Although hemodynamic stability is the norm, a small number of patients may demonstrate hypotension due to reduced stroke volume and LV outflow tract obstruction and require hemodynamic support during the acute phase. Mild-to-moderate congestive heart failure commonly accompanies the condition.16 Rarely, patients will report an episode of syncope or an out-of-hospital cardiac arrest.17 Rare complications of TTC are cardiogenic shock and formation of a thrombus at the LV apex due to apical ballooning akinesis.17,18
Diagnostic Studies
Electrocardiography (ECG) findings may demonstrate ST-segment elevation, although this occurs in only one-half of patients with TTC.17 The elevation is typically noted in the precordial leads,16 but the ECG can be normal or show nonspecific T-wave abnormalities.17 In patients with ST-segment elevation, the severity of ventricular dysfunction or prognosis does not correlate with the ECG changes noted on presentation.19 The ST-segment elevation is followed by T-wave inversions and QT prolongation.16 Torsades de pointes and QT prolongation in patients with TTC has been reported.20
Laboratory studies demonstrate mildly elevated cardiac troponin and brain natriuretic peptide levels.3,21,22 LV wall-motion abnormalities and a severely depressed ejection fraction have been noted on transthoracic echocardiography.23 Several case reports utilized cardiac magnetic resonance imaging in patients with TTC, resulting in findings of wall motion abnormalities, myocardial edema, and hyperenhancement on contrast-enhanced imaging.24,25
Diagnosis
Although universally accepted diagnostic criteria are currently unavailable,23 Bybee and colleagues have proposed criteria for the diagnosis of TTC.6 All four of the following criteria must be met:
• Transient hypokinesis, akinesis, or dyskinesis of the LV apical and midventricular segments with regional wall-motion abnormalities encompassing more than a single epicardial vascular distribution.
• Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
• New ECG abnormalities (either ST-segment or T-wave inversion) or modest elevation of cardiac troponin levels.
• Absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, and hypertrophic cardiomyopathy.
The diagnosis of TTC is often made in an emergency setting because of the presenting complaint of chest pain. Typically, patients with TTC have no associated significant atherosclerotic luminal narrowing7 despite the presence of transient apical and left midventricular systolic dysfunction.
Treatment and Management
Optimal management of TTC has yet to be established, but the general approach is supportive and conservative. Because the presenting chest pain is indistinguishable from AMI, initial management should focus on preventing ischemia. Continuous ECG monitoring and administration of nitrates, morphine for pain control, aspirin, IV heparin, and beta-blockers are recommended.26
Once the diagnosis of TTC is confirmed, if there is no coexisting coronary atherosclerosis, aspirin therapy can be discontinued.17 Treatment with beta-blockers (in hemodynamically stable patients) and ACE inhibitors (in the absence of outflow tract obstruction) is usually recommended, although randomized trials have not been conducted.27
Beta-blockers, which may inhibit the release of catecholamines, could be beneficial since they are hypothesized to mediate in TTC. Additionally, beta-blockers work to reduce LV outflow tract obstruction through basal segment hypercontractility.3 For patients with associated congestive heart failure, diuretics may be effective. For significant hypotension, phenylephrine helps to increase afterload and LV cavity size; note that inotropes are contraindicated in this situation. In the rare occurrence of LV thrombus, anticoagulation is recommended.16,18 Long-term administration of beta-blockers is recommended to reduce the likelihood of TTC recurrence.17
Prognosis
In the absence of underlying comorbid conditions, the prognosis in TTC is generally good. Cardiovascular symptoms—systolic dysfunction and regional wall-motion abnormality—usually resolve completely within days to one month; an alternative diagnosis should be considered if the cardiomyopathy does not resolve after this time. Close follow-up with a cardiologist, usually with serial echocardiograms, in the weeks after diagnosis is recommended to ensure complete resolution. At six-week follow-up, the ECG usually demonstrates complete resolution, although T-wave inversion may persist.17
Inpatient mortality rates associated with TTC range from 0% to 8%.18,28 The recurrence rate has been reported as less than 10%, but additional studies are needed to track recurrence, in addition to the longitudinal effects of this condition.29 Left-sided heart failure, with or without pulmonary edema, is the most common complication associated with TTC. Others are LV mural clot, systemic or pulmonic embolic events, mitral valve regurgitation, and ventricular arrhythmias.3
Conclusion
TTC is an entity of acute heart failure that can mimic AMI. It should be considered in symptomatic postmenopausal women with a normal heart and no history of cardiovascular disease. Providers should include TTC in the differential diagnosis, especially when patients present with acute chest pain after a stressful incident. While short-term management may suffice, providers should follow these patients over time to identify the potential for long-term impact and possible causes of this condition.