Myocardial injury in transient global amnesia: a case-control study.

BACKGROUND AND PURPOSE: Elevation of cardiac troponin (cTn), a sensitive biomarker of myocardial injury, is frequently observed in severe acute neurological disorders. Case reports suggest that cardiac dysfunction may also occur in patients with transient global amnesia (TGA). Until now, no study has systematically assessed this phenomenon. METHODS: We performed a case-control study using data of consecutive patients presenting with TGA from 2010 to 2015. Multiple logistic regression analysis accounting for age, sex and cardiovascular risk factors was performed to compare the likelihood of myocardial injury [defined as elevation of cTn > 99th percentile (≥14 ng/L); highly sensitive cardiac troponin T assay] in TGA with three reference groups: migraine with aura, vestibular neuritis and transient ischaemic attack (TIA). RESULTS: Cardiac troponin elevation occurred in 28 (25%) of 113 patients with TGA. Patients with TGA with cTn elevation were significantly older, more likely to be female and had higher blood pressure on admission compared with those without. The likelihood of myocardial injury following TGA was at least more than twofold higher compared with all three reference groups [adjusted odds ratio, 5.5; 95% confidence interval (CI), 1.2-26.4, compared with migraine with aura; adjusted odds ratio, 2.2; 95% CI, 1.2-4.4, compared with vestibular neuritis; adjusted odds ratio, 2.3; 95% CI, 1.3-4.2, compared with TIA]. CONCLUSIONS: One out of four patients with TGA had evidence of myocardial injury as assessed by highly sensitive cTn assays. The likelihood of myocardial injury associated with TGA was even higher than in TIA patients with a more pronounced cardiovascular risk profile. Our findings suggest the presence of a TGA-related disturbance of brain-heart interaction that deserves further investigation.

Plasma Catecholamine Profile of Subarachnoid Hemorrhage Patients with Neurogenic Cardiomyopathy.

PURPOSE: To investigate the connection between sympathetic function and neurogenic cardiomyopathy (NC), and to determine whether NC is mediated primarily by circulating adrenal epinephrine (EPI) or neuronally transmitted norepinephrine (NE), following subarachnoid hemorrhage (SAH). METHODS: This is a prospective observational investigation of consecutive severe-grade SAH patients. All participants had transthoracic echocardiography and serological assays for catecholamine levels - dopamine (DA), NE and EPI - within 48 h of hemorrhage onset. Clinical and serological independent predictors of NC were determined using multivariate logistic regression analyses, and the accuracy of predictors was assessed by receiver operating characteristic (ROC) curves. Multivariate linear regression analyses were used to evaluate correlations among the catecholamines. RESULTS: The investigation included a total of 94 subjects: the mean age was 55 years, 81% were female and 57% were Caucasian. NC was identified in approximately 10% (9/94) of cases. Univariate analyses revealed associations between NC and worse clinical severity (p = 0.019), plasma DA (p = 0.018) and NE levels (p = 0.024). Plasma NE correlated with DA levels (ρ = 0.206, p = 0.046) and EPI levels (ρ = 0.392, p < 0.001), but was predicted only by plasma EPI in bivariate [parameter estimate (PE) = 1.95, p < 0.001] and multivariate (PE = 1.89, p < 0.001) linear regression models. Multivariate logistic regression analyses consistently demonstrated the predictive value of clinical grade for NC (p < 0.05 for all analyses) except in models incorporating plasma NE, where NC was independently predicted by NE level (OR 1.25, 95% CI 1.01-1.55) over clinical grade (OR 4.19, 95% CI 0.874-20.1). ROC curves similarly revealed the greater accuracy of plasma NE [area under the curve (AUC) 0.727, 95% CI 0.56-0.90, p = 0.02] over clinical grade (AUC 0.704, 95% CI 0.55-0.86, p = 0.05) for identifying the presence or absence of NC. CONCLUSIONS: Following SAH, the development of NC is primarily related to elevated plasma NE levels. Findings implicate a predominantly neurogenic process mediated by neuronal NE (and not adrenal EPI), but cannot exclude synergy between the catecholamines.