Background Kinematically aligned TKA restores function by aligning the femoral and tibial components to the normal or prearthritic joint lines of the knee. However, aligning the components to the joint lines of the normal knee also aligns the tibial component in varus, creating concern that varus alignment might result in poor function and early catastrophic failure. Questions/Purposes We therefore determined whether function and the incidence of catastrophic failure were different when the tibial component, knee, and limb alignment were in a specified normal range, varus outlier, or valgus outlier. Methods We prospectively followed all 198 patients (214 knees) who underwent TKAs between February and October 2008. We treated each knee in this cohort of patients with a kinematically aligned, cruciate-retaining prosthesis implanted using patient-specific guides. From a long-leg scanogram, we measured and categorized alignment of the tibial component as in range (B 0°) or a varus outlier ([ 0°), alignment of the knee as in range (between À2.5°to À7.4°valgus) or a varus ([À2.5°) or valgus (\À7.4°) outlier, and alignment of the limb as in range (0°± 3°) or a varus ([3°) or valgus (\À3°) outlier. We assessed function using the Oxford Knee Score and WOMAC TM score, and reported catastrophic failure as the incidence of revision attributable to loosening, wear, and instability of the femoral or tibial components. The minimum followup was 31 months (mean, 38 months; range, 31-43 months). Results The mean Oxford Knee Score of 43 and WOMAC TM score of 92 were similar between the three alignment categories. The incidence of catastrophic failure in each alignment category was zero.

As determined by imaging of the femoral condyles perpendicular to the primary femoral axis of the knee, the asymmetry between the radii of the medial and lateral femoral condyles in varus and valgus knees with end-stage osteoarthritis was < or =0.2 mm, which is small enough to be considered clinically unimportant when aligning a total knee prosthesis.

Background: New-onset atrial fibrillation (AF) in patients hospitalized with COVID-19 has been reported and associated with poor clinical outcomes. We aimed to understand the incidence of and outcomes associated with new-onset AF in a diverse and representative US cohort of patients hospitalized with COVID-19. Methods: We used data from the American Heart Association COVID-19 Cardiovascular Disease Registry. Patients were stratified by the presence versus absence of new-onset AF. The primary and secondary outcomes were in-hospital mortality and major adverse cardiovascular events (MACE; cardiovascular death, myocardial infarction, stroke, cardiogenic shock, and heart failure). The association of new-onset AF and the primary and secondary outcomes was evaluated using Cox proportional-hazards models for the primary time to event analyses. Results: Of the first 30 999 patients from 120 institutions across the United States hospitalized with COVID-19, 27 851 had no history of AF. One thousand five hundred seventeen (5.4%) developed new-onset AF during their index hospitalization. New-onset AF was associated with higher rates of death (45.2% versus 11.9%) and MACE (23.8% versus 6.5%). The unadjusted hazard ratio for mortality was 1.99 (95% CI, 1.81–2.18) and for MACE was 2.23 (95% CI, 1.98–2.53) for patients with versus without new-onset AF. After adjusting for demographics, clinical comorbidities, and severity of disease, the associations with death (hazard ratio, 1.10 [95% CI, 0.99–1.23]) fully attenuated and MACE (hazard ratio, 1.31 [95% CI, 1.14–1.50]) partially attenuated. Conclusions: New-onset AF was common (5.4%) among patients hospitalized with COVID-19. Almost half of patients with new-onset AF died during their index hospitalization. After multivariable adjustment for comorbidities and disease severity, new-onset AF was not statistically significantly associated with death, suggesting that new-onset AF in these patients may primarily be a marker of other adverse clinical factors rather than an independent driver of mortality. Causality between the MACE composites and AF needs to be further evaluated.

BackgroundIn patients with end‐stage kidney disease, sudden cardiac death is more frequent after a long interdialytic interval, within 6 hours after the end of a hemodialysis session. We hypothesized that the occurrence of paroxysmal arrhythmias is associated with changes in heart rate and heart rate variability in different phases of hemodialysis.Methods and ResultsWe conducted a prospective ancillary study of the Predictors of Arrhythmic and Cardiovascular Risk in End Stage Renal Disease cohort. Continuous ECG monitoring was performed using an ECG patch, and short‐term heart rate variability was measured for 3 minutes every hour (by root mean square of the successive normal‐to‐normal intervals, spectral analysis, Poincaré plot, and entropy), up to 300 hours. Out of enrolled participants (n=28; age 54±13 years; 57% men; 96% black; 33% with a history of cardiovascular disease; left ventricular ejection fraction 70±9%), arrhythmias were detected in 13 (46%). Nonsustained ventricular tachycardia occurred more frequently during/posthemodialysis than pre‐/between hemodialysis (63% versus 37%, P=0.015). In adjusted for cardiovascular disease time‐series analysis, nonsustained ventricular tachycardia was preceded by a sudden heart rate increase (by 11.2 [95% CI 10.1–12.3] beats per minute; P<0.0001). During every‐other‐day dialysis, root mean square of the successive normal‐to‐normal intervals had a significant circadian pattern (Mesor 10.6 [ 95% CI 0.9–11.2] ms; amplitude 1.5 [95% CI 1.0–3.1] ms; peak at 02:01 [95% CI 20:22–03:16] am; P<0.0001), which was replaced by a steady worsening on the second day without dialysis (root mean square of the successive normal‐to‐normal intervals −1.41 [95% CI −1.67 to −1.15] ms/24 h; P<0.0001).ConclusionsSudden increase in heart rate during/posthemodialysis is associated with nonsustained ventricular tachycardia. Every‐other‐day hemodialysis preserves circadian rhythm, but a second day without dialysis is characterized by parasympathetic withdrawal.

Background-Sex 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. Methods-Participants from the Atherosclerosis Risk in Communities study with analyzableECGs (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. Cox proportional hazards and Fine-Gray competing risk models were constructed. Relative hazard ration (RHR) and relative subhazard ratio (RSHR) with 95% confidence interval for SCD and nonSCD risk for women relative to men was calculated. Model 1 was adjusted for prevalent cardiovascular disease (CVD) and risk factors. Time-updated model 2 was in addition adjusted for incident non-fatal CVD events.Results-Over a median follow-up of 24.4 years, there were 530 SCDs (incidence 1.72 (1.58-1.88)/1000 person-years). Women experienced a greater than men risk of SCD 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), which was explained by incident CVD. Furthermore, 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) were associated with higher risk of SCD in women than in men, independently from incident CVD.Conclusions-Sex modifies an association of EP substrate with SCD. In women, global EP substrate is associated with up to 27% greater competing risk of SCD than in men. Development of sex-specific risk scores of SCD is necessary.