Explore the vast range of titles available.

Chocolate consumption could hypothetically improve cognitive function not only in individuals but in whole populations. Could there be a correlation between a country's level of chocolate consumption and its total number of Nobel laureates per capita? Dietary flavonoids, abundant in plant-based foods, have been shown to improve cognitive function. Specifically, a reduction in the risk of dementia, enhanced performance on some cognitive tests, and improved cognitive function in elderly patients with mild impairment have been associated with a regular intake of flavonoids. 1 , 2 A subclass of flavonoids called flavanols, which are widely present in cocoa, green tea, red wine, and some fruits, seems to be effective in slowing down or even reversing the reductions in cognitive performance that occur with aging. Dietary flavanols have also been shown to improve endothelial function and to lower blood pressure . . .

This secondary analysis of findings from a trial that assessed the effect of low-density lipoprotein cholesterol levels in patients with coronary artery disease shows that body-weight fluctuation was associated with an increased risk of death and cardiovascular events. Obesity is an independent risk factor for cardiovascular death and disease. 1 , 2 Among participants in the Framingham Heart Study who were between 35 and 75 years of age and were followed for up to 44 years, overweight and obese participants were at a higher risk for the development of cardiovascular disease than participants of normal weight. 3 Weight gain is strongly associated with an increased risk of death and disease among participants without evident cardiovascular disease at baseline. 4 , 5 Indeed, in obese persons, bariatric surgery followed by weight loss reduces the risk of cardiovascular disease, including hypertension, hypercholesterolemia, and diabetes. 6 – . . .

Objective To evaluate the outcomes with use of renin angiotensin system (RAS) blockers compared with other antihypertensive agents in people with diabetes.Design Meta-analysis.Data sources and study selection PubMed, Embase, and the Cochrane central register of controlled trials databases for randomized trials of RAS blockers versus other antihypertensive agents in people with diabetes mellitus. Outcomes were death, cardiovascular death, myocardial infarction, angina, stroke, heart failure, revascularization, and end stage renal disease.Results The search yielded 19 randomized controlled trials that enrolled 25 414 participants with diabetes for a total of 95 910 patient years of follow-up. When compared with other antihypertensive agents, RAS blockers were associated with a similar risk of death (relative risk 0.99, 95% confidence interval 0.93 to 1.05), cardiovascular death (1.02, 0.83 to 1.24), myocardial infarction (0.87, 0.64 to 1.18), angina pectoris (0.80, 0.58 to 1.11), stroke (1.04, 0.92 to 1.17), heart failure (0.90, 0.76 to 1.07), and revascularization (0.97, 0.77 to 1.22). There was also no difference in the hard renal outcome of end stage renal disease (0.99, 0.78 to 1.28) (power of 94% to show a 23% reduction in end stage renal disease).Conclusions In people with diabetes, RAS blockers are not superior to other antihypertensive drug classes such as thiazides, calcium channel blockers, and β blockers at reducing the risk of hard cardiovascular and renal endpoints. These findings support the recommendations of the guidelines of the European Society of Cardiology/European Society of Hypertension and eighth Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure to also use other antihypertensive agents in people with diabetes but without kidney disease.

Essential hypertension can be defined as a rise in blood pressure of unknown cause that increases risk for cerebral, cardiac, and renal events. In industrialised countries, the risk of becoming hypertensive (blood pressure >140/90 mm Hg) during a lifetime exceeds 90%. Essential hypertension usually clusters with other cardiovascular risk factors such as ageing, being overweight, insulin resistance, diabetes, and hyperlipidaemia. Subtle target-organ damage such as left-ventricular hypertrophy, microalbuminuria, and cognitive dysfunction takes place early in the course of hypertensive cardiovascular disease, although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen after long periods of uncontrolled hypertension only. All antihypertensive drugs lower blood pressure (by definition) and this decline is the best determinant of cardiovascular risk reduction. However, differences between drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascular events. Most hypertensive patients need two or more drugs for blood-pressure control and concomitant statin treatment for risk factor reduction. Despite the availability of effective and safe antihypertensive drugs, hypertension and its concomitant risk factors remain uncontrolled in most patients.

To compare the efficacy and safety of angiotensin-converting enzyme inhibitors (ACEis) and angiotensin receptor blockers (ARBs) in patients without heart failure. Meta-analysis of randomized trials identified using PubMed, Embase, and Cochrane Central Register of Controlled Trials searches from January 1, 1980, through April 13, 2015, of ACEis and ARBs compared with placebo or active controls and corroborated with head-to-head trials of ARBs vs ACEis. Outcomes were all-cause mortality, cardiovascular death, myocardial infarction (MI), angina, stroke, heart failure, revascularization, and new-onset diabetes. Our search yielded 106 randomized trials that enrolled 254,301 patients. Compared with placebo, ACEis but not ARBs reduced the outcomes of all-cause mortality (ACEis vs placebo: relative risk [RR], 0.89; 95% CI, 0.80-1.00; ARBs vs placebo: RR, 1.01; 95% CI, 0.96-1.06; Pinteraction=.04), cardiovascular death (RR, 0.83; 95% CI, 0.70-0.99 and RR, 1.02; 95% CI, 0.92-1.14; Pinteraction=.05), and MI (RR, 0.83; 95% CI, 0.78-0.90 and RR, 0.93; 95% CI, 0.85-1.03; Pinteraction=.06). The meta-regression analysis revealed that the difference between ACEis and ARBs compared with placebo was due to a higher placebo event rate in the ACEis trials (most of these trials were conducted a decade earlier than the ARB trials) for the outcome of all-cause mortality (P=.001), cardiovascular death (P<.001), and MI (P=.02). Sensitivity analyses restricted to trials published after 2000 revealed similar outcomes with ACEis vs placebo and ARBs vs placebo (Pinteraction>.05). Head-to-head comparison trials of ARBs vs ACEis exhibited no difference in outcomes except for a lower risk of drug withdrawal due to adverse effects with ARBs (RR, 0.72; 95% CI, 0.65-0.81). In patients without heart failure, evidence from placebo-controlled trials (restricted to trials after 2000), active controlled trials, and head-to-head randomized trials all suggest ARBs to be as efficacious and safe as ACEis, with the added advantage of better tolerability.

Presence of left ventricular hypertrophy (LVH) has been reported to be associated with supraventricular and ventricular arrhythmias, but the association has not been systematically quantified and evaluated. A systematic search of studies in MEDLINE, EMBASE, CINAHL, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials databases was undertaken through April 2014. Studies reporting on LVH and sustained arrhythmias such as atrial fibrillation and supraventricular tachycardias (SVTs) and ventricular arrhythmias (tachycardia and fibrillation) were identified. Pooled effect estimates were calculated with random-effects models (DerSimonian and Laird). A total of 10 eligible studies with 27,141 patients were included in the analysis. The incidence of SVT in patients with LVH was 11.1% compared with 1.1% among patients without LVH (p <0.001). Patients with LVH had 3.4-fold greater odds of developing SVT (odds ratio 3.39, 95% confidence interval 1.57 to 7.31) than those without LVH, although significant heterogeneity was present (I2 = 98%). Meta-regression analyses revealed the heterogeneity to have originated from differences in the baseline covariates such as age, male gender, hypertension, and diabetes of the individual studies. The incidence of ventricular arrhythmias was 5.5% compared with 1.2% in patients without LVH (p <0.001). The occurrence of ventricular tachycardia or fibrillation was 2.8-fold greater, in the presence of LVH (odds ratio 2.83, 95% confidence interval 1.78 to 4.51), and there was no significant heterogeneity (I2 = 9%). Presence of LVH in hypertensive patients is associated with a greater risk of sustained supraventricular/atrial and ventricular arrhythmias, and there is an unmet need for identifying and refining risk stratification for this group. This systematic review and meta-analysis revealed that•Patients with left ventricular hypertrophy (LVH) had 3.4-fold greater odds of supraventricular tachycardia.•The patients with LVH had 2.8 times greater odds of ventricular tachycardia or fibrillation.•Patients with LVH should therefore be risk stratified and followed up closely for earlier detection of these arrhythmias.

Obesity has been shown to be associated with atrial enlargement and ventricular diastolic dysfunction, both of which are risk factors for atrial fibrillation (AF). However, the role of obesity as a risk factor for the development of AF is unknown. The study aims to evaluate the role of obesity as a risk factor for the development of AF. The MEDLINE/ PUBMED and Cochrane databases were searched for studies in human subjects published in English language between 1966 and May 2007. Studies were included in our analyses if they were population-based cohort or postcardiac surgery cohort and investigated the incidence of AF in relation to the body mass index (BMI) categories. Of the 468 articles identified, 16 studies that enrolled a total of 123 249 individuals met the inclusion criteria. These 16 articles included 5 population-based cohort studies that enrolled 78 602 adult individuals from the United States and 3 European countries and 11 postcardiac surgery studies that enrolled 44 647 patients. Based on the population-based cohort studies, obese individuals have an associated 49% increased risk of developing AF compared to nonobese individuals (relative risk 1.49, 95% CI 1.36-1.64). The risk of AF increased in parallel with greater BMI in this cohort. In contrast, in the postcardiac surgery studies, obese individuals do not have an associated increased risk of developing AF compared to nonobese individuals (relative risk 1.02, 95% CI 0.99-1.06). Our findings demonstrate that obesity increased the risk of developing AF by 49% in the general population, and the risk escalated in parallel with increased BMI. Thus, AF evolves as yet another pathogenetic factor by which obesity may increase cardiovascular and cerebrovascular events.

The risk of cancer from antihypertensive drugs has been much debated, with a recent analysis showing increased risk with angiotensin-receptor blockers (ARBs). We assessed the association between antihypertensive drugs and cancer risk in a comprehensive analysis of data from randomised clinical trials. We undertook traditional direct comparison meta-analyses, multiple comparisons (network) meta-analyses, and trial sequential analyses. We searched PubMed, Embase, and the Cochrane Central Register of Controlled Trials from 1950, to August, 2010, for randomised clinical trials of antihypertensive therapy (ARBs, angiotensin-converting-enzyme inhibitors [ACEi], β blockers, calcium-channel blockers [CCBs], or diuretics) with follow-up of at least 1 year. Our primary outcomes were cancer and cancer-related deaths. We identified 70 randomised controlled trials (148 comparator groups) with 324 168 participants. In the network meta-analysis (fixed-effect model), we recorded no difference in the risk of cancer with ARBs (proportion with cancer 2·04%; odds ratio 1·01, 95% CI 0·93–1·09), ACEi (2·03%; 1·00, 0·92–1·09), β blockers (1·97%; 0·97, 0·88–1·07), CCBs (2·11%; 1·05, 0·96–1·13), diuretics (2·02%; 1·00, 0·90–1·11), or other controls (1·95%, 0·97, 0·74–1·24) versus placebo (2·02%). There was an increased risk with the combination of ACEi plus ARBs (2·30%, 1·14, 1·02–1·28); however, this risk was not apparent in the random-effects model (odds ratio 1·15, 95% CI 0·92–1·38). No differences were detected in cancer-related mortality for ARBs (death rate 1·33%; odds ratio 1·00, 95% CI 0·87–1·15), ACEi (1·25%; 0·95, 0·81–1·10), β blockers (1·23%; 0·93, 0·80–1·08), CCBs (1·27%; 0·96, 0·82–1·11), diuretics (1·30%; 0·98, 0·84–1·13), other controls (1·43%; 1·08, 0·78–1·46), and ACEi plus ARBs (1·45%; 1·10, 0·90–1·32). In direct comparison meta-analyses, similar results were recorded for all antihypertensive classes, except for an increased risk of cancer with ACEi and ARB combination (OR 1·14, 95% CI 1·04–1·24; p=0·004) and with CCBs (1·06, 1·01–1·12; p=0·02). However, we noted no significant differences in cancer-related mortality. On the basis of trial sequential analysis, our results suggest no evidence of even a 5–10% relative risk (RR) increase of cancer and cancer-related deaths with any individual class of antihypertensive drugs studied. However, for the ACEi and ARB combination, the cumulative Z curve crossed the trial sequential monitoring boundary, suggesting firm evidence for at least a 10% RR increase in cancer risk. Our analysis refutes a 5·0–10·0% relative increase in the risk of cancer or cancer-related death with the use of ARBs, ACEi, β blockers, diuretics, and CCBs. However, increased risk of cancer with the combination of ACEi and ARBs cannot be ruled out. None.

Newer oral P2Y12 inhibitors are more potent and have faster onset of action than clopidogrel. However, the efficacy and safety in patients with non–ST-elevation acute coronary syndrome (NSTE-ACS) are not well studied. A systemic search of MEDLINE and EMBASE databases was performed to identify randomized clinical trials comparing newer oral P2Y12 inhibitors (prasugrel or ticagrelor) to clopidogrel in patients with NSTE-ACS. The primary outcome was a composite of cardiovascular death, myocardial infarction (MI), and stroke (major cardiovascular events [MACE]). Secondary outcomes were individual components of the primary outcome, all-cause mortality, and Thrombolysis In Myocardial Infarction (TIMI) major and minor bleeding. A total of 31,470 patients with NSTE-ACS from 4 randomized clinical trials were included (newer oral P2Y12 inhibitors: 15,951; clopidogrel: 15,519). Newer oral P2Y12 inhibitors significantly decreased MACE (relative risk [RR] 0.87, 95% confidence interval [CI] 0.80 to 0.95) and MI (RR 0.85, 95% CI 0.75 to 0.96) and showed a trend toward reduction of cardiovascular death (RR 0.89, 95% CI 0.71 to 1.01). There was a significant increase in TIMI major bleeding (RR 1.27, 95% CI 1.07 to 1.50) and TIMI major or minor bleeding (RR 1.20, 95% CI 1.02 to 1.42). Results were largely similar when stratified by ticagrelor versus prasugrel (pinteraction >0.05) except for increased TIMI major/minor bleeding with prasugrel than ticagrelor (pinteraction = 0.01). In conclusion, in patients with NSTE-ACS, newer oral P2Y12 inhibitors decrease MACE and MI at the expense of a significant increase in the risk of bleeding. Treatment of 1,000 patients with newer oral P2Y12 inhibitors will prevent 16 MACE and 13 MIs at the expense of increase in 6 major bleeding events.

American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative assessment recommend perioperative β blockers for non-cardiac surgery, although results of some clinical trials seem not to support this recommendation. We aimed to critically review the evidence to assess the use of perioperative β blockers in patients having non-cardiac surgery. We searched Pubmed and Embase for randomised controlled trials investigating the use of β blockers in non-cardiac surgery. We extracted data for 30-day all-cause mortality, cardiovascular mortality, non-fatal myocardial infarction, non-fatal stroke, heart failure, and myocardial ischaemia, safety outcomes of perioperative bradycardia, hypotension, and bronchospasm. 33 trials included 12 306 patients. β blockers were not associated with any significant reduction in the risk of all-cause mortality, cardiovascular mortality, or heart failure, but were associated with a decrease (odds ratio [OR] 0·65, 95% CI 0·54–0·79) in non-fatal myocardial infarction (number needed to treat [NNT] 63) and decrease (OR 0·36, 0·26–0·50) in myocardial ischaemia (NNT 16) at the expense of an increase (OR 2·01, 1·27–3·68) in non-fatal strokes (number needed to harm [NNH] 293). The beneficial effects were driven mainly by trials with high risk of bias. For the safety outcomes, β blockers were associated with a high risk of perioperative bradycardia requiring treatment (NNH 22), and perioperative hypotension requiring treatment (NNH 17). We recorded no increased risk of bronchospasm. Evidence does not support the use of β-blocker therapy for the prevention of perioperative clinical outcomes in patients having non-cardiac surgery. The ACC/AHA guidelines committee should soften their advocacy for this intervention until conclusive evidence is available. None.