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Cellular and Molecular Alterations in the Failing Human Heart (Paperback, Softcover reprint of the original 1st ed. 1992)
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Cellular and Molecular Alterations in the Failing Human Heart (Paperback, Softcover reprint of the original 1st ed. 1992)
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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.
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