Evaluation and treatment for angina in pulmonary arterial hypertension

Abstract

p e m t d m p i a f lthough angina is a frequent complaint in patients with ulmonary hypertension (1), its cause often remains unlear. In addition, angina is commonly ignored and may esult in irrevocable consequences. Many theories of the ause of this pain have been proposed, with right ventriclar ischemia (2) being one of the more commonly accepted echanisms. However, a dilated pulmonary artery trunk an compress the left main coronary artery (3,4), resulting in evere stenosis, causing left ventricular ischemia, and, subequently, causing left ventricular dysfunction. In this issue of The American Journal of Medicine, Mesuita et al (5) report on the likelihood of left main coroary artery compression in pulmonary hypertension ased on the pulmonary trunk diameter. In this study, the uthors reviewed their experience with 36 patients with ocumented pulmonary arterial hypertension. Twentyix of the patients had symptoms of chest pain; however, nly 7 of these patients, those with the largest pulmonary rtery trunk, had substantial left coronary artery compresion consistent with left ventricular ischemia. The cause of he angina in the remaining 19 patients is unclear and may e due to right ventricular ischemia. Right ventricular ischmia decreases the coronary driving pressure of the right entricle, thereby causing angina complaints (3). Regardless of the cause, evaluation of chest pain is andatory in patients with pulmonary hypertension, as reatment may differ considerably based on the cause of he chest pain. To prevent substantial left ventricular dysunction it is essential to exclude left main coronary arery compression. Mesquita and colleagues also suggest guidelines for valuating patients with pulmonary arterial hypertension ho have complaints of angina. Noninvasive measureent of the pulmonary trunk diameter may be helpful in etermining the likelihood of left coronary artery comression and in selecting patients for diagnostic coronary ngiography. However, in this paper, the only parameter hat significantly correlated with coronary artery comression due to dilated pulmonary trunk diameter was he ratio of the pulmonary trunk diameter to the aortic iameter. The threshold level for pulmonary trunk diamter, below which no cases of coronary artery compresion were seen, was 40 mm. Seven of 19 patients (37%) ith values above 40 mm had coronary artery compres-