The patient was treated with supportive care, psychotropic therapy, angiotensin-converting enzyme inhibitor (ACE-I), and beta blocker therapy. Within 9 days, NT-proBNP levels normalized (from peak 8,834 pg/mL to 191.5 pg/mL).
Six weeks later, an echocardiogram confirmed resolution of wall motion abnormalities (Figure 8). Follow-up cardiac MRI showed complete resolution of segmental wall motion abnormalities and the apical ballooning, normal wall thickness, and absent delayed enhancement (Figure 9). These findings further supported the diagnosis of ABS and excluded MI and myocarditis.
What is striking about takotsubo cardiomyopathy is that the clinical presentation resembles an AMI. Several studies have reported that 1.7% to 2.2% of patients who had suspected acute coronary syndrome were subsequently diagnosed with takotsubo cardiomyopathy.6-8 Nearly 90% of reported cases involved postmenopausal women, and this may be related to loss of the cardioprotective effect of estrogen.5,9
A preceding stressful emotional or physical event is usually identified in about two-thirds of the patients with ABS.9 Most common emotional triggers are death of a relative or friend, broken relationships, assaults, and rapes, among others. Physical triggers include severe sepsis, shock, acute respiratory failure, seizures, and intracranial bleeds. Sometimes a specific trigger cannot be identified from the history, but the absence of an emotional or physical trigger does not exclude the diagnosis.
Although the exact pathogenesis of ABS remains unclear, it is likely that multiple factors are involved. Some of the suggested mechanisms are high levels of catecholamines, multivessel epicardial spasm, or coronary microvascular dysfunction.4 The catecholamine hypothesis has been supported by the finding that several patients with pheochromocytoma and subarachnoid hemorrhage also present with high levels of catecholamine and a cardiomyopathy resembling ABS. Furthermore, ABS has been reported in patients on catecholamine infusions and those treated with agents that inhibit reuptake of catecholamines.5
The presence of multivessel coronary spasm was suggested by early small studies in Japan, but more recent case series have not validated this hypothesis.5 The microvascular dysfunction hypothesis is supported by the presence of myocardial ischemia, diagnosed by ECG changes and elevated troponins, in the absence of significant coronary disease. However, it remains unclear whether this is a primary mechanism or a manifestation of a primary process.4 Microvascular dysfunction may be more likely related to impairment of myocardial relaxation with extramural coronary compression.
Signs and symptoms of ABS mimic those of AMI, with angina-like chest pain as the main presenting symptom in about 50% of cases.10 Other symptoms include dyspnea and less commonly, syncope or sudden cardiac death. Decompensated left heart failure occurs in 50% of patients, with severe hemodynamic compromise and cardiogenic shock not being uncommon. Other complications that may occur are tachyarrhythmias (atrial or ventricular) and ventricular thromboembolism.4
Common ECG changes in ABS include precordial ST segment elevations, symmetric T wave inversions, and nonspecific T wave changes.4,10 QT interval prolongation may be seen during the first days. Transient pathologic Q waves may be seen at presentation or afterward. These ECG changes tend to revert after weeks or months of presentation.
Elevation of cardiac biomarkers is usually present in laboratory data. Levels peak at 24 hours, and the degree of elevation is usually less than that seen in patients with an AMI.10 Most important, the degree of cardiac biomarker elevation is disproportionately low for the extent of involved coronary territory and left ventricular dysfunction. Other laboratory tests that are frequently altered are the BNP and pro-BNP levels, which are usually elevated due to transient left ventricular dysfunction. C-reactive protein elevates in most patients and indicates the presence of an acute inflammatory response.
Early coronary angiography should be performed in all patients with ABS to rule out the presence of a significant obstructive coronary lesion. Patients with ABS often have luminal irregularities or normal coronary vessels. However, concomitant obstructive coronary lesions may be found, especially in elderly patients.
The hallmark of ABS is a characteristic transient contractility abnormality of the left ventricle causing ballooning of the apex, which can be detected on left ventricular angiography or echocardiography. There are 3 distinct variants of ABS, according to the left ventricular myocardial wall segments involved.10 The classic form of takotsubo is characterized by hypokinesis, dyskinesis, or akinesis of the middle and apical segments of the left ventricle. The basal segment is usually spared and may be hyperdynamic. In the midventricular or apical sparing variant, the wall motion abnormalities are restricted to the midventricular segments, and apical contraction is preserved. This case resembles the atypical variant, because the midventricular segments were affected, whereas apical and basal regions were preserved. A rare variant of takotsubo exists with hypokinesis or akinesis of the base and preserved apical function.