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Nitrates have been for many years the cornerstone of cardiovascular
therapy for various indications. Not only have nitrates stood the
test of time for treatment of chronic stable angina pectoris, but
the indications for them have markedly ex panded. They now include
all forms of angina pectoris and myocardial ischemia, congestive
heart failure and hypertensive emergencies. The beneficial effects
of nitrates in all these conditions result from their vasodilatory
properties, but it is still unclear whether the central or
peripheral effects predominate in the thera peutic mechanism.
Recently nitrates have been shown to fulfill the most important
requirement for each and every drug - to reduce mortality. A large
scale study revealed that isosorbide dinitrate, combined with
hydralazine, reduced long-term mortality by 28% in patients with
congestive heart failure. This finding will certainly stimulate
research on nitrates, and it might be expected that interest in
these drugs will markedly increase. The primarily used nitrates in
clinical practice are nitroglycerin and the com plex organic
nitrates, mainly isosorbide dinitrate. The organic mononitrates are
now under clinical investigation, and isosorbide-5-mononitrate
(IS-5-MN) appears to be especially promising.
A. Schneeweiss Although the syndrome of congestive heart failure
has been recognized many years ago, the approach for its evaluation
and treatment has until recently, been partial and 'fragmentary'.
Various aspects of the disease have been treated according to the
evaluation tools and therapeutic measures available at each period.
This approach resulted in some of the greatest achievements in the
management of heart failure but also left many aspects neglected
and also resulted in several paradoxes. Examples of the
achievements and limitations of the 'fragmentary' ap proach are the
use of diuretics and hemodynamic measurements. The devel opment of
diuretics has provided us with an important tool for helping pa
tients whose predominant problem was edema. The success of
diuretics masked the fact that their use may often be
hemodynamically unsound and that they may reduce cardiac output.
Only many years after their introduction has the use of diuretics
found its appropriate place. Hemodynamic monitoring has gone via
the same path. The great contribu tion of continuous bedside
hemodynamic measurements to understanding heart failure resulted in
over-usage by many clinicians, who found themselves treating
hemodynamic charts rather than patients. It took almost a decade to
realize that hemodynamic improvement, even in the chronic setting,
does not necessarily mean symptomatic improvement or an increase in
exercise capac ity."
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