Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction.

Abstract

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptorheart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n=16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 ±2.4 hours (mean± SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 ±0.5 vs. 5.9±0.6 msec/mm Hg, p<0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2±0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p<0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later. (Circulation 1990;81:939-948) E xperimental coronary occlusion or acutely induced damage of the myocardium is followed by an abrupt impairment of the baroreceptor control of the sinus node,1-4 which is still evident several weeks later.3 This is potentially harmful because baroreceptors increase and reduce vagal and sympathetic influences on the heart, respectively, thereby opposing the adverse effects of ischemia on the electrical stability of the myocardium.5-8 In patients with a previous myocardial infarction (MI), the Valsalva maneuver and the administration of vasoactive drugs cause small changes in heart rate.9-12 Furthermore, a recent study from our institution has shown that in some patients, injection of phenylephrine induced somewhat greater bradycardias months as compared with weeks after the occurrence of an MI.13 This suggests that MI impairs the baroreceptor control of heart rate in humans as well as experimentally, but that some recovery later appears.In all human studies, the baroreceptor-heart ra...

Cardiac cholinergic NO-cGMP signaling following acute myocardial infarction and nNOS gene transfer

“…Clinically MI may induce the disruption of autonomic balance as evidenced by decreased heart rate variability (3,38), baroreflex sensitivity (44), and other markers of vagal control (20). Furthermore, surgically induced MI decreases vagal activity in dogs (46) although the converse has been shown in rats (51).…”

“…This is correlated with impaired cardiac vagal transmission, which can be restored by targeted nNOS overexpression (25). In humans (20,38,44) and dogs (46), the parasympathetic control of the myocardium is diminished in the early phase of MI. However, in the rat, post-MI, there is a compensatory increase in cardiac vagal tone coupled with a rise in right atrial nNOS mRNA and expression (51).…”

Bradycardic Therapy Improves Left Ventricular Function and Remodeling in Dogs with Coronary Embolization-Induced Chronic Heart Failure

“…A greater heart rate reduction and lower baseline resting heart rates were both associated with improved survival in the Cardiac Insufficiency Bisoprolol Study (CIBIS) II (CIBIS II Investigators, 1999), similar to findings in the United States Carvedilol Study . Patients after myocardial infarction also suffer from autonomic dysregulation of heart rate (Osculati et al, 1990), contributing to higher rates at ASPET Journals on May 9, 2018 jpet.aspetjournals.org of mortality and ventricular arrhythmias (ATRAMI Investigators, 1998). As reported by Nagatsu et al (2000), dogs treated with ␤-blockade alone (and subsequently lower heart rates) were found to have enhanced contractility compared with ␤-blockade plus pacing (with higher heart rates).…”

Baroreflex Sensitivity: Measurement and Clinical Implications

“…The injection of 100-200 mcg of nitroglycerin determines an immediate and progressive fall in systolic arterial pressure of about 20 mmHg over the following 8-15 beats. 35 Baroreflex slopes obtained by vasodilators are lower than those obtained by increasing arterial pressure to a similar extent, suggesting that the two responses are not mirror images; 36 yet a direct effect of the vasodilator drug on pacemaker cells cannot be excluded. Figure 2.…”