Hemodynamics of cardiogenic shock in a Broken Heart Syndrome patient: paradoxical effect of ionotropic agents in apical ballooning
07 Mar 2011-Interventional Cardiology (Future Medicine Ltd London, UK)-Vol. 3, Iss: 1, pp 45-48
TL;DR: Stress-induced cardiomyopathy, also known as Broken Heart Syndrome, is an increasingly recognized syndrome characterized by transient apical or midventricular dysfunction that mimics myocardial infarction in the absence of significant coronary artery disease.
Abstract: Stress-induced cardiomyopathy, also known as Broken Heart Syndrome or Takotsubo cardiomyopathy, is an increasingly recognized syndrome characterized by transient apical or midventricular dysfunction that mimics myocardial infarction in the absence of significant coronary artery disease. This disorder is much more common in women compared with men, with a mean age of 62–75 years. Different morphologic patterns of left ventricular dysfunction have been observed, with apical ballooning and hypercontracting basal segments being the most common and are observed in 60% of patients. The exact mechanism of this disorder is not well understood. Catecholamines may play an important role in the genesis of this disorder, as illustrated by a small case series demonstrating significantly increased plasma epinephrine and norepinephrine. Patients with stress-induced cardiomyopathy also tend to be prone to coronary vasospasm, induced by excess catecholamines. Typically, ionotropic agents are avoided in apical ballooning d...
TL;DR: This is the first series of “apical ballooning” to be reported in white patients, and despite dramatic initial presentation, left ventricle function recovered completely within three weeks in the survivors.
Abstract: Background: A cardiac syndrome of “apical ballooning” was recently described, consisting of an acute onset of transient extensive akinesia of the apical and mid portions of the left ventricle, without significant stenosis on the coronary angiogram, accompanied by chest symptoms, ECG changes, and a limited release of cardiac markers disproportionate to the extent of akinesia. Until now, this syndrome has been reported only in Japanese patients. Objective: To describe 13 white patients who presented with this syndrome over the previous four years. Results: All but one of the patients were women with a mean age of 62 years. Eight of them presented with chest pain, of whom six had cardiogenic shock. In nine patients a triggering factor was identified: emotional stress in three, trauma in one, pneumonia in one, asthma crisis in one, exercise in two, and cerebrovascular accident in one. In all patients left ventriculography showed very extensive apical akinesia (“apical ballooning”) in the absence of a significant coronary artery stenosis, not corresponding with the perfusion territory of a single epicardial coronary artery. Mean maximal creatine kinase MB and troponin rise were 27.4 μg/l (range 5.2–115.7 μg/l, median 16.6 μg/l) and 18.7 μg/l (range 2.0–97.6 μg/l, median 14.5 μg/l), respectively. Six patients were treated with intra-aortic balloon counterpulsation. One patient died of multiple organ failure. On necropsy, no myocardial infarction was found. In the 12 survivors, left ventricular systolic function recovered completely within three weeks. Conclusions: This is the first series of “apical ballooning” to be reported in white patients. Despite dramatic initial presentation, left ventricle function recovered completely within three weeks in the survivors.
TL;DR: An up-to-date review of the clinical presentation of the stress-related cardiomyopathy syndromes is provided, possible causal mechanisms are discussed, and the similarities and differences between them are highlighted.
Abstract: The relationship between the heart and the brain is complex and integral in the maintenance of normal cardiovascular function. Certain pathological conditions can interfere with the normal brain-heart regulatory mechanisms and result in impaired cardiovascular function. The mechanisms through which the central and autonomic nervous systems regulate the heart and the manner in which their impairment adversely affects cardiovascular function have recently been reviewed by Samuels.1 The purpose of this article is to provide an up-to-date review of the clinical presentation of the stress-related cardiomyopathy syndromes, discuss possible causal mechanisms, and highlight the similarities and differences between them.2–16 The stress-related cardiomyopathies appear similar in that they seemingly occur during times of enhanced sympathetic tone and may be precipitated in part or entirely by excessive endogenous or exogenous catecholamine stimulation of the myocardium. Although significant clinical overlap exists in those presenting with stress-associated cardiomyopathy, it is unclear whether myocardial adrenergic hyperstimulation is the only pathophysiological mechanism responsible for these syndromes (Tables 1 and 2⇓). View this table: Table 1. Precipitants of Stress Cardiomyopathy View this table: Table 2. Morphological LV Variants of Stress Cardiomyopathy In the early 1990s, Japanese authors began reporting a unique, reversible cardiomyopathy that appeared to be precipitated by acute emotional stress.2,13,16 They found that these patients were usually postmenopausal women and often developed signs and symptoms of an acute coronary syndrome (ACS) proximate to a strong emotional stressor associated with a transient apical and midventricular wall motion abnormality despite the lack of obstructive coronary artery disease (CAD) at the time of emergent coronary angiography. This syndrome was initially given the name Takotsubo cardiomyopathy (TC) and has subsequently been referred to as the apical ballooning syndrome and broken heart syndrome. It is now recognized that TC can also occur in the setting of acute medical illness and after surgery. TC …
TL;DR: Echocardiography should be systematically performed for all patients presenting with Tako-Tsubo syndrome for the detection of LVOT obstruction, with specific characteristics as compared with patients withoutLVOT obstruction.
TL;DR: For the first time in a Tako‐tsubo patient with refractory cardiogenic shock, the use of ECLS treatment is reported in order to unload the heart, sustain circulation and end‐organ perfusion, and promote potential ventricular recovery.
Abstract: We report the use of extra-corporeal cardiopulmonary support (ECLS), in a case of complicating refractory severe cardiogenic shock, in a patient with Tako-tsubo cardiomyopathy (TC). Tako-tsubo cardiomyopathy syndrome is characterized by left ventricular (LV) wall motion abnormalities, usually without coronary artery disease, mimicking the diagnosis of acute coronary syndrome. This ventricular dysfunction is typically reversible in the acute phase, though it can progress into refractory cardiogenic shock with limited therapeutic options available. Here, we report for the first time in a Tako-tsubo patient with refractory cardiogenic shock, the use of ECLS treatment in order to unload the heart, sustain circulation and end-organ perfusion, and promote potential ventricular recovery. Extra-corporeal life support allowed inotropic drug weaning while maintaining end-organ function and supported the patient until myocardial recovery. The patient recovered completely, and a normal LV ejection fraction was documented by 2D echocardiography on day 7. From our experience, ECLS can be an appropriate treatment for severe refractory cardiogenic shock in patients with TC. Extra-corporeal life support was an effective ultimate solution.