[Afterload reduction and vasodilator therapy (author's transl)].
The concept of clinical application of the vasodilator therapy for the treatment of cardiac failure is based on the experimental findings that defined the inverse relationship between force and velocity or extent of muscle shortening at constant muscle lengths. In the intact heart, a new construct has recently been proposed in hopes of better understanding the behavior of the normal or depressed human ventricle in which the shortening during ejection is considered to reflect the appropriateness of the matching between the existing afterload and the level of inotropic state, as modulated by the preload (or Frank-Starling) reserve. In the normal left ventricle, if the preload is not allowed to compensate for an acute increase in afterload, or if the limit of preload reserve is reached, shortening of the ventricular wall will diminish; that is, afterload mismatch will ensue. The view that an afterload mismatch can exist in the basal state provides an explanation for the fact that cardiac output and ventricular function can be improved when afterload is reduced in patients with severe left ventricular failure complicated with acute myocardial infarction or with mitral or aortic regurgitation. However, in the ischemic myocardium, the effect of interventions which alter the afterload on the left ventricular ejection is also determined by the pre-existing ischemic status. Thus, depending on the magnitude of coronary flow reduction, a potentially beneficial drug can be detrimental to an ischemic myocardium.
D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D006321:Heart / Q000187:drug effects*; D006333:Heart Failure / Q000188:drug therapy; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000188:drug therapy; D013318:Stroke Volume / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology* / Q000627:therapeutic use
D014665:Vasodilator Agents