(Circulation. 1998;98:2098-2102.)
© 1998 American Heart Association, Inc.
Correspondence |
University of Patras Medical School, Department of Internal Medicine, Division of Cardiology, Rio, Patras, Greece
The Second Department of Internal Medicine, Ehime University School of Medicine
Internal Medicine Takanoko Hospital, Ehime, Japan
We appreciate the opportunity to respond the comments that Dr Hahalis et al have made regarding our recent article.1 In this article, we reported that the class Ia antiarrhythmic drug cibenzoline markedly reduced left ventricular pressure gradient mainly due to a decrease in left ventricular myocardial contractility in patients with hypertrophic obstructive cardiomyopathy (HOCM). In addition, in our study, isovolumic relaxation time (IRT) increased, peak E-wave velocity remained unchanged, peak A-wave velocity decreased, and thus, the E/A ratio increased. We interpreted that these changes might be due to a decrease in both left atrial and ventricular pressures caused by the administration of cibenzoline.
Hahalis et al are concerned about our results in this Doppler echocardiographic study. They state that cibenzoline caused an impairment of left ventricular relaxation, resulting in a longer IRT. Therefore, they interpret that the altered mitral flow pattern indicates an elevation rather than a decrease in left ventricular filling pressure. However, we do not agree with their interpretation.
First, their interpretation is based on the fact that left ventricular elastic recoil decreases at low contractility.2 This understanding fits the patients whose systolic dysfunction parallels their diastolic dysfunction. In patients with hypertrophic cardiomyopathy, systolic function is usually supernormal, but diastolic function is markedly disturbed. Thus, patients with hypertrophic cardiomyopathy, especially in HOCM, respond in a paradoxical manner to a variety of stimuli.3 In fact, Nishimura et al4 reported that Doppler mitral flow velocity curves were useful in predicting left ventricular filling pressure in patients with left ventricular systolic dysfunction, but these curves could not be used in patients with hypertrophic cardiomyopathy.
Second, the pattern of mitral flow velocity curve represents the relative pressure gradient between the left ventricle and left atrium during diastole. Thus, an increase in left atrial pressure results in a higher E-velocity, a shorter deceleration time, and a shorter IRT. After the administration of cibenzoline, E-velocity remained unchanged and IRT was significantly prolonged. The deceleration time in 10 patients1 was also significantly prolonged. Therefore, it is reasonable to interpret that our data may be due to a decrease in left atrial pressure. Gwathmey et al5 indicated that intracellular Ca2+ overload was closely related to diastolic dysfunction in hypertrophic cardiomyopathy. Experimental studies show that cibenzoline possesses a certain calcium channel-blocking property. The beneficial effect of cibenzoline on the Doppler mitral flow pattern in HOCM may be due to this property.
References
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