Cardiovascular Endocrinology

Cardiovascular disease (CVD) is a major cause of morbidity and mortality all over the world. Despite growing knowledge about the origins of CVD, only a modest decrease in cardiovascular mortality, as a percentage of total mortality, has been found in recent decades. Several factors have been proposed to explain this trend in the epidemiology of CVD, such as adaptation of a Western lifestyle and the abundant availability of dietary calories. Cardiovascular prevention programs that should decrease the occurrence of cardiovascular disease have less than expected results: Initial decrease in smoking behavior is again growing among young individuals, with weight gain and, subsequently, an alarming growth in obesity. Moreover, patients who have classic risk factors, such as hypertension and dyslipidemia, are still insufficiently treated, leading the intervention programs to consequently have a smaller effect. Most CVD programs focus on atherosclerotic disease and its direct consequences on restenosis, and on reevents of ischemic coronary artery disease. However, a shift in cardiovascular morbidity and mortality is observed in a trend away from acute ischemic coronary artery disease toward a more chronic cardiovascular disease, such as heart failure. Recently, better treatment options for complications related to acute ischemic coronary disease were introduced, such as fibrinolytic therapy, use of coronary stents events, and emergency percutaneous transluminal coronary arteriography. In contrast to primary and secondary prevention programs that act through reducing effects of classical atherogenic risk factors, additional processes are involved in chronic heart disease concerning, for example, remodeling of damaged cardiac muscle. More insight is obtained from recent studies about biological processes that are part of the origin of remodeling and adaptation in cardiac performance, such as paracrine and autocrine growth factors and components of hormonal systems. Indeed, these factors within cardiac tissue are closely integrated in several adaptive processes that have an effect on heart and hemodynamic properties. This progress in research creates an increase in cross talk between distinct clinical departments, such as endocrinology, internal medicine, and cardiology, with a subsequent development of research and clinical programs that cross classic clinical borders. These academic initiatives could be organized within a medical infrastructure named cardiovascular endocrinology. Recent progress in molecular biology offers us novel tools to create new therapeutic strategies and to redefine in more detail the origin of CV diseases. Elucidation of involved genes and related proteins that participate in cardiac physiology enable us to learn more about future interventions to treat heart failure and atherosclerotic disease more efficiently. Indeed, more sensitive techniques showed, for example, the role of apoptosis and postnatal differentiation of functional tissues in the pathophysiological processes involved in remodeling heart muscle, with regeneration of damaged regions in the left ventricular muscle. The recent clinical introduction of brain natriuretic peptide in risk stratification and in evaluation of treatment in the clinical follow-up of patients with heart failure may serve as an example of applying knowledge concerning cardiac adaptation and secretion of paracrine cardiac neuropeptides. Most pathology that is related to coronary arteries found its origin in atherosclerotic disease. For a long time, disturbances in lipid metabolism were considered to be a key factor in atherogenesis. In these atherogenic processes, lipids (such as oxidized low-density lipoprotein cholesterol and native lipoprotein remnants) were thought to act as a toxificans. However, recent insights reveal that paracrine actions of cholesterol esters (a component of which are low-density lipoprotein cholesterol particles), in the maturation and differentiation of fibroblasts and precursor cells, are involved in atherogenesis. Interestingly, a role of cholesterol as a paracrine growth factor was already recognized early in prenatal life in embryonic development. Deficiencies in cholesterol in embryonic growth fields result in disturbances in the development of functional tissues. Perhaps the early effects of lipid-lowering drugs (after only 30 days) on atherosclerotic plaques and mortality after an ischemic event, called a pleiotropic effect, could be explained by these kinds of metabolic pathways.