OBJECTIVE-The study evaluates lipids profile changes during gestation in pregnancies with and without preeclampsia and/or gestational diabetes.STUDY DESIGN-Lipid profiles were assessed between year prior and after pregnancy in 9911 women without cardiovascular comorbidities.RESULTS-Lipid levels during gestation varied substantially with a nadir following conception and a peak at delivery. Compared to preconception levels total cholesterol levels increased from 164.4 mg/dL to 238.6 mg/dL and triglycerides (TGs) from 92.6 mg/dL to 238.4 mg/dL. The composite endpoint (gestational diabetes mellitus or preeclampsia) occurred in 1209 women (12.2%). Its prevalence increased with levels of TG-from 7.2% in the group with low TGs (<25th percentile adjusted for the gestational month) to 19.8% in the group with high TGs (>75th percentile), but was not associated with high-density lipoprotein levels. In multivariate analysis higher TGs levels, but not low high-density lipoprotein, were associated with the primary endpoint.CONCLUSION-Lipid levels change substantially during gestation. Abnormal levels of TGs are associated with pregnancy complications. Keywords adverse outcomes; gestation; lipidsA number of diseases affecting the cardiovascular system emerge during pregnancy. Gestational diabetes mellitus is a risk factor for the development of type 2 diabetes and gestational hypertension is associated with an elevated risk for developing subsequent systemic hypertension. 1-3 Gestational diabetes and hypertension can contribute to maternal and fetal risk of developing peri-and postpartum complications. 4,5 Reprints: Victor Novack, MD, PhD,

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Therapy with statins may be associated with a reduced risk of infection-related mortality. This protective effect is independent of all known comorbidities and dissipates when the medication is discontinued. If this finding is supported by prospective controlled trials, statins may play an important role in the primary prevention of infection-related mortality.

This review article integrates empirical findings from various scientific disciplines into a proposed psychoneuroimmunological (PNI) model of the acute coronary syndrome (ACS). Our starting point is an existing, mild, atherosclerotic plaque and a dysfunctional endothelium. The ACS is triggered by three stages. (1) Plaque instability: Pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha) and chemoattractants (MCP-1, IL-8) induce leukocyte chemoattraction to the endothelium, and together with other triggers such as the CD40L-CD40 co-stimulation system activate plaque monocytes (macrophages). The macrophages then produce matrix metalloproteinases that disintegrate extra-cellular plaque matrix, causing coronary plaque instability. Acute stress, hostility, depression and vital exhaustion (VE) have been associated with elevated pro-inflammatory cytokines and leukocyte levels and their recruitment. (2) Extra-plaque factors promoting rupture: Neuro-endocrinological factors (norepinephrine) and cytokines induce vasoconstriction and elevated blood pressure (BP), both provoking a vulnerable plaque to rupture. Hostility/anger and acute stress can lead to vasoconstriction and elevated BP via catecholamines. (3) Superimposed thrombosis at a ruptured site: Increases in coagulation factors and reductions in anticoagulation factors (e.g. protein C) induced by inflammatory factors enhance platelet aggregation, a key stage in thrombosis. Hostility, depression and VE have been positively correlated with platelet aggregation. Thrombosis can lead to severe coronary occlusion, clinically manifested as an ACS. Thus, PNI processes might, at least in part, contribute to the pathogenesis of the ACS. This chain of events may endure due to lack of neuroendocrine-to-immune negative feedback stemming from cortisol resistance. This model has implications for the use of psychological interventions in ACS patients.

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With this method, CFD levels correlated with the levels of established markers of myocardial necrosis but not with EF. The kinetic pattern of CFD release after STEMI and its prognostic value require further investigation.