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Simultaneous assessment of left ventricular systolic and diastolic dysfunction during pacing-induced ischemia
Insights
Pacing-induced ischemia in coronary artery disease patients reveals early diastolic dysfunction precedes systolic impairment. Nonischemic responses show improved contractility, while ischemic responses indicate reduced left ventricular distensibility before systolic decline.
Area of Science:
- Cardiology
- Physiology
Background:
- Systolic and diastolic dysfunction are known complications of pacing-induced ischemia.
- The precise temporal sequence of these dysfunctions remains unclear.
Purpose of the Study:
- To establish the temporal sequence of systolic and diastolic impairment during pacing-induced ischemia in patients with coronary artery disease.
Main Methods:
- Twenty-two coronary artery disease patients underwent pacing at increasing heart rates.
- Simultaneous hemodynamic monitoring, electrocardiography, and radionuclide ventriculography were employed.
- Sequential left ventricular pressure-volume diagrams were constructed at baseline, intermediate, and maximum pacing levels.
Main Results:
- Nonischemic group (n=11) showed decreased left ventricular end-diastolic pressure (LVEDP) and volumes, preserved ejection fraction, and improved contractility.
- Ischemic group (n=11) experienced angina, ST depression, and elevated LVEDP, with initial decreases followed by increases in LVEDP and volumes.
- Ischemic group demonstrated reduced left ventricular distensibility before the onset of systolic dysfunction.
Conclusions:
- Diastolic dysfunction, specifically decreased left ventricular distensibility, precedes systolic dysfunction during pacing-induced ischemia.
- This study clarifies the temporal relationship between diastolic and systolic impairments in this clinical context.
Abstract:
Both systolic and diastolic dysfunction have been described during pacing-induced ischemia, but the temporal sequence of systolic and diastolic impairment has not been established. Accordingly, 22 patients with coronary artery disease were paced at increasing heart rates and studied with simultaneous hemodynamic monitoring, electrocardiographic recording, and radionuclide ventriculography. In addition, with synchronized left ventricular pressure tracings and radionuclide volume curves, three sequential pressure-volume diagrams were constructed for each patient corresponding to baseline, intermediate, and maximum pacing levels. Eleven patients (group I) demonstrated a nonischemic response to pacing tachycardia without chest pain, significant electrocardiographic changes, or significant rise in left ventricular end-diastolic pressure (LVEDP) in the immediate postpacing period. These patients demonstrated a progressive decrease in LVEDP, end-diastolic volume, and end-systolic volume, no change in cardiac output or left ventricular ejection fraction, and a progressive increase in left ventricular diastolic peak filling rate and the end-systolic pressure-volume ratio. Pressure-volume diagrams shifted progressively leftward and slightly downward, suggesting both an increase in contractility and a mild increase in left ventricular distensibility. The remaining 11 patients (group II) exhibited an ischemic response to pacing tachycardia, with each patient experiencing angina pectoris, demonstrating greater than 1 mm ST segment depression on the electrocardiogram, and exhibiting greater than 5 mm Hg rise in LVEDP immediately after pacing. LVEDP, end-diastolic volume, and end-systolic volume in these patients initially decreased and then subsequently increased during angina, with no change in cardiac output but a decrease in ejection fraction. Left ventricular peak diastolic filling rate and the left ventricular end-systolic pressure-volume ratio both increased at the intermediate pacing rate but fell at maximum pacing. Pressure-volume diagrams for these patients shifted leftward initially, then back to the right, during intermediate and peak pacing levels, often with an upward shift in the diastolic pressure-volume relationship. LVEDP in group II was significantly higher than that in group I at the intermediate pacing level with no difference in end-diastolic or end-systolic volumes, suggesting decreased left ventricular distensibility in these patients before the onset of systolic dysfunction at the maximum pacing level.(ABSTRACT TRUNCATED AT 400 WORDS)