Syndromes of cardiac cachexia and the cachectic heart: Current perspective

Abstract

T HE HUMAN HEART can be described as a chemodynamic machine that liberates energy stored in carbon-carbon and carbonhydrogen bonds of substrate fuels, such as carbohydrates, proteins, and fat, and uses this energy to perform the mechanical work positively and efficiently.’ In order to perform this task the human heart relies heavily on a reciprocal state of normal interdependence between its own nutritional state and that of the host. Any disturbance or aberration of this normal interdependence, such as hyperlipidemia, hypertension, alcohol abuse, and malnutrition, can result in disease states such as aortocoronary atherosclerosis, hypertensive cardiovascular disease, alcoholic cardiomyopathy, and nutritional cardiomyopathy. The purpose of this article is not to discuss the above-mentioned disease entities, regarding which an exhaustive amount of literature is already available. Instead, the intention is to discuss the diagnosis, recent developments in the pathogenesis, and management of cardiac cachexia and the cachectic heart. Normally, loss or gain of weight, body fat, and body mass results from an imbalance between energy intake and expenditure.2 However, for several decades it has been known that patients with chronic congestive cardiac failure (CCHF) with a prominent right-sided component may suffer from a symptom complex known as syndrome of cardiac cachexia (SOCC), evidenced by weight loss and wasting of body fat and lean body mass. Its precise pathogenesis and where the imbalance of energy intake and expenditure lies remain obscure, but the incidence and severity of resulting cachexia usually bears a direct relationship to the duration and the severity of underlying heart disease that is usually valvular in etiology. Similarly, patients with malignant epithelial and mesenchymal tumors, malignant lymphoma, far advanced pulmonary tuberculosis, advanced cirrhosis of liver, and severe malnutrition resulting from malabsorption of any cause also suffer severe weight loss and wasting of body fat and lean body mass due to calorie expenditure presumably exceeding the intake,3 and this pathologic process does not spare the cardiovascular system. The latter observation is contrary to the past notions of several noted physiologists who not only maintained but also preserved the long-standing myth that the human heart is resistant to chronic malnutrition and does not undergo atrophy and degeneration easily, as do other organs of the body.4 This earlier concept probably evolved from an erroneous belief. that “nature protects the most vital organs,” ie, the heart and brain, during chronic malnutrition. Though philosophically and theologically attractive, this concept is not supported by the clinicopathologic observations of the syndrome of the cachectic heart (SOCH). This entity, when first described in 1968 by Burch et al,’ was defined as an acquired pathologic decrease in the size and mass of the heart along with a decrease in the epicardial fat with little or no aortocoronary atherosclerosis. Certain clinical, ECG, roentgenographic, and pathologic correlations were required for the diagnosis to be made. Even though the terminology used to define SOCC and SOCH is sufficiently distinctive and descriptive, the possibility for confusion between them exists due to certain unavoidable overlapping terms. In order to avoid such confusion, the basic ingredients and concepts of these two different and distinct syndromes, which in author’s view represent two unique and fascinating experiments of nature, are schematically illustrated in Fig 1.