The Stressed Heart: Takotsubo Cardiomyopathy Following Percutaneous Coronary Intervention

Abstract

Takotsubo cardiomyopathy, otherwise known as “stress cardiomyopathy,” “apical ballooning syndrome,” or “broken heart syndrome,” is a transient dysfunction of the left-sided ventricle associated with stress, and it is often confused with acute myocardial infarction on an electrocardiogram. Diagnosis is made by excluding coronary artery disease by coronary angiography and followed by left ventricular angiography, which shows the pathognomonic apical ballooning characteristic of Takotsubo cardiomyopathy. This is a case of a 61-year-old female who presented with anterior wall myocardial infarction. A coronary angiogram showed a tight lesion in the ramus intermedius, and she underwent percutaneous coronary intervention to the ramus intermedius. On Day 2, she had chest pain, with an electrocardiogram showing re-emerging ST-elevation in the precordial leads, raising suspicion of stent thrombosis. Coronary angiography and left ventricular angiography showed a patent stent and features consistent with Takotsubo cardiomyopathy. Re ST-elevation following percutaneous coronary intervention is concerning, as there is a high chance of stent thrombosis in such patients. Takotsubo cardiomyopathy should be strongly suspected as one of the differential diagnoses, especially in elderly postmenopausal females who present with ST-segment elevation with a history of physical or emotional stress. Takotsubo cardiomyopathy following percutaneous coronary intervention is a very rare clinical entity, and its clinical presentation is often confused with complications arising from percutaneous coronary intervention.

Introduction

Takotsubo cardiomyopathy (TC) is an acute and rapidly reversible heart failure syndrome characterized by distinctive left ventricular (LV) dysfunction. It is usually associated with psychological or physical stress and mimics the symptoms of acute myocardial infarction (MI), with characteristic apical ballooning and basal hypercontractility, followed by the absence of obstructive coronary artery disease (CAD). ¹ Initially, what was thought to be a benign condition has been found to be associated with severe complications, such as life-threatening arrhythmias and cardiogenic shock. The incidence of TC has been increasing, and its cause may be multifactorial. Increased awareness, along with newer techniques, has helped in the diagnostic evaluation of TC. ² The incidence of TC is approximately 1%-2% of all patients presenting with an initial primary diagnosis of either acute coronary syndrome (ACS) or MI, and 6% of all women presenting with suspected ST-elevation myocardial infarction (STEMI) who undergo urgent angiography. The majority of these patients are elderly, above 50 years of age. TC after percutaneous coronary intervention (PCI) is rare, and its clinical characteristics are easily confused with complications following PCI. This is a case report of a patient with TC who underwent PCI 2 days earlier. The condition initially mimicked acute stent thrombosis, but after a systematic workup, a diagnosis of TC following PCI was confirmed.

Case Report

A 61-year-old female presented with typical angina of 5 h duration to the emergency department. The patient had associated profuse sweating and shortness of breath. On presentation, she was afebrile and hemodynamically stable, with a blood pressure of 130/68 mmHg and a pulse of 92 beats per minute. Physical examination revealed no features of heart failure. Electrocardiogram (ECG) showed ST-segment elevation in leads V2 and V3, with Q waves in leads II, III, and aVF (Figure 1A). Laboratory workup showed a normal complete blood count and a marginally increased troponin I level of 0.23 ng/mL. The patient was diagnosed with anterior wall myocardial infarction (AWMI). The patient was shifted to the cardiac catheterization laboratory, which demonstrated a 95% lesion in the ramus intermedius and a 50%-60% tubular lesion in the proximal left anterior descending (LAD) artery (Figure 1B). The ramus intermedius was wired with a Sion blue guidewire, and she underwent primary PCI with a drug-eluting stent (sirolimus-coated, 2.5 × 13 mm) to the ramus intermedius. Medical management was planned for the LAD (Figure 1C). The patient was given 7,500 IU of intravenous heparin during the procedure. She was then shifted to the cardiac care unit, and post-procedure ECG showed ST resolution (Figure 1D). Transthoracic echocardiography revealed a regional wall motion abnormality in the anterior and anterolateral walls at the mid and apical levels, with fair LV function. The patient was started on dual antiplatelet therapy (DAPT), statins, and beta-blockers. On the second day, the patient had recurrent angina-type of chest pain, with ECG showing recurrent ST elevation in leads V2 and V3 (Figure 2A). Blood parameters showed an elevated troponin I level (1.8 ng/mL) and an NT-proBNP level of 3,748 pg/mL. Repeat 2D echocardiography showed apical ballooning with basal hypercontractility and mild LV dysfunction (Figure 2B to 2D). In view of suspected stent thrombosis, the patient was shifted to the catheterization laboratory for a repeat coronary angiogram, which showed a patent stent in the ramus intermedius (Figure 3A). Left ventriculography was performed, which showed apical ballooning with basal hypercontractility, consistent with TC (Figure 3B and 3C). Cardiac magnetic resonance imaging (MRI) was not performed in this patient. Alternative diagnoses, such as pheochromocytoma, were ruled out, as the patient had no history of hypertension. The possibility of myocarditis was deemed unlikely, as the patient’s ECG and clinical symptoms were not suggestive of it. The patient was followed up after 6 weeks, and echocardiography showed an improvement in LV function. There was no apical ballooning, suggesting the transient nature of TC (Figure 4A and 4B).

Figure 1.

(A) Electrocardiogram (ECG) Showing ST-segment Elevation in Leads V2 and V3 With q in II, III, and avF. (B) Coronary Angiography Demonstrating a 95% Lesion in the Ramus Intermedius and a 50%-60% Tubular Lesion in the Proximal Left Anterior Descending Artery. (C) Drug-eluting Stent to Ramus Intermedius. (D) ECG Showing ST-resolution and T Inversion in Precordial Leads.

Figure 2.

(A) Electrocardiogram (ECG) Showing re-ST-segment Elevation in Leads V2 and V3. (B to D) 2D Echo Showing Apical Ballooning With Basal Hypercontractility and Mild Left Ventricular (LV) Dysfunction.

Figure 3.

(A) Coronary Angiography Showing a Patent Stent in Ramus Intermedius. (B and C) Left Ventriculogram Showing Apical Ballooning With Basal Hypercontractility.

Figure 4.

(A and B) Follow-up Echocardiography Showing No Apical Ballooning and Improvement of Left Ventricular (LV) Function.

Discussion

Takotsubo cardiomyopathy is seen in 0.7%-2.5% of patients with suspected ACS. ³ TC was first described in the Japanese population ⁴ and was named TC after the octopus-trapping pot, which has a narrow neck and round bottom resembling the left ventricle during systole in these patients. ⁵ TC has been reported in approximately 1%-2% of all troponin-positive suspected ACS presentations and in almost 6% of all women presenting with suspected STEMI who undergo urgent angiography. ⁶ It occurs predominantly in elderly individuals, more commonly in postmenopausal women. ⁷ About 80% of cases involve patients aged 50 years or older at the time of diagnosis. ⁸

Diagnosis is by criteria from Mayo Clinic, ⁹ which include:

Transient akinesia, hypokinesia, or dyskinesia of the mid-segment of left-sided ventricle, with or without apical involvement; regional wall motion abnormalities extending beyond a single vascular distribution.

Absence of obstructive CAD or acute plaque rupture on angiography.

New ECG changes (ST-segment elevation or T-wave inversion) or a modest rise in troponin I levels.

Exclusion of pheochromocytoma or myocarditis.

Clinical features of TC closely resemble those of ACS. About 50% of patients present with angina-like chest pain or dyspnea. Syncope or cardiac arrest is a very rare presentation. Hemodynamic compromise is uncommon, but heart failure is frequently encountered, with hypotension due to a reduction in stroke volume. The occurrence of cardiogenic shock in TC is quite rare.^{10, 11} Preceding the event, physical or emotional stress is identified in approximately two-thirds of patients. Other factors triggering TC include noncardiac surgeries, severe pain due to fractures or renal colic, stress tests (e.g., dobutamine stress echocardiography), and thyrotoxicosis. ¹² The pathophysiological mechanism of TC suggests that hyper-sympathetic activity and a catecholamine surge play a key role in its development. ¹³ These triggers activate the sympathetic nervous system, leading to an increase in norepinephrine, epinephrine, cortisol, and catecholamine bioavailability. Animal model studies have shown that high intravenous epinephrine levels produce the characteristic reversible apical depression of myocardial contraction with basal hypercontractility.^{14, 15} Based on the ballooning pattern, TC is classified into four groups ¹⁶ :

Takotsubo type

Mid-ventricular type

Reverse Takotsubo type

Localized type

Right ventricular involvement is classified separately due to its extreme clinical manifestations. ¹⁷ A similar case was reported by Lu et al., in which TC was induced by psychological and physical stress following a successful PCI. ¹⁸ In that case report, the patient developed symptoms comparable to PCI-related complications. Coronary angiography and LV angiography were performed to confirm the diagnosis of TC following PCI. In addition, cardiac MRI was used as an added diagnostic tool to rule out differential diagnoses such as myocarditis. This case describes a postmenopausal woman who presented with AWMI and underwent a successful percutaneous transluminal coronary angioplasty (PTCA), with no complications such as coronary artery dissection or incomplete stent apposition. However, 2 days later, she developed recurrent chest pain, and 2D echocardiography showed apical ballooning with basal hypercontractility. Coronary angiography showed a patent ramus intermedius stent, while LV angiography showed features typical of TC. The probable cause in this patient was procedural stress, which resulted in a catecholamine surge leading to TC. This case highlights the difficulty in diagnosing TC after PCI, as its presentation can mimic PCI-related complications. However, TC is generally a benign condition with a favorable prognosis. The mortality and morbidity following the acute phase of TC are low, with an all-cause mortality rate of 5%-6% at 1 year. ⁸ The initial treatment of TC is same as acute MI till a final or definite diagnosis is established. Management is mostly supportive, which includes beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and diuretics. Beta-blockers help control the excessive catecholamine effects but should be administered only after pulmonary edema has resolved. Other heart failure medications may be started as needed. The most commonly used therapeutic approach is a combination of ACE inhibitors and beta-blockers. This combination is beneficial because ACE inhibitors prevent vasospasm and reduce hypertension, while beta-blockers inhibit the Gs-protein metabolic pathway, preventing recurrence of TC. ¹⁹ A newer therapeutic option, levosimendan, is a non-catecholamine inotrope that does not increase myocyte oxygen uptake. It is considered a rational treatment for cardiogenic shock associated with TC. ²⁰ Congestive heart failure is the most common complication of TC, occurring in approximately 20% of patients. This case emphasizes about unusual and interesting link between CAD and TC syndrome.

Conclusion

Post-ST-elevation myocardial infarction Takotsubo cardiomyopathy is a rare and uncommon presentation and is one of the differential diagnoses along with other post-PCI complications, such as acute stent thrombosis. In our case, given the post-PCI status, our initial differential diagnosis was acute stent thrombosis due to recurrent ST elevation. However, echocardiography provided a clue for TC, as it showed basal hypercontractility and apical ballooning, which was then confirmed by LV angiography. Therefore, a systematic workup should be performed to avoid misdiagnosis. This case also reminds us that when patients experience unexplained ECG changes and elevated troponin levels after PCI, we cannot overlook the possibility of TC while evaluating PCI-related complications. During the perioperative period, patients undergoing interventional treatment should receive proper communication and psychological support to reduce anxiety and fear associated with the procedure. This approach can improve postoperative recovery and lower the incidence of TC.