Right ventricular pacing increased systolic blood pressure from 60 mmHg to 98 mmHg and decreased left ventricular outflow tract pressure gradient from 160 mmHg to 107 mmHg, resulting in recovery from cardiogenic shock.
Does right ventricular pacing improve hemodynamics and reverse cardiogenic shock in a patient with Takotsubo cardiomyopathy complicated by left ventricular outflow tract obstruction?
Right ventricular pacing may serve as an effective, easily accessible rescue therapy for cardiogenic shock in Takotsubo cardiomyopathy complicated by left ventricular outflow tract obstruction by intentionally inducing left ventricular desynchrony.
Absolute Event Rate: 98% vs 60%
Takotsubo cardiomyopathy (TC) is a disease characterized by chest pain that must be differentiated from acute coronary syndrome, yet the coronary arteries are normal, and left ventricular systolic function is impaired. Historically, it had been recognized as a disease with a relatively favorable prognosis that improved spontaneously, but recent reports have made it clear that this is not necessarily the case. Particularly challenging situations arise when left ventricular outflow tract obstruction (LVOTO) is present, and this tendency is especially pronounced when accompanied by cardiogenic shock. In such cases, beta-agonists and nitrates are contraindicated, and beta-blockers cannot be used due to hypotension, leaving limited treatment options. This report describes the first successful treatment of cardiogenic shock due to TC with LVOTO using right ventricular (RV) pacing. A 79-year-old woman presented with chest pain; coronary angiography was normal. She subsequently developed cardiogenic shock. Echocardiography revealed akinesis from the apex to the septum, hyper-contraction at the base, severe LVOTO with associated systolic anterior movement of the mitral anterior leaflet, leading to mitral regurgitation. Peak pressure gradient (PG) was 160 mmHg in the left ventricular outflow tract, and an ejection fraction (EF) was 30%. Despite fluid therapy and norepinephrine administration, there was little improvement, and systolic blood pressure dropped to 60 mmHg. Upon initiating emergency temporary RV pacing, systolic blood pressure rose from 68 mmHg to 98 mmHg, and the left ventricular outflow tract PG decreased from 160 mmHg to 107 mmHg. Basal hyper-contractility also decreased. On the following day, a permanent dual-chamber pacemaker was implanted to achieve atrioventricular synchrony, leading to further stabilization of hemodynamics. By day 21, cardiac function normalized (EF 60%, PG 7 mmHg). The acetylcholine stress test ruled out coronary vasospastic angina. We diagnosed this patient with TC with LVOTO. The patient was discharged in good condition. Intentional induction of left ventricular desynchrony via RV pacing reduced hyper-contractility, rapidly lessened LVOTO, and facilitated recovery from cardiogenic shock. To the best of our knowledge, this is the first report demonstrating the efficacy of RV pacing in shock patients with TC complicated by LVOTO. In this highly critical situation, it may provide an easily accessible and clinically useful treatment option.
Mori et al. (Fri,) conducted a other in Takotsubo Cardiomyopathy with Left Ventricular Outflow Tract Obstruction (n=1). Right Ventricular Pacing was evaluated on Systolic blood pressure and left ventricular outflow tract pressure gradient improvement. Right ventricular pacing increased systolic blood pressure from 60 mmHg to 98 mmHg and decreased left ventricular outflow tract pressure gradient from 160 mmHg to 107 mmHg, resulting in recovery from cardiogenic shock.