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Objective: To test whether information simply obtained from adults can identify those who are likely to have blood cholesterol levels higher than 6.5 mmol/L (250 mg/dl).Design: Cross-sectional study.Setting: Seven general practices in the lower Hunter Region of Australia.Participants: Of 693 men and women 25 to 65 years old attending the general practices, 616 (89%) participated. Twelve pregnant women and four without blood samples were excluded, leaving 600 subjects (208 men, 392 women).Measurements and Main Results: Twenty-two percent of subjects had blood cholesterol higher than 6.5 mmol/L (250 mg/dl). In women, high cholesterol was mainly found among those over 40 years of age, but in men high cholesterol was more evenly spread across the different age groups. Stepwise logistic regression identified age, history of hypertension, and a past history of heart attack as significant independent predictors of high cholesterol. A simple model developed from these variables identified 81% of men and women (95% CI = 72-90%) with high cholesterol while testing only 49% of the population (95% CI = 44-54%). This model was developed in a random subset of 331 of the 600 subjects, and when applied to the remaining 269 subjects, it identified 77% of those with high cholesterol (95% CI = 67-87%) after testing 48% (95% CI = 42-54%).Conclusions: Selective screening using this simple model can identify adults who are likely to have high blood cholesterol and could complement case-finding or provide an alternative high-risk strategy for communities that cannot afford to screen all individuals. [ABSTRACT FROM AUTHOR]

Study Question: Patients with acute coronary syndrome (ACS) have elevated plasma levels of the proinflammatory, prothrombotic cytokine CD40 ligand (sCD40L). The present analysis examined the relationship between sCD40L and the risk of recurrent cardiovascular events soon after an ACS in the MIRACL study and tested whether the clinical benefit from statin therapy was related to a reduction in proinflammatory and prothrombotic stimuli associated with sCD40L.Methods: The investigators measured sCD40L in subjects with an ACS enrolled in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study. Subjects were randomized in this double-blind trial either to atorvastatin 80 mg/d or placebo for 16 weeks.Results: Plasma CD40L was measured from 2908 (94%) of 3086 subjects at baseline and 2352 (76%) subjects at 16 weeks. Odds ratios (ORs) and 95% CIs from logistic regression models assessed the risk of recurrent cardiovascular events over 16 weeks (death, nonfatal myocardial infarction, cardiac arrest, and worsening angina requiring rehospitalization) in the placebo group from baseline sCD40L and the effect of atorvastatin on the risk associated with CD40L in all subjects. The effects of atorvastatin on plasma concentrations of CD40L were assessed by Wilcoxon tests. There was a threshold effect, with only high sCD40L (>90th centile) being a risk factor for a recurrent cardiovascular event (OR 1.86, 95% CI 1.25–2.77). This risk was abolished by atorvastatin (OR 1.09, 95% CI 0.69–1.76), which reduced the risk by 48%. Atorvastatin had only a modest effect on sCD40L (p=0.08).Conclusions: The investigators state that, in patients with ACS, atorvastatin abrogated the risk of recurrent cardiovascular events associated with high sCD40L.Perspective: Patients presenting with ACS with highly elevated sCD40L have a higher risk of recurrent coronary events. In this setting, intensive statin therapy may reduce the risk of recurrent events associated with high sCD40L levels without affecting plasma concentrations of this cytokine. The present study points to anti-inflammatory and antithrombotic actions of statins as an additional mechanism of benefit after ACSs. DM [Copyright &y& Elsevier]

Abstract Background Little is known about the influence of the site of research or publication on the impact of the research findings on clinical practice, particularly in developing countries. The International Clinical Epidemiology Network (INCLEN) is dedicated to improving the quality of health research in the Developing World through institutional capacity building for evidence based medicine, and provided the opportunity to examine the likely impact of research location and journal location on physicians' practice in a number of the participating countries. Methods Physicians from secondary and tertiary hospitals in six cities located in China, Thailand, India, Egypt and Kenya were enrolled in a cross-sectional questionnaire survey. The primary outcome measures were scores on a Likert scale reflecting stated likelihood of changing clinical practice depending on the source of the research or its publication. Results Overall, local research and publications were most likely to effect change in clinical practice, followed by North American, European and regional research/publications respectively, although there were significant variations between countries. The impact of local and regional research would be greater if the perceived research quality improved in those settings. Conclusion Conducting high quality local research is likely to be an effective way of getting research findings into practice in developing countries.

Inflammation plays a crucial role in the cell biology of atherosclerosis. Coronary risk factors, and particularly low-density lipoprotein (LDL) cholesterol, injure the endothelium and decrease the bioavailability of nitric oxide to promote the expression of proinflammatory genes, cellular adhesion molecules, cytokines, chemokines, and growth factors. For example, the expression of CD40/CD40 ligand increases cell-mediated immune responses to activate a number of inflammatory cells and destabilize atherosclerosis. As part of this response, soluble markers of inflammation that are released into the blood offer insights into the cell biology of inflammation in atherosclerosis. In groups of patients, these markers have provided a means to study inflammatory mechanisms and have supported the value of many of our interventions that prevent cardiovascular disease. Statins have potent effects to reduce LDL cholesterol in the plasma and the artery wall and also appear to have a number of nonlipid effects that decrease inflammatory stimuli. Because statins also reduce some soluble markers of inflammation, it is likely that at least part of their benefit reflects a reduction in vascular inflammation in stable and unstable coronary syndromes. Although these inflammatory markers are valuable tools for studying the mechanisms of atherosclerosis, their use in clinical practice to stratify cardiovascular risk or assess treatment in individual patients requires further evaluation. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a complex process that is characterized by the accumulation of modified low-density lipoprotein (LDL), local inflammatory and immune responses, and reduced nitric oxide bioavailability within the arterial wall. These cellular changes lead to endothelial vasomotor dysfunction, plaque instability, and the development of clinical events such as stable angina and the acute coronary syndromes. The vascular endothelium plays a critical role in modulating both the inflammatory response and vasomotor abnormalities that occur in those with coronary artery disease or risk factors for disease. In these conditions, endothelial cells are activated by cytokines to express cellular adhesion molecules that facilitate the adhesion of leukocytes to the endothelium, and their migration into the subintimal space. Cytokines stimulate inflammatory and smooth muscle cells in the intima to produce degradative enzymes, including metalloproteinases that can weaken the fibrous cap of atherosclerotic lesions and make them vulnerable to rupture. Endothelial cells also regulate vascular tone by the synthesis of nitric oxide. Atherosclerosis and other conventional risk factors for coronary artery disease are associated with endothelial vasodilator dysfunction in the coronary epicardial and resistance vessels, which likely contributes to myocardial ischemia. Several studies have demonstrated that lowering serum total and LDL cholesterol reverses endothelial vasomotor dysfunction, reduces myocardial ischemia, and lowers the risk of the acute coronary syndromes or need for revascularization. Improving endothelial function, for example, by lowering blood cholesterol should now be regarded as a goal of therapy in the treatment of coronary artery disease. [ABSTRACT FROM AUTHOR]

The uncertain significance of hazy areas at the margins of coronary stents may lead to further, at times unnecessary, stenting. However, the risk of restenosis increases substantially when additional stents are deployed. We used intravascular ultrasound (IVUS) to identify the causes of hazy segments adjacent to stents. We identified 13 cases with hazy regions adjacent to coronary stents and 20 controls without hazy regions matched by age, gender, and vessel stented. Hazy regions were defined from the angiogram as reduced contrast density without a clearly defined intimal tear, dissection, thrombus, or stenosis (> 50%). IVUS images were obtained from the reference, stent, and hazy and control regions adjacent to the stent. Computerized planimetery was used to measure the vessel, lumen, and plaque cross-sectional areas (CSAs), the maximum arc of calcium, and the eccentricity ratio (minimum:maximum lumen diameter). There were no significant differences between hazy and control segments in the vessel, lumen, and plaque CSAs. All lumen CSAs were >4.0 mm2. Compared with control regions, the hazy regions had calcified plaque more often (69% vs 25%; odds ratio [OR] 6.75, 95% confidence intervals [CI] 1.82 to 25.0]) and more frequent intimal tears (23% vs 0%, OR 6.67, 95% CI 1.98 to 35.0). Haziness was particularly associated with calcified plaque and eccentric lumen (p = 0.037). Thus, haziness at the margins of coronary stents is often caused by calcified plaque. IVUS can differentiate calcified plaques from intimal tears and thereby obviate unnecessary stenting. [ABSTRACT FROM AUTHOR]

Discusses the quantitative angiographic outcome after intracoronary pullback atherectomy. Study design and population; Acute procedural success rate; Angiographic evidence of dissection or spasm; Relation of various factors to major angiographic complications after pullback atherectomy.

Atherosclerosis is often asymptomatic, unrecognized, and undertreated. Lumen irregularities are important angiographic findings that should be addressed aggressively through risk factor modification, medical therapy, and coronary revascularization. Both angiographic and clinical benefits have been demonstrated with lipid reduction therapy in randomized clinical trials. Coronary revascularization is indicated for symptom relief and improvement in quality of life in patients with acute coronary syndromes at "intermediate" and "high" risk of subsequent death or myocardial infarction. In patients following percutaneous coronary intervention (PCI), future cardiac events may be related to lumen renarrowing or to progression of atherosclerotic disease at sites remote from the site of coronary revascularization. The time course of restenosis is relatively self-limiting, generally occurring within 6-12 months after the procedure. Clinical events occurring > 1 year after PCI generally relate to new lesions or progression of existing atherosclerotic disease. Patients with diabetes mellitus may be at higher risk for late coronary events than nondiabetic patients. In post-coronary artery bypass surgery (CABG) patients, the majority of late events relate to degeneration of saphenous vein grafts. Lipid lowering therapy after coronary revascularization has been shown to prevent clinical events related to plaque instability and inhibit progression of saphenous vein graft disease. Thus, there are 2 goals in management of patients with symptomatic coronary artery disease: (1) to relieve the flow-limiting stenosis, and (2) to prevent future clinical events with aggressive lipid lowering and modification of other risk factors. Patients, specialists, and primary care physicians each need to take accountability for this risk-factor modification. [ABSTRACT FROM AUTHOR]

We sought to explore the relation between Chlamydia pneumoniae, cytomegalovirus (CMV), and cardiac transplant-associated arteriosclerosis. Serologic evidence of past Chlamydia pneumoniae infection was investigated in 3 patient groups at the time of cardiac catheterization: cardiac transplant recipients (n=49), patients having coronary artery bypass grafting (CABG) (n=39), and a control group free of angiographic coronary artery disease (n=21). High Chlamydia pneumoniae immunoglobulin G titers (> or =1:160) were more frequently observed in cardiac transplant recipients (odds ratio[OR] 13.7; 95% confidence intervals [CI] 1.6 to 117.4, p <0.05) and CABG patients (OR 21.7; 95% CI 1.6 to 287.0, p <0.05) than in controls. However, high Chlamydia pneumoniae titers did not distinguish between cardiac transplant recipients with or without angiographic transplant-associated arteriosclerosis or CABG patients with or without bypass vein graft disease. Furthermore, there was no significant relation between elevated Chlamydia pneumoniae titers and the presence or progression of transplant-associated arteriosclerosis in the subgroup of patients who were also CMV positive. Yet, analysis of the same angiograms demonstrated an association between CMV infection and the recent progression of transplant-associated arteriosclerosis. Thus, patients with cardiac transplantation have evidence of past Chlamydia pneumoniae and CMV infection but Chlamydia pneumoniae does not appear to have an independent role or synergistic relation to CMV in the development of transplant-associated arteriosclerosis. [ABSTRACT FROM AUTHOR]

The absorption of sublingual nitrate tablets is sometimes variable. We performed a randomized controlled trial to determine whether wetting the mouth improved the decrease in aortic systolic blood pressure (BP) from sublingual nitrate tablet or spray. The 100 patients undergoing routine diagnostic cardiac catheterization were allocated to control (no nitrate), 0.3 mg sublingual nitrate tablet, 0.4 mg sublingual nitrate spray, water + 0.3 mg sublingual nitrate tablet, or water + 0.4 mg sublingual nitrate spray. Aortic systolic and diastolic BP were recorded using a fluid-filled catheter and measured off-line blind to the treatment group. Compared with control subjects, there were significant decreases in aortic systolic BP with both nitrate preparations (tablet = -7.1 mm Hg, 95% confidence interval [CI] = -12.5 to -1.6 mm Hg; spray = -8.0 mm Hg, 95% CI = -13.4 to -2.5 mm Hg). On average, water significantly increased the fall in aortic systolic BP with nitrate tablets (-5.5 mm Hg, 95% CI = -10.9 to -0.1 mm Hg, p = 0.044) but did not significantly enhance the effect of nitrate spray (-2.8 mm Hg, 95% CI = -8.3 to 2.6 mm Hg). Water significantly increased the fall in aortic diastolic BP with tablets only (-2.9 mm Hg, 95% CI = -5.5 to -0.2), and had no significant effect on heart rate. Water had a consistently larger influence on the hemodynamic effects of nitrate tablets than on the effects of nitrate spray. Patients with a dry mouth will have an increased effect from sublingual nitrate tablets if they wet their mouth before using sublingual nitrate tablets. Water does not appear to assist in the action of sublingual spray. [ABSTRACT FROM AUTHOR]

Examines the use of the thrombolysis in myocardial infarction frame count for the quantitative assessment of transplant-associated arteriosclerosis (TAA). Reliance on surveillance coronary angiography of clinical practice for the assessment of TAA; Quantitative approach to assessing TAA; Absence of severe structural narrowings in epicardial arteries.

Examines the effect of endogenous vitamin C on nitric oxide bioavailability and coronary endothelial vasomotor function in cardiac transplant recipients. Relation between plasma vitamin C concentration and coronary vasomotor response (CVR) to acetylcholine and nitroglycerin; Relation of plasma F(sub 2)-isoprostanes and CVR to acetylcholine and nitroglycerine.