W Gregory Hundley

Wake Forest School of Medicine, Winston-Salem, North Carolina, United States

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Publications (184)1248.92 Total impact

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    ABSTRACT: Background Abnormal resting arterial stiffness is present in middle‐aged and elderly persons with abnormalities of fasting glucose (diabetes or impaired fasting glucose) and is associated with exercise intolerance. We sought to determine whether these same persons exhibited stress‐related abnormalities of arterial stiffness. Methods and Results We analyzed dobutamine magnetic resonance stress imaging results from 373 consecutively recruited persons aged 55 to 85 years with normal fasting glucose, impaired fasting glucose, or diabetes who were at risk for but without symptomatic heart failure. Personnel blinded to participant identifiers measured arterial stiffness (brachial pulse pressure/left ventricular stroke volume indexed to body surface area, the aortic elastance index [brachial end‐systolic pressure/left ventricular stroke volume indexed to body surface area], and thoracic aortic distensibility) at 80% of the maximum predicted heart rate response for age. Participants averaged 69±8 years of age; 79% were white, 92% were hypertensive, and 66% were women. After accounting for hypertension, sex, coronary artery disease, smoking, medications, hypercholesterolemia, and visceral fat, we observed an effect of glycemic status for stress measures of arterial stiffness in those with diabetes and impaired fasting glucose relative to those with normal fasting glucose (P=0.002, P=0.02, and P=0.003, respectively). Conclusion Middle‐ and older‐aged individuals with diabetes or impaired fasting glucose have higher stress measures of arterial stiffness than those with normal fasting glucose. These data emphasize the need for future studies with larger sample sizes to determine whether stress‐related elevations in arterial stiffness are related to exercise intolerance and future episodes of heart failure experienced by those with abnormalities of fasting glucose. Clinical Trial Registration URL: http://clinicaltrials.gov/. Unique identifier: NCT00542503.
    Journal of the American Heart Association 12/2015; 4(1). DOI:10.1161/JAHA.114.000991 · 4.31 Impact Factor
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    ABSTRACT: Dobutamine associated left ventricular (LV) wall motion analyses exhibit reduced sensitivity for detecting inducible ischemia in individuals with increased LV wall thickness. This study was performed to better understand the mechanism of this reduced sensitivity in the elderly who often manifest increased LV wall thickness and risk factors for coronary artery disease. During dobutamine cardiovascular magnetic resonance (DCMR) stress testing, we assessed rate pressure product (RPP), aortic pulse wave velocity (PWV), LV myocardial oxygen demand (pressure volume area, PVA, mass, volumes, concentricity, and the presence of wall motion abnormalities (WMA) and first pass gadolinium enhanced perfusion defects (PDs) indicative of ischemia in 278 consecutively recruited individuals aged 69 ± 8 years with pre-existing or known risk factors for coronary artery disease. Each variable was assessed independently by personnel blinded to participant identifiers and analyses of other DCMR or hemodynamic variables. Participants were 80% white, 90% hypertensive, 43% diabetic and 55% men. With dobutamine, 60% of the participants who exhibited PDs had no inducible WMA. Among these participants, myocardial oxygen demand was lower than that observed in those who had both wall motion and perfusion abnormalities suggestive of ischemia (p = 0.03). Relative to those with PDs and inducible WMAs, myocardial oxygen demand remained different in these individuals with PDs without an inducible WMA after accounting for LV afterload and contractility (p = 0.02 and 0.03 respectively), but not after accounting for either LV stress related end diastolic volume index (LV preload) or resting concentricity (p = 0.31-0.71). During dobutamine stress testing, elderly patients experience increased LV concentricity and declines in LV preload and myocardial oxygen demand, all of which are associated with an absence of inducible LV WMAs indicative of myocardial ischemia. These findings provide insight as to why dobutamine associated wall motion analyses exhibit reduced sensitivity for identifying inducible ischemia in elderly. Trial registration This study was registered with Clinicaltrials.gov (NCT00542503).
    Journal of Cardiovascular Magnetic Resonance 12/2015; 17(1). DOI:10.1186/s12968-015-0131-3 · 4.56 Impact Factor
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    ABSTRACT: Myocardial injury because of oxidative stress manifesting through reductions in left ventricular ejection fraction (LVEF) may occur after the administration of anthracycline-based chemotherapy (A-bC). We hypothesized that bilirubin, an effective endogenous antioxidant, may attenuate the reduction in LVEF that sometimes occurs after receipt of A-bC. We identified 751 consecutively treated patients with cancer who underwent a pre-A-bC LVEF measurement, exhibited a serum total bilirubin level <2 mg/dl, and then received a post-A-bC LVEF assessment because of symptomatology associated with heart failure. Analysis of variance, Tukey's Studentized range test, and chi-square tests were used to evaluate an association between bilirubin and LVEF changes. The LVEF decreased by 10.7 ± 13.7%, 8.9 ± 11.8%, and 7.7 ± 11.5% in group 1 (bilirubin at baseline ≤0.5 mg/dl), group 2 (bilirubin 0.6 to 0.8 mg/dl), and group 3 (bilirubin 0.9 to 1.9 mg/dl), respectively. More group 1 patients experienced >15% decrease in LVEF compared with those in group 3 (p = 0.039). After adjusting for age, coronary artery disease/myocardial infarction, diabetes mellitus, hematocrit, and the use of cardioactive medications, higher precancer treatment bilirubin levels and lesser total anthracycline doses were associated with LVEF preservation (p = 0.047 and 0.011, respectively). In patients treated with anthracyclines who subsequently develop symptoms associated with heart failure, pre-anthracycline treatment serum bilirubin levels inversely correlate with subsequent deterioration in post-cancer treatment LVEF. In conclusion, these results suggest that increased levels of circulating serum total bilirubin, an intrinsic antioxidant, may facilitate preservation of LVEF in patients receiving A-bC for cancer.
    The American journal of cardiology 10/2015; DOI:10.1016/j.amjcard.2015.08.042 · 3.28 Impact Factor
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    ABSTRACT: The Multi-Ethnic Study of Atherosclerosis (MESA), initiated in July 2000, is a six-center longitudinal population-based study that included 6,814 men and women at baseline study. Cardiac MRI was part of the study procedures, representing the first large-scale application of cardiac MRI in a multi-center and multi-ethnic population study in the USA. To date, this is the largest ever MRI study. Such effort would come with a great potential for variability due to the number of professionals involved; therefore, an intensive quality control process was implemented since the very beginning. A workflow for process control was used to match image protocols in different types of MRI scanners, transfer images to the reading center, train technicians, and implement image quality scorecards. This article reviews the influence of research management for quality control and work standardization processes in cardiac magnetic MRI results at the 10th year of follow-up in MESA.
    Current Cardiovascular Imaging Reports 05/2015; 8(5). DOI:10.1007/s12410-015-9329-x
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    ABSTRACT: Visceral fat (VF) is a source of pro-inflammatory adipokines implicated in cardiac remodeling. We sought to determine the impact of visceral fat and subcutaneous fat (SQ) depots on left ventricular (LV) structure, function, and geometry in the Multi-Ethnic Study of Atherosclerosis (MESA). We performed a post-hoc analysis on 1151 participants from MESA with cardiac magnetic resonance quantification of LV mass and LV mass-to-volume ratio (LVMV, an index of concentricity) and computed tomographic-derived SQ and VF area. Multivariable regression models to estimate association between height-indexed SQ and VF area (per cm(2)/m) with height-indexed LV mass (per height(2.7)) and LVMV were constructed, adjusted for clinical, biochemical, and demographic covariates. We found that both VF and SQ area were associated with height-indexed LV mass (ρ = 0.36 and 0.12, P < 0.0001, respectively), while only VF area was associated with LVMV (ρ = 0.28, P < 0.0001). Individuals with above-median VF had lower LV ejection fraction, greater indexed LV volumes and mass, and higher LVMV (all P < 0.001). In multivariable models adjusted for weight, VF (but not SQ) area was associated with LV concentricity and LV mass index, across both sexes. Visceral adiposity is independently associated with LV concentricity, a precursor to heart failure. Further study into the role of VF in LV remodeling as a potential therapeutic target is warranted. Copyright © 2015 Elsevier B.V. All rights reserved.
    Nutrition Metabolism and Cardiovascular Diseases 04/2015; 25(7). DOI:10.1016/j.numecd.2015.03.016 · 3.32 Impact Factor
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    ABSTRACT: The study was performed to determine age, sex, and time-dependent changes in aortic wall thickness (AWT) and to evaluate cross-sectional associations between AWT and arterial stiffness in older adults. Three hundred seventy-one longitudinal and 426 cross-sectional measurements of AWT from cardiovascular magnetic resonance imaging studies conducted within the Multi-Ethnic Study of Atherosclerosis were analyzed at 2 points in time, in 2000 to 2002 and then again from follow-up examinations in 2010 to 2012. Aortic wall thickness was determined from a double inversion recovery black-blood fast spin-echo sequence, and aortic stiffness was measured from a phase-contrast cine gradient echo sequence. The thickness of the midthoracic descending aortic wall was measured and correlated to distensibility of the ascending aorta and aortic pulse wave velocity. The average rate of AWT change was 0.032 mm/y. The increase in AWT was greater for those aged 45 to 54 years relative to individuals older than 55 years (P trend<0.001). Ascending aortic distensibility was lower (P<0.001) and pulse wave velocity was higher (P=0.012) for hypertensive subjects. After adjustment for traditional risk factors, distensibility of the ascending aorta was significantly related to AWT in participants without hypertension. Hypertension was associated with increased aortic stiffness independent of aortic wall thickness. © 2015 American Heart Association, Inc.
    Hypertension 03/2015; 65(5). DOI:10.1161/HYPERTENSIONAHA.114.05080 · 6.48 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(17). DOI:10.1016/j.jacc.2015.03.022 · 16.50 Impact Factor
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    ABSTRACT: We sought to assess the impact of smoking status, cumulative pack-years, and time since cessation (the latter in former smokers only) on 3 important domains of cardiovascular disease: inflammation, vascular dynamics and function, and subclinical atherosclerosis. The Multi-Ethnic Study of Atherosclerosis (MESA) cohort enrolled 6814 adults without prior cardiovascular disease. Smoking variables were determined by self-report and confirmed with urinary cotinine. We examined cross-sectional associations between smoking parameters and (1) inflammatory biomarkers (high-sensitivity C-reactive protein [hsCRP], interleukin-6, and fibrinogen); (2) vascular dynamics and function (brachial flow-mediated dilation and carotid distensibility by ultrasound, as well as aortic distensibility by MRI); and (3) subclinical atherosclerosis (coronary artery calcification, carotid intima-media thickness, and ankle-brachial index). We identified 3218 never smokers, 2607 former smokers, and 971 current smokers. Mean age was 62 years and 47% were male. There was no consistent association between smoking and vascular distensibility or flow-mediated dilation outcomes. In contrast, compared with never smokers, the adjusted association between current smoking and measures of either inflammation or subclinical atherosclerosis was consistently stronger than for former smoking (eg, odds ratio for hsCRP>2 mg/L of 1.7 [95% confidence interval, 1.5-2.1] versus 1.2 [1.1-1.4], odds ratio for coronary artery calcification>0 of 1.8 [1.5-2.1] versus 1.4 [1.2-1.6], respectively). Similar associations were seen for interleukin-6, fibrinogen, carotid intima-media thickness, and ankle-brachial index. A monotonic relationship was also found between increasing pack-years exposure and elevated inflammatory markers. Furthermore, current smokers with hsCRP>2 mg/L were more likely to have increased carotid intima-media thickness, abnormal ankle-brachial index, and coronary artery calcification>75th percentile for age, sex, and race (relative to smokers with hsCRP<2 mg/L, interaction P<0.05 for all 3 outcomes). In contrast, time since quitting in former smokers was independently associated with lower inflammation and atherosclerosis (eg, odds ratio for hsCRP>2 mg/L of 0.91 [0.88-0.95] and odds ratio for coronary artery calcification>0 of 0.94 [0.90-0.97] for every 5-year cessation interval). These findings expand our understanding of the harmful effects of smoking and help explain the cardiovascular benefits of smoking cessation. © 2015 American Heart Association, Inc.
    Arteriosclerosis Thrombosis and Vascular Biology 03/2015; 35(4). DOI:10.1161/ATVBAHA.114.304960 · 6.00 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A1089. DOI:10.1016/S0735-1097(15)61089-0 · 16.50 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A1075. DOI:10.1016/S0735-1097(15)61075-0 · 16.50 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A1081. DOI:10.1016/S0735-1097(15)61081-6 · 16.50 Impact Factor
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    ABSTRACT: To examine the contemporary effect of smoking in a multiethnic sample, and to explore the respective contributions of inflammation and subclinical atherosclerosis to the cardiovascular consequences of smoking. We studied 6814 participants free of cardiovascular disease and coronary heart disease (CHD) from Multiethnic Study of Atherosclerosis. Smoking status and cumulative exposure were determined by self-report and confirmed by urinary cotinine. Multivariable Cox regression was used to estimate the association between smoking parameters and all-cause cardiovascular disease, all-cause CHD, and hard CHD events. We further adjusted for high-sensitivity C-reactive protein and coronary artery calcium (CAC) in hierarchical Cox models. We identified 3218 never smokers, 2607 former smokers, and 971 current smokers. Median follow-up was 10.2 years. Compared with never smokers, adjusted hazard ratios in current smokers were 1.7 (95% confidence interval, 1.3-2.2) for all-cause cardiovascular disease, 1.6 (1.1-2.1) for all-cause CHD, and 1.7 (1.2-2.4) for hard CHD. Similarly, among current smokers, hazard ratios were higher in the 4th versus 1st quartile of pack-years (eg, all-cause CHD hazard ratio=2.7 [1.1-6.6]). Both CAC>100 and high-sensitivity C-reactive protein ≥3 mg/L identified higher relative risk among current smokers (eg, all-cause CHD hazard ratio of 3.0 [1.5-6.0, compared with CAC=0] and 2.6 [1.4-4.8, compared with high-sensitivity C-reactive protein <2 mg/L], respectively). However, CAC was a stronger mediator of events and adversely modified the effect of smoking on events (eg, P-interaction=0.02 for hard CHD). Compared with never smokers, former smokers (median cessation interval=22 years) had similar adjusted hazard for events. In this multiethnic cohort, current smoking and cumulative exposure remain important modifiable determinants of cardiovascular disease. Both high-sensitivity C-reactive protein ≥3 mg/L and, particularly, CAC>100 identified high-risk smokers who may benefit from more intensive smoking-cessation efforts. © 2015 American Heart Association, Inc.
    Arteriosclerosis Thrombosis and Vascular Biology 01/2015; 35(3). DOI:10.1161/ATVBAHA.114.304562 · 6.00 Impact Factor
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    ABSTRACT: Recent studies show an association between statin therapy and a reduced risk of heart failure among breast cancer survivors. Our goal was to evaluate whether statin therapy for prevention of cardiovascular disease (CVD) would ameliorate declines in left ventricular ejection fraction (LVEF) often observed during anthracycline-based chemotherapy (Anth-bC).Methods In 51 participants (33 women and 18 men; aged 48±2 years), we performed CV magnetic resonance (CMR) measurements of LVEF before and 6 months after initiation of Anth-bC for patients with breast cancer, leukemia, or lymphoma. Fourteen individuals received statin therapy, and 37 received no statin. MR image analysts were blinded to participant identifiers.ResultsThose receiving statins were older and often had diabetes (DM), hypertension (HTN), and hyperlipidemia (HLD). For those receiving statins, LVEF was 56.6±1.4% at baseline and 54.1±1.3% 6 months after initiating anthracycline (p=0.15). For those not receiving a statin, LVEF was 57.5±1.4% at baseline and decreased to 52.4±1.2% over a similar 6 month interval (p=0.0003). In a multivariable model accounting for age, sex, DM, HTN, HLD, and cumulative amount of anthracycline received, LVEF remained unchanged in participants receiving a statin (+ 1.1±2.6%) versus a -6.5±1.5% decline among those not receiving a statin (p=0.03).Conclusion In conclusion, these data highlight that individuals receiving statin therapy for prevention of CVD may experience less deterioration in LVEF upon early receipt of Anth-bC than individuals not receiving a statin. Further studies with large numbers of participants are warranted to determine if statins protect against LVEF decline in patients receiving Anth-bC.
    The Canadian journal of cardiology 11/2014; 31(3). DOI:10.1016/j.cjca.2014.11.020 · 3.94 Impact Factor
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    ABSTRACT: The assessment of right ventricular (RV) perfusion defects has remained challenging during vasodilator stress perfusion with cardiovascular magnetic resonance (CMR). The significance of RV signal abnormalities during vasodilator stress perfusion and late gadolinium-enhanced CMR is yet uncertain. Among 61 individuals who underwent adenosine CMR stress testing before cardiac catheterization, we assessed the severity of coronary artery stenoses, mortality, the presence of stress and rest perfusion defects, as well as the presence of late gadolinium enhancement (LGE). Right ventricular stress-induced perfusion defects were positively associated with left anterior descending artery and proximal right coronary artery stenoses but were negatively associated with left circumflex artery stenoses. The presence of RVLGE was associated with mortality, but 77% of those with RVLGE also had left ventricular LGE. Proximal right coronary artery and left anterior descending artery stenoses are positively associated, whereas left circumflex artery stenoses are negatively associated with RV stress-induced perfusion defects. Right ventricular LGE was associated with mortality, but further study is needed to determine whether this is independent of left ventricular LGE.
    Journal of Cardiovascular Magnetic Resonance 11/2014; 16(Suppl 1). DOI:10.1097/RCT.0000000000000175 · 4.56 Impact Factor
  • R Brandon Stacey · Augustus J Caine · W Gregory Hundley
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    ABSTRACT: Left ventricular (LV) noncompaction cardiomyopathy (LVNC) is a form of cardiomyopathy in which trabeculations fail to "compact" with the left ventricular endocardium during fetal cardiac development and is classically associated with subsequent impairment of LV function, significant mortality, ventricular dysrhythmias, and embolic phenomena. As awareness and medical imaging quality have improved, it is becoming easier to identify trabeculations that traverse the LV cavity and serve as a distinguishing feature of this disorder. Differentiating true noncompaction from mild increases in trabeculations requires prudent imaging and clinical correlation. This review seeks to discuss the potential methods of evaluating left ventricular trabeculations, the role of increased trabeculations in cardiovascular disease, and how their presence may affect clinical management.
    Current Heart Failure Reports 11/2014; 12(1). DOI:10.1007/s11897-014-0237-1
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    ABSTRACT: BACKGROUND Left ventricular (LV) trabeculation is highly variable among individuals and is increased in some diseases (e.g., congenital heart disease or cardiomyopathies), but its significance in population-representative individuals is unknown. OBJECTIVES The goal of this study was to determine if excessive LV trabeculation in population-representative individuals is associated with preceding changes in cardiac volumes and function. METHODS For technical reasons, the extent of trabeculation, which is expressed as the ratio of noncompacted to compacted (NC/C) myocardium, was measured on cardiac magnetic resonance (CMR) long-axis cine images in 2,742 participants in the MESA (Multi-Ethnic Study of Atherosclerosis) (mean age 68.7 years; 52.3% women; 56.4% with hypertension; 16.8% with diabetes) at examination 5. These were considered in quintiles of trabeculation extent; the NC/ C ratio of quintile 5 was 2.46 to 5.41. We determined the relationship between the maximal NC/C ratio and the preceding change (9.5 years between examinations 1 and 5) in end-systolic volume indexed (ESVi) to body surface area. Secondary analyses assessed the associations between the maximal NC/C ratio and preceding changes in end-diastolic volume indexed (EDVi) to body surface area and the ejection fraction (EF). RESULTS Over 9.5 years, the ESVi decreased by 1.3 ml/m2, the EDVi decreased by 5.1 ml/m2, and the EF decreased by 0.6% (p < 0.0001). Even in subjects with excessive trabeculation, there were no clinically relevant differences in LV volumes and systolic function changes among the quintiles of trabeculation extent. CONCLUSIONS Greater extent of, and even excessive, LV trabeculation measured in end-diastole in asymptomatic population-representative individuals appeared benign and was not associated with deterioration in LV volumes or function during an almost 10-year period. (J Am Coll Cardiol 2014;64:1971–80) © 2014 by the American College of Cardiology Foundation.
    Journal of the American College of Cardiology 11/2014; 64(19):1971-1980. DOI:10.1016/j.jacc.2014.08.035 · 16.50 Impact Factor
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    ABSTRACT: Background: In a murine anthracycline-related cardiotoxicity model, increases in cardiovascular magnetic resonance myocardial contrast-enhanced T1-weighted signal intensity are associated with myocellular injury and decreases with left ventricular ejection fraction. We sought to determine whether T1- and T2-weighted measures of signal intensity associate with decreases in left ventricular ejection fraction in human subjects receiving potentially cardiotoxic chemotherapy. Methods and results: In 65 individuals with breast cancer (n=51) or a hematologic malignancy (n=14), we measured left ventricular volumes, ejection fraction, and contrast-enhanced T1-weighted and T2-weighted signal intensity before and 3 months after initiating potentially cardiotoxic chemotherapy using blinded, unpaired analysis of cardiovascular magnetic resonance images. Participants were aged 51 ± 12 years, of whom 55% received an anthracycline, 38% received a monoclonal antibody, and 6% received an antimicrotubule agent. Overall, left ventricular ejection fraction decreased from 57 ± 6% to 54 ± 7% (P<0.001) because of an increase in end-systolic volume (P<0.05). T1-weighted signal intensities also increased from 14.1 ± 5.1 to 15.9 ± 6.8 (P<0.05), with baseline values trending higher among individuals who received chemotherapy before study enrollment (P=0.06). Changes in T1-weighted signal intensity did not differ within the 17 LV myocardial segments (P=0.97). Myocardial edema quantified from T2-weighted images did not change significantly after 3 months (P=0.70). Conclusions: Concordant with previous animal studies, cardiovascular magnetic resonance measures of contrast-enhanced T1-weighted signal intensity occur commensurate with small but significant left ventricular ejection fraction declines 3 months after the receipt of potentially cardiotoxic chemotherapy. These data indicate that changes in T1-weighted signal intensity may serve as an early marker of subclinical injury related to the administration of potentially cardiotoxic chemotherapy in human subjects.
    Circulation Cardiovascular Imaging 10/2014; 7(6). DOI:10.1161/CIRCIMAGING.114.002217 · 5.32 Impact Factor
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    ABSTRACT: Background: Limited data exist on the association between left ventricular (LV) dilation/remodeling and incident heart failure (HF), especially in adults without prior myocardial infarction (MI) and valvular heart disease. We assessed the association between LV dilation and remodeling and incident HF in a multiethnic cohort. Methods and results: A total of 4,974 of 6,814 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) had cardiac magnetic resonance imaging and complete data. Kaplan-Meier and Cox proportional hazard analyses were used to assess the association between LV end-diastolic diameter (LVEDD) and adjudicated HF. During the 12 years of follow-up (mean 9.4 y), 177 (3.6%) HF events occurred, 126 (71.2%) in HF with reduced ejection fraction (EF) and 51 (28.8%) in HF with preserved EF. LV dilation (LVEDD >52 mm or >95th percentile) was associated with HF in univariate (hazard ratio [HR] 1.21, 95% confidence interval [CI] 1.08-1.46; P = .007) and multivariable Cox models (HR 1.28, 95% CI 1.09-1.57; P = .01) adjusting for traditional risk factors, medication use, LV EF, and interim MI. We found a significant multiplicative interaction between LVEDD and LV EF in our full multivariable models. Participants with dilated LV and preserved EF had increased risk [HR 2.22, 95% CI 1.46-3.37; P = .006) and those with dilated LV and reduced EF had worse prognosis (HR 7.35, 95% CI 2.36-22.85; P = .0006) compared with normal-size LV and preserved EF. A high proportion of participants with LV dilation had eccentric remodeling, a risk factor for HF. Concentric hypertrophy, also a risk factor for HF, was common in the normal-size LV group. Conclusions: LV dilation predicts incident HF independently from risk factors, LV EF, and interim MI.
    Journal of Cardiac Failure 09/2014; 20(12). DOI:10.1016/j.cardfail.2014.09.002 · 3.05 Impact Factor
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    ABSTRACT: Previous case reports have described patients with left ventricular noncompaction cardiomyopathy (LVNC) with significant mitral regurgitation (MR). The study aim was to determine if LVNC is associated with MR, as assessed by cardiac magnetic resonance imaging (cMRI). LVNC, assessed with cMRI, was observed retrospectively among 122 consecutive cases, 31 of whom had an end-systolic noncompacted-to-compacted ratio (ESNCCR) ≥ 2. In addition, 40 normal subjects undergoing cMRI and 40 with moderate to severe MR were included as controls. Using cine images, the ESNCCR and left ventricular (LV) and right ventricular (RV) stroke volumes were measured. The mitral regurgitant fraction (MRF) was calculated by dividing the difference between the RV and LV stroke volumes by the LV stroke volume. The total papillary muscle (TPM) area was measured from the mid short-axis view. Adjusting for age, race, gender and body surface area, an analysis of covariance was conducted to determine whether MRF and TPM were associated with ESNCCR ≥ 2. Adjusted means were presented with 95% confidence intervals. After adjustment, the MRF in patients with ESNCCR ≥ 2 was higher than in controls, but did not differ from that in patients with significant MR (21 ± 6.5% versus 2.7 ± 12% versus 29.2 ± 11%, p = 0.039 and p = 0.3, respectively). Further, patients with ESNCCR ≥ 2 had a lower TPM than normal controls or those with moderate to severe MR (1.89 ± 0.28 cm2 versus 3.6 ± 0.26 cm2 versus 3.7 ± 0.24 cm2; p < 0.001 and p < 0.001, respectively). LVNC is associated with increased MR, as assessed using cMRI. LVNC is also associated with abnormalities in the papillary muscle anatomy, which may predispose to MR.
    The Journal of heart valve disease 09/2014; 23(5):591-7. · 0.75 Impact Factor
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    ABSTRACT: This is a case of a 48-year-old man who presented with a pulmonary embolism and was found to have left ventricular non-compaction cardiomyopathy. Initial echocardiograms demonstrated prominent apical trabeculations with reduced biventricular function. These findings were further confirmed and characterized by cardiac magnetic resonance imaging. He met all major criteria used to identify left ventricular non-compaction cardiomyopathy. He underwent medical management for heart failure and during follow-up was noted to have significant improvement in left ventricular systolic function and symptoms. While most management attention is focused on rhythm disturbances or embolic risk, particular attention should also be exercised to ensure that heart failure medical therapy is optimized. While many with left ventricular non-compaction cardiomyopathy have irreversible dysfunction, this case highlights that there may be some who will respond well to aggressive medical therapy. The diagnosis and medical management of left ventricular non-compaction cardiomyopathy are reviewed in light of our patient and his clinical course. <Learning objective: Historically, left ventricular non-compaction cardiomyopathy (LVNC) has been associated with significant morbidity and mortality. Discussion often focuses on sudden cardiac death and prevention of embolisms. Many of the initial reports and case series were written in an era when standard medical therapy for congestive heart failure was not yet defined. While many do not respond as this case did, this case emphasizes that optimal medical therapy can make a substantial difference, even for LVNC.
    Journal of Cardiology Cases 09/2014; 10(6). DOI:10.1016/j.jccase.2014.08.004

Publication Stats

5k Citations
1,248.92 Total Impact Points


  • 2001–2015
    • Wake Forest School of Medicine
      • • Department of Internal Medicine
      • • Section on Cardiology
      • • Department of Radiology
      Winston-Salem, North Carolina, United States
  • 1999–2015
    • Wake Forest University
      • • Department of Cardiology
      • • Department of Internal Medicine
      • • School of Medicine
      Winston-Salem, North Carolina, United States
  • 2009
    • Winston-Salem State University
      Winston-Salem, North Carolina, United States
  • 2008
    • University of Dallas
      Irving, Texas, United States
  • 1995–1998
    • University of Texas Southwestern Medical Center
      • Department of Internal Medicine
      Dallas, Texas, United States
  • 1995–1996
    • University of Texas at Dallas
      Richardson, Texas, United States