Patients with nonobstructive hypertrophic cardiomyopathy showed a significantly greater increase in fractional shortening (12% vs 7%, p<0.05) during low-dose epinephrine infusion compared to healthy controls.
Case-Control (n=42)
No
Absolute Event Rate: 12% vs 7%
p-value: p=<0.05
To study the role of catecholamines in the pathogenesis of hypertrophic cardiomyopathy (HCM), hemodynamic responses to low and high dose infusions of epinephrine (0.037 and 0.074 micrograms/Kg/min) were compared between 21 patients with nonobstructive HCM and 21 healthy controls, matched for age and sex. During low dose infusion, patients with HCM showed significantly greater responses (p less than 0.05) than controls in echocardiographic left ventricular (LV) end-systolic dimension (-8 +/- 1% vs -4 +/- 1%, mean +/- SEM), fractional shortening (12 +/- 2% vs 7 +/- 1%) and peak systolic velocity of the LV posterior wall (32 +/- 5% vs 15 +/- 4%), but the differences disappeared during high dose infusion. Thus, patients with HCM started to respond to epinephrine earlier than controls and seemed to have an increased sensitivity of beta-adrenergic receptors in the cardiovascular system. As the augmented responses were more evident in younger patients (less than 35 years) who manifested frequent familial occurrences of HCM, the increased sensitivity to catecholamine was postulated to be genetically determined and to be related to the abnormal myocardial hypertrophy of HCM.
Koga et al. (Tue,) conducted a case-control in Nonobstructive hypertrophic cardiomyopathy (n=42). Epinephrine infusion vs. Healthy controls was evaluated on Percent change in fractional shortening during low dose epinephrine infusion (p=<0.05). Patients with nonobstructive hypertrophic cardiomyopathy showed a significantly greater increase in fractional shortening (12% vs 7%, p<0.05) during low-dose epinephrine infusion compared to healthy controls.
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