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La enfermedad cardiovascular (ECV), en particular, la cardiopatía coronaria (CC) y la enfermedad cerebrovascular (ECeV), es un problema grave y creciente en las poblaciones debajos y medianos ingresos. Los pacientes con ECV establecida están expuestos a un riesgo muy alto de sufrir otros episodios de enfermedad potencialmente mortales. La prevención secundaria (las medidas que se toman para reducir el riesgo de episodios vasculares recurrentes en los pacientes con ECV) es un elemento importante y de costo asequible de la estrategia de control de la ECV en las poblaciones de bajos y medianos ingresos. Varios elementos de la prevención secundaria, incluidos los cambios del modo de vida, el tratamiento farmacológico y los procedimientos quirúrgicos, pueden reducir mucho el riesgo de ECV recurrente.

Of all cardiovascular causes of mortality, coronary heart disease (CHD) remains the leading cause of death. Our objectives were to establish trends in the prevalence and incidence of CHD in the province of Quebec, and to determine the proportion of CHD mortality that had no previous CHD diagnosis. Trends in prevalence, incidence and mortality were examined with a population-based study using the Quebec Integrated Chronic Disease Surveillance System, which links several health administrative databases. Data are presented using two case definitions for Quebecers aged 20 years and over: 1) a validated definition, and 2) CHD causes of death codes added to estimate the proportion of deaths that occurred without any previous CHD diagnosis as a proxy for sudden cardiac death (SCD). In 2012/2013, the crude prevalence of CHD was 9.4% with the first definition (593 000 people). Between 2000/2001 and 2012/2013, the age-standardized prevalence increased by 14%, although it has been decreasing slightly since 2009/2010. Age-standardized incidence and mortality rates decreased by 46% and 26% respectively, and represented a crude rate of 6.9 per 1000 and 5.2% in 2012/2013. The proportion identified only by CHD mortality, our SCD proxy, was only significant for the incident cases (0.38 per 1000 in 2009/2010) and declined over the study period. The prevalence of CHD has tended to decrease in recent years, and incidence and mortality have been declining in Quebec. Most CHD mortality occurs in previously diagnosed patients and only a small proportion of incident cases were not previously identified.

Coronary thromboembolism is a rare cause of acute coronary syndromes (ACS). The information regarding ACS in patients with prosthetic heart valves is scarce and based mainly on case reports. Although plaque rupture is the most common cause of acute myocardial infarction, coronary embolism (CE) is not a rare cause of acute myocardial infarction. There is no consensus regarding the treatment in such a situation. We present three cases of prosthetic valve thrombosis complicated with CE causing non-ST elevation ACS, who were successfully treated with thrombolytic therapy (TT). We administered low-dose (25 mg), slow-infusion (6 hours) tissue plasminogen activator (t-PA), which was shown to be safe and effective in our group in a large study. The patients benefited from TT with respect to the coronary flow, as shown by the lysis of thrombi in all three patients on coronary angiogram.

While comorbidity between coronary heart disease (CHD) and depression is evident, it is unclear whether the two diseases have shared underlying mechanisms. We performed a range of analyses in 367,703 unrelated middle-aged participants of European ancestry from UK Biobank, a population-based cohort study, to assess whether comorbidity is primarily due to genetic or environmental factors, and to test whether cardiovascular risk factors and CHD are likely to be causally related to depression using Mendelian randomization. We showed family history of heart disease was associated with a 20% increase in depression risk (95% confidence interval [CI] 16–24%, p < 0.0001), but a genetic risk score that is strongly associated with CHD risk was not associated with depression. An increase of 1 standard deviation in the CHD genetic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0–3%; p = 0.11). Mendelian randomization analyses suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are likely causal risk factors for depression. The odds ratio for depression per standard deviation increase in genetically-predicted triglycerides was 1.18 (95% CI 1.09–1.27; p = 2 × 10−5); per unit increase in genetically-predicted log-transformed IL-6 was 1.35 (95% CI 1.12–1.62; p = 0.0012); and per unit increase in genetically-predicted log-transformed CRP was 1.18 (95% CI 1.07–1.29; p = 0.0009). Our analyses suggest that comorbidity between depression and CHD arises largely from shared environmental factors. IL-6, CRP and triglycerides are likely to be causally linked with depression, so could be targets for treatment and prevention of depression.

The benefit of CT coronary angiography (CTCA) in patients presenting with stable chest pain has not been systematically studied. We aimed to assess the effect of CTCA on the diagnosis, management, and outcome of patients referred to the cardiology clinic with suspected angina due to coronary heart disease. In this prospective open-label, parallel-group, multicentre trial, we recruited patients aged 18–75 years referred for the assessment of suspected angina due to coronary heart disease from 12 cardiology chest pain clinics across Scotland. We randomly assigned (1:1) participants to standard care plus CTCA or standard care alone. Randomisation was done with a web-based service to ensure allocation concealment. The primary endpoint was certainty of the diagnosis of angina secondary to coronary heart disease at 6 weeks. All analyses were intention to treat, and patients were analysed in the group they were allocated to, irrespective of compliance with scanning. This study is registered with ClinicalTrials.gov, number NCT01149590. Between Nov 18, 2010, and Sept 24, 2014, we randomly assigned 4146 (42%) of 9849 patients who had been referred for assessment of suspected angina due to coronary heart disease. 47% of participants had a baseline clinic diagnosis of coronary heart disease and 36% had angina due to coronary heart disease. At 6 weeks, CTCA reclassified the diagnosis of coronary heart disease in 558 (27%) patients and the diagnosis of angina due to coronary heart disease in 481 (23%) patients (standard care 22 [1%] and 23 [1%]; p<0·0001). Although both the certainty (relative risk [RR] 2·56, 95% CI 2·33–2·79; p<0·0001) and frequency of coronary heart disease increased (1·09, 1·02–1·17; p=0·0172), the certainty increased (1·79, 1·62–1·96; p<0·0001) and frequency seemed to decrease (0·93, 0·85–1·02; p=0·1289) for the diagnosis of angina due to coronary heart disease. This changed planned investigations (15% vs 1%; p<0·0001) and treatments (23% vs 5%; p<0·0001) but did not affect 6-week symptom severity or subsequent admittances to hospital for chest pain. After 1·7 years, CTCA was associated with a 38% reduction in fatal and non-fatal myocardial infarction (26 vs 42, HR 0·62, 95% CI 0·38–1·01; p=0·0527), but this was not significant. In patients with suspected angina due to coronary heart disease, CTCA clarifies the diagnosis, enables targeting of interventions, and might reduce the future risk of myocardial infarction. The Chief Scientist Office of the Scottish Government Health and Social Care Directorates funded the trial with supplementary awards from Edinburgh and Lothian's Health Foundation Trust and the Heart Diseases Research Fund.

Cardiometabolic co-morbidities, diabetes (DM), hypertension (HTN), and obesity contribute to cardiovascular disease. Circulating biomarkers facilitate prognostication for patients with cardiovascular disease. We explored the relation between cardiometabolic co-morbidity burden in patients with chronic coronary disease and biomarkers of myocardial stretch, injury, inflammation, and platelet activity. We analyzed participants from the International Study of Comparative Health Effectiveness with Medical and Invasive Approaches (ISCHEMIA) trials biorepository with plasma biomarkers (N-terminal probrain natriuretic peptide, high-sensitivity cardiac troponin T, high-sensitivity C-reactive protein, interleukin-6, soluble CD40 ligand, and growth differentiation factor-15) and clinical risk factors (hemoglobin A1c [HbA1c], systolic blood pressure [SBP], and body mass index [BMI]) at baseline. We defined cardiometabolic co-morbidities as DM, HTN, and obesity at baseline. Co-morbidity burden is characterized by the number and severity of co-morbidities. Controlled co-morbidities were defined as HbA1c <7% for those with DM, SBP <130 mm Hg for those with HTN, and BMI <30 kg/m2. Severely uncontrolled was defined as HbA1c ≥8%, SBP ≥160 mm Hg, and BMI ≥35 kg/m2. We performed linear regression analyses to examine the association between co-morbidity burden and log-transformed biomarker levels, adjusting for age, gender, estimated glomerular filtration rate controlled for hemodialysis, and left ventricular ejection fraction. A total of 752 participants (mean age 66 years, 19% women, 84% White) were included in this analysis. Self-reported Black race, current smokers, history of myocardial infarction, and heart failure had a greater cardiometabolic co-morbidity burden. The presence of ≥1 severely uncontrolled co-morbidity was associated with significantly higher baseline levels of high-sensitivity cardiac troponin T, high-sensitivity C-reactive protein, interleukin-6, and growth differentiation factor-15 than participants with no co-morbidities. In conclusion, increasing cardiometabolic co-morbidity burden in patients with chronic coronary disease is associated with higher levels of circulating biomarkers of myocardial injury and inflammation. •Greater cardiometabolic co-morbidity burden was associated with increased levels of biomarkers of inflammation.•Greater cardiometabolic co-morbidity burden was associated with increased levels of biomarkers of myocardial injury.•Cardiometabolic co-morbidity burden was not associated with increased levels of a natriuretic peptide.•Future studies should determine the role of co-morbidity optimization in reducing myocardial injury and inflammation.

Research has shown that a greater adherence to the Mediterranean diet is associated with a reduced risk of major chronic disease. However, the existing literature leads to debate for different issues, such as the measurement of the adherence to the Mediterranean diet, the use of a wide variety of dietary indices with various food components and the large heterogeneity across the studies. In order to summarise the evidence and evaluate the validity of the association between the adherence to the Mediterranean diet and multiple health outcomes, an umbrella review of the evidence across meta-analyses of observational studies and randomised clinical trials (RCTs) was performed. Thirteen meta-analyses of observational studies and 16 meta-analyses of RCTs investigating the association between the adherence to the Mediterranean diet and 37 different health outcomes, for a total population of over than 12 800 000 subjects, were identified. A robust evidence, supported by a P-value<0.001, a large simple size, and not a considerable heterogeneity between studies, for a greater adherence to the Mediterranean diet and a reduced the risk of overall mortality, cardiovascular diseases, coronary heart disease, myocardial infarction, overall cancer incidence, neurodegenerative diseases and diabetes was found. For most of the site-specific cancers, as well as for inflammatory and metabolic parameters, the evidence was only suggestive or weak and further studies are needed to draw firmer conclusions. No evidence, on the other hand, was reported for bladder, endometrial and ovarian cancers, as well as for LDL (low density lipoprotein)-cholesterol levels.

In this trial involving patients with atherosclerotic disease who were receiving effective statin therapy, those who were assigned to receive anacetrapib, a CETP inhibitor, had a lower risk of major coronary events than did those in the placebo group.

Coronary artery disease is a major cause of morbidity and mortality worldwide, and is a consequence of acute thrombotic events involving activation of platelets and coagulation proteins. Factor Xa inhibitors and aspirin each reduce thrombotic events but have not yet been tested in combination or against each other in patients with stable coronary artery disease. In this multicentre, double-blind, randomised, placebo-controlled, outpatient trial, patients with stable coronary artery disease or peripheral artery disease were recruited at 602 hospitals, clinics, or community centres in 33 countries. This paper reports on patients with coronary artery disease. Eligible patients with coronary artery disease had to have had a myocardial infarction in the past 20 years, multi-vessel coronary artery disease, history of stable or unstable angina, previous multi-vessel percutaneous coronary intervention, or previous multi-vessel coronary artery bypass graft surgery. After a 30-day run in period, patients were randomly assigned (1:1:1) to receive rivaroxaban (2·5 mg orally twice a day) plus aspirin (100 mg once a day), rivaroxaban alone (5 mg orally twice a day), or aspirin alone (100 mg orally once a day). Randomisation was computer generated. Each treatment group was double dummy, and the patients, investigators, and central study staff were masked to treatment allocation. The primary outcome of the COMPASS trial was the occurrence of myocardial infarction, stroke, or cardiovascular death. This trial is registered with ClinicalTrials.gov, number NCT01776424, and is closed to new participants. Between March 12, 2013, and May 10, 2016, 27 395 patients were enrolled to the COMPASS trial, of whom 24 824 patients had stable coronary artery disease from 558 centres. The combination of rivaroxaban plus aspirin reduced the primary outcome more than aspirin alone (347 [4%] of 8313 vs 460 [6%] of 8261; hazard ratio [HR] 0·74, 95% CI 0·65–0·86, p<0·0001). By comparison, treatment with rivaroxaban alone did not significantly improve the primary outcome when compared with treatment with aspirin alone (411 [5%] of 8250 vs 460 [6%] of 8261; HR 0·89, 95% CI 0·78–1·02, p=0·094). Combined rivaroxaban plus aspirin treatment resulted in more major bleeds than treatment with aspirin alone (263 [3%] of 8313 vs 158 [2%] of 8261; HR 1·66, 95% CI 1·37–2·03, p<0·0001), and similarly, more bleeds were seen in the rivaroxaban alone group than in the aspirin alone group (236 [3%] of 8250 vs 158 [2%] of 8261; HR 1·51, 95% CI 1·23–1·84, p<0·0001). The most common site of major bleeding was gastrointestinal, occurring in 130 [2%] patients who received combined rivaroxaban plus aspirin, in 84 [1%] patients who received rivaroxaban alone, and in 61 [1%] patients who received aspirin alone. Rivaroxaban plus aspirin reduced mortality when compared with aspirin alone (262 [3%] of 8313 vs 339 [4%] of 8261; HR 0·77, 95% CI 0·65–0·90, p=0·0012). In patients with stable coronary artery disease, addition of rivaroxaban to aspirin lowered major vascular events, but increased major bleeding. There was no significant increase in intracranial bleeding or other critical organ bleeding. There was also a significant net benefit in favour of rivaroxaban plus aspirin and deaths were reduced by 23%. Thus, addition of rivaroxaban to aspirin has the potential to substantially reduce morbidity and mortality from coronary artery disease worldwide. Bayer AG.