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Relationship between exercise-induced myocardial ischemia and reduced left ventricular distensibility in patients
Satoshi Isobe1, Hideo Izawa, Yasushi Takeichi
1Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan. sisobe@med.nagoya-u.ac.jp
Insights
Myocardial ischemia contributes to reduced left ventricular (LV) diastolic distensibility in hypertrophic cardiomyopathy (HCM) patients. This study clarifies the link between exercise-induced ischemia and impaired LV diastolic function in HCM.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Medical Imaging
Background:
- Reduced left ventricular (LV) diastolic distensibility is a key factor in hypertrophic cardiomyopathy (HCM) pathophysiology.
- The precise relationship between myocardial ischemia and impaired LV distensibility in HCM remains incompletely understood.
Purpose of the Study:
- To investigate the association between exercise-induced myocardial ischemia and reduced LV diastolic distensibility in patients diagnosed with HCM.
Main Methods:
- Utilized stress-redistribution (201)Tl myocardial scintigraphy, biventricular cardiac catheterization, and echocardiography in 20 HCM patients and 5 controls.
- Analyzed scintigraphic defects using Berman's 20-segment model, calculating Summed Stress Score (SSS) and Summed Difference Score (SDS).
- Assessed hemodynamic parameters including LV end-diastolic pressure (LVEDP) and LV pressure half-time during rest and peak exercise.
Main Results:
- Patients were categorized into ischemic (SSS ≥10, SDS ≥5) and non-ischemic groups.
- The ischemic HCM group exhibited significantly greater increases in LVEDP and pulmonary artery wedge pressure during exercise compared to the non-ischemic group.
- The ischemic group showed significantly smaller percentage changes in LV pressure first derivative and LV pressure half-time, indicating impaired diastolic function, without differences in end-diastolic dimensions.
Conclusions:
- Elevated LVEDP without chamber dilation in some HCM patients signifies reduced LV diastolic distensibility.
- Exercise-induced myocardial ischemia appears to be a contributing factor to the reduced LV diastolic distensibility observed in HCM.
Unlabelled:
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 (201)Tl 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 (201)Tl defect as follows: 9 patients with an SSS on (201)Tl of >or=10 and an SDS on (201)Tl of >or=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 (201)Tl scintigraphy, showed increased (18)F-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.
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