Biosensors, Aarhus University Hospital, and participating sites.

AstraZeneca, Biosensors, and The Medicines Company.

Myocardial and vascular endothelial tissues have receptors for thyroid hormones and are sensitive to changes in the concentrations of circulating thyroid hormones. The importance of thyroid hormones in maintaining cardiovascular homeostasis can be deduced from clinical and experimental data showing that even subtle changes in thyroid hormone concentrations - such as those observed in subclinical hypothyroidism or hyperthyroidism, and low triiodothyronine syndrome - adversely influence the cardiovascular system. Some potential mechanisms linking the two conditions are dyslipidaemia, endothelial dysfunction, blood pressure changes, and direct effects of thyroid hormones on the myocardium. Several interventional trials showed that treatment of subclinical thyroid diseases improves cardiovascular risk factors, which implies potential benefits for reducing cardiovascular events. Over the past 2 decades, accumulating evidence supports the association between abnormal thyroid function at the time of an acute myocardial infarction (MI) and subsequent adverse cardiovascular outcomes. Furthermore, experimental studies showed that thyroid hormones can have an important therapeutic role in reducing infarct size and improving myocardial function after acute MI. In this Review, we summarize the literature on thyroid function in cardiovascular diseases, both as a risk factor as well as in the setting of cardiovascular diseases such as heart failure or acute MI, and outline the effect of thyroid hormone replacement therapy for reducing the risk of cardiovascular disease.

P reeclampsia is a major cause of maternal mortality worldwide 1 and affects 2% to 8% of all pregnancies. 2,3 It is confined to pregnancy and defined as onset of hypertension after 20-week gestation with proteinuria, organ dysfunction, or uteroplacental dysfunction. 4 The pathogenesis of preeclampsia remains poorly understood and is thought to be because of the failure of spiral artery remodeling in the placenta causing placental hypoperfusion and hypoxia. The resultant oxidative stress triggers an excessive systemic inflammatory response, which causes endothelial dysfunction and vasoconstriction leading to systemic hypertension and end-organ hypoperfusion. 2,5 There is growing evidence that these effects on end organs persist after pregnancy.Cardiovascular disease is a leading cause of mortality globally and also of maternal death in the United Kingdom and United States. 6,7 Several studies have examined the relationship between preeclampsia and future incident cardiovascular disease, although the literature has been inconsistent. Some studies reported significantly higher risks of composite cardiovascular events or heart failure, 8,9 whereas others have not demonstrated such relationships. 10,11 It is unclear whether preeclampsia is an independent risk factor for future cardiovascular disease or an early marker of women with high-risk profiles for future cardiovascular disease. Factors that predispose women to preeclampsia are also found in the risk profile for cardiovascular diseases. These include obesity, 12 metabolic abnormalities, dyslipidemia, insulin resistance, 13 heightened inflammatory responses, hypercoagulable states, and endothelial dysfunction.14 Alternatively, the body may not fully recover from the damage to the Background-Preeclampsia is a pregnancy-specific disorder resulting in hypertension and multiorgan dysfunction. There is growing evidence that these effects persist after pregnancy. We aimed to systematically evaluate and quantify the evidence on the relationship between preeclampsia and the future risk of cardiovascular diseases. Methods and Results-We studied the future risk of heart failure, coronary heart disease, composite cardiovascular disease, death because of coronary heart or cardiovascular disease, stroke, and stroke death after preeclampsia. A systematic search of MEDLINE and EMBASE was performed to identify relevant studies. We used random-effects meta-analysis to determine the risk. Twenty-two studies were identified with >6.4 million women including >258 000 women with preeclampsia. Meta-analysis of studies that adjusted for potential confounders demonstrated that preeclampsia was independently associated with an increased risk of future heart failure (risk ratio ). Conclusions-Preeclampsia is associated with a 4-fold increase in future incident heart failure and a 2-fold increased risk in coronary heart disease, stroke, and death because of coronary heart or cardiovascular disease. Our study highlights the importance of lifelong monitoring of cardiovascular risk f...

A combination of prolonged SAPD, advanced age, and male sex identifies patients at high risk for development of AF after CABG.

Thyroid hormone (TH) receptors are present in the myocardium and vascular tissue, and minor alterations in TH concentration can affect cardiovascular (CV) physiology. The potential mechanisms that link CV disease with thyroid dysfunction are endothelial dysfunction, changes in blood pressure, myocardial systolic and diastolic dysfunction, and dyslipidemia. In addition, cardiac disease itself may lead to alterations in TH concentrations (notably, low triiodothyronine syndrome) that are associated with higher morbidity and mortality. Experimental data and small clinical trials have suggested a beneficial role of TH in ameliorating CV disease. The aim of this review is to provide clinicians dealing with CV conditions with an overview of the current knowledge of TH perturbations in CV disease.

In ambulant outpatients with chronic HF, low serum sodium and SDNN and high serum creatinine identify patients at increased risk of death due to progressive HF.

Anomalous radial artery anatomy is relatively common and is a significant cause of procedural failure. Within each specific anomalous pattern there is a differential procedural failure rate. This has implications for clinical practice and suggests a need for imaging of the radial artery after sheath insertion.