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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.
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.
Im vorliegenden Band wird die vielschichtige klinische Problematik
von Herzmuskel- und Perikarderkrankungen sowie der Herz- und
Perikardtumoren ausfuhrlich dargestellt. Die Klassifizierung der
Myokarderkrankungen folgt der derzeitigen Einteilung in (primare)
Kardiomyopathien und (sekundare) spezifische
Herzmuskelerkrankungen. Besondere Schwerpunkte liegen in der
Darstellung der Immunpathogenese myokardialer Erkrankungen und der
Anwendung neuer diagnostischer Verfahren wie Myokardbiopsie und
bildgebender Verfahren. Breiter Raum ist in der Therapie neben den
klassischen Methoden der Anwendung von Vasodilatantien,
Betablockern, Kalziumantagonisten und Immunsuppressiva gewidmet.
Erstmalig werden Myokardalterationen bei genetischen Erkrankungen
und neurologischen Systemkrankheiten zusammenfassend dargestellt.
Von besonderer Aktualitat sind toxische Einwirkungen auf das
Myokard sowie Strahlenschaden. Internisten und allen kardiologisch
interessierten Arzten vermittelt dieser Band umfassende
Basisinformationen uber die diagnostischen und therapeutischen
Fortschritte unter Einschluss der jeweils aktuellen Probleme in
Pathogenese und Therapie."
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