Physiologic basis of vasodilator therapy for heart failure.
In congestive heart failure, an increase in impedance to left ventricular ejection appears to be an important factor in impairing left ventricular performance. Arteriolar narrowing and decreased arterial compliance will decrease the left ventricular ejection fraction, whereas reduction in venous capacitance will shift blood centrally and increase cardiac filling. These vascular events may result from activation of the sympathetic nervous system and the renin-angiotensin system. Vasodilator drugs, by relaxing the increased vascular tone, will reduce ventricular volume and increase stroke volume, and thus improve the patient's hemodynamic and myocardial metabolic state. Translation of this acute hemodynamic response into a therapeutic benefit from long-term therapy is an attractive but not yet entirely proved thesis. Long-term controlled trials must eventually establish the place of vasodilator drug therapy in the management of different types of congestive heart failure. Furthermore, additional insight is needed into the potential for selective therapy that is tailored to counteract specific mechanisms of vasoconstriction in individual patients.
D006333:Heart Failure / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D009638:Norepinephrine / Q000097:blood; D012083:Renin / Q000097:blood; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000627:therapeutic use*
D014665:Vasodilator Agents; D012083:Renin; D009638:Norepinephrine