Transient Stress Cardiomyopathy
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- Transient stress cardiomyopathy (TSC) is a unique cause of reversible left ventricle (LV) dysfunction with a presentation indistinguishable from the acute coronary syndromes (ACSs), particularly ST-segment elevation myocardial infarction (MI) (1).
- Typically, the patient is a postmenopausal woman who presents with acute chest pain or dyspnea after an identifiable “trigger” (i.e., an acute emotional or physiologic stressor).
- First reported by authors from Japan, TSC was known initially as the takotsubo syndrome because the typical LV morphology (i.e., apical ballooning) resembled that of a Japanese octopus trap or takotsubo.
- Presenting clinical features include the following:
- Chest symptoms and/or dyspnea
- ECG changes, including ST-segment elevations or diffuse T-wave inversions
- Mild elevation in cardiac biomarkers (creatine kinase [CK], troponin)
- Transient wall motion abnormalities that may involve the base, midportion, and/or lateral walls of the LV.
- The apex of the right ventricle (RV) may be affected in up to 25% of cases (2)[B].
- Clinical features may vary on a case-by-case basis, and formal diagnostic criteria have not been established.
- Authors from the Mayo Clinic have proposed that 3 of the 4 following criteria establish the diagnosis (1)[A]:
- Transient akinesis or dyskinesis of the LV apical and midventricular segments with regional wall motion abnormalities extending beyond a single epicardial vascular distribution
- Absence of obstructive coronary artery disease (CAD) or angiographic evidence of acute plaque rupture
- New ECG abnormalities, either ST-segment elevation or T-wave inversion
- Absence of
- Recent significant head trauma
- Intracranial bleeding
- Obstructive epicardial CAD
- Hypertrophic cardiomyopathy
- Synonym(s): takotsubo cardiomyopathy; apical ballooning syndrome; stress cardiomyopathy; broken heart syndrome; ampulla cardiomyopathy
- TSC accounts for a small percentage (1–3%) of ACS.
- In a recent prospective evaluation of patients admitted to the ICU, as many as 28% had apical ballooning, often in association with sepsis.
- Predominant sex: 82–100% of cases occur in women.
- Predominant age: Mean age of patients is 62 to 75 years.
2.2% of patients presenting to a referral hospital with ST-segment MIs were found to have TSC.
Etiology and Pathophysiology
- The exact pathophysiology is not known.
- A perturbation in the brain–heart axis, originating in the insular cortex, may be the inciting event (3).
- Subsequent overwhelming activation of the sympathetic nervous system initiates a cascade of events, including the following:
- Catecholamine-induced LV dysfunction: “biased agonism” of epinephrine for β2-adrenergic receptors, located predominantly at the cardiac apex
- Endothelial dysfunction and vasospasm
- Cellular metabolic injury
- Myocardial norepinephrine release
- Calcium overload
- Contraction band necrosis
No genetic associations have been described to date.
- Female sex
- Postmenopausal state
- Emotional stress (i.e., argument, death of family member)
- Physiologic stress (i.e., acute medical illness)
- Chronic neurologic or psychiatric disease (3)
Commonly Associated Conditions
Death from TSC is rare, and most cases resolve rapidly, within 2 to 3 days. Reported complications include:
- Left-sided heart failure
- Pulmonary edema
- Cardiogenic shock and hemodynamic compromise
- Dynamic LV outflow tract gradient complicated by hypotension
- Mitral regurgitation
- Ventricular arrhythmias
- LV thrombus formation
- LV free wall rupture
- Death (rare, 0–8%)