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Subclinical atherosclerosis can be quantified by coronary artery calcium (CAC) scoring. Due to its high specificity for atherosclerosis, CAC is an excellent phenotypic tool for the evaluation of emerging risk markers. Lipoprotein(a) [Lp(a)] is atherogenic due to the presence of apoB and may be thrombogenic through its apo(a) component. Lp(a) has been linked to cardiovascular events in Caucasians; however, its link to atherosclerosis in various ethnicities remains unclear. We evaluated the ability of Lp(a) mass to predict subclinical atherosclerosis in Southeast Asians and Caucasians, as measured by CAC. Traditional lipid measurements, Lp(a) measurements, and CAC by 64-slice multidetector computed tomography was performed in 103 consecutive patients in the USA and in 104 consecutive patients in Jakarta, Indonesia. Proportion of positive CAC and median CAC in Southeast Asians and in Caucasians was 61.5% and 63.1%, and 23.5 (interquartile range, 0-270) and 13 (interquartile range, 0-388), respectively. Significantly higher proportion of Southeast Asians had elevated Lp(a) levels, compared to Caucasians (51.0% vs. 29.2%; p = 0.005). In Southeast Asians, Lp(a) remained an independent predictor of CAC with an odds ratio of 4.97 (95% confidence interval, 1.56-15.88; p < 0.0001), but not in Caucasians. Receiver operating characteristic analysis showed an improvement in area under the curve from 0.81 to 0.86 (p = 0.05) when including Lp(a) in the predictive model in Southeast Asians. This translated to 7% of Southeast Asians reclassified to correct CAC status. Lp(a) measurements may have a role in risk stratification of Southeast Asians. Ethnic variation should be taken into account when considering the use of Lp(a) measurements in risk assessment.

Background: The relationship between chest lateral width, tube current, image noise, and radiation exposure on 320-detector row CT has not been reported., Objective: We investigated the relationships between chest lateral width, estimated radiation exposure (DLPe), and image noise in 300 patients undergoing clinical coronary calcium scanning., Methods: Patients undergoing coronary calcium scanning with 320-detector row CT (prospective, volumetric mode, 120 kV of tube voltage, 100-550 mA of tube current, 0.5-mm detector width) were grouped by chest lateral width (small, medium, and large) from anteroposterior topograms and 100 consecutive patients were selected from each group (n = 300). Tube current, DLPe, and noise were compared among groups with Kruskal-Wallis or one-way ANOVA. Phantom experiments were performed to evaluate the accuracy of calcium quantification as a function of size and tube current., Results: Median tube current in small, medium, and large patients was 130, 200, and 250 mA, respectively (P < 0.0001). Despite the use of higher tube current settings, noise levels also increased with size (20.2 ± 4.5 HU, 22.0 ± 3.9 HU, and 25.1 ± 4.9 HU, respectively; global P < 0.001). DLPe was significantly higher with increasing size (54, 83, and 104 mGy · cm, respectively; P < 0.0001). Phantom experiments showed that 50-100 mA, 150-200 mA, and approximately 300 mA in small, medium, and large phantoms were associated with stable estimate of calcium., Conclusions: Increasing chest lateral width is associated with increasing radiation exposure and image noise. The use of 50-100 mA in small and 150-200 mA in medium patients is associated with acceptable noise and stable estimate of coronary artery calcium. In large patients, precise identification of individual calcified lesions remains difficult despite increasing tube current and radiation exposure., (Copyright © 2011 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

:, Opinion Statement: Currently, there are significant data to support a link between lipoprotein(a) [Lp(a)] levels and cardiovascular risk. However, there has not been a clinical trial examining the effects of Lp(a) reduction on cardiovascular risk in a primary prevention population. Until such a trial is conducted, current consensus supports using an Lp(a) percentile greater than 75% for race and gender as a risk stratification tool to target more aggressive low-density lipoprotein cholesterol (LDL-C) or apolipoprotein B (apoB) goals. Therefore, Lp(a) measurements should be considered in the following patients: individuals with early-onset vascular disease determined by clinical presentation or subclinical imaging, intermediate and high Framingham risk patients with a family history of premature coronary disease, and low Framingham risk patients with a family history and low high-density lipoprotein cholesterol (HDL-C) levels. Once LDL-C goals are met, Lp(a) levels may be taken into account in selecting secondary agents to reach more aggressive secondary goals, including non-HDL-C and apoB. To achieve Lp(a) reduction, one evidence-based approach is to initiate therapy with low-dose aspirin and extended-release niacin, titrated from 0.5 g up to 2 g over several weeks. If higher doses of niacin are desired, crystalline niacin allows for titration to a dosage as high as 2 g three times a day; however, the flushing side effect usually is quite prominent. Although hormone replacement therapy (HRT) has been shown to lower Lp(a), there are no indications for using HRT for primary or secondary prevention; therefore, we do not advocate initiating it solely for Lp(a) reduction. LDL apheresis is an option to lower LDL-C levels in patients with homozygous familial hypercholesterolemia who are not responsive to medical therapy. Although it does lower Lp(a), there is no treatment indication for this. A recent study supports the cholesterol absorption inhibitor ezetimibe's ability to lower Lp(a), a finding that deserves further investigation as it has not been previously reported in multiple ezetimibe trials. Additionally, the apoB messenger RNA antisense therapy mipomersen currently is in phase 3 trials and may serve as a potential inhibitor of Lp(a) production. Ultimately, more trial evidence is needed to determine whether lowering Lp(a) actually reduces cardiovascular risk, although this may be difficult to isolate without a specific Lp(a)-lowering therapy.

Whether combination lipoprotein therapy targeting apolipoprotein B (apoB)- and apoA-containing lipoprotein particles and triglycerides (TGs) in low-risk, asymptomatic subjects with coronary atherosclerosis alters the natural progression of plaques is unknown. This study was designed to compare the progression of coronary atherosclerosis in asymptomatic, low-risk subjects without previously known coronary artery disease but with the presence of plaque on a combination of atorvastatin 40 mg plus fenofibric acid 135 mg daily for 18 months, using cardiovascular computed tomography (CCT). This is an investigator-initiated, single-center, prospective, double-blind, randomized, placebo-controlled, parallel-arm study. Asymptomatic subjects at low risk of cardiovascular events defined as <10% 10-year risk based on the Framingham Risk Score will be recruited, if they do not qualify for lipoprotein-lowering therapy based on the National Cholesterol Education Panel Adult Treatment Panel III guidelines. Subjects will qualify based on lipid parameters if their low-density lipoprotein cholesterol is >/=100 mg/dL and <190 mg/dL, TGs are >150 mg/dL, and the TGs/high-density lipoprotein cholesterol ratio is >3.5. Patients must have nonobstructive plaque based on CCT. Randomization will be 1:1 to either a combination of atorvastatin 40 mg plus fenofibric acid 135 mg daily or placebo for 18 months. Patients will undergo CCT at baseline and at the end of the treatment period. The primary end point will be the between-group difference in percent atheroma volume. Ultimately, this study can guide physicians about the use of a statin-fibric acid derivative combination in asymptomatic, low-risk persons with atherosclerosis., (Copyright 2010 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

Cardiovascular disease remains the leading cause of morbidity and mortality in developed nations. Inflammation plays an increasingly important role in the cardiovascular disease process. Recent statin trials have demonstrated a correlation between the inflammatory biomarker high-sensitivity C-reactive protein (hsCRP) and cardiovascular risk. This review describes the results of changes in hsCRP in the major statin outcome trials and the concept of a "dual target" for both low-density lipoprotein cholesterol and hsCRP. The effect on hsCRP of combination statin therapy with ezetimibe, fenofibric acid, niacin, and colesevelam is reviewed. Although some statin combination therapies have additional effects on CRP and other atherogenic lipids, evidence for their effect on cardiovascular risk beyond statin monotherapy is lacking. Ongoing placebo-controlled trials investigating statin combination therapy versus statin monotherapy may provide additional clues to the role of additional changes in lipids versus markers of inflammation on cardiovascular risk reduction. Until these trials are completed, current evidence suggests focusing on low-density lipoprotein cholesterol targets.

Intraarterial vasopressin has been reported to be effective in the treatment of massive upper gastrointestinal hemorrhage. A prospective, controlled clinical trial comparing conventional treatment with conventional therapy plus intraarterial vasopressin was undertaken. Sixty episodes of upper gastrointestinal hemorrhage were evaluated during a 40-month period; 32 received conventional and 28 conventional plus vasopressin therapy. The two groups of patients were similar in type and severity of their bleeding lesions and in their underlying diseases. Vasopressin was more effective in controlling hemorrhage from nonvariceal lesions (P less than 0.05) and from varices (P less than 0.01) than conventional therapy. Transfusion requirements were significantly reduced in those patients who received vasopressin. Paradoxically, survival was not affected by vasopressin administration. The failure of cessation of hemorrhage to improve survival is thought to be due to the degree of advancement of the underlying disease, to the torrential nature of the hemorrhage, to the frequency of recurrent hemorrhage, and to the use of intraarterial vasopressin in some patients in the conventional treatment group in whom conventional therapy had failed.

In a prospective, randomized, double-blind study of prednisolone therapy of acute alcoholic hepatitis, 39% of the total group of 28 patients died. Mortality and cumulative survival were similar in steroid- and placebo-treated patients. After 14 days of therapy, the serum albumin concentration and white blood count were significantly higher in the steroid group, but all other parameters were similar. An increased risk of fungal infection appeared to be associated with steroid therapy.