Nd-stage heart failure and cancer are associated with wasting syndrome, an I irreversible catabolic state involving I complex interaction between immune and neurohumoral factors. In heart failure, where it is also known as cardiac cachexia, it is characterized clinically by anorexia, malnutrition, muscle wasting, reduced bone mass, and impaired performance. It is associated with multiple neurohumoral, cytokine, and catabolic abnormalities.
Tissue loss in heart failure
Patients with cardiac cachexia show major changes in key tissues such as muscle, fat, and bone. Limb muscle mass is strikingly reduced; the microscopic and ultra-structural changes in the muscle fibers favor anaerobic metabolism. Whereas fat tissue increases in noncachec-tic patients with heart failure, it decreases in cachexia, reducing energy reserves. The reductions in bone mass and bone density expose patients to osteoporosis.
The catabolic effects are associated with profound neurohumoral changes. The increased lipolysis and resting metabolic rate observed in these patients could be explained by the increased plasma levels of catecholamines and cortisol, and a reduced insulin drive (decreased inhibition of free fatty acid release from adipose tissue and absence of protein anabolism).
Cytokine inflammatory activation
Given the overlap between the clinical characteristics of cardiac and malignant cachexia, the similarities in the underlying cytokine inflammatory response come as no surprise. Table I lists the cytokines involved in cardiac cachexia and their catabolic effects. Thus, wasting syndrome is a significant feature of end-stage cardiac failure, with neurohumoral and cytokine activation playing a major role in the catabolism affecting the major tissue groups.
Tumor necrosis factor-a (TNF-a) Soluble TNF receptor I (sTNFR-I)4Interleukin-1 Interleukin-6
Muscle wasting and fat loss Muscle wasting and fat loss Muscle catabolism Osteoclastogenesis
Table I. Wasting syndrome cytokines and their tissue effects.
“Anker et al showed significant correlations between increases in TNF-a and sTNFR-I levels and decreases in muscle, fat, and bone mass.
Aypertrophic cardiomyopathy (HCM) progresses to nonobstructive left ventricular dilatation and dysfunction in 10% to 15% of patients, particularly in those with marked septal hypertrophy, and generally carries a poor prognosis. Biventricular systolic dysfunction eventually develops due to myocardial fibrosis (end-stage HCM), as a result either of fibrous transformation of the loose intercellular connective tissue interspersed between areas of myocyte disarray, or of myocardial ischemia and infarction due to small-vessel disease more rarely, it results from concomitant coronary artery disease. Myocardial fibrosis causes wall thinning, loss of outflow obstruction, uncoordinated and impaired systolic function with a decreased ejection fraction, and increased end-systolic volume. Ventricular dilatation
Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A Textbook of Cardiovascular Medicine. 6tfi ed. Philadelphia, Pa: WB Saunders Co; 2001.1769. Spirit© P, Seidman CE, McKenna WJ, Maron BJ. The management of hypertrophic cardiomyopathy. N Engl J Med. 1997;336:775-785. is usually moderate, less than in typical dilated cardiomyopathy.
The treatment of end-stage nonobstructive HCM differs diametrically from that of obstructive HCM, where negative inotropes are indicated to decrease obstruction, and digitalis, diuretics, and afterload reduction are contraindicated because they increase obstruction. End-stage nonobstructive HCM requires digitalis, diuretics, and afterload reduction; negative inotropes such as verapamil are contraindicated. In obstructive HCM, patients refractory to medical therapy require dual-chamber pacing or myomectomy. In end-stage nonobstructive HCM, on the other hand, the pacemaker indication is purely electrophysiologi-cal; within the broad spectrum of the disease, such patients are ultimately the only potential candidates for heart transplantation.
Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment. Circulation. 1995;92:1680-1692.
pathophysiology; hypertrophic cardiomyopathy; left ventricular dilatation; treatment
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