Cardiovascular Sciences

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  • ItemOpen Access
    Laparoscopic Peritoneopericardial Herniorrhaphy in 2 Dogs
    (2022-09) Iannettoni, Mark; Anciano, Carlos; Scharf, Valery F.
  • ItemOpen Access
    Unusual Cause of Hepatic Vein Systolic Flow Reversal
    (2022-01-26) Shah, Neeraj; Naniwadeka, Aditi
  • ItemOpen Access
    A Genotype–Phenotype Analysis of Glutathione Peroxidase 4 in Human Atrial Myocardium and Its Association with Postoperative Atrial Fibrillation
    (2022-04-06) Akhter, Shahab A.; Berdaweel, Islam A.; Hart, Alexander A.; Jatis, Andrew J.; Karlan, Nathan; Gaine, Marie E.; Smith, Ryan M.; Anderson, Ethan
  • ItemOpen Access
    Comparison of a New bioprosthetic Mitral Valve to Other Commercially Available Devices Under Controlled Conditions in a Porcine Mode
    (2021) Chitwood, W. Randolph; Wang, Dee Dee; Caranasos, Thomas G.; O'Neill, Brian P.; Stack, Richard S.; O'Neill, William W.
  • ItemOpen Access
    Sex Differences in Arrhythmic Burden with the Wearable Cardioverter-Defibrillator
    (2021) Burch, Ashley E.; Goldenberg, Ido; Erath, Julia W.; Russo, Andrea M.; Assmus, Birgit; Bonderman, Diana; McNitt, Scott; Kutyifa, Valentina
  • ItemOpen Access
    Sipuleucel-T Associated Inflammatory Cardiomyopathy: A Case Report and Observations from a Large Pharmacovigilance Database
    (2021) Moey, Melissa Y.Y.; Kreeger, R. Wayne; Marcu, C. Bogdan; Morris, D. Lynn; Ardhanari, Sivakumar; Jiwani, Rahim A.; Takeda, Kotaro; Prenshaw, Karyn; Inzerillo, John; Liles, Darla K.; Lebrun-Vignes, Bénédicte; Salem, Joe-Elie
  • ItemOpen Access
    The Impact of Chest Pain Center on Treatment Delay of STEMI Patients: a Time Series Study
    (2021) Sun, Xiaolin; Yao, Bo; Shi, Kexin; Xue, Yajiong; Liang, Huigang
  • ItemOpen Access
    Methods of using carnosinol and analogs thereof
    (2015-12-17) Anderson, Ethan; Katunga, Lalage; Aldini, Giancarlo
    Embodiments of the present invention relate to methods of preventing or treating diabetes, an obesity/diabetes-related condition, insulin sensitivity, heart disease, mitochondrial dysfunction or liver disease comprising administering carnosinol or an analog thereof to a subject in need thereof.
  • ItemOpen Access
    Methods of Reducing Myocardial Injury Following Myocardial Infarction
    (2014-02-27) Virag, Jitka; Dries, Jessica L.
  • ItemOpen Access
    Monoamine Oxidase is a Major Determinant of Redox Balance in Human Atrial Myocardium and is Associated With Postoperative Atrial Fibrillation
    (2014-02) Anderson, Ethan; Efird, Jimmy T.; Davies, Stephen W.; O'Neal, Wesley T.; Darden, Timothy M.; Thayne, Kathleen A.; Katunga, Lalage Adalaide; Kindell, Linda C.; Ferguson, T. Bruce; Anderson, Curtis A.; Chitwood, W. Randolph; Koutlas, Theodore C.; Williams, J. Mark; Rodriguez, Evelio; Kypson, Alan P.
    BACKGROUND: Onset of postoperative atrial fibrillation (POAF) is a common and costly complication of heart surgery despite major improvements in surgical technique and quality of patient care. The etiology of POAF, and the ability of clinicians to identify and therapeutically target high-risk patients, remains elusive. METHODS AND RESULTS: Myocardial tissue dissected from right atrial appendage (RAA) was obtained from 244 patients undergoing cardiac surgery. Reactive oxygen species (ROS) generation from multiple sources was assessed in this tissue, along with total glutathione (GSHt) and its related enzymes GSH-peroxidase (GPx) and GSH-reductase (GR). Monoamine oxidase (MAO) and NADPH oxidase were observed to generate ROS at rates 10-fold greater than intact, coupled mitochondria. POAF risk was significantly associated with MAO activity (Quartile 1 [Q1]: adjusted relative risk [ARR]=1.0; Q2: ARR=1.8, 95% confidence interval [CI]=0.84 to 4.0; Q3: ARR=2.1, 95% CI=0.99 to 4.3; Q4: ARR=3.8, 95% CI=1.9 to 7.5; adjusted Ptrend=0.009). In contrast, myocardial GSHt was inversely associated with POAF (Quartile 1 [Q1]: adjusted relative risk [ARR]=1.0; Q2: ARR=0.93, 95% confidence interval [CI]=0.60 to 1.4; Q3: ARR=0.62, 95% CI=0.36 to 1.1; Q4: ARR=0.56, 95% CI=0.34 to 0.93; adjusted Ptrend=0.014). GPx also was significantly associated with POAF; however, a linear trend for risk was not observed across increasing levels of the enzyme. GR was not associated with POAF risk. CONCLUSIONS: Our results show that MAO is an important determinant of redox balance in human atrial myocardium, and that this enzyme, in addition to GSHt and GPx, is associated with an increased risk for POAF. Further investigation is needed to validate MAO as a predictive biomarker for POAF, and to explore this enzyme's potential role in arrhythmogenesis.
  • ItemOpen Access
    Acute Adverse Effects of Fine Particulate Air Pollution on Ventricular Repolarization
    (2010-07) Liao, Duanping; Shaffer, Michele L.; Rodriguez-Colon, Sol; He, Fan; Li, Xian; Wolbrette, Deborah L.; Yanosky, Jeff D.; Cascio, Wayne E.
    Background The mechanisms for the relationship between particulate pollution and cardiac disease are not fully understood. Objective We examined the effects and time course of exposure to fine particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) on ventricular repolarization of 106 nonsmoking adults who were living in communities in central Pennsylvania. Methods The 24-hr beat-to-beat electrocardiogram (ECG) data were obtained using a high-resolution 12-lead Holter system. After visually identifying and removing artifacts and arrhythmic beats, we summarized normal beat-to-beat QTs from each 30-min segment as heart rate (HR)-corrected QT measures: QT prolongation index (QTI), Bazett’s HR-corrected QT (QTcB), and Fridericia’s HR-corrected QT (QTcF). A personal PM2.5 monitor was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data and used 30-min time-specific average PM2.5 exposures. Results The mean age of the participants was 56 ± 8 years, with 41% male and 74% white. The means ± SDs for QTI, QTcB, and QTcF were 111 ± 6.6, 438 ± 23 msec, and 422 ± 22 msec, respectively; and for PM2.5, the mean ± SD was 14 ± 22 μg/m3. We used distributed lag models under a framework of linear mixed-effects models to assess the autocorrelation-corrected regression coefficients (β) between 30-min PM2.5 and the HR-corrected QT measures. Most of the adverse ventricular repolarization effects from PM2.5 exposure occurred within 3–4 hr. The multivariable adjusted β (SE, p-value) due to a 10-μg/m3 increase in lag 7 PM2.5 on QTI, QTcB, and QTcF were 0.08 (0.04, p < 0.05), 0.22 (0.08, p < 0.01), and 0.09 (0.05, p < 0.05), respectively. Conclusions Our results suggest a significant adverse effect of PM2.5 on ventricular repolarization. The time course of the effect is within 3–4 hr of elevated PM2.5.
  • ItemOpen Access
    Increased Coronary Artery Disease Severity in Black Women Undergoing Coronary Bypass Surgery
    (2015-02) Efird, Jimmy T.; O'Neal, Wesley T.; Griffin, William F.; Anderson, Ethan; Davies, Stephen W.; Landrine, Hope; O'Neal, Jason B.; Shiue, Kristin Y.; Kindell, Linda C.; Bruce Ferguson, T.; Randolph Chitwood, W.; Kypson, Alan P.
    Race and sex disparities are believed to play an important role in heart disease. The purpose of this study was to examine the association between race, sex, and number of diseased vessels at the time of coronary artery bypass grafting (CABG), and subsequent postoperative outcomes. The 13,774 patients undergoing first-time, isolated CABG between 1992 and 2011 were included. Trend in the number of diseased vessels between black and white patients, stratified by sex, were analyzed using a Cochran-Armitage trend test. Models were adjusted for age, procedural status (elective vs. nonelective), and payor type (private vs. nonprivate insurance). Black female CABG patients presented with an increasingly greater number of diseased vessels than white female CABG patients (adjusted P(trend) = 0.0021). A similar trend was not observed between black and white male CABG patients (adjusted P(trend) = 0.18). Black female CABG patients were also more likely to have longer intensive care unit and hospital lengths of stay than other race-sex groups.Our findings suggest that black female CABG patients have more advanced coronary artery disease than white female CABG patients. Further research is needed to determine the benefit of targeted preventive care and preoperative workup for this high-risk group.
  • ItemOpen Access
    Acute Effects of Fine Particulate Air Pollution on Cardiac Arrhythmia: The APACR Study
    (2011-03) He, Fan; Shaffer, Michele L.; Rodriguez-Colon, Sol; Yanosky, Jeff D.; Bixler, Edward O.; Cascio, Wayne E.; Liao, Duanping
    Background: The mechanisms underlying the relationship between particulate matter (PM) air pollution and cardiac disease are not fully understood. Objectives: We examined the effects and time course of exposure to fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] on cardiac arrhythmia in 105 middle-age community-dwelling healthy nonsmokers in central Pennsylvania. Methods: The 24-hr beat-to-beat electrocardiography data were obtained using a high-resolution Holter system. After visually identifying and removing artifacts, we summarized the total number of premature ventricular contractions (PVCs) and premature atrial contractions (PACs) for each 30-min segment. A personal PM2.5 nephelometer was used to measure individual-level real-time PM2.5 exposures for 24 hr. We averaged these data to obtain 30-min average time–specific PM2.5 exposures. Distributed lag models under the framework of negative binomial regression and generalized estimating equations were used to estimate the rate ratio between 10-μg/m3 increases in average PM2.5 over 30-min intervals and ectopy counts. Results: The mean ± SD age of participants was 56 ± 8 years, with 40% male and 73% non-Hispanic white. The 30-min mean ± SD for PM2.5 exposure was 13 ± 22 μg/m3, and PAC and PVC counts were 0.92 ± 4.94 and 1.22 ± 7.18. Increases of 10 μg/m3 in average PM2.5 concentrations during the same 30 min or the previous 30 min were associated with 8% and 3% increases in average PVC counts, respectively. PM2.5 was not significantly associated with PAC count. Conclusion: PM2.5 exposure within approximately 60 min was associated with increased PVC counts in healthy individuals.
  • ItemOpen Access
    Association of cardiac and vascular changes with ambient PMin diabetic individuals
    (2010) Schneider, Alexandra; Neas, Lucas M.; Graff, Donald W.; Herbst, Margaret C.; Cascio, Wayne E.; Schmitt, Mike T.; Buse, John B.; Peters, Annette; Devlin, Robert B.
    Background and Objective Exposure to fine airborne particles (PM2.5) has been shown to be responsible for cardiovascular and hematological effects, especially in older people with cardiovascular disease. Some epidemiological studies suggest that individuals with diabetes may be a particularly susceptible population. This study examined effects of short-term exposures to ambient PM2.5 on markers of systemic inflammation, coagulation, autonomic control of heart rate, and repolarization in 22 adults (mean age: 61 years) with type 2 diabetes. Methods Each individual was studied for four consecutive days with daily assessments of plasma levels of blood markers. Cardiac rhythm and electrocardiographic parameters were examined at rest and with 24-hour ambulatory ECG monitors. PM2.5 and meteorological data were measured daily on the rooftop of the patient exam site. Data were analyzed with models adjusting for season, weekday, meteorology, and a random intercept. To identify susceptible subgroups, effect modification was analyzed by clinical characteristics associated with insulin resistance as well as with oxidative stress and by medication intake. Results Interleukin (IL)-6 and tumor necrosis factor alpha showed a significant increase with a lag of two days (percent change of mean level: 20.2% with 95%-confidence interval [6.4; 34.1] and 13.1% [1.9; 24.4], respectively) in association with an increase of 10 μg/m3 in PM2.5. Obese participants as well as individuals with elevated glycosylated hemoglobin, lower adiponectin, higher ferritin or with glutathione S-transferase M1 null genotype showed higher IL-6 effects. Changes in repolarization were found immediately as well as up to four days after exposure in individuals without treatment with a beta-adrenergic receptor blocker. Conclusions Exposure to elevated levels of PM2.5 alters ventricular repolarization and thus may increase myocardial vulnerability to arrhythmias. Exposure to PM2.5 also increases systemic inflammation. Characteristics associated with insulin resistance or with oxidative stress were shown to enhance the association.