Gun Ownership and Firearm-related Deaths

BACKGROUND: A variety of claims about possible associations between gun ownership rates, mental illness burden, and the risk of fi rearm-related deaths have been put forward. However, systematic data on this issue among various countries remain scant. Our objective was to assess whether the popular notion "guns make a nation safer" has any merits.METHODS: Data on gun ownership were obtained from the Small Arms Survey, and for fi rearm-related deaths from a European detailed mortality database (World Health Organization), the National Center for Health Statistics, and others. Crime rate was used as an indicator of safety of the nation and was obtained from the United Nations Surveys of Crime Trends. Age-standardized disability-adjusted life- year rates due to major depressive disorder per 100,000 inhabitants with data obtained from the World Health Organization database were used as a putative indicator for mental illness burden in a given country.RESULTS: Among the 27 developed countries, there was a significant positive correlation between guns per capita per country and the rate of fi rearm-related deaths ( r ¼ 0.80; P < .0001). In addition, there was a positive correlation (r ¼ 0.52; P ¼ .005) between mental illness burden in a country and fi rearm-related deaths. However, there was no significant correlation (P ¼ .10) between guns per capita per country and crime rate ( r ¼ .33), or between mental illness and crime rate ( r ¼ 0.32; P ¼ .11). In a linear regression model with fi rearm-related deaths as the dependent variable with gun ownership and mental illness as independent covariates, gun ownership was a significant predictor ( P < .0001) of fi rearm-related deaths, whereas mental illness was of borderline significance ( P ¼ .05) only.CONCLUSION: The number of guns per capita per country was a strong and independent predictor of fi rearm-related death in a given country, whereas the predictive power of the mental illness burden was of borderline significance in a multivariable model. Regardless of exact cause and effect, however, the current study debunks the widely quoted hypothesis that guns make a nation safer

Resistant hypertension: what the cardiologist needs to know

Treatment-resistant hypertension (TRH) affects between 3 and 30% of hypertensive patients, and its presence is associated with increased cardiovascular morbidity and mortality. Until recently, the interest on these patients has been limited, because providing care for them is difficult and often frustrating. However, the arrival of new treatment options [i.e. catheter-based renal denervation (RDN) and baroreceptor stimulation] has revitalized the interest in this topic. The very promising results of the initial uncontrolled studies on the blood pressure (BP)-lowering effect of RDN in TRH seemed to suggest that this intervention might represent an easy solution for a complex problem. However, subsequently, data from controlled studies have tempered the enthusiasm of the medical community (and the industry). Conversely, these new studies emphasized some seminal aspects on this topic: (i) the key role of 24 h ambulatory BP and arterial stiffness measurement to identify ‘true' resistant patients; (ii) the high prevalence of secondary hypertension among this population; and (iii) the difficulty to identify those patients who may profit from device-based interventions. Accordingly, for those patients with documented TRH, the guidelines suggest to refer them to a hypertension specialist/centre in order to perform adequate work-up and treatment strategies. The aim of this review is to provide guidance for the cardiologist on how to identify patients with TRH and elucidate the prevailing underlying pathophysiological mechanism(s), to define a strategy for the identification of patients with TRH who may benefit from device-based interventions and discuss results and limitations of these interventions, and finally to briefly summarize the different drug-based treatment strategie

Efficacy and safety of dual blockade of the renin-angiotensin system: meta-analysis of randomised trials

Objective To compare the long term efficacy and adverse events of dual blockade of the renin-angiotensin system with monotherapy. Design Systematic review and meta-analysis. Data sources PubMed, Embase, and the Cochrane central register of controlled trials, January 1990 to August 2012. Study selection Randomised controlled trials comparing dual blockers of the renin-angiotensin system with monotherapy, reporting data on either long term efficacy (≥1 year) or safety events (≥4 weeks), and with a sample size of at least 50. Analysis was stratified by trials with patients with heart failure versus patients without heart failure. Results 33 randomised controlled trials with 68 405 patients (mean age 61 years, 71% men) and mean duration of 52 weeks were included. Dual blockade of the renin-angiotensin system was not associated with any significant benefit for all cause mortality (relative risk 0.97, 95% confidence interval 0.89 to 1.06) and cardiovascular mortality (0.96, 0.88 to 1.05) compared with monotherapy. Compared with monotherapy, dual therapy was associated with an 18% reduction in admissions to hospital for heart failure (0.82, 0.74 to 0.92). However, compared with monotherapy, dual therapy was associated with a 55% increase in the risk of hyperkalaemia (P less than 0.001), a 66% increase in the risk of hypotension (P less than 0.001), a 41% increase in the risk of renal failure (P=0.01), and a 27% increase in the risk of withdrawal owing to adverse events (P less than 0.001). Efficacy and safety results were consistent in cohorts with and without heart failure when dual therapy was compared with monotherapy except for all cause mortality, which was higher in the cohort without heart failure (P=0.04 v P=0.15), and renal failure was significantly higher in the cohort with heart failure (P less than 0.001 v P=0.79). Conclusion Although dual blockade of the renin-angiotensin system may have seemingly beneficial effects on certain surrogate endpoints, it failed to reduce mortality and was associated with an excessive risk of adverse events such as hyperkalaemia, hypotension, and renal failure compared with monotherapy. The risk to benefit ratio argues against the use of dual therapy

Body-Weight Fluctuations and Outcomes in Coronary Disease.

BackgroundBody-weight fluctuation is a risk factor for death and coronary events in patients without cardiovascular disease. It is not known whether variability in body weight affects outcomes in patients with coronary artery disease.MethodsWe determined intraindividual fluctuations in body weight from baseline weight and follow-up visits and performed a post hoc analysis of the Treating to New Targets trial, which involved assessment of the efficacy and safety of lowering low-density lipoprotein cholesterol levels with atorvastatin. The primary outcome was any coronary event (a composite of death from coronary heart disease, nonfatal myocardial infarction, resuscitated cardiac arrest, revascularization, or angina). Secondary outcomes were any cardiovascular event (a composite of any coronary event, a cerebrovascular event, peripheral vascular disease, or heart failure), death, myocardial infarction, or stroke.ResultsAmong 9509 participants, after adjustment for risk factors, baseline lipid levels, mean body weight, and weight change, each increase of 1 SD in body-weight variability (measured according to average successive variability and used as a time-dependent covariate) was associated with an increase in the risk of any coronary event (2091 events; hazard ratio, 1.04; 95% confidence interval [CI], 1.01 to 1.07; P=0.01), any cardiovascular event (2727 events; hazard ratio, 1.04; 95% CI, 1.02 to 1.07; P&lt;0.001), and death (487 events; hazard ratio,1.09; 95% CI, 1.07 to 1.12; P&lt;0.001). Among patients in the quintile with the highest variation in body weight, the risk of a coronary event was 64% higher, the risk of a cardiovascular event 85% higher, death 124% higher, myocardial infarction 117% higher, and stroke 136% higher than it was among those in the quintile with the lowest variation in body weight in adjusted models.ConclusionsAmong participants with coronary artery disease, fluctuation in body weight was associated with higher mortality and a higher rate of cardiovascular events independent of traditional cardiovascular risk factors. (Funded by Pfizer; ClinicalTrials.gov number, NCT00327691 .)

Renin Angiotensin System Inhibitors for Patients with Stable Coronary Artery Disease without heart failure: Systematic Review and Meta-Analysis of Randomized Trials

Objective: To critically evaluate the efficacy of renin angiotensin system inhibitors (RASi) in patients with coronary artery disease without heart failure, compared with active controls or placebo. Design: Meta-analysis of randomized trials. Data sources: PubMed, EMBASE, and CENTRAL databases until 1 May 2016. Eligibility criteria for selecting studies: Randomized trials of RASi versus placebo or active controls in patients with stable coronary artery disease without heart failure (defined as left ventricular ejection fraction ≥40% or without clinical heart failure). Each trial had to enroll at least 100 patients with coronary artery disease without heart failure, with at least one year’s follow-up. Studies were excluded if they were redacted or compared use of angiotensin converting enzyme inhibitors with angiotensin receptor blockers. Outcomes were death, cardiovascular death, myocardial infarction, angina, stroke, heart failure, revascularization, incident diabetes, and drug withdrawal due to adverse effects. Results: 24 trials with 198 275 patient years of follow-up were included. RASi reduced the risk of all cause mortality (rate ratio 0.84, 95% confidence interval 0.72 to 0.98), cardiovascular mortality (0.74, 0.59 to 0.94), myocardial infarction (0.82, 0.76 to 0.88), stroke (0.79, 0.70 to 0.89), angina, heart failure, and revascularization when compared with placebo but not when compared with active controls (all cause mortality, 1.05, 0.94 to 1.17; Pinteraction=0.006; cardiovascular mortality, 1.08, 0.93 to 1.25, Pinteraction14.10 deaths and >7.65 cardiovascular deaths per 1000 patient years) but not in those with low control event rates. Conclusions: In patients with stable coronary artery disease without heart failure, RASi reduced cardiovascular events and death only when compared with placebo but not when compared with active controls. Even among placebo controlled trials in this study, the benefit of RASi was mainly seen in trials with higher control event rates but not in those with lower control event rates. Evidence does not support a preferred status of RASi over other active controls