Key result
Transient cardiac ballooning mimics acute MI but typically normalizes within 1 to 6 weeks.
This review provides a comprehensive overview of the pathophysiology, diagnosis, and management of transient cardiac ballooning syndrome.
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Recognizes transient cardiac ballooning as a reversible MI mimic warranting conservative care; leaves optimal long-term strategies open.
Transient cardiac ballooning is usually a reversible clinical entity. A patient typically presents with chest pain, electrocardiogram (ECG) abnormalities like ST-segment elevation (most commonly reported) or depression, and elevated cardiac enzymes, but has no or nonobstructive coronary artery disease. Left ventriculography reveals transient akinesis of the involved portion of the myocardial wall with compensatory hyperkinesis of the remaining myocardium, leading to ballooning of the noncontracting myocardial wall during systole. Acute regional myocardial dysfunction ensues, which normalizes on average within 1 to 6 weeks. The hypotheses for these pathophysiologic changes range from direct cardiac myocyte injury to postischemic myocardial stunning to neurotransmitter actions. The objective of this article is to present a succinct description of a small case series accompanied with various recently reported presentations and morphology by left ventriculogram and a detailed review of available data on underlying pathophysiology. In addition, a discussion on current diagnostic guidelines, treatment, prognosis, and potential future investigations is included.
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Gupta et al. (2009) conducted a review in Transient cardiac ballooning. Transient cardiac ballooning was evaluated. Transient cardiac ballooning presents with acute regional myocardial dysfunction mimicking myocardial infarction but typically normalizes within 1 to 6 weeks.
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