Key result
Myocardial infarction reduces endocardial monophasic action potential amplitude by ~32% with unchanged repolarization duration.
Why the study?
The study aimed to characterise monophasic action potentials recorded from subacutely infarcted myocardial regions displaying fractionated bipolar electrograms.
This preclinical study demonstrates the feasibility of recording monophasic action potentials in subacutely infarcted canine myocardium, providing a technique to study electrophysiological mechanisms of ventricular arrhythmias.
Enables mechanistic study of post-MI arrhythmogenic substrate in canines; clinical translation of these electrophysiologic changes remains untested.
Study objective The aim was to characterise monophasic action potentials recorded from subacutely infarcted myocardial regions, where fractionated bipolar electrograms could be obtained. Design Dogs underwent ligation of the left anterior descending coronary artery. Before and 8-12 d after ligation, monophasic action potentials and local electrograms were recorded endocardially from the apex of the left ventricle. Experimental material 15 anaesthetised mongrel dogs (30 mg pentobarbitone.kg-1) were used. Measurements and main results Multiphasic fractionated bipolar electrograms could be recorded from infarcted sites of the left ventricle with a mean duration of 69(SD 10) ms and a mean amplitude of 3.7(1.6) mV, compared to control values of 42(7) ms (p less than 0.05) and 9.4(2.2) mV (p less than 0.05), respectively. Endocardial monophasic action potentials recorded from these areas were similar to action potentials obtained from non-infarcted sites before coronary ligation. The fractionated extracellular potentials were superimposed on the monophasic action potential upstroke. MAP90 was 189(31) ms, MAP30 138(12) ms, versus control values of 182(27) ms and 139(10) ms (NS). Monophasic action potential amplitude was significantly reduced at infarcted sites compared to control, at 26(7) mV v 38(6) mV. Histological specimens were taken to confirm that measurements were obtained from infarcted tissue. Conclusions It is possible to record monophasic action potential in subacutely infarcted canine ventricular myocardium; this technique might help in further studies to characterise electrophysiological mechanisms of ventricular arrhythmias in chronic myocardial infarction in man.
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Schmitt et al. (1991) studied Subacutely infarcted canine ventricular myocardium (n=15). Left anterior descending coronary artery ligation and endocardial monophasic action potential recording vs. Non-infarcted control values before coronary ligation was evaluated on Monophasic action potential amplitude and duration (MAP90, MAP30) and fractionated bipolar electrogram duration and amplitude (p=<0.05). Endocardial monophasic action potential recording in infarcted canine myocardium showed reduced amplitude (26 vs 38 mV) but similar MAP90 (189 vs 182 ms, NS) compared to pre-ligation control.
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