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Ischemia-induced changes in human endocardial electrograms during percutaneous transluminal coronary angioplasty
P T Vaitkus1, J M Miller, A E Buxton
1Division of Cardiology, Hospital of the University of Pennsylvania, Philadelphia.
Insights
Acute myocardial ischemia in humans slows heart electrical conduction, decreasing electrogram amplitude and increasing duration. A preconditioning effect was observed, suggesting repeated ischemia may offer protection.
Area of Science:
- Cardiology
- Electrophysiology
- Ischemic Heart Disease
Background:
- The electrophysiologic effects of acute myocardial ischemia in humans are not well understood.
- Previous experimental models showed slowed conduction in ischemic heart tissue, but human data were lacking.
Purpose of the Study:
- To analyze regional endocardial electrogram changes during reversible myocardial ischemia.
- To investigate if prior ischemia (preconditioning) affects the response to subsequent ischemia.
Main Methods:
- Bipolar left ventricular endocardial electrograms were recorded during percutaneous transluminal coronary angioplasty in 11 patients.
- Changes in electrogram amplitude and duration were measured during balloon occlusions of varying lengths.
Main Results:
- Myocardial ischemia caused a significant decrease in electrogram amplitude and an increase in duration.
- These electrogram changes returned to baseline after reperfusion.
- In a preconditioning protocol, the second ischemic episode showed a reduced increase in electrogram duration compared to the first.
Conclusions:
- Acute transmural myocardial ischemia in humans leads to slowed electrical conduction, evidenced by reduced electrogram amplitude and prolonged duration.
- Findings align with animal studies and suggest a potential protective preconditioning effect on electrogram duration with repeated ischemia.
Abstract:
The electrophysiologic sequelae of acute reversible transmural myocardial ischemia in humans are poorly understood. Experimental models have demonstrated slowing of conduction in ischemic myocardium, but similar evidence in humans is lacking. We used percutaneous transluminal coronary angioplasty as a model for reversible ischemia to (1) analyze the regional endocardial electrogram response to ischemia and (2) determine whether an initial episode of ischemia may mitigate the effects of a subsequent bout of ischemia (preconditioning). We recorded bipolar left ventricular endocardial electrograms during elective angioplasty in 11 patients and examined changes in amplitude and duration on the electrogram. Each of the 11 patients underwent two to seven balloon inflations. The electrogram amplitude at 90 seconds of balloon occlusion fell to 86% +/- 17% of the control value, and the electrogram duration increased to 109% +/- 12% of the control value. These variables returned to baseline values by 30 and 120 seconds, respectively, after balloon deflation. Among the six patients in the preconditioning protocol, the electrogram duration at 90 seconds was less with the second inflation (106% +/- 7%) than with the first (115% +/- 17%, p < 0.05). The difference in electrogram amplitude between the first and the second inflation was not significant (88% +/- 17% vs 85% +/- 13%, p = NS). At 60 seconds of ischemia there was no difference between normal sinus rhythm and paced complexes in the magnitude of change in electrogram amplitude or duration. We conclude that acute transmural myocardial ischemia in humans is associated with a decrease in local bipolar endocardial electrogram amplitude and an increase in electrogram duration. These findings are consistent with slowed conduction in the ischemic zone and are in agreement with experimental findings in animals. Furthermore, a preconditioning effect on electrogram duration suggests a possible protective effect for repeated bouts of ischemia.