Editorial: How to Treat — The Hemodynamic Approach

Abstract

The prognosis of patients with congestive heart failure can be estimated by clinical symptomatology, left ventricular volume and ejection fraction, complex ventricular arrhythmias, and neuroendocrine activation. The cause of heart failure may be biochemical abnormalities of the myocytes responsible for the depressed contractility, which may involve alterations in the receptor population and regulatory proteins, changes in the properties of the sarcolemma and sarcoplasmatic reticulum, and unfavourable alterations of mitochondrial function. The structural basis of the ventricle is also influenced by changes in the non-myocyte compartment, the interstitium and intramural coronary vasculature. Remodeling of the existing fibrillar collagen network and disproportionate accumulation of collagen in the interstitium and around intramyocardial coronary arteries may have important implications for ventricular function, influencing the geometry of the ventricle and diastolic and systolic myocardial stiffness. A third important factor in heart failure, especially with regard to exercise capacity, is blood flow to the vasculature of exercising skeletal muscle, which is reduced by several factors the nature of which is not precisely defined. The most promising therapeutic approach to congestive heart failure is use of angiotensin converting enzyme inhibitors, which due to their multiple sites of action interfere with some of the above-mentioned mechanisms, thereby significantly improving exercise capacity, well-being, and prognosis of patients with heart failure.