Table 2.

Summary of biomarkers of cardiac dysfunction following stroke in patients

	Subarachnoid hemorrhage (SAH)	Ischemic stroke (IS)	Comments
Creatine kinase-MB (CK-MB)	CK-MB level is associated with poor outcome¹⁸¹	CK-MB elevation after stroke may not be of cardiac origin³¹ Modest and progressive increase in expression Elevated for a few days	CK-MB is not completely cardiac specific and may increase in skeletal muscle injury, kidney failure, intramuscular injection, strenuous exercise, and after exposure to several toxins and drugs³¹
Cardiac Troponins (cTn) (cTn T and cTn I)	cTnI level peaks within 24 to 36 hours after SAH³⁷ High cTnT levels correlated with LV hypokinesia¹⁸² Elevated cTnI levels is associated with increased risk of LVDD, in-hospital morbidity and mortality^{45, 178, 183} May indicate delayed cerebral ischemia from vasospasm	Elevated cTn’s are observed in 5–8% of IS patients^{39, 40} Circulating cTn I level is an independent predictor of stroke prognosis³⁹ Serum cTn T expression helps to evaluate myocardial injury and estimate ischemic lesion volume, is closely associated with the risk of death in patients with acute IS, and severe neurological deficits at stroke onset and damage to the insular cortex⁴¹ May indicate coincidence of acute coronary syndrome or coronary artery disease⁴³	cTn T is a specific and sensitive biomarker for cardiac damage The American Stroke Association recommends a routine examination of cardiac Troponin in patients with acute stroke
C-Reactive Protein (CRP)	Elevated CRP level is an independent predictor of future stroke and transient ischemic attack¹⁸⁴ Patients with an increased plasma CRP level within 72 hours of stroke onset battle high mortality due to cardiovascular complications¹⁸⁵ Stroke patients with CRP levels >1.5 mg/dL (optimum sensitivity and specificity for adverse outcome) have a worse prognosis¹⁸⁵ Patients with elevated CRP levels beyond the inflammatory acute phase and at time of hospital discharge, face a danger of subsequent cardiovascular complications, death and severe neurological deficit and disability which should be carefully factored in their follow up treatment¹⁸⁵		CRP is a plasma protein that increases in response to inflammation during the acute phase of brain injury¹⁸⁶ CRP may serve as a clinically useful risk marker for the development of unstable atherosclerotic disease, as well as a predictor of future cardiovascular morbidity and mortality¹⁸⁶
N-terminal pro-brain natriuretic peptide (NT-proBNP)	NT-proBNP increases the risk of death and delayed cerebral ischemia⁴⁰	NT-proBNP levels is increased after ischemic stroke⁴⁰ Increased NT-proBNP levels is an independent risk factor for stroke⁴⁰ Increased NT-proBNP levels is associated with unfavorable functional outcome and mortality rates after stroke⁴³ NT-proBNP is an indicator of ischemic stroke of cardioembolic cause About 10 fold increase in NT-proBNP when TTC develops after stroke¹⁵	NT-proBNP is the product of brain natriuretic peptide precursor (pro-BNP) being cleaved into BNP and is mainly found in myocardial cells NT-proBNP is synthesized and secreted by normal cardiac muscle cells, and levels can rapidly increase after myocardial injury or necrosis

Abbreviations: CK-MB: Creatine kinase-MB; CRP: C-Reactive Protein; cTn: Cardiac Troponin; IS: Ischemic stroke; LV: Left ventricular; LVDD: Left ventricular diastolic dysfunction; NT-proBNP: N-terminal pro-brain natriuretic peptide; SAH: Subarachnoid hemorrhage; TTC: Takotsubo cardiomyopathy.