Key result
In dogs, acute LV dysfunction and beta-adrenergic desensitization induced by excess isoproterenol were almost totally prevented by ARB but only partially prevented by ACEI.
Why the study?
Does ACEI or ARB prevent isoproterenol-induced acute left ventricular dysfunction in dogs?
Does ACEI or ARB prevent isoproterenol-induced acute left ventricular dysfunction in dogs?
In a canine model, ARBs were superior to ACE inhibitors in preventing isoproterenol-induced acute left ventricular dysfunction, a difference partly attributable to bradykinin pathway activation by ACE inhibitors.
Answers are grounded in this paper and cite their sources.
Does not support changing ACEI/ARB use in patients; leaves open whether ARBs confer superior protection against catecholamine-induced LV dysfunction.
Several clinical trials have demonstrated that angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II type 1 receptor blocker (ARB) are equally effective in the treatment of chronic heart failure. However, this has not been confirmed for acute cardiac dysfunction. We examined whether ACEI or ARB prevents isoproterenol-induced acute left ventricular (LV) dysfunction in dogs. LV dysfunction induced by a large dose of isoproterenol (1 microg.kg(-1).min(-1), 3-h infusion) was compared in dogs treated with ACEI (temocaprilat) or ARB (olmesartan). Atrial pacing induced a constant heart rate and use of adjustable aortic banding provided a nearly constant afterload. LV systolic function (LV dP/dt, fractional shortening, and ejection fraction) and diastolic function (tau and LV end-diastolic pressure) were significantly deteriorated after isoproterenol infusion. The LV dysfunction was almost totally prevented by ARB but was only partially prevented by ACEI. The partial effect of ACEI was complemented by cotreatment with HOE-140, a bradykinin B2 receptor antagonist. At baseline, the response to low doses of isoproterenol was significantly attenuated by ACEI but not by ARB, and the ACEI-induced attenuation was totally abolished by cotreatment with HOE-140. The response to isoproterenol was significantly attenuated after 3 h of excess isoproterenol loading, and it was almost completely preserved by ARB but not by ACEI. In conclusion, acute LV dysfunction and beta-adrenergic desensitization induced by excess isoproterenol administration were almost totally prevented by ARB but only partially prevented by ACEI. These differences were attributable at least in part to bradykinin pathways activated by ACEI administration in acute LV dysfunction.
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Ohta et al. (2004) studied Acute left ventricular dysfunction. ARB (olmesartan) vs. ACEI (temocaprilat) was evaluated on Left ventricular systolic and diastolic function. In dogs, acute LV dysfunction and beta-adrenergic desensitization induced by excess isoproterenol were almost totally prevented by ARB but only partially prevented by ACEI.
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