Abstract WP176: Electrocardiographic Left Atrial Abnormality and Silent Vascular Brain Injury: The Northern Manhattan Study

Abstract

Background: Increased P-wave terminal force in lead V1 (PTFV1) of a standard 12-lead electrocardiogram (EKG), a marker of left atrial dilatation and possibly fibrosis, has been associated with stroke risk in the absence of atrial fibrillation (AF), and with subclinical infarcts in some cohorts. We hypothesized that PTFV1 would be associated with an increased prevalence of subclinical infarcts, especially cortical ones, and leukoaraiosis in a population-based, multi-ethnic cohort. Methods: PTFV1 was collected manually from baseline EKGs of participants in the population-based, prospective Northern Manhattan Study (NOMAS) who had remained clinically stroke-free and undergone brain MRI (n=1,290). MRIs were read for superficial and deep infarcts and white matter hyperintensity volume adjusted for head size (WMHV). Logistic regression models were used for the association of PTFV1 with all subclinical infarcts and with cortical infarcts, and linear regression models with logWMHV. Models were adjusted for demographics and risk factors. Results: Among the 1174 participants with PTFV1, mean age was 70 + 9 SD years at the time of MRI, 40.3% were male, and 14.4% were white, 17.6% black, and 65.8% Hispanic. Hypertension was present in 68.0%. Mean PTFV1 was 3587.35 ± 2315.62 μV-ms. MRIs were performed a mean of 6.0 + 3.4 years after EKG. Subclinical infarcts were present in 170 (15.1%) participants, and were cortical in 40 (3.6%). PTFV1 >5000 μV-ms was associated with greater WMHV even after adjusting for demographics and risk factors, including baseline AF (mean difference in logWMHV 0.14, 95% CL 0.01-0.28). There was a trend toward an association of PTFV1 with cortical (unadjusted OR per SD change logPTFV1 1.30, 95% CI 0.94-1.81) but not with all subclinical infarcts (unadjusted OR 1.00, 95% CI 0.85-1.18). Conclusion: EKG evidence of left atrial abnormality was associated with leukoaraiosis, and possibly with subclinical cortical infarcts, though the limited number of outcomes did not permit us to confirm this finding. Left atrial cardiopathy may be a source of emboli, but may also cause cerebral hypoperfusion-related injury. Further studies in large cohorts are needed to determine the relationship of PTFV1 to risk of subclinical cerebrovascular disease.