Suppression of acute heart failure rehospitalization by biventricular pacing in wide QRS and mid-range ejection fraction
A 66-year-old man with complete left bundle branch block and mid-range left ventricular EF at rest had he had recurrent hospitalization (three times within a 6 month period) due to clinical scenario 1 acute HF. Treatment with a nitrovasodilator immediately compensated his HF. He had been diagnosed with symptomatic sick sinus syndrome 2 years prior and was treated with the implantation of a dual-chamber pacemaker. After a thorough review of the examination results, he was diagnosed with dilated cardiomyopathy. The right ventricular pacing burden was marginal (<0.1%) owing to his normal atrioventricular conduction and the use of an algorithm of Intrinsic rhythm support (IRSplus) and Ventricular pacing suppression (VpS) of Biotronik pacemaker. The patient had progressive dyspnoea on exertion [New York Heart Association (NYHA) Class III] even though he had received an implant of a rate-responsive pacemaker and optimal medical therapy (beta-blocker with a vasodilator activity, angiotensin receptor blocker and aldosterone antagonist at maximally tolerated doses) for the treatment of hypertension and heart failure. His home blood pressure at rest was 110/70 mmHg on average. Electrocardiogram showed an atrial pacing rhythm (60 ppm) with a complete left bundle branch block (QRS duration: 185 ms; Figure\n). A transthoracic echocardiogram showed moderate left ventricular systolic dysfunction with a mid-range EF of 42%, trivial to mild MR, with a structurally normal valve at rest. Remarkable left ventricular (LV) dyssynchrony was observed between the septal and postero-lateral walls on speckle-tracking echocardiography (Figure\n). However, the exercise stress echocardiogram demonstrated a decrease in LVEF with exercise to 33%, with an increase in systolic blood pressure (from 110 to 190 mmHg) and MR from mild to severe as the QRS width slightly increased (from 185 ms to 195 ms; Figure\n). In addition, LV dyssynchrony was further worsened (Figure\n) compared with the findings of resting echocardiography (Figure\n). Interestingly, a phenylephrine-induced increase of afterload enhanced the elevation of left ventricular end-diastolic pressure (LVEDP), pulmonary capillary wedge pressure (PCWP), pulmonary arterial V-wave augmentation and MR, which was confirmed via intra-cardiac pressure measurement and echocardiography (Figure\n) and QRS widening appeared.\nTaking into consideration the patient's debilitating symptoms, we offered him the option of a biventricular pacemaker. His paced electrocardiogram is demonstrated in Figure\n (QRS duration: 155 ms). A follow-up evaluation using the same methods as used previously demonstrated that LV dyssynchrony at rest was attenuated by biventricular pacing (Figure\n) and stress echocardiography did not show exacerbation of dyssynchrony (Figure\n); further, biventricular pacing reduced phenylephrine-induced MR and elevation of LVEDP, PCWP and pulmonary arterial V-wave augmentation (Figure\n).\nDuring the 2 year follow-up period, the patient reported a dramatic improvement in his exercise capacity, with NYHA Class I symptoms. We also noted an improvement in resting EF to 55%. The patient has not had any recurrent hospitalization due to HF.