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  • There are several limitations to the

    2019-04-28

    There are several limitations to the procedure described herein. The present GC was developed for engaging the coronary sinus via a right-sided approach. However, this GC was bent dorsally and had the shortest tip and most acute tip angle among the Attain™ family, which facilitated its placement into the inferior IAS via a left-sided approach. Because the size and rotation of the Rapamycin is individual and variable, several combinations with various shapes, lengths, and Fr sizes may be required. At present, a recently developed active fixation lead (CapSureFix MRI™ 5086; Medtronic) with magnetic resonance imaging (MRI) capability is too thick (7.0 Fr) to insert in the current 9.0 Fr (7.2 Fr inner) system. However, the technique described herein will become an attractive option when a much thinner active fixation lead with MRI capability is developed. Although the tip of the present GC is sufficiently soft and safely facilitates bare manipulation in the right heart, careful and gentle manipulation was required to avoid mechanical injury inside the RA. Detailed three-dimensional anatomical knowledge combined with fluoroscopic biplane cardiac imaging is believed to be essential for such procedures. To avoid any complications, this technique should not be applied to sites other than the IAS. The SelectSecure™ system involves the use of a lumenless deflectable GC-delivered bipolar lead [13]; however, the deflectable GC curve is too large for IAS selection, and its tip is much harder compared with the GC used in the present case. Since a significantly high rate of complications was reported in domestic initial clinical experience with the above-mentioned system, it is not routinely used in Japan.
    Conflict of interest
    Acknowledgments
    Introduction
    Case history History of current illness: the patient was a 77-year-old woman. She was treated for hypertension and dyslipidemia. She had no siblings with heart disease or who had experienced sudden death. She began to feel exertional chest discomfort beginning in Octobar 2000. From about March 2005, the chest discomfort started to occur frequently, and she was examined in our department. Asymmetric septal hypertrophy (ASH), systolic anterior motion (SAM), and left ventricular outflow tract (LVOT) stenosis (PG max=124mmHg) were seen on echocardiography (Fig. 1), and the patient was hospitalized with a diagnosis of suspected hypertrophic obstructive cardiomyopathy. No significant stenosis was seen on coronary angiography, and the lumen was banana shaped in systole on left ventriculography. The maximum LV-Ao gradient was 130mmHg with pullback pressure. On histopathological examination of a myocardial biopsy specimen obtained at the same time, myocardial disarray was seen, and hypertrophic obstructive cardiomyopathy was diagnosed. The outflow tract gradient was judged to be the cause of the chest discomfort. With the aim of relieving the pressure gradient, oral cibenzoline 300mg/day and apical DDD pacing were started. The patient had no episode of syncope, but considering the proarrhythmic effect of cibenzoline (there are some case reports regarding class Ic antiarrhythmic drug-induced ventricular tachycardia and fibrillation in patients with hypertrophic cardiomyopathy) [1,2], an implantable cardioverter defibrillator (ICD) (PRIZM2, Boston scientific, St. Paul, MN) was implanted. The atrial pacing lead was located in the right atrial appendage, and the defibrillation lead was located in the right ventricular apex, with a set-rate of 60bpm and a paced AV delay of 70ms. With these findings, both the gradient (124mmHg→24.6mmHg) and subjective symptoms were resolved. The patient\'s symptoms improved from the New York Heart Association (NYHA) class III to class I after which she was discharged from the hospital. A hypoglycemic attack occurred in January 2008, and cibenzoline was discontinued. Afterward, no changes in the LVOT gradient were seen on echocardiography, but enlargement of the cardiothoracic ratio was seen on plain chest radiographs from May 2009. No changes occurred in chest symptoms (NYHA class I), but an effect from left ventricular remodeling was suspected, and pacing off was considered. Acute changes in the LVOT gradient were evaluated with echocardiography before and after pacing on–off. No changes were seen before and after pacing on–off (6.8mmHg and 8.1mmHg, respectively), and so the patient\'s course was observed in a pacing-off state after March 2009. New functional stenosis (PG max=36mmHg) in the center of the left ventricle (Fig. 2), which had not been seen previously, was seen on echocardiography in May 2009, but outflow tract stenosis did not recur. The outflow tract gradient gradually increased (9–16mmHg) from October 2009. A small cavity was seen in the left ventricular apex in December 2009. The gradient decreased again with the restart of pacing, and reverse remodeling was judged to be the cause of the repeat increase in the outflow tract gradient in this case. The course of the outflow tract gradient is shown in Fig. 3. A deep negative T wave was seen immediately after pacing off on electrocardiogram in March 2009, but the negative T wave improved with partial induction on electrocardiogram in October 2009 (Fig. 4). The reverse remodeling after pacing off was judged to be due to this improvement in the T wave, and DDD pacing therapy is currently under way.