Abstract

Although well documented drug therapies are available for the management of ventricular hypertrophy (VH) and heart failure (HF), most patients nonetheless experience a downhill course, and further therapeutic measures are needed. Nutraceutical, dietary, and lifestyle measures may have particular merit in this regard, as they are currently available, relatively safe and inexpensive, and can lend themselves to primary prevention as well. A consideration of the pathogenic mechanisms underlying the VH/HF syndrome suggests that measures which control oxidative and endoplasmic reticulum (ER) stress, that support effective nitric oxide and hydrogen sulfide bioactivity, that prevent a reduction in cardiomyocyte pH, and that boost the production of protective hormones, such as fibroblast growth factor 21 (FGF21), while suppressing fibroblast growth factor 23 (FGF23) and marinobufagenin, may have utility for preventing and controlling this syndrome. Agents considered in this essay include phycocyanobilin, N-acetylcysteine, lipoic acid, ferulic acid, zinc, selenium, ubiquinol, astaxanthin, melatonin, tauroursodeoxycholic acid, berberine, citrulline, high-dose folate, cocoa flavanols, hawthorn extract, dietary nitrate, high-dose biotin, soy isoflavones, taurine, carnitine, magnesium orotate, EPA-rich fish oil, glycine, and copper. The potential advantages of whole-food plant-based diets, moderation in salt intake, avoidance of phosphate additives, and regular exercise training and sauna sessions are also discussed. There should be considerable scope for the development of functional foods and supplements which make it more convenient and affordable for patients to consume complementary combinations of the agents discussed here. Research Strategy: Key word searching of PubMed was employed to locate the research papers whose findings are cited in this essay.

Highlights

  • Well documented drug therapies are available for the management of ventricular hypertrophy (VH) and heart failure (HF), most patients experience a downhill course, and further therapeutic measures are needed

  • It compromises the swift systolic rise and rapid diastolic rise of intracellular free calcium, leading to decreased efficiency of contraction and relaxation, as well as an increased risk for arrhythmias. This is associated with a depletion of calcium in the sarcoplasmic reticulum, giving rise to endoplasmic reticulum (ER) stress, a mediator of the cardiomyocyte apoptosis that contributes to progressive heart failure

  • This pathological stew, which is self-reinforcing in many ways, is typically triggered by chronic mechanical strain—induced by uncontrolled hypertension, volume overload, valvular stenosis or failure, or loss of viable myocardium following myocardial infarctions or infections—and neurohormonal stimuli associated with the systemic stress reaction and/or kidney failure, such as adrenergic activity, angiotensin II, endothelin, and fibroblast growth factor 23 (FGF23)

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Summary

Sketch of the Pathogenesis of Ventricular Hypertrophy and Heart Failure

Ventricular hypertrophy (VH) progressing to heart failure (HF) is considered the leading cause of death in the U.S today. PKG, via phosphorylation of the G protein RhoA, blunts the ability of mechanical strain to promote cardiomyocyte synthesis and release of TGFβ and connective tissue growth factor (CTGF), which act in a paracrine manner on cardiac fibroblasts to trigger cardiac fibrosis; loss of effective NO bioactivity makes a key contribution to the pathogenesis of HFpEF, both by promotion of cardiac fibrosis and by loss of lusitropic activity [49,50,69]. Flow-mediated dilation tends to be impaired in heart failure owing the reduction in pulsatile shear associated with decreased cardiac output; episodic increases in shear stress associated with exercise training or regular sauna sessions help to correct this problem [73,74,75] For all of these reasons, measures which support efficient NOS activity can be beneficial in VH/HF. Other measures which appear likely to be beneficial include: optimizing magnesium (Mg) status; supplementing with taurine, carnitine, copper, and orotate; a whole-food plant-based diet, low in saturated fats, moderate in salt, and rich in potassium; regular exercise training; and sauna

Attenuating Oxidative Stress
Inhibiting ER Stress
Optimizing Omega-3 Status
Protective Diet and Lifestyle Measures
Findings
Summing Up
Full Text
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