Authors:
Kim G. Jackson, Anne Marie Minihane
Abstract:
case–control studies have further qualitatively established nonfasting TAG as a CVD risk factor [16,17], with information on the quantitative relationship limited to a small number of studies [6,8,9,18,19]. In the Copenhagen Heart Study, nonfasting TAG levels of more than or equal to 5, 4–4.99, 3–3.99, 2–2.99 and 1–1.99 mmol/l versus less than 1 mmol/l were shown to predict a 16.8-, 5.1-, 3.9-, 4.4and 2.2-fold increase in risk of myocardial infarction in females, respectively, with equivalent values in males of 4.6-, 3.3-, 3.6-, 2.3an (...)
case–control studies have further qualitatively established nonfasting TAG as a CVD risk factor [16,17], with information on the quantitative relationship limited to a small number of studies [6,8,9,18,19]. In the Copenhagen Heart Study, nonfasting TAG levels of more than or equal to 5, 4–4.99, 3–3.99, 2–2.99 and 1–1.99 mmol/l versus less than 1 mmol/l were shown to predict a 16.8-, 5.1-, 3.9-, 4.4and 2.2-fold increase in risk of myocardial infarction in females, respectively, with equivalent values in males of 4.6-, 3.3-, 3.6-, 2.3and 1.6-fold, respectively [8]. This greater ‘penetrance’ in females is consistent with an earlier meta-ana lysis that considered fasting TAG data [4].
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