Revised task force criteria for arrhythmogenic right ventricular cardiomyopathy.
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
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Of all the water resources present on earth, only 2.5% exists as freshwater. Fresh water can exist in the form of ground water, surface water and water present in glaciers and ice. A major fraction of fresh water is present in glaciers with only a tiny fraction available as surface water.
\nIncreasing population and urbanization has increased our water demands and place undue stress on the existing water resources. Studies indicate that by 2030 there will be a 40% deficit between the world water demand and the available water resources [1]. People in the developing world are most vulnerable to climate changes; changes in rainfall pattern as a consequence of climate change have largely affected the world in recent years. Extreme changes in the rainfall patterns have increased the frequency of floods and droughts. Exploitation of the available water resources affects all aspects of human existence in addition to disrupting the fine balance in the ecosystem. Erratic and unseasonal rainfall largely affects agricultural activity which mainly sustains the economy of most of the developing countries. Sustainable water management practices are therefore critical to ensure conservation of the existing water resources. Development of policies on smart water practices and its implementation need to go hand in hand to promote conservation of water resources. Many countries around the world have adopted different strategies to reduce the pressure on their available water resources and interesting case studies on their success stories exist.
\nSome of the strategies that can be adopted for sustainable water management are: (i) re-use of treated water for various end uses such as agriculture, horticulture, ground water recharge, aqua culture etc., (ii) revival of water bodies; (iii) reduction in non-revenue water losses. These strategies need to be executed in parallel to conserve and sustain the water resources.
\nTreated water from the Sewage Treatment Plants (STPs) can be used to cater to horticultural needs, irrigation and partly for the daily water requirements. The city of Delhi for example has three sources of water: (1) Surface water supplied by river basins; (2) groundwater; (3) Treated water- the status of which will depend on the quality of treatment. The daily water requirement for Delhi is around 1120 MGD, of which 840 MGD is extracted from River Yamuna and 80 MGD is extracted from groundwater. Currently most of the treated water from STPs are discharged into the major drains and reach River Yamuna. As of 2019, out of 720 MGD generated as raw sewage, only 90 MGD is currently being utilized by various agencies for non-potable purposes like horticulture and in STPs. Some of the advantages of utilizing treated wastewater are:
It will reduce the ever-increasing gap of Potable Water Supply and Demand in Urban Cities.
It can bring down billing charges of fresh water which are a result of long-distance transportation, gradient and higher energy costs.
It can mitigate conflicts of water resource allocation between the Domestic and Agriculture/ Industry.
It can reduce groundwater extraction and also aid in conservation of water resources.
It can make water and sanitation sector sustainable.
Water bodies are an excellent source to conserve rain water which otherwise can lead to flooding due to complete concretization of cities. Revival of existing water bodies and creation of new water bodies can have many advantages; few of which are mentioned below:
Additional Reserves of water can be created within the city which can be utilized in case of scarcity
Ground water recharge
Treated water coming from STPs can be utilized which currently discharge into drains
Rain water can be captured and stored at massive level
Excess water can be utilized to meet needs of the people
Social and Cultural connected – Community owned space – Protection of water bodies
Non-revenue water loss refers to the produced water that is lost during distribution without generating revenue and comprises of components such as real losses, apparent losses and unbilled water consumption [2]. Real losses and apparent losses in a distribution network can be reduced considerably by efficient water auditing. Water flow meters play a critical role in water auditing and give an idea on water losses and usage during each stage. Electromagnetic flow meters can be fitted at different stages of the water supply and a typical scheme of attached flow meters is shown in Figure 1. Water from the source water body reaches a Water Treatment Plant (WTPs) and following treatment is diverted to various primary underground reservoirs. Water from the primary underground reservoir can be tapped to various locations and can also be stored in a number of secondary underground reservoirs. Water flow meters installed at different stages can help identify water losses, water consumption patterns and enable better water accounting. The capital city of Delhi for example has Ten WTPs and until 2015 had a total of 350 water flow meters. Sustainable water management practices in the recent years have led to better water accounting and until 2019, a total of 2000 water flow meters have been installed. This has enabled efficient distribution of available water resources and decreased water losses during distribution and water theft.
\nInstallation of flow meters in a water distribution network.
Sustainable management of water resources to provide safe drinking water to all and to protect the natural reserves is one of the major goals of the SDGs put forth by the United Nations. In the current scenario of climate change and water scarcity, it is of utmost importance to strategize urban water management focusing of water use and reuse, conservation of available water resources and sustainable plans to reduce water losses. Sustaining a low water footprint can effectively reduce water scarcity. The developing world is already taking considerable measures to achieve sustainable use of available water resources while many nations in the developing world have started taking initiatives to adopt sustainable water management. Sustainable water management practices can go a long way in protecting the available water resources and preserving the fragile ecosystem for the future generations.
\nNaxos disease is an arrhythmogenic cardiomyopathy, considered to represent a form of ARVC [1]. It is of genetic origin and two main proteins have been associated with the disease. The clinical manifestations include wooly hair, keratosis of the extremities, and right ventricular dysfunction. Albeit rare, the disease can cause advanced heart failure and life-threatening arrhythmias, even in the young [2]. Data on Naxos disease are limited, and current patient management follows the guidelines for heart failure and ARVC. In recent years, research has focused on the field of bioengineering, illuminating some of the aspects of the disease and cultivating future perspectives regarding its management. In this chapter we present current knowledge regarding the clinical presentation, epidemiology, genetic substrate, pathophysiology, current guidelines for patient management, and future paths for Naxos disease.
Naxos disease manifests with a typical phenotype including both cardiac and extracardiac characteristics. The extracardiac manifestation of the disease involves tight, wooly and rough hair, commonly present from birth [3]. In addition, Naxos patients exhibit diffuse palmoplantar non-epidermolytic keratosis, with clear borders, manifesting as soon as the child starts using hands and feet [3, 4]. Small arms and hands, short fingers, curved nails and hypo/oligodontia have also been reported in some cases [5, 6]. Notably, heterozygous carriers do not display certain aspects of the disease, such as palmoplantar keratoderma but wooly hair may manifest [7].
Regarding the cardiac characteristics, the disease resembles the ARVC phenotype. Echocardiography frequently portrays right ventricular dysfunction. In more detail, prominent dilation is often present along with hypokinesia and aneurysms that affect mainly the outflow tract, apex, and inferior wall of the right ventricle [3, 7]. In a quarter of the cases, the left ventricle is also affected, exhibiting the same characteristics as seen in dilated cardiomyopathy [4]. The term ‘triangle of dysplasia’ has been suggested in Naxos disease, which refers to aneurysms of the outflow tract, apex, and posterior wall of the right ventricle [8]. The disease prognosis is generally adverse [8]. The annual cardiac mortality reaches 3.0% [7].
While the extra-cardiac manifestations are prominent from a young age, symptoms suggestive of cardiac involvement usually occur in adolescence and in young adulthood. Heart failure and life-threatening ventricular arrhythmias may occur in adolescence [4]. Palpitations, syncope, and atrial arrhythmias are frequently encountered [5]. Arrhythmic events involve a wide range of patterns, from numerous premature ventricular complexes to sustained ventricular tachycardia (VT) and are present in half of the patients [7]. Events of VT, most commonly of a left bundle branch block (LBBB) pattern suggestive of right ventricular origin [9], have been documented in Naxos disease, even being drug-refractory in some cases [5]. Symptomatic patients tend to exhibit inducible VT in electrophysiology studies [3].
Symptoms suggestive of right ventricular dysfunction occur in advanced heart failure [8], while heart failure, either right- or bi-ventricular affects half of the patients after 10-year follow-up after diagnosis [7]. When severe hypokinesia is present in the context of progression of heart failure, intra-cardiac thrombi may occur [10]. Heterozygous carriers do not display ventricular arrhythmias or late potentials on signal-averaged electrocardiography (ECG), but atypical ECG or echocardiographic discrepancies may occur [7]. Similarly, they did not display symptoms or echocardiographic abnormalities in follow-up, in a paper by Protonotarios et al. [7].
Naxos disease has been identified as a form of ARVC inherited in an autosomal recessive pattern by the World Health Organization since 1995 [11]. However, the disease was first described in 1986, when Protonotarios and associates first documented the disease manifestations and clinical course [5]. The name “Naxos” originates from this original description of the disease; nine patients, aged 7 to 41 years, from four families of Naxos island in Greece, were presented. All these patients had wooly hair and palmoplantar keratosis as well as a range of arrhythmic events, including VT. Interestingly, all patients had echocardiographic signs of right ventricular (RV) dysfunction, while in some the left ventricle (LV) was also affected [5]. Since then, more patients have been found not only in Greece, but in Israel, Saudi Arabia, Italy, and Turkey [12]. Sporadic cases of the disease have also been identified in Bangladesh and in Canada [13, 14]. The prevalence of the disease in the Greek islands has been calculated to 1:1000 [3]. Officially, the disease was first named “Naxos disease” in a 1994 abstract [15]. Of interest, since ARVC and its clinical spectrum has been found to manifest with biventricular or mainly LV dysfunction, the term arrhythmogenic cardiomyopathy (ACM) has been proposed as more accurate [1]. Prevalence of heterozygous carriers is up to 5% in the Naxos population [8].
The proposed recessive hereditary pattern and the resemblance of the disease to ARVC [5, 16], was confirmed in 1998, when its locus was identified in chromosome 17 in position q21 [17], and in 2000 when plakoglobin was identified as the mutated protein attributed to the disease [18]. Since then, research has concluded that the causative mutation (Pk2157del2TG) is in the gene truncating the C-terminal of the protein plakoglobin [3, 12]. In addition, another mutation, the homozygous 2-bp deletion (c.2157delTG) (also in the protein plakoglobin) has been associated with the disease [18]. Furthermore, mutations of the protein desmoplakin have been identified to cause cardiocutaneous ARVC [19, 20]. Early data suggested that Naxos disease was a more severe form of ARVC [12], while a more recent comparison between the two entities indicates a similar cardiac phenotype, easily identified through non-invasive screening [2, 21]. In 2017, a novel homozygous mutation was discovered to cause Naxos disease, in unrelated patients of French-Canadian families. This is a mutation of the exon 5 of the JUP gene (p.Glu301 Gly) [14]. Two mutations of the desmoplakin gene have been implicated; Dsp7901del1G and DspG2375R [19, 20]. All aforementioned mutations follow an autosomal recessive pattern [2]. However, in 2011 a mutation (c.1790 C > T, p.Ser597Leu) was reported to be causative of the disease associated with hypo/oligodontia, that follows an autosomal dominant pattern [6].
A syndrome resembling Naxos disease, known as Carvajal syndrome, has been described in families from Ecuador and India as well as in Arab-Palestinian families [8, 22, 23]. Truncated proteins of desmoplakin, plakoglobin and desmocollin-2 have been implemented in the genetic substrate [23]. This syndrome was first described by Carvajal-Huerta [22]. Patients present with epidermolytic keratoderma while the disease usually manifests at a younger age and the LV is commonly affected [3, 8]. Notably, the replacement of the myocytes by fatty tissue is not apparent in Carvajal syndrome [24].
Both plakoglobin (γ-catenin) and desmoplakin, that are linked with Naxos disease are associated with myocardial cell adhesion [3, 25]. Plakoglobin has a two-fold role in both mechanical contraction and electrical signal conduction; it is a component of the desmosomes, interconnecting with the intermediate filaments of desmin, and constitutes a component of the adherens junctions where it is connected to the actin skeleton [3, 26]. Similarly, desmoplakin is a cytoplasmic protein that links plakoglobin to the intermediate filaments of desmin [3]. The defective cell adhesion in the case of the truncated plakoglobin protein, also causes a reduction in the connexin-43 levels, a major gap junction protein. The associated myocardial gap-junction remodeling, creates a substrate for arrhythmogenic events [27]. Furthermore, the defective cell adhesion of the cardiomyocytes leads to their apoptosis which is then followed by fibrofatty replacement in the affected ventricles [18]. The associated conduction disturbances created can induce arrhythmogenic events and sustain re-entry circuits [3].
In the landmark paper Protonotarios et al., all patients were reported to have signs of intra-ventricular conduction delay ECG as well as echocardiographic findings of right- or bi-ventricular dysfunction. In more detail, the ECG abnormalities that were reported include a wide QRS ≥120 ms and abnormal T-wave inversions in seven out of nine patients [5]. The most common abnormalities documented in Naxos patients are wide QRS and inverted T-waves in V1-V3 or in all precordial leads, while epsilon waves may also be present [3]. An incomplete right bundle branch block may also be apparent, while the extrasystoles tend to manifest with an LBBB morphology [7]. Flattened T-waves appear in the case of biventricular involvement [3]. Late potentials in Naxos disease are more often abnormal than in other forms of cardiomyopathies [28]. In echocardiography, dysfunction, hypokinesia and aneurysms are prominent [3, 7]. In histological specimens fibrofatty patterns are prominent, while focal myocarditis has also been reported in follow-up histology specimens [4]. Both the subepicardial and the mediomural myocardium of the involved ventricles is replaced by fibrofatty tissue, while healthy myocytes are surrounded by fatty tissue [3, 29]. In immunohistochemical specimens the signal of plakoglobin and connexin-43 in the intracellular junctions is diminished [24, 27].
Since the disease belongs in the ARVC spectrum and there are currently no specific diagnostic criteria for the cardiac manifestations of Naxos disease, the diagnostic criteria of ARVC are widely used [30, 31]. However, while the specificity of the revised task force criteria is high, sensitivity has been shown to be as low as 13–20% [32]. Since then, progress has been made regarding tissue characterization through cardiac magnetic resonance (CMR), possibly providing a tool of higher diagnostic accuracy, high specificity and high sensitivity [32, 33]. The revised task force criteria for ARVC are depicted in Table 1. In November 2020 the Padua criteria for the diagnosis of ACM was published. The Padua diagnostic criteria introduce tissue characterization by contrast enhanced cardiac magnetic resonance for detection of fibro-fatty myocardial replacement of both ventricles. It also adds new ECG criteria, including depolarization/ repolarization abnormalities and ventricular arrhythmias, specific for the LV involvement [34]. The proposed Padua diagnostic criteria need to be validated by further clinical studies in large cohorts of patients.
Category | Criteria |
---|---|
Global or regional dysfunction and structural alterations | Major By 2-D echocardiography:
By CMR:
By RV angiography:
Minor By 2-D echocardiography:
By CMR:
|
Wall tissue characterization | Major Residual myocytes <60% by morphometric analysis (or < 50% if estimated), with fibrous replacement of the RV free wall myocardium in ≥1 sample, with or without fatty replacement of tissue on endomyocardial biopsy Minor Residual myocytes 60–75% by morphometric analysis (or 50–65% if estimated), with fibrous replacement of the RV free wall myocardium in ≥1 sample, with or without fatty replacement of tissue on endomyocardial biopsy |
Repolarization abnormalities | Major Inverted T waves in right precordial leads (V1, V2, and V3), or beyond in individuals >14 years old (in the absence of complete RBBB ≥QRS 120 ms) Minor
|
Depolarization/conduction abnormalities | Major Epsilon wave (reproducible low-amplitude signals between end of QRS complex to onset of the T wave) in the right precordial leads (V1 to V3) Minor
V3, in the absence of complete RBBB |
Arrhythmias | Major Nonsustained or sustained ventricular tachycardia of LBBB morphology with superior axis (negative or indeterminate QRS in leads II, III, and aVF and positive in lead aVL) Minor
|
Family history | Major
Minor
|
Revised task force criteria for arrhythmogenic right ventricular cardiomyopathy.
Required for definite diagnosis: 2 major or 1 major and 2 minor criteria or 4 minor from different categories; borderline: 1 major and 1 minor or 3 minor criteria from different categories
Possible diagnosis: 1 major or 2 minor criteria from different categories.
ARVC, arrhythmogenic right ventricular cardiomyopathy; BSA, body surface area; CMR, cardiac magnetic resonance imaging; LBBB, left bundle branch block; PLAX, parasternal long-axis view; PSAX, parasternal short-axis view; RBBB, right bundle branch block; RV, right ventricular; RVOT, RV outflow tract; SAEG, signal averaged ECG.
Adapted from Marcus et al. [31].
Naxos disease is predominantly a condition affecting the right ventricle, causing right ventricular failure. Unlike for LV failure, less is known regarding the optimal pharmacological therapy. However, the expert consensus regarding the management of ACMs suggests that when treating left or right ventricular dysfunction, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, beta-blockers, mineralocorticoid receptor antagonists, and diuretics, in the case of fluid overload, should be considered [35]. Despite the lack of Naxos-specific guidelines, ACE inhibitors, betablockers, and diuretics are reasonable prescribing choices [2]. Dapagliflozine and empagliflozine have been introduced in the treatment of heart failure, even in non-diabetic patients [36, 37], while sacubitril/valsartan is indicated for patients with left ventricular ejection fraction (EF) ≤35% [38]. Anticoagulation treatment is indicated in the case of atrial fibrillation/flutter, in the event of intra-cardiac thrombi and can also be considered in patients with ventricular aneurysms, either left or right [35, 39]. In the case of advanced heart failure, patients may benefit from devices such as cardiac resynchronization therapy (CRT), often combined with an implantable cardioverter-defibrillator (ICD), left ventricular assist devices (LVAD) and assist devices for the right ventricle (RVAD or BiVAD) in the setting of an LVAD implantation and considered as bridge to transplant [38].
The prognosis of the disease is adverse, especially in the young and annual SCD mortality is 2.3% [7, 8]. As risk factors for SCD, the following have been identified: history of syncope, onset of symptoms before the age of 35, structural progression before the age of 35, and left-ventricular involvement [7]. However, risk stratification of SCD constitutes a challenge. ARVC guidelines and position papers on ICD implantation, guide the same decisions in the management of Naxos disease [35, 40]. Criteria for risk stratification for SCD is presented in Table 2. A clear indication for an ICD implantation is aborted SCD and VT with haemodynamic instability, while in the case of VT without haemodynamic compromise it should also be considered [35, 40]. An ICD protects from SCD in ARVC either in secondary prevention or is justified as primary prevention based on careful judgment of risk factors [40, 41, 42]. However, the clinical presentation should play a major part in the decision making; unexplained syncope, risk markers associated with medical history, family history and severity of clinical presentation and deterioration should be considered [40]. An ICD is indicated for ACM patients with low ejection fraction ≤35% and New York Heart Association (NYHA) class II or III, provided that the patient’s estimated survival exceeds one year [35]. The same guidelines apply for Naxos patients. The first implantation of an ICD in a Naxos patient was reported in 2000 [43]. Naxos-specific guidelines are rare. Among those, an ICD is indicated for patients who are symptomatic or present structural progression especially before the age of 35 [8, 44]. Naxos patients, like ARVC patients, should abstain from competitive sports as myocardial stress can exacerbate the dysplasia [40]. Regarding drug therapy, beta-blockers (Class I), and possibly amiodarone (Class IIb) and sotalol (Class IIb) in special cases have been suggested for patients with ACMs for the control of arrhythmias and the reduction of ICD shocks [35, 45]. Specifically for Naxos patients with recurrent sustained VTs, anti-arrhythmic drugs should be prescribed as per the general guidelines of arrhythmias, while amiodarone or sotalol alone or in combination with beta-blockers have been suggested [8, 40, 45]. As far as catheter ablation is concerned, it should be considered in ACM cases with amiodarone-refractory recurrent monomorphic VT, recurrent symptomatic drug-refractory sustained VT, symptomatic nonsustained VT or a high ectopic burden (≥1000 premature ventricular contractions/day) refractory to beta-blockers [35]. Beta-blockers are also recommended for patients without an ICD (Class IIa) [35].
Estimated Risk | Parameters |
---|---|
High risk (>10% / year) | Major arrhythmic events
|
Intermediate risk (1–10% / year) | Major risk factors
|
Low risk (<1% / year) | No events/no risk factor
|
On the front of cellular and molecular engineering, advances have been made that may create a substrate with therapeutic potentials in the future. The pharmaceutical substance SB216763 (SB21) (an inhibitor of the glycogen synthase kinase GSK-3β) prevented heart failure and reduced mortality when administered early on to zebrafish models with induced plakoglobin mutations that resulted in Naxos disease. The effect could possibly be attributed to the prevention of the formation of an arrhythmic substrate on the intercalated disk level [47]. Further data on mammalian models are, however, needed [2, 48].
On the front of induced pluripotent stem cells (iPSCs) that enable the in-vitro study of human genetic disorders like ARVC through the induction of mutant cardiomyocytes, albeit a challenging field, promising results have been reported [49, 50, 51]. Researchers have been able to re-create the ARVC phenotype using adultlike metabolic energetics, proving that adultlike metabolism plays a crucial role in establishing ARVC models through iPSCs [49]. Furthermore, cultured ARVC cardiomyocytes manifest with adipogenic phenotype and reduced cell surface localization of desmosomal proteins, characteristic features of ARVC [50]. Also Naxos-ARVC has been created in mice models through a homozygous mutation of the plakoglobin gene [52] and of the desmoplakin gene, the latter causing human-like cardiac arrhythmias, palmoplantar keratosis, and alopecia [53]. Interestingly, cardiac function was restored in mice through the normalization of Naxos plakoglobin levels, indicating that it is the downregulation of the protein that causes the cardiac dysfunction, rather than the mutation itself [54]. This conclusion, if further supported, could have clinical applications in Naxos disease [2]. The article suggests that an approach to this would be to use antisense technology to specifically block nonsense-mediated decay of mutant plakoglobin mRNA, enabling the expression of the truncated protein at increased levels [54, 55].
In this chapter key aspects of Naxos disease are presented. Due to its rarity, the condition follows the general guidelines for arrhythmias and heart failure, as disease-specific criteria is lacking. However, due to its uniqueness, larger Naxos registries are needed, as they would illuminate the individual characteristics of the disease as well as guide the way to designated guidelines for the management of Naxos patients. Possibly, the thorough study of the origins of the disease, the genetic substrate and pathogenesis, can offer insights with therapeutic potential.
IK and ML reports no conflicts of interest. GM has received speaker’s fee from Alnylam, MSD, and Internetmedicin. PM is on the advisory board of Coala Life and has received speaker’s fees or grants from Abbott, Alnylam, Amicus Therapeutics, AstraZeneca, Bayer, Boehringer-Ingelheim, Internetmedicin, Lilly, MSD, Novo Nordisk, Octopus Medical, OrionPharma, Pfizer, Vifor Pharma, and Zoll.
angiotensin-converting enzyme arrhythmogenic cardiomyopathy arrhythmogenic right ventricular cardiomyopathy cardiac magnetic resonance cardiac resynchronization therapy electrocardiography induced pluripotent stem cell implantable cardioverter-defibrillator left bundle branch block left ventricle left ventricular assist device New York Heart Association sudden cardiac death ventricular tachycardia
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