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Left ventricular volumes and function during atrial pacing in coronary artery disease: a radionuclide angiographic
Insights
Atrial pacing in coronary artery disease patients causes reversible left ventricular dysfunction, reducing ejection fraction. Stroke volume is maintained by relative ventricular dilation, highlighting impaired cardiac response during rapid heart rates.
Area of Science:
- Cardiology
- Physiology
Background:
- Coronary artery disease (CAD) can impair left ventricular function.
- Atrial pacing is a method to assess cardiac response to increased heart rates.
Purpose of the Study:
- To investigate pathophysiologic changes in the left ventricle during atrial pacing in patients with CAD.
- To compare ventricular function during pacing in CAD patients versus healthy individuals.
Main Methods:
- Twenty-two patients with CAD underwent graduated right atrial pacing up to 160 beats/min or until angina/ST depression occurred.
- Radionuclide angiography measured ventricular volumes at rest and various pacing rates (100, 120, 140, 160 bpm).
- A control group of 10 healthy subjects was also studied.
Main Results:
- In CAD patients, left ventricular end-diastolic volume, stroke volume, and ejection fraction (EF) significantly decreased with pacing.
- End-systolic volume initially decreased then increased at higher pacing rates.
- Compared to controls, CAD patients showed less decrease in end-diastolic and end-systolic volumes, while EF decreased.
- Cardiac output and blood pressure remained stable in CAD patients during pacing.
Conclusions:
- Atrial pacing-induced tachycardia leads to reversible left ventricular dysfunction in CAD patients, characterized by reduced EF.
- Despite reduced EF, stroke volume is maintained due to relative ventricular dilation.
- CAD patients exhibit altered ventricular volume dynamics compared to healthy individuals under pacing stress.
Abstract:
This study set out to determine the pathophysiologic changes in the left ventricle during atrial pacing in 22 patients with coronary artery disease. Graduated right atrial pacing to a rate of 160 beats/min, or the induction of angina pectoris or significant ST depression was undertaken. Ventricular volumes were measured at rest and at rates of 100, 120, 140 and 160 beats/min using radionuclide angiography. The volumes at a pacing rate of 100 beats/min were used as a reference standard (100%). In the 22 patients with coronary artery disease, left ventricular end-diastolic volume decreased from 118 +/- 3% at rest to 80 +/- 5% at a rate of 160 beats/min; stroke volume from 121 +/- 3% to 54 +/- 5%; and ejection fraction (EF) from 49 +/- 3% to 37 +/- 5%. End-systolic volume decreased from 118 +/- 4% at rest, reached its minimal value of 94 +/- 5% at a rate of 120 beats/min and then increased slightly to 106 +/- 9% at 160 beats/min. Cardiac output and blood pressure did not change significantly. Compared to the control group of 10 normal subjects, the patients had a significantly smaller decrease in end-diastolic volume and end-systolic volume than in normal control subjects. EF in the normal subjects did not change. Blood pressure, cardiac output and stroke volume were similar in both groups. Atrial pacing tachycardia induced reversible ventricular dysfunction with a decrease in EF. Stroke volume was maintained because of relative ventricular dilatation.