the development of strength, you should use resistance (weight), which allows you to perform 8–12 repetitions of each exercise, which leads to strong-willed fatigue. (c) Dose of activity. Activity of intensive intensity can have a greater benefit than physical activity of medium intensity.
\nWalks have been reported as useful for primary prevention; this should be done by individuals who do not adhere to current recommendations.
\nBased on this and taking into account the individual choice, it is possible to give advice on the most appropriate activities, on how to move forward, about what goals should be set to achieve and maintain health benefits from active lifestyles. It is necessary to identify barriers to achieving a more active lifestyle, perceived by the individual, and to explore ways of overcoming them. For people at work, it is recommended to recommend an active trip, as well as active breaks from long periods of sitting. In people who are not able to perform a minimum, or in inactive subjects who are just beginning to engage in any activity, even the lowest recommended level should be recommended. It should be emphasized that any increase in activity will be associated with a beneficial health impact, even before the learning effect becomes apparent, and that it is normal for gradual work for any given purpose.
\nThere are several plausible mechanisms for the association of obesity and an increased risk of heart failure. Indirect but well-known and documented mechanism is the effect of obesity in heart failure with the help of other risk factors. The increase in BMI is a risk factor for the development of hypertension, diabetes mellitus, and dyslipidemia, all of which increase the risk of myocardial infarction, which is an important precursor of heart failure. In addition, hypertension and diabetes mellitus independently increase the risk of HF occurrence. It has also been shown that increased BMI is associated with altered left ventricular remodeling, possibly due to increased hemodynamic loading, neurohormonal activation, and increased oxidative stress. Studies have shown that obesity can have a direct effect on the myocardium, demonstrating a loss of cardiac function through cardiac steatosis and lipoapoptosis.
\nThe body mass index is associated with heart failure in a positive and linear way in both sexes. Although the body mass index in the obesity area (≥30 kg/m2) is clearly associated with an increased risk of heart failure, there are disputes regarding the body mass index in the overweight range (25–29.9 kg/m2). However, recent data confirm that overweight is also associated with heart failure. Abdominal obesity may be a stronger predictor of heart failure than complete obesity, even in the absence of coronary heart disease. Several mechanisms have been proposed that increase the body mass index, the risk of heart failure, including (a) changes in the cardiac load, (b) changes in cardiac structure and function, (c) activation of neurohumoral and inflammatory pathways, (d) promotion of atherogenic conditions, (e) a predisposition to breathing with sleep disorders, and (f) a chronic kidney disease.
\nAlthough elevated BMI is well known as a risk factor for heart failure, this study showed that an elevated BMI is not a risk factor for increasing mortality but rather is associated with a trend toward improved survival. This counterintuitive epidemiological link between survival outcomes and traditional risk factors is called reverse epidemiology or “paradoxical obesity,” and it is now well documented in numerous studies and in the literature on heart failure.
\nThe exact mechanisms underlying the paradox of obesity have not been clearly defined. There are several theories. A common explanation for the increase in survival in obese patients with heart failure is that additional fatty tissue provides greater reserves against catabolic changes associated with the disease process that can lead to cardiac cachexia. Cardiac cachexia is a syndrome that includes progressive weight loss and changes in the body composition, which carries a destructive prognosis for heart failure, as well as in other painful conditions.
\nThe basic approach to risk reduction for obese patients should include weight control and physical activity, as well as control of related risk factors such as hypertension, diabetes, sleep disorders, and metabolic syndrome components. Changes in the myocardium with nonsurgical or surgical weight loss are possible, and a slight weight loss is effective; weight loss of 10% reduces systolic dysfunction, and a weight loss of 8–10 kg leads to a significant decrease in the size of the left ventricle and the mass index and improves diastolic function. Significant weight loss reduces the thickness and volume of the wall of the left ventricle, filling pressure, improves diastolic parameters, and improves systolic function of the left ventricle. The role of metabolic and neurohumoral modification may take precedence over hemodynamic effects, since left ventricular mass or functional improvement occurs independently of load changes.
\nAlthough epidemiological data constantly demonstrate the harmful effects on health associated with alcohol use, current literature cites some evidence of reducing the risk of heart failure with mild and moderate alcohol consumption. However, in order to fully understand the relationship between mild to moderate alcohol consumption and heart failure, several gaps need to be filled, especially the role of alcohol samples, beverage types, and genetic variations affecting alcohol metabolism and the effect of light on moderate drinking in predicting mortality and concomitant morbidity among people with heart failure. In the absence of large randomized studies of moderate alcohol consumption and heart failure, residual mixing or immeasurable confusion cannot be ruled out as possible explanations of the observed relationships. Thus, for patients who do not consume alcohol, it would be premature to recommend mild to moderate alcohol consumption as a means to reduce the risk of HF, given the possible risk of abuse and the resulting consequences.
\nExcessive consumption of alcohol is associated with alcoholic cardiomyopathy. Interestingly, other data are consistent with the possible benefits of moderate alcohol consumption for the risk of heart failure. In addition, it was reported that mild to moderate alcohol consumption is associated with a 40–50% lower risk of heart failure than with a previous myocardial infarction, whereas in the same study, the risk of heart failure without previous myocardial infarction among people who use heavy drinks was 1.7 times higher than that of abstained. Similar results were presented in the study of the health of doctors. The favorable effects of alcohol on the risk of developing hypertension, myocardial infarction, and diabetes mellitus have also been reported, while alcohol increases the level of high-density lipoprotein cholesterol, increases insulin sensitivity, reduces the level of inflammatory markers and clotting factors in plasma, and increases the level of adiponectin.
\nAll current guidelines on the prevention of CVD in clinical practice recommend the assessment of total CVD risk because atherosclerotic CVD is usually the product of a number of risk factors. Prevention of CVD in a given person should be adapted to his or her total CVD risk: the higher the risk, the more intensive the action should be. The stratification of the community into different levels of total CVD risk was given in recent guidelines.
\nThe treatment goals for LDL-C depend on the total CVD risk of the patient and of the baseline LDL-C level. In patients at very high CVD risk, an LDL-C goal of <1.8 mmol/L (70 mg/dL), or a reduction of at least 50% if the baseline LDL-C level is between 1.8 and 3.5 mmol/L (70 and 135 mg/dL), is recommended.
\nIn patients at high CVD risk, an LDL-C goal of <2.6 mmol/L (100 mg/dL), or a reduction of at least 50% if the baseline LDL-C level is between 2.6 and 5.2 mmol/L (100 and 200 mg/dL), is recommended. In subjects at moderate risk, an LDL-C goal of <3.0 mmol/L (115 mg/dL) should be considered.
\nStatins have proven effective in patients with coronary heart disease; however, their usefulness in staging left ventricular dysfunction remains under investigation. The role of statins in the prevention of heart failure is shown.
\nBased on the results of the IMPROVE-IT study, further reduction in LDL-C by the addition of ezetimibe should be considered in patients with cardiovascular diseases with LDL-C ≥ 70 mg/dl (≥1.8 mmol/L), despite the maximum allowable dose of statin. Now a new family of drugs that lower lipid levels is available. These inhibitors of subtilisin/kexin type 9 retardate convertase (PCSK9) further reduce LDL-C in addition to what can be achieved with statins. In a FOURIER study, inhibition of PCSK9 with evolocumab against statins lowered LDL-C to a median of 30 mg/dL (0.78 mmol/L) and reduced cardiovascular events. The use of this drug should be considered in patients with a very high risk of cardiovascular disease, in which LDL-C remains elevated, despite the fact that it is treated with a maximum dose of statins in combination with ezetimibe or in patients with statin intolerance.
\nElevated blood pressure (BP) is one of the most powerful modifiable risk factors for cardiovascular disease. The beneficial effects of lowering blood pressure on the reduction of stroke, myocardial infarction, heart failure, and death have been shown in numerous RCTs and in various meta-analyses. BP reduction can be achieved through lifestyle changes and drug therapy [17, 18, 19].
\nProgression progresses from hypertension to structural changes in the ventricles and systolic and diastolic ventricular dysfunction. The increase in chronic load, left ventricular mass, and stress, accompanied by a deterioration in the properties of diastolic filling, occurs in a chronic environment. Disproportionately increased left ventricular mass leads to inadequate microcirculation for perfusion of the hypertrophied myocardium, which leads to subendocardial hypoperfusion, ischemia. These changes increase the risk of developing coronary thrombosis and a heart attack characterized by loss of contractile function, neurohormonal activation, and ventricular remodeling, which leads to the development of systolic dysfunction. Anomalies in neurohormonal activation and the balance of water and electrolyte also play a role in the cascade, which leads to hypertension to heart failure [20, 21, 22].
\nIn people with impaired glucose tolerance, the development of type 2 diabetes mellitus (DM) can be delayed or prevented. In patients with type 2 diabetes, cardiovascular disease can be prevented by good control of risk factors for cardiovascular disease. Intensive management of hyperglycemia also reduces the risk of microvascular complications.
\nDiabetes mellitus is an independent risk factor for heart failure in all age groups. The relative risk of heart failure in patients with diabetes varies from 1.3 to 2.7, increasing to 4 in patients under the age of 65 and 11 in individuals younger than 45 years. Several mechanisms have been proposed to explain the increased risk. Combinations associated with heart failure, including obesity, hypertension, and coronary artery disease, are common among people with diabetes. Insulin resistance itself can cause disturbances in the cardiac structure and function [23, 24, 25].
\nUnfortunately, the prevalence of type 2 DM increases in most parts of the world, mainly because of unbalanced diets and lack of physical activity. The diagnosis of DM is also problematic in a large number of people and even in patients with established CVD. Screening should be considered by evaluating HbA1c or fasting blood glucose levels. When there is any doubt, you should offer a test for glucose tolerance orally.
\nFor most nonpregnant adults with type 1 or type 2 DM, it is recommended to reduce HbA1c < 7.0% (<53 mmol / mol) to reduce the risk of cardiovascular disease and the risk of microvascular complications. When diagnosed or at the beginning of a DM, the target HbA1c ≤ 6.5% (≤48 mmol/mol) should be considered in patients who are not brittle and do not have CVD.
\nMetformin is recommended as first-line therapy if it is tolerated and not contraindicated after assessing kidney function. In patients with diabetes and cardiovascular disease, the use of sodium glucose-based cotransporter-2 (SGCT2) inhibitors reduced cardiovascular and total mortality without significant adverse effects. These drugs should be considered at an early stage of treatment of DM in these patients. Optimal management of LDL-C and BP levels is of great importance for all patients with DM [3, 24, 25].
\nAppropriate care for heart failure and adequate provision of care and research require recognition of its clinical, social, and economic importance not only by health authorities and providers of health services but also by the general public. Without recognition of the symptoms and their severity, people with heart failure will not seek immediate treatment—patients often present with a long history of dyspnea. Awareness of the causes of HF can help to make appropriate lifestyle changes to reduce the risk. In addition, awareness of the benefits of treatment can help compliance and encourage patients to seek appropriate care. However, there is a lack of information about public awareness of HF. Studies have shown a relatively low understanding and treatment of heart failure by general practitioners. If doctors are not aware of the importance of HF, it is unlikely that the general public will have a good understanding [26, 27, 28].
\nA large number of premature deaths are due to ignorance of the causes and symptoms of heart failure. There is an urgent need for public information programs that determine heart failure in a simple and accessible language, explain how to recognize symptoms, and stress the need for emergency medical care. Other important messages are that most types of heart failure can be prevented and a healthy lifestyle can reduce the risk. Policymakers should support the development and implementation of public awareness programs targeted at these messages. The public understanding of the symptoms of heart failure is dangerously low.
\nCost-effective information, education, and support programs to reduce the risk of heart failure should be at the forefront of public health guidelines. Lifestyle events can have a significant impact on the health of the world, because obesity, diabetes, cigarette smoking, and high blood pressure significantly increase the likelihood of heart failure. Renewing commitment to public education, the importance of healthy nutrition and weight, regular exercise, and prevention of smoking should be a priority for policymakers [29, 30].
\nIn low- and middle-income countries, lifestyle-based measures to prevent heart failure were calculated as more cost-effective than pharmaceutical interventions. The acute need to take risks into life throughout the world is recognized by the United Nations, including in regions such as sub-Saharan Africa, where noncommunicable diseases associated with western lifestyles are not yet the leading causes of death or disease. Given the increasing number of patients with heart failure in economically developing regions, governments should be encouraged to combine lifestyle-based preventive measures with their programs to combat hunger and the epidemic. One could consider the issue of regulating aggressive marketing of high-calorie foods by large global corporate enterprises, especially schoolchildren and adolescents [31, 32, 33].
\nCompliance with the recommendations of clinical practice is often associated with improved outcomes for patients with heart failure. However, in many countries there are significant differences in how closely hospitals follow the recommendations of national recommendations for heart failure. In response, policymakers must protect the fairness of care for all patients. First, it is important to promote heart failure training programs that raise awareness of the guidelines among all relevant health professionals. Secondly, better care should be encouraged, using performance indicators and incentives appropriate to local conditions. Funding is needed to research evidence-based health-care performance indicators that reflect improvements in clinical outcomes for patients with heart failure. By improving health care, policymakers can provide a health system that provides timely access to the diagnosis and treatment of heart failure and then a consistent transition to long-term management.
\nDiagnosis of heart failure can be difficult, even for skilled professionals. Not all patients with heart failure have typical symptoms, and the same symptoms can be experienced by patients who do not have heart failure. For an accurate diagnosis, a number of diagnostic tools and information are required in combination with clinical judgment and expert knowledge.
\nMany patients initially do not see an expert in heart failure due to the fact that they are part of the health-care system. Those with severe symptoms, such as dyspnea at rest, are most often evaluated by paramedics or emergency doctors in the hospital, whereas those with less obvious life-threatening symptoms are more likely to go to their family doctor or outpatient clinic. Educational programs are needed to raise awareness about clinical practice recommendations among health professionals from a wide range of specialties that may be the first to encounter patients with undiagnosed heart failure.
\nRecommendations for the use of drugs for the treatment of heart failure are based on clinical trials conducted mainly in Europe and the United States. In other parts of the world, the underlying causes of heart failure are different, and it is not safe to assume that drugs will be equally effective in all patient groups. A further clinical study to investigate the efficacy of treating heart failure in different patient groups around the world should be maintained [32, 33, 34].
\nThe world survey showed the need to improve patients’ self-care. Most patients reported taking medication as prescribed, but few reported having control of their weight or regular training. Educational programs are a priority, but they need to be developed carefully, because it is reported that patients with a deeper knowledge of heart failure are more likely to delay treatment. This may reflect false optimism and a lack of understanding that controlling the symptoms of heart failure does not slow the progression of the disease. The learning environment should also be carefully considered. Short video clips, text messages, and social networks can be used to deliver simple but accurate messages. Currently, according to estimates, 6 billion people own a mobile phone; technology can be an important way to reach remote and socially economically disadvantaged [27, 28, 29, 30, 31].
\nTeaching people how to support a partner, family member, or friend with heart failure is also an important part of encouraging self-help. Patients are more likely to engage in useful self-help if they have someone who will help them than if they were socially isolated. This emphasizes the need to improve support for communities of socioeconomically disadvantaged patients and those who live alone. Policymakers should provide resources to educate and support people with heart failure and their caregivers, allowing them to actively engage in long-term care.
\nPrevention of disease and death due to heart failure should be a priority in the field of health. Despite the increasing number of people living and dying of heart failure, awareness of this disease is low among the public, politicians, and even some health professionals. Despite the lack of treatment for heart failure, many cases can be prevented, and most patients can effectively be treated to improve quality of life and survival. Policymakers are responsible for ensuring that as many people as possible can take advantage of affordable prevention, diagnosis, treatment, and long-term treatment of heart failure. At the same time, research should be supported in areas where immediate unmet needs exist.
\nAll current recommendations for the prevention of cardiovascular disease in clinical practice recommend an estimate of the overall risk of cardiovascular disease, since atherosclerotic cardiovascular risk is usually the result of a number of risk factors. Prevention of cardiovascular disease in this person should be adapted to his or her overall risk of cardiovascular disease: the higher the risk, the more intense the action should be.
\nThe positive impact of specialized management programs on survival suggests that these factors also lead to a significant number of preventable deaths. Many of the factors listed above are often considered in “normal conditions” of clinical trials with increased monitoring and individualized observation. It is therefore not surprising that patients in clinical trials usually have lower than expected morbidity and mortality rates.
\nAny program aimed at improving long-term management must recognize that patients with heart failure play a key role in their own care. Self-service includes maintenance, monitoring, and management. Maintenance involves taking medication as prescribed, regular meals, and a healthy diet. Monitoring involves monitoring of symptoms and weight (which can serve as a warning sign of increasing fluid accumulation). Management involves responding to changes in symptoms by adjusting the doses of certain drugs if they are prescribed for “use as needed” (e.g., drugs that increase urine production to reduce fluid accumulation) or by seeking medical help if symptoms worsen.
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",metaTitle:"What Does It Cost?",metaDescription:"Open Access publishing helps remove barriers and allows everyone to access valuable information, but article and book processing charges also exclude talented authors and editors who can’t afford to pay. The goal of our Women in Science program is to charge zero APCs, so none of our authors or editors have to pay for publication.",metaKeywords:null,canonicalURL:null,contentRaw:'[{"type":"htmlEditorComponent","content":"We are currently in the process of collecting sponsorship. If you have any ideas or would like to help sponsor this ambitious program, we’d love to hear from you. Contact us at info@intechopen.com.
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