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Prehypertension is a frequent condition and has been demonstrated to increase cardiovascular risk. However, the association with coronary atherosclerosis as part of target organ damage is not well understood. We investigated the cross-sectional relationship and longitudinal outcome between blood pressure categories and coronary artery calcification (CAC), quantified by electron beam computed tomography, in 4181 participants from the population-based Heinz Nixdorf Recall Study cohort. At baseline, we observed a continuous increase in calcium scores with increasing blood pressure categories. During a median follow-up period of 7.18 years, 115 primary end points (2.8%; fatal and nonfatal myocardial infarction) and 152 secondary end points (3.6%; stroke and coronary revascularization) occurred. We observed a continuous increase in age- and risk factor-adjusted secondary endpoints (hazard ratios [95% CI]) with increasing blood pressure categories (referent: normotension) in men: prehypertension, 1.80 (0.53-6.13); stage 1 hypertension, 2.27 (0.66-7.81); and stage 2 hypertension, 4.10 (1.27-13.24) and in women: prehypertension, 1.13 (0.34-3.74); stage 1 hypertension, 2.14 (0.67-6.85); and stage 2 hypertension, 3.33 (1.24-8.90), respectively, but not in primary endpoints. Cumulative event rates were determined by blood pressure categories and the CAC. In prehypertension, the adjusted hazard ratios for all of the events were, for CAC 1 to 99, 2.05 (0.80-5.23; P=0.13); 100 to 399, 3.12 (1.10-8.85; P=0.03); and ≥400, 7.72 (2.67-22.27; P=0.0002). Risk of myocardial infarction and stroke in hypertension but also in prehypertension depends on the degree of CAC. This marker of target-organ damage might be included, when lifestyle modification and pharmacotherapeutic effects in prehypertensive individuals are tested to avoid exposure to risk and increase benefit. [ABSTRACT FROM AUTHOR]

The article presents a study which aimed to quantify the release of vasoconstrictors during stent implantation into atherosclerotic plaques and to determine the efficacy of coronary dilators to attenuate their action. Results showed serotonin as the main coronary vasoconstrictor released after stenting with thromboxane and tumor necrosis factor (TNF)α potentiating the response. Nitroprusside and verapamil were found to be more potent than adenosine in attenuating the aspirate plasma-induced vasoconstriction.

Long-term exposure to particulate air pollution has been associated with increased cardiovascular disease. Biologic pathways for this association are not fully understood.We examined the association of urban air pollution with atherosclerosis of the peripheral vascular bed, using baseline data (2000-2003) from 4348 participants in a population-based cohort study in the German Ruhr Area. Levels of annual fine particulate matter (PM2.5) exposure, derived from a dispersion and chemistry transport model, were assigned to the participants’ home addresses. Residential traffic exposure was assessed by the distance between residence and major roads (federal and state highways). Using multiple regression analyses and controlling for individual level risk factors, we examined the association of PM2.5 and traffic with the ankle-brachial index and prevalence of peripheral arterial disease, defined as an index of less than 0.9 or a history of treatment for peripheral artery disease.Living within 101-200, 51-100, and 50 m of a major road was associated with an adjusted absolute decrease in ankle-brachial index of -0.015 (95% confidence interval [CI] = -0.030 to 0.0), -0.002 (-0.021 to 0.016) and -0.024 (-0.047 to -0.001), respectively. Stronger associations were seen in women, whereas no clear association was found in men. Individuals living within 50 m of a major road had an OR of 1.77 (1.01-2.1) for peripheral arterial disease compared with those living more than 200 m away. Associations with PM2.5 were inconsistent.This study adds to the evidence that long-term residential exposure to traffic is associated with atherosclerosis. [ABSTRACT FROM AUTHOR]

Objective: To examine the association between genomewide association study-based diabetes mellitus-related single-nucleotide polymorphisms (SNPs) and coronary artery calcification (CAC), a valid risk factor for coronary heart disease, in a large, unselected, population-based cohort., Methods and Results: We genotyped 11 validated genomewide association study-based diabetes SNPs in 4459 participants of the Heinz Nixdorf Recall Study. We applied generalized linear regression models to explore the impact of the diabetes SNPs on CAC and to jointly model the effect of the SNPs and CAC on diabetes status. We observed a significant association between cyclin-dependent kinase inhibitor 2A/2B (CDKN2A/2B) variant rs564398 and quantitative CAC (P=1.81 x 10(-5) and adjusted P=4.02 x 10(-4); odds ratio for the presence of CAC, 1.12 [95% CI, 1.02 to 1.25]). Moreover, we observed no strong impact of CAC on diabetes risk in the presence of the other genetic variants., Conclusions: We show that a genetic variant near CDKN2A/2B that has been reported to be strongly associated with diabetes is strongly associated with CAC. In contrast, variants near insulin-like growth factor-binding protein 2 (IGFBP2), CDK5 regulatory subunit associated protein 1-like 1 (CDKAL1), solute carreir family 30 (zinc transporter), member 8 (SLC30A8), hematopoietically-expressed homeobox (HHEX), and transcription factor 7-like2 (TCF7L2) were clearly associated with diabetes; no evidence for an association to CAC was observable. This differential association pattern underlines the potential of endophenotypes, such as CAC, to extend the scope of disease outcome associations.