Broken Heart Syndrome: Evolving Molecular Mechanisms and Principles of Management

Abstract

Broken Heart Syndrome, also known as Takotsubo Syndrome (TS), is sudden and transient dysfunction of the left and/or right ventricle which often mimics Acute Coronary Syndrome (ACS). Japan was the first country to describe this syndrome in the 1990s, and since then it has received a lot of attention from researchers all around the world. Although TS was once thought to be a harmless condition, recent evidence suggests that it may be linked to serious complications and mortality on par with Acute Coronary Syndrome (ACS). The understanding of TS has evolved over the past few years. However, its exact etiology is still poorly understood. It can be classified into two main types: Primary and Secondary TS. Primary TS occurs when the symptoms of myocardial damage, which is typically preceded by emotional stress, are the reason for hospitalization. Secondary TS is seen in patients hospitalized for some other medical, surgical, obstetric, anesthetic, or psychiatric conditions, and the dysfunction develops as a secondary complication due to the activation of the sympathetic nervous system and the release of catecholamines. The etiopathogenesis is now proposed to include adrenergic hormones/stress, decreased estrogen levels, altered microcirculation, endothelial dysfunction, altered inflammatory response via cardiac macrophages, and disturbances in the brain-heart axis. The role of genetics in disease progression is becoming the focus of several upcoming studies. This review focuses on potential pathophysiological mechanisms for reversible myocardial dysfunction observed in TS, and comprehensively describes its epidemiology, clinical presentation, novel diagnostic biomarkers, and evolving principles of management. We advocate for more research into molecular mechanisms and promote the application of current evidence for precise individualized treatment.

Stroke Related Brain–Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms

“…[49,[70][71][72] The incidence of significant cardiac arrhythmias surges within the first day of care for 501 acute neurovascular patients. [35,73,74] Autonomic dysfunction, [30,75] myocardial infarction, [59,76] cardiac arrhythmias, [77] takotsubo syndrome (TTS) [15,78] and higher BPV, [79][80][81] are prevalent clinical features signifying dysregulation of brain-heart axis. Heart rate variability analysis using continuous ECG signals has shown promise in predicting outcomes in patients with acute stroke.…”

Review on the neuron damage parameters in patients with end-stage renal disease

“…GFAP has also been found to be expressed in glomeruli and peritubular fibroblasts taken from kidneys [57]. GFAP is thought to help to maintain astrocyte mechanical strength [58] as well as the shape of cells, but its exact function remains poorly understood, despite the number of studies using it as a cell marker [59]. The initial GFAP dimers combine to make staggered tetramers, which are the basic subunits of an intermediate filament.…”

Effects of pharmacological interventions on mortality in patients with Takotsubo syndrome: a report from the SWEDEHEART registry

“…1,7 However, pharmacological therapeutic approaches, such as betablockers, antiplatelets, statins, and angiotensin-converting enzyme inhibitors (ACE-Is), are frequently used. 8,9 Medical professionals may assume that treatments used for other conditions, such as MI and acute heart failure, will yield similar outcomes in TS. 10 However, the efficacy and safety of pharmacological treatments such as inotropes, beta-blockers, antiplatelets, statins, and ACE-Is in TS remain unclear.…”

“…Due to the transient nature of the disorder, it will be prudent to concentrate on supportive treatment 1,7 . However, pharmacological therapeutic approaches, such as beta‐blockers, antiplatelets, statins, and angiotensin‐converting enzyme inhibitors (ACE‐Is), are frequently used 8,9 . Medical professionals may assume that treatments used for other conditions, such as MI and acute heart failure, will yield similar outcomes in TS 10 .…”