Cardiac Resynchronisation Therapy in Chronic Heart Failure

Cardiac Resynchronisation Therapy in Chronic Heart Failure

Flesch Markus
European Cardiology 2005
Published: May 2005
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Introduction
Chronic heart failure (HF) is a common, malignant disease and is a major economic burden for healthcare systems in developed nations. It affects 5% to 10% of all people. In Germany, approximately 150,000 people are newly diagnosed with HF per year. Fifteen per cent of approximately 1.6 million HF patients in Germany are in advanced HF status, being classified as stage III–IV according to the HF criteria of the New York Heart Association (NYHA). The prognosis of these patients is poor, despite major advances in HF therapy during the last 20 years. The one-year mortality is 10% in patients with HF class II–III, 20% to 40% in patients with HF class III–IV and up to 50% in patients with HF class IV. Since HF incidence increases with age, and because of the increasing number of elderly in modern industrialised societies, HF is regarded as one of the major epidemics of the 21st century.

The aetiology of HF is diverse. It can develop as a consequence of long-standing arterial hypertension and can be a consequence of coronary artery disease (CAD). Besides these two major aetiological factors, there are other reasons leading to HF such as primary cardiomyopathies, anaemia, hyper- and hypothyroidism, diabetes mellitus, valve defects, cardiac arrythmias, such as atrial fibrillation, and drug or alcohol intoxication.

Pharmacological Therapy of Chronic HF
In some cases, specific therapy of the underlying disease leads to an improvement of HF status or a complete cure. Examples are hyperthyroidism, atrial fibrillation or coronary artery occlusion; however, most patients with systolic and diastolic HF are treated with a similar combination of pharmacological substances independent of the primary cause of HF. In this respect, ACE-inhibitors, B-blockers, aldosterone antagonists and AT1-receptor antagonists have been demonstrated to be highly potent substances decreasing the morbidity, and especially the mortality, of HF patients. The convincing results of large clinical trials on the effects of these neurohormonal antagonists in HF patients have underlined the pathophysiological concept that chronic activation of the reninangiotensin system and the sympathetic nervous system are major reasons for the progression of HF.

Despite optimal standard therapy, progression of HF therapy cannot be antagonised completely and HF mortality remains high. Unfortunately, new pharmacological approaches in the therapy of HF, such as the introduction of endothelin antagonists or the treatment with tumour necrosis factor (TNF) inhibitors, have not been successful.1,2 Only one AT1-receptor antagonist, candesartan, has so far been demonstrated to decrease the combined incidence of HF deterioration and death when given in combination with ACE-inhibitors and ß-blockers.3 Others might even have adverse effects when added to these drugs.4 These experiences suggest that a further extension of neurohormonal blockade might not be very efficient at improving morbidity and mortality in HF patients and other therapeutical approaches might be necessary.

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