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Effects of induced asynchrony on left ventricular diastolic function in patients with coronary artery disease
S Betocchi1, F Piscione, B Villari
1Department of Cardiology and Cardiac Surgery, Federico II University School of Medicine, Naples, Italy.
Insights
Atrioventricular (AV) pacing increases left ventricular asynchrony, slowing isovolumetric relaxation and rapid filling. This highlights the impact of pacing on diastolic function in patients with coronary artery disease.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Diastolic Function
Background:
- Left ventricular (LV) mechanical dispersion significantly impacts diastolic function.
- Understanding LV diastolic mechanics is crucial for managing cardiac conditions.
Purpose of the Study:
- To investigate the effects of induced left ventricular asynchrony via sequential atrioventricular (AV) pacing.
- To assess the impact of AV pacing on LV isovolumetric relaxation, rapid filling, and chamber stiffness.
Main Methods:
- Studied 13 coronary artery disease patients using radionuclide angiography and cardiac catheterization.
- Evaluated systolic and diastolic asynchrony using regional time-activity curves.
- Measured cardiac index, LV pressure, and derived relaxation time constant and chamber stiffness.
Main Results:
- Atrioventricular (AV) pacing decreased cardiac index and peak filling rate.
- Isovolumetric relaxation time constant increased, indicating slower relaxation.
- Global diastolic pressure-volume relationship shifted upward, suggesting increased stiffness.
Conclusions:
- Sequential AV pacing induces left ventricular asynchrony.
- This asynchrony is linked to impaired isovolumetric relaxation and reduced rapid filling rates.
- Pacing-induced asynchrony negatively affects diastolic function parameters.
Objectives:
This study was designed to increase asynchrony with sequential atrioventricular (AV) pacing and to study its effects on left ventricular isovolumetric relaxation, rapid filling and stiffness.
Background:
Left ventricular nonuniformity is a major determinant of diastolic function.
Methods:
Thirteen patients with coronary artery disease were studied by simultaneous equilibrium radionuclide angiography and cardiac catheterization during atrial and AV pacing. Ejection fraction and peak filling rate were measured by radionuclide angiography. Regional analysis was obtained by analyzing time-activity curves of four left ventricular sectors; systolic and diastolic asynchrony were evaluated as the coefficient of variation of time to end-systole and, respectively, time to peak filling rate in the four sectors. Cardiac index and left ventricular pressure were measured with high fidelity catheters at cardiac catheterization. The time constant of isovolumetric relaxation was derived from left ventricular pressure. Pressure-volume loops were assembled and constants of chamber stiffness were computed.
Results:
Atrioventricular pacing led to a decrease in cardiac index (3.7 +/- 0.9 to 3.3 +/- 0.8 liters/min per m2, p = 0.01) and peak filling rate (352 +/- 125 to 287 +/- 141 ml/s, p = 0.03; 2.4 +/- 0.8 to 2.0 +/- 0.8 end-diastolic counts/s, p = 0.02; 4 +/- 1.3 to 3.2 +/- 1.0 stroke counts/s, p = 0.008). The time constant of isovolumetric relaxation increased (57 +/- 10 to 64 +/- 12 ms, p = 0.04) and the global diastolic pressure-volume relation shifted upward.
Conclusions:
Atrioventricular pacing induces left ventricular asynchrony, which is associated with a slower rate of isovolumetric relaxation. The isovolumetric relaxation lasts after the filling phase has begun, thereby reducing the rate of rapid filling.