Takotsubo Cardiomyopathy (TTC) is an uncommon cause of acute reversible ventricular systolic dysfunction in the absence of obstructive Coronary Artery Disease (CAD). Typically manifesting as apical wall ballooning, TTC can rarely present atypically with apical wall sparing.

A 62-year-old female presented with complaints of chest pain and features mimicking acute coronary syndrome. Coronary angiogram revealed no obstructive CAD and left ventriculogram showed reduced ejection fraction, normal left ventricular apex and hypokinetic mid-ventricles consistent with atypical TTC. The patient was discharged home on heart failure medications and a follow-up transthoracic echocardiogram demonstrated improved left ventricular function with no wall motion abnormality.

This case report provides an insight into the diagnosis and management of TTC in the absence of pathognomic features.

Stress-induced cardiomyopathy is an acute disease characterized by a large left ventricular apical dyskinesia ("apical ballooning"), triggered by intense emotional or physical stress, acute illnesses or, rarely, by alcohol or opiates withdrawal. Connection to stress and apical asynergy suggest a catecholamine-mediated pathogenesis. We recently observed a typical apical stress-induced cardiomyopathy, arising two weeks after a long-lasting antidepressant treatment withdrawal and recurring, a week later, with evidence of inferior wall akinesia. The reported case has several unusual features: 1) both episodes were not preceded by relevant triggering event (except antidepressant discontinuation); 2) early heterozonal relapse was observed; 3) the latency between antidepressant discontinuation and stress-induced cardiomyopathy onset is unusually long. The lack of relevant triggering stress and the evidence of multifocal asynergies could support the hypothesis of a non-catecholaminergic pathogenesis. Moreover, the long latency after antidepressant withdrawal may suggest that prolonged antidepressant treatments may have delayed pathological consequences, possibly related to their known neuroplastic effects.

Reversible left ventricular apical ballooning, without coronary artery stenosis, is a novel heart syndrome mimicking acute myocardial infarction, and is very rare in Taiwan. A 74-year-old Taiwanese woman returned from travelling abroad for one week and suffered from persistent, severe jet lag with sleep disturbance. She had a cold exacerbated by bronchial asthma for three days. She presented with sudden onset of chest pain after drinking three cups of coffee and taking a sauna for more than 1 h. On admission, an electrocardiogram showed ST segment elevation in leads II, III, aVF and V(3-6), and cardiac enzyme tests revealed minimal elevation. An echocardiogram showed apical ballooning and basal hyperkinesias of the left ventricle (LV) in systole. A coronary angiogram on the second day was normal, while the ST segment was still elevated, and the patient continued to experience chest pain. A negative T wave developed three days later. The electrocardiogram abnormality and LV dysfunction resolved completely six months later. A takotsubo (ampulla) cardiomyopathy was diagnosed. The activated myocardial adrenergic nervous system, stimulated by acute and marked stress in this patient, with more adrenergic innervations distributed in the apex of the LV, may be the trigger for this novel cardiac syndrome.

Although takotsubo cardiomyopathy (TTC) typically affects the apical and/or midventricular segments, several recent cases have reported a reverse or inverted variant of TTC. The aim of this study was to investigate the clinical characteristics, laboratory parameters, electrocardiographic, and echocardiographic findings in patients presenting as inverted TTC and compare those parameters to those presenting as mid or apical variant.

The clinical features of inverted TTC are different from those of other types of TTC.

Of 103 patients enrolled from the TTC registry database, 20 showed inverted TTC (inverted TTC group), and 83 showed mid or apical variant (other TTC group).

Clinical presentations and in-hospital courses were mostly similar between the groups. However, the inverted TTC group was younger (median, 54.5 vs 64.0 years; P = 0.006) than other TTC and had a higher prevalence of triggering stress (100% vs 77%, P = 0.018), whereas other TTC group had higher prevalence of dyspnea (58% vs 30%, P = 0.025), pulmonary edema (46% vs 20%, P = 0.035), cardiogenic shock (36% vs 10%, P = 0.023), T-wave inversion (81% vs 60%, P = 0.049), and significant reversible mitral regurgitation (MR) (19% vs 0%, P = 0.033). Also, the inverted TTC group had significantly higher creatine kinase MB fraction (CK-MB); CK-MB (median, 30.7 vs 7.6 ng/mL; P = 0.001) and troponin-I (median, 13.1 vs 1.6 ng/mL; P = 0.001), but lower N-terminalpro-brain natriuretic peptide (NT-proBNP) levels (median, 613.3 vs 4987.0 pg/mL; P = 0.020).

Inverted TTC presents at a younger age and has a higher prevalence of triggering stress, whereas other TTC has a higher prevalence of heart failure symptoms, significant reversible MR, and T-wave inversion and higher NT-proBNP levels despite other clinical features that are mostly similar.

Stress cardiomyopathy is characterised by reversible left ventricular dysfunction. It simulates an acute coronary syndrome (ACS), presenting with precordial pain or dyspnoea, changes of the ST segment, T wave, or QTc interval on electrocardiogram, and raised cardiac enzymes. Typical findings are disturbances of segmental contractility (apical hypokinesia or akinesia), with normal epicardial coronary arteries. The true prevalence is unknown, as the syndrome may be under-diagnosed; it is more common in postmenopausal women. There is usually a trigger in the form of physical or psychological stress. The electrocardiographic, echocardiographic, and ventriculographic changes resolve spontaneously over a variable period of time (from days to months). There are a number of pathophysiological theories, none of which has been shown to be definitive, suggesting that all of them may be involved to some extent. The prognosis is generally favourable, and recurrence is very rare.

Although takotsubo cardiomyopathy (TTC) has been reported to have an excellent clinical recovery, there are few data regarding clinical, laboratory, and echocardiographic findings in TTC presenting as cardiogenic shock. We aimed to assess the differences in these parameters between TTC presenting with and without cardiogenic shock.

Fifty patients were enrolled from the TTC registry database and divided according to the presence of cardiogenic shock. Sixteen patients presented with cardiogenic shock as initial presentation (S group), and 34 did not (NS group).

The S group had a higher prevalence of dyspnea (81% vs 38%, P = .005), pulmonary edema (69% vs 29%, P = .009), and significant reversible mitral regurgitation (44% vs 15%, P = .025) than the NS group. In addition, the S group had significantly higher troponin-I (median, 8.2 vs 1.4 pg/mL; P = .043) and N-terminal prohormone brain natriuretic peptide levels (median, 8831 vs 2348 pg/mL; P = .046). During follow-up (median, 3.1 years), cardiac deaths associated with TTC itself and recurrences of TTC were not noted in both groups.

The S group has a higher prevalence of heart failure symptoms, significant reversible mitral regurgitation, and troponin-I and N-terminal prohormone brain natriuretic peptide levels. However, with meticulous therapeutic strategies, prognosis of this syndrome may be excellent irrespective of hemodynamic instability.

Tako-Tsubo syndrome is a clinical entity mimicking acute coronary syndrome (ACS). Left ventricular outflow tract (LVOT) obstruction may occur in Tako-Tsubo syndrome. The aim of this study was to determine the prevalence and features of LVOT obstruction in Tako-Tsubo syndrome in a population presenting with ACS.

This study included consecutive patients admitted to 2 catheterization laboratories for suspected ACS. All patients underwent echocardiography, coronary arteriography, and left ventricular angiography if no significant coronary lesions were found.

Among 10,366 patients referred for coronary angiography, the study population consisted of 3,909 patients with suspected ACS. Thirty-two patients (mean age 71 +/- 13 years old) presented with Tako-Tsubo syndrome, resulting in a prevalence of 0.8% in our population of ACS and 5% of patients without significant coronary lesions. Eight women (mean age 81 +/- 4 years old, P = .01) exhibited LVOT obstruction, a prevalence of 25% among Tako-Tsubo syndrome cases. All patients with intraventricular pressure gradient had systolic anterior motion of the mitral valve and septal bulge. Prevalence of septal bulge was 100% in patients with Tako-Tsubo syndrome and LVOT obstruction versus 29% in patients without LVOT obstruction (P = .002). Mean degree of mitral regurgitation was 2.1 +/- 0.7 in cases of LVOT obstruction versus 0.9 +/- 0.7 in patients without LVOT (P = .0003) and significantly decreased during follow-up (1 +/- 0.8, P = .002). Recovery of left ventricular ejection fraction was similar in patients with and without LVOT obstruction (P = .58).

The present study demonstrates that the prevalence of LVOT obstruction in Tako-Tsubo syndrome is high, with specific characteristics as compared with patients without LVOT obstruction. Echocardiography should be systematically performed for all patients presenting with Tako-Tsubo syndrome for the detection of LVOT obstruction.

Takotsubo or ampulla transient left ventricular apical ballooning (LVAB) cardiomyopathy has been described as a clinical syndrome characterized by the sudden onset of chest pain, cardiac failure, ischemic changes on electrocardiography, and apical severe myocardial dysfunction in the presence of "normal" coronary arteries on angiography. All features last from a few days to a few weeks.

On the basis of previous knowledge and in light of our recent experience with acetylcholine testing in this condition, the cases of four patients are described and preliminary but sound arguments are given to support the theory that LVAB is caused by severe, sustained spasm of many or all of the coronary vessels. In one of these patients, experimental reproduction of LVAB occurred in the catheterization laboratory during acetylcholine testing (as evidenced by echocardiographic monitoring), while in two other patients, the test provoked similar, extensive angiographic vasospasm and suggestive symptoms. In addition, the similarities and differences that exist between LVAB and Prinzmetal angina are discussed.

To evaluate the pathogenesis of LVAB, it is proposed that acetylcholine testing be routinely performed under specific, prospective, investigational protocols at specialized centers.

Apical ballooning syndrome (ABS) is a unique reversible cardiomyopathy that is frequently precipitated by a stressful event and has a clinical presentation that is indistinguishable from a myocardial infarction. We review the best evidence regarding the pathophysiology, clinical features, investigation, and management of ABS. The incidence of ABS is estimated to be 1% to 2% of patients presenting with an acute myocardial infarction. The pathophysiology remains unknown, but catecholamine mediated myocardial stunning is the most favored explanation. Chest pain and dyspnea are the typical presenting symptoms. Transient ST elevation may be present on the electrocardiogram, and a small rise in cardiac troponin T is invariable. Typically, there is hypokinesis or akinesis of the mid and apical segments of the left ventricle with sparing of the basal systolic function without obstructive coronary lesions. Supportive treatment leads to spontaneous rapid recovery in nearly all patients. The prognosis is excellent, and a recurrence occurs in <10% of patients. Apical ballooning syndrome should be included in the differential diagnosis of patients with an apparent acute coronary syndrome with left ventricular regional wall motion abnormality and absence of obstructive coronary artery disease, especially in the setting of a stressful trigger.

Transient apical dysfunction syndrome, ballooning or Takotsubo cardiomyopathy is a recently described syndrome. It is a disease with a partially known mechanism, characterized by the morphology adopted by the left ventricle secondary to hypokinesis and dyskinesis of the apical segments and hypercontractibility of the basal segments. In most of the cases published, it is a syndrome with ST segment elevation in the precordial leads, whose presentation form is also thoracic pain or dyspnea, with the possible existence of moderate elevation of cardiac biomarkers. On the contrary to the acute coronary syndrome, patients with left ventricle dysfunction do not have atherothrombotic disease in the coronary arteries. Furthermore, the alterations described have a reversible character. Some diagnostic clinical criteria have been proposed and there is presently some controversy on them and on the complementary examination needed to diagnose it.

Transient left ventricular apical ballooning syndrome (TLVABS) is an acute cardiac syndrome mimicking ST-segment elevation myocardial infarction characterized by transient wall-motion abnormalities involving apical and mid-portions of the left ventricle in the absence of significant obstructive coronary disease.

Searching the MEDLINE database 28 case series met the eligibility criteria and were summarized in a narrative synthesis of the demographic characteristics, clinical features and pathophysiological mechanisms.

TLVABS is observed in 0.7-2.5% of patients with suspected ACS, affects women in 90.7% (95% CI: 88.2-93.2%) with a mean age ranging from 62 to 76 years and most commonly presents with chest pain (83.4%, 95% CI: 80.0-86.7%) and dyspnea (20.4%, 95% CI: 16.3-24.5%) following an emotionally or physically stressful event. ECG on admission shows ST-segment elevations in 71.1% (95% CI: 67.2-75.1%) and is accompanied by usually mild elevations of Troponins in 85.0% (95% CI: 80.8-89.1%). Despite dramatic clinical presentation and substantial risk of heart failure, cardiogenic shock and arrhythmias, LVEF improved from 20-49.9% to 59-76% within a mean time of 7-37 days with an in-hospital mortality rate of 1.7% (95% CI: 0.5-2.8%), complete recovery in 95.9% (95% CI: 93.8-98.1%) and rare recurrence. The underlying etiology is thought to be based on an exaggerated sympathetic stimulation.

TLVABS is a considerable differential diagnosis in ACS, especially in postmenopausal women with a preceding stressful event. Data on longterm follow-up is pending and further studies will be necessary to clarify the etiology and reach consensus in acute and longterm management of TLVABS.

A 77-year-old female was admitted in our hospital for uterine prolapse surgery. She developed ventricular tachycardia during induction of general anaesthesia and after initial symptomatic measures, she was transferred to the coronary care unit. Heart failure persisted and electrocardiographic changes mimicking acute myocardial infarction appeared. Coronary angiography was normal and left ventriculography revealed akinesis of the apical region of the left ventricle and apical ballooning during systole, with relative sparing of the base of the heart. Complete recovery of left ventricular function occurred 8 days after the initial onset of symptoms. A diagnosis of Takotsubo syndrome was made on the basis of consistent clinical and laboratory findings, typical echocardiography and angiography findings, and reversible course. This case emphasises the importance of being aware of uncommon causes of cardiac dysfunction in stressful situations, especially during induction of general anaesthesia.

Transient left ventricular apical ballooning syndrome, known as the japanese name of tako-tsubo was recently described and is characterised at the acute period by a large apical dyskinesia of the left ventricule apex. This syndrome usually mimics an acute coronary syndrome, sometime a cardiac failure or arrhythmias. We report a typical case of a seventy-seven years old women struck by a tako-tsubo syndrome revealed by an acute chest pain after an emotional stress. The diagnosis was proposed because angiography didn't shown any abnormality in spite of a large left ventricular dysfunction at the ventriculography. Actuality and strong points: Tako-tsubo syndrome is more and more published due to a better knowledge of this syndrome, specially in the acute coronary syndrome without coronary abnormality. His physiopathology is not well known but is clearly in relation with an acute stress. Several hypothesis are discussed, helped by some experimental animal model. With an excellent prognosis at a middle-course, his discovery allow an adapted take care especially of the complications.

The setting up of clinic and electrocardiographic reliable and well-tried criteria will allowed an early diagnosis to avoid harmful treatment. His specific treatment is not reached by consensus but will develop by a better knowledge of the physiopathology.