Left ventricular regional systolic function in patient with hypertrophic cardiomyopathy by quantitative tissue velocity imaging

Abstract

The left ventricular regional systolic functions in patients with hypertrophic cardiomyopathy (HCM) were assessed by using quantitative tissue velocity imaging (QTVD). Left ventricular (LV) regional myocardial velocity along long- and short-axis in 31 HCM patients and 20 healthy subjects were analyzed by QTVI, and the regional myocardial systolic peak velocities (MVS) were measured. Mean MVS at each level including mitral annular, basal, middle and apical segments were calculated. The ratio of MVS along long-axis to that along short-axis (Ri) at basal and middle segments of the LV posterior wall and ventricular septum were calculated. The results showed that mean MVS was slower at each level including mitral annular, basal, middle and apical segments in the HCM patients than that in the healthy subjects (P<0.01). There were no significant differences in mean MVS between obstructive and non-obstructive groups in HCM patients. MVS of all regional myocardial segments along long-axis in the HCM patients were significantly slower than regional myocardial segments along long-axis in the HCM patients were significantly slower than that in the healthy subjects (P<0.05), but there was no significant difference in MVS of all regional myocardial segments along long-axis between hypertrophied and non-hypertrophied group in the HCM patients. Ri was significantly lower in the HCM patients than that in the healthy subjects. The LV regional myocardial contractility along long-axis was impaired not only in the hypertrophied wall but also in the non-hypertrophied one in patients with HCM, suggesting that QTVI can assess accurately LV regional systolic function in patient with HCM and provides a novel means for an early diagnosis before and independent of hypertrophy.

Keywords

quantitative tissue velocity imaging / hypertrophic cardiomyopathy / left ventricular regional systolic function

References

[1] RustE M, AlbayyaF P, MetzgerJ M. Identification of a contractile deficit in adult cardiac myocytes expressing hypertrophic cardiomyopathy-associated mutant troponin T proteins. J Clin Invest, 1999, 103: 1459-1467

[2] MarianA J. Pathogenesis of diverse clinical and pathological phenotypes in hypertrophic cardiomyopathy. Lancet, 2000, 355(9197): 58-60

[3] KimS J, IizukaK, KellyR A, et al.. An α-cardiac myosin heavy chain gene mutation impairs contraction and relaxation function of cardiac myocytes. Am J Physiol, 1999, 276: H1780-H1787

[4] NaguehS F, KopelenH A, LimD S, et al.. Tissue Doppler imaging consistently detects myocardial contraction and relaxation abnormalities, irrespective of cardiac hypertrophy, in a transgenic rabbit model of human hypertrophic cardiomyopathy. Circulation, 2000, 102(12): 1346-1350

[5] YamadaH, OkiT, TabataT, et al.. Assessment of the systolic left ventricular myocardial velocity profile and gradient using tissue Doppler imaging in patients with hypertrophic cardiomyopathy. Echocardiography, 1999, 16(8): 775-775

[6] NaguehS F, BachinskiL L, MeyerD, et al.. Tissue Doppler imaging consistently detects myocardial abnormalities in patients with hypertrophic cardiomyopathy and provides a novel means for an early diagnosis before and independently of hypertrophy. Circulation, 2001, 104(2): 128-130

[7] CardimN, PerrotA, FerreiraT, et al.. Usefulness of Doppler myocardial imaging for identification of mutation carriers of familial hypertrophic cardiomyopathy. Am J Cardiol, 2002, 90(2): 128-132

[8] OnoseY, OkiT, MishiroY, et al.. Influence of aging on systolie left ventricular wall motion velocities along the long and short axis in clinically normal patients determined by pulse tissue Doppler imaging. J Am Soc Echocardiogr, 1999, 12(11): 921-926

[9] CardimN, TorresD, MotaisH, et al.. Tissue Doppler imaging in hypertrophic cardiomyopathy: impact of intraventricular obstruction on longitudinal left ventricular function. Rev Port Cardiol, 2002, 21(3): 271-297