Cardiac Vulnerability to Cerebrogenic Stress as a Possible Cause of Troponin Elevation in Stroke

Abstract

BackgroundTroponin elevation with electrocardiography changes is not uncommon in patients with acute ischemic stroke; however, it is still unclear whether the mechanism of these changes is due to cardiac problems or neurally mediated myocytic damage. Thus, we investigated cardiac and neurological predictors of troponin elevation in those patients.Methods and ResultsWe retrospectively analyzed medical data of the prospectively registered ischemic stroke patients on stroke registry who were admitted and underwent a serum cardiac troponin I and 12‐lead electrocardiography within 24 hours of symptom onset. However, patients with well‐known troponin‐elevating comorbidities were excluded from the analysis. Among 1404 ischemic stroke patients, 121 (8.7%) had elevated troponin, which was defined as more than 0.04 mg/mL. Multivariable analysis identified electrocardiography abnormalities such as QTc‐prolongation (odds ratio [OR]: 1.52, 95% CI: 1.02–2.28), left ventricular hypertrophy (OR: 2.14, 95% CI 1.43–3.19), Q‐wave (OR: 2.53, 95% CI: 1.48–4.32), and ST elevation (OR: 2.74, 95% CI: 1.12–6.72) as cardiac variables associated with troponin elevation, and higher National Institutes of Health Stroke Scale score (OR: 1.04, 95% CI: 1.01–1.07) and insular cortical lesions (OR: 2.78, 95% CI: 1.85–4.19) as neurological variables associated with troponin elevation. Incidence of troponin elevation as well as QTc‐prolongation was increased further in combination with cardiac and neurological factors.ConclusionsCertain cardiac and neurological conditions in acute ischemic stroke may contribute to troponin elevation. The proposed concept of cardiac vulnerability to cerebrogenic stress can be a practical interpretation of troponin elevation and electrocardiography abnormalities in stroke patients.

Cardiac troponin for predicting all-cause mortality in patients with acute ischemic stroke: a meta-analysis

“…One possible explanation of troponin elevation in acute ischemic stroke patients may be the coincidence of acute coronary syndrome, triggering a rise in circulating troponin level [ 38 ]. Cardiac vulnerability to cerebrogenic stress can be an alternate explanation interpretation of troponin elevation [ 39 , 40 ]. Activation of the sympathoadrenal system may be an important contributor to myocardial damage in acute ischemic stroke patients [ 41 ].…”

Prognostic Significance of Troponin Elevation for Long-Term Mortality after Ischemic Stroke

“…Although our findings show that troponin elevation can indicate various vascular and non-vascular problems and consequently predict future vascular and non-vascular death, the clinical value of measuring troponin is still limited due to an additional diagnostic challenge to discriminate various conditions for troponin elevation [ 35 ]. Currently, we proposed a concept that synergistic effect on troponin elevation in a combination of the cardiac vulnerability (e.g., hypertrophic or damaged myocardium by ischemia, and possibly tachycardia) to cerebrogenic stress (e.g., by severe neurological deficits or insular cortical lesion) could be a practical interpretation of troponin elevation in stroke patients [ 36 ]. In our study, the median score of NIHSS and prevalence of comorbidities (e.g., mainly due to a gradual increase in cardiac-comorbidities including AF, IHD, and CHF) was gradually increased in a dose-dependent manner with increase in four levels of troponin ( Figure 4 ).…”

Preliminary investigation of serum cardiac troponin I in dogs with acute ischaemic stroke

“…Recently, the concept of cardiac vulnerability to cerebrogenic stress has been suggested as an explanation for cTnI elevation after ischaemic stroke in humans (Ahn et al . ). In acute ischaemic stroke, several ECG abnormalities as well as the lesion location and stroke severity were predictors of cTnI elevation.…”