Yoshihiro J. Akashi

Takotsubo Cardiomyopathy A New Form of Acute, Reversible Heart Failure

Several relatively recent case reports and series have described a condition featuring symptoms and signs of acute myocardial infarction without demonstrable coronary artery stenosis or spasm in which the heart takes on the appearance of a Japanese octopus fishing pot called a takotsubo (Figure 1). In takotsubo cardiomyopathy (also called transient apical ballooning and stress cardiomyopathy), left ventricular dysfunction, which can be remarkably depressed, recovers within a few weeks.1–4 Figure 1 Left ventriculogram (A, end-diastolic phase; B, end-systolic phase) in the right anterior oblique projection. The extensive area around the apex shows akinesis, and the basal segments display hypercontraction, especially in the end-diastolic phase. C, ... Takotsubo cardiomyopathy occurs predominantly in post-menopausal women soon after exposure to sudden, unexpected emotional or physical stress. For instance, the incidence of takotsubo cardiomyopathy increased substantially in elderly women living near the epicenter of the Niigata earthquake.4 Although the left ventricular dysfunction is transient and there is no evidence of obstructive epicardial coronary disease, an increasing number of angioplasty procedures have been performed for presumed acute coronary syndromes. Concepts about the demographics, clinical features, prognosis, and management of this reversible form of left ventricular failure are still evolving. In this brief review, we summarize recent clinical reports and discuss an animal model that may clarify the pathogenesis of this condition.

Current state of knowledge on Takotsubo syndrome: a Position Statement from the Taskforce on Takotsubo Syndrome of the Heart Failure Association of the European Society of Cardiology

Takotsubo syndrome is an acute reversible heart failure syndrome that is increasingly recognized in modern cardiology practice. This Position Statement from the European Society of Cardiology Heart Failure Association provides a comprehensive review of the various clinical and pathophysiological facets of Takotsubo syndrome, including nomenclature, definition, and diagnosis, primary and secondary clinical subtypes, anatomical variants, triggers, epidemiology, pathophysiology, clinical presentation, complications, prognosis, clinical investigations, and treatment approaches. Novel structured approaches to diagnosis, risk stratification, and management are presented, with new algorithms to aid decision‐making by practising clinicians. These also cover more complex areas (e.g. uncertain diagnosis and delayed presentation) and the management of complex cases with ongoing symptoms after recovery, recurrent episodes, or spontaneous presentation. The unmet needs and future directions for research in this syndrome are also discussed.

Mechanisms of stress (Takotsubo) cardiomyopathy

Stress cardiomyopathy, also referred to as Takotsubo cardiomyopathy, transient apical ballooning or broken heart syndrome, is a disorder associated with transient left ventricular dysfunction. Symptoms include acute chest pain and dyspnea accompanied by electrocardiographic changes, such as ST-segment elevation and T-wave inversions, minimal elevation of cardiac enzyme levels and transient wall-motion abnormalities in the absence of substantial coronary artery obstruction. Complete recovery of contractile function has been documented in nearly all cases, but the mechanisms of disease remain unclear and the cause has not been established. Coronary artery vasospasm, microcirculation dysfunction, and transient obstruction of the left ventricular outflow tract have been proposed as possible causes of this disorder. An excessive release of catecholamines also seems to have a pivotal role in the development of stress cardiomyopathy. This Review summarizes published data on stress cardiomyopathy, focusing primarily on the most likely causes of this cardiac entity.

Left Ventricular Rupture Associated With Takotsubo Cardiomyopathy

A 70-year-old woman was admitted to the hospital with chest discomfort after quarreling with her neighbors. Electrocardiography revealed ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6. Coronary angiography demonstrated normal arteries, but left ventriculography showed apical akinesis and basal hyperkinesis. Takotsubo cardiomyopathy was diagnosed on the basis of these characteristic findings. The creatine kinase and creatine kinase-MB concentrations were elevated at admission and reached maximum levels 6 hours after admission. The plasma level of brain natriuretic peptide was 10.7 pg/mL (reference range, <18.4 pg/mL) on the first hospital day. ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6 persisted at 72 hours after admission. On the third hospital day, sudden rupture of the left ventricle occurred, and despite extensive resuscitation efforts, the patient died. Takotsubo cardiomyopathy presents in a manner similar to that of acute myocardial infarction, but ventricular systolic function usually returns to normal within a few weeks. To our knowledge, this is the first reported case of fatal left ventricular rupture associated with takotsubo cardiomyopathy. We suggest that takotsubo cardiomyopathy may be a newly recognized cause of sudden cardiac death.

Epidemiology and pathophysiology of Takotsubo syndrome

Takotsubo syndrome is an acute cardiac syndrome first described in 1990 and characterized by transient left ventricular dysfunction affecting more than one coronary artery territory, often in a circumferential apical, mid-ventricular, or basal distribution. Several pathophysiological explanations have been proposed for this syndrome and its intriguing appearance, and awareness is growing that these explanations might not be mutually exclusive. The reversible apical myocardial dysfunction observed might result from more than one pathophysiological phenomenon. The pathophysiology of Takotsubo syndrome is complex and integrates neuroendocrine physiology, potentially involving the cognitive centres of the brain, and including the hypothalamic–pituitary–adrenal axis. Cardiovascular responses are caused by the sudden sympathetic activation and surge in concentrations of circulating catecholamines. The multiple morphological changes seen in the myocardium match those seen after catecholamine-induced cardiotoxicity. The acute prognosis and recurrence rate are now known to be worse than initially thought, and much still needs to be learned about the epidemiology and the underlying pathophysiology of this fascinating condition in order to improve diagnostic and treatment pathways.

Reversible ventricular dysfunction takotsubo cardiomyopathy

Recently, many cardiologists have recognized the existence of a rapidly reversible form of heart failure of unknown origin characterized by a takotsubo‐shaped, dyskinetic left ventricle on left ventriculography.

Takotsubo cardiomyopathy — The current state of knowledge

Takotsubo cardiomyopathy is defined as acute chest pain during stressful incidents which is associated with ST-segment abnormalities and/or increased serum troponin levels. There is also regressive systolic dysfunction which is usually localized in the apical and medial left ventricles but there are no significant coronary artery lesions. The ventricular asynergy is also described in the right ventricle but is less common. Almost all the patients are women. The onset of this disease is typically triggered by an acute emotional or stress event or by an accumulation of trivial and repetitive stresses. The etiology of this syndrome remains unclear. Myocardial ischemia and reperfusion due to microvascular spasm, aborted myocardial infarction and related no-reflow phenomenon have been proposed as inducers of Takotsubo cardiomyopathy. The temporal relationship between the stressful event and the triggering of the clinical syndrome as well as the report of elevated catecholamine plasma levels during the acute phase suggest a possible involvement of the sympathetic nervous system. A smaller left ventricular size and hormonal disturbances in women may also play a role.

Prognosis and therapy approaches of cardiac cachexia

Purpose of review This review focuses on the prognostic implications and therapeutic approaches in cardiac cachexia – a syndrome that has been recognized for a long time, although it has only received increased attention lately. Recent findings Cardiac cachexia is a common and serious complication of chronic heart failure and associated with very poor prognosis, yet is often recognized by the clinicians only at late stage. Approximately 15% of heart failure patients will develop cardiac cachexia, defined by a 6% non-edematous, non-voluntary weight loss over a period of 6 months. Several studies have demonstrated that cardiac cachexia is a multi-factorial disease, which involves increased neurohormonal activity and immune abnormalities, resulting in hormonal and metabolic catabolic/anabolic imbalance of the body, leading to the loss of fat and lean mass and ultimately death. So far, there are no standardized therapies available for this disease. Summary Cardiac cachexia in heart failure patients is under-recognized and there is currently no causal therapy available. Several interesting treatment options exist, however, which have emerged recently, including appetite stimulants, hormones and ‘classical’ drugs, such as beta-blockers and ACE inhibitors.

Cachexia in chronic heart failure: Prognostic implications and novel therapeutic approaches

Cachexia in patients with chronic heart failure (CHF) has been recognized for a long time; however, it has not received much attention until recently. Cardiac cachexia, a common and serious complication of CHF, is associated with very poor prognosis. Several studies have demonstrated that increased neurohormonal and immune abnormalities may play a crucial role in the pathophysiology of cardiac cachexia. Hormonal and catabolic/anabolic imbalances of the body are likely to be responsible for the development of cachexia in CHF. Recently, ghrelin, a novel growth hormone-releasing peptide, has been widely noticed to have potential in the treatment of severe CHF and cardiac cachexia. However, further research will be necessary to identify the exact pathways involved and to find the best therapeutic strategies of using ghrelin to fight the wasting process.

Reversible left ventricular dysfunction “takotsubo” cardiomyopathy associated with pneumothorax

An 83 year old woman presented to the emergency department with chest pain and dyspnoea. Chest radiography showed pneumothorax of the left lung. Arteries were normal on coronary angiography. Left ventriculography showed asynergy of apical akinesis and basal hyperkinesis. Within 18 days, the asynergy improved without any specific treatment. In the present case the left ventricular dysfunction may have been induced by altered catecholamine dynamics as a result of pneumothorax.