Thomas Budde

Psychological and quality-of-life outcomes from a comprehensive stress reduction and lifestyle program in patients with coronary artery disease: results of a randomized trial.

Background: Stress reduction and comprehensive lifestyle modification programs have improved atherosclerosis and cardiac risk factors in earlier trials. Little is known about the impact of such programs on quality-of-life (QoL) and psychological outcomes. Given recent significant improvements in cardiac care, we evaluated the current benefit of stress reduction/lifestyle modification on QoL and emotional distress in patients with coronary artery disease (CAD). Methods: 101 patients (59.4 ± 8.6 years, 23 female) with CAD were randomized to a 1-year lifestyle/stress management program (n = 48) or written advice (n = 53). QoL and psychological outcomes were assessed with the SF-36, Beck Depression, Spielberger State/Trait Anxiety, Spielberger State/Trait Anger and Perceived Stress Inventories. Group repeated-measures analyses of variance were performed for all measures. Results: Adherence to the program was excellent (daily relaxation practice 39 ± 5vs. 5 ± 8 min, respectively; p < 0.001). Both groups improved comparably in most dimensions of QoL, and significantly greater improvements for the lifestyle group were found for physical function and physical sum score (p = 0.046 and p = 0.045). Depression, anxiety, anger and perceived stress were reduced similarly in both groups. However, intervention × gender interaction effects revealed greater benefits among women in the lifestyle intervention vs. advice group for depression and anger (p = 0.025 and p = 0.040), but no effects for men. Conclusions: A comprehensive lifestyle modification and stress management program did not improve psychological outcomes in medically stable CAD patients. The program did appear to confer psychological benefits for women but not men. Further trials should investigate gender-related differences in coronary patient responses to behavioral interventions.

Progression of coronary artery calcification seems to be inevitable, but predictable - results of the Heinz Nixdorf Recall (HNR) study

Aim Coronary artery calcification (CAC), as a sign of atherosclerosis, can be detected and progression quantified using computed tomography (CT). We develop a tool for predicting CAC progression. Methods and results In 3481 participants (45–74 years, 53.1% women) CAC percentiles at baseline (CACb) and after five years (CAC5y) were evaluated, demonstrating progression along gender-specific percentiles, which showed exponentially shaped age-dependence. Using quantile regression on the log-scale (log(CACb+1)) we developed a tool to individually predict CAC5y, and compared to observed CAC5y. The difference between observed and predicted CAC5y (log-scale, mean±SD) was 0.08±1.11 and 0.06±1.29 in men and women. Agreement reached a kappa-value of 0.746 (95% confidence interval: 0.732–0.760) and concordance correlation (log-scale) of 0.886 (0.879–0.893). Explained variance of observed by predicted log(CAC5y+1) was 80.1% and 72.0% in men and women, and 81.0 and 73.6% including baseline risk factors. Evaluating the tool in 1940 individuals with CACb>0 and CACb<400 at baseline, of whom 242 (12.5%) developed CAC5y>400, yielded a sensitivity of 59.5%, specificity 96.1%, (+) and (−) predictive values of 68.3% and 94.3%. A pre-defined acceptance range around predicted CAC5y contained 68.1% of observed CAC5y; only 20% were expected by chance. Age, blood pressure, lipid-lowering medication, diabetes, and smoking contributed to progression above the acceptance range in men and, excepting age, in women. Conclusion CAC nearly inevitably progresses with limited influence of cardiovascular risk factors. This allowed the development of a mathematical tool for prediction of individual CAC progression, enabling anticipation of the age when CAC thresholds of high risk are reached.

Coronary atherosclerosis burden, but not transient troponin elevation, predicts long-term outcome in recreational marathon runners

AbstractnWe determined the prognostic value of transient increases in high-sensitive serum troponin I (hsTnI) during a marathon and its association with traditional cardiovascular risk factors and imaging-based risk markers for incident coronary events and all-cause mortality in recreational marathon runners. Baseline data of 108 marathon runners, 864 age-matched controls and 216 age- and risk factor-matched controls from the general population were recorded and their coronary event rates and all-cause mortality after 6xa0±xa01xa0years determined. hsTnI was measured in 74 marathon finishers before and after the race. Other potential predictors for coronary events, i.e., Framingham Risk Score (FRS), coronary artery calcium (CAC) and presence of myocardial fibrosis as measured by magnetic resonance imaging-based late gadolinium enhancement (LGE), were also assessed. An increase beyond the 99xa0% hsTnI-threshold, i.e., 0.04xa0μg/L, was observed in 36.5xa0% of runners. FRS, CAC, or prevalent LGE did not predict hsTnI values above or increases in hsTnI beyond the median after the race, nor did they predict future events. However, runners with versus without LGE had higher hsTnI values after the race (median (Q1/Q3), 0.08xa0μg/L (0.04/0.09) versus 0.03xa0μg/L (0.02/0.06), pxa0=xa00.039), and higher increases in hsTnI values during the race (median (Q1/Q3), 0.05xa0μg/L (0.03/0.08) versus 0.02xa0μg/L (0.01/0.05), pxa0=xa00.0496). Runners had a similar cumulative event rate as age-matched or age- and risk factor-matched controls, i.e., 6.5 versus 5.0xa0% or 4.6xa0%, respectively. Event rates in runners with CAC scores <100, 100–399, and ≥400 were 1.5, 12.0, and 21.4xa0% (pxa0=xa00.002 for trend) and not different from either control group. Runners with coronary events had a higher prevalence of LGE than runners without events (57 versus 8xa0%, pxa0=xa00.003). All-cause mortality was similar in marathon runners (3/108, 2.8xa0%) and controls (26/864, 3.0xa0% or 5/216, 2.4xa0%, respectively). Recreational marathon runners with prevalent myocardial fibrosis develop higher hsTnI values during the race than those without. Increasing coronary artery calcium scores and prevalent myocardial fibrosis, but not increases in hsTnI are associated with higher coronary event rates. All-cause mortality in marathon runners is similar to that in risk factor-matched controls.

Effect of smoking and other traditional risk factors on the onset of coronary artery calcification: Results of the Heinz Nixdorf recall study

BACKGROUNDnCoronary artery calcium (CAC) indicates coronary atherosclerosis and can be present in very early stages of the disease. The conversion from no CAC to any CAC reflects an important step of the disease process as cardiovascular risk is increased in persons even with mildly elevated CAC. We sought to identify risk factors that determined incident CAC>0 in men and women from an unselected general population with a special focus on the role of smoking.nnnMETHODSnAll 4814 persons that were initially studied in the Heinz Nixdorf Recall Study were invited to participate in the follow-up examination after 5.1 ± 0.3 years. All traditional Framingham risk factors were quantified using standard techniques. Smokers were categorized in never, former and present smokers. The CAC scores were measured from EBCT using the Agatston method.nnnRESULTSnOverall, out of 342 men and 919 women with zero CAC at baseline, 107 (31.3%) men and 210 (22.9%) women had CAC>0 at second examination. In multivariable analysis, age (OR estimate per 5 years: 1.34 (95%CI: 1.21-1.47)), LDL cholesterol (per 10 mg/dL: 1.05 (95%CI: 1.01-1.10)), systolic blood pressure (per 10 mmHg: 1.19 (95%CI: 1.11-1.28)) and current smoking (1.49 (95%CI: 1.04-2.15)) were independent predictors of CAC onset. The probability of CAC onset steadily increased with age from 23.3% (men) and 15.3% (women) at age 45-49 years to 66.7% (men) and 42.9% (women) at age 70-74 years. The difference in age-dependent conversion rates was quantified by years between reaching a given level of CAC onset probability. We found a consistent pattern with respect to smoking status: presently (formerly) smoking middle-aged men convert to positive CAC 10 (5) years earlier than never smokers, for women (middle-aged to elderly) this time span is 8 (5) years.nnnCONCLUSIONnSeveral traditional CVD risk factors are associated with CAC onset during 5 years follow-up. CAC onset is accelerated by approximately 10 (5) years for present (former) compared to never smokers.

Carotid and peripheral atherosclerosis in male marathon runners.

PURPOSEnWe measured extracoronary atherosclerotic plaque burden and its association with cardiovascular risk factors and with coronary atherosclerosis in male marathon runners.nnnMETHODSnWe studied 100 male presumably healthy runners, aged 50-75 yr, who completed at least five marathons during the preceding 3 yr. Presence of plaque in the carotid, abdominal, and lower limb arteries was imaged using B-mode ultrasound. In all runners, traditional cardiovascular risk factors and the electron beam computed tomography-based coronary artery calcium (CAC) score were determined.nnnRESULTSnTen runners were free from any plaque in the carotid or peripheral arteries. Runners with plaque were older (58±6 vs 54±5 yr, P=0.04), had a higher 10-yr Framingham risk score (7.2±3.8 vs 5.0±1.9, P=0.026), and tended to have a higher prevalence of CAC (76.7% vs 50.0%, P=0.07) compared with those without. Runners with CAC≥100 had larger peripheral artery diameters (aorta and iliac and common femoral arteries) but smaller lumen than runners with CAC<100, indicating atherosclerotic remodeling. A stepwise model selection process to predict CAC on the basis of age and peripheral atherosclerosis yielded a model as follows: log2(CAC+1)=0.181 age (yr)+0.435 maximum carotid plaque thickness (mm)-6.487, with a coefficient of determination of 22.8%. However, positive and negative predictive values were too low to predict CAC≥100 with sufficient accuracy.nnnCONCLUSIONSnThe prevalence of carotid and peripheral atherosclerosis in marathon runners is high and is related to cardiovascular risk factors and the coronary atherosclerotic burden. Remodeling of peripheral arteries is greatest in runners with the most evidence of atherosclerosis. These data support an increased awareness of atherosclerosis prevalence and cardiovascular risk factors in marathon runners.

Statin Medication Enhances Progression of Coronary Artery Calcification: The Heinz Nixdorf Recall Study

Statins are suggested to stabilize plaque by decreasing lipid-rich and necrotic plaque components and increasing plaque calcification [(1,2)][1]. However, to date the relationship between statin administration and progression of coronary artery calcification (CAC) is poorly understood, and existing

Accelerated progression of coronary artery calcification in hypertension but also prehypertension

Objective: To determine the role of hypertension for coronary artery calcification (CAC) progression. Methods: The population-based Heinz Nixdorf Recall study recruited 4814 participants from a German urban population in 2000–2003. CAC was measured using electron-beam computed tomography at baseline and after 5 years. The present analyses refer to 3481 participants with repeat scan (coronary heart disease until 5 years excluded, age at baseline 45–74 years, and 53.1% women). Blood pressure (BP), Framingham risk factors, and antihypertensive medication were recorded at baseline. BP was staged according to Joint National Committee 7 guidelines. Participants under antihypertensive medication were classified as stage 2. CAC at 5 years was predicted from baseline using our dedicated, publicly available algorithm. CAC progression was accordingly classified as slow, expected, or rapid. Results: Normotension was found in 20.5%, prehypertension in 27.2%, stage 1 hypertension in 15.8%, and stage 2 (ST2) in 36.5%. The frequency of rapid progression increases with BP stage (normotension: 16.7% to ST2: 21.1%, Pu200a=u200a0.004). Risk factor adjusted relative risk [RR (95% confidence interval), reference: normotension] of rapid progression was for prehypertension: 1.22 (0.98;1.51), stage 1: 1.29 (1.01;1.65), and ST2: 1.45 (1.17;1.79). Risk factor adjusted measures of CAC progression per 10u200ammHg SBP were already elevated in women with BP below 140/90u200ammHg: CAC onset, RRu200a=u200a1.22 (1.07;1.40), rapid progression, RRu200a=u200a1.17 (1.05;1.31), 5-year CAC progression, 6.7% (0.5;13.4). In men below 140/90u200ammHg, only RR of rapid progression was considerably increased [RRu200a=u200a1.11 (0.96;1.29)]. Conclusion: CAC progression, a sign of ongoing target organ damage, is already accelerated in prehypertensive patients, a substantial proportion of our urban population.

Comparison of dual-source and electron-beam CT for the assessment of coronary artery calcium scoring.

OBJECTIVEnCardiac CT allows the detection and quantification of coronary artery calcification (CAC). Electron-beam CT (EBCT) has been widely replaced by high-end CT generations in the assessment of CAC. The aim of this study was to compare the CAC scores derived from an EBCT with those from a dual-source CT (DSCT).nnnMETHODSnWe retrospectively selected 92 patients (61 males; mean age, 60.7 ± 12 years) from our database, who underwent both EBCT and DSCT. CAC was assessed using the Agatston score by two independent readers (replicates: 1, 2; 3=mean of reading 1 and 2).nnnRESULTSnEBCT scores were on average slightly higher than DSCT scores (281 ± 569 vs 241 ± 502; p<0.05). In regression analysis R(2)-values vary from 0.956 (1) to 0.966 (3). We calculated a correction factor as EBCT=(DSCT+1)(1.026)-1. When stratifying into CAC categories (0, 1-99, 100-399, 400-999 and ≥1000), 79 (86%) were correctly classified. From those with positive CAC scores, 7 out of 61 cases (11%, κ=0.81) were classified in different categories. Using the corrected DSCT CAC score, linear regression analysis for the comparison to the EBCT results were r=0.971 (p<0.001), with a mean difference of 6.4 ± 147.8. Five subjects (5.4%) were still classified in different categories (κ=0.84).nnnCONCLUSIONnCAC obtained from DSCT is highly correlated with the EBCT measures. Using the calculated correction factor, agreement only marginally improved the clinical interpretation of results. Overall, for clinical purposes, face value use of DSCT-derived values appears as useful as EBCT for CAC scoring.

Progression of coronary artery calcification is stronger in poorly than in well controlled diabetes: Results from the Heinz Nixdorf Recall Study

AIMnTo assess associations between HbA1c and progression of coronary artery calcification (CAC) in persons with and without diabetes.nnnMETHODSnIn the Heinz Nixdorf Recall Study, a population-based cohort study in Germany (N=3453, aged 45-74years), CAC was assessed by electron-beam tomography at baseline and at 5-year follow-up. At baseline, participants were divided into five groups: poorly (HbA1c≥7.0%) and well (HbA1c<7.0%) controlled previously known diabetes (group I/II); no previously known diabetes with HbA1c ≥6.5% (group III), HbA1c 5.7-6.4% (group IV), and HbA1c <5.7% (group V). We fitted linear, logistic and robust Poisson regression models to assess associations between diabetes group and PF5 (factor by which CAC after 5-year follow-up is larger than baseline CAC), and categories of CAC change, respectively.nnnRESULTSnRelative to group V, adjusted percentage increase of the geometric mean of PF5 (95% CI) was: 69.1% (33.9%;113.6%), 15.4% (-5.6%;41.1%), -4.1% (-22.2%;18.2%), 4.2% (-5.4%;14.8%) for groups I-IV, respectively. The corresponding odds ratios for annual CAC increase ≥100 Agatston units (reference: <10) were 10.0 (4.8;20.6), 4.0 (2.1;7.6), 1.5 (0.7;3.2), and 1.1 (0.7;1.8).nnnCONCLUSIONSnIn known diabetes, CAC progression was stronger in poor diabetes control. For newly detected diabetes diagnosed by HbA1c ≥6.5%, associations with CAC progression were weak.

Sleep characteristics and progression of coronary artery calcification: Results from the Heinz Nixdorf Recall cohort study

BACKGROUND AND AIMSnSleep characteristics are associated with incident cardiovascular diseases (CVD), but there is a lack of studies on the association between sleep characteristics and incidence/progression of coronary artery calcification (CAC).nnnMETHODSnIn the Heinz Nixdorf Recall Study, a population-based cohort study in Germany, CAC was assessed by electron-beam tomography at baseline and at 5-year follow-up. In an analysis set of 3043 subjects (age at baseline 45-74 years; 47% men), we fitted logistic and linear regression models to assess associations between self-rated sleep characteristics (nocturnal and total sleep duration; napping; various sleep disorders) and CAC incidence/CAC progression. Progression was measured as 5-year progression factor, as categories of absolute CAC change, and additionally characterized as rapid or slow compared to an extrapolation of baseline CAC values.nnnRESULTSnWe observed barely any association between sleep characteristics and CAC progression regardless of the chosen statistical approach; associations between sleep and CAC incidence were slightly larger, e.g., the geometric mean of the 5-year CAC progression factor was 6.8% (95% confidence interval:xa0-9.5; 25.9) larger for ≤5u202fh, 2.9% (-7.3; 14.3) larger for 5.1-6.9u202fh and 7.1% (-2.4; 15.7) smaller for ≥7.5u202fh total sleep compared to 7- <7.5u202fh total sleep. For subjects with any regular sleep disorder, the geometric mean of the 5-year CAC progression was 3.5% (-4.7; 11.2) smaller compared to subjects without any regular sleep disorder.nnnCONCLUSIONSnIn this German cohort study, sleep characteristics were barely associated with CAC progression.