Dobutamine Stress-Induced Ischemic Right Ventricular Dysfunction and Its Relation to Cardiac Output in Patients With Three-Vessel Coronary Artery Disease With Angina-Like Symptoms

We investigated markers of ischemic dysfunction and their relation to overall right ventricular (RV) performance during dobutamine stress echocardiography in patients who had coronary artery disease. Thirty-three patients (58 ± 10 years old) who had 3-vessel coronary artery disease were compared with 17 age-matched controls (58 ± 11 years old). RV long-axis amplitude (M mode), systolic and diastolic myocardial tissue Doppler velocities, and filling and ejection velocities were measured, and cardiac output (CO) was calculated at rest and during peak stress. There was no difference in RV size (inlet dimension <3.5 cm), RV systolic long-axis amplitude, systolic and diastolic velocities, peak early/late diastolic velocity ratio, and RV CO between patients and controls at rest. During stress, RV systolic long-axis amplitude increased in controls (from 24 ± 6 to 30 ± 5 mm) and CO increased significantly (from 4.9 ± 1.2 to 12.5 ± 2.1 L/min, p <0.001 for the 2 items). In contrast, RV amplitude did not change with stress in patients (from 24 ± 5 to 22 ± 6 mm, p = NS), and the stress-increment in CO was augmented (from 4.2 ± 1.2 to 8.3 ± 2.0 L/min, p <0.001 vs control stress increment). Failure to increase RV systolic amplitude >2 mm was 79% sensitive and 88% specific for detecting ischemic RV dysfunction, and there was a close correlation between stress-induced change in RV systolic amplitude and change in CO in patients (r = 0.56, p <0.001). Early diastolic velocity increased in controls (from 10.8 ± 3.2 to 13.1 ± 3.6 cm/s, p <0.01) but did not change in patients (from 11.5 ± 3.7 to 11.3 ± 4.8 cm/s, p = NS). RV shortening after ejection did not appear in any control subject but did develop in 8 of 33 patients, thus contributing to the decrease in RV peak early/late diastolic velocity ratio in patients (from 1.1 ± 0.3 to 0.76 ± 0.4, p <0.001) compared with that in controls (1.3 ± 0.3 to 1.0 ± 0.2, p <0.001). In conclusion, markers of RV dysfunction are not related to left ventricular wall motion score index or long-axis changes with stress.