Related Experiment Video
Updated: Jun 18, 2026

Echocardiographic Evaluation of Atrial Communications before Transcatheter Closure
Published on: February 8, 2022
Transient cardiac ballooning--the syndrome
Raghav Gupta1, Candice Sech, Ralph Lazzara
1Section of Cardiovascular Diseases, Department of Internal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. raghav-gupta@ouhsc.edu
Insights
Transient cardiac ballooning, a reversible heart condition, causes chest pain and ECG changes but no blocked arteries. Myocardial dysfunction typically resolves within weeks, with ongoing research into its causes.
Area of Science:
- Cardiology
- Pathophysiology
Background:
- Transient cardiac ballooning is a reversible condition mimicking myocardial infarction.
- Patients present with chest pain, ECG abnormalities, and elevated cardiac enzymes without obstructive coronary artery disease.
Observation:
- Left ventriculography shows transient myocardial wall akinesis and systolic ballooning.
- Acute regional myocardial dysfunction is observed.
Findings:
- The condition typically normalizes within 1 to 6 weeks.
- Hypotheses for pathophysiology include direct myocyte injury, postischemic stunning, and neurotransmitter actions.
Implications:
- This review details case series, pathophysiology, diagnostic guidelines, treatment, and prognosis.
- Further investigation into the underlying mechanisms of transient cardiac ballooning is warranted.
Abstract:
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.
Related Concept Videos
Aortic Regurgitation II: Clinical Features and Diagnostic Tests
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy I: Introduction and Classification
Mitral Valve Prolapse I: Introduction
Transient Ischemic Attack l: Introduction
Aneurysm I: Introduction
