Cardiac Troponin Elevation and Outcome in Subarachnoid Hemorrhage

Abstract

Many cardiopulmonary complications occur after aneurysmal subarachnoid hemorrhage. This is due to sympathetic nervous system activation which results in release of norepinephrine from myocardial sympathetic nerves. Cardiac troponin I is a marker for diagnosis of cardiac injury. Elevated levels of troponin in these patients are associated with worse clinical outcomes. PubMed was searched for literature using regular and Medical Subject Heading (MeSH) keywords for data collection. Papers published in English language involving human subjects within the last 20 years focusing on cardiac troponin elevation following subarachnoid hemorrhage were included. Systemic complications that occur after subarachnoid hemorrhage worsen the clinical outcome of patients and have negative effects on the mortality and morbidity of these patients. Cardiac troponin I elevation is significantly associated with the severity of the stroke, poor neurological status, longer ICU stay, and death. Cardiac troponin I should be measured in patients presented with acute stroke. Hemodynamic monitoring and appropriate supportive care can improve clinical outcomes.

Clinical study of aneurysmal subarachnoid hemorrhage complicated with neurogenic pulmonary edema

“…This can lead to a decrease in the oxygenation index and an increase in lactic acid (LAC) anaerobic metabolism, which in turn can cause an increase in BNP and hs-cTnI levels, it is important to note that these effects are not related to coronary artery disease [19,20]. In this study, it was found that BNP and hs-cTnI levels were signi cantly increased in all patients.…”

The elevation of different myocardial biomarkers on admission is associated with disease features and different outcomes in aneurysmal subarachnoid hemorrhage

“…Before performing this study, we assumed that there would be a difference in the distribution of the sites of aneurysms. This assumption comes from functional dissection of innervation of the heart 15 and the theory mentioned before that sympathetic nervous system activation causes the change of myocardial biomarkers 16 . Since cortex, subcortical forebrain, brain stem all play roles in the central reflex and sympathetic control of the heart, it's reasonable to find a difference when an aneurysm's rupture affects different parts of the brain.…”

Clinical Interpretation of Serum Troponin in the Era of High-Sensitivity Testing

“…It is thought that Tn elevations in stroke are a result of the activation of the sympathoadrenal system and increased catecholamine release, which can lead to direct myocardial toxicity, demand ischemia, LV dysfunction, arrhythmias, possible plaque instability causing MI, and neurogenic sudden cardiac death [ 177 , 186 , 187 , 188 ].…”