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Reduced muscular strength, as measured by grip strength, has been associated with an increased risk of all-cause and cardiovascular mortality. Grip strength is appealing as a simple, quick, and inexpensive means of stratifying an individual's risk of cardiovascular death. However, the prognostic value of grip strength with respect to the number and range of populations and confounders is unknown. The aim of this study was to assess the independent prognostic importance of grip strength measurement in socioculturally and economically diverse countries. The Prospective Urban-Rural Epidemiology (PURE) study is a large, longitudinal population study done in 17 countries of varying incomes and sociocultural settings. We enrolled an unbiased sample of households, which were eligible if at least one household member was aged 35–70 years and if household members intended to stay at that address for another 4 years. Participants were assessed for grip strength, measured using a Jamar dynamometer. During a median follow-up of 4·0 years (IQR 2·9–5·1), we assessed all-cause mortality, cardiovascular mortality, non-cardiovascular mortality, myocardial infarction, stroke, diabetes, cancer, pneumonia, hospital admission for pneumonia or chronic obstructive pulmonary disease (COPD), hospital admission for any respiratory disease (including COPD, asthma, tuberculosis, and pneumonia), injury due to fall, and fracture. Study outcomes were adjudicated using source documents by a local investigator, and a subset were adjudicated centrally. Between January, 2003, and December, 2009, a total of 142 861 participants were enrolled in the PURE study, of whom 139 691 with known vital status were included in the analysis. During a median follow-up of 4·0 years (IQR 2·9–5·1), 3379 (2%) of 139 691 participants died. After adjustment, the association between grip strength and each outcome, with the exceptions of cancer and hospital admission due to respiratory illness, was similar across country-income strata. Grip strength was inversely associated with all-cause mortality (hazard ratio per 5 kg reduction in grip strength 1·16, 95% CI 1·13–1·20; p<0·0001), cardiovascular mortality (1·17, 1·11–1·24; p<0·0001), non-cardiovascular mortality (1·17, 1·12–1·21; p<0·0001), myocardial infarction (1·07, 1·02–1·11; p=0·002), and stroke (1·09, 1·05–1·15; p<0·0001). Grip strength was a stronger predictor of all-cause and cardiovascular mortality than systolic blood pressure. We found no significant association between grip strength and incident diabetes, risk of hospital admission for pneumonia or COPD, injury from fall, or fracture. In high-income countries, the risk of cancer and grip strength were positively associated (0·916, 0·880–0·953; p<0·0001), but this association was not found in middle-income and low-income countries. This study suggests that measurement of grip strength is a simple, inexpensive risk-stratifying method for all-cause death, cardiovascular death, and cardiovascular disease. Further research is needed to identify determinants of muscular strength and to test whether improvement in strength reduces mortality and cardiovascular disease. Full funding sources listed at end of paper (see Acknowledgments).

Global estimates of the effect of common modifiable risk factors on cardiovascular disease and mortality are largely based on data from separate studies, using different methodologies. The Prospective Urban Rural Epidemiology (PURE) study overcomes these limitations by using similar methods to prospectively measure the effect of modifiable risk factors on cardiovascular disease and mortality across 21 countries (spanning five continents) grouped by different economic levels. In this multinational, prospective cohort study, we examined associations for 14 potentially modifiable risk factors with mortality and cardiovascular disease in 155 722 participants without a prior history of cardiovascular disease from 21 high-income, middle-income, or low-income countries (HICs, MICs, or LICs). The primary outcomes for this paper were composites of cardiovascular disease events (defined as cardiovascular death, myocardial infarction, stroke, and heart failure) and mortality. We describe the prevalence, hazard ratios (HRs), and population-attributable fractions (PAFs) for cardiovascular disease and mortality associated with a cluster of behavioural factors (ie, tobacco use, alcohol, diet, physical activity, and sodium intake), metabolic factors (ie, lipids, blood pressure, diabetes, obesity), socioeconomic and psychosocial factors (ie, education, symptoms of depression), grip strength, and household and ambient pollution. Associations between risk factors and the outcomes were established using multivariable Cox frailty models and using PAFs for the entire cohort, and also by countries grouped by income level. Associations are presented as HRs and PAFs with 95% CIs. Between Jan 6, 2005, and Dec 4, 2016, 155 722 participants were enrolled and followed up for measurement of risk factors. 17 249 (11·1%) participants were from HICs, 102 680 (65·9%) were from MICs, and 35 793 (23·0%) from LICs. Approximately 70% of cardiovascular disease cases and deaths in the overall study population were attributed to modifiable risk factors. Metabolic factors were the predominant risk factors for cardiovascular disease (41·2% of the PAF), with hypertension being the largest (22·3% of the PAF). As a cluster, behavioural risk factors contributed most to deaths (26·3% of the PAF), although the single largest risk factor was a low education level (12·5% of the PAF). Ambient air pollution was associated with 13·9% of the PAF for cardiovascular disease, although different statistical methods were used for this analysis. In MICs and LICs, household air pollution, poor diet, low education, and low grip strength had stronger effects on cardiovascular disease or mortality than in HICs. Most cardiovascular disease cases and deaths can be attributed to a small number of common, modifiable risk factors. While some factors have extensive global effects (eg, hypertension and education), others (eg, household air pollution and poor diet) vary by a country's economic level. Health policies should focus on risk factors that have the greatest effects on averting cardiovascular disease and death globally, with additional emphasis on risk factors of greatest importance in specific groups of countries. Full funding sources are listed at the end of the paper (see Acknowledgments).

Participants without cardiovascular disease who were at increased risk were randomly assigned to receive a polypill (containing a statin and three blood-pressure–lowering drugs) or placebo and to receive aspirin or placebo. At 4.6 years, the incidence of cardiovascular events was lower among participants receiving both the polypill and aspirin than among those receiving both placebos.

In this large, international study, investigators found that participants with a broad range of carbohydrate intakes and diverse dietary patterns who consumed a diet with a high glycemic index had an increased risk of cardiovascular disease and death.

Although most cardiovascular disease occurs in low-income and middle-income countries, little is known about the use of effective secondary prevention medications in these communities. We aimed to assess use of proven effective secondary preventive drugs (antiplatelet drugs, β blockers, angiotensin-converting-enzyme [ACE] inhibitors or angiotensin-receptor blockers [ARBs], and statins) in individuals with a history of coronary heart disease or stroke. In the Prospective Urban Rural Epidemiological (PURE) study, we recruited individuals aged 35–70 years from rural and urban communities in countries at various stages of economic development. We assessed rates of previous cardiovascular disease (coronary heart disease or stroke) and use of proven effective secondary preventive drugs and blood-pressure-lowering drugs with standardised questionnaires, which were completed by telephone interviews, household visits, or on patient's presentation to clinics. We report estimates of drug use at national, community, and individual levels. We enrolled 153 996 adults from 628 urban and rural communities in countries with incomes classified as high (three countries), upper-middle (seven), lower-middle (three), or low (four) between January, 2003, and December, 2009. 5650 participants had a self-reported coronary heart disease event (median 5·0 years previously [IQR 2·0–10·0]) and 2292 had stroke (4·0 years previously [2·0–8·0]). Overall, few individuals with cardiovascular disease took antiplatelet drugs (25·3%), β blockers (17·4%), ACE inhibitors or ARBs (19·5%), or statins (14·6%). Use was highest in high-income countries (antiplatelet drugs 62·0%, β blockers 40·0%, ACE inhibitors or ARBs 49·8%, and statins 66·5%), lowest in low-income countries (8·8%, 9·7%, 5·2%, and 3·3%, respectively), and decreased in line with reduction of country economic status (p trend<0·0001 for every drug type). Fewest patients received no drugs in high-income countries (11·2%), compared with 45·1% in upper middle-income countries, 69·3% in lower middle-income countries, and 80·2% in low-income countries. Drug use was higher in urban than rural areas (antiplatelet drugs 28·7% urban vs 21·3% rural, β blockers 23·5% vs 15·6%, ACE inhibitors or ARBs 22·8% vs 15·5%, and statins 19·9% vs 11·6%; all p<0·0001), with greatest variation in poorest countries (p interaction<0·0001 for urban vs rural differences by country economic status). Country-level factors (eg, economic status) affected rates of drug use more than did individual-level factors (eg, age, sex, education, smoking status, body-mass index, and hypertension and diabetes statuses). Because use of secondary prevention medications is low worldwide—especially in low-income countries and rural areas—systematic approaches are needed to improve the long-term use of basic, inexpensive, and effective drugs. Full funding sources listed at end of paper (see Acknowledgments).

The contribution of various risk factors to the burden of stroke worldwide is unknown, particularly in countries of low and middle income. We aimed to establish the association of known and emerging risk factors with stroke and its primary subtypes, assess the contribution of these risk factors to the burden of stroke, and explore the differences between risk factors for stroke and myocardial infarction. We undertook a standardised case-control study in 22 countries worldwide between March 1, 2007, and April 23, 2010. Cases were patients with acute first stroke (within 5 days of symptoms onset and 72 h of hospital admission). Controls had no history of stroke, and were matched with cases for age and sex. All participants completed a structured questionnaire and a physical examination, and most provided blood and urine samples. We calculated odds ratios (ORs) and population-attributable risks (PARs) for the association of all stroke, ischaemic stroke, and intracerebral haemorrhagic stroke with selected risk factors. In the first 3000 cases (n=2337, 78%, with ischaemic stroke; n=663, 22%, with intracerebral haemorrhagic stroke) and 3000 controls, significant risk factors for all stroke were: history of hypertension (OR 2·64, 99% CI 2·26–3·08; PAR 34·6%, 99% CI 30·4–39·1); current smoking (2·09, 1·75–2·51; 18·9%, 15·3–23·1); waist-to-hip ratio (1·65, 1·36–1·99 for highest vs lowest tertile; 26·5%, 18·8–36·0); diet risk score (1·35, 1·11–1·64 for highest vs lowest tertile; 18·8%, 11·2–29·7); regular physical activity (0·69, 0·53–0·90; 28·5%, 14·5–48·5); diabetes mellitus (1·36, 1·10–1·68; 5·0%, 2·6–9·5); alcohol intake (1·51, 1·18–1·92 for more than 30 drinks per month or binge drinking; 3·8%, 0·9–14·4); psychosocial stress (1·30, 1·06–1·60; 4·6%, 2·1–9·6) and depression (1·35, 1·10–1·66; 5·2%, 2·7–9·8); cardiac causes (2·38, 1·77–3·20; 6·7%, 4·8–9·1); and ratio of apolipoproteins B to A1 (1·89, 1·49–2·40 for highest vs lowest tertile; 24·9%, 15·7–37·1). Collectively, these risk factors accounted for 88·1% (99% CI 82·3–92·2) of the PAR for all stroke. When an alternate definition of hypertension was used (history of hypertension or blood pressure >160/90 mm Hg), the combined PAR was 90·3% (85·3–93·7) for all stroke. These risk factors were all significant for ischaemic stroke, whereas hypertension, smoking, waist-to-hip ratio, diet, and alcohol intake were significant risk factors for intracerebral haemorrhagic stroke. Our findings suggest that ten risk factors are associated with 90% of the risk of stroke. Targeted interventions that reduce blood pressure and smoking, and promote physical activity and a healthy diet, could substantially reduce the burden of stroke. Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Pfizer Cardiovascular Award, Merck, AstraZeneca, and Boehringer Ingelheim.

In one comparison from a 2-by-2 factorial trial, 12,705 persons at intermediate cardiovascular risk were assigned to either rosuvastatin or placebo. At 5.6 years, there were significantly fewer participants with cardiovascular events in the rosuvastatin group than in the placebo group. Cardiovascular diseases cause 18 million deaths per year globally and a similar number of nonfatal cardiovascular events. 1 Elevated low-density lipoprotein (LDL) cholesterol levels account for approximately half the population-attributable risk of myocardial infarction 2 and approximately one quarter of the risk of ischemic stroke. 3 In previous trials, lowering LDL cholesterol levels with statins has been shown to reduce the risk of cardiovascular diseases, but most of the patients enrolled in those trials had vascular disease, elevated lipid levels, elevated inflammatory markers, hypertension, or diabetes. 4 , 5 The association between LDL cholesterol level and cardiovascular disease is graded and has no documented threshold. . . .

In a large study in 17 countries, an estimated sodium intake that was either higher or lower than the average estimated sodium intake was associated with an increased risk of cardiovascular events. A higher-than-average potassium intake was associated with reduced risk. Most of the global population consumes between 3.0 and 6.0 g of sodium per day (7.5 to 15.0 g of salt per day). 1 , 2 Guidelines on cardiovascular disease prevention recommend a maximum sodium intake of 1.5 to 2.4 g per day, but achieving this target will require a substantial change in diet for most people. 3 – 5 Although clinical trials have shown a reduction in blood pressure with a reduced sodium intake, to our knowledge, no large randomized trial has been conducted to document reductions in the risk of cardiovascular disease with low sodium intake. 6 Prospective cohort studies have shown inconsistent . . .

In one comparison from a 2-by-2 factorial trial, over 12,000 participants with a mean baseline blood pressure of 138/82 mm Hg were assigned to candesartan plus hydrochlorothiazide or to placebo. At 5.6 years, there was no between-group difference in the rates of cardiovascular events. High blood pressure is the leading risk factor for cardiovascular disease globally 1 and affects more than 1 billion adults worldwide. 2 Observational studies involving persons without cardiovascular disease show a graded increase in risk at systolic blood-pressure levels above 115 mm Hg. 3 It has been suggested that lowering blood pressure at any level above this value will reduce the risk of cardiovascular events. 4 Antihypertensive therapy has been clearly shown to reduce the risk of cardiovascular disease among people with vascular or renal disease, diabetes, or hypertension with end-organ damage or, in the absence of these conditions, among persons with a systolic . . .

High sodium intake was found to be associated with increased blood pressure. Decreasing dietary sodium intake can effectively reduce blood pressure, especially among hypertensive individuals, but the extent of reduction remains debatable. The effectiveness of different sodium reduction strategies on blood pressure reduction was identified in the current review. Randomized controlled trials and clinical trials on dietary sodium intake and blood pressure published from 23 March 2008 to 23 March 2021 were collected from the PubMed database. Twenty-six studies were included and divided into four subgroups based on the types of interventions identified. Subgroups included a low-sodium diet (1) in a group with or without added sodium, (2) through food substitutes, (3) through health education and behavior change, and (4) through salt substitutes. Reduction of dietary sodium intake resulted in a mean difference of 4.51 mmHg (95% CI: 3.35-5.67) in systolic blood pressure and 2.42 mmHg (95% CI: 1.61-3.23) in diastolic blood pressure. The effectiveness of these strategies was approximated from the difference in 24-h urinary sodium excretion between the intervention and control groups, which was 53.74 mmol/day (95% CI: 31.95-75.53). When analyzed, the low-sodium diet without added sodium showed the greatest significant differences in blood pressure (7.58/4.01 mmHg) and 24-h urinary sodium excretion (101.49 mmol/day), whereas the low-sodium diet through food substitutes yielded the lowest significant differences in blood pressure (2.26/0.81 mmHg) and 24-h urinary sodium excretion (25.78 mmol/day). Thus, reducing sodium intake can be an effective strategy for the prevention and treatment of hypertension.