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Showing papers by "Ana Barac published in 2012"



Journal ArticleDOI
TL;DR: In a population with a high prevalence of obesity, MS, and diabetes, elevated CRP and fibrinogen increased HF risk, but these associations are attenuated by the adjustments for conventional risk factors suggesting that inflammation acts in concert with metabolic and clinical risk factors in increasing HF risk.
Abstract: Inflammation may play a role in increased risk of heart failure (HF) that is associated with obesity, metabolic syndrome (MS), and diabetes. This study investigated associations between inflammatory markers, MS, and incident HF in a population with a high prevalence of diabetes, obesity, and MS. The cohort consisted of 3098 American Indians without prevalent cardiovascular disease who had C-reactive protein (CRP) and fibrinogen measured at the Strong Heart Study phase II examination. Independent associations between inflammatory markers, MS, and HF were analyzed by Cox hazard models. During a mean follow-up of 11 years, 218 participants developed HF. After the adjustment for cardiovascular risk factors, fibrinogen, (hazard ratio [HR], 1.36; 95% confidence interval [CI], 1.15-1.59) but not CRP (HR, 1.25; 95% CI, 0.97-1.32) remained a significant HF predictor. In individuals without diabetes, concomitant presence of MS and elevated CRP or fibrinogen increased HF risk (for MS and CRP: HR, 2.02; 95% CI, 0.95-4.31; for CRP and fibrinogen: HR, 1.75; 95% CI, 0.83-3.72). In a population with a high prevalence of obesity, MS, and diabetes, elevated CRP and fibrinogen increased HF risk. These associations are attenuated by the adjustments for conventional risk factors suggesting that inflammation acts in concert with metabolic and clinical risk factors in increasing HF risk.

24 citations


Journal ArticleDOI
TL;DR: The genetic findings to date in the area of arterial stiffness and blood pressure in African Americans are reviewed with an emphasis on the current limitations and new efforts to move the field forward.
Abstract: The prevalence of hypertension in African Americans in the USA is among the highest in the world and increasing. The identification of genes and pathways regulating blood pressure in African Americans has been challenging. An early predictor of hypertension is arterial stiffness. The prevalence of arterial stiffness is significantly higher in African Americans compared to Caucasians. Approximately 20 % of the variance in arterial stiffness is estimated to be heritable. Identifying genes and biological pathways regulating arterial stiffness may provide insight into the genetics underlying the increased risk of hypertension in African Americans. This paper reviews the genetic findings to date in the area of arterial stiffness and blood pressure in African Americans with an emphasis on the current limitations and new efforts to move the field forward.

23 citations


Journal ArticleDOI
TL;DR: WRITING COMMITTEE MEMBERS* Thomas M. Bashore, MD, FACC, FSCAI, chair, Stephen Balter, PhD, FAAPM, FACR, FSIR, Ana Barac,MD, PhD; and Jeffrey J. Oliver-McNeil, DNP, ACNP-BC, AACC.
Abstract: WRITING COMMITTEE MEMBERS* Thomas M. Bashore, MD, FACC, FSCAI, chair, Stephen Balter, PhD, FAAPM, FACR, FSIR, Ana Barac, MD, PhD, John G. Byrne, MD, FACC, Jeffrey J. Cavendish, MD, FACC, FSCAI, Charles E. Chambers, MD, FACC, FSCAI, James Bernard Hermiller, Jr, MD, FACC, FSCAI, Scott Kinlay, MBBS, PhD, FACC, FSCAI, Joel S. Landzberg, MD, FACCk, Warren K. Laskey, MD, MPH, FACC, FSCAI, Charles R. McKay, MD, FACC, Julie M. Miller, MD, FACC, David J. Moliterno, MD, FACC, FSCAI, John W.M. Moore, MD, MPH, FACC, FSCAI, Sandra M. Oliver-McNeil, DNP, ACNP-BC, AACC, Jeffrey J. Popma, MD, FACC, FSCAI, and Carl L. Tommaso, MD, FACC, FSCAI

19 citations


Journal ArticleDOI
TL;DR: Global longitudinal and circumferential strain was assessed by echo in 15 patients after acute MI and MRI parameters including ventricular volumes, scar, and area at risk were assessed 3+/-2 days post STEMI and at 30 day follow up.
Abstract: Summary Global longitudinal and circumferential strain was assessed by echo in 15 patients after acute MI. MRI parameters including ventricular volumes, scar, and area at risk were assessed 3+/-2 days post STEMI and at 30 day follow up. Echo strain measures correlated most strongly with LVEF (r=0.81 and 0.88 longitudinal ad circumferential strain, p<0.0001) and infarct size (r=-0.68 and r=-0.69, p<0.001). There were moderate correlations between longitudinal strain and change in LVEDV (r=0.61, p<0.05). Background Cardiac MR (CMR) is a powerful tool in the evaluation myocardial scar and volumes. Speckle tracking by echo is used to evaluate myocardial strain. The correlation between strain measures and MR measures of scar is not well defined. Hypothesis CMR parameters, area at risk (AAR), infarct size (IS), and salvage area (SA), correlate with global echo strain in patients with a ST elevation MI (STEMI). Methods Contrast enhanced(CE) CMR and 2-D echocardiography imaging were performed in patients within 3+/-2 days post STEMI. CMR-derived IS was measured from the late CE images and AAR was measured from T2 black blood images. SA was calculated as AAR/IS. Global longitudinal (LS) and circumferential (CS) strain were assessed from standard apical (16 segment model for LS) or midventricular short axis views using 2-D speckle-tracking software (2D CPA, TomTec, Germany). Results 15 patients with STEMI completed the protocol. Age was 50.8+/-12.6 years (86.7% male). Baseline LVEDV was 203.4 +/- 51.7ml and EF was 51.1% +/- 14.7% with follow up LVEDV 219.9 +/- 72.2ml (p=0.15) and EF 50.8% +/- 13.8% (p=0.8). Average IS was 16.4+/-10.4%, AAR was 23.4+/-12.2%, and SA was 7.0+/-5.7% at baseline. Baseline LS was -13.5 +/- 4.1 and CS was -19.4 +/6.3. Global longitudinal strain was associated with peak troponin I levels (r=-0.74, P<0.001). Correlating LS and CS to baseline MRI parameters showed a strong correlation to LVEF (r=0.81 and 0.88 respectively, p<0.0001) and IS (r=-0.68 and r=-0.69, p<0.001). There was moderate correlation of LS and CS to LVEDV (r=-0.55 and -0.57), p<0.05) and AAR (r=-0.61 and r=-0.57, p<0.05). There was no correlation between strain and SA. There were modest correlations between initial LS and change in LVEDV but not with CS and change in LVEDV (r=0.61, p<0.05 and r=-0.48, p=0.07). Conclusions Echo strain measurements correlated most strongly with LVEF and IS. There were modest associations between strain at baseline and early LV remodeling. Funding None.

1 citations