No abstract

The mechanism for dynamic left ventricular outflow tract obstruction (LVOTO) after acute coronary syndromes (ACS) is thought to be apical infarction with compensatory hyperkinesia of the residual normally perfused basal segments of the myocardium. However, herein, we report a patient with ACS and dynamic LVOTO (peak gradient of 250 mm Hg at rest) that could not be secondary to apical akinesia. We propose a potential alternative mechanism leading to dynamic LVOTO in ACS, namely, the interplay between sigmoid septum, basal hyperkinesis, and outflow tract narrowing induced by afterload reduction due to acute myocardial ischemia itself.

Background Atrial infarction, usually concurrent with ventricular infarction, is underrecognized. Although most patients with atrial infarction have complicated supraventricular tachyarrhythmias, its mechanism is still unknown. We report a case of atrial tachycardia related to atrial infarction treated with catheter ablation. Case summary A 51-year-old man was referred for acute chest pain. Electrocardiography showed a junctional rhythm with ST depression in the precordial leads. Emergency coronary angiography revealed an occluded dominant left circumflex coronary artery (LCX). A drug-eluting stent was deployed; however, the atrial branch from the distal side of the LCX was jailed by the stent and became occluded. On the 7th day, the premature atrial contractions (PAC) became frequent and changed to atrial tachycardia (AT). Due to its resistance to medication, we performed catheter ablation. The electro-anatomical map revealed counter-clockwise macro-reentrant tachycardia at the tricuspid valve annulus, with low-voltage and fragmented potential (FP) areas at the posterior wall of the right atrium (RA). After terminating the AT through linear ablation for the cavotricuspid isthmus, multiple-focus PACs originating from the FP area in the RA posterior wall were documented. Coronary angiography revealed that these damaged areas were perfused by the atrial branch of the LCX. Defragmentation in the FP area could eliminate PACs. The patient was discharged with sinus rhythm and without any complications. Discussion We can perform electro-anatomical mapping to identify tachycardia circuit and PACs arising from the FP area in the posterior RA, where the atrial branch was perfusing. Multiple PACs from infarcted myocardium result in tachycardia.