The Heart Is at Risk: Understanding Stroke-Heart-Brain Interactions with Focus on Neurogenic Stress Cardiomyopathy—A Review

Abstract

In recent years, it has been convincingly demonstrated that acute brain injury may cause severe cardiac complications-such as neurogenic stress cardiomyopathy (NSC), a specific form of takotsubo cardiomyopathy. The pathophysiology of these brain-heart interactions is complex and involves sympathetic hyperactivity, activation of the hypothalamic-pituitary-adrenal axis, as well as immune and inflammatory pathways. There have been great strides in our understanding of the axis from the brain to the heart in patients with isolated acute brain injury and more specifically in patients with stroke. On the other hand, in patients with NSC, research has mainly focused on hemodynamic dysfunction due to arrhythmias, regional wall motion abnormality, or left ventricular hypokinesia that leads to impaired cerebral perfusion pressure. Comparatively little is known about the underlying secondary and delayed cerebral complications. The aim of the present review is to describe the stroke-heart-brain axis and highlight the main pathophysiological mechanisms leading to secondary and delayed cerebral injury in patients with concurrent hemorrhagic or ischemic stroke and NSC as well as to identify further areas of research that could potentially improve outcomes in this specific patient population.

Stroke-heart syndrome: A case report and mini literature review

“…Both regions regulate the central autonomic function and play an integral role in the pathophysiology of the "stroke-heart syndrome." 2,6 In the case of our patient and based on the absence of clinical symptoms, ECG-changes, and wall motion abnormalities, we estimate that cTn-elevation was due to a stroke-induced neurocardiogenic non-ischemic myocardial injury caused either by microcirculatory dysfunction (i.e. endothelial or oxidative stress) or by myocardial demand ischemia precipitated by hypertensive crisis, tachycardia, and respiratory distress.…”

“…Indeed, it is convincingly recognized that AIS may cause severe cardiac dysfunction, which refers to neurocardiogenic interactions in this population 2 and represents more complex pathophysiological mechanisms than traditional vascular risk factors. 6 Cardiac injury is a common medical problem during the acute phase of AIS 9 and includes a variety of clinical manifestations, that is, post-stroke acute coronary syndromes (ACS; type 1 and 2 myocardial infarction, MI), acute myocardial injury-ischemic and non-ischemic-as presented by cTn-elevation, left ventricular dysfunction of varying severity up to heart failure, and stroke-associated Takotsubo Syndrome, 2 ECG-alterations such as QT-interval prolongation, T-wave inversion, and ST-depression, tachyarrhythmias including atrial fibrillation, 2 and sudden cardiac death. 6 In order to early detect the cardioembolic origin of stroke and to identify patients at high risk of cardiac complications and poor outcomes, quantitative cTn-determination in all patients with suspected stroke is strongly recommended.…”

“…15,25,26 In addition, an excess of catecholamines, particularly epinephrine, may be characterized by a negative inotropic effect as they mediate the switching of β-2 adrenergic receptors from the physiological G-protein-activated cardiostimulant to inhibitory G-proteinactivated cardiodepressant pathways. 2,27 Therefore, targeting local cardiac catecholamine using β-blockers during an ischemic event's acute phase seems conclusive and should be further examined in well-designed randomized and blinded therapy studies. 6 Besides sympathetic overdrive, pro-inflammatory cascades are well-recognized contributors to the stroke-heart syndrome.…”

“…6 Besides sympathetic overdrive, pro-inflammatory cascades are well-recognized contributors to the stroke-heart syndrome. 2 The inflammatory response occurs immediately after the onset of stroke and represents a pathophysiological cornerstone of stroke progression. 28 Even though pro-inflammatory and procoagulative mediators are released within minutes after the ischemic event, their plasma elevation is only temporary.…”

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

“…[20,21,37,189] Arrhythmias, when coupled with acute hemo-dynamic dysfunction, compromise cerebral perfusion pressure, correlating with elevated post-stroke mortality. [1,126] In a retrospective cross-sectional study from Wira et al, AIS patients admitted from an urban emergency department were assessed within 24 h of symptom onset. Results indicated that troponin elevation, systolic dysfunction, AF, and ischemic changes on ECG may be linked to increased in-hospital mortality rates, highlighting the importance of monitoring cardiac complications in AIS presentation.…”