Why the study?
Does an abnormal blood pressure response during exercise predict malignant arrhythmias and reflect altered hemodynamics in patients with hypertrophic cardiomyopathy?
Does an abnormal blood pressure response during exercise predict malignant arrhythmias and reflect altered hemodynamics in patients with hypertrophic cardiomyopathy?
An abnormal blood pressure response during exercise in patients with nonobstructive HCM is driven by an inability to increase stroke volume and is associated with a significantly higher risk of malignant arrhythmias.
Abnormal exercise BPR may flag higher arrhythmia risk in nonobstructive HCM; leaves open prospective validation for risk stratification.
BACKGROUND: An abnormal blood pressure response (BPR) during exercise has been proposed as a risk factor for sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). Some patients with HCM show systolic dysfunction during exercise. HYPOTHESIS: The aim of this study was to clarify the hemodynamic response during exercise and prognosis in patients with HCM and abnormal BPR. METHODS: Sixty-five patients with HCM underwent radionuclide monitoring of left ventricular function and measurement of blood pressure during supine ergometer exercise. Thereafter, cardiac events were recorded for an average period of 76 months. RESULTS: Seven of 65 patients had abnormal BPR, while the others had normal BPR. Changes of heart rate and systemic vascular resistance during exercise did not differ between the two groups. Stroke volume did not increase in the abnormal BPR group but did in the normal BPR group. During a mean follow-up period of 76 months, three of the seven patients (43%) with abnormal but only one patient (2%) with normal BPR suffered a malignant arrhythmia. CONCLUSIONS: Abnormal BPR occurred in about 11% of patients with nonobstructive HCM and was associated with a high prevalence of cardiac events. The predictor of abnormal BPR during exercise may not be an abnormal response of systemic vascular resistance and heart rate, but the lack of an appropriate increase in stroke volume.
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Nagata et al. (2003) studied this question.
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