Cardiovascular Disease - Cardiomyopathy (Heart Failure)

Congestive heart failure (CHF), congestive cardiac failure (CCF) or just heart failure, is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood through the body. It is not to be confused with "cessation of heartbeat", which is known as asystole, or with cardiac arrest, which is the cessation of normal cardiac function with subsequent hemodynamic collapse leading to death.

Cardiomyopathy, which literally means "heart muscle disease", is the deterioration of the function of the myocardium (i.e., the actual heart muscle) for any reason. People with cardiomyopathy are often at risk of arrhythmia or sudden cardiac death or both

Cardiomyopathy has a number of causes including drug and alcohol toxicity, certain infections (including Hepatitis C), and various genetic and idiopathic (i.e., unknown) causes. Cardiomyopathies are generally classified into four type, but additional types are also recognized:

• Dilated cardiomyopathy (DCM), the most common form, and one of the leading indications for heart transplantation. In DCM the heart (especially the left ventricle) is enlarged and the pumping function is diminished. Approximately 40% of cases are familial, but the genetics are poorly understood compared with HCM. In some cases it manifests as peripartum cardiomyopathy, and in other cases it may be associated with alcoholism.
• Hypertrophic cardiomyopathy (HCM or HOCM), a genetic disorder caused by various mutations in genes encoding sarcomeric proteins. In HCM the heart muscle is thickened, which can obstruct blood flow and prevent the heart from functioning properly.
• Arrhythmogenic right ventricular cardiomyopathy (ARVC) arises from an electrical disturbance of the heart in which heart muscle is replaced by fibrous scar tissue. The right ventricle is generally most affected.
• Restrictive cardiomyopathy (RCM) is an uncommon cardiomyopathy. The walls of the ventricles are stiff, but may not be thickened, and resist the normal filling of the heart with blood. A rare form of restrictive cardiomyopathy is the obliterative cardiomyopathy, seen in the hypereosinophilic syndrome. In this type of cardiomyopathy, the myocardium in the apices of the left and right ventricles becomes thickened and fibrotic, causing a decrease in the volumes of the ventricles and a type of restrictive cardiomyopathy.
• Noncompaction cardiomyopathy has been recognized as a separate type since the 1980s. The term refers to a cardiomyopathy where the left ventricle wall has failed to grow properly from birth and has a spongy appearance when viewed during an echocardiogram.

Source: Wikipedia

Conditioned nutritional requirements: therapeutic relevance to heart failure

Herz. 2002 Mar;27(2):174-8

Sole MJ, Jeejeebhoy KN.

BACKGROUND: The advent of disease, genetic predisposition or certain drug therapies may significantly alter the nutritional demands of specific organs. Several specific metabolic deficiencies have been found in the failing myocardium: (1) a reduction in L-carnitine, coenzyme Q10, creatine, and thiamine--nutrient cofactors important for myocardial energy production; (2) a relative deficiency of taurine, an amino acid integral to intracellular calcium homeostasis; (3) increased myocardial oxidative stress and a reduction of antioxidant defenses. Deficiencies of carnitine or taurine alone are well documented to result in dilated cardiomyopathy in animals and humans. Each of these deficiencies is amenable to restoration through dietary supplementation. A variety of nutrients have been investigated as single therapeutic agents in pharmacologic fashion, but there has been no broad-based approach to nutritional supplementation in congestive heart failure to correct this complex of metabolic abnormalities. METHOD AND RESULTS: We have demonstrated deficiencies in carnitine, taurine and coenzyme Q10 in cardiomyopathic hamster hearts during the late stage of the cardiomyopathy. In another study, we randomized placebo diet against a supplement containing taurine, coenzyme Q10, carnitine, thiamine, creatine, vitamin E, vitamin C, and selenium to cardiomyopathic hamsters during the late stages of the disease. Supplementation for 3 months markedly improved myocyte sarcomeric structure, developed pressure, +dp/dt, and -dp/dt. We also documented carnitine, taurine and coenzyme Q10 in biopsies taken from human failing hearts, the levels correlating with ventricular function. A double-blind, randomized, placebo-controlled trial of a supplement containing these nutrients, given for 30 days, restored myocardial levels and resulted in a significant decrease in left ventricular end-diastolic volume. CONCLUSION: These experiments suggest that a comprehensive restoration of adequate myocyte nutrition may be important to any therapeutic strategy designed to benefit patients suffering from congestie heart failure. Future studies in this area are of clinical importance.

Publication Types:

• Review

The management of conditioned nutritional requirements in heart failure

Heart Fail Rev. 2006 Mar;11(1):75-82

Allard ML, Jeejeebhoy KN, Sole MJ.

Patients suffering from congestive heart failure exhibit impaired myocardial energy production, myocyte calcium overload and increased oxidative stress. Nutritional factors known to be important for myocardial energy production, calcium homeostasis and the reduction of oxidative stress, such as thiamine, riboflavin, pyridoxine, L-carnitine, coenzyme Q10, creatine and taurine are reduced in this patient population. Furthermore, deficiencies of taurine, carnitine, and thiamine are established primary causes of dilated cardiomyopathy.Studies in animals and limited trials in humans have shown that dietary replacement of some of these compounds in heart failure can significantly restore depleted levels and may result in improvement in myocardial structure and function as well as exercise capacity. Larger scale studies examining micronutrient depletion in heart failure patients, and the benefits of dietary replacement need to be performed. At the present time, it is our belief that these conditioned nutritional requirements, if unsatisfied, contribute to myocyte dysfunction and loss; thus, restoration of nutritional deficiencies should be part of the overall therapeutic strategy for patients with congestive heart failure.

Publication Types:

• Review

The importance of lost minerals in heart failure

Cardiovasc Hematol Agents Med Chem. 2007 Oct;5(4):295-9

Newman KP, Neal MT, Roberts M, Goodwin KD, Hatcher EA, Bhattacharya SK.

The clinical syndrome congestive heart failure (CHF) has its origins rooted in a salt-avid state mediated largely by effector hormones of the renin-angiotensin-aldosterone system (RAAS). In addition, a systemic illness accompanies chronic RAAS activation. Its features include: the presence of oxidative stress in diverse tissues coupled with a reduction in activity of endogenous oxidoreductases, such as Cu/Zn-superoxide dismutase and Se-glutathione peroxidase; a proinflammatory phenotype with activated immune cells and increased circulating levels of proinflammatory cytokines; and a catabolic state with loss of soft tissues and bone that eventuates in a wasting syndrome termed cardiac cachexia. Pathogenic mechanisms and pathophysiologic expressions of this illness are under active investigation. In this context and less well appreciated is the importance of a dyshomeostasis of various minerals, including Ca2+, Mg2+, Zn, and Se, and their impact on the systemic and progressive nature of CHF. A convergence of multiple factors, some hormonal (e.g., aldosteronism, secondary hyperparathyroidism, hypovitaminosis D), others pharmacologic (e.g., loop diuretics, angiotensin-converting enzyme inhibitors), predispose to the heightened excretion of these minerals in urine and feces while parathyroid hormone promotes intracellular Ca2+ overloading in diverse tissues. The importance of these macro- and micronutrients to the appearance of oxidative stress, compromised antioxidant defenses, an immunostimulatory state and tissue wasting needs to be critically addressed. So, too, must the potential for nutriceuticals, complementary to today's

Publication Types:

• Review

Publication Types:

• Review