Sepsis-Induced Takotsubo Cardiomyopathy Mimicking ST-Elevation Myocardial Infarction: A Clinical Case.

Takotsubo cardiomyopathy (TCM) was first initially reported in 1990 in Japan and has been increasingly recognized in clinical practice. It is characterized by transient regional left ventricular dysfunction without evidence of obstructive coronary artery disease, often precipitated by emotional and physical stressors. Although TCM does occur in young women and men, it is most commonly seen in postmenopausal women. Sepsis induced TCM is an infrequently encountered entity. We present a case of TCM in a middle age gentleman who presented with septic shock due to acute cholecystitis. Two days later, the patient developed clinical features of acute myocardial infarction. Echocardiography revealed hypokinesis of the left ventricle. Coronary angiography revealed normal arteries without any obstruction. Diagnosis of sepsis induced TCM was finally made. The patient made a dramatic recovery and discharged home in stable condition. Follow-up echocardiography showed improvement in left ventricular systolic function. Copyright:

INTRODUCTION

Takotsubo cardiomyopathy (also called apicalballooning syndrome, stress cardiomyopathy, and broken-heart syndrome) is an acute clinical syndrome that often mimicking the presentation of anterior wall acute myocardial infarction. It was first described in Japan in the early 1990s and has been most frequently observed in postmenopausal women after exposure to intense emotional or physical stress. It is characterized by symptoms such as chest pain and shortness of breath, electrocardiography (ECG) changes with ST-segment elevation, elevated myocardial enzymes, diverse range of transient wall motion abnormalities on echocardiography, in the absence of obstructive coronary artery disease.[1] Takotsubo cardiomyopathy accounts for 1%–2% of patients presenting with symptoms suggestive of acute coronary syndrome.[23] The exact pathogenesis of Takotsubo cardiomyopathy is not well understood. However, the postulated mechanism includes catecholamine excess, microvascular dysfunction, and coronary artery spasm.[4] Patients with TCM usually have a favorable prognosis, and almost complete resolution of ventricular function usually occurs 4–8 weeks after presentation in 96% of the cases.[5]

Patients admitted to high dependency units experience extreme physical, emotional stress and catecholamine surges, which could potentially precipitate TCM. According to a case series, cardiomyopathy is seen in 50% and 25% of patients with septic shock and sepsis, respectively.[5] Nevertheless, the takotsubo pattern is not a well-described entity in this setting. We, therefore, sought to present a case of Takotsubo cardiomyopathy following admission for septic shock secondary to acute cholecystitis.

CASE PRESENTATION

A 63-year-old male, with a past medical history (PMHx) of recurrent abdominal adhesions requiring multiple surgeries, presently with Abcarian stoma and mucus fistula, presented with a history of abdominal pain and fever. The results of his initial physical examination revealed a body temperature of 36.8°C, a blood pressure of 109/54 mmHg, a pulse rate of 109 beats/min, and a respiratory rate of 18 breaths/min. The breathing sound was coarse; his heartbeats were regular without audible murmur; the abdomen was soft with tenderness in the right upper quadrant, with positive murphy signs. There was no palpable mass or hepatosplenomegaly noted.

The initial blood investigations revealed mild anemia, hemoglobin level of 10.6g/dl, with marked neutrophilic leuocytosis, white blood cell count of 28,000/ml. The C-reactive protein level was 100 mg/L. His troponin I level was mildly elevated at 48 ng/L. Renal function was deranged with a creatinine level of 176 umol/L and urea of 19 mmol/L. Other laboratory findings, including electrolytes, liver function tests, serology, and urinalysis, were all within normal limits. Chest X-ray findings were unremarkable, as was the initial ECG. Ultrasound of abdomen showed thick gallbladder wall greater than 3mm, with pericholecystic fluid. There was also evidence of sludge and cholelithiasis.

He was admitted with the impression of sepsis secondary to acute cholecystitis. He was started on antibiotics along with other supportive measures. On the next day, the patient continued to be highly febrile and became hypotensive requiring intensive care unit (ICU) admission and inotropic support.

On the 2nd day of ICU admission, he started complaining of retrosternal chest pain which was associated with profuse sweating. ECG was notable for ST-segment elevation on leads V2–V4 [Figure 1]. The patient's troponin-T level was elevated at 781 ng/L. A diagnosis of anterior wall ST-segment elevation myocardial infarction was considered. An emergent coronary angiography was done which demonstrated nonobstructive CAD. Echocardiographic evaluation revealed dilated left ventricular cavity with extensive apical dyskinesis and relative preservation of the basal to midseptal and basal-lateral wall contraction [Figure 2]. Estimated left ejection fraction was approximately 25%. Sepsis-induced TCM was the final diagnosis in this patient. The patient recovered after antibiotics and other conservative therapies, and finally, he was discharged from the hospital. He had repeated echocardiogram 4 weeks later which showed complete resolution of left ventricular systolic function, estimated ejection fraction was >55%.

Figure 1

Electrocardiography: sinus rhythm, ST-segment elevation on leads V2–V5

Figure 2

Echocardiography: Four chamber view showing evidence of classic takotsubo cardiomyopathy, the apical type. (a) Represents systole and (b) represents diastole

DISCUSSION

Takosubo cardiomypathy is a reversible cardiomyopathy that is usually precipitated by intense emotional or physical stress in the absence of significant coronary disease. Complete resolution of ventricular function usually occurs 4–8 weeks after presentation. Although the true prevalence of this syndrome is not well known, Gianni, and colleagues have reported that it may account for between 1% and 2% of all the patients suspected cases of acute coronary syndrome.[6] Moreover, it has a striking female predominance, mainly affecting the postmenopausal age group. For instance, Templin et al. stated that 90% of TCM patients were female in a multinational registry of 1750 patients, with 79% aged above 50 years.[7] The most frequently reported symptoms are chest pain and dyspnea, which mimics that of the acute coronary syndrome.

The diagnosis of TCM remains challenging. The most widely accepted diagnostic criteria was published by the Mayo Clinic in 2004. It includes 4 major criteria which are: “(1) transient hypokinesia, akinesia, or dyskinesia of the left ventricular mid segment with or without apical involvement; (2) an absence of obstructive coronary artery or angiographic absence of acute plaque rupture; (3) a new ECG abnormality (either ST-segment elevation and/or T wave inversion) or elevated cardiac troponin; and (4) the absence of a recent significant heart trauma, intracranial bleeding, pheochromocytoma, myocarditis, or hypertrophic cardiomyopathy.”[4] Our patient had met all four proposed diagnostic criteria. Pheochromocytoma and myocarditis were excluded clinically. He was normotensive and did not have history of palpitations, or excessive diaphoresis. Thus, pheochromocytoma was not a concern. Moreover, our patient did not have a history of a recent viral illness; therefore, we had a lower index of suspicion for viral myocarditis.

Although the exact pathophysiological mechanism of TCM remains poorly understood, the proposed mechanisms include multivessel coronary vasospasm, coronary microvascular dysfunction, and catecholamine cardiotoxicity. Of these, the most favored explanation is catecholamine-mediated myocardial injury. Stress causes activation of the sympathetic nervous system, which in turn, causes elevation in the catecholamine level in the circulation. For instance, Wittstein and colleagues found that the concentration of serum catecholamine in TCM patients was two to three times higher than that in myocardial infarction patients. This surge in catecholamine level results into a decline in myocyte contractile function.[8] Severe sepsis can cause this physiological response and theoretically may precipitate TTC in predisposed individuals.

In a systematic review, De Giorgi et al. documented 27 published cases of sepsis-induced TCM. Bacterial infections were the most frequent cause (23 of 27 cases, 85.2%) and females were more predominantly affected than males (74% vs. 26%).[9] Our patient had septic shock secondary to acute cholecystitis.

Unlike other forms of cardiomyopathies, TCM lacks well-established guideline-based therapies and its treatment is primarily supportive. In acute phase, initial management usually focuses on treating myocardial ischemia (MI) as it is difficult to distinguish for certain TCM from acute coronary syndrome (ACS). This including administration of acetylsalicylic acid, clopidogrel, heparin, and beta-blocker or angiotensin-converting enzyme (ACE)-inhibitor. Once acute MI has been excluded by angiography, antiplatelet duo therapy is usually withdrawn.[4]

In our case, the patient was treated initially as ACS and he underwent angiography which showed non obstructive disease. After having suspected the diagnosis of TCM, the patient was monitored closely for development of complications such as cardiogenic shock and malignant arrhythmias. He was also treated using intravenous hydration, noradrenaline infusion, and empiric antibiotics. His hospital stay was uneventful and he was discharged after 10 days of hospital stay. Left ventricular function recovered within 4 weeks.

CONCLUSION

Takotsubo cardiomyopathy is a type of acquired cardiomyopathy usually occur in patients with stressful event including sepsis. The clinical profile closely mimics that of an acute coronary syndrome. Overall prognosis is good with appropriate supportive management in the acute phases. This case signify the importance of keeping this syndrome a part of differential diagnosis in patients with acute heart failure syndrome.

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