Key result
In patients with dilated cardiomyopathy, left ventricular hypertrophy was associated with significantly higher fractional shortening during isoproterenol infusion (29% vs 17%; p<0.025).
Why the study?
Does the presence of left ventricular hypertrophy improve systolic reserve and alter catecholamine response in patients with dilated cardiomyopathy?
Observational (n=17)
Does the presence of left ventricular hypertrophy improve systolic reserve and alter catecholamine response in patients with dilated cardiomyopathy?
In patients with dilated cardiomyopathy, the presence of left ventricular hypertrophy is associated with greater systolic reserve and lower sympathetic activation during exercise, potentially explaining their better prognosis.
Answers are grounded in this paper and cite their sources.
LVH may mark preserved systolic reserve in dilated cardiomyopathy; leaves open causal links to prognosis and need for prospective studies.
BACKGROUND AND HYPOTHESIS: Patients with dilated cardiomyopathy (DCM) with left ventricular hypertrophy (LVH) have been found to have a better prognosis than patients without LVH. However, the pathophysiologic mechanism for that has not been investigated. We sought to clarify the pathophysiologic significance of LVH in DCM. METHODS: We performed isoproterenol infusion echocardiography (0.02 micrograms/kg/min) in 17 patients with DCM, and measured plasma epinephrine and norepinephrine levels at rest and at the end of ergometer exercise in 14 of the 17 patients. Patients were classified into groups according to the presence (9 patients) (LVH+) or absence (8 patients) (LVH-) of LVH. Left ventricular hypertrophy was defined as an inter-ventricular thickness or posterior wall thickness > or = 13 mm. RESULTS: Although there was no significant difference between groups in fractional shortening at rest during isoproterenol infusion, fractional shortening was significantly higher in the LVH(+) group than in the LVH(-) group (29 +/- 9 vs. 17 +/- 8%; p < 0.025). Although there was no significant difference in plasma norepinephrine level, it was significantly lower in the LVH(+) group than in the LVH(-) group (233 +/- 169 vs. 519 +/- 258 pg/ml; p < 0.05) at the end point of the exercise. CONCLUSION: Systolic reserve, represented by the response to isoproterenol, is greater in patients with DCM with LVH than in those without LVH, and a lower plasma level of norepinephrine is needed to activate the myocardium during exercise in patients with DCM with LVH. This pathophysiologic characteristic could be one of the mechanisms which explain a better prognosis in patients with DCM with LVH.
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Iida et al. (1996) conducted an observational in Dilated cardiomyopathy (n=17). Left ventricular hypertrophy vs. Absence of left ventricular hypertrophy was evaluated on Fractional shortening during isoproterenol infusion (p=<0.025). In patients with dilated cardiomyopathy, left ventricular hypertrophy was associated with significantly higher fractional shortening during isoproterenol infusion (29% vs 17%; p<0.025).
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