Browsing by Subject "Coronary Artery Disease"

Now showing 1 - 7 of 7
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    Depressive symptom clusters as predictors of incident coronary artery disease: a 15-year prospective study
    (Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins, 2014-01) Hawkins, Misty A. W.; Callahan, Christopher M.; Stump, Timothy E.; Stewart, Jesse C.; Department of Psychology, School of Science
    OBJECTIVE: Because it is not known whether particular clusters of depressive symptoms are associated with a greater risk of adverse cardiac outcomes, we compared the utility of four clusters in predicting incident coronary artery disease (CAD) events during a 15-year period in a large cohort of primary care patients 60 years and older. METHODS: Participants were 2537 primary care patients 60 years or older who were screened for depression between 1991 and 1993 and had no existing CAD diagnosis. Depressive symptoms cluster scores (depressed affect, somatic symptoms, interpersonal distress, and positive affect) were computed from responses on the Center for Epidemiologic Studies Depression Scale administered at baseline. CAD events, defined as the occurrence of a nonfatal acute myocardial infarction or CAD death during the follow-up period, were identified using electronic medical record and National Death Index data. RESULTS: There were 678 CAD events. In separate fully adjusted Cox proportional hazard models (controlling for demographics and cardiovascular risk factors), the depressed affect (hazard ratio [HR] = 1.11, 95% confidence interval [CI] = 1.04-1.20), somatic (HR = 1.17, 95% CI = 1.08-1.26), and positive affect (HR = 0.88, 95% CI = 0.82-0.95) clusters each predicted CAD events. When the depressive symptom clusters were entered simultaneously into the fully adjusted model, however, only the somatic cluster remained predictive of CAD events (HR = 1.13, 95% CI = 1.03-1.23). CONCLUSIONS: Our findings suggest that the longitudinal relationship between overall depressive symptom severity and incident CAD events may be driven primarily by the somatic cluster.
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    Epicardial Adipose Tissue Removal Potentiates Outward Remodeling and Arrests Coronary Atherogenesis
    (Elsevier, 2017-05) McKenney-Drake, Mikaela L.; Rodenbeck, Stacey D.; Bruning, Rebecca S.; Kole, Ayeeshik; Yancey, Kyle W.; Alloosh, Mouhamad; Sacks, Harold S.; Sturek, Michael; Cellular and Integrative Physiology, School of Medicine
    BACKGROUND: Pericoronary epicardial adipose tissue (cEAT) serves as a metabolic and paracrine organ that contributes to inflammation and is associated with macrovascular coronary artery disease (CAD) development. Although there is a strong correlation in humans between cEAT volume and CAD severity, there remains a paucity of experimental data demonstrating a causal link of cEAT to CAD. The current study tested the hypothesis that surgical resection of cEAT attenuates inflammation and CAD progression. METHODS: Female Ossabaw miniature swine (n = 12) were fed an atherogenic diet for 8 months and randomly allocated into sham (n = 5) or adipectomy (n = 7) groups. Both groups underwent a thoracotomy, opening of the pericardial sac, and placement of radioopaque clips to mark the proximal left anterior descending artery. Adipectomy swine underwent removal of 1 to 1.5 cm2 of cEAT from the proximal artery. After sham or adipectomy, CAD severity was assessed with intravascular ultrasonography. Swine recovered for an additional 3 months on an atherogenic diet, and CAD was assessed immediately before euthanasia. Artery sections were processed for histologic and immunohistochemical analysis. RESULTS: Severity of CAD as assessed by percent stenosis was reduced in the adipectomy cohort compared with shams; however, plaque size remained unaltered, whereas larger plaque sizes developed in sham-operated swine. Adipectomy resulted in an expanded arterial diameter, similar to the Glagov phenomenon of positive outward remodeling. No differences in inflammatory marker expression were observed. CONCLUSIONS: These data indicate that cEAT resection did not alter inflammatory marker expression, but arrested CAD progression through increased positive outward remodeling and arrest of atherogenesis.
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    Fragmented ECG as a risk marker in cardiovascular diseases
    (Bentham Science, 2014-08) Jain, Rahul; Singh, Robin; Yamini, Sundermurthy; Das, Mithilesh K.; Department of Medicine, IU School of Medicine
    Various noninvasive tests for risk stratification of sudden cardiac death (SCD) were studied, mostly in the context of structural heart disease such as coronary artery disease (CAD), cardiomyopathy and heart failure but have low positive predictive value for SCD. Fragmented QRS complexes (fQRS) on a 12-lead ECG is a marker of depolarization abnormality. fQRS include presence of various morphologies of the QRS wave with or without a Q wave and includes the presence of an additional R wave (R') or notching in the nadir of the R' (fragmentation) in two contiguous leads, corresponding to a major coronary artery territory. fQRS represents conduction delay from inhomogeneous activation of the ventricles due to myocardial scar. It has a high predictive value for myocardial scar and mortality in patients CAD. fQRS also predicts arrhythmic events and mortality in patients with implantable cardioverter defibrillator. It also signifies poor prognosis in patients with nonischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and Brugada syndrome. However, fQRS is a nonspecific finding and its diagnostic prognostic should only be interpreted in the presence of pertinent clinical evidence and type of myocardial involvement (structural vs. structurally normal heart).
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    Higher usual alcohol consumption was associated with a lower 41-y mortality risk from coronary artery disease in men independent of genetic and common environmental factors: the prospective NHLBI Twin Study
    (American Society for Nutrition, 2015-07) Dai, Jun; Mukamal, Kenneth J.; Krasnow, Ruth E.; Swan, Gary E.; Reed, Terry; Department of Medical and Molecular Genetics, IU School of Medicine
    BACKGROUND: Evidence that alcohol consumption is inversely associated with long-term coronary artery disease (CAD) mortality independent of genetic and early life environmental factors is lacking. OBJECTIVE: We evaluated whether alcohol consumption was prospectively associated with CAD mortality risk independent of familial factors. DESIGN: In total, 843 male twins (396 pairs and 51 unpaired twins) aged 42-55 y (mean: 48 y) without baseline CAD reported beer, wine, and spirits consumption at baseline (1969-1973) and were followed up to 2010 in the prospective National Heart, Lung, and Blood Institute Twin Study. Data on usual alcohol consumption over the past year were collected. Outcome was time to event, where the primary event was death from CAD and secondary events were death from cardiovascular disease and all causes. HRs were estimated by using frailty survival models, both overall and within-pair. RESULTS: There were 129 CAD deaths and 219 cardiovascular deaths during 41 y of follow-up. In the whole cohort, after adjustment for caloric intake and cardiovascular disease risk factors, overall HRs per 10-g increment in alcohol intake were 0.94 (95% CI: 0.89, 0.98) for CAD and 0.97 (95% CI: 0.93, 1.00) for cardiovascular mortality. The within-pair adjusted HRs for a twin with 10-g higher daily alcohol consumption than his co-twin were 0.90 (95% CI: 0.84, 0.97) for CAD and 0.95 (95% CI: 0.90, 1.00) for cardiovascular disease mortality in the cohort pooled by zygosity, which remained similar among monozygotic twins. All 3 beverage types tended to be associated with lower CAD mortality risk within-pair to a similar degree. Alcohol consumption was not associated with total mortality risk overall or within-pair. CONCLUSION: Higher usual alcohol consumption is associated with lower CAD mortality risk, independent of germline and early life environment and adulthood experience shared among twins, supporting a possible causal role of alcohol consumption in lowering CAD death risk. This trial was registered at clinicaltrials.gov as NCT00005124.
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    The Impact of Tele-Health Education in Decreasing the Knowledge Deficit Regarding Coronary Artery Disease in a Rural Area
    (2014-04-14) Crecelius, Teela D.
    Background: The objective of this study was to evaluate if using an educational tele-health intervention will reduce the knowledge deficit by a significant amount. Methods: Using a pre-test post-test design, the study examined the effect of a brief multimedia health education curriculum on knowledge related to coronary artery disease. Specifically, each participant experienced an educational intervention consisting of a 5-minute tele-health video as well as a pamphlet explaining the pathophysiology, risk factors, and prevention of coronary artery disease. To assess change, the project included a pre- and post-survey that assessed participant knowledge related to coronary artery disease. Results: Upon determining that the data followed a normal distribution, a paired-sample t-test was performed to compare mean scores from pre- to post-test. Post-test scores (M = 6.38, SD = 1.04) were significantly greater than pre-test scores (M = 5.54, SD = 1.20), t(12) = -2.51, p = 0.03, d = 0.75.Cohen’s d indicates that participants improved their knowledge by three-fourths of a standard deviation, which, according to Cohen (1988), is classified as a medium-sized effect. Conclusion: Tele-health does significantly improve knowledge base when comparing pre-test and post-test scores. Using tele-health could potentially be a useful avenue to provide medical education to rural populations in the United States.
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    Perivascular adipose tissue and coronary vascular disease
    (Ovid Technologies Wolters Kluwer -American Heart Association, 2014-08) Owen, Meredith Kohr; Noblet, Jillian N.; Sassoon, Daniel J.; Conteh, Abass M.; Goodwill, Adam G.; Tune, Johnathan D.; Department of Cellular & Integrative Physiology, IU School of Medicine
    Coronary perivascular adipose tissue is a naturally occurring adipose tissue depot that normally surrounds the major coronary arteries on the surface of the heart. Although originally thought to promote vascular health and integrity, there is a growing body of evidence to support that coronary perivascular adipose tissue displays a distinct phenotype relative to other adipose depots and is capable of producing local factors with the potential to augment coronary vascular tone, inflammation, and the initiation and progression of coronary artery disease. The purpose of the present review is to outline previous findings about the cardiovascular effects of coronary perivascular adipose tissue and the potential mechanisms by which adipose-derived factors may influence coronary vascular function and the progression of atherogenesis.