Prevalence, associated factors and management implications of left ventricular outflow tract obstruction in Takotsubo cardiomyopathy: a two-year, two-center experience

Background: Some patients with Takotsubo cardiomyopathy (TTC) develop cardiogenic shock due to left ventricular outflow tract (LVOT) obstruction -there is, however, a paucity of data regarding this condition. Methods: Prevalence, associated factors and management implications of LVOT obstruction in TTC was explored, based on two-year data from two Belgian heart centres. Results: A total of 32 patients with TTC were identified out of 3,272 patients presenting with troponin-positive acute coronary syndrome. In six patients diagnosed with TTC (19%), a significant LVOT obstruction was detected by transthoracic echocardiography. Patients with LVOT obstruction were older and had more often septal bulging, and presented more frequently in cardiogenic shock as compared to those without LVOT obstruction (P < 0.05). Moreover, all patients with LVOT obstruction showed systolic anterior motion (SAM) of the anterior mitral valve leaflet, which was associated with a higher grade of mitral regurgitation (2.2 +/- 0.7 vs. 1.0 +/- 0.6, P< 0.001). Adequate therapeutic management including fluid resuscitation, cessation of inotropic therapy, intravenous beta-blocker, and the use of intra-aortic balloon pump resulted in non-inferior survival in TTC patients with LVOT obstruction as compared to those without LVOT obstruction. Conclusions: TTC is complicated by LVOT obstruction in approximately 20% of cases. Older age, septal bulging, SAM-induced mitral regurgitation and hemodynamic instability are associated with this condition. Timely and accurate diagnosis of LVOT obstruction by echocardiography is key to successful management of these TTC patients with LVOT obstruction and results in a non-inferior outcome as compared to those patients without LVOT obstruction

Pathophysiological Mechanisms of Takotsubo Cardiomyopathy - a Systematic Review

Takotsubo cardiomyopathy, also referred to as stress-induced cardiomyopathy, is an acute condition associated with transient left ventricular dysfunction. Since it can be induced by increased emotional stress (such as losing a loved oneor constant anxiety) it is also called the broken heart syndrome. This type of cardiomyopathy occurs in all age groups and both sexes, but it is most common in postmenopausal women. There are several clinical manifestations such as chest pain, sometimes with heart failure, and often with ST-segment changes that may present as acute coronary syndrome. It is characterized by absence of coronary artery obstruction, with transient regional wall motion abnormalities and minimal elevation of cardiac enzyme levels. Although wall motion abnormalities are reversible in almost all cases, and long-term prognosis is excellent, this condition is important because in the acute phase it may cause sudden cardiac death. Mechanisms and cause of this disease still remain unclear. Some possible causes of the disorder include: 1) coronary artery vasospasm, 2) microcirculatory dysfunction, 3) transient obstruction of the left ventricular outflow tract, and 4) excessive release of catecholamine, which seems to have the most important role. The aim of this review is to summarize the most important pathophysiological mechanisms that may be responsible for the development of this type of cardiomyopathy

Neurocardiogenic injury in subarachnoid hemorrhage: A wide spectrum of catecholamin-mediated brain-heart interactions

Background: The purpose of this review was to summarize the up-to-date knowledge on clinical presentation and management of neurocardiogenic injury and to deliver the evidence of common pathophysiology of this broad spectrum of disorders.Methods: Medline and EmBase databases were searched to obtain original research articles and review papers using the following key words: neurocardiogenic injury, stress cardiomyopathy,tako-tsubo, subarachnoid hemorrhage, ECG abnormalities, catecholamine toxicity, neuropulmonary edema.Results: Various forms of cerebral pathology, most importantly subarachnoid hemorrhage (SAH), are accompanied by transient cardiac dysfunction with ST-segment elevation and QT interval prolongation and T wave inversion with simultaneous release of cardiac troponin. In the past 20 years a great deal of data emerged concerning stress cardiomyopathy (‘tako-tsubo’) presenting as a rare transient apical ballooning syndrome following stressful life events with symptoms and signs resembling acute myocardial infarction (AMI), yet without significant coronary artery stenosis. Both forms of cardiac dysfunction are mediated by catecholamine toxicity, triggered by physical and psychological distress, leading to a specific type of neurogenic myocardial stunning reflected by histopathological image of contraction band necrosis.Conclusions: Neurocardiogenic injury should be carefully differentiated from AMI. Cardiac dysfunction in SAH heralds increased mortality. The criteria for the diagnosis of stress cardiomyopathy should be revised to comprise the diversity of its clinical symptomatology and to include cardiac dysfunction accompanying cerebral pathology.

Takotsubo cardiomyopathy and neurogenic stunned myocardium: similar albeit different

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Indications of beta-adrenoceptor blockers in Takotsubo syndrome and theoretical reasons to prefer agents with vasodilating activity

Takotsubo syndrome (TTS) is estimated to account for 1–3% of all patients presenting with suspected ST-segment elevation myocardial infarction. A sudden surge in sympathetic nervous system is considered the cause of TTS. Nonetheless, no specific recommendations have been provided regarding β-blocking therapy. Apart from specific contra-indications (severe LV dysfunction, hypotension, bradycardia and corrected QT interval &gt;500 ms), treatment with a β-blocker seems reasonable until full recovery of LV ejection fraction, though evidence is limited to a few animal studies, case reports or observational studies. In this review, we will reappraise the rationale for β-blocker therapy in TTS and speculate on the pathophysiologic basis for preferring non-selective agents with vasodilating activity over β1-selective drugs

Mechanisms of Myocardial Stunning in Stress-Induced Cardiomyopathy

Stress-induced cardiomyopathy, in contrast to acute myocardial infarction, is a type of acute heart failure characterized by reversible left ventricular dysfunction. Cardiac imaging primarily reveals left ventricle myocardial stunning, 81.7% of which is apical type. Emotional or psychological stress usually precedes the onset of stress-induced cardiomyopathy, which is increasingly being recognized as a unique neurogenic myocardial stunning disease. To distinguish between acute myocardial infarction and acute viral or auto-immune myocarditis, this review summarizes specific mechanisms of myocardial stunning in stress-induced cardiomyopathy, such as calcium disorders, metabolic alterations, anatomical and histological variations in different parts of the left ventricle, and microvascular dysfunction