Key result
Metabolic syndrome was associated with significantly reduced longitudinal contractile reserve during peak exercise compared to controls (2.00 vs 2.90 cm/sec, p=0.015) in non-diabetic hypertensive patients.
Why the study?
Does metabolic syndrome reduce myocardial contractile reserve during exercise in non-diabetic hypertensive subjects?
Observational (n=112)
No
Does metabolic syndrome reduce myocardial contractile reserve during exercise in non-diabetic hypertensive subjects?
Absolute Event Rate: 2% vs 2.9%
p-value: p=0.015
Metabolic syndrome is independently associated with reduced myocardial contractile reserve during exercise in non-diabetic hypertensive patients, indicating early LV systolic dysfunction.
MS may impair exercise LV reserve in treated hypertension; hypothesis-generating and requires prospective validation before clinical consideration.
BACKGROUND: Metabolic syndrome (MS) is associated with increased left ventricular (LV) mass and diastolic dysfunction. This study uses relatively load-independent Doppler tissue echocardiography to examine whether MS is associated with decreased longitudinal contractile reserve during dynamic exercise. METHODS: A total of 112 patients with relatively well-controlled, treated hypertension who complained of exertional dyspnea were enrolled (average age: 56.7 ± 10.5 years). Fifty-six were non-diabetic patients with MS (Group 1), and 56 were age-sex matched hypertensive patients without MS (Group 2). Exercise stress echo was performed using a symptom-limited, multistage, supine bicycle exercise test. Multiple Doppler parameters were obtained at baseline, at each stage of exercise, and during recovery. RESULTS: There was no significant difference between the two groups in terms of age, gender, and hemodynamic variables. E/E', an index of LV filling pressure, was significantly higher in the MS group at rest and during exercise. The longitudinal contractile reserve, the change in S' (longitudinal tissue velocity) from baseline to peak exercise, was significantly lower in the MS group (2.00 ± 1.65 vs. 2.90 ± 1.66, p = 0.015). Multiple regression analysis showed independent association of MS with longitudinal contractile reserve when controlled for confounding factors, such as LV mass index, gender, blood pressure, and age (β = -0.235, p = 0.035). CONCLUSION: Longitudinal contractile reserve was reduced in MS patients compared to others, although both groups demonstrated similar longitudinal contractile function at rest. We present the first demonstration that metabolic syndrome is independently associated with LV systolic dysfunction during exercise in hypertensive patients.
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Ha et al. (2011) conducted an observational in Hypertension with exertional dyspnea (n=112). Metabolic syndrome vs. Hypertensive patients without metabolic syndrome was evaluated on Longitudinal contractile reserve (change in S' from baseline to peak exercise) (p=0.015). Metabolic syndrome was associated with significantly reduced longitudinal contractile reserve during peak exercise compared to controls (2.00 vs 2.90 cm/sec, p=0.015) in non-diabetic hypertensive patients.
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