Journal of internal medicine
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The prognosis of patients with congenital heart defects has improved significantly: more and more patients reach adulthood and old age. At the same time, the possibility of cardiovascular morbidity increases. The conventional risk factors for coronary artery disease are at least as high or even higher in patients than in the general population. ⋯ Fontan), the incidence of CAD might be lower, but it usually returns to the average level or higher after correction of the defect. Coronary artery disease is one of the most important reasons for mortality also in ACHD patients, and the consequences of a coronary event might be more fateful in a patient with a corrected congenital heart defect than in her/his peer. There should be a paradigm shift from operative mortality and short-term outcome to long-term morbidity and prevention of cardiovascular disease - a task that often has been forgotten during follow-up visits.
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Renewed interest in triglyceride-rich lipoproteins as causative agents in cardiovascular disease mandates further exploration of the integrated metabolism of chylomicrons and very low-density lipoproteins (VLDL). ⋯ The intestine secretes apoB48-containing particles not only as chylomicrons but also directly into the VLDL1 and VLDL2 density ranges both in the basal state and during dietary lipid absorption. Over the day, apoB48-containing particles appear to comprise about 20-25% of circulating VLDL and, especially in those with elevated triglycerides, form part of a slowly cleared 'remnant' particle population, thereby potentially increasing CHD risk. These findings provide a metabolic understanding of the potential consequences for increased CHD risk when slowed lipolysis leads to the accumulation of remnants, especially in individuals with hypertriglyceridemia.
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The carnitine precursor trimethyllysine (TML) is associated with progression of atherosclerosis, possibly through a relationship with trimethylamine-N-oxide (TMAO). Riboflavin is a cofactor in TMAO synthesis. We examined prospective relationships of circulating TML and TMAO with acute myocardial infarction (AMI) and potential effect modifications by riboflavin status. ⋯ Amongst patients with suspected stable angina pectoris, plasma TML, but not TMAO, independently predicted risk of AMI. Our results motivate further research on metabolic processes determining TML levels and their potential associations with cardiovascular disease. We did not adjust for multiple comparisons, and the subgroup analyses should be interpreted with caution.