928-81 Importance of Holter Monitoring, as Compared to Exercise Testing, in Revealing ST-segment Changes in Patients with Syndrome X

Abstract

Despite growing interest and a large body of studies on syndrome X (anginal chest pain and angiographically normal coronary arteries), there are no data concerning the respective diagnostic value of exercise testing (ExT) and ambulatory Holter monitoring (HM) in revealing ischemic ST-segment changes in these patients. To address this problem, we performed ExT and 24-hour HM, off therapy, in 38 syndrome X patients (27 women, age 54 ± 8 years). ExT showed ST-segment depression (STd) in 28 patients (74% Group 1), whereas it was normal in 10 patients (26%, Group 2). Anginal chest pain during ExT was reported by 10 patients (36%) of Group 1 and 9 patients (90%) of Group 2 (p < 0.01). On the other hand, STd episodes were detected on HM in 22 patients (59%), 17 (61%) of whom belonging to Group 1 and 5 (50%) to Group 2 (p = NS). On the whole, 129 STd episodes, 14 (11%) of which associated to anginal pain, were found in the 22 patients (mean 5.8 ± 4.6 episodes/patient). A total of 21 STd episodes (5 associated to anginal pain) were detected on HM in the 5 patients with negative ExT (mean 4.3 ± 3.5 episodes/patient, range 1–10). In these 5 patients, heart rate at 1 mm STd during HM was significantly lower than that achieved at peak exercise during ExT (111 ± 19 vs. 136 ± 22 bpm, p = 0.01). The prevalence of positive HM in patients with negative ExT in our syndrome X patients was significantly higher than that observed in an unselected group of 76 patients with stable angina, significant coronary artery disease and negative ExT (50% vs 8%, p < 0.01). Thus, our data show that HM, with respect to ExT, has a significant additional diagnostic value in revealing the occurrence of ischemic ST-segment changes in patients with syndrome X. These findings also support the hypothesis that a microvascular vasoconstriction, rather than an impaired vasodilation, plays a major role in the pathophysiologic mechanisms leading to transient ischemia in these patients.