Background: Tako-tsubo syndrome (TTS) in its typical (apical) and atypical (non-apical) forms is being increasingly recognized in the West owing to early systematic coronary angiography in acute coronary syndromes (ACS).
Aim of the study: To assess the incidence, the clinical characteristics and the outcome of TTS in a single high volume cath lab in Southern Italy over the last 6 years.
Methods: Among 1674 consecutive patients (pts) referred to our coronary care units in the last 6 years (2001–2006) for ACS we selected 6 (0.5%) pts (6 women; age 57 ± 6 years) who fulfilled the following 4 criteria: 1) transient left ventricular wall motion abnormalities resulting in ballooning at contrast ventricolographic or echocardiographic evaluation; 2) normal coronary artery on coronary angiography performed 5 ± 9 hours from hospitalization; 3) new electrocardiographic ischemic-like abnormalities (either ST-segment elevation or T-wave inversion) and 4) emotional or physical trigger event.
Results: At admission all pts had presumptive diagnosis of ACS and ECG revealed ST elevation in 3 (50%) and T wave inversion with QT elongation in 3 (50%). In the acute phase cardiogenic shock occurred in 2 (33%) and heart failure in 1(16%). Presenting symptoms were chest pain in 6 (100%), dyspnoea in 2 (33%) and lipotimia in 1 (16%). At echocardiographic-ventricolographic assessment, the mechanical dysfunction (ballooning) was apical in all 6 pts ("classic" TTS). In all patients wall motion abnormalities completely reversed within 4.5 ± 1.5 days. The region of initial recovery was the anterior and lateral wall in 4 cases and the lateral wall in 2 cases. Ejection fraction was 35 ± 8% in the acute phase and increased progressively at discharge (55 ± 6%) and at 41 ± 20 months follow-up (60 ± 4%, p < 0.001 vs. baseline). All patients remained asymptomatic with minimal (aspirin, beta blockers, antihypertensive and antidislipidemic therapy) treatment.
Conclusion: Classic TTS is a frequent serendipitous diagnosis after coronary angiography showed "surprisingly" normal findings in a clinical setting mimicking an ACS. Despite its long-term good prognosis life threatening complications in the acute phase can occur.
Introduction
Stress induced cardiomyopathy is described as an acute cardiomyopathy characterized by acute, but rapidly reversible, left ventricle systolic dysfunction in the absence of atherosclerotic coronary artery disease which appears to be triggered by intense psychological and physical stress [1]. This syndrome has been firstly described in Japan in 1990 by Sato et al, who proposed the term 'Tako-Tsubo', the name used by Japanese fishermen for the fishing pot with a narrow neck and a wide base that is used to trap octopus. In fact, the left ventricle with Tako-tsubo cardiomyopathy shows the peculiar appearance of a rounded bottom an a narrow neck on the end-systolic left ventriculogram [2]. Various definitions have been proposed in order to describe this syndrome such as apical ballooning syndrome (ABS), broken heart syndrome and stress or ampulla cardiomyopathy [2]. The exact incidence of ABS appears to be unclear, it ranges form 1 to 2% of patients who present, at admission, a clinical scenario which often mimics acute myocardial infarction. The occurrence of ABS syndrome seems to be significantly recurrent in postmenopausal women although it has been described also in younger women and males. The most frequent finding on the admission ECG is a mild ST-segment elevation which appears to occur in approximately 50–60% of the patients [2]. The 12-lead ECG alone in not helpful in differentiating ABS from ST-elevation myocardial infarction.
Characteristic evolutionary changes that occur over 2 to 3 days include resolution of the ST-segment elevation and subsequent development of diffuse and often deep T-wave inversion that involves most leads. New pathological Q waves may occasionally be observed and, furthermore, it has been possible to observe a prolongation of the corrected QT interval [2]. Although there are rare exceptions, the proposed Echocardiographic Mayo Clinic Criteria for the clinical diagnosis of ABS underline a transient apical regional wall motion abnormalities, usually extending beyond a single epicardial vascular distribution. Most, if not all of the patients, appear to have a mild increase of cardiac biomarkers. Typically, no obstructive coronary artery disease has been found. Although the pathogenesis still remains unclear, a common element appears to be an exaggerated sympathetic activation. The mechanism underlying the association between sympathetic stimulation and myocardial stunning in unknown. One possibility is ischemia resulting from epicardial coronary arterial spasm. An alternative mechanism is microvascular spasm. A third possible mechanism is direct myocyte injury [3]. Activation of cardiac adrenoreceptors is experimentally proven to induce left ventricular (apical) dysfunction. In fact, there is evidence that apical myocardium has enhanced responsiveness to symphatetic stimulation [4], potentially making the apex more vulnerable to sudden surges in circulating catecholamine levels. Aim of the present study was to describe a case series of 6 ABS observed in the last 6 years in a tertiary care referral center with high volume cardiac cath lab in Mercogliano, Southern Italy.
Methods
During the last 6 years (2001–2006), among 1674 consecutive patients (pts) referred to our coronary care units for ACS, 6 patients (age 57 ± 6 years; all women) presenting at admission with acute onset of cardiovascular event have been retrospectively selected. All fulfilledthe following 4 predetermined criteria to define Tako-Tsubo cardiomyopathy [2]: 1) transientleft ventricularwall motion abnormalities resulting in ballooning at contrast ventricolographic or echocardiographic evaluation; 2) normal coronary artery on coronary angiography (performed 5 ± 9 hours from the hospitalization); 3) new electrocardiographic ischemic-like abnormalities (either ST-segment elevation or T-wave inversion) and 4) emotional or physical trigger event.
All patients underwent, at admission, two-dimensional transthoracic echocardiography, 12 lead electrocardiogram, serial measurements of cardiac isoenzymes including creatine kinase, creatine kinase MB fraction, and troponin. Transthoracic echocardiography has again been repeated at discharge. All patients have been followed-up for a median period of 40 months.
