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."