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  • Title: Use of angiotensin II stress pulsed tissue Doppler imaging to evaluate regional left ventricular contractility in patients with hypertrophic cardiomyopathy.
    Author: Mishiro Y, Oki T, Yamada H, Onose Y, Matsuoka M, Tabata T, Wakatsuki T, Ito S.
    Journal: J Am Soc Echocardiogr; 2000 Dec; 13(12):1065-73. PubMed ID: 11119273.
    Abstract:
    There is controversy concerning whether contract-ility in the nonhypertrophied region of the left ventricular (LV) wall is impaired or normal in patients with hypertrophic cardiomyopathy (HCM). Global LV systolic function decreases with increases in afterload in this disease. This study was performed to identify abnormalities in regional LV contractility along the long and short axes in the setting of HCM with the use of angiotensin II (AT-II) stress pulsed tissue Doppler imaging (PTDI). Angiotensin II was administered intravenously to patients with asymmetric septal hypertrophy (HCM group, n = 21) and age-matched normal volunteers (N group, n = 12). We then measured the percent LV fractional shortening (%FS) and end-systolic circumferential LV wall stress by M-mode echocardiography, LV ejection fraction (LVEF) by 2-dimensional echocardiography, and time-velocity integral (TVI) of LV outflow velocity by pulsed Doppler echocardiography. The peak first and second systolic LV wall motion velocities along the long (L-Sw(1) and L-Sw(2)) and short (S-Sw(1) and S-Sw(2)) axes were measured in the LV posterior wall and ventricular septum with the use of PTDI. The end-systolic circumferential LV wall stress at baseline was significantly lower in the HCM group. The L-Sw(1) and L-Sw(2) for the posterior wall were significantly lower in the HCM group, but the S-Sw(1) and S-Sw(2) for the posterior wall and ventricular septum were similar in the two groups. The %FS, LVEF, TVI, and systolic PTDI variables along both axes for the posterior wall decreased significantly, and end-systolic circumferential LV wall stress increased significantly at AT-II doses of 0.005 or 0.010 microg/kg per minute in the HCM group. No significant changes were found in either group in the systolic PTDI variables (except for L-Sw(1)) for the ventricular septum with AT-II infusion. Contractility along the long and short axes of the nonhypertrophied LV wall is easily impaired with increases in afterload in patients with HCM, resulting in a decrease in global LV systolic function. We found AT-II stress PTDI to be a safe and useful technique for evaluating the regional LV systolic function in this disease.
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