There are two types of hypertrophic cardiomyopathy (HCM): hypertrophic obstructive cardiomyopathy (HOCM) and hypertrophic non-obstructive cardiomyopathy. It is also known that there are two types of HOCM; obstruction at the subaorta, called idiopathic hypertrophic subaortic stenosis (IHSS), and obstruction at the mid left ventricle (1, 2). Unlike in patients with IHSS, systolic murmur in patients with midventricular obstruction is generally not loud, and specific markers, such as systolic anterior motion of the mitral valve and a spike-and-dome pattern on carotid pulse tracing are not found. Thus, in the clinical setting, patients with midventricular obstruction may often be overlooked. Mitral regurgitation associated with systolic anterior motion of the anterior leaflet of the mitral valve usually exists in most patients with IHSS, and its severity is known to be correlated with the severity of left ventricular pressure gradient (LVPG). A recent study elucidated that LVPG observed in patients with HOCM was related to the prognosis in patients with HCM (3). Therefore, it is an important strategy to attenuate LVPG and to decrease mitral regurgitation in patients with HOCM, especially in patients with IHSS. However, both -blockers and calcium antagonists are often insufficient for attenuating LVPG. In 1982, Pollick (4) reported the usefulness of the antiarrhythmic drug disopyramide in attenuating LVPG in IHSS. Unfortunately sustained use of disopyramide is difficult owing to thirst, dysuria due to its strong anticholinergic action. We previously reported the usefulness of the antiarrhythmic drug, cibenzoline, the anticholinergic action of which is very weak, to attenuate LVPG and to improve left ventyricular diastolic functions in IHSS (5).A manuscript in this journal by Inada et al (6) reported a patient with IHSS whose severe LVPG and mitral regurgitation disappeared by an intravenous administration of cibenzoline.Takada et al (7) also reported the same effect of intravenous administration of cibenzoline on LVPG and mitral regurgitation in a patient with IHSS. We can estimate at least two mechanisms for these beneficial effects of cibenzoline on hemodynamics in patients with IHSS. One mechanism for these effects is the negative inotropic action by cibenzoline (5). This negative inotropic action of cibenzoline may be related to the suppression of left ventricular systolic function as reflected by a decrease of fractional shortening and by an increase of left ventricular end-systolic dimension. The other mechanism is the direct effect of cibenzoline through a marked decrease in the intracellular Ca 2+ concentration of myocytes through Na + and Ca 2+ channel blocking actions of cibenzoline (8). We indicated that left ventricular diastolic dysfunctions estimated by the transmitral Doppler flow pattern, left ventricular wall motion, apex cardiography and gated radionuclide angiography were all improved after the treatment by cibenzoline even in hypertrophic nonobstructive cardiomyopathy (9). This is the reason why we...
