Vagal reflexes and survival during acute myocardial ischemia in conscious dogs with healed myocardial infarction

The role of vagal tone and reflexes in the genesis of life-threatening arrhythmias was investigated in a clinically relevant animal model for sudden cardiac death. Forty-five dogs with a healed anterior myocardial infarction in which transient myocardial ischemia during exercise did not induce malignant arrhythmias were utilized for the study. They underwent a further exercise and ischemia test in which atropine (75 micrograms/kg) was injected before coronary artery occlusion. Novel occurrence of ventricular arrhythmia, or worsening of the type of arrhythmia present in the control test, occurred in 23 of 45 dogs (51%) and ventricular fibrillation occurred in 11 of 45 (24%, P = 0.001). Analysis of heart rate response to acute ischemia in the control test indicates that these 11 animals had powerful vagal reflexes during coronary artery occlusion, compared with the 34 survivors (-32 +/- 35 vs. +2 +/- 27 beats/min, P = 0.003). This study indicates that approximately 75% of animals resistant to ventricular fibrillation are characterized by weak sympathetic reflexes in response to acute myocardial ischemia. In the remaining 25% powerful vagal reflexes counteract concomitant reflex sympathetic hyperactivity, decrease heart rate, and are essential for survival.

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Myocardial infarction and ventricular fibrillation due to iatrogenic right coronary artery occlusion following tricuspid valve annuloplasty: a case report

European Heart Journal - Case Reports ◽

10.1093/ehjcr/ytaa328 ◽

2020 ◽

Author(s):

Shi Sum Poon ◽

Joseph George ◽

Daniel Obaid ◽

Pankaj Kumar

Keyword(s):

Myocardial Infarction ◽

Coronary Artery ◽

Ventricular Fibrillation ◽

Tricuspid Valve ◽

Right Coronary Artery ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Left Ventricular ◽

Haemodynamic Instability ◽

Tricuspid Valve Annuloplasty

Abstract Background Iatrogenic right coronary artery (RCA) injury is a rare complication of tricuspid valve annuloplasty. Given that surgical intervention is increasingly favoured for tricuspid regurgitation, it is of great importance to recognize potential complications following tricuspid valve surgery. Case summary A 72-year-old man underwent surgical mitral and tricuspid valve repair. The early post-operative course was complicated by recurrent ventricular fibrillation episodes. Due to haemodynamic instability, a re-sternotomy and another cardiopulmonary bypass run were required. The patient subsequently underwent coronary angiography study which confirmed RCA occlusion. The occluded posterior left ventricular (PLV) branch was reopened by balloon angioplasty. However, despite multiple attempts it was not possible to pass a coronary guide wire into the posterior descending artery (PDA). An intravascular ultrasound examination revealed that the ostium of the PDA was compressed by external factors leaving a narrow slit-like appearance with no accessible lumen. Subsequently, a drug-eluting stent was placed into the PLV branch. The PDA was not accessible on repeated re-canalization attempts. The patient later successfully recovered from the right ventricular myocardial infarction. Discussion Right coronary artery occlusion should be considered as a differential diagnosis for significant rhythm disturbances and haemodynamic instability in the peri- and post-operative period following tricuspid valve annuloplasty. A low threshold for diagnostic angiography is needed to avoid potential delay in life-saving revascularization.

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Effects of ortho-lodo sodium benzoate on acute myocardial ischemia, hemodynamic function, and infarct size after coronary artery occlusion in dogs

The American Journal of Cardiology ◽

10.1016/0002-9149(83)90323-5 ◽

1983 ◽

Vol 51 (8) ◽

pp. 1422-1427 ◽

Cited By ~ 11

Author(s):

Robert E. Rude ◽

John Tumas ◽

Marcel Gunst ◽

Robert A. Kloner ◽

Laurence W.V. DeBoer ◽

...

Keyword(s):

Coronary Artery ◽

Myocardial Ischemia ◽

Infarct Size ◽

Sodium Benzoate ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Acute Myocardial Ischemia ◽

Hemodynamic Function

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Hypothermia reduces ischemia- and stimulation-induced myocardial interstitial norepinephrine and acetylcholine releases

Journal of Applied Physiology ◽

10.1152/japplphysiol.00622.2006 ◽

2007 ◽

Vol 102 (2) ◽

pp. 622-627 ◽

Cited By ~ 12

Author(s):

Toru Kawada ◽

Hirotoshi Kitagawa ◽

Toji Yamazaki ◽

Tsuyoshi Akiyama ◽

Atsunori Kamiya ◽

...

Keyword(s):

Coronary Artery ◽

Myocardial Ischemia ◽

Nerve Stimulation ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Acute Myocardial Ischemia ◽

Autonomic Nerves ◽

Ach Release ◽

Ischemic Region

Although hypothermia is one of the most powerful modulators that can reduce ischemic injury, the effects of hypothermia on the function of the cardiac autonomic nerves in vivo are not well understood. We examined the effects of hypothermia on the myocardial interstitial norepinephrine (NE) and ACh releases in response to acute myocardial ischemia and to efferent sympathetic or vagal nerve stimulation in anesthetized cats. We induced acute myocardial ischemia by coronary artery occlusion. Compared with normothermia ( n = 8), hypothermia at 33°C ( n = 6) suppressed the ischemia-induced NE release [63 nM (SD 39) vs. 18 nM (SD 25), P < 0.01] and ACh release [11.6 nM (SD 7.6) vs. 2.4 nM (SD 1.3), P < 0.01] in the ischemic region. Under hypothermia, the coronary occlusion increased the ACh level from 0.67 nM (SD 0.44) to 6.0 nM (SD 6.0) ( P < 0.05) and decreased the NE level from 0.63 nM (SD 0.19) to 0.40 nM (SD 0.25) ( P < 0.05) in the nonischemic region. Hypothermia attenuated the nerve stimulation-induced NE release from 1.05 nM (SD 0.85) to 0.73 nM (SD 0.73) ( P < 0.05, n = 6) and ACh release from 10.2 nM (SD 5.1) to 7.1 nM (SD 3.4) ( P < 0.05, n = 5). In conclusion, hypothermia attenuated the ischemia-induced NE and ACh releases in the ischemic region. Moreover, hypothermia also attenuated the nerve stimulation-induced NE and ACh releases. The Bezold-Jarisch reflex evoked by the left anterior descending coronary artery occlusion, however, did not appear to be affected under hypothermia.

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Complexity of the autonomic heart rate control in coronary artery occlusion in patients with and without prior myocardial infarction

Medical Engineering & Physics ◽

10.1016/j.medengphy.2012.11.004 ◽

2013 ◽

Vol 35 (8) ◽

pp. 1070-1078 ◽

Cited By ~ 4

Author(s):

R. Magrans ◽

P. Gomis ◽

P. Caminal ◽

G.S. Wagner

Keyword(s):

Myocardial Infarction ◽

Heart Rate ◽

Coronary Artery ◽

Rate Control ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Heart Rate Control ◽

Prior Myocardial Infarction

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Sabiporide Reduces Ischemia-Induced Arrhythmias and Myocardial Infarction and Attenuates ERK Phosphorylation and iNOS Induction in Rats

BioMed Research International ◽

10.1155/2013/504320 ◽

2013 ◽

Vol 2013 ◽

pp. 1-9 ◽

Cited By ~ 7

Author(s):

Henri Doods ◽

Dongmei Wu

Keyword(s):

Myocardial Infarction ◽

Coronary Artery ◽

Myocardial Ischemia ◽

Infarct Size ◽

Troponin I ◽

Ischemia Reperfusion ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Myocardial Infarct Size ◽

Myocardial Ischemia And Reperfusion

The aim of the present study was to investigate the effects of sabiporide, a potent and selective NHE1 inhibitor, on myocardial ischemia-induced arrhythmias and myocardial infarction and the possible pathways related to the cardioprotection afforded by sabiporide treatment. Anesthetized rats were subjected to myocardial ischemia via left main coronary artery occlusion for 30 minutes, followed by 2 hours of reperfusion. Administration of sabiporide (0.01–3.0 mg/kg) prior to coronary artery occlusion dose-dependently reduced ischemia-induced arrhythmias and infarct size with an ED50 value of 0.14 mg/kg. Administration of sabiporide (1.0 mg/kg) prior to reperfusion also reduced infarct size by 38.6%. The reduction in infarct size was accompanied by a decrease in circulating levels of creatine phosphokinase and troponin I. In addition, sabiporide (1.0 mg/kg) given prior to coronary artery occlusion or immediately before reperfusion significantly reduced phosphorylation of the extracellular signal-regulated kinase (ERK1/2) and the expression of the inducible nitric oxide synthase (iNOS) following myocardial ischemia-reperfusion. This study demonstrates that sabiporide is a potent and effective cardioprotective agent during myocardial ischemia and reperfusion, by reducing serious ventricular arrhythmias and myocardial infarct size. The cardioprotection afforded by sabiporide is attributed in part to inhibition of ERK1/2 phosphorylation and suppression of iNOS expression.

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