The Biochemistry of Myocardial Failure

Abstract

Almost twenty years ago, Richard Bing and colleagues [1] addressed the question, “What is cardiac failure?” These authors concluded that we had no answer to this question, partly because of limitations in our techniques, but more likely because there is not one single answer to the complex array of changes associated with the heart’s failure to pump blood. Recently, Mall and O’Rourke [2] noted that the relationship between biochemical changes and depressed myocardial contractility associated with failure remain unclear and a subject of continuing investigation. Despite tremendous advances in techniques and knowledge, our understanding of the fundamental biochemical mechanisms underlying myocardial contractile function and its regulation is still limited. These limitations make the understanding of myocardial failure all the more difficult and congestive heart failure continues to be a major clinical problem [3]. Although major deficiencies still exist in our knowledge of cause and effect relationships between biochemical “defects” and myocardial failure, it is clear that prolonged hemodynamic stress leads to decreased myocardial contractility [4]. Sustained hemodynamic stress can be caused by a variety of factors including hypertension, valvular heart disease and loss of functional myocardium following ischemic injury. Clinical congestive heart failure, in the vast majority of cases, results from hypertensive or coronary artery disease (ischemic injury). The focus of this chapter will be on those biochemical changes related to these two general types of hemodynamic stress.