Advanced left ventricular hypertrophy (wall thickness ≥1.3 cm) in systemic hypertension exhibited a right-shifted wall stress-diameter relation, indicating depressed myocardial contractility.
Observational (n=32)
To assess the contractile state of the hypertrophied ventricle induced by long-standing systemic hypertension in 22 patients, we used echocardiography for the measurement of the ventricular diameter and posterior wall thickness, together with simultaneous recording of brachial arterial pressure. Meridional wall stress (WSt) was used for the expression of the force per unit cross-sectional area. The WSt-diameter relation obtained during dynamic responses to acute pressure reduction by nitroprusside infusion was compared with the same relation obtained in 10 normal subjects (posterior wall thickness averaged 0.7 cm range 0.6-0.9 cm) over a range of matched systolic pressure induced by methoxamine administration. In 15 patients in whom end-diastolic wall thickness increased to 1.1 cm (range 1.0-1.2 cm), the linear WSt-diameter relation at end-systole did not differ from the control group, indicating a normal level of inotropic state. In the seven patients with an end-diastolic wall thickness of 1.3 cm or more, the end-systolic WSt-diameter relation was clearly shifted to the right and had a less steep slope. These findings indicate that in advanced left ventricular hypertrophy induced by pressure overload, myocardial contractility may be depressed.
Takahashi et al. (Tue,) conducted a observational in Systemic hypertension with left ventricular hypertrophy (n=32). Acute pressure reduction by nitroprusside infusion vs. Normal subjects receiving methoxamine administration was evaluated on End-systolic meridional wall stress (WSt)-diameter relation. Advanced left ventricular hypertrophy (wall thickness ≥1.3 cm) in systemic hypertension exhibited a right-shifted wall stress-diameter relation, indicating depressed myocardial contractility.