Tako-tsubo cardiomyopathy in a radical operation for carcinoma of colon patient with PCI history

Tako-tsubo cardiomyopathy (TTC), also known as “stress-induced cardiomyopathy”, “broken heart syndrome” or “apical ballooning syndrome”, often presents as an acute coronary syndrome (ACS) with ST segment changes and shows transient left ventricular dysfunction.[1]^,[2]

TTC usually affects postmenopausal women, who often get a psychological or physical incident as a trigger.[3] There were about 0.7%–2.5% patients are TTCs among those who were alleged to have ACS.[4] The pathogenesis continues to be unknown. TTC patients with relevant coronary artery disease (CAD) were more likely to be older in age, to have diabetes, a familial history of CAD, and acute functional mitral regurgitation compared with those without relevant CAD.[5] We presented a case of TTC complicating CAD, diabetes, hypertension. What's more, we first introduced the case of TTC after a radical operation for carcinoma of colon.

An 81-year-old woman was transferred to intensive care unit (ICU) for complaint of dyspnea and whooping pink frothy sputum ten hours from coloproctological department, who had a history of hypertension, diabetes mellitus (DM) type II, and percutaneous coronary intervention (PCI) history within one year, and suffered exploratory laparotomy and sigmoid colon carcinoma radical resection twelve days before. During this period, her plasma glucose was poorly controlled after surgery. Physical examination, moist rale was heard at the bottom of both lung. As noninvasive support for treatment received little effect, she accepted bedside emergency treatment with tracheal intubation via oral cavity and mechanical ventilation. Cardiac enzymes were slightly elevated (Hypersensitive-Troponin I (Hs-TnI) 94.8 pg/mL, creatine phosphokinase-MB (CK-MB) within normal limits 16 U/L) and N-terminal pro-brain natriuretic peptide (NT-ProBNP) was significantly elevated (16100.0 pg/mL). Electrocardiogram (ECG) showed sinus tachycardia (149 bpm), limb leads low voltage. Four hours later, cardiac enzymes were notably elevated (Hs-TnI 16568.5 pg/mL, CK-MB 56 U/L). ECG showed sinus rhythm (97 bpm), Q wave in II, III, aVF, T-inversion and ST-depression in V2–V4. Combined her ECG and cardiac enzymes' dynamic changes, we'd prone to diagnose it as acute myocardial infraction (AMI). But echocardiogram showed left ventricular dysfunction with systolic apical ballooning distension and akinesia, we could not exclude TTC. After communicating the illness with her family and obtaining their consent of emergency coronary angiography, we did emergency interventional surgery eight hours later. Coronary angiography showed patency of the left main coronary artery (LAM), diffuse in-stent restenosis of the left anterior descending artery (LAD) for 70%–90%, and stent intimal thickening of circumflex artery (LCX) as well the right coronary artery (RCA). Left ventriculograms showed apical ballooning distension, apical akinesia, and basal hypercontractility (Figure 1). Beta-blockers, cardiac stimulant, a diuretic and dual antiplatelet therapy were started. Soon afterwards, her tracheal intubation was pulled out, and Hs-TnI (3849.8 pg/mL) and NT-ProBNP (4000.0 pg/mL) were markedly decreased. She was sent back to coloproctological department and left hospital with Hs-TnI 199.2 pg/mL. Four months later, the patient came to vasculocardiology department for complaint of chest distress and palpitation. ECG showed sinus rhythm, T-inversion in some leads (V2–6). Cardiac enzymes were slightly elevated (Hs-TnI 60.8 pg/mL, CK-MB within normal limits 11 U/L) and NT-ProBNP was negative (940.0 pg/mL). Echocardiogram showed a bit thickness of the interventricular septum (12 mm) and ejection fraction 55%. A coronary angiogram documented diffuse in-stent restenosis of the proximal-middle segment of LAD to 90%, and no significant stenosis of LCX and RCA. Left ventriculography showed normal apical walls motion. In the end, we put two coronary stents at the site of LAD critical stenosis. During the follow-up period, the patient is in excellent health.

Figure 1. Coronary angiography of the patient.

(A): normal left main coronary artery, diffuse in-stent restenosis of the left anterior descending artery for 70%–90%; (B, C): stent intimal thickening of circumflex artery as well the right coronary artery; (D, E): Left ventriculography shows initial recovery of basal contractility and persistent akinesia of the apical segments.

TTC is a reversible acute heart failure syndrome that is increasingly recognized in modern cardiology practice. According to diagnostic criteria made by European Society of Cardiology (ESC),[6] the woman had an operation history as a trigger, this case could be diagnosed as TTC. As the local and blood-borne release of catecholamines as mediators of myocyte injury in TTC,[7] DM probably shows a “protective” influence via an associated neuropathy involving autonomic sympathetic nerves, and the prevalence of DM in patients with TTC is low.[8]

The patient's ECG showed acute anteroseptal, lateral and inferior myocardial infraction, but coronary angiogram showed significant stenosis of the LAD. We cannot purely diagnose it as AMI. A retrospective case series showed that ST-elevation in –aVR was characteristic of ST-elevation-TTC with a specificity 95%, ST-elevation in –aVR with T-inversion in any lead was also specific for non ST-elevation-TTC (specificity 100%).[9] When the presence of significant coronary artery stenosis (≥ 50%) does not supply the area and extension of the myocardial dysfunction, it should not be considered an exclusion criterion for TTC.[5] As we know, troponin elevations are relatively lower in TTC, compared with AMI. In this case, her cardiac enzymes took a dynamic development, we can't exclude it complicated with AMI. Just recall this case, we should do cardiac magnetic resonance (CMR) imaging. CMR is a useful, noninvasive instrument for the assessment of myocardial motion abnormalities because it may provide different manifestations towards a particular cause. In particular, the presence and pattern of any late gadolinium enhancement may point towards a vascular or non-vascular cause. And CMR performed early after admission to hospital would in many TTC cases help to establish the diagnosis based on a typical pattern of oedema.[10]

Various diseases may be linked to TTC, like intracranial hemorrhage, pneumothorax, small bowel necrotic ischemia, and asthma. Surgery may represent a major stressing trauma and, therefore, could be responsible for triggering a massive catecholamine release. So many departments may meet the challenge to treat this disease. Nevertheless, no randomized trials exist to define the optimal treatment of these patients despite the rapid growth of the medical literature in this area over the past two decades. Empiric therapeutic strategies, the use of cardio-selective b-blockers, ACE inhibitors, mechanical support, and consideration of short-term anti-thrombotic medications could be chosen based on the actual situation.[10] However, it's challenging to distinguish between TTC, CAD and other forms of myocardial infraction in numerous cases. And patients may have received unjustified aggressive therapies, resulting in increased complications and cost. Above all, there are still a lot of problems about TCC's pathogenesis, diagnosis and therapy to be solved.