Assessment of the myocardial perfusion pattern in patients with multivessel coronary artery disease.

We studied 42 symptomatic patients with coronary artery disease involving two or three vessels using exercise thallium-201 myocardial scintigraphy. Qualitative analysis of the images predicted multivessel disease in 75% of the patients with two-vessel disease and in 82% of the patients with three-vessel disease. Quantitative analysis of the size of the perfusion defect indicated that approximately 40% of the left ventricular perimeter showed abnormal perfusion pattern during stress in these patients, and there was no significant difference in the size of the defect in patients with two-vessel disease or three-vessel disease (41 +/- 17% vs 42 +/- 14%, respectively, mean +/- SD). The exercise heart rate, exercise ECG response, and severity of narrowing did not correlate with the size of the perfusion defect. Patients with anterior infarction had larger defects in the distribution of the left anterior descending artery than those without infarction. Collaterals offered partial protection during exercise only when they were not jeopardized. This study confirms the value of qualitative analysis of exercise thallium-201 imaging in predicting multivessel disease, and describes a simple method of assessing the extent of perfusion abnormalities during stress in patients with multivessel disease. The results may be important in patient management and prognosis.

Quantitative radionuclide angiography in assessment of hemodynamic changes during upright exercise: observations in normal subjects, patient with coronary artery disease and patients with aortic regurgitation.

Quantitative radionuclide angiography (with the first pass technique and a computerized multicrystal camera) was used to evaluate hemodynamic changes in three subject groups during symptom-limited upright exercise. The 12 normal subjects had significant increases in heart rate, stroke volume, left ventricular ejection fraction and cardiac output during exercise; changes in end-diastolic and end-systolic volumes were not significant. In the 24 patients with coronary artery disease there were significant increases in heart rate and cardiac output during exercise, but insignificant changes in end-diastolic, end-systolic and stroke volumes and ejection fraction. The change in diastolic volume in these patients was determined by the extent of coronary artery disease, propranolol therapy, end point of exercise and presence of collateral vessels. Furthermore, patients with previous myocardial infarction had a lower ejection fraction and higher end-diastolic and end-systolic volumes during exercise than those without myocardial infarction. In the 12 patients with chronic aortic regurgitation of moderate to severe degree, there was a decrease in the end-diastolic volume during exercise. This response was distinctly different from that of the normal subjects or the patients with coronary artery disease. All three groups had a significant decrease in pulmonary transit time during exercise. It is concluded that changes in cardiac output in normal subjects during upright exercise are related to augmentation of stroke volume and tachycardia, whereas in patients with coronary artery disease they are related mainly to tachycardia. Left ventricular dilatation during exercise occurred in some normal subjects and in patients with coronary artery disease but was not a consistent finding. However, a decrease in left ventricular end-diastolic volume is common in patients with aortic regurgitation. Such a decrease may be explained by a reduction in the regurgitant volume per beat caused by shortening of the diastolic filling period or a decrease in systemic vascular resistance, or both.