Hansjorg Just – författare

The myocardium in heart failure: Cellular and subcellular alterations in the failing human myocardium. H. Just Medizinische Universitatsklinik Freiburg i. Br., Innere Medizin III - Kardiologie, FRG The syndrome of heart failure continues to be a major challenge to clinicians and scientists. Incidence and mortality of the disease are high, the patient is disabled, and is permanently threatened by the high morbidity and mortality. The clinician faces a syndrome of complex pathophysiology. Multiple causes or underlying disorders of the heart have to be differentiated from heart failure itself, which often results in exceedingly difficult diagnoses. Likewise, prognostication meets with difficulties due to problems in separating influences of the underlying disease and the heart failure syndrome itself. In chronic refractory failure annual mortality may exceed 50%. If aortic stenosis or ischemic cardiomyopathy with main­ stem lesions are present, this percentage may be even higher. The situation becomes particularly threatening to the patient when the reduction in cardiac performance goes along with complex ventricular arrhythmias. Therapy has remained difficult and of limited effectiveness. Major progress was achieved with the introduction of diuretic substances. Of similar importance was the introduction of va so dilating drugs into the treatment of heart failure. The principle of vasodilation has greatly improved our understanding of the disease, and has brought about a major improvement of symptoms, increase of exercise capacity, and reduc­ tion of mortality. This is especially true for the introduction of the angiotensin converting enzyme inhibitors.

Traditionally, cardiac hypertrophy is regarded as an adaptation of the heart to permanent mechanical overload. Regardless of the fact that many different and often unknown primary causes can result in heart failure, mechanical overload and myocardial hypertrophy is found in almost all forms of manifest chronic heart failure (apart from failure due to extramyocardial hindrances to inflow or to relaxation). However, the reactive enlargement of myocardial mass in response to an enhanced hemodynamic burden appears to be a double-edged sword. Obviously, the hypertrophy helps to reduce the enhanced ventricular wall stress in heart failure by adding contractile units to the overdistended chamber wall. However, in recent years it became clear that this adaptive hypertrophic process is rather complex and may include problematic facets. The adaptive hypertrophy includes proliferation of the nonmyocyte cardiac cells as well as substantial alterations in the phenotype of the growing myocytes due to differential changes in gene expression.

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