[Modern therapy of cardiac insufficiency].
Heart failure is a lethal, end-stage cardiovascular disease. Recent decrease in mortality rates from cardiovascular diseases has not been accompanied by a reduced mortality from heart failure. Survival, once the heart has used up all its reserves and compensatory mechanisms, is a little better than in cancer. That makes heart failure one of the most important world health problems.


METHODS
This paper briefly reviews history, present and future of heart failure therapy, as a worldwide problem. Definition and diagnosis of heart failure, mechanism of deterioration of heart function, clinical use of present drugs in heart failure therapy and need for prevention of heart failure are, briefly pointed out. Results of clinical studies are presented, as well as the recommended indication for drug use. Heart failure is not readily identified, defined and evaluated. There is an absence of clear definition. To find a new definition which complies best with clinical practice is an important challenge cardiologists must face. Heart failure is a progressive disease and once the process has started it continues with further deterioration of cardiac function or ends in sudden death. In many patients changes within heart develop long before clinical symptoms occur. The left ventricle goes through a number of adaptations remodeling to compensate increased pressure or volume load or subsequent myocardial infarction.


CONCLUSIONS
For decades therapy has been focused on relieving symptoms, whereas preventive aspects and prolonging survival received less attention. Conventional therapy with diuretics and cardiotonic glycosides causes regression of symptoms and signs of heart failure, but there is no evidence that these drugs slow down the progression of the disease and reduce mortality. Currently, angiotensin-converting enzyme inhibitors plus diuretics are considered first line therapy for all degrees of heart failure, except for heart failure with atrial fibrillation and a rapid ventricular rate. They are, currently, the only agents with proven ability to decrease mortality. There is evidence about the efficacy of angiotensin-converting enzyme inhibitors in asymptomatic left ventricular dysfunction. It is likely that not only patients with significant reduction of systolic function but also other signs of impaired left ventricular dysfunction will benefit from treatment with ACE inhibitors. However, only preventive treatment may decrease the number of patients with new onset of clinical heart failure. Therefore treatment should be introduced early, rather than waiting for heart failure to progress to a more severe stage. Based on these facts ACE inhibitors should be considered as treatment of choice, a first line therapy in most cases of heart failure. A substantial reduction in cardiovascular mortality requires detection and correction of presymptomatic left ventricular dysfunction and risk factors, which predispose to its occurrence. Major contributors to the development of cardiac failure have been delineated and quantified. Identification of high-risk individuals is difficult since signs and symptoms of heart failure are often lacking. A strategy to find these patients must use objective methods to characterize the state of the left ventricle. Despite this, methods for efficient identification presymptomatic candidates for cardiac failure for preventive measures have been developed. High-risk candidates can now be costly-effectively targeted for treatment to delay failure. Early diagnosis and subsequent aggressive medical or surgical treatment are therefore fundamental to improve adverse outcome of heart failure. It is necessary to allow a rational approach to the clinician, indicating the effectiveness of these drugs in patients with evidence of impaired ventricular function.


CONCLUSIONS
Further reduction of morbidity and mortality from heart failure and diseases associated with heart failure is to be expected by early
Stojsić
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Klinika za kardiologiju, Sremska Kamenica, Institut za kardiovaskularne bolesti, Medicinski fakultet, Novi Sad.
Jelkić
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N
D006333:Heart Failure / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans