Key result
Syncope or NSVT in HCM patients shows no association with worse coronary vasodilator reserve.
Why the study?
Coronary vasodilator reserve is impaired in hypertrophic cardiomyopathy despite normal coronaries, prompting evaluation of whether its severity correlates with syncope and non-sustained ventricular tachycardia.
Is the severity of coronary vasodilator reserve impairment correlated with the occurrence of syncope and non-sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy?
Observational (n=84)
Is the severity of coronary vasodilator reserve impairment correlated with the occurrence of syncope and non-sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy?
Syncope and non-sustained ventricular tachycardia in hypertrophic cardiomyopathy are not related to the severity of coronary microvascular dysfunction, but NSVT is associated with greater left ventricular dilation.
Does not support coronary vasodilator reserve as a determinant of syncope or NSVT in hypertrophic cardiomyopathy; leaves open other contributors to sudden death risk.
UNLABELLED: Non-sustained ventricular tachycardia on Holter and syncope have been considered risk factors for sudden death in hypertrophic cardiomyopathy. AIMS: In these patients the coronary vasodilator reserve is impaired despite normal coronaries, so we evaluated the correlation between the severity of coronary vasodilator reserve impairment and the occurrence of syncope and non-sustained ventricular tachycardia. METHODS AND RESULTS: Eighty-four patients with hypertrophic cardiomyopathy (62 males, age 43 +/- 12 years) had a two-dimensional echocardiographic study and a 48-h Holter. Myocardial blood flow was measured by positron emission tomography, at baseline and after dipyridamole, and the coronary vasodilator reserve was computed as dipyridamole myocardial blood flow/baseline myocardial blood flow. In 27 patients, subendocardial and subepicardial myocardial blood flow was measured in the septum and the subendocardial/subepicardial ratio was computed. Twenty of 84 patients had at least one syncopal episode, and 26 had at least one run of non-sustained ventricular tachycardia on Holter. Baseline and dipyridamole myocardial blood flow, coronary vasodilator reserve, and baseline and dipyridamole subendocardial/subepicardial myocardial blood flow ratio were similar in patients with and without syncope and with and without non-sustained ventricular tachycardia on Holter. However, patients with non-sustained ventricular tachycardia had larger left ventricular end-diastolic (47 +/- 6 vs 44 +/- 5 mm, P < 0.05) and end-systolic diameters (30 +/- 6 vs 27 +/- 4 mm, P < 0.05). CONCLUSIONS: (1) Coronary vasodilation is not more severely impaired in patients with hypertrophic cardiomyopathy and syncope or non-sustained ventricular tachycardia. (2) The left ventricle is more dilated in hypertrophic cardiomyopathy with non-sustained ventricular tachycardia.
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Lorenzoni et al. (1997) conducted an observational in Hypertrophic cardiomyopathy (n=84). Syncope or non-sustained ventricular tachycardia vs. Absence of syncope or non-sustained ventricular tachycardia was evaluated on Coronary vasodilator reserve and myocardial blood flow. Coronary vasodilator reserve was not more severely impaired in hypertrophic cardiomyopathy patients with syncope or non-sustained ventricular tachycardia compared to those without.
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