Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.

Thames, Marc D.; Klopfenstein, H S; Abboud, François M.; Mark, Allyn L.; Walker, John L.

doi:10.1161/01.res.43.4.512

Cited by 196 publications

(68 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These results were expected since a reflex increase in vagal tone occurs more frequently in association with inferior myocardial ischemia than in association with anterior myocardial ischemia'4 15 19 However, the discontinuation of calcium blockers should be attempted with caution, particularly in patients with recent acceleration of vasospastic angina, since myocardial infarction and sudden death occurred in three of our patients shortly after calcium blockers were discontinued.…”

Section: Discussionmentioning

confidence: 55%

Clinical characteristics associated with myocardial infarction, arrhythmias, and sudden death in patients with vasospastic angina.

Nakamura¹,

Takeshita²,

Nose³

1987

Circulation

250

146

View full text Add to dashboard Cite

A total of 349 patients with vasospastic angina were followed in eight centers in Japan for a period of 3.4 + 0.1 years (mean ± SE). Ninety-eight percent of patients were treated with calcium blockers. Twenty-one episodes of myocardial infarction occurred in 18 patients (5%), including two fatal myocardial infarctions. The rate of myocardial infarction was higher (p < .01) in patients with a fixed stenosis of 90% or greater than in patients with a fixed stenosis of less than 90% or normal coronary arteries. Myocardial infarctions occurred predominantly during hospital stays or at a time when the frequency of vasospastic angina increased. There were five sudden deaths (2%). Only one patient suffering sudden death had a fixed stenosis of 75% or greater. Serious arrhythmias were noted in 49 patients (14%). The risk of arrhythmias did not depend on the presence of a fixed stenosis of 75% or greater. These results suggest that cardiac events are rather infrequent in Japanese patients with vasospastic angina who are receiving treatment with calcium blockers and that the presence of a severe fixed stenosis markedly increases the risk of myocardial infarction but not the risk of arrhythmias.

show abstract

Section: Discussionmentioning

confidence: 55%

Clinical characteristics associated with myocardial infarction, arrhythmias, and sudden death in patients with vasospastic angina.

Nakamura¹,

Takeshita²,

Nose³

1987

Circulation

250

146

View full text Add to dashboard Cite

show abstract

“…The cardioinhibitory vagal afferents modulate the arterial baroreflex. 4 18 Therefore, one might expect that the slope of the relationship of arterial pressure and heart rate response would be steeper with right coronary perfusion. Our findings show that the interaction of the two opposing reflexes resulted in a similar slope, but a significantly different intercept, in the reperfused right coronary group.…”

Section: Resultsmentioning

confidence: 99%

Cardiovascular reflexes stimulated by reperfusion of ischemic myocardium in acute myocardial infarction.

Wei¹,

Markis²,

Malagold³

et al. 1983

Circulation

118

View full text Add to dashboard Cite

SUMMARY Acute myocardial infarction (AMI), especially of the inferior left ventricular wall, where most cardiac receptors with vagal afferents that are stimulated during coronary occlusion are located, is commonly associated with reflex hypotension and sinus bradycardia. To determine whether reperfusion of an acutely ischemic area can activate cardiac reflexes, changes in the heart rate, arterial pressure and rhythm were correlated with the time course and location of intracoronary thrombolytic therapy in 41 patients with AMI. Of the 27 patients with successful reperfusion, 17 developed significant transient bradycardia and hypotension and one became tachycardic and hypertensive at the time of recanalization. Spontaneous reversion of the bradycardia and hypotension occurred definitely in six patients and possibly in more (nine reverted after atropine and two after fluids). A positive correlation existed between the changes in heart rate and blood pressure, in contrast to the usual inverse relationship when baroreceptors are stimulated. Two of the three patients in whom reperfusion was transient also developed hypotension and bradycardia. In contrast, all 11 patients with persistent occlusion demonstrated no reflex cardiovascular changes during intracoronary thrombolytic therapy. Thus, successful reperfusion in AMI stimulates cardioinhibitory and vasodepressor (Bezold-Jarisch) reflexes. These findings raise the possibility that the transient hypotension and bradycardia observed during AMI, particularly inferior MI, may sometimes reflect the occurrence of spontaneous reperfusion of the acutely ischemic myocardium.ACUTE myocardial infarction (AMI), especially of the inferior left ventricular wall, is often associated with transient hypotension and sinus bradycardia.' 2 Experimental evidence suggests that this cardiac reflex may result from activation of inhibitory cardiac receptors with vagal afferents located predominantly in the inferoposterior wall of the left ventricle.3'5 Acute occlusion of the coronary artery and restoration of flow after prolonged occlusion have been associated with abrupt increases in discharge of left ventricular receptors in the cat.' Whether reperfusion of ischemic myocardium also influences cardiac reflexes is not established. In the past, this question has not lent itself easily to investigation in humans, largely because reperfusion after acute coronary occlusion has not been widely studied until recently.7-9 However, the use of thrombolytic agents in conscious patients in the early hours of AMI permits an evaluation of the reflex effects associated with coronary reperfusion. The present study was undertaken to assess the effect of reestablishment of coronary flow to ischemic myocardium on blood pressure and heart rate in humans. Because coronary spasm'0 "1 and perhaps its reversal'0 as well as intracoronary contrast injection'2 -4 have elicited the hypotensive-bradycardic response, we hypothesized that reperfusion of acutely ischemic myocardium might activate cardiac reflexes. We sou...

show abstract

“…The mechanism of the decreased inferior distribution of 123 I-MIBG could be explained by the experimental observations that the inferior wall of the left ventricle has predominantly parasympathetic innervation, and that the anterior wall shows primarily sympathetic innervation. 1,18 Therefore, a patchy distribution of nerve terminals was observed in the present study, which raises the possibility that sympathetic imbalance may occur in regions of exercise-induced silent ischemia.…”

Section: Myocardial Mibg Kinetics In the Athlete's Heartmentioning

confidence: 45%

Cardiac Sympathetic Dysfunction in an Athlete's Heart Detected by 123I-Metaiodobenzylguanidine Scintigraphy.

et al. 2001

View full text Add to dashboard Cite

Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.

Cited by 196 publications

References 30 publications

Clinical characteristics associated with myocardial infarction, arrhythmias, and sudden death in patients with vasospastic angina.

Clinical characteristics associated with myocardial infarction, arrhythmias, and sudden death in patients with vasospastic angina.

Cardiovascular reflexes stimulated by reperfusion of ischemic myocardium in acute myocardial infarction.

Cardiac Sympathetic Dysfunction in an Athlete's Heart Detected by 123I-Metaiodobenzylguanidine Scintigraphy.

Contact Info

Product

Resources

About