Background: Plasma cardiac troponin (cTnI) elevation has been associated with death after ischemic stroke and elevation has been theorized to result from an exaggerated sympathetic response. To our knowledge, no investigation into the cardiac effects of cerebral venous thrombosis (CVT) has been conducted. We hypothesized that acute CVT could result in similar cardiac stress manifesting as electrocardiogram (ECG) changes or cTnI elevation.
Methods: In this retrospective cohort study of all consecutive patients admitted to Johns Hopkins Hospital from 2005-2015 with CVT by ICD9/10 code, patient data (sex, race, risk factors, CVT location/number, venous bleed/stroke, cTnI, ECG) were obtained from hospital records.
Results: Of 81 patients identified with CVT, 53 (66%) had clot in at least one vein and had available ECG data; this group constituted our study population. Included patients had an average age of 41 years (range 1-80); 71% were white and 66% female. The left transverse sinus was most commonly involved (47%) and 66% of patients had >2 clots. 22(41%) had cTnI elevation, defined as >0.06. Odds of cTnI elevation increased per each additional vein involved (age-adjusted OR 2.64, 95%CI 1.14, 6.13] Of those with deep clots (deep veins, straight sinus; n=8), 37.5% had cTnI elevation compared to 4.44% without deep clots (p=0.02). The mean cTnI of those individuals with venous infarct (n=15) was higher than those without (0.14 vs 0.02, p=0.009) but lost significance after adjusting for age/race. cTnI elevation was not associated with venous hemorrhage. No significant association was found between ECG parameters and clot number/venous infarct.
Conclusions: Clots in multiple veins and deep veins increased odds of cTnI elevation in a retrospective cohort of acute CVT patients irrespective of age and race. The cardiac effects of acute CVT should be recognized and further investigated to elucidate pathophysiology, and significance.