Relationship between exercise-induced myocardial ischemia and reduced left ventricular distensibility in patients with nonobstructive hypertrophic cardiomyopathy

Many studies have demonstrated that reduced left ventricular (LV) diastolic distensibility plays a key role in the pathophysiology of hypertrophic cardiomyopathy (HCM). However, the relationship between myocardial ischemia and reduced LV distensibility in HCM remains unclear. We aimed to clarify the relationship between exercise-induced ischemia and reduced LV distensibility in patients with HCM. Methods: Twenty patients with HCM and 5 age-matched control subjects underwent stress-redistribution ²⁰¹Tl myocardial scintigraphy and biventricular cardiac catheterization and echocardiography at rest and during exercise. Scintigraphic defect analysis was interpreted using Berman's 20-segment model. The summed stress score (SSS) was calculated as the sum of scores of the 20 LV segments and the summed difference score (SDS) was calculated as the sum of differences between each of the 20 LV segments on stress and rest images. Results: Patients were divided into 2 groups according to the ²⁰¹Tl defect as follows: 9 patients with an SSS on ²⁰¹Tl of >10 and an SDS on ²⁰¹Tl of >5 (ischemic group) and 11 patients with an SSS of <10 or an SDS of <5 (nonischemic group). The absolute increases from rest to peak exercise in LV end-diastolic pressure (LVEDP) and pulmonary artery wedge pressure were significantly greater (15.5 ± 5.2 vs. 7.6 ± 5.5 mm Hg and 17.3 ± 5.0 vs. 8.9 ± 5.0 mm Hg, P < 0.01, respectively), and the percentage changes from rest to peak exercise in the maximum first derivative of LV pressure and LV pressure half-time were significantly smaller in the ischemic HCM group compared with the nonischemic HCM group (70% ± 24% vs. 123% ± 43% and -32% ± 6.4% vs. -44% ± 9.4%, P < 0.01, respectively). However, the end-diastolic dimensions did not differ between the 2 HCM groups. One of the 9 patients in the ischemic group, as revealed by fill-in on ²⁰¹Tl scintigraphy, showed increased ¹⁸F-FDG uptake in the anteroseptal wall. Conclusion: Some HCM patients show a significant increase in LVEDP without chamber dilatation, indicating reduced LV diastolic distensibility. Myocardial ischemia may at least in part contribute to this condition.