Akosah K, Olsovsky M, Mohanty P K
Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, VA 23249, USA.
Chest. 1995 Sep;108(3):695-700. doi: 10.1378/chest.108.3.695.
The clinical consequences of cardiac denervation include the inability of the heart transplant recipient to sense cardiac pain. This is due mainly to interruption of ventricular sympathetic afferents normally responsible for transmission of cardiac pain. Although angina has been reported in transplant recipients, to our knowledge, its temporal relationship to myocardial ischemia has not been previously demonstrated.
Eighty-two patients with heart transplants were serially evaluated by dobutamine stress echocardiography (DSE). In patients who developed angina during DSE, we sought to determine if the onset of angina was related to myocardial ischemia as demonstrated by stress-induced wall motion abnormalities. Coronary angiography was performed within 48 h of DSE in 45 of 82 patients.
Mean patient age and time since transplant were 53.1 +/- 1.1 years and 57.7 +/- 30.4 months, respectively (mean +/- SEM). Eleven patients developed typical angina during DSE. Three of the 11 (27%) had diagnostic ECG changes. All 11 had stress-induced regional wall motion abnormalities (WMA). Nine of the 11 patients (82%) had coronary angiographic data available that demonstrated significant coronary artery disease (CAD) in 8 (89%). All coronary lesions matched the observed segmental WMA. There was no difference between the angina (n = 11) and no angina (n = 71) groups with respect to peak heart rate (HR) (141 +/- 7 vs 145 +/- 3 beats/min; p = NS), peak systolic blood pressure (SBP) (155 +/- 8 vs 149 +/- 3 mm Hg; p = NS), or rate pressure product (21,699 +/- 1,490 vs 21,646 +/- 621 mm Hg x beats/min; p = NS). However, the mean time since transplant was significantly higher in patients with DSE-induced angina (80.3 +/- 6.2 vs 57.3 +/- 3.5 months; p < 0.05).
These data suggest that (1) the occurrence of angina in long-term transplant recipients with CAD is directly related to myocardial ischemia despite anatomic ventricular denervation, and (2) sympathetic reinnervation in the long-term may account for the occurrence of angina in cardiac transplant recipients.
