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  • Title: Longitudinal Strain Patterns in Stress (Takotsubo) Cardiomyopathy: Evidence of Global Myocardial Injury and Incomplete Recovery.
    Author: Gibson LE, Davis EF, Ponzini F, Wood MJ.
    Journal: Am J Cardiol; 2024 Jan 15; 211():193-198. PubMed ID: 37949337.
    Abstract:
    Stress cardiomyopathy develops after abrupt sympathetic stimulation, likely from catecholamine-induced myocardial toxicity. The evolution of myocardial strain during and after an episode have not been previously characterized. We aimed to determine whether preexisting contractile abnormalities may explain the observed regional dysfunction during an acute episode and to investigate the persistence of strain abnormalities after clinical recovery. We identified patients who were diagnosed with stress cardiomyopathy and had an echocardiogram performed before their episode, during their episode, and within 1 year after. The diagnosis was confirmed based on the absence of obstructive coronary lesions. Left ventricular (LV) longitudinal strain was calculated using speckle-tracking software and compared between baseline, episode, and follow-up echocardiograms. The LV strain analysis was performed on 23 patients. The LV ejection fraction was 64 ± 8.7% at baseline, 45 ± 12% during the episode, and 5 9 ± 10% after a median follow-up of 46 days. The LV global longitudinal strain was 24 ± 4.7% at baseline, 11 ± 4.9% during the episode, and 19 ± 4.6% after the follow-up. The mean ejection fraction (p <0.01) and global longitudinal strain (p <0.001) remained below baseline levels at follow-up. Longitudinal strain was reduced (<18%) in 80 ± 23% of myocardial segments during an episode and 41 ± 21% of myocardial segments at follow-up. During the acute episode, 35 ± 6% of the abnormal segments were in the base, outside of the region of ballooning. Our findings suggests that stress cardiomyopathy is associated with global rather than regional myocardial injury and that contractile abnormalities persist after clinical improvement. These findings challenge our previous understanding of stress cardiomyopathy and may guide future pathophysiologic understanding of this complex disease.
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