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Antiarrhythmic effect of repeated coronary occlusion during balloon angioplasty
1Cardiovascular Laboratory, Department of Medicine, University of Oulu, Finland. kari.airaksinen@.oulu.fi
Insights
Brief coronary artery occlusions during angioplasty may protect against ventricular ectopy. Repeated occlusions reduced the incidence of these abnormal heart rhythms, suggesting increased electrical stability in ischemic heart tissue.
Area of Science:
- Cardiology
- Electrophysiology
- Ischemic Heart Disease
Background:
- Sudden cardiac death is often caused by ventricular arrhythmias from myocardial ischemia.
- Animal studies show ischemic preconditioning protects against arrhythmias, but human data is lacking.
Purpose of the Study:
- To determine if brief, repeated coronary artery occlusions during angioplasty can prevent ischemia-induced ventricular ectopy in humans.
Main Methods:
- 156 patients undergoing balloon angioplasty had continuous ECG, heart rate, and blood pressure monitoring.
- Two identical coronary artery occlusions (mean 111s) were performed, separated by a 5-minute equilibration period.
Main Results:
- Ventricular ectopy occurred in 24 patients during occlusion.
- The incidence of ventricular ectopy was significantly lower during the second occlusion compared to the first (7% vs. 13.5%, p=0.02).
- No significant differences in ischemia signs or hemodynamics were noted between occlusions.
Conclusions:
- A short occlusion-reperfusion cycle appears to enhance the electrical stability of ischemic myocardium.
- This suggests a potential protective effect of ischemic preconditioning in humans during angioplasty.
Objectives:
The purpose of the present study was to assess whether brief, repeated coronary artery occlusions during balloon angioplasty protect against ischemia-induced ventricular ectopy.
Background:
Most sudden cardiac deaths are caused by fatal ventricular arrhythmias precipitated by early myocardial ischemia of acute coronary occlusion. In animals, a preceding 3- to 5-min coronary occlusion protects against malignant ventricular arrhythmias during a subsequent prolonged coronary occlusion. Whether such an antiarrhythmic effect caused by ischemic preconditioning occurs in humans is not known.
Methods:
To assess the effects of a preceding, brief vessel occlusion-reperfusion cycle on the occurrence of ventricular ectopy, continuous electrocardiographic, heart rate and blood pressure recordings were performed in 156 patients before and during two identical balloon occlusions of a coronary artery (mean 111 s) separated by a 5-min equilibration period.
Results:
The occluded vessel was the left anterior descending coronary artery in 94 patients, the left circumflex branch in 29 patients and the right coronary artery in 33 patients. Balloon occlusion of a coronary artery caused ventricular ectopy in 24 patients. The incidence of ventricular ectopy was higher during the first occlusion than during the second occlusion (21 patients [13.5%] vs. 11 patients [7%], p = 0.02). In 13 patients, ventricular ectopy was observed only during the first occlusion; in 8 patients during both occlusions; and in 3 patients only during the second occlusion. Bigeminal or repetitive ectopic beats were observed in eight patients during the first coronary occlusion and in four patients during the second occlusion. Atrial premature beats occurred during the first occlusion in three patients, but in none of the patients during the second occlusion. The 24 patients with ventricular ectopy during coronary occlusion had milder stenosis than the rest of the patients (mean [+/- SD] 74 +/- 12% vs. 81 +/- 12%, p = 0.01). The 13 patients with ventricular ectopy only during the first occlusion did not, however, differ significantly with respect to any clinical or angiographic features from the rest of the patients with ventricular ectopy. There were no significant differences in the signs of myocardial ischemia or hemodynamic variables between the sequential occlusions.
Conclusions:
A preceding, short vessel occlusion-reperfusion cycle seems to increase the electrical stability of ischemic myocardium.