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1.  The Adverse Events and Hemodynamic Effects of Adenosine-Based Cardiac MRI 
Korean Journal of Radiology  2011;12(4):424-430.
Objective
We wanted to prospectively assess the adverse events and hemodynamic effects associated with an intravenous adenosine infusion in patients with suspected or known coronary artery disease and who were undergoing cardiac MRI.
Materials and Methods
One hundred and sixty-eight patients (64 ± 9 years) received adenosine (140 µg/kg/min) during cardiac MRI. Before and during the administration, the heart rate, systemic blood pressure, and oxygen saturation were monitored using a MRI-compatible system. We documented any signs and symptoms of potential adverse events.
Results
In total, 47 out of 168 patients (28%) experienced adverse effects, which were mostly mild or moderate. In 13 patients (8%), the adenosine infusion was discontinued due to intolerable dyspnea or chest pain. No high grade atrioventricular block, bronchospasm or other life-threatening adverse events occurred. The hemodynamic measurements showed a significant increase in the heart rate during adenosine infusion (69.3 ± 11.7 versus 82.4 ± 13.0 beats/min, respectively; p < 0.001). A significant but clinically irrelevant increase in oxygen saturation occurred during adenosine infusion (96 ± 1.9% versus 97 ± 1.3%, respectively; p < 0.001). The blood pressure did not significantly change during adenosine infusion (systolic: 142.8 ± 24.0 versus 140.9 ± 25.7 mmHg; diastolic: 80.2 ± 12.5 mmHg versus 78.9 ± 15.6, respectively).
Conclusion
This study confirms the safety of adenosine infusion during cardiac MRI. A considerable proportion of all patients will experience minor adverse effects and some patients will not tolerate adenosine infusion. However, all adverse events can be successfully managed by a radiologist. The increased heart rate during adenosine infusion highlights the need to individually adjust the settings according to the patient, e.g., the number of slices of myocardial perfusion imaging.
doi:10.3348/kjr.2011.12.4.424
PMCID: PMC3150669  PMID: 21852902
MRI; Adenosine; Coronary artery disease; Hemodynamics; Adverse events
2.  Non‐invasive screening for coronary artery disease: calcium scoring 
Heart  2007;93(12):1620-1629.
doi:10.1136/hrt.2005.071258
PMCID: PMC2095743  PMID: 18003695
3.  Use of automatic exposure control in multislice computed tomography of the coronaries: comparison of 16‐slice and 64‐slice scanner data with conventional coronary angiography 
Heart  2007;93(9):1040-1043.
Objective
To evaluate the radiation‐dose‐reduction potential of automatic exposure control (AEC) in 16‐slice and 64‐slice multislice computed tomography (MSCT) of the coronary arteries (computed tomography angiography, CTA) in patients. The rapid growth in MSCT CTA emphasises the necessity of adjusting technique factors to reduce radiation dose exposure.
Design
A retrospective data analysis was performed for 154 patients who had undergone MSCT CTA. Group 1 (n = 56) had undergone 16‐slice MSCT without AEC, and group 2 (n = 51), with AEC. In group 1, invasive coronary angiography (ICA) had been performed in addition. Group 3 (n = 47) had been examined using a 64‐slice scanner (with AEC, without ECG‐triggered tube current modulation).
Results
In group 1, the mean (SD) effective dose (ED) for MSCT CTA was 9.76 (1.84) mSv and for ICA it was 2.6 (1.27) mSv. In group 2, the mean ED for MSCT CTA was 5.83 (1.73) mSv, which signifies a 42.8% dose reduction for CTA by the use of AEC. In comparison to ICA, MSCT CTA without AEC shows a 3.8‐fold increase in radiation dose, and the radiation dose of CTA with AEC was increased by a factor of 1.9. In group 3, the mean ED for MSCT CTA was 13.58 (2.80) mSV.
Conclusions
This is the first study to show the significant dose‐reduction potential (42.8%) of AEC in MSCT CTA in patients. This relatively new technique can be used to optimise the radiation dose levels in MSCT CTA.
doi:10.1136/hrt.2006.103838
PMCID: PMC1955015  PMID: 17395667
4.  Chronic Residential Exposure to Particulate Matter Air Pollution and Systemic Inflammatory Markers 
Environmental Health Perspectives  2009;117(8):1302-1308.
Background
Long-term exposure to urban air pollution may accelerate atherogenesis, but mechanisms are still unclear. The induction of a low-grade systemic inflammatory state is a plausible mechanistic pathway. Objectives: We analyzed the association of residential long-term exposure to particulate matter (PM) and high traffic with systemic inflammatory markers.
Methods
We used baseline data from the German Heinz Nixdorf Recall Study, a population-based, prospective cohort study of 4,814 participants that started in 2000. Fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] exposure based on a small-scale dispersion and chemistry transport model was assigned to each home address. We calculated distances between residences and major roads. Long-term exposure to air pollution (annual PM2.5 and distance to high traffic) and concentration of inflammatory markers [high-sensitivity C-reactive protein (hs-CRP) and fibrinogen] on the day of the baseline visit were analyzed with sex-stratified multiple linear regression, controlling for individual-level risk factors.
Results
In the adjusted analysis, a cross-sectional exposure difference of 3.91 μg/m3 in PM2.5 (interdecile range) was associated with increases in hs-CRP of 23.9% [95% confidence interval (CI), 4.1 to 47.4%] and fibrinogen of 3.9% (95% CI, 0.3 to 7.7%) in men, whereas we found no association in women. Chronic traffic exposure was not associated with inflammatory markers. Short-term exposures to air pollutants and temperature did not influence the results markedly.
Conclusions
Our study indicates that long-term residential exposure to high levels of PM2.5 is associated with systemic inflammatory markers in men. This might provide a link between air pollution and coronary atherosclerosis.
doi:10.1289/ehp.0800362
PMCID: PMC2721876  PMID: 19672412
air quality; cardiovascular disease; epidemiology; inflammation; roadway proximity
5.  Comparison of Subclinical Coronary Atherosclerosis and Risk Factors in Unselected Populations in Germany and US-America 
Atherosclerosis  2007;195(1):e207-e216.
Background
On the basis of the Framingham risk algorithm, overestimation of clinical events has been reported in some European populations. Electron-beam computed tomography-derived quantification of coronary artery calcification (CAC) allows for noninvasive assessment of coronary atherosclerosis in the general population and may thus add important in vivo information on the path from risk factor exposure to formation of clinical events. The current study was undertaken to compare the relationship between risk factors and subclinical coronary atherosclerosis between non-Hispanic white cohorts in Germany and US-America, the hypothesis being that subclinical coronary atherosclerosis might be less prevalent in Europe at the same level of classical risk factor exposure.
Methods
The Heinz Nixdorf Recall (HNR) study, conducted in the German Ruhr area and the Epidemiology of Coronary Calcification (ECAC) study, conducted in Olmsted County, Minnesota, both recruited large unselected cohorts, men and women aged 45 – 74 years, from the general population. All subjects with no history of coronary artery disease (CAD) or stroke were included (n = 3,120 in HNR, n = 703 in ECAC). Coronary risk factors were assessed by personal and computer-assisted interviews and direct laboratory measurements. Cardiovascular medication use (antihypertensive, lipid-lowering, and anti-diabetic) was noted. CAC scores were determined using the Agatston method in an identical fashion in both studies.
Results
Adverse levels of risk factors were more prevalent, and the Framingham risk score was higher (10.6 ± 7.6 vs. 9.3 ± 7.1, p < 0.001) in HNR than ECAC, respectively. There was no difference in body mass index (BMI). CAC scores were greater in HNR than in ECAC (mean values, 155.7 ± 423.0 versus 107.2 ± 280.0; median values, 11.9 versus 2.4; p < 0.001, respectively). When subjects were matched on CAD risk factors, presence and quantity of CAC were similar in the 2 cohorts. Risk factors significantly associated with CAC score in both studies included: age, male sex, current and former smoking, systolic blood pressure, and non HDL-cholesterol. Inferences were similar after excluding subjects using lipid- or blood pressure-lowering medications. Using the same risk factor variables for modelling, the predicted CAC scores were comparable in both cohorts.
Conclusions
In the higher-risk German cohort, presence and quantity of CAC were greater than in the lower-risk US-American cohort. Risk factor associations, however, with CAC were very similar in both unselected populations. As opposed to studies concerning clinical endpoints, we could not demonstrate a relative increase in subclinical coronary atherosclerosis in the US-American cohort.
doi:10.1016/j.atherosclerosis.2007.04.009
PMCID: PMC2293130  PMID: 17532322
6.  Signs of subclinical coronary atherosclerosis in relation to risk factor distribution in the Multi-Ethnic Study of Atherosclerosis (MESA) and the Heinz Nixdorf Recall Study (HNR) 
European Heart Journal  2008;29(22):2782-2791.
Aims
Modern imaging technology allows us the visualization of coronary artery calcification (CAC), a marker of subclinical coronary atherosclerosis. The prevalence, quantity, and risk factors for CAC were compared between two studies with similar imaging protocols but different source populations: the Multi-Ethnic Study of Atherosclerosis (MESA) and the Heinz Nixdorf Recall Study (HNR).
Methods and results
The measured CAC in 2220 MESA participants were compared with those in 3126 HNR participants with the inclusion criteria such as age 45–75 years, Caucasian race, and free of baseline cardiovascular disease. Despite similar mean levels of CAC of 244.6 among participants in MESA and of 240.3 in HNR (P = 0.91), the prevalence of CAC > 0 was lower in MESA (52.6%) compared with HNR (67.0%) with a prevalence rate ratio of CAC > 0 of 0.78 [95% confidence interval (CI): 0.72–0.85] after adjustment for known risk factors. Consequently, among participants with CAC > 0, the participants in MESA tended to have higher levels of CAC than those in HNR (ratio of CAC levels: 1.39; 95% CI: 1.19–1.63), since many HNR participants have small (near zero) CAC values.
Conclusions
The CAC prevalence was lower in the United States (MESA) cohort than in the German (HNR) cohort, which may be explained by more favourable risk factor levels among the MESA participants. The predictors for increased levels of CAC were, however, similar in both cohorts with the exception that male gender, blood pressure, and body mass index were more strongly associated in the HNR cohort.
doi:10.1093/eurheartj/ehn439
PMCID: PMC2582985  PMID: 18845666
Epidemiology; Atherosclerosis; Coronary artery calcium; Risk factors; Screening

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