Temperature and repeated catecholamine surges modulate regional wall motion abnormalities in a rodent takotsubo syndrome model.

Transient regional wall motion abnormalities (RWMA) after stress are a hallmark of experimental and clinical Takotsubo Syndrome (TS). The mechanisms driving RWMA remain incompletely understood. This study investigates these mechanisms in a small-animal model of TS, validating the model's complication profile, recovery dynamics, and recurrence, while assessing the predictive value of echocardiography. Male, 7-9-week-old rats underwent TS induction via isoprenaline infusion. The effects of body temperature and repeated catecholaminergic surges on RWMA were assessed using high-resolution speckle-tracking echocardiography. Complications were evaluated through ECG, autopsy, and blood gas analysis. The TS phenotype showed reduced longitudinal strain with RWMA characterized by apical end-systolic akinesia/dyskinesia, a contracting base, and a narrow transition zone, resulting in apical ballooning. RWMA originated from the apex and recovered in the opposite direction. Hyperthermia increased RWMA incidence, while hypothermia attenuated RWMA (p = 0.008). A repeated catecholamine surge exacerbated RWMA in the acute phase (p = 0.042) but not during recovery (p = 0.308), with reduced RWMA susceptibility after recovery (RR 0.45, 95%CI; 0.27-0.76). Systolic function at initial echocardiography predicted worse outcomes (odds ratio 0.73; 95%CI 0.57-0.85), and RWMA extent correlated with recovery time (Rho = 0.772). TS rats developed complications similar to patients, including heart failure, arrhythmias, and thrombus formation. This study validates the small-animal TS model by replicating patient findings, and emphasizing the importance of controlling body temperature and limiting adrenergic drug use in managing TS. RWMA analysis offers promise as a diagnostic and prognostic tool in TS, and the delayed adaptive response presents a potential pathway for therapeutic intervention.