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Background Oxidative stress (OS) may be a key mechanism underlying the development of atrial fibrillation (AF) in experimental studies, but data in humans remain limited. Objective Systemic OS can be estimated by measurements of circulating levels of the aminothiols including glutathione, cysteine, and their oxidized products. We tested the hypothesis that the redox potentials of glutathione (E h GSH) and cysteine will be associated with prevalent and incident AF. Methods Plasma levels of aminothiols were measured in 1439 patients undergoing coronary angiography, of whom 148 (10.3%) had a diagnosis of AF. After a median follow-up of 6.3 years, 104 of 917 patients (11.5%) developed incident AF. Multivariate logistic regression and Cox regression models were used to determine whether OS markers were independent predictors of prevalent and incident AF after adjustment for traditional risk factors, heart failure, coronary artery disease, and high-sensitivity C-reactive protein level. Results For each 10% increase in E h GSH, the odds of prevalent AF was 30% higher (odds ratio [OR] 1.3; 95% confidence interval [CI] 1.1–1.7; P = .02) and 90% higher (OR 1.9; 95% CI 1.3–2.7; P = .004) when the median was used as a cutoff. The E h GSH level above the median was more predictive of chronic AF (OR 4.0; 95% CI 1.3–12.9; P = .01) than of paroxysmal AF (OR 1.7; 95% CI 1.1–2.7; P = .03). Each 10% increase in E h GSH level was associated with a 40% increase in the risk of incident AF (hazard ratio 1.4; 95% CI 1.1–1.7; P = .01). Conclusion Increased OS measured by the redox potentials of glutathione is associated with prevalent and incident AF. Therapies that modulate OS need to be investigated to treat and prevent AF.

Introduction Soluble urokinase-type plasminogen activator receptor (suPAR) strongly predicts outcomes and incident chronic kidney disease (CKD) in patients with cardiovascular disease (CVD). Whether the association between suPAR and CKD is a reflection of its overall association with chronic inflammation and poor CVD outcomes is unclear. We examined whether CVD biomarkers, including high-sensitivity C-reactive protein (hs-CRP), fibrin-degradation products (FDPs), heat-shock protein 70 (HSP-70), and high-sensitivity troponin I (hs-TnI) were associated with a decline in kidney function in the Emory Cardiovascular Biobank cohort, in which suPAR levels were shown to be predictive of both incident CKD and CVD outcomes. Methods We measured suPAR, hs-CRP, HSP-70, FDP, and hs-TnI plasma levels in 3282 adults (mean age 63 years, 64% male, 75% estimated glomerular filtration rate [eGFR] >60 ml/min per 1.73 m 2 ). Glomerular filtration rate was estimated using Chronic Kidney Disease–Epidemiology Collaboration (eGFR) at enrollment (n = 3282) and follow-up (n = 2672; median 3.5 years). Urine protein by dipstick at baseline was available for 1335 subjects. Results There was a weak correlation among biomarkers (r range: 0.17−0.28). hs-CRP, FDPs, hs-TnI, and suPAR were independently associated with baseline eGFR and proteinuria. The median yearly decline in eGFR was −0.6 ml/min per 1.73 m 2 . hs-CRP (β: −0.04; P = 0.46), FDPs (β: −0.13; P = 0.08), HSP-70 (β: 0.05; P = 0.84), or hs-TnI (β: −0.01; P = 0.76) were associated with eGFR decline. suPAR remained predictive of eGFR decline even after adjusting for all biomarkers. Discussion hs-CRP, FDP, HSP-70, and hs-TnI were not associated with eGFR decline. The specific association of suPAR with eGFR decline supported its involvement in pathways specific to the pathogenesis of kidney disease.

Background Endogenous regenerative capacity, assessed as circulating progenitor cell (PC) numbers, is an independent predictor of adverse outcomes in patients with cardiovascular disease. However, their predictive role in heart failure (HF) remains controversial. We assessed the relationship between the number of circulating PCs and the pathogenesis and severity of HF and their impact on incident HF events. Methods and Results We recruited 2049 adults of which 651 had HF diagnosis. PCs were enumerated by flow cytometry as CD45med + blood mononuclear cells expressing CD34, CD133, vascular endothelial growth factor receptor-2, and chemokine (C-X-C motif) receptor 4 epitopes. PC subsets were lower in number in HF and after adjustment for clinical characteristics in multivariable analyses, a low CD34 + and CD34 + /CXCR + cell count remained independently associated with a diagnosis of HF ( P + , CD34 + /CD133 + , and CD34 + /CXCR4 + ) were independent predictors of all-cause death (hazard ratio 2.0, 1.6, 1.6-fold higher mortality, respectively; P + /VEGF + ) were independent predictors of mortality in patients with HF with preserved ejection fraction only (hazard ratio, 5.0; P =0.001). Conclusions PC levels are lower in patients with HF, and lower PC counts are strongly and independently predictive of mortality. Strategies to increase PCs and exogenous stem cell therapies designed to improve regenerative capacity in HF, especially, in HF with preserved ejection fraction, need to be further explored.

This study sought to determine the cardiovascular physiologic correlates of sleep-disordered breathing (SDB) in American-style football (ASF) participants using echocardiography, vascular applanation tonometry, and peripheral arterial tonometry. Forty collegiate ASF participants were analyzed at pre- and postseason time points with echocardiography and vascular applanation tonometry. WatchPAT (inclusive of peripheral arterial tonometry) used to assess for SDB was then performed at the postseason time point. Twenty-two of 40 (55%) ASF participants demonstrated SDB with an apnea-hypopnea index (pAHI) ≥5. ASF participants with SDB were larger (109 ± 20 vs 92 ± 14 kg, p = 0.004) and more likely linemen position players (83% vs 50%, p = 0.03). Compared with those without SDB, ASF participants with SDB demonstrated relative impairments in left ventricular diastolic and vascular function as reflected by lower lateral e' (14 ± 3 vs 17 ± 3 cm/s, p = 0.007) and septal e' (11 ± 2 vs 13 ± 2 cm/s, p = 0.009) tissue velocities and higher pulse wave velocity (5.4 ± 0.9 vs 4.8 ± 0.5 m/s, p = 0.02). In the total cohort, there were significant positive correlations between pAHI and pulse wave velocity (r = 0.42, p = 0.008) and inverse correlations between pAHI and the averaged e' tissue velocities (r = -0.42, p = 0.01). In conclusion, SDB is highly prevalent in youthful collegiate ASF participants and associated with relative impairments in cardiac and vascular function. Targeted efforts to identify youthful populations with SDB, including ASF participants, and implement SDB treatment algorithms, represent important future clinical directives.

Objective Exercise-induced cardiac dysfunction and corollary biomarker release have been documented following long-distance running events. To what degree these processes occur during shorter distance running events is unknown. Methods 72 healthy recreational runners (54% male/46% female) recruited by age (group 1 (18–20 years old, N=19); group 2 (45–50 years old, N=27); group 3 (70–75 years old, N=26)) were studied with echocardiography and biochemical profiling during participation in a 10 km running race. Results Despite age-dependent baseline differences in ventricular size and diastolic tissue velocities, there were no significant within group or across group decrements in ventricular systolic or diastolic function following race completion. Postrace increases in cardiac troponin-I (cTnI), B-type natriuretic peptide (BNP) and high-sensitivity C-reactive protein (hs-CRP) were common and demonstrated distinct age dependent profiles. Specifically, BNP increases were most pronounced among older runners (group 3Δ: 16±22 pg/mL, p=0.001), hs-CRP increased only among younger runners (group 1Δ: 1.5±2.7 mg/L, p=0.03) and cTnI increased in both younger (group 1Δ: 0.01±0.02 ng/mL, p=0.028) and older (group 3Δ: 0.01±0.01 ng/mL, p=0.007) runners, but not middle aged runners (group 2Δ: 0.00±0.00 ng/mL, p=0.57). Conclusions Moderate distance recreational running leads to distinct age-dependent biomarker release but is not associated with cardiac fatigue, a proposed stimulus for pathologic cardiac remodelling that has been observed following longer distance running events.

Acute myocardial infarction (AMI) is rare among women of childbearing age. Spontaneous coronary artery dissection (SCAD), a rare cause of AMI, is the leading cause of pregnancy-associated acute myocardial infarction (PAMI), and is associated with critical complications, including pump failure, ventricular arrhythmias, and sudden death. Optimal treatment strategies for SCAD and PAMI remain unclear. In this report, we describe a case of PAMI due to SCAD presenting as cardiopulmonary arrest. After comprehensive treatment including advanced cardiovascular life support, emergent percutaneous coronary intervention (PCI), therapeutic hypothermia, and emergent Cesarian section for intrauterine fetal death, she survived without neurological sequelae. Intensive medication for pump failure was subsequently required, and she was discharged with adequately controlled heart failure, despite revealing stent lumen obstruction by cardiac computed tomography. On close follow-up for one year, she has remained free of further cardiac events. .

Background: Circulating hematopoietic enriched progenitor cells (PCs) predict adverse cardiovascular outcomes in patients with coronary artery disease (CAD). The additive predictive role of endothelial enriched PCs expressing vascular endothelial growth factor receptor (VEGF) remains controversial.

High-sensitivity Troponin-I (hs-TnI) as a marker of myocardial injury is predictive of adverse outcomes in patients with coronary artery disease (CAD). Whether the relationship between hs-TnI and outcomes is dependent on underlying CAD severity is unknown. 2826 patients without AMI (mean age 62, 64

Participation in ultra-endurance exercise is associated with transient cardiac dysfunction, or cardiac fatigue. The effects of aging and participation in a moderate distance running race on changes in cardiac function have not been studied. 73 healthy runners spanning a wide age spectrum [(Group 1

Seventy-two unipolar QRS-inhibited demand pacemakers were examined by provoking myopotential interference by exercise. Filter characteristics of 5 kinds of generators were tested by the use of sin wave pulse. Each myosignal of the major pectoral muscle and the abdominal rectus muscle was subjected to Fourier transform for analyses of amplitude and frequencies. Pacemaker inhibition was observed in 42 (58 per cent) of 72 with the highest frequency in the push up test. In this test, the incidence of myopotential inhibition was significantly lower (p less than 0.01) on the pacemaker implantations in the abdominal wall than that in the anterior chest wall. The myosignals of the major pectoral muscle had sufficient frequency and power density for triggering the QRS sensing mechanism but the abdominal muscular signals did not. To avoid myopotential inhibition of unipolar ventricular inhibited demand pacemakers it is most effective to implant multiprogrammable pacemakers subcutaneously in the abdominal wall and to select the optimal sensitivity according to the myopotential inhibition tests.