\r\n\tThe development of the interpersonal model and the Kleinian school in the second half of the last century allowed the emergence of an original understanding of the unconscious mind. Within the intersubjective paradigm, the psychoanalytic situation is conceptualized as an interpersonal field to which both the analyst and the patient contribute substantially. We have shown elsewhere how the failure to give a full account of such an intersubjective dimension in both psychoanalytic theory and practice amounts to a core liability in contemporary psychoanalytic discourse.
\r\n\r\n\tThe present book will focus on a few areas where the insufficient development of our discipline is currently apparent: five wounds that mark the body of the psychoanalytic enterprise.
\r\n\r\n\tNew contributions are particularly needed in the following areas: Current conceptualization of the unconscious mind is mechanistic and not suited to incorporate the full network of interpersonal exchanges which unfolds in the analytic room; Furthermore, the development of interpersonal psychoanalysis and the theory of the object relations warrants a greater appreciation of the impact of extratranference relations (e.g., couple, family, peers) on the patient's inner life both within and without the psychoanalytic situation.
\r\n\r\n\tAn integration of theories and models from other psychological paradigms is clearly in order here; the book will also focus on Barangers’ theory of the bi-personal field that makes traditional unipersonal models of the psychoanalytic process untenable. Also, it will help in the understanding of the reciprocal interactions of the two partners in the psychoanalytic dyad in most psychoanalytic institutes the training format relies naively on models from the academic or the professional domains. This fosters rigidity, conformism, and a hierarchical organizational style in the institutional life; e) all over the long span of his creative life Freud showed consistent interest in the application of psychoanalysis to literature, the arts, religion, and politics. Contemporary psychoanalysis is getting more and shyer and is pressed at the margins of social and political debate. The psychoanalytic theory includes unique lore of knowledge about the conscious and unconscious mind. Without it, a comprehensive understanding of human reality will stay out of the reach of contemporary culture.
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C. Ronco distinguished 5 clinical types of CRS [1]:
Type 1: Acute worsening of heart function leading to kidney injury and/or dysfunction.
Type 2: Chronic abnormalities in heart function leading to kidney injury or dysfunction. This subtype refers to a more chronic state of kidney disease complicating chronic heart disease, the so-called chronic kidney disease (CKD).
Type 3: Acute worsening of kidney function leading to heart injury and/or dysfunction (acute heart failure).
Type 4: Chronic kidney disease causing cardiac overload, leading to progressive chronic cardiac dysfunction.
Type 5: Systemic condition (e.g., sepsis, vasculitis) leading to simultaneous injury and/or dysfunction of heart and kidney.
We can see the interplay of decreased glomerular filtration rate and impaired cardiac contractile function early in chronic kidney disease (CKD) worsening as renal failure increases. However, the existing classification of CRS does not consider the population of patients on renal replacement therapy (RRT), where the effect of dialysis treatment itself engages additional mechanisms of pathogenesis of cardiac pathology. Thus, the progression of cardiac dysfunction with decreasing ejection fraction reduces the effectiveness of hemodialysis (HD), while reducing the intensity of dialysis regimen and gradual loss of residual renal function speeds up the atherosclerosis and cardiomyopathy progression.
Thus, one can consider the cardiorenal relationships in patients on RRT, reflecting progression and myocardial damage in dialysis patients, as a separate type of CRS where the renal component implies end stage renal disease (ESRD) with complicating metabolic and endocrine disorders, complete loss of residual renal function, and dialysis therapy.
The features of cardiac dysfunction in patients on RRT include its widespread prevalence and severity [2]. The incidence of left ventricular myocardial hypertrophy (LVH) increases with increasing stage of CKD, reaching 90% in stages 4–5 [3]. Prevalence and severity of cardiac pathology, both coronary and non-coronary, increases rapidly in the dialysis stage of renal failure, correlating with dialysis experience. In 75–80% of patients with CKD stage 5D, secondary cardiomyopathy develops predisposing to congestive heart failure (CHF), acute coronary syndrome, or complex rhythm and conduction abnormalities. In patients on RRT, progressive atherosclerosis is associated with activation of inflammatory reactions and high frequency of protein-energy malnutrition (PEM) [4]. Thus, PEM is diagnosed in 20–50% of patients with pre-dialysis stages of CKD, increasing to 50–80% in patients on regular HD and permanent PD.
The cardiac function in patients on RRT deteriorates progressively under several pathogenetic mechanisms. These include bio-incompatibility of dialysis membranes and solutions, ineffective dialysis, PEM, dialysis hypotension, rapid decline and subsequent complete loss of residual renal function, vascular calcification, excessive shunt from arterio-venous hemodialysis fistula (AVF).
CKD in RRT is characterized by higher level of uremia and the impact of dialysis procedure itself. Despite the successes of modern hemodialysis therapy, the problem of hemodialysis membranes’ bio-incompatibility is still unresolved. A key inducer of blood cell activation is dialyzer membrane material, along with the endotoxin contamination of dialysis solutions. Membrane contact with blood causes pro-inflammatory and pro-oxidant stress, thrombosis, and release of oxidative stress biomarkers, inflammatory and anti-inflammatory cytokines (IFN-γ, TNF-α, IL -1β, IL-4, IL-6, IL-10, IL-12, and IL-18), and acute phase proteins (C-reactive protein, fibrinogen) [5]. Other consequences of bio-incompatibility are complement [6] and platelet activation [7].
The oxidative events induced by extracorporeal treatment are thought to affect the concomitant pathology. Chronic inflammation, besides cardiovascular dysfunction, contributes to worsening renal anemia by reducing sensitivity to the erythropoietin-stimulating agent and shortening the life span of red blood cells [8, 9]. Also, blood leukocyte activation, oxidative stress, and mechanical factors damage the red blood cells. Leukocytes in contact with bio-incompatible dialysis membranes re-activate. The resultant leukopeniais considered a major cause of defective cellular immune response in patients on hemodialysis (HD) [10, 11]. Changes in lymphocyte phenotype (from Th1 to Th2) cause this response and excessive synthesis of pro-inflammatory cytokines [5]. Bio-incompatible membranes release pyrogens and active inflammatory mediators (histamine and bradykinin). These contribute to fever and hemodialysis-induced hypotension [12]. The latter is a key factor in residual renal function reducing in patients on regular HD [13].
Dialysate composition for peritoneal dialysis (PD) can also cause oxidative stress and inflammation [14, 15]. High concentrations of glucose and lactate, and low pH or hyperosmolality of dialysate for PD contribute to excessive production of reactive oxygen species and accumulation of oxidative damage products in the peritoneum, increasing calcification and fibrosis. The relationship between the preserved residual renal function and oxidative stress has been shown to correlate with cardiovascular risk and survival in patients on PD [14]. Given the longer preservation of residual renal function in patients on PD treatment, this method can be considered more favorable for patients with cardiovascular diseases (CVD). Also, several studies have shown a higher accumulation of oxidants and depletion of antioxidant reserves in patients on HD compared with those on PD [15, 16].
The accumulation of oxidative stress products is the highest in patients with ESRD. Peroxidizing agents oxidize unsaturated lipids [17, 18, 19] and endogenous pro-oxidants damage plasma proteins with the formation of glycation products [20, 21, 22]. Small reactive carbonyls and larger posttranslational uremic-modified proteins form many inflammatory mediators, reflecting uremic toxicity that is little dependent on the method of dialysis therapy [23]. However, all modern diffusion, convective, or mixed methods do not remove medium- and high-molecular-weight dissolved substances modified by reactive oxygen species (ROS) and reactive carbonyls effectively from blood [24, 25, 26].
Oxidative stress plays a key role in the development of cardiac dysfunction in patients on RRT. In patients with ESRD, the balance between nitric oxide (NO) and ROS is shifted toward the latter by increasing ROS production and decreasing NO availability [27]. Pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α can stimulate renin synthesis and norepinephrine secretion [28, 29]. IL-6 induces AT-1 receptors and angiotensin II-mediated ROS production in cultured rat smooth muscle cells, supporting the link between inflammation, renin-angiotensin-aldosterone system (RAAS) activation, and oxidative stress [30]. Volume overload on RRT and venous stasis are additional sources of inflammatory mediators [31, 32]. Because of intravascular overload, the vascular endothelium may be a major source of cytokine production in response to biomechanical stress [33]. Thus, the above data confirms the potential role of circulating cellular precursors of ROS and/or local agonists of ROS synthesis in the development of CRS in dialysis patients.
C. Vida et al. have shown in dialysis patients the activation of peripheral blood polymorphonuclear and mononuclear leukocytes, which leads to excess production of oxidative compounds such as reactive oxygen species, and it is this process that plays the leading role [34].
The imbalance between the RAAS, sympathetic nervous system, and inflammation speeds up the CRS formation in dialysis patients. To prevent and slow the cardiac pathology in HD treatment, highly purified dialysis solutions and synthetic dialysis membranes are being developed to reduce the risk of oxidative stress and other manifestations caused by low biocompatibility of membranes. For example, dialysis membranes made of regenerated cellulose that interact with the β-D-glucose hydroxyl groups of blood components cause activation of the complement system and leukopenia. To improve the biocompatibility of these membranes, hydroxyl groups are modified chemically by acetylation to produce triacetate cellulose or addition of D-α-tocopherol polyethylene glycol-1000 succinate chains, an esterified form of α-tocopherol. HD and PD in CKD permanently excrete antioxidants through the membranes. To normalize their blood levels and suppress ROS generation in patients on HD, vitamins C, E, and glutathione are supplemented orally [27].
PEM should be noted among the factors influencing the progression of cardiovascular pathology and the formation of CRS in patients on dialysis [35, 36]. Progressive blood pressure instability with LVH and diastolic dysfunction, acidosis, coronary atherosclerosis, as well as increasing hypoalbuminemia and severe anemia early lead to ineffective HD and loss of residual renal function. These exacerbate hyperhydration with overload and ischemia of myocardial muscle, oxidative stress, and heart chamber dilatation.
The causes of PEM in dialysis patients include protein hypercatabolism with decreased synthesis of albumin and essential amino acids and their subsequent losses (more on PD), L-carnitine deficiency, anorexia with depression, and chronic inflammation with hyperproduction of pro-inflammatory cytokines [37]. Uremic hyperparathyroidism with deficiency of anabolic hormones (insulin, erythropoietin) plays an important role in the PEM development. Progression of PEM is fixed by monitoring of anthropometry (BMI, shoulder muscle circumference, and triceps skinfold), levels of albumin, lymphocytes, TNF-α, transferrin, and CRP.
In the advanced stage of dialysis CRS, PEM progresses to MIA-syndrome (Malnutrtion, Inflammation, Atherosclerosis). This is manifested by ischemic cardiomyopathy provoking arrhythmias, stenotic atherosclerosis with diffuse calcification of arteries and heart valves, and treatment-resistant anemia and hypoalbuminemia [38].
Preservation of residual kidney function in dialysis patients improves their survival and prognosis. For example, Dutch joint NECOSAD study [40] in 740 patients on HD showed an increase in residual kidney function (Kt/V by 1 unit) associated with a 66% reduction in the relative risk of death. Prospective analysis by W. Van der Wal et al., which included 1800 dialysis patients (1191 patients were on HD and 609 on PD), found a 1.5-fold death risk increase after loss of residual renal function compared to patients with preserved residual renal function [41]. Y. Obi et al. found that higher and more stable residual renal function (GFR) was associated with better patient survival one year after initiation of regular HD. Mortality related inversely with residual renal function measured by urea clearance and daily urine output [42]. In several other multicenter studies [43, 44] residual function has been an independent predictor of survival in patients on PD. The Canadian-American Study (CANUSA) [45] showed on 601 patients on PD that residual renal function rather than peritoneal creatinine clearance and peritoneal ultrafiltration (UF) correlate with patient survival. A study of residual renal function in PD patients showed a 36% reduction in the relative risk of death with an increase in daily urine output by 250 mL.
Preservation of residual renal function provides better control of hyperhydration, dyselectrolytemia, inflammatory activity, and clearance of protein-bound low molecular weight toxins and medium-molecular-weight molecules. Even a small amount of residual function reduces the level of plasma dissolved uremic toxins and β2-microglobulin [46, 47, 48].
The residual renal function allows to reduce cardiac mortality and progression of cardiovascular disease in dialysis patients primarily through better hydration control. Both on regular and continuous PD, CKD patients with uncorrected hyperhydration are at high risk of developing cardiovascular complications: volume/sodium-dependent hypertension, left ventricular hypertrophy, arrhythmias, and congestive heart failure [49, 50, 51]. The expansion of intravascular volume leads to elongation of myocardial cells, and eccentric or asymmetrical left ventricular remodeling [52].
In patients on intermittent HD, UF causes post-ischemic impairment of myocardial contractile function (myocardial stunning) even in the absence of angiographically significant coronary disease [53]. Recurrent UF-induced ischemia provokes chronic left ventricular dysfunction, a cause of CHF progression in patients on HD [54]. Preserved residual renal function in patients on regular PD allows to reduce UF volumes during dialysis session, thus reducing risk of recurrent myocardial ischemia or systolic pressure drop during the session (hemodialysis-induced hypotension) [54, 55, 56, 57]. In patients on PD, maintenance of residual renal function and significant diuresis attenuates the damaging effects of dextrose on the peritoneal membrane and reduces hyperglycemia and the risk of obesity and diabetes.
The residual renal function not only increases survival but also improves hormonal, mineral-bone, and nutritional disorders and the quality of life in patients on HD and PD, as confirmed by the CHOICE study [58]. Higher quality of life in patients with diuresis over 250 ml per day is also associated with a less restriction in diet and fluid intake, and better nutritional status [59] and control of hyperphosphatemia, renal osteodystrophy, and anemia. The latter depend on a renal synthesis of erythropoietin and active forms of vitamin D3 in kidneys [60, 61]. Several data have shown an association between the preserved residual renal function and decreased production of inflammatory markers: C-reactive protein and interleukin-6 [62, 63].
In patients with end stage CKD, fluid removal is achieved by extracorporeal UF with HD or intracorporeal UF with continuous PD. Unlike intermittent HD, continuous PD is not associated with “stunned” myocardium, which largely explains the slower progression of CHF in patients treated with PD [64]. However, clinical studies showed contradictory results on the benefits of PD.
The development of intradialysis hypotension on regular HD is caused by uremic polyneuropathy and CHF, when, in response to dialysis UF, the vascular bed fills inadequately slowly, causing hypovolemia and hypotension. Dialysis CRS with hypotension is often complicated by thrombosis of vascular access, resulting in rapid formation of underdialysis syndrome with hypercatabolism. Blood loss and sinus tachycardia combined with hemodialysis-induced hypotension significantly increase the risk of acute coronary syndrome and cerebrovascular accident (CVA). Patients with diabetic nephropathy often develop severe hemodialysis-induced hypotension refractory to conservative therapy. The hypotension can provoke target organ ischemia. Vasopressors and alpha-adrenergic agonists are not safe in treating hemodialysis-induced hypotension. Controlled UF with “dry weight” monitoring by bio-impedance, transfer to PD, or daily (nighttime) HD are recommended.
Metabolic acidosis is common in patientswith ESRD because of a decreased ability to excrete acids and reduced renal synthesis of bicarbonate. It leads to malnutrition, inflammation, bone disease disorders, and even a higher death risk [69]. Significant acid–base variations during dialysis may play an important role in CVD development in HD patients. One study [70] has shown an association between low serum bicarbonate concentrations and cardiovascular disease in patients on dialysis. It is important to avoid large variations in serum bicarbonate levels in dialysis patients because these variations can increase CVD.
MIA syndrome is characterized by rapid stenosing of the major arteries by the progressing atherosclerosis combined with calcinosis. Frequent complications are ischemic kidney disease with uncontrolled renin-dependent hypertension, stenotic atherosclerosis of cerebral arteries with the risk of CVA, ischemic occlusive enteropathy with malabsorption syndrome aggravating PEM and anemia.
In dialysis CRS with the expanded PEM, coronary heart disease (CHD) is typical with unstable angina and elevated blood CRP correlating with LDL levels [71, 72]. Hyperparathyroidism is associated with progressive coronary artery calcification, increasing atherosclerosis [73, 74]. Stenosis of the proximal coronary artery is typical, which causes high mortality in patients on dialysis [75]. Early diagnosis of myocardial infarction in dialysis CRS is difficult because of confounding uremic polyneuropathy, dyselectrolitemia, myocardial calcification, and coronary calcinosis. Coronarography in 60% of patients with CKD stage 5 admitted for regular HD treatment in Japan reveals low-symptomatic stenosis of one coronary artery and of several coronary arteries (multivessel disease) in some patients.
To prevent acute coronary syndrome, risk factors should be addressed in HD: hemodialysis-induced hypotension, sinus tachycardia, blood loss, and anemia. ACE inhibitors reduce the cardiac mortality [76]. Nitrates and beta-blockers are tolerated worse in dialysis CRS because of hemodynamic instability.
Hemodialysis-induced myocardial ischemiamight regress with the use of beta-blockers, which have substantially improved survival in patients with acute coronary syndromes and heart failure. In dialysis patients, carvedilol significantly improved cardiovascular mortality, LV function, and LV morphology. Dialysis patients treated with carvedilol had a 50% lower mortality rate than patients receiving placebo [77, 78]. The efficacy of statins on regular HD has not been proven conclusively, and the incidence of side effects is higher than in the early stages of CKD [79].
Current guidelines by KDIGO recommend not starting lipid-lowering therapy in dialysis patients. These recommendations are based on clinical trials which failed to show that statin therapy is beneficial in reducing cardiovascular mortality indialysis patients, in contrast to the general population [80]. High-density lipoprotein cholesterol (HDL-C) from HD patients compared to healthy controls has been much less effective in cholesterol efflux and regulation of inflammation [81]. HDL-C from HD patients promotes endothelial dysfunction via accumulation of symmetric dimethylarginine (SDMA), which is associated with increased all-cause and cardiovascular mortality [82].
Erythropoietin drugs cannot fully realize their cardioprotective effect because of more frequent side effects of the high doses. Survival rate after acute myocardial infarction is extremely low at conservative therapy of CHD on hemodialysis (by the end of the 1st year, 41%, after 2 years, 27%, after 3 years, 10%). This causes intolerance of uremic myocardium to ischemia with small coronary artery remodeling (uremic small vessel disease) and myocardial stunning on HD. In coronary angioplasty in patients with dialysis-related CRS, the acute postoperative mortality is over 3.5 times higher than the statistical average, and the long-term survival rate after stenting is significantly higher than in conservative therapy [83].
CHF in patients on HD is manifested by worsening chronic hypervolemia, causing both circuits decompensation and a significant decrease in ejection fraction preventing effective HD, and development of critical progressive hyponatremia with a high risk of cerebral edema. The 3-year survival rate of patients with CHF on regular HD does not exceed 20%, and sudden cardiac death is most frequent fatality in this group of patients on HD [84].
The rate of sudden cardiac death is 59 deaths in 1000 patient-years in the CKD stage 5D population, whereas it is 1 death in 1000 patient-years in the general population [85]. Patients on dialysis have a high incidence of coronary heart disease, but the rate of sudden cardiac death is disproportionately high compared with the incidence of coronary heart disease in these patients. Even a complete revascularization reduce the risk of sudden cardiac death only in part [86]. Dialysis, especially HD, is a risk factor for sudden cardiac death, providing the highest risk within the first 12 hours after dialysis and after a long dialysis-free interval [87]. Potential mechanisms include volume and sudden electrolyte shifts after dialysis, volume overload, and electrolyte disturbance.
These outcomes largely depend not on the severity of CHD, but on the value of the corrected QT-interval and QT dispersion and are caused by complex rhythm disturbances in dialysis malnutrition (hypercatabolism, acidosis, imbalance of potassium, sodium and calcium in dialysis solution, and hypomagnesemia) [88]. Cardioprotectors, antiarrhythmics, and vasopressors provide only short-term effect; myocardial reperfusion, artificial pacemaker, implanted cardioverter-defibrillator are more effective [84, 88].
PD may be the method of choice in the treatment of patients with CHF, providing effective UF and sodium excretion in the required volumes, especially when using icodextrin solution. In patients with CRS and severe ascites, PD can reduce intra-abdominal pressure. PD in patients with CHF has several advantages: continuous “mild” UF with minimal impact on hemodynamics and reduction of volume overload symptoms; weight reduction and correction of hypervolemia; increase in left ventricular ejection fraction; sodium “sieving” effect and better control of hypernatremia; removal of acute phase proteins, medium-molecular-weight molecules, abscence of pro-inflammatory activation of cytokines; reduction of intraabdominal pressure and improved quality of life in patients with severe ascites; and better control of serum potassium level with the possibility of using aldosterone receptor blockers and ACE inhibitors. Heart transplantation should be used in refractory cases, sometimes in combination with the kidney transplantation.
Hyperparathyroidism, frequent in RRT patients, is prognostically unfavorable [89]. Elevation of serum fibroblast growth factor-23 (FGF-23) with the development of resistance to it precedes Mineral Bone Disease (MBD). Elevated FGF23 levels were independently associated with LVH.FGF23 caused LVH via FGF receptor-dependent activation of the calcineurin-nuclear factor of activated T-cells signaling pathway [90]. Klotho deficiency and FGF23 elevation are associated with poor outcomes and complications in dialysispatients. Klotho deficiency cause vascular calcification, cardiac fibrosis, and cardiac hypertrophy in patients with CKD [91].
Hyperphosphatemia and parathyroid hormone elevation increase with increasing stage of CKD and correlate with cardiac mortality [92]. This is largely because of vascular calcification, especially pronounced in dialysis patients, which is associated with the use of solutions for PD and HD with increased calcium content.
Vascular calcification (VC) is defined as vascular deposition of calcium-phosphate mineral complexes. Traditionally, two forms of calcification are pointed out: 1) intimal calcification in proximity to lipid deposits, clinically relevant in obstructive arterial disease and 2) medial calcification with differentiation of smooth muscle cells into osteoblast-like cells is akin to bone formation, related to several genes as BMP2, Msh Homeobox 2, and gene of alkaline phosphatase [93]. Medial calcification is common in dialysis patients with CKD.VC has a clearrelationship with atherosclerotic vascular disease [94]. Calcification of arterial vessels leads to arterial stiffness, contributes to increased pulse wave velocity, increased cardiac afterload, and thus heart failure [95]. Arterial stiffness is an independent predictor of cardiovascular mortality [96]. Arterial stiffness and medial calcification intensify each other, to create a vicious cycle [97]. Heart valve calcification occurs in stage 5 CKD in up to 88–99% of patients, increasing from 40% of patients in CKD stage 3 [98].
Calcinosis of heart valves leads to the formation of acquired heart valvular disease (aggravating CHF) and increases the risk of infective endocarditis. The extent of vascular calcifications in CKD herald a poor prognosis [99]. Resulting hemodynamic alterations induce left ventricular hypertrophy associated with a decrease in coronary perfusion [100].
In dialysis CRS, active vitamin D metabolites are contraindicated because of the risk of soft tissue calcification (including skin calcification with sepsis). Calcium-free phosphate binders are advisable: sevelamer, lanthanum carbonate [101]. Sevelamer corrects hyperphosphatemia and decreases mortality in dialysis patients by 1.5 times, slowing coronary calcification, reducing blood levels of atherogenic lipids, FGF-23, and pro-inflammatory cytokines [102]. Iron-containing phosphate binders effectively lower blood phosphate levels, but are often complicated by diarrhea and nutritional disorders exacerbation in PEM [103]. Total parathyroidectomy in patients with dialysis cachexia is effective in MBD and CHF progression but carries a risk of acute postoperative complications [104]. An alternative to parathyroidectomy is administration of calcimimetics. Prolonged-release cinalcet reduces the need for parathyroidectomy, slows arterial and cardiac valve calcification, and reduces cardiovascular mortality [105, 106].
In dialysis-associated CRS, infection is severe, both induced by thrombosis of sclerosed AVF or not associated with vascular access. Pneumonia risk factors in dialysis CRS with malnutrition include immune deficiency with activation of opportunistic infections and Staphylococcus carrying in the nasopharynx, CHF with chronic hyperhydration and hypoxia of lung tissue, hydrothorax, hyperparathyroidism with lung tissue calcification, obstructive night apnea syndrome, and epoetin-resistant anemia.
Pathogens of acute pneumonia on dialysis include staphylococcus, opportunistic bacteria (
Antibiotic therapy is carried out after removal of the infected fistula with the formation of a new AVF or with transfer to PD [109]. Treatment with broad-spectrum antibiotics should be started immediately and corrected by the blood culture results. Antibiotic therapy is ineffective in CHF, recurrent thromboembolism, fungal endocarditis, tricuspid or pulmonary artery valves lesions (frequent in HD patients). In these cases, surgery is necessary to replace the affected valve [108].
Anemia in CKD patients induces eccentric LVH and exacerbates myocardial ischemia, increasing cardiovascular mortality in dialysis CRS [110, 111]. Erythropoietin drugs improve the quality of life of dialysis patients. However, the mortality-reducing effect of erythropoietin in dialysis CRS has not been proven, and the most effective and safe target Hb level is not established. The currently recommended target Hb level of 10–12 g/dL does not stimulate sufficiently neo-angiogenesis and endothelial stem cells activity.
Resistant anemia often develops within MIA syndrome (under the influence of chronic inflammation, acidosis, iron malabsorption, vit. B12 and folic acid deficiency), as well as because of ineffective HD syndrome and hyperparathyroidism, requiring the unusually high doses of erythropoietin. Since this therapy is often complicated by poorly controlled hypertension and thrombosis, combined antihypertensive therapy, complete correction of iron deficiency, vit. B12 and metabolic acidosis, and control of the coagulation system are indicated [112]. Intensification of HD regimen, correction of hyperparathyroidism, influence on chronic inflammation syndrome (anti-cytokine drugs, etc.) are of great importance for overcoming resistance to epoetin. At critically low hemoglobin, blood transfusions can be used.
Recently, a new group of drugs has been proposed to treat anemia, the so called hypoxia-inducible factor-prolyl hydroxylase inhibitors (HIF-PHIs). HIF-PHIs promote erythropoiesis primarily through increased endogenous EPO production and modulation of iron metabolism. The results of phase 2 and 3 clinical trials have shown their advantages, such as decreased hepcidin levels, better iron utilization and thus less need for iron, the ability to influence the background of inflammation without increasing the dose [113]. These drugs will probably find their use in patients with epoetin-resistant anemia associated with both inflammation and iron metabolism disorders.
In dialysis patients, one can assume the relationship between CHF and recent AVF formation in slight reduction of cardiac output, absence of pulmonary hypertension and other causes of heart failure progression (severe CHD, cardiomyopathy).
After AVF formation, peripheral vascular resistance decreases rapidly, leading to compensatory increase of cardiac output and possibly to acute CHF decompensation. Because of the increase of blood inflow to the heart, the diastolic size of the left ventricleand pulmonary pressure increase [114]. Subsequently, progressing myocardial hypertrophy and dilatation of heart cavities cause diastolic LV dysfunction and CHF development [115]. Pulmonary hypertension, found in 40–50% of patients on HD [116], joins soon after AVF formation and is associated with the size of arterio-venous shunt [117]. The inadequate pulmonary vasodilation in response to the AVF-induced increase in blood flow rate is thought to be caused by decreased NO synthesis in the endothelium or accumulation of uremic NO inhibitors, such as asymmetric dimethyl arginine [118].
In all patients on regular HD, AVF with a large shunt should be considered as a factor aggravating the CHD and CHF development. Normalization of blood flow in AVF can lead to delay in cardiovascular pathology progression. In peripheral bypass syndrome, blood flow and perfusion in the limb distal to the fistula reduce dramatically because of shunt redistribution of blood flow. Less known is coronary bypass syndrome, where left-sided AVF, bypassing the left internal thoracic artery, reduces coronary blood flow, which can lead to myocardial ischemia, especially during the HD session [119].
After the AVF formation, the blood volume increases to maintain a higher cardiac output and can be complicated by severe (refractory) hypertension. In several “preload (end-diastolic pressure)-dependent” dialysis patients, poorly controlled dialysis-induced hypotension accompanies inter-dialysis hypertension in the first 15–20 min of HD even with moderate volumes of UF. Among other complications, fistula infection with outcome in progressing CHF and thromboembolic syndrome provokes prognostically unfavorable bacterial endocarditis.
Thus, AVF, being essentially an iatrogenic vascular anomaly formed to treat HD, can contribute to cardiac mortality. The negative effect of AVF on cardiovascular mortality is directly proportional to blood flow in the fistula and severity of initial cardiovascular pathology. Thus, AVF should not be used in patients with LV ejection fraction <40% and significant pulmonary hypertension. Therefore, the AVF formation should be preceded by cardiac assessment (ECG and Echo-CG monitoring) involving a consultation with a cardiologist.
AVF formation should be planned 2–3 months before the expected start of HD. It is unwise to form AVF a year or more before the start of HD and at Hb levels >12 g/dL because of high risk of fistula thrombosis. Blood flow in the fistula should be targeted at 400–600 ml/min; for blood flow over 800 ml/min, surgical reduction of arterio-venous blood shunt is reasonable. Ultrasonography, venography, and arteriography (fistulography) are used to monitor AVF.
In patients with refractory CHF, CHD with unstable angina, coronary or peripheral bypass syndrome, or severe pulmonary hypertension, AVF ligation with transfer to CAPD is indicated. In endocarditis after removal of infected AVF is recommended temporary transfer of a patient with HD to CAPD or low-flow dialysis, increasing the effectiveness of antibiotic therapy, followed by prosthetic heart valves insertion. PD can be used also for the period of standard AVF formation and maturation instead of AVF with excessive shunt.
Further study is important of cardiorenal relationships in patients on RRT with the isolation of a separate “dialysis-related” type of CRS reflecting the progression of cardiac dysfunction during dialysis treatment. To analyze the features of dialysis CRS, a comprehensive approach should be developed for its treatment and prevention.
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He has published more than 50 papers in journals and 2 books.",institutionString:null,institution:{name:"Universitas Internasional Batam",country:{name:"Indonesia"}}},{id:"314576",title:"Dr.",name:"Ibai",middleName:null,surname:"Laña",slug:"ibai-lana",fullName:"Ibai Laña",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/314576/images/system/314576.jpg",biography:"Dr. Ibai Laña works at TECNALIA as a data analyst. He received his Ph.D. in Artificial Intelligence from the University of the Basque Country (UPV/EHU), Spain, in 2018. He is currently a senior researcher at TECNALIA. His research interests fall within the intersection of intelligent transportation systems, machine learning, traffic data analysis, and data science. He has dealt with urban traffic forecasting problems, applying machine learning models and evolutionary algorithms. He has experience in origin-destination matrix estimation or point of interest and trajectory detection. Working with large volumes of data has given him a good command of big data processing tools and NoSQL databases. He has also been a visiting scholar at the Knowledge Engineering and Discovery Research Institute, Auckland University of Technology.",institutionString:"TECNALIA Research & Innovation",institution:{name:"Tecnalia",country:{name:"Spain"}}},{id:"314575",title:"Dr.",name:"Jesus",middleName:null,surname:"L. Lobo",slug:"jesus-l.-lobo",fullName:"Jesus L. Lobo",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/314575/images/system/314575.png",biography:"Dr. Jesús López is currently based in Bilbao (Spain) working at TECNALIA as Artificial Intelligence Research Scientist. In most cases, a project idea or a new research line needs to be investigated to see if it is good enough to take into production or to focus on it. That is exactly what he does, diving into Machine Learning algorithms and technologies to help TECNALIA to decide whether something is great in theory or will actually impact on the product or processes of its projects. So, he is expert at framing experiments, developing hypotheses, and proving whether they’re true or not, in order to investigate fundamental problems with a longer time horizon. He is also able to design and develop PoCs and system prototypes in simulation. He has participated in several national and internacional R&D projects.\n\nAs another relevant part of his everyday research work, he usually publishes his findings in reputed scientific refereed journals and international conferences, occasionally acting as reviewer and Programme Commitee member. Concretely, since 2018 he has published 9 JCR (8 Q1) journal papers, 9 conference papers (e.g. ECML PKDD 2021), and he has co-edited a book. He is also active in popular science writing data science stories for reputed blogs (KDNuggets, TowardsDataScience, Naukas). Besides, he has recently embarked on mentoring programmes as mentor, and has also worked as data science trainer.",institutionString:"TECNALIA Research & Innovation",institution:{name:"Tecnalia",country:{name:"Spain"}}},{id:"103779",title:"Prof.",name:"Yalcin",middleName:null,surname:"Isler",slug:"yalcin-isler",fullName:"Yalcin Isler",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRyQ8QAK/Profile_Picture_1628834958734",biography:"Yalcin Isler (1971 - Burdur / Turkey) received the B.Sc. degree in the Department of Electrical and Electronics Engineering from Anadolu University, Eskisehir, Turkey, in 1993, the M.Sc. degree from the Department of Electronics and Communication Engineering, Suleyman Demirel University, Isparta, Turkey, in 1996, the Ph.D. degree from the Department of Electrical and Electronics Engineering, Dokuz Eylul University, Izmir, Turkey, in 2009, and the Competence of Associate Professorship from the Turkish Interuniversity Council in 2019.\n\nHe was Lecturer at Burdur Vocational School in Suleyman Demirel University (1993-2000, Burdur / Turkey), Software Engineer (2000-2002, Izmir / Turkey), Research Assistant in Bulent Ecevit University (2002-2003, Zonguldak / Turkey), Research Assistant in Dokuz Eylul University (2003-2010, Izmir / Turkey), Assistant Professor at the Department of Electrical and Electronics Engineering in Bulent Ecevit University (2010-2012, Zonguldak / Turkey), Assistant Professor at the Department of Biomedical Engineering in Izmir Katip Celebi University (2012-2019, Izmir / Turkey). He is an Associate Professor at the Department of Biomedical Engineering at Izmir Katip Celebi University, Izmir / Turkey, since 2019. In addition to academics, he has also founded Islerya Medical and Information Technologies Company, Izmir / Turkey, since 2017.\n\nHis main research interests cover biomedical signal processing, pattern recognition, medical device design, programming, and embedded systems. He has many scientific papers and participated in several projects in these study fields. He was an IEEE Student Member (2009-2011) and IEEE Member (2011-2014) and has been IEEE Senior Member since 2014.",institutionString:null,institution:{name:"Izmir Kâtip Çelebi University",country:{name:"Turkey"}}},{id:"339677",title:"Dr.",name:"Mrinmoy",middleName:null,surname:"Roy",slug:"mrinmoy-roy",fullName:"Mrinmoy Roy",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/339677/images/16768_n.jpg",biography:"An accomplished Sales & Marketing professional with 12 years of cross-functional experience in well-known organisations such as CIPLA, LUPIN, GLENMARK, ASTRAZENECA across different segment of Sales & Marketing, International Business, Institutional Business, Product Management, Strategic Marketing of HIV, Oncology, Derma, Respiratory, Anti-Diabetic, Nutraceutical & Stomatological Product Portfolio and Generic as well as Chronic Critical Care Portfolio. A First Class MBA in International Business & Strategic Marketing, B.Pharm, D.Pharm, Google Certified Digital Marketing Professional. Qualified PhD Candidate in Operations and Management with special focus on Artificial Intelligence and Machine Learning adoption, analysis and use in Healthcare, Hospital & Pharma Domain. Seasoned with diverse therapy area of Pharmaceutical Sales & Marketing ranging from generating revenue through generating prescriptions, launching new products, and making them big brands with continuous strategy execution at the Physician and Patients level. Moved from Sales to Marketing and Business Development for 3.5 years in South East Asian Market operating from Manila, Philippines. Came back to India and handled and developed Brands such as Gluconorm, Lupisulin, Supracal, Absolut Woman, Hemozink, Fabiflu (For COVID 19), and many more. In my previous assignment I used to develop and execute strategies on Sales & Marketing, Commercialization & Business Development for Institution and Corporate Hospital Business portfolio of Oncology Therapy Area for AstraZeneca Pharma India Ltd. Being a Research Scholar and Student of ‘Operations Research & Management: Artificial Intelligence’ I published several pioneer research papers and book chapters on the same in Internationally reputed journals and Books indexed in Scopus, Springer and Ei Compendex, Google Scholar etc. Currently, I am launching PGDM Pharmaceutical Management Program in IIHMR Bangalore and spearheading the course curriculum and structure of the same. I am interested in Collaboration for Healthcare Innovation, Pharma AI Innovation, Future trend in Marketing and Management with incubation on Healthcare, Healthcare IT startups, AI-ML Modelling and Healthcare Algorithm based training module development. I am also an affiliated member of the Institute of Management Consultant of India, looking forward to Healthcare, Healthcare IT and Innovation, Pharma and Hospital Management Consulting works.",institutionString:null,institution:{name:"Lovely Professional University",country:{name:"India"}}},{id:"310576",title:"Prof.",name:"Erick Giovani",middleName:null,surname:"Sperandio Nascimento",slug:"erick-giovani-sperandio-nascimento",fullName:"Erick Giovani Sperandio Nascimento",position:null,profilePictureURL:"https://intech-files.s3.amazonaws.com/0033Y00002pDKxDQAW/ProfilePicture%202022-06-20%2019%3A57%3A24.788",biography:"Prof. Erick Sperandio is the Lead Researcher and professor of Artificial Intelligence (AI) at SENAI CIMATEC, Bahia, Brazil, also working with Computational Modeling (CM) and HPC. He holds a PhD in Environmental Engineering in the area of Atmospheric Computational Modeling, a Master in Informatics in the field of Computational Intelligence and Graduated in Computer Science from UFES. He currently coordinates, leads and participates in R&D projects in the areas of AI, computational modeling and supercomputing applied to different areas such as Oil and Gas, Health, Advanced Manufacturing, Renewable Energies and Atmospheric Sciences, advising undergraduate, master's and doctoral students. He is the Lead Researcher at SENAI CIMATEC's Reference Center on Artificial Intelligence. In addition, he is a Certified Instructor and University Ambassador of the NVIDIA Deep Learning Institute (DLI) in the areas of Deep Learning, Computer Vision, Natural Language Processing and Recommender Systems, and Principal Investigator of the NVIDIA/CIMATEC AI Joint Lab, the first in Latin America within the NVIDIA AI Technology Center (NVAITC) worldwide program. He also works as a researcher at the Supercomputing Center for Industrial Innovation (CS2i) and at the SENAI Institute of Innovation for Automation (ISI Automação), both from SENAI CIMATEC. He is a member and vice-coordinator of the Basic Board of Scientific-Technological Advice and Evaluation, in the area of Innovation, of the Foundation for Research Support of the State of Bahia (FAPESB). He serves as Technology Transfer Coordinator and one of the Principal Investigators at the National Applied Research Center in Artificial Intelligence (CPA-IA) of SENAI CIMATEC, focusing on Industry, being one of the six CPA-IA in Brazil approved by MCTI / FAPESP / CGI.br. He also participates as one of the representatives of Brazil in the BRICS Innovation Collaboration Working Group on HPC, ICT and AI. He is the coordinator of the Work Group of the Axis 5 - Workforce and Training - of the Brazilian Strategy for Artificial Intelligence (EBIA), and member of the MCTI/EMBRAPII AI Innovation Network Training Committee. He is the coordinator, by SENAI CIMATEC, of the Artificial Intelligence Reference Network of the State of Bahia (REDE BAH.IA). He leads the working group of experts representing Brazil in the Global Partnership on Artificial Intelligence (GPAI), on the theme \"AI and the Pandemic Response\".",institutionString:"Manufacturing and Technology Integrated Campus – SENAI CIMATEC",institution:null},{id:"1063",title:"Prof.",name:"Constantin",middleName:null,surname:"Volosencu",slug:"constantin-volosencu",fullName:"Constantin Volosencu",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/1063/images/system/1063.png",biography:"Prof. Dr. Constantin Voloşencu graduated as an engineer from\nPolitehnica University of Timișoara, Romania, where he also\nobtained a doctorate degree. He is currently a full professor in\nthe Department of Automation and Applied Informatics at the\nsame university. Dr. Voloşencu is the author of ten books, seven\nbook chapters, and more than 160 papers published in journals\nand conference proceedings. He has also edited twelve books and\nhas twenty-seven patents to his name. He is a manager of research grants, editor in\nchief and member of international journal editorial boards, a former plenary speaker, a member of scientific committees, and chair at international conferences. His\nresearch is in the fields of control systems, control of electric drives, fuzzy control\nsystems, neural network applications, fault detection and diagnosis, sensor network\napplications, monitoring of distributed parameter systems, and power ultrasound\napplications. He has developed automation equipment for machine tools, spooling\nmachines, high-power ultrasound processes, and more.",institutionString:'"Politechnica" University Timişoara',institution:null},{id:"221364",title:"Dr.",name:"Eneko",middleName:null,surname:"Osaba",slug:"eneko-osaba",fullName:"Eneko Osaba",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/221364/images/system/221364.jpg",biography:"Dr. Eneko Osaba works at TECNALIA as a senior researcher. He obtained his Ph.D. in Artificial Intelligence in 2015. He has participated in more than twenty-five local and European research projects, and in the publication of more than 130 papers. He has performed several stays at universities in the United Kingdom, Italy, and Malta. Dr. Osaba has served as a program committee member in more than forty international conferences and participated in organizing activities in more than ten international conferences. He is a member of the editorial board of the International Journal of Artificial Intelligence, Data in Brief, and Journal of Advanced Transportation. He is also a guest editor for the Journal of Computational Science, Neurocomputing, Swarm, and Evolutionary Computation and IEEE ITS Magazine.",institutionString:"TECNALIA Research & Innovation",institution:{name:"Tecnalia",country:{name:"Spain"}}},{id:"275829",title:"Dr.",name:"Esther",middleName:null,surname:"Villar-Rodriguez",slug:"esther-villar-rodriguez",fullName:"Esther Villar-Rodriguez",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/275829/images/system/275829.jpg",biography:"Dr. Esther Villar obtained a Ph.D. in Information and Communication Technologies from the University of Alcalá, Spain, in 2015. She obtained a degree in Computer Science from the University of Deusto, Spain, in 2010, and an MSc in Computer Languages and Systems from the National University of Distance Education, Spain, in 2012. Her areas of interest and knowledge include natural language processing (NLP), detection of impersonation in social networks, semantic web, and machine learning. Dr. Esther Villar made several contributions at conferences and publishing in various journals in those fields. Currently, she is working within the OPTIMA (Optimization Modeling & Analytics) business of TECNALIA’s ICT Division as a data scientist in projects related to the prediction and optimization of management and industrial processes (resource planning, energy efficiency, etc).",institutionString:"TECNALIA Research & Innovation",institution:{name:"Tecnalia",country:{name:"Spain"}}},{id:"49813",title:"Dr.",name:"Javier",middleName:null,surname:"Del Ser",slug:"javier-del-ser",fullName:"Javier Del Ser",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/49813/images/system/49813.png",biography:"Prof. Dr. Javier Del Ser received his first PhD in Telecommunication Engineering (Cum Laude) from the University of Navarra, Spain, in 2006, and a second PhD in Computational Intelligence (Summa Cum Laude) from the University of Alcala, Spain, in 2013. He is currently a principal researcher in data analytics and optimisation at TECNALIA (Spain), a visiting fellow at the Basque Center for Applied Mathematics (BCAM) and a part-time lecturer at the University of the Basque Country (UPV/EHU). His research interests gravitate on the use of descriptive, prescriptive and predictive algorithms for data mining and optimization in a diverse range of application fields such as Energy, Transport, Telecommunications, Health and Industry, among others. In these fields he has published more than 240 articles, co-supervised 8 Ph.D. theses, edited 6 books, coauthored 7 patents and participated/led more than 40 research projects. He is a Senior Member of the IEEE, and a recipient of the Biscay Talent prize for his academic career.",institutionString:"Tecnalia Research & Innovation",institution:{name:"Tecnalia",country:{name:"Spain"}}},{id:"278948",title:"Dr.",name:"Carlos Pedro",middleName:null,surname:"Gonçalves",slug:"carlos-pedro-goncalves",fullName:"Carlos Pedro Gonçalves",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRcmyQAC/Profile_Picture_1564224512145",biography:'Carlos Pedro Gonçalves (PhD) is an Associate Professor at Lusophone University of Humanities and Technologies and a researcher on Complexity Sciences, Quantum Technologies, Artificial Intelligence, Strategic Studies, Studies in Intelligence and Security, FinTech and Financial Risk Modeling. He is also a progammer with programming experience in:\n\nA) Quantum Computing using Qiskit Python module and IBM Quantum Experience Platform, with software developed on the simulation of Quantum Artificial Neural Networks and Quantum Cybersecurity;\n\nB) Artificial Intelligence and Machine learning programming in Python;\n\nC) Artificial Intelligence, Multiagent Systems Modeling and System Dynamics Modeling in Netlogo, with models developed in the areas of Chaos Theory, Econophysics, Artificial Intelligence, Classical and Quantum Complex Systems Science, with the Econophysics models having been cited worldwide and incorporated in PhD programs by different Universities.\n\nReceived an Arctic Code Vault Contributor status by GitHub, due to having developed open source software preserved in the \\"Arctic Code Vault\\" for future generations (https://archiveprogram.github.com/arctic-vault/), with the Strategy Analyzer A.I. module for decision making support (based on his PhD thesis, used in his Classes on Decision Making and in Strategic Intelligence Consulting Activities) and QNeural Python Quantum Neural Network simulator also preserved in the \\"Arctic Code Vault\\", for access to these software modules see: https://github.com/cpgoncalves. He is also a peer reviewer with outsanding review status from Elsevier journals, including Physica A, Neurocomputing and Engineering Applications of Artificial Intelligence. Science CV available at: https://www.cienciavitae.pt//pt/8E1C-A8B3-78C5 and ORCID: https://orcid.org/0000-0002-0298-3974',institutionString:"University of Lisbon",institution:{name:"Universidade Lusófona",country:{name:"Portugal"}}},{id:"241400",title:"Prof.",name:"Mohammed",middleName:null,surname:"Bsiss",slug:"mohammed-bsiss",fullName:"Mohammed Bsiss",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/241400/images/8062_n.jpg",biography:null,institutionString:null,institution:null},{id:"276128",title:"Dr.",name:"Hira",middleName:null,surname:"Fatima",slug:"hira-fatima",fullName:"Hira Fatima",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/276128/images/14420_n.jpg",biography:"Dr. Hira Fatima\nAssistant Professor\nDepartment of Mathematics\nInstitute of Applied Science\nMangalayatan University, Aligarh\nMobile: no : 8532041179\nhirafatima2014@gmal.com\n\nDr. Hira Fatima has received his Ph.D. degree in pure Mathematics from Aligarh Muslim University, Aligarh India. Currently working as an Assistant Professor in the Department of Mathematics, Institute of Applied Science, Mangalayatan University, Aligarh. She taught so many courses of Mathematics of UG and PG level. Her research Area of Expertise is Functional Analysis & Sequence Spaces. She has been working on Ideal Convergence of double sequence. She has published 17 research papers in National and International Journals including Cogent Mathematics, Filomat, Journal of Intelligent and Fuzzy Systems, Advances in Difference Equations, Journal of Mathematical Analysis, Journal of Mathematical & Computer Science etc. She has also reviewed few research papers for the and international journals. She is a member of Indian Mathematical Society.",institutionString:null,institution:null},{id:"414880",title:"Dr.",name:"Maryam",middleName:null,surname:"Vatankhah",slug:"maryam-vatankhah",fullName:"Maryam Vatankhah",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Borough of Manhattan Community College",country:{name:"United States of America"}}},{id:"414879",title:"Prof.",name:"Mohammad-Reza",middleName:null,surname:"Akbarzadeh-Totonchi",slug:"mohammad-reza-akbarzadeh-totonchi",fullName:"Mohammad-Reza Akbarzadeh-Totonchi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Ferdowsi University of Mashhad",country:{name:"Iran"}}},{id:"414878",title:"Prof.",name:"Reza",middleName:null,surname:"Fazel-Rezai",slug:"reza-fazel-rezai",fullName:"Reza Fazel-Rezai",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"American Public University System",country:{name:"United States of America"}}},{id:"426586",title:"Dr.",name:"Oladunni A.",middleName:null,surname:"Daramola",slug:"oladunni-a.-daramola",fullName:"Oladunni A. Daramola",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Federal University of Technology",country:{name:"Nigeria"}}},{id:"357014",title:"Prof.",name:"Leon",middleName:null,surname:"Bobrowski",slug:"leon-bobrowski",fullName:"Leon Bobrowski",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Bialystok University of Technology",country:{name:"Poland"}}},{id:"302698",title:"Dr.",name:"Yao",middleName:null,surname:"Shan",slug:"yao-shan",fullName:"Yao Shan",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Dalian University of Technology",country:{name:"China"}}},{id:"354126",title:"Dr.",name:"Setiawan",middleName:null,surname:"Hadi",slug:"setiawan-hadi",fullName:"Setiawan Hadi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Padjadjaran University",country:{name:"Indonesia"}}},{id:"125911",title:"Prof.",name:"Jia-Ching",middleName:null,surname:"Wang",slug:"jia-ching-wang",fullName:"Jia-Ching Wang",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"National Central University",country:{name:"Taiwan"}}},{id:"332603",title:"Prof.",name:"Kumar S.",middleName:null,surname:"Ray",slug:"kumar-s.-ray",fullName:"Kumar S. Ray",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Indian Statistical Institute",country:{name:"India"}}},{id:"415409",title:"Prof.",name:"Maghsoud",middleName:null,surname:"Amiri",slug:"maghsoud-amiri",fullName:"Maghsoud Amiri",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Allameh Tabataba'i University",country:{name:"Iran"}}},{id:"357085",title:"Mr.",name:"P. Mohan",middleName:null,surname:"Anand",slug:"p.-mohan-anand",fullName:"P. Mohan Anand",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Indian Institute of Technology Kanpur",country:{name:"India"}}},{id:"356696",title:"Ph.D. Student",name:"P.V.",middleName:null,surname:"Sai Charan",slug:"p.v.-sai-charan",fullName:"P.V. Sai Charan",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Indian Institute of Technology Kanpur",country:{name:"India"}}},{id:"357086",title:"Prof.",name:"Sandeep K.",middleName:null,surname:"Shukla",slug:"sandeep-k.-shukla",fullName:"Sandeep K. Shukla",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Indian Institute of Technology Kanpur",country:{name:"India"}}}]}},subseries:{item:{id:"22",type:"subseries",title:"Applied Intelligence",keywords:"Machine Learning, Intelligence Algorithms, Data Science, Artificial Intelligence, Applications on Applied Intelligence",scope:"This field is the key in the current industrial revolution (Industry 4.0), where the new models and developments are based on the knowledge generation on applied intelligence. The motor of the society is the industry and the research of this topic has to be empowered in order to increase and improve the quality of our lives.",coverUrl:"https://cdn.intechopen.com/series_topics/covers/22.jpg",hasOnlineFirst:!0,hasPublishedBooks:!0,annualVolume:11418,editor:{id:"27170",title:"Prof.",name:"Carlos",middleName:"M.",surname:"Travieso-Gonzalez",slug:"carlos-travieso-gonzalez",fullName:"Carlos Travieso-Gonzalez",profilePictureURL:"https://mts.intechopen.com/storage/users/27170/images/system/27170.jpeg",biography:"Carlos M. Travieso-González received his MSc degree in Telecommunication Engineering at Polytechnic University of Catalonia (UPC), Spain in 1997, and his Ph.D. degree in 2002 at the University of Las Palmas de Gran Canaria (ULPGC-Spain). He is a full professor of signal processing and pattern recognition and is head of the Signals and Communications Department at ULPGC, teaching from 2001 on subjects on signal processing and learning theory. His research lines are biometrics, biomedical signals and images, data mining, classification system, signal and image processing, machine learning, and environmental intelligence. He has researched in 52 international and Spanish research projects, some of them as head researcher. He is co-author of 4 books, co-editor of 27 proceedings books, guest editor for 8 JCR-ISI international journals, and up to 24 book chapters. He has over 450 papers published in international journals and conferences (81 of them indexed on JCR – ISI - Web of Science). He has published seven patents in the Spanish Patent and Trademark Office. He has been a supervisor on 8 Ph.D. theses (11 more are under supervision), and 130 master theses. He is the founder of The IEEE IWOBI conference series and the president of its Steering Committee, as well as the founder of both the InnoEducaTIC and APPIS conference series. He is an evaluator of project proposals for the European Union (H2020), Medical Research Council (MRC, UK), Spanish Government (ANECA, Spain), Research National Agency (ANR, France), DAAD (Germany), Argentinian Government, and the Colombian Institutions. He has been a reviewer in different indexed international journals (<70) and conferences (<250) since 2001. He has been a member of the IASTED Technical Committee on Image Processing from 2007 and a member of the IASTED Technical Committee on Artificial Intelligence and Expert Systems from 2011. \n\nHe has held the general chair position for the following: ACM-APPIS (2020, 2021), IEEE-IWOBI (2019, 2020 and 2020), A PPIS (2018, 2019), IEEE-IWOBI (2014, 2015, 2017, 2018), InnoEducaTIC (2014, 2017), IEEE-INES (2013), NoLISP (2011), JRBP (2012), and IEEE-ICCST (2005)\n\nHe is an associate editor of the Computational Intelligence and Neuroscience Journal (Hindawi – Q2 JCR-ISI). 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We encourage the submission of manuscripts that provide novel and mechanistic insights that report significant advances in the fields. Topics can include but are not limited to: Biotechnology such as biotechnological products and process engineering; Biotechnologically relevant enzymes and proteins; Bioenergy and biofuels; Applied genetics and molecular biotechnology; Genomics, transcriptomics, proteomics; Applied microbial and cell physiology; Environmental biotechnology; Methods and protocols. Moreover, topics in biosensor technology, like sensors that incorporate enzymes, antibodies, nucleic acids, whole cells, tissues and organelles, and other biological or biologically inspired components will be considered, and topics exploring transducers, including those based on electrochemical and optical piezoelectric, thermal, magnetic, and micromechanical elements. Chapters exploring biomaterial approaches such as polymer synthesis and characterization, drug and gene vector design, biocompatibility, immunology and toxicology, and self-assembly at the nanoscale, are welcome. Finally, the tissue engineering subcategory will support topics such as the fundamentals of stem cells and progenitor cells and their proliferation, differentiation, bioreactors for three-dimensional culture and studies of phenotypic changes, stem and progenitor cells, both short and long term, ex vivo and in vivo implantation both in preclinical models and also in clinical trials.",annualVolume:11405,isOpenForSubmission:!0,coverUrl:"https://cdn.intechopen.com/series_topics/covers/9.jpg",editor:{id:"126286",title:"Dr.",name:"Luis",middleName:"Jesús",surname:"Villarreal-Gómez",fullName:"Luis Villarreal-Gómez",profilePictureURL:"https://mts.intechopen.com/storage/users/126286/images/system/126286.jpg",institutionString:null,institution:{name:"Autonomous University of Baja California",institutionURL:null,country:{name:"Mexico"}}},editorTwo:null,editorThree:null,editorialBoard:[{id:"35539",title:"Dr.",name:"Cecilia",middleName:null,surname:"Cristea",fullName:"Cecilia Cristea",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYQ65QAG/Profile_Picture_1621007741527",institutionString:null,institution:{name:"Iuliu Hațieganu University of Medicine and Pharmacy",institutionURL:null,country:{name:"Romania"}}},{id:"40735",title:"Dr.",name:"Gil",middleName:"Alberto Batista",surname:"Gonçalves",fullName:"Gil Gonçalves",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYRLGQA4/Profile_Picture_1628492612759",institutionString:null,institution:{name:"University of Aveiro",institutionURL:null,country:{name:"Portugal"}}},{id:"211725",title:"Associate Prof.",name:"Johann F.",middleName:null,surname:"Osma",fullName:"Johann F. 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