[Left ventricular remodeling: pathophysiological mechanisms and therapeutic recommendations].
Hospital mortality from acute myocardial infarction has decreased in the last two decades. Left ventricular dysfunction therefore have been mainly due to ischemia. After extensive myocardial infarction, there are processes of adaptation (remodeling) which result in altered geometry of the left ventricle. The effects of this on neurohormonal systems (organ regulation), on the changed ratio of myocyte mass and collagen content owing to reactive and reparative fibrosis (organ texture) and on the molecular and cellular mechanisms (organ structure) are of crucial importance. Depending on the structural changes, the myocardial contractility decreases. This is associated with an activation of the circulating renin-angiotensin-aldosterone system (RAAS). The fundamental knowledge available has led to the therapeutic use of ACE inhibitors in the post-infarct period. This treatment enabled a sustained reduction of mortality in several large-scale randomized studies. The effect of early administration in patients with clinical signs of heart failure and/or left ventricular dysfunction was very much greater compared to unselected controls. Only 17 and 13 patients had to be treated after selection in order to save one life in the AIRE and TREACE Study respectively (NNT: number needed to treat), whereas e.g. in the ISIS-4 study 200 unselected patients had to be treated. In clinical practice, however, this life-saving therapy is only used in every second patient requiring treatment. With consideration of an individual form of treatment (anterior infarction, large infarct area, reinfarction, clinical signs of heart failure as well as arterial hypertension and diabetes mellitus), a greater acceptance of evidence-based guidelines is thus desirable. Treatment with a high dose may be expected to be of additional benefit.
Völler
H
H
Klinik am See Fachklinik für Herz- und Kreislauferkrankungen, Rüdersdorf.
Dietz
R
R
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D012084:Renin-Angiotensin System / Q000502:physiology; D016896:Treatment Outcome; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors