Background-The CD14 receptor of monocytes is an important mediator for the activation of monocytes/macrophages by endotoxins from the envelope of Gram-negative bacteria (lipopolysaccharides). We identified a polymorphism in the CD14 receptor and examined whether this genetic marker influenced the expression of the CD14 receptor on monocytes and affected the predisposition to myocardial infarction. Methods and Results-We identified a C(Ϫ260)3 T nucleotide change, creating a HaeIII polymorphism in the promoter of the CD14 gene. The polymorphism was determined in 178 male patients Ͻ65 years old (cases; average age, 55.9Ϯ6.3 years) at the time of their first myocardial infarction and in 135 representative selected male control subjects (controls; average age, 55.2Ϯ11.5 years). The frequency of the T allele (absence of the cutting site) was 0.49 in cases and 0.35 in controls (Pϭ0.0005; OR, 1.781; 95% CI, 1.286 to 2.465). Subsequently, we measured the expression of monocyte CD14 by flow cytometry in 18 volunteers with different CD14 genotypes. A significantly higher density of the CD14 receptor was shown in the T/T homozygotes than in the others (Pϭ0.0028). Conclusions-A higher frequency of allele T(Ϫ260) in the promoter of the CD14 receptor gene was found in myocardial infarction survivors than in controls. At the same time, this variation was associated with a higher density of CD14 receptors in healthy volunteers. Therefore, we can conclude that in addition to the well-established risk factors, a genetically determined reaction of monocytes/macrophages to infectious stimuli could play an important role in the process of atherosclerosis. (Circulation. 1999;99:3218-3220.)

Aims The aim of the present paper was to provide an up-to-date view on epidemiology and risk factors of heart failure (HF) development after myocardial infarction. Methods and results Based on literature review, several clinical risk factors and biochemical, genetic, and imaging biomarkers were identified to predict the risk of HF development after myocardial infarction. Conclusions Heart failure is still a frequent complication of myocardial infarction. Timely identification of subjects at risk for HF development using a multimodality approach, and early initiation of guideline-directed HF therapy in these patients, can decrease the HF burden.

Although Dynamic Registry patients had more unstable and complex coronary disease than those in the 1985-1986 Registry, their rate of procedural success was higher whereas rates of complications and subsequent CABG were lower. Results of percutaneous coronary intervention have improved substantially over the past decade.