Lesson of the month 1: Broken heart in the intensive care unit

Discussion

TCM, also known as apical ballooning syndrome, broken heart syndrome or stress-induced cardiomyopathy, is observed in 1.7–2.2% of patients presenting with acute coronary symptoms (ACS).^1,2 It is characterised by transient systolic dysfunction of the apical and/or mid segments of the LV that mimics myocardial infarction, but occurs in the absence of obstructive CAD.1,³ Although the modified Mayo criteria are commonly used for diagnosing TCM, there is currently no consensus on the diagnostic criteria for TCM; therefore, its diagnosis can be difficult.²

TCM most commonly affects women aged 50 years or older, and generally starts abruptly and unpredictably.^1,4 It is associated with symptoms of chest pain and frequently also with shortness of breath, usually triggered by an emotionally or physically stressful event.^1,4 Other less common, but likely, triggers of TCM include cocaine and methamphetamine use, opiate withdrawal, excessive phenylephrine use, stress testing using dobutamine, phaeochromocytoma, acute brain injury, lightning strike, ergonovine injections and thyrotoxicosis.^1,4 However, a triggering event is not always present.

The ECG findings of TCM are often confused with those found during an acute anterior wall STEMI. Most ST elevations (95%) involve the precordial leads and are usually maximal in leads V₂–V₃. However, the amplitude of ST-segment elevations is substantially lower in patients with TCM compared with patients with STEMI caused by LAD occlusion.^5,6 Initially, normal or nonspecific ECG findings are observed in approximately 15% of patients with TCM.^1,2,⁴ Furthermore, cardiac markers are usually elevated in patients with TCM. However, these levels tend to be lower, and normalise sooner compared with ACS.^1,2 Apical ballooning (typical variant) and/or midventricular hypokinesis are usually seen on echocardiography. In a subset of cases, the transient left ventricular hypokinesis is restricted to the midventricular segments (‘atypical variant’ or ‘apical sparing variant’) without involvement of the apex.^3,4 Perhaps most importantly, these wall motion abnormalities extend beyond the distribution of any single coronary artery. Angiography is required for diagnosis, because there is no accurate method to distinguish TCM from ACS reliably using ECG or cardiac markers.^1,2,⁴

There are currently no controlled data on the optimal treatment regimen for TCM, but it is reasonable to treat these patients with standard medication for LV systolic dysfunction, including ACEi, BBs and diuretics.^1,2,⁴ The benefits of other standard outpatient post-STEMI medications, such as statins, aspirin, and clopidogrel, are currently unknown. The prognosis of TCM is excellent, with nearly 95% of patients experiencing complete recovery within 4–8 weeks; however, a small subset of patients experience potentially life-threatening complications during the initial presentation, including left ventricular outflow tract (LVOT) obstruction.^1,4 LVOT obstruction has been described in 10–25% of all patients with TCM. As highlighted by the present case, TCM can occur after an acute medical illness; therefore, physicians should be aware of this condition as a potential cause of inotrope-resistant hypotension. In patients with hypotension and moderate-to-severe LVOT obstruction, inotropic agents should be avoided, because they can worsen the degree of obstruction. Instead, BBs are preferred, because they are capable of resolving the obstruction and consequently improve the hemodynamics.^1,4