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Severe diastolic dysfunction with preserved energy conversion efficiency after countershock

S Yasuda¹, T Shishido, Y Goto

¹Department of Internal Medicine, National Cardiovascular Center, Osaka, Japan.

The American Journal of Physiology

|August 1, 1997

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Direct current (DC) countershocks cause diastolic dysfunction in the heart, leading to myocardial edema. However, DC shocks do not significantly impair the heart

Area of Science:

Cardiovascular Physiology
Cardiac Electrophysiology
Myocardial Metabolism

Background:

Direct current (DC) countershocks are used to treat cardiac arrhythmias.
The impact of DC countershocks on left ventricular (LV) mechanical performance and myocardial oxygen consumption is not fully understood.
Myocardial stunning following ischemia is known to increase the energy cost of excitation-contraction coupling.

Purpose of the Study:

To investigate the effects of DC countershocks on LV mechanical performance and myocardial oxygen consumption (VO2) in relation to pressure-volume area (PVA).
To assess the oxygen cost of contractility and contractile efficiency after DC countershocks.
To determine the potential mechanisms underlying diastolic dysfunction induced by DC countershocks.

Main Methods:

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Isolated blood-perfused dog hearts were used to measure LV mechanical performance and VO2-PVA relationships.
Measurements were taken before and after the application of DC countershocks.
Parameters analyzed included LV end-diastolic pressure, LV end-systolic pressure-volume relationship, time constant of LV pressure decay, and the oxygen cost of contractility.

Main Results:

DC countershocks progressively increased LV end-diastolic pressure and prolonged the time constant of LV pressure decay, indicating diastolic dysfunction.
Myocardial interstitial edema was observed to correlate with the progression of diastolic dysfunction.
Neither LV end-systolic pressure-volume relationship slope nor contractile efficiency (VO2-PVA relationship) was significantly altered by DC shocks.
The oxygen cost of contractility increased by 27% after DC shocks, which is considerably less than that observed in postischemic stunned myocardium.

Conclusions:

Despite inducing severe diastolic dysfunction and myocardial edema, DC countershocks have a relatively minor impact on the energy cost of excitation-contraction coupling.
DC countershocks do not substantially impair cross-bridge cycling or calcium cycling efficiency.
Myocardial interstitial edema is identified as a likely mechanism responsible for the diastolic dysfunction observed after DC countershocks.