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Impaired Left Ventricular Contractile Reserve in Patients With Hypertrophic Cardiomyopathy and Abnormal Blood
Mayumi Takeoka1, Michiyo Yamano1,2, Sakiko Honda1
1Department of Cardiology, Matsushita Memorial Hospital, Moriguchi, JPN.
Insights
Abnormal blood pressure response during exercise in hypertrophic cardiomyopathy (HCM) patients is linked to reduced left ventricular contractile reserve. This finding suggests impaired cardiac function may underlie exercise blood pressure abnormalities in HCM.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Exercise Physiology
Background:
- Abnormal blood pressure response (ABPR) is a known risk factor for sudden cardiac death in hypertrophic cardiomyopathy (HCM).
- The relationship between ABPR during exercise and left ventricular (LV) contractile reserve in HCM patients requires further investigation.
Purpose of the Study:
- To investigate the association between ABPR during exercise stress echocardiography (ESE) and impaired LV contractile reserve in HCM patients.
- To determine if reduced two-dimensional strain parameters correlate with ABPR during ESE in HCM.
Main Methods:
- 26 HCM patients underwent ESE with treadmill exercise.
- ABPR was defined as a blood pressure increase <20 mmHg from baseline at maximum workload.
- LV global longitudinal strain and other echocardiographic parameters were compared between patients with and without ABPR.
Main Results:
- Nine out of 26 HCM patients exhibited ABPR.
- No significant differences in cardiac output or E/e' ratio changes were observed between groups.
- Patients with ABPR showed a significantly lower percent change in LV global longitudinal strain compared to those without ABPR (12±17% vs. 27±15%, P=0.02).
Conclusions:
- Impaired LV contractile reserve during exercise may contribute to ABPR in HCM patients.
- Reduced LV global longitudinal strain during exercise is associated with ABPR in HCM.
Background:
Abnormal blood pressure response (ABPR) has been reported to be a risk factor for sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). We aimed to elucidate the relationship between ABPR during exercise stress echocardiography (ESE) and impaired left ventricular (LV) contractile reserve based on two-dimensional strain in patients with HCM.
Methods:
Patients with HCM underwent ESE with treadmill exercise. Patients whose blood pressure elevation at maximum workload was lower than 20 mmHg from baseline were classified as having ABPR. Echocardiographic parameters were compared between patients with and without ABPR. Results: Of 26 patients with HCM, nine patients were diagnosed with ABPR. Significant LV outflow tract obstruction (>50 mmHg) was provoked only in one patient with ABPR (baseline to the conclusion of the exercise, 15.2 mmHg to 63.0 mmHg). Change in cardiac output (CO) and the ratio of early diastolic velocity to early annular velocity (E/e') from baseline to just after the conclusion of exercise did not differ between patients with and without ABPR (CO, 102±40% vs. 122±45%, P = 0.19; E/e', 4±22% vs. 2±20%, P = 0.86). Change in systemic vascular resistance change was not significant (patients with vs. without ABPR, -52±10% vs. -46±13%, P = 0.24). Percent change in LV global longitudinal strain was lower in patients with ABPR than patients without ABPR (12±17% vs. 27±15%, P = 0.02).
Conclusion:
In conclusion, impaired LV contractile reserve during exercise might contribute to ABPR in patients with HCM.
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