Stress Induced Cardiomyopathy Triggered by Acute Myocardial Infarction: A Case Series Challenging the Mayo Clinic Definition

Background

Stress induced cardiomyopathy (SIC) is a form of acute heart failure that commonly presents with signs and symptoms that mimic acute coronary syndrome [1]. It usually presents in elderly females after an emotional or physical trigger, although cases have been reported with no obvious trigger [2]. The classic echocardiographic appearance is apical to mid segment hypokinesia/akinesia with hyper contractile basal segments; however, more recently, other variations have been described [3,4]. Typically, wall motion abnormalities (WMAs) are transient with subsequent resolution of the left ventricular (LV) function within weeks [3].

The most widely accepted criteria for diagnosing SIC is the Mayo Clinic criteria that consist of the following parameters (all should be present): (a) transient WMA that extends beyond a single vessel distribution; (b) absence of obstructive coronary artery disease (CAD) or angiographic evidence of acute plaque rupture; (c) electrocardiographic changes or mild elevation in cardiac troponin; and (d) absence of pheochromocytoma or myocarditis. Stressful event is often but not always present [2]. Although these criteria are the most commonly used for diagnosing SIC, subsequent reports have challenged them, especially with regards to the mandatory absence of obstructive CAD [5–7]. Adding to the controversy, we present the first case series of patients presenting with acute myocardial infarction (AMI) triggering SIC.

Case Report

CASE 1:

A 56-year-old male with no significant past medical history (PMH) was admitted with sudden onset chest pain radiating to his left arm. On arrival to the emergency department the patient had ventricular fibrillation which was successfully managed by electrical defibrillation. His ECG revealed ST elevations in the anterior leads. Emergent cardiac catheterization revealed 98% thrombotic occlusion of the mid LAD that was successfully treated with a bare metal stent. There was no other obstructive CAD (Figure 1A, 1B). The patient was admitted to the intensive care unit in stable condition and chest pain free. Initial transthoracic echocardiography (TTE) showed left ventricular ejection fraction (LVEF) of 45% with apical hypokinesia. On the second day of admission, the patient became hypotensive. His ECG revealed diffuse T-wave inversions and QTc prolongation (561 ms). A follow-up TTE showed global LV-dysfunction with LVEF of 25%. Repeat coronary angiography showed patent stent to the LAD. The LV gram was consistent with SIC (Figure 2A, 2B).

CASE 2:

A 70-year-old female with no significant PMH presented with sudden onset chest pressure occurring at rest with associated dyspnea. Her initial ECG revealed antero-lateral ST segment elevations. Emergency cardiac angiography showed 99% stenosis in the mid LAD (culprit lesion) and 90% stenosis in the proximal portion of the obtuse marginal branch. Both lesions were successfully treated with drug eluting stents. Post-procedure, the patient was pain free and was transferred to the telemetry unit for observation. Her troponin level was mildly elevated at 2.2 ng/mL. Overnight she developed repeat episodes of chest pain with associated nausea. Repeat ECG revealed diffuse T-wave inversions with prolonged QTc interval of 484 ms. Bedside TTE revealed akinesia of all apical segments with sparing of the basal segments and severely reduced ejection fraction. Follow-up ECG the next day revealed diffuse T-wave inversions with further prolongation of QTc interval to 525 ms. Subsequent TTE three days later revealed that her LVEF had improved to 45–50%.

CASE 3:

A 55-year-old female with PMH of depression and generalized anxiety disorder was admitted with complaints of intermittent episodes of chest pressure radiating to the left shoulder for one day. Her initial ECG did not show any acute ischemic changes. Laboratory data was remarkable for an NT-pro BNP of 6,730 pg/mL and troponin of 6.3 ng/mL. TTE revealed akinesia of mid anterior, mid antero-septal, mid infero-septal and all apical segments with LVEF of 35–40%. Coronary angiography revealed 98% stenosis in the proximal LAD that was treated with drug eluting stent. Three was no other obstructive CAD. Her procedure was uneventful; however, 30 minutes later she complained of nausea and became hypotensive requiring fluids and inotropes. Her emergent repeat TTE was unchanged from her prior TTE. Serial ECGs did not reveal any ischemic changes but were notable for marked prolongation of QT interval >500 ms. Prior to discharge, TTE was repeated showing significant improvement of the LVEF to 50%. QT interval normalized within the next week.

CASE 4:

A 55-year-old female with a 30 pack per year smoking history and history of domestic abuse was admitted with an episode of acute onset precordial chest pain radiating to the left arm and neck for six hours. ECG revealed significant ST elevation in leads V2–V5 and initial troponin was 0.532 ng/mL. Subsequent coronary angiography revealed complete occlusion of mid LAD treated successfully with a drug eluting stent. Angiography was also remarkable for 50% stenosis of the proximal right coronary artery and 50% stenosis of the proximal left circumflex (which were not intervened). Her TTE was significant for severely reduced LVEF of 25–30% with akinesia in all segments except for the basal inferior and basal anterior. This case was also suspicious for LV thrombus and the patient was hence placed on warfarin. Subsequent ECGs were remarkable for markedly prolonged QT interval of 609 ms. Repeated TTE one month later revealed improvement in systolic function to an LVEF of 50–55%.

Discussion

LIMITATIONS:

Cardiac MRI can be very helpful when trying to differentiate SIC from other types of cardiomyopathy [14] and would have been invaluable in our case study. Unfortunately, a cardiac MRI was not performed for our patients to confirm our hypothesis. However, even in the absence of cardiac MRI, we believe that the body of evidence seen in our patients strongly indicated the presence of SIC superimposed on AMI.

Conclusion

AMI can trigger SIC. Extensive reversible wall motion abnormalities, beyond the ones expected from an angiography, accompanied by modest elevation in troponin and marked QTc prolongation suggests SIC superimposed on AMI. If this can be proven in further studies, especially with concomitant use of cardiac MRI, the criteria for SIC should be modified.