Spironolactone prevents the inducibility of ventricular tachyarrhythmia in rats with aldosteronism.

Myocardial fibrosis is considered a substrate for fatal ventricular arrhythmias (VAs). In rats receiving aldosterone/salt treatment (ALDOST) for ≥4 weeks, foci of myocardial scarring that replace necrotic cardiomyocytes appear scattered throughout the right and left sides of the heart. We hypothesized that this adverse structural remodeling would promote the inducibility of VA, which could be prevented by cotreatment with spironolactone (A+Spiro), an aldosterone receptor antagonist and cardioprotective agent. In controls and each treatment group, we monitored: (1) electrocardiogram, ventricular electrogram, and arterial pressure before, during, and after bipolar electrical stimulation of the right ventricular outflow tract and apex at a strength 3× the pacing threshold, using both programmed stimulation with premature extra stimuli and 50-Hz burst pacing for 3 different durations; and (2) myocardial collagen volume fraction (CVF) as a marker of cardiac fibrosis. We found that VA (duration >200 ms accompanied by declining arterial pressure) was more inducible (P < 0.05) at 4 weeks (4 of 6) and with even greater frequency at 6 weeks (9 of 10) of ALDOST versus controls (0 of 6) and A+Spiro for 6 weeks (2 of 11). CVF (%) was proportionally increased (P < 0.05) at 4 and 6 weeks (8.4 ± 0.74 and 13.9 ± 1.9, respectively) of ALDOST compared with control group (2.6 ± 0.4) and A+Spiro group (5.3 ± 0.7). However, the effective refractory period was indistinguishable between groups, whereas the probability of VA was nonlinearly related to CVF. Thus, in rats with aldosteronism, in which a reduction in effective refractory period was not evident, the mechanism for VA susceptibility is presumably linked to a decrease in conduction velocity and/or increased dispersion of refractoriness, probably caused by consequential myocardial fibrosis.

Exercise-induced atrial and ventricular tachycardias in a patient with left ventricular noncompaction and normal ejection fraction.

We report a patient with ventricular and atrial tachycardias reproducibly induced during exercise testing. Atrial tachycardia, but no sustained ventricular tachycardia, was induced during electrophysiological study. Catecholaminergic polymorphic ventricular tachycardia was considered because of normal echocardiogram, family history of sudden death, and polymorphic appearance of some of the nonsustained ventricular tachycardia episodes. However, most episodes of ventricular tachycardia were monomorphic. Cardiac magnetic resonance diagnosed isolated left ventricular noncompaction.

Central cyanosis and clubbing in an 18-year-old postpartum woman presenting with a stroke.

An 18-year-old woman without previously documented medical history delivered a healthy 32-week-old preterm infant. Severe bleeding occurred during week 1 postpartum secondary to ruptured vaginal condylomas. The consequent anemia was accompanied by complaints of exercise intolerance that resolved with blood transfusion. Six weeks later, the patient was brought to the emergency department of the regional medical center, where she was found to be unresponsive, with a left-sided hemiparesis and with hypoxemia that failed to correct with assisted ventilation and 100% oxygen. A cardiology consultation was obtained, which identified the patient as having central cyanosis and heretofore unappreciated marked clubbing of fingers and toes. This suggested a diagnosis of right-to-left shunting, likely at the cardiac level, together with presumptive embolic stroke, which was documented by magnetic resonance imaging and magnetic resonance angiography as a left pontine infarct. Transthoracic and transesophageal echocardiography identified anomalous drainage of the inferior vena cava into the left atrium, which was confirmed by a three-dimensional computed tomographic angiogram. Corrective surgery in the form of atrial septostomy and redirection of the inferior vena cava to the right atrium was performed. The patient was subsequently discharged and is in stable condition 3 months later without effort intolerance and with normal arterial oxygen saturation on room air.