Stretch-induced ventricular arrhythmias during acute ischemia and reperfusion

2004 ◽  
Vol 97 (1) ◽  
pp. 377-383 ◽  
Author(s):  
Kevin Kit Parker ◽  
James A. Lavelle ◽  
L. Katherine Taylor ◽  
Zifa Wang ◽  
David E. Hansen
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Mechanical Stretch ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Acute Ischemia ◽  
Ischemia And Reperfusion ◽  
A Value ◽  
Action Potential Waveform ◽  
Electrophysiological Effects

Mechanical stretch has been demonstrated to have electrophysiological effects on cardiac muscle, including alteration of the probability of excitation, alteration of the action potential waveform, and stretch-induced arrhythmia (SIA). We demonstrate that regional ventricular ischemia due to coronary artery occlusion increases arrhythmogenic effects of transient diastolic stretch, whereas globally ischemic hearts showed no such increase. We tested our hypothesis that, during phase Ia ischemia, regionally ischemic hearts may be more susceptible to triggered arrhythmogenesis due to transient diastolic stretch. During the first 20 min of regional ischemia, the probability of eliciting a ventricular SIA ( PSIA) by transient diastolic stretch increased significantly. However, after 30 min, PSIA decreased to a value comparable with baseline measurements, as expected during phase Ib, where most ventricular arrhythmias are of reentrant mechanisms. We also suggest that mechanoelectrical coupling may contribute to the nonreentrant mechanisms underlying reperfusion-induced arrhythmia. When coronary artery occlusion was relieved after 30 min of ischemia, we observed an increase in PSIA and the maintenance of this elevated level throughout 20 min of reperfusion. We conclude that mechanoelectrical coupling may underlie triggered arrhythmogenesis during phase 1a ischemia and reperfusion.

scholarly journals Electrophysiological Effects of Late Percutaneous Coronary Intervention for Infarct-Related Coronary Artery Occlusion

Circulation ◽  
2009 ◽  
Vol 119 (6) ◽  
pp. 779-787 ◽  
Author(s):  
Eric J. Rashba ◽  
Gervasio A. Lamas ◽  
Jean-Philippe Couderc ◽  
Sharri M. Hollist ◽  
Vladimir Dzavik ◽  
...  
Keyword(s):  
Percutaneous Coronary Intervention ◽  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Coronary Intervention ◽  
Artery Occlusion ◽  
Percutaneous Coronary ◽  
Electrophysiological Effects

Early time course of myocardial electrical impedance during acute coronary artery occlusion in pigs, dogs, and humans

2005 ◽  
Vol 99 (4) ◽  
pp. 1576-1581 ◽  
Author(s):  
Carlos L. del Rio ◽  
Patrick I. McConnell ◽  
Bradley D. Clymer ◽  
Roger Dzwonczyk ◽  
Robert E. Michler ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Time Course ◽  
Electrical Impedance ◽  
Early Time ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Acute Ischemia ◽  
Collateral Flow ◽  
Total Occlusion ◽  
Interspecies Differences

Changes in myocardial electrical impedance (MEI) and physiological end points have been correlated during acute ischemia. However, the importance of MEI's early time course is not clear. This study evaluates such significance, by comparing the temporal behavior of MEI during acute total occlusion of the left anterior descending coronary artery in anesthetized humans, dogs, and pigs. Here, interspecies differences in three MEI parameters (baseline, time to plateau onset, and plateau value normalized by baseline) were evaluated using Kruskal-Wallis ANOVA and post hoc tests ( P < 0.05). Noteworthy differences in the MEI time to plateau onset were observed: In dogs, MEI ischemic plateau was reached after 46.3 min (SD 12.9) min of occlusion, a significantly longer period compared with that of pigs and humans [4.7 (SD 1.2) and 4.1 min (SD 1.9), respectively]. However, no differences could be observed between both animal species regarding the normalized MEI ischemic plateau value (15.3% (SD 4.7) in pigs, vs. 19.6% (SD 2.6) in dogs). For all studied MEI parameters, only swine values resembled those of humans. The severity of myocardial supply ischemia, resulting from coronary artery occlusion, is known to be dependent on collateral flow. Thus, because dogs possess a well-developed collateral system (unlike humans or pigs), they have shown superior resistance to occlusion of a coronary artery. Here, the early MEI time course after left anterior descending coronary artery occlusion, represented by the time required to reach ischemic plateau, was proven to reflect such interspecies differences.

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

1991 ◽  
Vol 261 (1) ◽  
pp. H63-H69 ◽  
Author(s):  
G. M. De Ferrari ◽  
E. Vanoli ◽  
M. Stramba-Badiale ◽  
S. S. Hull ◽  
R. D. Foreman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Myocardial Ischemia ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Acute Myocardial Ischemia ◽  
Acute Ischemia ◽  
Control Test

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.

scholarly journals CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis

2012 ◽  
Vol 44 (2) ◽  
pp. 173-182 ◽  
Author(s):  
Jan Neckář ◽  
Jan Šilhavý ◽  
Václav Zídek ◽  
Vladimír Landa ◽  
Petr Mlejnek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Artery ◽  
Circadian Rhythms ◽  
Infarct Size ◽  
Ventricular Arrhythmias ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Transgenic Rats ◽  
Spontaneously Hypertensive ◽  
Long Chain

CD36 fatty acid translocase plays a key role in supplying heart with its major energy substrate, long-chain fatty acids (FA). Previously, we found that the spontaneously hypertensive rat (SHR) harbors a deletion variant of Cd36 gene that results in reduced transport of long-chain FA into cardiomyocytes and predisposes the SHR to cardiac hypertrophy. In the current study, we analyzed the effects of mutant Cd36 on susceptibility to ischemic ventricular arrhythmias and myocardial infarction in adult SHR- Cd36 transgenic rats with wild-type Cd36 compared with age-matched SHR controls. Using an open-chest model of coronary artery occlusion, we found that SHR- Cd36 transgenic rats showed profound arrhythmogenesis resulting in significantly increased duration of tachyarrhythmias (207 ± 48 s vs. 55 ± 21 s, P < 0.05), total number of premature ventricular complexes (2,623 ± 517 vs. 849 ± 250, P < 0.05) and arrhythmia score (3.86 ± 0.18 vs. 3.13 ± 0.13, P < 0.001). On the other hand, transgenic SHR compared with SHR controls showed significantly reduced infarct size (52.6 ± 4.3% vs. 72.4 ± 2.9% of area at risk, P < 0.001). Similar differences were observed in isolated perfused hearts, and the increased susceptibility of transgenic SHR to arrhythmias was abolished by reserpine, suggesting the involvement of catecholamines. To further search for possible molecular mechanisms of altered ischemic tolerance, we compared gene expression profiles in left ventricles dissected from 6-wk-old transgenic SHR vs. age-matched controls using Illumina-based sequencing. Circadian rhythms and oxidative phosphorylation were identified as the top KEGG pathways, while circadian rhythms, VDR/RXR activation, IGF1 signaling, and HMGB1 signaling were the top IPA canonical pathways potentially important for Cd36-mediated effects on ischemic tolerance. It can be concluded that transgenic expression of Cd36 plays an important role in modulating the incidence and severity of ischemic and reperfusion ventricular arrhythmias and myocardial infarct size induced by coronary artery occlusion. The proarrhythmic effect of Cd36 transgene appears to be dependent on adrenergic stimulation.

Antifibrillatory effects of α1-adrenoceptor blocking drugs in experimental coronary artery occlusion and reperfusion

1993 ◽  
Vol 71 (2) ◽  
pp. 103-111 ◽  
Author(s):  
B. G. Benfey
Keyword(s):  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Guinea Pig ◽  
Ventricular Arrhythmias ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Coronary Reperfusion ◽  
Isolated Hearts ◽  
Anesthetized Dogs

The myocardium of animals and man possesses α1-adrenoceptors in addition to β-adrenoceptors. Ischemia increases sympathetic tone, and ventricular arrhythmias can occur by β- and α1-adrenoceptor stimulation. I believe that α1-adrenoceptor blocking drugs have antifibrillatory effects and will review the data that support this condition. The effect of α1,-adrenoceptor blocking drugs on the incidence of ventricular fibrillation in acute coronary artery occlusion and (or) reperfusion has been determined in 24 studies in conscious and anesthetized dogs and rats, anesthetized cats and pigs, and rat and guinea-pig isolated hearts. The drugs reduced the incidence of fibrillation from 35 to 24% in coronary occlusion and from 61 to 29% in reperfusion.Key words: heart, coronary occlusion, coronary reperfusion, ventricular fibrillation, α1-adrenoceptor blocking drugs.

Ventricular arrhythmias following coronary artery occlusion in the streptozotocin diabetic rat

1988 ◽  
Vol 66 (3) ◽  
pp. 312-317 ◽  
Author(s):  
G. N. Beatch ◽  
J. H. McNeill
Keyword(s):  
Coronary Artery ◽  
Ventricular Arrhythmias ◽  
Streptozotocin Diabetes ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Diabetic Rat ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Conscious Rat ◽  
Streptozotocin Diabetic Rat

The following investigation was designed to assess whether or not streptozotocin diabetes has an influence on the number and severity of ventricular arrhythmias following coronary artery occlusion in the conscious rat. In addition, electrocardiogram and haemodynamic data were compared between streptozotocin diabetic groups and control. Diabetes was induced in male Sprague–Dawley rats with streptozotocin (55 mg/kg iv) and left anterior descending coronary artery ligation was performed either 6 or 9 weeks later. Rats were allowed to recover from preparative surgery for 1 week prior to ligation. Streptozotocin diabetes (untreated or insulin controlled) appeared to have little influence on the variables tested. When exposed to equivalent degrees of ischaemia (the rat is a microangiopathy-resistant species), the streptozotocin diabetic rat heart was not appreciably more prone to arrhythmias of any type compared with control.

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