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Aims Heart failure (HF) confers potentially negative effects on the brain and autonomic nervous system. The measurement cerebral tissue oxygen saturation (SctO2) may aid in understanding such effects. We aimed to investigate if compensated HF affects SctO2 at rest and during orthostatic challenge. Methods and results Non‐invasive haemodynamic monitoring and near‐infrared spectroscopy were applied during head‐up tilt (HUT) in 61 HF patients [mean (SD) 71 (11) years, 82% male, New York Heart Association (NYHA) class I–III] and 60 controls [60 (12) years, 42% male). Group differences in continuous variables were compared using Student's t‐test. Associations between HF and SctO2 were studied using multivariable linear regression models adjusted for age, sex, diabetes, smoking, systolic blood pressure (SBP), and heart rate in supine position and after 10 min of HUT. Mean SctO2 was lower in HF patients compared with controls both in the supine position (67 vs. 71%; P

Background Vasovagal reflex is the most common form of syncope, but the pathophysiological mechanisms that initiate the reflex are not well understood. We aimed to study supine and early orthostatic levels of the neurohormones involved in control of circulatory homeostasis in relation to the onset of tilt‐induced vasovagal syncope (VVS). Methods and Results A total of 827 patients who were investigated for unexplained syncope with head‐up tilt test (HUT) and optional nitroglycerin provocation (Italian protocol) had blood samples collected while supine and after 3‐minutes of HUT. Of these, 173 (20.9%) patients developed VVS during drug‐free HUT, 161 of whom (males 44.7%; age 45±21 years) had complete data. We analyzed levels of epinephrine, norepinephrine, C‐terminal pro–arginine vasopressin, C‐terminal endothelin‐1, and midregional fragments of pro–atrial natriuretic peptide and pro‐adrenomedullin in relation to time from tilt‐up to onset of VVS. We applied a linear regression model adjusted for age and sex. The mean time to syncope was 11±7 minutes. Older age (β=0.13; SE=0.03, P P =0.02), and higher supine midregional fragment of pro‐adrenomedullin predicted longer time to syncope (β=2.31; SE=0.77, P =0.003), whereas supine levels of other neurohormones were not associated with time to syncope. Among 151 patients who developed VVS later than 3 minutes of HUT, increase in epinephrine (β=−3.24; SE=0.78, P P =0.001) at 3 minutes of HUT were related to shorter time to syncope. Conclusions Older age, higher blood pressure, and higher level of pro‐adrenomedullin are associated with later onset of VVS during tilt testing, whereas greater increase of tilt‐induced epinephrine and vasopressin release correlate with shorter time to syncope.

BACKGROUND: Risk factors included in the cardiovascular (CHA2 DS2 -VASc) score, currently used for atrial fibrillation (AF), may predispose to cardiovascular events whether or not AF is present. The aim was to explore the predictive role of CHA2 DS2 -VASc score on cardiovascular outcomes in diabetic patients without AF. METHODS: We accessed individual data from 610 diabetic patients without AF at baseline included in the prospective cohort of the Malmö Diet and Cancer study. Main outcome measure was the occurrence of cardiovascular events (stroke, coronary events) and death. Mean follow-up was 14.5 ± 5 years (8845 person/years). RESULTS: The CHA2 DS2 -VASc score significantly predicted the risk of all outcome measures. There was a significant increase in stroke, coronary events, and death risk by each point of CHA2 DS2 -VASc score elevation [stroke: adjusted hazard ratio (aHR) 1.43, 95% CI 1.14-1.79, P = 0.001; coronary events: aHR 1.55, 95% CI 1.34-1.80, P

Atherosclerotic cardiovascular disease (CVD) is a leading cause of mortality and morbidity worldwide, with coronary artery disease (CAD) being the single leading cause of death. Better control of risk factors, enhanced diagnostic techniques and improved medical therapies have all substantially decreased the mortality of CAD in developed countries. However, CAD and other forms of atherosclerotic CVD are projected to remain the leading cause of death by 2030 and we face a number of challenges if the outcomes of CAD are to be further improved. The fact that a substantial fraction of high-risk subjects do not reach treatment goals for important risk factors is one of these challenges. At the same time, there is also a non-negotiable fraction of 'concealed' high-risk subjects who are not detected by current risk algorithms and diagnostic modalities. In recent years, we have started to rapidly increase our knowledge of the framework of common genetics underlying CAD and atherosclerotic CVD in the population. In conjunction with modern diagnostic and therapeutic options, this new genetic knowledge may provide a valuable tool for further improvements in prevention. This review summarizes the recent findings from the search for common genetic risk factors for CAD. Furthermore, the author discusses how such recent findings could potentially be used in a number of clinical applications within CAD prevention, including in clinical risk stratification, in prediction of drug treatment response and in the search for targets for novel preventive therapies.

Objective: To assess whether a genetic risk score that was previously shown to be associated with myocardial infarction and coronary artery disease is also associated with markers of carotid atherosclerosis. Design: A total of 4022 middle-aged subjects from the general Swedish population were genotyped and individually assigned a genetic risk score based on 13 single-nucleotide polymorphisms (SNPs), previously associated with myocardial infarction and coronary artery disease. The genetic score (Score-MI) was then related to carotid bulb intima-media thickness (IMT), common carotid artery IMT and to the occurrence of carotid plaques in the study population. Results: Score-MI was associated with IMT of the bulb (P