Stroke–Heart Syndrome: Recent Advances and Challenges

Abstract

After ischemic stroke, there is a significant burden of cardiovascular complications, both in the acute and chronic phase. Severe adverse cardiac events occur in 10% to 20% of patients within the first few days after stroke and comprise a continuum of cardiac changes ranging from acute myocardial injury and coronary syndromes to heart failure or arrhythmia. Recently, the term stroke–heart syndrome was introduced to provide an integrated conceptual framework that summarizes neurocardiogenic mechanisms that lead to these cardiac events after stroke. New findings from experimental and clinical studies have further refined our understanding of the clinical manifestations, pathophysiology, and potential long‐term consequences of the stroke–heart syndrome. Local cerebral and systemic mediators, which mainly involve autonomic dysfunction and increased inflammation, may lead to altered cardiomyocyte metabolism, dysregulation of (tissue‐resident) leukocyte populations, and (micro‐) vascular changes. However, at the individual patient level, it remains challenging to differentiate between comorbid cardiovascular conditions and stroke‐induced heart injury. Therefore, further research activities led by joint teams of basic and clinical researchers with backgrounds in both cardiology and neurology are needed to identify the most relevant therapeutic targets that can be tested in clinical trials.

14-day Holter monitoring for atrial fibrillation after ischemic stroke: The yield of guideline-recommended monitoring duration

“…Although data suggesting this association is limited, time to Holter initiation is likely related to the probability of AF detection after stroke. 2 , 43 – 45 Research on the Stroke-Heart Syndrome (SHS) has indicated that post-stroke major adverse cardiovascular events and AF peak in the first 3–30 days after stroke onset. 45 Our data showed no significant difference in time to Holter between patients with and without detected AF as reported in previous work.…”

“… 2 , 43 – 45 Research on the Stroke-Heart Syndrome (SHS) has indicated that post-stroke major adverse cardiovascular events and AF peak in the first 3–30 days after stroke onset. 45 Our data showed no significant difference in time to Holter between patients with and without detected AF as reported in previous work. 28 , 46 However, with median time to Holter of 35 days in our sample, we largely included patients outside the peak window for potential SHS cases.…”

“…incomplete data on MRI for stroke location particularly insular cortex, echocardiography for presence of patent foramen ovale, or biomarkers such as cardiac troponin) impaired our ability to assess the significance of risk factors and biomarkers associated with post-stroke AF detection. 34 , 45 , 57 By still presenting baseline data stratified by AF detection during Holter monitoring, we aimed to contribute to potential future work on personalized monitoring approaches. 2 While adherence to our 14-day study design was high among included patients, recent evidence points to the superiority implantable devices in detecting silent AF, which is reflected in the current ESO guideline’s recommendations.…”

Cardiac dysfunction in patients affected by subarachnoid haemorrhage affects in-hospital mortality

“…A proposed mechanism behind them is a sympathetically mediated myocardial cell calcium overload and a subsequent catecholamineinduced contraction band necrosis. 6,7 Sugimoto et al 41 evaluated plasma catecholamine levels and found greater norepinephrine levels in the group with RWMAs as compared with those without (2.098 AE 1.773 vs. 963 AE 839 pg ml À1 , respectively); conversely, the same authors found no differences in the plasma levels of epinephrine. Interestingly, norepinephrine levels were inversely correlated with LVEF.…”

“…Cardiovascular function and mental stress are closely linked, and the so-called ‘stroke–heart syndrome’ refers to a wide spectrum of cardiac dysfunction related to all the acute brain injuries, including SAH 4–7 . Independent predictors of SAH-related neurogenic stress cardiomyopathy may include the severity of neurological injury, elevated cardiac enzymes or brain natriuretic peptide elevation, and female gender 4,8,9 .…”