John A Rumberger

The Ohio State University, Columbus, Ohio, United States

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Publications (204)1514.52 Total impact

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    Malkanthi Evans · William V Judy · Dale Wilson · John A Rumberger · Najla Guthrie ·
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    ABSTRACT: This study investigated the efficacy of Diabetinol(®) in people with diabetes on medication but not meeting the American Association of Clinical Endocrinologists and American Diabetes Association glycemic, blood pressure, and lipid targets. Fifty subjects, aged 18-75 years, with fasting blood glucose ≤15.4 mmol/L, hemoglobin A1c levels ≤12%, and a body mass index between 25 and 40 kg/m(2), were enrolled in a 24-week, randomized, double-blind, placebo-controlled, parallel study. Diabetinol(®) or placebo was administered as 2×525 mg capsules/day. In the Diabetinol(®) group, 14.3% versus 0% in the placebo group, 33.3% versus 15.4% in placebo, 20.0% versus 12.5% in placebo, and 83.3% versus 60% in placebo achieved the American Association of Clinical Endocrinologists and American Diabetes Association targets for hemoglobin A1c, low-density lipoprotein, total cholesterol, and systolic blood pressure, respectively. There was no difference in the maximum concentration (Cmax) of serum glucose or area under the curve (AUC)0-240 minutes. The time to Cmax was longer for participants on Diabetinol(®) than placebo group at week 12 (P=0.01). Fasting blood glucose increased from baseline to week 24 in both groups; however, this increase was 14.3 mg/dL lower in the Diabetinol(®) group versus placebo. The Diabetinol(®) group showed an increase of 5.53 mg/dL in fasting insulin at week 12 (P=0.09) and 3.2 mg/dL at week 24 (P=0.41) over and above the placebo group. A decrease of 1.5% in total cholesterol, 5.8% in low-density lipoprotein, and a 1.6% increase in high-density lipoprotein concentrations were seen in the Diabetinol(®) group. Diabetinol(®) improved 6-month oral glucose tolerance test and 2-hour postprandial glucose profiles in participants between 40 and 60 years of age. The current study suggests a role for Diabetinol(®) as an adjunctive therapy for glycemic maintenance and for decreasing the risk of diabetes-associated comorbidities in type 2 diabetic patients on conventional therapies.
    Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 06/2015; 8:275-86. DOI:10.2147/DMSO.S79450
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    ABSTRACT: Although the traditional Agatston coronary artery calcium (CAC) score is a powerful predictor of mortality, it is unknown if the regional distribution of CAC further improves cardiovascular risk prediction. We retrospectively studied 23,058 patients referred for Agatston CAC scoring, of whom 61% had CAC (n = 14,084). CAC distribution was defined as the number of vessels with CAC (0 to 4, including left main). For multivessel CAC, "diffuse" CAC was defined by decreasing percentage of CAC in the single most affected vessel and by ≤75% total Agatston CAC score in the most calcified vessel. All-cause mortality was ascertained through the social security death index. The mean age was 55 ± 11 years, with 69% men. There were 584 deaths (2.5%) over 6.6 ± 1.7 years. Considerable heterogeneity existed between the Agatston CAC score group and the number of vessels with CAC. In each CAC group, increasing number of vessels with CAC was associated with an increased mortality rate. After adjusting for age, gender, Agatston CAC score, and cardiovascular risk factors, increasing number of vessels with CAC was associated with higher mortality risk compared with single-vessel CAC (2-vessel: HR 1.61 [95% CI 1.14 to 2.25], 3-vessel: 1.99 [1.44 to 2.77], and 4-vessel: 2.22 [1.53 to 3.23]). "Diffuse" CAC was associated with a higher mortality rate in the CAC 101 to 400 and >400 groups. Left main CAC was associated with increased mortality risk. In conclusion, increasing number of vessels with CAC and left main CAC predict increased all-cause mortality and improve the prognostic power of the traditional Agatston CAC score. Copyright © 2015 Elsevier Inc. All rights reserved.
    The American Journal of Cardiology 02/2015; 115(9). DOI:10.1016/j.amjcard.2015.01.555 · 3.28 Impact Factor
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    ABSTRACT: Risk assessment in the extensive calcified plaque phenotype has been limited by small sample size. We studied all-cause mortality rates among asymptomatic patients with markedly elevated Agatston scores > 1000. We studied a clinical cohort of 44,052 asymptomatic patients referred for coronary calcium scans. Mean follow-up was 5.6 years (range, 1-13 years). All-cause mortality rates were calculated after stratifying by Agatston score (0, 1-1000, 1001-1500, 1500-2000, and >2000). A multivariable Cox regression model adjusting for self-reported traditional risk factors was created to assess the relative mortality hazard of Agatston scores 1001 to 1500, 1501 to 2000, and >2000. With the use of post-estimation modeling, we assessed for the presence of an upper threshold of risk with high Agatston scores. A total of 1593 patients (4% of total population) had Agatston score > 1000. There was a continuous graded decrease in estimated 10-year survival across increasing Agatston score, continuing when Agatston score > 1000 (Agatston score 1001-1500, 78%; Agatston score 1501-2000, 74%; Agatston score > 2000, 51%). After multivariable adjustment, Agatston scores 1001 to 1500, 1501 to 2000, and >2000 were associated with an 8.05-, 7.45-, and 13.26-fold greater mortality risk, respectively, than for Agatston score of 0. Compared with Agatston score 1001 to 1500, Agatston score 1501 to 2000 had a similar all-cause mortality risk, whereas Agatston score > 2000 had an increased relative risk (Agatston score 1501-2000: hazard ratio [HR], 1.01 [95% CI, 0.67-1.51]; Agatston score > 2000: HR, 1.79 [95% CI, 1.30-2.46]). Graphical assessment of the predicted survival model suggests no upper threshold for risk associated with calcified plaque in coronary arteries. Increasing calcified plaque in coronary arteries continues to predict a graded decrease in survival among patients with extensive Agatston score > 1000 with no apparent upper threshold.
    Journal of cardiovascular computed tomography 03/2014; 8(1):26-32. DOI:10.1016/j.jcct.2013.12.002 · 2.29 Impact Factor
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    ABSTRACT: High serum concentration of low-density lipoprotein cholesterol (LDL-C) is a major risk factor for coronary heart disease. The efficacy of pantethine treatment on cardiovascular risk markers was investigated in a randomized, triple-blinded, placebo-controlled study, in a low to moderate cardiovascular disease (CVD) risk North American population eligible for statin therapy, using the National Cholesterol Education Program (NCEP) guidelines. A total of 32 subjects were randomized to pantethine (600 mg/day from weeks 1 to 8 and 900 mg/day from weeks 9 to16) or placebo. Compared with placebo, the participants on pantethine showed a significant decrease in total cholesterol at 16 weeks (P=0.040) and LDL-C at 8 and 16 weeks (P=0.020 and P=0.006, respectively), and decreasing trends in non-high-density lipoprotein cholesterol at week 8 and week 12 (P=0.102 and P=0.145, respectively) that reached significance by week 16 (P=0.042). An 11% decrease in LDL-C from baseline was seen in participants on pantethine, at weeks 4, 8, 12, and 16, while participants on placebo showed a 3% increase at week 16. This decrease was significant between groups at weeks 8 (P=0.027) and 16 (P=0.010). The homocysteine levels for both groups did not change significantly from baseline to week 16. Coenzyme Q10 significantly increased from baseline to week 4 and remained elevated until week 16, in both the pantethine and placebo groups. After 16 weeks, the participants on placebo did not show significant improvement in any CVD risk end points. This study confirms that pantethine lowers cardiovascular risk markers in low to moderate CVD risk participants eligible for statins according to NCEP guidelines.
    Vascular Health and Risk Management 02/2014; 10:89-100. DOI:10.2147/VHRM.S57116
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    ABSTRACT: Objective We studied all-cause mortality rates among asymptomatic patients with markedly elevated coronary artery calcium scores (CAC) above 1000. Background Risk assessment in the extensive CAC phenotype has been limited by small sample size. Methods We studied a clinical cohort of 44,052 asymptomatic patients referred for CAC scans. Mean follow-up was 5.6 years (range 1-13). All-cause mortality rates were calculated after stratifying by CAC score group (0, 1-1000, 1001-1500, 1500-2000, and >2000). A multivariable Cox regression model adjusting for self-reported traditional risk factors was created to assess the relative mortality hazard of CAC 1001-1500, CAC 1501-2000, and CAC >2000. Using post-estimation modeling, we assessed for the presence of an upper threshold of risk with high CAC scores. Results: A total of 1593 patients (4% of total population) had CAC >1000. There was a continuous graded decrease in estimated 10-year survival across increasing CAC, continuing when CAC >1000 (CAC 1001-1500: 78%, CAC 1501-2000 74%, CAC>2000 51%). After multivariable adjustment, CAC scores >1001-1500, 1501-2000, and >2000 were associated with an 8.05, 7.45, and 13.26 fold greater mortality risk, respectively, compared to CAC=0. Compared to CAC 1001-1500, CAC 1501-2000 had a similar all-cause mortality risk while CAC>2000 demonstrated an increased relative risk [CAC 1501-2000: HR 1.01 (95% CI 0.67-1.51), CAC>2000: HR 1.79 (95% CI 1.30-2.46)]. Graphical assessment of the predicted survival model suggests no upper threshold for risk associated with CAC. Conclusion Increasing CAC continues to predict a graded decrease is survival among patients with extensive CAC >1000 with no apparent upper threshold.
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    John A Rumberger ·

    JACC. Cardiovascular imaging 10/2012; 5(10):1000-2. DOI:10.1016/j.jcmg.2012.08.004 · 7.19 Impact Factor
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    ABSTRACT: The aim of this study was to further explore the interplay between smoking status, coronary artery calcium (CAC), and all-cause mortality. Prior studies have not directly compared the relative prognostic impact of CAC in smokers versus nonsmokers. In particular, although a calcium score of zero (CAC = 0) is a known favorable prognostic marker, whether smokers with CAC = 0 have as good a prognosis as nonsmokers with CAC = 0 is unknown. Given that computed tomography (CT) screening for lung cancer appears effective in smokers, the relative prognostic implications of visualizing any CAC versus no CAC on such screening also deserve study. Our study cohort consisted of 44,042 asymptomatic individuals referred for noncontrast cardiac CT (age 54 ± 11 years, 54% men). Subjects were followed for a mean of 5.6 years. The primary endpoint was all-cause mortality. Approximately 14% (n = 6,020) of subjects were active smokers at enrollment. There were 901 deaths (2.05%) overall, with increased mortality in smokers versus nonsmokers (4.3% vs. 1.7%, p < 0.0001). Smoking remained a risk factor for mortality across increasing strata of CAC scores (1 to 100, 101 to 400, and >400). At each stratum of elevated CAC score, mortality in smokers was consistently higher than mortality in nonsmokers from the CAC stratum above. In multivariable analysis within these strata, we found mortality hazard ratios of 3.8 (95% confidence interval [CI]: 2.8 to 5.2), 3.5 (95% CI: 2.6 to 4.9), and 2.7 (95% CI: 2.1 to 3.5), respectively, in smokers compared with nonsmokers. However, among the 19,898 individuals with CAC = 0, the mortality hazard ratio for smokers without CAC was 3.6 (95% CI: 2.3 to 5.7), compared with nonsmokers without CAC. Smoking is a risk factor for death across the entire spectrum of subclinical coronary atherosclerosis. Smokers with any CAC had significantly higher mortality than smokers without CAC, a finding with implications for smokers undergoing lung cancer CT-based screening. However, the absence of CAC might not be as useful a "negative risk factor" in active smokers, because this group has mortality rates similar to nonsmokers with mild-to-moderate atherosclerosis.
    JACC. Cardiovascular imaging 10/2012; 5(10):1037-45. DOI:10.1016/j.jcmg.2012.02.017 · 7.19 Impact Factor
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    ABSTRACT: Background: Coronary artery calcium (CAC) has emerged as an important prognostic indicator for coronary heart disease risk. The purpose of this study was to assess the impact of increasing CAC burden among those with and without hypertension (HTN). Methods: The study cohort consisted of 44,052 consecutive asymptomatic individuals free of known coronary heart disease referred for electron beam computed tomography (EBT) for the assessment of subclinical atherosclerosis. Patients were followed for a mean of 5.6 ± 2.6 years (range 1-13 years). The primary endpoint for the study cohort was mortality from any cause. Results: About one third (34%) of the subjects were affected by hypertension. There were 901 deaths (2.05%) in the total study population over a mean follow-up of 5.6 ± 2.6 years (range 1-13 years). The lowest event rate was observed in those with no CAC among those without hypertension (1.6 events per 1000 person years), whereas those with CAC ≥400 and hypertension had the highest all fatality rate (9.8 per 1000 person years). Compared to a CAC score of 0, increasing CAC scores (1-99, 100-399, and ≥400) were associated with increases in all-cause mortality. The hazard ratio was 2.19-7.74-fold among those without HTN and 3.00-5.83 fold among those with HTN. Overall likelihood ratio chi square statistics demonstrated that the addition of CAC scores increased mortality prediction beyond traditional risk among those with hypertension. Conclusion: Addition of CAC scores contributed significantly in predicting mortality in addition to just traditional risk factors alone among those with and without hypertension.
    Atherosclerosis 09/2012; 225(2). DOI:10.1016/j.atherosclerosis.2012.08.014 · 3.99 Impact Factor
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    ABSTRACT: AimsTo determine if coronary artery calcium (CAC) scoring is independently predictive of mortality in young adults and in the elderly population and if a young person with high CAC has a higher mortality risk than an older person with less CAC.Methods and resultsWe studied a cohort of 44 052 asymptomatic patients referred for CAC scans for cardiovascular risk stratification. All-cause mortality rates (MRs) were calculated after stratifying by age groups (<45, 45-54, 55-64, 65-74, and ≥75) and CAC score (0, 1-100, 100-400, and >400). Multivariable Cox regression models were constructed to assess the independent value of CAC for predicting all-cause mortality in the <45- and ≥75-year-old age groups. The MR increased in both the <45- and ≥75-year-old age groups with an increasing CAC group. After multivariable adjustment, increasing CAC remained independently predictive of increased mortality compared with CAC = 0 [<45 age group, hazard ratio (95% confidence interval): CAC = 1-100, 2.3 (1.2-4.2); CAC = 100-400, 7.4 (3.3-16.6); CAC > 400, 34.6 (15.5-77.4); ≥75 age group: CAC = 1-100, 7.0 (2.4-20.8); CAC = 100-400, 9.2 (3.2-26.5); CAC > 400, 16.1 (5.8-45.1)]. Persons <45 years old with CAC = 100-400 and CAC > 400 had 2- and 10-fold increased MRs, respectively, compared with persons ≥75 with no CAC. Individuals ≥75 years old with CAC = 0 had a 5.6-year survival rate of 98%, similar to those in other age groups with CAC = 0 (5.6-year survival, 99%).Conclusion The value of CAC for predicting mortality extends to both elderly patients and those <45 years old. Elderly persons with no CAC have a lower MR than younger persons with high CAC.
    European Heart Journal 07/2012; 33(23). DOI:10.1093/eurheartj/ehs230 · 15.20 Impact Factor
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    ABSTRACT: Current guidelines recommend the use of coronary artery calcium (CAC) scoring for intermediate-risk patients; however, the potential role of CAC among individuals who have no risk factors (RFs) is less established. We sought to examine the relationship between the presence and burden of traditional RFs and CAC for the prediction of all-cause mortality. The study cohort consisted of 44,052 consecutive asymptomatic individuals free of known coronary heart disease referred for computed tomography for the assessment of CAC. The following RFs were considered: (1) current cigarette smoking, (2) dyslipidemia, (3) diabetes mellitus, (4) hypertension, and (5) family history of coronary heart disease. Patients were followed for a mean of 5.6 ± 2.6 years for the primary end point of all-cause mortality. Among individuals who had no RF, Cox proportional model adjusted for age and sex identified that increasing CAC scores were associated with 3.00- to 13.38-fold higher mortality risk. The lowest survival rate was observed in those with no CAC and no RF, whereas those with CAC ≥ 400 and ≥3 RFs had the highest all-cause fatality rate. Notably, individuals with no RF and CAC ≥ 400 had a substantially higher mortality rate compared with individuals with ≥3 RFs in the absence of CAC (16.89 versus 2.72 per 1000 person-years). By highlighting that individuals without RFs but elevated CAC have a substantially higher event rates than those who have multiple RFs but no CAC, these findings challenge the exclusive use of traditional risk assessment algorithms for guiding the intensity of primary prevention therapies.
    Circulation Cardiovascular Imaging 06/2012; 5(4):467-73. DOI:10.1161/CIRCIMAGING.111.964528 · 5.32 Impact Factor
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    ABSTRACT: It is unclear whether coronary artery calcium (CAC) is effective for risk stratifying patients with diabetes in whom treatment decisions are uncertain. Of 44,052 asymptomatic individuals referred for CAC testing, we studied 2,384 individuals with diabetes. Subjects were followed for a mean of 5.6 ± 2.6 years for the end point of all-cause mortality. There were 162 deaths (6.8%) in the population. CAC was a strong predictor of mortality across age-groups (age <50, 50-59, ≥60), sex, and risk factor burden (0 vs. ≥1 additional risk factor). In individuals without a clear indication for aspirin per current guidelines, CAC stratified risk, identifying patients above and below the 10% risk threshold of presumed aspirin benefit. CAC can help risk stratify individuals with diabetes and may aid in selection of patients who may benefit from therapies such as low-dose aspirin for primary prevention.
    Diabetes care 03/2012; 35(3):624-6. DOI:10.2337/dc11-1773 · 8.42 Impact Factor
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    ABSTRACT: Safety and efficacy of a biologically active derivative of vitamin B(5) (pantethine) on total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) metabolism was studied in North American subjects at conventional low to moderate cardiovascular disease (CVD) risk. A total of 120 subjects initiated a therapeutic lifestyle change (TLC) diet 4 weeks before randomization (baseline) and maintained the diet throughout a 16-week study period; at baseline, subjects were randomized in a triple-blinded manner to either pantethine (600 mg/d, baseline to week 8, and 900 mg/d, weeks 9-16) or identically labeled, nonbiologically active placebo (n = 60 per group). We hypothesized that pantethine would lower TC and low-density lipoprotein in low-CVD-risk North American subjects in a similar manner as reported in high-CVD-risk subjects studied mainly in Italy and Japan. While sustaining a TLC diet and in comparison with placebo, pantethine demonstrated significant (P < .005) and sustained reductions (from baseline to week 16) in TC (6 mg/dL, 0.16 mmol/L, 3%), LDL-C (4 mg/dL, 0.10 mmol/L, 4%), and apolipoprotein B (4 mg/dL, 0.04 g/L, 5%). Our data suggest that pantethine supplementation for 16 weeks (600 mg/d for weeks 1-8 then 900 mg/d for weeks 9-16) is safe and significantly lowers TC and LDL-C over and above the effect of TLC diet alone. Although the absolute magnitude of these effects was small in these low- to moderate-risk North Americans (4-6 mg/dL), the results are noteworthy as prior studies have shown that, for each 1 mg/dL (0.026 mmol/L) reduction in LDL-C, there is a concomitant 1% reduction in overall future CVD risk.
    Nutrition research 08/2011; 31(8):608-15. DOI:10.1016/j.nutres.2011.08.001 · 2.47 Impact Factor

  • Journal of the American College of Cardiology 04/2011; 57(14). DOI:10.1016/S0735-1097(11)60640-2 · 16.50 Impact Factor
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    ABSTRACT: Elevated low-density lipoprotein cholesterol (LDL-C) levels are a major cardiovascular disease risk factor. Genetic factors are an important determinant of LDL-C levels. To identify single nucleotide polymorphisms associated with LDL-C and subclinical coronary atherosclerosis, we performed a genome-wide association study of LDL-C in 841 asymptomatic Amish individuals aged 20 to 80 years, with replication in a second sample of 663 Amish individuals. We also performed scanning for coronary artery calcification (CAC) in 1018 of these individuals. From the initial genome-wide association study, a cluster of single nucleotide polymorphisms in the region of the apolipoprotein B-100 gene (APOB) was strongly associated with LDL-C levels (P < 10(-68)). Additional genotyping revealed the presence of R3500Q, the mutation responsible for familial defective apolipoprotein B-100, which was also strongly associated with LDL-C in the replication sample (P < 10(-36)). The R3500Q carrier frequency, previously reported to be 0.1% to 0.4% in white European individuals, was 12% in the combined sample of 1504 Amish participants, consistent with a founder effect. The mutation was also strongly associated with CAC in both samples (P < 10(-6) in both) and accounted for 26% and 7% of the variation in LDL-C levels and CAC, respectively. Compared with noncarriers, R3500Q carriers on average had LDL-C levels 58 mg/dL higher, a 4.41-fold higher odds (95% confidence interval, 2.69-7.21) of having detectable CAC, and a 9.28-fold higher odds (2.93-29.35) of having extensive CAC (CAC score ≥400). The R3500Q mutation in APOB is a major determinant of LDL-C levels and CAC in the Amish.
    Archives of internal medicine 11/2010; 170(20):1850-5. DOI:10.1001/archinternmed.2010.384 · 17.33 Impact Factor
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    ABSTRACT: Aortic valve calcium (AVC) can be quantified on the same computed tomographic scan as coronary artery calcium (CAC). Although CAC is an established predictor of cardiovascular events, limited evidence is available for an independent predictive value for AVC. We studied a cohort of 8,401 asymptomatic subjects (mean age 53 ± 10 years, 69% men), who were free of known coronary heart disease and were undergoing electron beam computed tomography for assessment of subclinical atherosclerosis. The patients were followed for a median of 5 years (range 1 to 7) for the occurrence of mortality from any cause. Multivariate Cox regression models were developed to predict all-cause mortality according to the presence of AVC. A total of 517 patients (6%) had AVC on electron beam computed tomography. During follow-up, 124 patients died (1.5%), for an overall survival rate of 96.1% and 98.7% for those with and without AVC, respectively (hazard ratio 3.39, 95% confidence interval 2.09 to 5.49). After adjustment for age, gender, hypertension, dyslipidemia, diabetes mellitus, smoking, and a family history of premature coronary heart disease, AVC remained a significant predictor of mortality (hazard ratio 1.82, 95% confidence interval 1.11 to 2.98). Likelihood ratio chi-square statistics demonstrated that the addition of AVC contributed significantly to the prediction of mortality in a model adjusted for traditional risk factors (chi-square = 5.03, p = 0.03) as well as traditional risk factors plus the presence of CAC (chi-square = 3.58, p = 0.05). In conclusion, AVC was associated with increased all-cause mortality, independent of the traditional risk factors and the presence of CAC.
    The American journal of cardiology 11/2010; 106(12):1787-91. DOI:10.1016/j.amjcard.2010.08.019 · 3.28 Impact Factor
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    John A Rumberger ·
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    ABSTRACT: The presence of mural calcification has, for decades, been recognized as a marker for atheromatous plaque in the coronary arteries and the aorta, but only in the past decade has the application of noncontrast computed tomography (CT) been shown to be a reproducible, safe, and convenient test, which now is available worldwide. However, awareness of coronary artery calcium scanning is insufficient and the practitioner must be aware of the available literature as well as understanding clinical recommendations for applications and interpretation. It is best applied in the medium/intermediate risk, asymptomatic adult regardless of ethnicity across broad age ranges for both men and women; additional prognostic information is also afforded from the calcium distribution in the coronary artery system. Additionally, information can also be derived from the same CT scan regarding heart and aorta size and assessment of the epicardial fat pad (an anatomic marker for the metabolic syndrome). Details of how this test can aid in cardiovascular risk assessment and management in adults are provided.
    Vascular Health and Risk Management 07/2010; 6(1):579-91. DOI:10.2147/VHRM.S7457
  • David A Fein · John Rumberger ·

    Journal of cardiovascular computed tomography 03/2010; 4(2):116-8. DOI:10.1016/j.jcct.2010.03.002 · 2.29 Impact Factor
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    ABSTRACT: The effect of aggressive medical therapy on quantitative coronary plaque burden is not generally known, especially in ethnic Chinese. We reasoned that Cardiac CT could conveniently quantify early coronary atherosclerosis in our patient population, and hypothesized that serial observation could differentiate the efficacy of aggressive medical therapy regarding progression and regression of the atherosclerotic process, as well as evaluating the additional impact of life-style modification and the relative effects of the application of statin therapy. We employed a standardized Cardiac CT protocol to serially scan 113 westernized Hong Kong Chinese individuals (64 men and 49 women) with Chest Pain and positive coronary risk factors. In all cases included for this serial investigation, subsequent evaluation showed no significantly-obstructive coronary disease by functional studies and angiography. After stringent risk factor modification, including aggressive statin therapy to achieve LDL-cholesterol lowering conforming to N.C.E.P. ATP III guidelines, serial CT scans were performed 1-12 years apart for changes in coronary artery calcification (CAC), using the Agatston Score (AS) for quantification. At baseline, the mean AS was 1413.6 for males (mean age 54.4 years) and 2293.3 for females (mean age 62.4 years). The average increase of AS in the entire study population was 24% per year, contrasting with 16.4% per year on strict risk factor modification plus statin therapy, as opposed to 33.2% per year for historical control patients (p < 0.001). Additionally, 20.4% of the 113 patients demonstrated decreasing calcium scores. Medical therapy also yielded a remarkably low adverse event rate during the follow-up period --- 2 deaths, 2 strokes and only 1 case requiring PCI. This study revealed that aggressive medical therapy can positively influence coronary plaque aiding in serial regression of calcium scores.
    Cardiovascular Ultrasound 03/2010; 8(1):5. DOI:10.1186/1476-7120-8-5 · 1.34 Impact Factor
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    ABSTRACT: Screening for early-stage asymptomatic cancers (e.g., breast and colon) to prevent late-stage malignancies has been widely accepted. However, although atherosclerotic cardiovascular disease (e.g., heart attack and stroke) accounts for more death and disability than all cancers combined, there are no national screening guidelines for asymptomatic (subclinical) atherosclerosis, and there is no government or healthcare-sponsored reimbursement for atherosclerosis screening. Parts I and II of this consensus statement elaborated on new discoveries in the field of atherosclerosis that led to the concept of the vulnerable patient. These landmark discoveries, along with the new diagnostic and therapeutic options, have set the stage for the next step: translation of this knowledge into a new practice of preventive cardiology. The identification and the treatment of the vulnerable patient are the focus of this consensus statement. In this report, the Screening for Heart Attack Prevention and Education (SHAPE) Task Force presents a new practice guideline for cardiovascular screening in the asymptomatic at-risk population. In summary, the SHAPE Guideline calls for noninvasive screening of all asymptomatic men 45–75 years of age and asymptomatic women 55–75 years of age (except those defined as very low risk) to detect and treat those with subclinical atherosclerosis. A variety of screening tests are available, and the cost effectiveness of their use in a comprehensive strategy must be validated. Some of these screening tests, such as measurement of coronary artery calcification (CAC) by computed tomography (CT) scanning and carotid artery intima-media thickness and plaque by ultrasonography, have been available longer than others and are capable of providing direct evidence for the presence and extent of atherosclerosis. Both these imaging methods provide prognostic information of proven value regarding the future risk of heart attack and stroke. Careful and responsible implementation of these tests as part of a comprehensive risk assessment and reduction approach is warranted and outlined by this report. Other tests for the detection of atherosclerosis and abnormal arterial structure and function, such as magnetic resonance imaging (MRI) of the great arteries, studies of small and large artery stiffness, and assessment of systemic endothelial dysfunction, are emerging and need to be further validated. The screening results (severity of subclinical arterial disease) combined with risk factor assessment are used for risk stratification to identify the vulnerable patient and secure appropriate therapy. The higher the risk, the more vulnerable an individual is to a near-term adverse event. Since less than 10% of the population who test positive for atherosclerosis will experience a near-term event, additional risk stratification based on reliable markers of disease activity is needed and is expected to further focus the search for the vulnerable patient in the future. All individuals with asymptomatic atherosclerosis should be counseled and treated to prevent progression to overt clinical disease. The aggressiveness of the treatment should be proportional to the level of risk. Individuals with no evidence of subclinical disease may be reassured of the low risk of a future near-term event, yet encouraged to adhere to a healthy lifestyle and maintain appropriate risk factor levels. Early heart attack care education is urged for all individuals with a positive test for atherosclerosis. The SHAPE Task Force reinforces existing guidelines for the screening and treatment of risk factors in younger populations. Cardiovascular healthcare professionals and policymakers are urged to adopt the SHAPE proposal and its attendant cost effectiveness as a new strategy to contain the epidemic of atherosclerotic cardiovascular disease and the rising cost of therapies associated with this epidemic. Key wordsCardiovascular Screening-Atherosclerosis-Asymptomatic Atherosclerosis-Subclinical Atherosclerosis-Noninvasive Imaging-Coronary Artery Calcium Score-Carotid Intima Media Thickness-CAC-IMT-Vascular Function-Primary Prevention-Vulnerable Plaque-Vulnerable Patient-Acute Coronary Syndromes-Sudden Cardiac Death-Preventive Cardiology
    12/2009: pages 517-535;
  • John A. Rumberger ·
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    ABSTRACT: Cardiac CT began with electron beam CT in the early 1980s and continues now with multidetector CT in the twenty-first century. The major applications of noncontrast cardiac CT are currently for the quantification of coronary artery calcium – a reliable and repeatable means to estimate atherosclerotic plaque burden. The major applications of contrast-enhanced CT (CT angiography) is for more detailed estimation of total plaque burden by qualitatively defining “noncalcified” and complex plaque as well as ruling out obstructive coronary artery disease. Both of these applications are discussed, along with historical perspectives, in this review. Key wordsAtherosclerotic Plaque-Coronary Angiography-Coronary Artery-Coronary Calcification-Electron beam CT (EBT)-Multidetector CT (MDCT)
    Asymptomatic Atherosclerosis, 12/2009: pages 335-349;

Publication Stats

13k Citations
1,514.52 Total Impact Points


  • 2000-2009
    • The Ohio State University
      • • Division of Cardiology
      • • Division of Medical Oncology
      • • Department of Internal Medicine
      Columbus, Ohio, United States
  • 2008
    • University of Maryland, Baltimore
      • Division of Endocrinology, Diabetes and Nutrition
      Baltimore, MD, United States
  • 2004-2007
    • Johns Hopkins University
      • • Department of Medicine
      • • Division of Cardiology
      Baltimore, MD, United States
    • Johns Hopkins Medicine
      Baltimore, Maryland, United States
  • 2004-2006
    • George Washington University
      Washington, Washington, D.C., United States
  • 2003
    • Harbor-UCLA Medical Center
      Torrance, California, United States
  • 1989-2001
    • Mayo Clinic - Rochester
      • Department of Cardiovascular Diseases
      Rochester, Minnesota, United States
  • 1998
    • University of Minnesota Rochester
      Рочестер, Minnesota, United States
  • 1995
    • University of Michigan
      • Department of Epidemiology
      Ann Arbor, Michigan, United States
  • 1992
    • Medical College of Wisconsin
      • Division of Cardiology
      Milwaukee, Wisconsin, United States
  • 1988
    • University of Wisconsin - Milwaukee
      Milwaukee, Wisconsin, United States
  • 1987
    • University of Iowa Children's Hospital
      Iowa City, Iowa, United States