Case Report. An 82-year-old male with ischemic cardiomyopathy underwent permanent pacemaker implantation because of symptomatic intermittent second-degree Mobitz II heart block. Immediately after implantation and while the patient was still in the operating room, he developed acute pulmonary edema requiring intubation. Emergency echocardiography did not show any pericardial effusion and no pneumothorax was seen on fluoroscopy. Right-heart catheterization showed increased capillary wedge pressure with small V-waves while in sinus rhythm, but with pacing the amplitude of V-waves markedly increased with a concomitant significant decrease in the systemic arterial pressure (Figure 1). When pacing stopped, the arterial pressure increased and the V-waves decreased (Figure 2). The pacemaker was reprogrammed to a rate of 40 beats per minute, minimizing the amount of pacing. A biventricular pacemaker was subsequently implanted with resolution of the patient’s heart failure symptoms.

Discussion. Acute hemodynamic deterioration during pacemaker implantation is usually due to pneumothorax, tamponade or pulmonary embolism.¹ Right ventricular pacing may exacerbate mitral regurgitation by causing left ventricular dyssynchrony.² In the past, pacemaker-induced functional mitral regurgitation was considered part of the pacemaker syndrome, which is currently defined as the clinical consequences of suboptimal atrioventricular synchrony.³ Our case demonstrates that right ventricular pacing may immediately induce severe mitral regurgitation, leading to sudden hemodynamic collapse. Lowering the pacemaker rate or upgrading to biventricular pacing, which allows for simultaneous activation of the left and right ventricle, can significantly reduce the severity of mitral regurgitation,⁴ and lead to recovery.