Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.
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Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) has primarily been described in Japan and is characterized by transient left ventricular apical ballooning in the absence of coronary artery disease, associated with chest symptoms, electrocardiographic changes and minimal cardiac enzymes release. Aim of the present review is to summarize the current knowledge about TTP. TTP has been described predominantly in females. TTP occurs also outside Japan. Clinical symptoms comprise anginal chest pain, dyspnea and syncope. TTP occurs frequently after acute emotional or physical stress. Electrocardiographic ST- elevations may be present only for several hours. Then, normalization of the ST-segment occurs, followed by negative T waves, which persist for months. Arterial hypertension in TTP is found in up to 76%, hyperlipidaemia in up to 57%, diabetes mellitus in up to 12% and smoking in up to 18% of the patients. Several pathomechanisms have been proposed: myocardial stunning due to increased catecholamine levels, coronary vasospasm, atherosclerotic plaques rupture, myocarditis, catecholamine-induced hyperkinesis of the basal left ventricular segments and genetic. Patients with TTP should be monitored like patients with myocardial infarction. Care should be taken in the application of catecholamines and nitrates. Betablockers should be given in the acute and chronic phase, and possibly indefinitely to prevent recurrences. The prognosis of TTP is assumed to be good, but in the acute phase there are deaths due to multisystem organ failure, cardiogenic shock, ventricular fibrillation and ventricular rupture. The long term prognosis of TTP patients is largely unknown. (+info)
An unusual presentation of "tako-tsubo cardiomyopathy".
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We report a case of tako-tsubo cardiomyopathy, complicated by left ventricular apical thrombus. (+info)
Subaortic dynamic obstruction: a contributing factor to haemodynamic instability in tako-tsubo syndrome?
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We present a case of transient apical ballooning with haemodynamic instability in a female patient with normal coronaries and a history of poorly controlled systemic arterial hypertension. There was dynamic obstruction of the outflow tract and moderate secondary mitral regurgitation at presentation. These were due to systolic anterior motion of the mitral valve, which normalised gradually with the recovery of left ventricular function, and to a 'sigmoid' septum. Mid-cavity obstruction is potentially an important contributory factor to the haemodynamic instability sometimes encountered in this syndrome. (+info)
Apical ballooning syndrome complicated by acute severe mitral regurgitation with left ventricular outflow obstruction--case report.
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BACKGROUND: Apical ballooning syndrome (or Takotsubo cardiomyopathy) is a syndrome of transient left ventricular apical ballooning. Although first described in Japanese patients, it is now well reported in the Caucasian population. The syndrome mimicks an acute myocardial infarction but is characterised by the absence of obstructive coronary disease. We describe a serious and poorly understood complication of Takotsubo cardiomyopathy. CASE PRESENTATION: We present the case of a 65 year-old lady referred to us from a rural hospital where she was treated with thrombolytic therapy for a presumed acute anterior myocardial infarction. Four hours after thrombolysis she developed acute pulmonary oedema and a new systolic murmur. It was presumed she had acute mitral regurgitation secondary to a ruptured papillary muscle, ischaemic dysfunction or an acute ventricular septal defect. Echocardiogram revealed severe mitral regurgitation, left ventricular apical ballooning, and systolic anterior motion of the mitral valve with significant left ventricular outflow tract gradient (60-70 mmHg). Coronary angiography revealed no obstructive coronary lesions.She had an intra-aortic balloon pump inserted with no improvement in her parlous haemodynamic state. We elected to replace her mitral valve to correct the outflow tract gradient and mitral regurgitation. Intra-operatively the mitral valve was mildly myxomatous but there were no structural abnormalities. She had a mechanical mitral valve replacement with a 29 mm St Jude valve. Post-operatively, her left ventricular outflow obstruction resolved and ventricular function returned to normal over the subsequent 10 days. She recovered well. CONCLUSION: This case represents a serious and poorly understood association of Takotsubo cardiomyopathy with acute pulmonary oedema, severe mitral regurgitation and systolic anterior motion of the mitral valve with significant left ventricular outflow tract obstruction. The sequence of our patient's presentation suggests that the apical ballooning caused geometric alterations in her left ventricle that in turn led to acute and severe mitral regurgitation, systolic anterior motion of the mitral valve and left ventricular outflow tract obstruction. The left ventricular outflow tract obstruction and mitral regurgitation were corrected by mechanical mitral valve replacement. We describe a variant of Takotsubo cardiomyopathy with acute mitral regurgitation, systolic anterior motion of the mitral valve leaflet and left ventricular outflow tract obstruction of a dynamic nature. (+info)
Assessment of coronary flow reserve by transthoracic Doppler echocardiography in left apical ballooning syndrome.
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We present the time course of transthoracic coronary flow reserve in the left anterior descending artery in a patient who suffered a transient left apical ballooning syndrome. (+info)
Tako-Tsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery.
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AIMS: To gain more insight into the phenomenon of Tako-Tsubo cardiomyopathy (TTC), the purpose of the present study was to investigate the myocardial structure in the acute phase of TTC and after functional recovery. METHODS AND RESULTS: We studied eight patients presenting with TTC diagnosed by coronary angiography, ventriculography, magnetic resonance imaging, and echocardiography. Serial myocardial biopsies were taken during the phase of severely impaired left ventricular function and after functional recovery. Specimens were examined by light and electron microscope as well as immunohistochemistry. Additionally, specific methods detecting different types of cell death and measurements of virus titer were performed. All patients showed the typical contractile pattern of TTC and complete functional recovery within 12 +/- 3 days. In 'acute' biopsies, many vacuoles of different size were found contributing to cellular hypertrophy. PAS staining revealed intracellular accumulation of glycogen. Additionally, structural deteriorations characterized by disorganization of contractile and cytoskeletal proteins could be detected. The extracellular matrix proteins were increased. Signs of oncotic and apoptotic cell death were absent. After functional recovery, all described alterations showed a nearly complete reversibility. CONCLUSION: TTC is accompanied by severe morphological alterations potentially resulting from catecholamine excess followed by microcirculatory dysfunction and direct cardiotoxicity. However, the affected myocardium represents a high potential of structural reconstitution which correlates with the rapid functional recovery. (+info)
The role of cardiovascular magnetic resonance in patients presenting with chest pain, raised troponin, and unobstructed coronary arteries.
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AIMS: Troponin measurement is used in the assessment and risk stratification of patients presenting acutely with chest pain when the main cause of elevation is coronary artery disease. However, some patients have no coronary obstruction on angiography, leading to diagnostic uncertainty. We evaluated the incremental diagnostic value of cardiovascular magnetic resonance (CMR) in these patients. METHODS AND RESULTS: Sixty consecutive patients (mean age 44 years, 72% male) with a troponin-positive episode of chest pain and unobstructed coronary arteries were recruited within 3 months of initial presentation. All patients underwent CMR with cine imaging, T2-weighted imaging for detection of inflammation, and late gadolinium enhancement imaging for detection of infarction/fibrosis. An identifiable basis for troponin elevation was established in 65% of patients. The commonest underlying cause was myocarditis (50%), followed by myocardial infarction (11.6%) and cardiomyopathy (3.4%). In the 35% of patients where no clear diagnosis was identified by CMR, significant myocardial infarction/fibrosis was excluded. CONCLUSION: CMR is a valuable adjunct to conventional investigations in a diagnostically challenging and important group of patients with troponin-positive chest pain and unobstructed coronary arteries. (+info)
Left ventricular apical rupture caused by takotsubo cardiomyopathy--comprehensive pathological heart investigation.
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An 81-year-old woman with emotionally-induced takotsubo cardiomyopathy developed a fatal left ventricular (LV) apical rupture. During the hospitalization persistent ST-segment elevation with no electrocardiographic time evolution was observed on the ECG, characteristic for takotsubo cardiomyopathy. Histopathologically, transmural myocardial necrosis with hemorrhage was found at the rupture site, but there were foci of coagulation and contraction band necrosis with mononuclear lymphocyte infiltrations in other heart regions, and the intensity and distribution of these pathological changes corresponded to the distribution of the LV contraction abnormalities seen on ventriculography. The article concludes that: the LV functional disorder in takotsubo cardiomyopathy may be caused by distracted foci of coagulation and contraction band necrosis in the myocardium; contraction band necrosis (a sign of catecholamine cardiotoxicity) may reflect the sympathetic hyperactivity in this disease; persistent myocardial damage expressed by persistent ST-segment elevation without an electrocardiographic time evolution should be carefully observed with sequential echocardiographic examinations because of the possibility of cardiac rupture. (+info)