Biology subjects

Tereshchenko, L. G.

Publications and source records attributed to Tereshchenko, L. G..

3 recordsLinked to original sources

bioRxiv2019

Does Sex Modify an Association of Electrophysiological Substrate with Sudden Cardiac Death? The Atherosclerosis Risk in Communities (ARIC) Study

BackgroundSex is a well-recognized risk factor for sudden cardiac death (SCD). Sex differences in electrophysiological (EP) substrate of SCD are known. However, it remains unknown whether sex can modify an association of EP substrate with SCD.\n\nMethodsParticipants from the Atherosclerosis Risk in Communities study with analyzable ECGs (n=14,725; age, 54.2{+/-}5.8 yrs; 55% female, 74% white) were included. EP substrate was characterized by traditional 12-lead ECG (heart rate, QRS, QTc, Cornell voltage), spatial ventricular gradient (SVG) and sum absolute QRST integral (SAI QRST) metrics. Two competing outcomes were adjudicated SCD and nonSCD. Interaction of ECG metrics with sex was studied in Cox proportional hazards and Fine-Gray competing risk models. Relative hazard ratio (RHR) and relative sub-hazard ratio (RSHR) with a 95% confidence interval for SCD and nonSCD risk for women relative to men were calculated. Model 1 was adjusted for prevalent cardiovascular disease (CVD) and risk factors. Time-updated model 2 was additionally adjusted for incident non-fatal CVD.\n\nResultsOver a median follow-up of 24.4 years, there were 530 SCDs (incidence 1.72 (1.58-1.88)/1000 person-years) and 2,178 nonSCDs (incidence 7.09; (6.80-7.39)/ 1000 person-years). Women experienced a greater than men risk of SCD associated with Cornell voltage (RHR 1.18(1.06-1.32); P=0.003), SAI QRST (RHR 1.16(1.04-1.30); P=0.007), area SVG magnitude (RHR 1.24(1.05-1.45); P=0.009), and peak SVG magnitude (RHR 1.22(1.04-1.44); P=0.018), independently from incident CVD. Greater risk of SCD for women than men associated with QRS duration (RHR 1.24(1.07-1.44); P=0.004) and QTc (RSHR 1.15(1.02-1.30); P=0.025) was explained by incident CVD. Furthermore, women had greater odds of SCD associated with heart rate (RSHR 1.19(1.01-1.40); P=0.036), independently of incident CVD.\n\nConclusionsSex modifies an association of EP substrate with SCD. In women, global EP substrate is associated with up to 27% greater risk of SCD than in men. Development of sex-specific risk scores of SCD is necessary. Further studies of mechanisms behind sex differences in EP substrate of SCD are warranted.

epidemiology↗

bioRxiv2019

The Dialysis Procedure Triggers Autonomic Imbalance and Cardiac Arrhythmias: Insights from Continuous 14-day ECG Monitoring

BackgroundIn end-stage kidney disease the dialytic cycle relates to the rate of sudden cardiac death. We hypothesized that circadian, dialytic cycles, paroxysmal arrhythmias, and cardiovascular risk factors are associated with periodic changes in heart rate and heart rate variability (HRV) in incident dialysis patients.\n\nMethodsWe conducted a prospective ancillary study of the Predictors of Arrhythmic and Cardiovascular Risk in End Stage Renal Disease cohort (n=28; age 54{+/-}13 y; 57% men; 96% black; 33% with a history of structural heart disease; left ventricular ejection fraction 70{+/-}9%). Continuous ECG monitoring was performed using an ECG patch (Zio Patch, iRhythm) and short-term HRV was measured for three minutes every hour. HRV was measured by root mean square of the successive normal-to-normal intervals (rMSSD), high and low frequency power, Poincare plot, and sample and Renyi entropy.\n\nResultsArrhythmias were detected in 46% (n=13). Non-sustained ventricular tachycardia (VT) was more frequent during dialysis or within 6 hours post-dialysis, as compared to pre-or between-dialysis (63% vs. 37%, P=0.015), whereas supraventricular tachycardia was more frequent pre-/ between-dialysis, as compared to during-/ post-dialysis (84% vs. 16%, P=0.015). In adjusted for cardiovascular disease and its risk factors autoregressive conditional heteroscedasticity panel (ARCH) model, VT events were associated with increased heart rate by 11.2 (95%CI 10.1-12.3) bpm (P<0.0001). During regular dialytic cycle, rMSSD demonstrated significant circadian pattern (Mesor 10.6(0.9-11.2) ms; Amplitude 1.5(1.0-3.1) ms; Peak at 02:01(20:22-03:16) am; P<0.0001), which was abolished on a second day interdialytic extension (adjusted ARCH trend for rMSSD -1.41(-1.67 to -1.15) ms per 24h; P<0.0001).\n\nConclusionCardiac arrhythmias associate with dialytic phase. Regular dialytic schedule preserves physiological circadian rhythm, but the second day without dialysis is characterized by parasympathetic withdrawal and a steady increase in sympathetic predominance.\n\nSubject TermsArrhythmias, Autonomic Nervous System, Electrocardiology (ECG), Treatment.

epidemiology↗

bioRxiv2019

Prevention of heart failure in hypertension: disentangling the role of evolving left ventricular hypertrophy and blood pressure lowering: the ALLHAT study

BackgroundHypertension (HTN) is a known risk factor for heart failure (HF), possibly via the mechanism of cardiac remodeling and left ventricular hypertrophy (LVH). We studied how much blood pressure (BP) change and evolving LVH contribute to the effect that lisinopril, doxazosin, amlodipine have on HF compared to chlorthalidone.\n\nMethodsWe conducted causal mediation analysis of Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) data. ALLHAT participants with available serial ECGs and BP measurements were included (n=29,892; mean age 67{+/-}4 y; 32% black; 56% men): 11,008 were randomized to chlorthalidone, 5,967 - to doxazosin, 6,593 - to amlodipine, and 6,324 - to lisinopril. Evolving ECG-LVH, and BP-lowering served as mediators. Incident symptomatic HF was the primary outcome. Linear regression (for mediator) and logistic regression (for outcome) models were adjusted for mediator-outcome confounders (demographic and clinical characteristics known to be associated both with both LVH/HTN and HF).\n\nResultsA large majority of participants (96%) had ECG-LVH status unchanged; 4% developed evolving ECG-LVH. On average, BP decreased by 11/7 mmHg. In adjusted Cox regression analyses, progressing ECG-LVH [HR 1.78(1.43-2.22)], resolving ECG-LVH [HR 1.33(1.03-1.70)], and baseline ECG-LVH [1.17(1.04-1.31)] carried risk of incident HF. After full adjustment, evolving ECG-LVH mediated 4% of the effect of doxazosin on HF. Systolic BP-lowering mediated 12% of the effect of doxazosin, and diastolic BP-lowering mediated 10% effect of doxazosin, 7% effect of amlodipine, and borderline 9% effect of lisinopril on HF.\n\nConclusionsEvolving ECG-LVH and BP change account for 4-13% of the mechanism by which antihypertensive medications prevent HF.

clinical trials↗