br Discussion There are many reports on the effectiveness

Discussion There are many reports on the effectiveness of pacing therapy for hypertrophic obstructive cardiomyopathy. Fananapazir et al. reported that long-term right ventricular apical pacing improved both the left ventricular outflow tract gradient and subjective symptoms [3]. Maron et al. reported improvement in quality of life scores with long-term DDD pacing, but no relationship with gradient decrease was seen, and the improvements in subjective symptoms were considered a placebo effect from pacemaker dopamine receptor antagonist [4]. Hosoda et al. reported a case of hypertrophic obstructive cardiomyopathy treated with DDD pacing therapy. In that report, cardiac catheterization study was performed 7 years after ICD implantation, and LVOT gradient was significantly low (10mmHg) and this state continued more than 60min after pacing was turned off [5]. In the current case, no changes in the left ventricular outflow tract gradient were seen for 7 months after pacing off. Pacing therapy is reported to not only reduce myocardial constriction around the pacing site, but also produce constriction from mechanical dyssynchrony, with remodeling in the long term [6–10]. It has also been reported that an abnormal excitation pattern in the left ventricle continues for some time after pacing off [6]. In the current case, long-term right ventricular apical pacing brought about left ventricular myocardial remodeling, and it is thought that the gradient did not increase because this state continued for some time even after pacing off. Over time, after pacing off, the LVOT tract gradient increased again. It was therefore judged that reverse remodeling had occurred. A new stenosis in the center of the left ventricle and apical ventricular aneurysm-like changes were seen at this time. There have been no other similar reports. Stenosis in the center of the left ventricle is a relatively rare condition even in hypertrophic cardiomyopathy, and it is reported to often be accompanied by apical ventricular aneurysm from the frequently increased pressure load in the apex [11,12]. Although there are no reports of stenosis in the center of the left ventricle during the course of hypertrophic cardiomyopathy accompanied by LVOT stenosis, this may be the natural course of hypertrophic cardiomyopathy.
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Introduction
Case report A 76-year-old female with New York Heart Association class III congestive heart failure was referred to our hospital for cardiac resynchronization therapy (CRT). Echocardiography showed severe LV dysfunction (LV ejection fraction=23%, LV end-diastolic diameter=69mm, LV end-systolic diameter=59mm, and LV end-systolic volume=124mL) and significant LV dyssynchrony. A 12-lead ECG showed sinus rhythm and complete left bundle block with a QRS duration of 184ms (Fig. 1A). Coronary angiography showed no significant stenosis, and we diagnosed her as having dilated cardiomyopathy. Holter ECG monitoring detected non-sustained ventricular tachycardia. The patient was scheduled for implantation of a defibrillator with biventricular pacing capability (CRT-D). A transvenous approach was utilized to position an active-fixation lead (1888TC, 52cm, St. Jude Medical, St. Paul, MN, USA) in the right atrial appendage and a right ventricular shocking lead (DURATA 7122Q, St. Jude Medical, St. Paul, MN, USA) in the lower septum of the right ventricle (Fig. 2C and D). The LV lead (QuickFlex 1158T-86 cm, St. Jude Medical, St. Paul, MN, USA) was introduced via the right subclavian vein and advanced through the coronary sinus into the posterolateral vein (Fig. 2B–D). A coronary sinus angiogram revealed that the lateral vein was too small (Fig. 2A), and the LV lead could not be inserted. We inserted the LV lead into the posterolateral vein (Fig. 2B). The LV pacing threshold at implantation was 0.7V at 0.4ms, and the impedance was 1174Ω. The R-wave sensing threshold was 22.9mV. Diaphragm stimulation was not observed on fluoroscopy during pacing at outputs of up to 10V. A CRT-D generator (PROMOTE+CD3211-36Q, St. Jude Medical, St. Paul, MN, USA) was implanted in the left pectoral region.