Rosuvastatin did not reduce the primary outcome or the number of deaths from any cause in older patients with systolic heart failure, although the drug did reduce the number of cardiovascular hospitalizations. The drug did not cause safety problems. (ClinicalTrials.gov number, NCT00206310.)

Polymorphisms in the CRP gene are associated with marked increases in CRP levels and thus with a theoretically predicted increase in the risk of ischemic vascular disease. However, these polymorphisms are not in themselves associated with an increased risk of ischemic vascular disease.

A strategy for reperfusion involving the transfer of patients to an invasive-treatment center for primary angioplasty is superior to on-site fibrinolysis, provided that the transfer takes two hours or less.

AZD6140 exhibited greater mean inhibition of platelet aggregation than a standard regimen of clopidogrel in ACS patients. In addition, AZD6140 further suppressed platelet aggregation in clopidogrel pretreated patients.

PIDEMIOLOGICAL STUDIES CONSIStently demonstrate that a low plasma level of high-density lipoprotein (HDL) cholesterol is associated with increased risk of ischemic heart disease (IHD). 1 However, whether HDL cholesterol is a primary causal factor in the pathogenesis of IHD is unclear. Data from observational studies are potentially confounded by other factors related to low HDL cholesterol levels that may contribute independently to increases in cardiovascular events. One such factor is plasma triglycerides, 2 a marker for the presence of atherogenic remnant lipoproteins. 3-5 Mendelian randomization, which is the random assortment of genes from parents to offspring that occurs during gamete formation, provides a method of assessing whether modifiable exposures are causally related to increased risk of IHD. 6 Thus, studies of genetic disorders that lower HDL cholesterol without increases in plasma triglycerides and remnant lipoproteins provide an ideal system in which to assess the consequences of isolated, lifelong low HDL cholesterol levels. A genetic disorder that fulfills such a criterion is Tangier disease, which is due to loss-of-function mutations in the adenosine triphosphatebinding cassette transporter A1 (ABCA1; GenBank No. AF275948) gene and results in unmeasurable HDL cholesterol levels in homozygotes and half-normal HDL cholesterol levels in heterozygotes. Family studies of homozygotes or heterozygotes for these severe HDL de-Author Affiliations are listed at the end of this article.

These data are consistent with a causal association between elevated levels of remnant cholesterol in hypertriglyceridaemia and an increased risk of MI. Limitations include that remnants were not measured directly, and that APOA5 genetic variants may influence other lipoprotein parameters.

Patients who survive the first month after an STEMI treated with primary PCI have an excellent prognosis, with a <1.5% annual risk of successive cardiac death. Noncardiac causes are responsible for the majority of later deaths in these patients.

The PCSK9 46L allele was associated with reductions in LDL-C from 20 to 80+ years in the general population. The reduction in risk of IHD was larger than predicted by the observed reduction in LDL-C alone. This could be because genotype is a better predictor of lifelong exposure to LDL-C than LDL-C measured in adult life.