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Coronary Artery Disease: HELP
Articles by Karina W. Davidson
Based on 5 articles published since 2008

Between 2008 and 2019, Karina W. Davidson wrote the following 5 articles about Coronary Artery Disease.
+ Citations + Abstracts
1 Guideline Risk Assessment for Cardiovascular Disease With Nontraditional Risk Factors: US Preventive Services Task Force Recommendation Statement. 2018

Anonymous2681075 / Curry, Susan J / Krist, Alex H / Owens, Douglas K / Barry, Michael J / Caughey, Aaron B / Davidson, Karina W / Doubeni, Chyke A / Epling, John W / Kemper, Alex R / Kubik, Martha / Landefeld, C Seth / Mangione, Carol M / Silverstein, Michael / Simon, Melissa A / Tseng, Chien-Wen / Wong, John B. ·University of Iowa, Iowa City. · Fairfax Family Practice Residency, Fairfax, Virginia. · Virginia Commonwealth University, Richmond. · Veterans Affairs Palo Alto Health Care System, Palo Alto, California. · Stanford University, Stanford, California. · Harvard Medical School, Boston, Massachusetts. · Oregon Health & Science University, Portland. · Columbia University, New York, New York. · University of Pennsylvania, Philadelphia. · Virginia Tech Carilion School of Medicine, Roanoke. · Nationwide Children's Hospital, Columbus, Ohio. · Temple University, Philadelphia, Pennsylvania. · University of Alabama at Birmingham. · University of California, Los Angeles. · Boston University, Boston, Massachusetts. · Northwestern University, Evanston, Illinois. · University of Hawaii, Honolulu. · Pacific Health Research and Education Institute, Honolulu, Hawaii. · Tufts University, Medford, Massachusetts. ·JAMA · Pubmed #29998297.

ABSTRACT: Importance: Cardiovascular disease (CVD) is the most common cause of death among adults in the United States. Treatment to prevent CVD events by modifying risk factors is currently informed by the Framingham Risk Score, the Pooled Cohort Equations, or similar CVD risk assessment models. If current CVD risk assessment models could be improved by adding more risk factors, treatment might be better targeted, thereby maximizing the benefits and minimizing the harms. Objective: To update the 2009 US Preventive Services Task Force (USPSTF) recommendation on using nontraditional risk factors in coronary heart disease risk assessment. Evidence Review: The USPSTF reviewed the evidence on using nontraditional risk factors in CVD risk assessment, focusing on the ankle-brachial index (ABI), high-sensitivity C-reactive protein (hsCRP) level, and coronary artery calcium (CAC) score; the health benefits and harms of CVD risk assessment and treatment guided by nontraditional risk factors combined with the Framingham Risk Score or Pooled Cohort Equations compared with using either risk assessment model alone; and whether adding nontraditional risk factors to existing CVD risk assessment models improves measures of calibration, discrimination, and risk reclassification. Findings: The USPSTF found adequate evidence that adding the ABI, hsCRP level, and CAC score to existing CVD risk assessment models results in small improvements in discrimination and risk reclassification; however, the clinical meaning of these changes is largely unknown. Evidence on adding the ABI, hsCRP level, and CAC score to the Pooled Cohort Equations is limited. The USPSTF found inadequate evidence to assess whether treatment decisions guided by the ABI, hsCRP level, or CAC score, in addition to risk factors in existing CVD risk assessment models, leads to reduced incidence of CVD events or mortality. The USPSTF found adequate evidence to conceptually bound the harms of early detection and interventions as small. The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of using the ABI, hsCRP level, or CAC score in risk assessment for CVD in asymptomatic adults to prevent CVD events. Conclusions and Recommendation: The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of adding the ABI, hsCRP level, or CAC score to traditional risk assessment for CVD in asymptomatic adults to prevent CVD events. (I statement).

2 Review The 'perfect storm' and acute coronary syndrome onset: do psychosocial factors play a role? 2013

Burg, Matthew M / Edmondson, Donald / Shimbo, Daichi / Shaffer, Jonathan / Kronish, Ian M / Whang, William / Alcántara, Carmela / Schwartz, Joseph E / Muntner, Paul / Davidson, Karina W. ·Department of Medicine, Center for Cardiovascular Behavioral Health, Columbia University, New York, NY 10032, USA. ·Prog Cardiovasc Dis · Pubmed #23621970.

ABSTRACT: The revolution in cardiac care over the past two decades, characterized by emergent revascularization, drug eluting stents, anti-platelet medications, and advanced imaging has had little impact on overall ACS recurrence, or ACS prevention. The "Perfect Storm" refers to a confluence of events and processes, including atherosclerotic plaque, coronary flow dynamics, hemostatic and fibrinolytic function, metabolic and inflammatory conditions, neurohormonal dysregulation, and environmental events that give rise to, and result in an ACS event. In this article we illustrate the limits of the traditional main effect research model, giving a brief description of the current state of knowledge regarding the development of atherosclerotic plaque and the rupturing of these plaques that defines an ACS event. We then apply the Perfect Storm conceptualization to describe a program of research concerning a psychosocial vulnerability factor that contributes to increased risk of recurrent ACS and early mortality, and that has defied our efforts to identify underlying pathophysiology and successfully mount efforts to fully mitigate this risk.

3 Article Parathyroid hormone is related to QT interval independent of serum calcium in patients with coronary artery disease. 2018

Palmeri, Nicholas O / Davidson, Karina W / Whang, William / Kronish, Ian M / Edmondson, Donald / Walker, Marcella D. ·Columbia University Medical Center, New York, NY, USA. · Mount Sinai Medical Center, New York, NY, USA. ·Ann Noninvasive Electrocardiol · Pubmed #28949082.

ABSTRACT: BACKGROUND: Elevated serum parathyroid hormone (PTH) is associated with increased risk of cardiovascular death, including sudden cardiac death, in patients with and without parathyroid disease. In small studies, PTH levels have been associated with changes in cardiac conduction and repolarization. Changes in the corrected QT interval (QTc) in particular are thought to be mediated by the effect of PTH on serum calcium. There is limited evidence to suggest PTH may affect cardiac physiology independent of its effects on serum calcium, but there is even less data linking PTH to changes in electrical conduction and repolarization independent of serum calcium. METHODS: ECG data were examined from the PULSE database-an observational cohort study designed to examine depression after acute coronary syndromes (ACS) at a single, urban American medical center. In all, 407 patients had PTH and ECG data for analysis. RESULTS: The QTc was longer in patients with elevated PTH levels compared with those without elevated PTH levels (451 ± 38.6 ms vs. 435 ± 29.8 ms; p < .001). The difference remained statistically significant after controlling for calcium, vitamin D, and estimated glomerular filtration rate (p = .007). Inclusion of left ventricular ejection fraction in the model attenuated the association (p = .054), suggesting that this finding may be partly driven by changes in cardiac structure. CONCLUSIONS: In one of the largest series to examine PTH, calcium, and QT changes, we found that elevated PTH is associated with longer corrected QT interval independent of serum calcium concentration in ACS survivors.

4 Article Differential Association of Psychosocial Comorbidities With Subclinical Atherosclerosis in Rheumatoid Arthritis. 2015

Liu, Ying L / Szklo, Moyses / Davidson, Karina W / Bathon, Joan M / Giles, Jon T. ·College of Physicians and Surgeons, Columbia University, New York, New York. · Johns Hopkins School of Public Health, Baltimore, Maryland. ·Arthritis Care Res (Hoboken) · Pubmed #26274015.

ABSTRACT: OBJECTIVE: Rheumatoid arthritis (RA) is associated with an elevated risk of cardiovascular disease (CVD) events and subclinical atherosclerosis, but the reasons for the excess risk are unclear. We explored whether psychosocial comorbidities, which may be associated with CVD in the general population, are differentially associated with subclinical atherosclerosis in RA compared to controls. METHODS: Data were from a longitudinal cohort study of 195 RA patients and 1,073 non-RA controls. Using validated scales, heterogeneity in the associations of psychosocial measures (depression, stress, anxiety/anger, support, discrimination/hassles) with measures of subclinical atherosclerosis (coronary artery calcium [CAC] and carotid intima-media thickness [IMT]/plaque) were compared in RA and non-RA groups using multivariable generalized linear models. Computed tomography and ultrasound were used to identify CAC and IMT/plaque, respectively. CAC >100 units was used to define moderate/severe CAC. RESULTS: In RA, per-unit higher anxiety scores (odds ratio [OR] 1.10, P = 0.029), anger scores (OR 1.14, P = 0.037), depressive symptoms (OR 3.41, P = 0.032), and caregiver stress (OR 2.86, P = 0.014) were associated with increased odds of CAC >100 units after adjustment for relevant covariates. These findings persisted despite adjustment for markers of inflammation (C-reactive protein and interleukin-6 levels) and were seen only in RA, not in controls (adjusted multiplicative interaction P = 0.001-0.077). In RA, job stress was associated with an increased risk of carotid plaque (adjusted OR = 3.21, P = 0.019), and increasing social support was associated with lower internal carotid IMT (adjusted P = 0.024). CONCLUSION: Depressive symptoms, stress, anger/anxiety, and social support may preferentially affect CVD risk in RA, and screening/treatment for psychosocial morbidities in RA may help ameliorate the additional CVD burden.

5 Minor Antidepressant use is associated with reduced myocardial mIBG uptake in CAD patients. 2015

Peacock, James / Whang, William / Burg, Matthew / Onyeji, Ifeanyi / Davidson, Karina W / Bokhari, Sabahat. ·622 West 168th Street, PH 9-309, New York, NY 10032, United States. Electronic address: JP2341@cumc.columbia.edu. · 622 West 168th Street, PH 9-309, New York, NY 10032, United States. ·Int J Cardiol · Pubmed #26301662.

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