Uric Acid—An Emergent Risk Marker for Thrombosis?

Hyperuricemia is nowadays an established cardiovascular risk factor. Experimental studies linked elevated serum uric acid (SUA) levels with endothelial dysfunction (ED), inflammation, and prothrombotic state. The purpose of this review is to summarize the current evidence that emphasizes the possible role of uric acid as a biomarker for a prothrombotic state. A large number of clinical trials correlated SUA levels with both incident and recurrent cases of venous thromboembolism (VTE), independent of other confounding risk factors. Moreover, increased SUA levels may be an important tool for the risk stratification of patients with pulmonary embolism (PE). Left atrial thrombosis was correlated with high SUA levels in several studies and its addition to classical risk scores improved their predictive abilities. In patients with acute myocardial infarction (MI), hyperuricemia was associated with increased mortality, and the idea that hyperuricemia may be able to act as a surrogate to unstable coronary plaques was advanced. Finally, SUA was correlated with an increased risk of thromboembolic events in different systemic diseases. In conclusion, uric acid has been considered a marker of a thrombotic milieu in several clinical scenarios. However, this causality is still controversial, and more experimental and clinical data is needed.

Serotonin: a platelet hormone modulating cardiovascular disease

Cardiovascular diseases and depression are significant health burdens and increasing evidence suggests a causal relationship between them. The incidence of depression among patients suffering from cardiovascular disease is markedly elevated, and depression itself is an established cardiovascular risk factor. Serotonin 5-hydroxytryptamin (5-HT), a biogenic amine acting as a neurotransmitter and a peripheral hormone, is involved in the pathogenesis of both, cardiovascular disease and depression. Novel cardiovascular functions of 5-HT have recently been described and will be summarized in this review. 5-HT has a broad spectrum of functions in the cardiovascular system, yet the clinical or experimental data are partly conflicting. There is further research needed to characterize the clinical effects of 5-HT in particular tissues to enable targeted pharmacological therapies.

Preeclampsia Is Associated With Increased Preclinical Carotid Atherosclerosis in Women With Type 1 Diabetes

Purpose Although preeclampsia (PE) is a well-established cardiovascular risk factor (CVRF) in the general population, its role in type 1 diabetes (T1D) has been scarcely studied. We assessed the association between PE and preclinical atherosclerosis in T1D. Methods We recruited 112 women without cardiovascular disease and last pregnancy ≥5 years before: (1) T1D and previous PE (T1D+/PE+; n = 28); (2) T1D without preeclampsia (T1D+/PE–; n = 28); (3) previous PE without T1D (T1D–/PE+; n = 28); and (4) controls (without T1D or PE; T1D–/PE–; n = 28). Groups were matched by age, several CVRFs, and diabetes duration and retinopathy (in T1D participants). Carotid intima-media thickness (IMT) and the presence of plaque (IMT ≥ 1.5 mm) were assessed by standardized ultrasonography protocol. Results Mean age of the participants was 44.9 ± 7.8 years (14.3% hypertension and 21.4% active smokers). Groups including T1D (T1D+/PE+ and T1D+/PE–) more frequently presented hypertension and statin treatment (23.2% vs 5.4% and 37.5% vs 8.9%; respectively; P < 0.01), without differences in other CVRFs. Carotid plaques were observed in 20.5%. In multivariate models adjusted for age, CVRF, and statins, both T1D and PE showed a similar impact on the presence of plaque, with odds ratios (95% confidence interval), 5.45 (1.36–21.9) and 4.24 (1.04–17.3), respectively. Both entities showed an additive effect when combined, both in common carotid-IMT (T1D+/PE– or T1D–/PE+, β = 0.198; T1D+/PE+, β = 0.297) and in the presence of plaque (8.53 [1.07–68.2] and 28.1 [2.67–296.4], respectively). Conclusions Previous PE was independently associated with preclinical atherosclerosis in T1D. Further studies are needed to ascertain its usefulness for stratifying risk in T1D women.

Body Mass Index and Hospital Mortality in Patients with Acute Coronary Syndrome Receiving Care in a University Hospital

Although obesity is a well-established cardiovascular risk factor, some controversy has arisen with regard to its effect on hospital mortality in patients admitted for acute coronary syndrome.Methods. Clinical and anthropometric variables were analyzed in patients consecutively admitted for acute coronary syndrome to a university hospital between 2009 and 2010, and the correlation of those variables with hospital mortality was examined.Results. A total of 824 patients with a diagnosis of myocardial infarction or unstable angina were analyzed. Body mass index was an independent factor in hospital mortality (odds ratio 0.739 (IC 95%:0.597-0.916),P=0.006). Mortality in normal weight(n=218), overweight(n=399), and obese(n=172)subjects was 6.1%, 3.1%, and 4.1%, respectively, with no statistically significant differences between the groups.Conclusions. There is something of a paradox in the relationship between body mass index and hospital mortality in patients with acute coronary syndrome in that the mortality rate decreases as body mass index increases. However, no statistically significant differences have been found in normal weight, overweight, or obese subjects.