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Introduction Mortality from cardiovascular disease (CVD) has dramatically reduced over the past 50 years in the UK. While this trend should be celebrated, it is important to consider mortality alongside trends in morbidity to gain a full understanding of how healthcare resources and prevention schemes should be directed. This paper reported trends in mortality, incidence and prevalence of coronary heart disease (CHD), stroke, heart attack, angina and heart failure over the past 50 years. Methods Mortality data were provided by the UK national statistics agencies. For morbidity data we reviewed the peer-reviewed and grey literature for comparable estimates from different time points over the last 50 years. Results Around half of the UK population died from CVD in the 1960s; by 2009 this had dropped to a third. CHD mortality rates have remained 30%–40% higher in Scotland than in England since 1961. Incidence rates for heart attack have decreased since the 1960s, while survival has improved; prevalence in those over 75 has increased by around 40% since the mid-1990s. Over the past 20 years heart failure incidence decreased by over a third in Scotland. Between 1970 and 1991, prevalence of angina nearly tripled for men over 75 and has continued to rise. Conclusion Mortality from CVD has declined over the past 50 years, but striking geographic inequalities have remained. Incidence of two major CVD conditions have declined, but continuing increases in prevalence and an ageing population mean that the burden of CVD is still a major issue for the UK.

Background Blood pressure reduction is an important target for the prevention of coronary heart disease (CHD). In 1982, Rose proposed that small population-wide reductions in blood pressure, through public health measures to reduce salt intake, might deliver larger reductions in CHD mortality than by treating hypertensive patients. We aimed to estimate the potential for each strategy to reduce future CHD deaths in England and Wales. Methods We used the Stock of Health (SoH) model, where each individual is born with a 100% stock which then depreciates year-by-year, reflecting fixed and modifiable risk factors. A CHD death occurs when the individual’s CHD’s SoH falls below a critical point. Births, deaths and risk factor distributions were obtained from the Office of National Statistics and the Health Survey for England. Model parameters were calibrated using data from the US Cardiovascular Lifetime Risk Pooling Project. We modelled ten policy scenarios: population-wide, individual-based and combination strategies. The population-wide strategies were: a systolic blood pressure (SBP) reduction of 0.1 mmHg achieved by health promotion media strategies (Pop1), a 1.3 mmHg reduction achieved by mandatory salt reformulation (Pop2) and an attainable goal where SBP levels fall to those observed in the US population (Pop3). The individual-based strategies assumed that in currently uncontrolled hypertensive patients, control was then achieved in 30% (Indi1) and 50% (Indi2) of them. Results We forecast that approximately 467,200 CHD (95% CI 466,900–467,600) deaths may occur between 2013 and 2030. By controlling 30% and 50% of hypertensive patients, we predict approximately 3800 (3200–4300) and 6200 (5700–6800) fewer deaths respectively. Conversely, we predict approximately 1300 (800–1900) fewer deaths by health promotion; some 16,400 (15,800–16,900) fewer deaths by mandatory reformulation and approximately 25,400 (24,900–25,900) fewer deaths by gradual SBP declines to US levels. Combining Pop1 and Indi1 might achieve approximately 5100 (4500–5600) fewer deaths in 2030; whereas combining Pop1 and Indi2 could achieve some 7500 (2000–13,000) fewer deaths. Combining Pop2 and Indi1 might prevent approximately 19,700 (19,200–20,300) deaths; while combining Pop2 and Indi2 could prevent or postpone some 21,900 (21,400–22,400) deaths by 2030. Conclusion Both population-wide salt reduction policies and individual-based treatment strategies could substantially reduce CHD deaths in England and Wales. Even greater reductions in mortality might be achieved by reducing SBP to US levels. However, there is no clear single successful intervention, but both types of strategies are needed to maximise our chances of controlling the burden of mortality attributable to blood pressure.

Background Between 2000 and 2010, coronary heart disease (CHD) mortality rates in Scotland fell by over one third. Important contributions came from reductions in blood pressure and serum cholesterol (primary prevention). However, the relative contributions from preventive medications (anti-hypertensives and statins) in individuals and from population-wide dietary changes remain unclear. We therefore examined the impact of differential effects on health inequalities. Methods We used the previously validated IMPACTsec model to estimate the contributions of population-level risk factor changes and treatment changes to the CHD mortality decline in Scotland between 2000 and 2010 for adults aged over 25. Data were stratified using the Scottish Index of Multiple Deprivation (SIMD), a small area measure of deprivation. Model outputs were quantified as deaths prevented or postponed (DPPs) by each intervention. Sensitivity analyses were conducted using Ersatz-based Monte Carlo simulations. Results Between 2000 and 2010, 5770 fewer CHD deaths than expected occurred in Scotland; an estimated 3570 (62%) were attributable to reductions in blood pressure and serum cholesterol. Declines in blood pressure were responsible for approximately 2285 DPPs (minimum estimate 1630, maximum estimate 2915). The vast majority (2130 DPPs) came from population-wide blood pressure falls, with bigger absolute mortality decreases in the most deprived quintile compared with the least deprived (460 vs. 340 DPPs respectively); relative contributions were similar (37.2% and 37.5%). Anti-hypertension medications resulted in only 155 fewer deaths, with similar DPPs in the most (35) and least (30) deprived quintiles. Reductions in serum cholesterol resulted in 1280 fewer deaths; approximately 515 of these were attributable to population-wide changes in diet with more deaths prevented in the most deprived quintile compared with the least deprived (170 vs. 45 DPPs; relative contribution 13.8% and 4.7%). Conversely, approximately 770 fewer deaths were attributable to statin use, with very similar absolute numbers of deaths prevented in most (140) and least (140) deprived quintiles, but relatively greater contributions in the least deprived (15.4% vs 11.2%). Statin uptake was higher in the most deprived areas (17% vs 13.2%). Conclusion Population-wide falls in blood pressure helped to reduce CHD mortality; however the benefit from hypertension treatment was small. Improved diet and statins for high-risk individuals both made important contributions to the fall in population cholesterol. Population-wide falls in blood pressure and reductions due to medical treatments for hypertension were equitable between socio-economic groups. Higher socio-economic groups appeared to benefit more from statins, probably due to better compliance; this may perpetuate inequalities.

Background Coronary heart disease (CHD) deaths in the UK have plummeted since the 1970s. However, CHD remains the biggest single cause of premature mortality, particularly in deprived social groups. But have all social groups benefited equally from these declines? Or do the headline figures conceal differences in rates of decline among social strata, potentially generating conflicting views on inequalities? Our analysis therefore aimed to examine whether the rapid declines in overall CHD mortality have benefited all socio-economic groups, and explore the implications for future projections. Methods We used a Bayesian analysis of an age-period-cohort model for the English population with data from Office for National Statistics (ONS). We projected age-specific CHD mortality by gender and deprivation status for the period 2007–2035, using 1982–2006 as the input. We converted the age-specific values to premature CHD death rates (ages 35–74). Deprivation status was measured by Index of Multiple Deprivation quintiles, which aggregate seven types of deprivation, including health and income. We first analysed the influence of the population-level trend in premature CHD mortality on absolute inequality, and second investigated the contributions to change in relative inequality. We quantified inequality by the variance in the probability of premature death among deprivation quintiles. Furthermore, we introduced a method to analyse the contribution of each group to the change in variance over time. Results We found that overall mortality trends conceal heterogeneities. Our models predict more rapid declines in premature CHD death for the most affluent than for the most deprived quintiles (annualised rate of decline 2006–2025, 7.9% [95% CI 4.7–11.0% ] versus 6.0% [ 1.9–10.0% ] for men, and 6.3% [ 3.5–9.0% ] versus 5.9% [ 2.2–9.5% ] for women). Absolute inequality was projected to decrease by 87% ( 29–98% ) among men and by 89% ( 48–98% ) among women. This decrease was particularly driven by the most deprived groups, reflecting their higher premature death rates. However, relative inequality was projected to rise by 60% among men ( 26–107% ) and by 10% ( -15–42% ) among women. Because premature death is declining more slowly in the most deprived, these increases are also mostly influenced by the most deprived. Conclusion Overall, premature coronary death rates in England continue to decline steeply, regardless of deprivation status. Furthermore, absolute inequalities are decreasing, reflecting declines in the high premature mortality burden in deprived groups. However, relative inequalities are projected to widen further, reflecting slower mortality declines in the most deprived groups. We suggest that more aggressive and progressive prevention policies are urgently needed.

Background Coronary Heart Disease (CHD) disease remains a leading cause of UK mortality, generating a large and unequal burden of disease. Dietary trans fats represent a powerful CHD risk factor. However, UK efforts to reduce the dietary intake of industrial trans fats (currently approximately 1% of daily energy) have been less successful than some other nations, such as Denmark, Iceland, Austria, Switzerland and the USA. Furthermore, the potential outcomes of such measures, and the effects upon health inequalities, have not been well quantified. We therefore aimed to model the potential effects of specific reductions in trans fats intake on CHD mortality, CHD related admissions, and further examined the potential distribution of these effects by socio-economic position up to 2030. Methods We extended the previously validated IMPACTsec model, to estimate the potential effects of reductions in trans fats intake upon the England and Wales population aged 25 years and above. We stratified these estimates by age, sex and socio-economic circumstances (SEC). We estimated a reduction in expected CHD deaths in 2030 attributable to a modest reduction in industrial trans fats intake (-0.5% energy) and a complete ban (-1% energy). Main output measures were deaths prevented or postponed, life years gained and hospital admissions. Results were tested in a probabilistic sensitivity analysis. Results Reducing trans fats consumption in the England and Wales population by 0.5% of daily energy intake would result in approximately 1900 fewer deaths per year (minimum estimate 1700, maximum estimate 2200), some 5000 fewer hospital admissions (min 4300, max 5700), and approximately 18,000 additional life years (min 15,000, max 22,000). This would also reduce health inequalities, preventing about six times as many deaths and gaining six times as many life years in the most deprived quintile compared with the most affluent. Complete elimination of industrial trans fats (a 1% reduction in energy) would generate approximately 3900 (min 3300, max 4400) fewer deaths, 10,000 (min 8800, max 10,300) fewer hospital admissions, and approximately 37,000 (min 30,000, max 45,000) life years gained. Reductions in inequalities would be correspondingly large. Discussion Reducing dietary intake of industrial trans fats could substantially decrease CHD mortality and hospital admissions, and gain tens of thousands of life years. Crucially, this policy could also reduce health inequalities. UK strategies should therefore aim to minimise industrial trans fats intakes, as successfully achieved in many other European countries.

Background Coronary Heart Disease (CHD) remains a major cause of mortality in the United Kingdom. Yet predictions of future CHD mortality are potentially problematic due to population ageing and increase in obesity and diabetes. Here we explore future projections of CHD mortality in England & Wales under two contrasting future trend assumptions. Methods In scenario A, we used the conventional counterfactual scenario that the last-observed CHD mortality rates from 2011 would persist unchanged to 2030. The future number of deaths was calculated by applying those rates to the 2012–2030 population estimates. In scenario B, we assumed that the recent falling trend in CHD mortality rates would continue. Using Lee-Carter and Bayesian Age Period Cohort (BAPC) models, we projected the linear trends up to 2030. We validate our methods using past data to predict mortality from 2002–2011. Then, we computed the error between observed and projected values. Results In scenario A, assuming that 2011 mortality rates stayed constant by 2030, the number of CHD deaths would increase 62% or approximately 39,600 additional deaths. In scenario B, assuming recent declines continued, the BAPC model (the model with lowest error) suggests the number of deaths will decrease by 56%, representing approximately 36,200 fewer deaths by 2030. Conclusions The decline in CHD mortality has been reasonably continuous since 1979, and there is little reason to believe it will soon halt. The commonly used assumption that mortality will remain constant from 2011 therefore appears slightly dubious. By contrast, using the BAPC model and assuming continuing mortality falls offers a more plausible prediction of future trends. Thus, despite population ageing, the number of CHD deaths might halve again between 2011 and 2030. This has implications for how the potential benefits of future cardiovascular strategies might best be calculated and presented.

R A L A B ST R A C T S Results: There is a positive correlation between SFA and CHD mortality in both HIC (Figure 1) and LMIC (Figure 2). With the exception of Russia, CHD mortality trends in HIC are decreasing. Patterns of SFA in HIC is divergent with Southern Europe and East Asia (excluding China) showing increasing trends (but from a low base), compared to Australia/New Zealand, Northern and Western Europe and North America where trends are falling (from high levels). Eastern Europe and Russian SFA increases to around 1990, from when consumption falls. CHD mortality trends in LMIC have increased, particularly in Central Asia. SFA intake in LMIC has changed little, except China where SFA intake has increased significantly (from a low base). Conclusion: Changes in SFA consumption and CHD mortality patterns are generally similar. SFA patterns reflect changes in global food production that have occurred over the past half century. A 2008 FAO publication reported per capita/per day supply of vegetable oils increased 112% in HIC and 191% in LMIC between 1961 and 2003. Per capita/per day supply of animal fats decreased 26% in HIC and increased 109% in LMIC. However, consumption of vegetable oils was still 1.9 times higher and animal fats 3.4 times higher in HIC than LMIC, reflected in the higher (x2) CHD mortality and SFA consumption in HIC than LMIC. Despite reductions in HIC SFA consumption, it is still a significant population determinant for CHD. Increasing SFA consumption in LMIC will likely correspond with increasing CHD. Research is currently underway to examine time lag relationships between population changes in dietary fat intake and CHD mortality. Disclosure of Interest: None Declared

Hyperlipidemia and the atherosclerotic conditions that result from it are well recognized as major contributors to coronary heart disease (CHD). Fortunately, several large-scale clinical trials have shown that there are effective treatments that can substantially lower atherogenic lipid levels and thereby reduce the risk of CHD mortality and morbidity. However, duplication of these dramatic trial results can be negatively affected in "real life" clinical practice by an important issue: compliance. No medications will work if patients do not take them. Unfortunately, patients who need lipid-lowering therapy are likely to need it long-term, perhaps for a lifetime. Yet, many do not adhere to the prescribed medication regimen. This article reviews some major studies of compliance for lipid-lowering drugs. The reasons why patients do not take them as prescribed vary: poor education, lack of understanding, cost, provider indifference, and others. Achieving compliance requires a multifaceted approach. It can be enhanced by encouraging patients to talk openly about their medication habits and by convincing them of the long-term benefits of reaching and maintaining target low-density lipoprotein cholesterol levels. Although more studies focusing on compliance specifically regarding CHD are needed, the current literature does provide some guidance. Arch Fam Med. 2000;9:1169-1175

Since the overall risks and benefits of hormonal replacement therapy (HRT) in breast cancer survivors are not clearly established, and it is unlikely that a definitive answer will be available in the near future, we developed a decision analytic computer model for individualizing decisions, using the best available literature estimates for all currently known or suspected benefits and adverse outcomes. In addition, the model allows input of individual risk factors for breast cancer recurrence, coronary artery disease, osteoporosis, etc., and allows weighting of patients' preferences for these outcomes. We found that women at average risk for coronary heart disease (CHD) and hip fracture lose 4.3 quality-adjusted life months (QALMs) by taking HRT. Women who value the CHD and hip fracture states as having the worst impact on health and breast cancer recurrence as having the mildest impact on health lose the least from HRT, 3.6 QALMs. Women who value the CHD and hip fracture states as having the mildest impact and breast cancer recurrence as having the worst impact on health lose 5.3 QALMS. Therefore, unless future studies show a larger benefit on CHD mortality or other health states, HRT decisions for breast cancer survivors should include careful consideration of individual preferences for all of the potential outcomes. The model can readily incorporate data on new treatments and other outcomes as they become available.

Coronary heart disease (CHD) is the leading cause of death for women in the United States. There has been a substantial decrease in CHD mortality in the past few decades in the United States for both women and men. The change in lifestyle after World War II may affect the incidence of and mortality from CHD in a more recent birth cohort, such as the 45-54-year-old age group. CHD mortality among women aged 45-54 by state and race in the United States and other countries in 1994 was evaluated. Correlation of the CHD mortality with state-specific and race-specific educational attainment (% of not a high school graduate) and state-specific prevalence of smoking was examined. There was a 2.5-fold difference in CHD mortality (ICD 410-414, 429.2) between black and white women aged 45-54: 78/100,000 for black versus 31/100,000 for white women; a 3-fold difference in CHD mortality among white women by state: 16/100,000 in Colorado versus 53/100,000 in Louisiana; and a 3-fold difference in CHD mortality among black women by state: 45/100,000 in New Jersey versus 124/100,000 in Arkansas. CHD mortality was correlated with educational attainment among white women (r = 0.62, p = 0.001) and with prevalence of smoking (r = 0.39, p = 0.021). There is a large variation in CHD mortality among women aged 45-54 in the United States by race and state. These differences may reflect variations in coronary risk factors. More detailed evaluation of determinants of CHD mortality by area is needed, as are public health programs that can reduce the marked disparity in CHD mortality in the United States.

This review identifies coronary heart disease (CHD) as the leading cause of mortality among postmenopausal women and highlights the well-documented problem of underrecognition and undertreatment of women who are at risk for or who already have CHD. This undertreatment encompasses both preventive care (i.e., drug treatment for lipid management) and more invasive treatments (e.g., revascularization procedures). Preventive interventions to reduce dyslipidemia and control other coronary risk factors can lessen CHD mortality and morbidity in the postmenopausal woman.

Objective: Although all-cause mortality and coronary heart disease (CHD) mortality is declining in Sweden, as in most other countries in the industrialised world, we have limited information about the distribution and trends of mortality in deprived and affluent neighbourhoods. Design: This study analyses the extent to which the decline in all-cause mortality and CHD mortality (over the age range 25–74 y) differs between affluent and deprived neighbourhoods during the decade 1984–1993. Incidence density ratios (IDR), estimated by Poisson regression, were calculated for small areas, grouped into population deciles, by both the care need index (CNI) and the Townsend deprivation score. On average, there were about 14 500 residents and 560 deaths in each decile over the period. Setting: A large Swedish city. Main outcome measures: All-cause mortality and mortality from CHD. Results: The most deprived neighbourhoods had the highest IDR for all-cause mortality and CHD mortality. Over the period from 1984–1988 to 1989–1993 there was an overall decrease in all-cause mortality and CHD mortality, which was significantly higher in the most affluent areas. The mortality ratios for the most deprived neighbourhoods were almost three times higher than those of the most affluent areas. Conclusions: People liviing in more affluent neighbourhoods have had the benefit of most of the last decade's decline in CHD mortality.

In the current issue of Heart , Gray et al report the results of a pilot study to identify patients with familial hypercholesterolaemia (FH) in general practice ( see article on page 754 ).1 Why is this important and how did they do it? FH is a common disorder where subjects have markedly raised low-density lipoprotein-cholesterol (LDL-C), and consequently have premature coronary heart disease (CHD) and myocardial infarction. Studies carried out in the 1970s in the UK and the USA2 3 suggest that, if untreated, 50% of men with FH will have developed CHD by the age of 55 years and 50% of women by the age of 65 years (women show the same degree of elevation of LDL-C but are protected somewhat from the atherosclerosis until after the menopause). Thankfully, patients with FH are now well treated by statins and their overall standardised CHD mortality rate has fallen from 8.1 in 20–59-year-olds before statins to 3.7 after statins.4 This translates into roughly 9 life-years gained, and models have shown that treatment of patients with FH, even at a young age, is highly cost effective as measured by the cost for each life-year gained.5 Management of other CHD risk factors is also important in patients with FH, the dietary and lifestyle advice, particular smoking cessation, being a benefit, and with the new and more powerful statins now available, it is a realistic possibility for people with FH to have a normal life expectancy. How many patients with FH are there in the UK, and are they being well managed? The estimated prevalence of FH is 1 in 500, suggesting that there are probably more than 100 000 people with FH in the UK. A recent survey of the 130 lipid clinics currently active in the UK suggests that …

References 1 Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ 2004;328:1519. 2 Belanger C, Speizer FE, Hennekens CH, Rosner B, Willett W, Bain C. The nurses’ health study: current findings. Am J Nurs 1980;80:1333. 3 Keys A, Aravanis C, Blackburn HW et al. Epidemiological studies related to coronary heart disease: characteristics of men aged 40–59 in seven countries. Acta Med Scand Suppl 1966;460:1–392. 4 Mariotti S, Capocaccia R, Farchi G, Menotti A, Verdecchia A, Keys A. Differences in the incidence rate of coronary heart disease between north and south European cohorts of the Seven Countries Study as partially explained by risk factors. Eur Heart J 1982;3:481–87. 5 Rose G. Incubation period of coronary heart disease. Br Med J (Clin Res Ed) 1982;284:1600–1. (Reprinted Int J Epidemiol 2005;34:242–44.) 6 Ross SD, Allen IE, Connelly JE et al. Clinical outcomes in statin treatment trials: a meta-analysis. Arch Intern Med 1999;159: 1793–1802. 7 Vartiainen E, Puska P, Pekkanen J, Tuomilehto J, Jousilahti P. Changes in risk factors explain changes in mortality from ischaemic heart disease in Finland. BMJ 1994;309:23–27. 8 Rose G. Sick individuals and sick populations. Int J Epidemiol 2001;30:427–32. 9 Tuomilehto J, Kuulasmaa K. WHO MONICA Project: assessing CHD mortality and morbidity. Int J Epidemiol 1989;18:S38–S45. 10 The INTERSALT Co-operative Research Group. Sodium, potassium, body mass, alcohol and blood pressure: the INTERSALT Study. J Hypertens Suppl 1988;6:S584–S586. 11 Ounpuu S, Negassa, A,Yusuf S. INTER-HEART: a global study of risk factors for acute myocardial infarction. Am Heart J 2001;141:711–21. 246 INTERNATIONAL JOURNAL OF EPIDEMIOLOGY

Background Despite rapidly declining coronary heart disease (CHD) mortality rates over the last two decades, CHD mortality rates in the British Isles are still amongst the highest in Europe. Greater risk factor reductions have been achieved in many other countries in Europe and beyond. This study aimed to use a modelling approach to assess the potential impact of alternative future risk factor scenarios relating to smoking and physical activity levels, dietary salt and saturated fat intakes on future CHD mortality in three countries: Northern Ireland (NI), Republic of Ireland (RoI) and Scotland. Methods CHD mortality models previously developed and validated in each country were extended to predict potential reductions in CHD mortality from 2010 (baseline year) to 2030. For each country, using risk factor data from recent surveys as a baseline, we modelled alternative future risk factor scenarios: Absolute decreases in (i) smoking prevalence and (ii) physical inactivity rates of up to 15% by 2030; (iii) relative decreases in dietary salt intake of up to 30% by 2030 & (iv) relative decreases in% energy from dietary saturated fat of up to 6% by 2030 (replacing by polyunsaturated fats). Sensitivity analyses were then conducted. Results Projected populations by 2030 (adults aged 25-84) were 1.3, 3.9 and 3.9 million in NI, RoI and Scotland respectively. By 2030: assuming continuing declines in mortality: 15% absolute reductions in smoking could decrease CHD deaths by 6–8% (approximately 40, 130 and 210 fewer deaths In NI, RoI and Scotland respectively). 15% absolute declines in physical inactivity levels might decrease CHD deaths by 4% (approximately 30, 90 and 90 fewer deaths respectively). Relative reductions in salt intake of 30% could decrease CHD deaths by 3–4% (approximately 25, 75 and 110 fewer deaths respectively) and 6% in saturated fat intake might decrease CHD deaths by some 9–10% (approximately 65, 170 and 265 fewer deaths In NI, RoI and Scotland respectively). These projections remained stable under a wide range of sensitivity analyses. Conclusion Modest and feasible reductions in four CHD risk factors (which have already been achieved elsewhere) could translate into substantial reductions in future CHD deaths. More aggressive polices are therefore needed in the British Isles to control tobacco, promote healthy food and increase physical activity.

Previous reports from the Russian Lipid Research Clinics (LRC) study showed no association between the level of high-density-lipoprotein (HDL) cholesterol and mortality from coronary heart disease (CHD), while US LRC data indicated a strong negative association between HDL cholesterol and CHD mortality. This report investigated the association of HDL cholesterol and mortality in these same population samples with follow-up extended to 12 years. The association between HDL cholesterol and mortality remained inverse and significant in the US sample. In the Russian sample, high levels of HDL cholesterol were associated with higher risk of all-cause and cancer mortality, although adjustment for known risk factors reduced the strength of the association. The association between HDL cholesterol and CHD mortality was negative in the Russian sample, although the strength of the association was less than that for the US sample. Extended follow-up reduced the difference in the association between HDL cholesterol and mortality between the two countries; however, important differences remained. Further research will be required to clearly determine the cause for their differences.

Finland has marked regional differences in the occurrence of coronary heart disease (CHD). Although the causes for these differences in CHD mortality and morbidity in the Finnish population are unknown, it offers an excellent opportunity to investigate the effects of non-insulin-dependent diabetes mellitus (NIDDM) on CHD risk in two populations differing significantly with respect to the occurrence of CHD. Therefore, we carried out a 7-year prospective population-based study including a large number of patients with NIDDM (East Finland: 253 men and 257 women; West Finland: 328 men, 221 women) and corresponding non-diabetic subjects (East Finland: 313 men, 336 women; West Finland: 325 men, 399 women). In both study populations the presence of NIDDM increased significantly the risk for CHD events (CHD mortality or all CHD events including CHD mortality or non-fatal myocardial infarction). Diabetic men had 3–4 fold higher and diabetic women 8–11-fold higher risk for CHD than corresponding non-diabetic subjects. Both non-diabetic and diabetic subjects had odds ratios (East vs West) for CHD events of about 2 indicating a similar East-West difference in the CHD risk. Regional difference was quite similar in men and women. These results imply that factors related to NIDDM, independently of conventional risk factors and the occurrence of atherothrombosis in the background population, must play a major role in the pathogenesis of atherosclerotic vascular disease in NIDDM diabetes.

Background Despite advances made in treating coronary heart disease (CHD), mortality due to CHD in Syria has been increasing for the past two decades. This study aims to assess CHD mortality trends in Syria between 1996 and 2006 and to investigate the main factors associated with them. Methods The IMPACT model was used to analyze CHD mortality trends in Syria based on numbers of CHD patients, utilization of specific treatments, trends in major cardiovascular risk factors in apparently healthy persons and CHD patients. Data sources for the IMPACT model included official statistics, published and unpublished surveys, data from neighboring countries, expert opinions, and randomized trials and meta-analyses. Results Between 1996 and 2006, CHD mortality rate in Syria increased by 64%, which translates into 6370 excess CHD deaths in 2006 as compared to the number expected had the 1996 baseline rate held constant. Using the IMPACT model, it was estimated that increases in cardiovascular risk factors could explain approximately 5140 (81%) of the CHD deaths, while some 2145 deaths were prevented or postponed by medical and surgical treatments for CHD. Conclusion Most of the recent increase in CHD mortality in Syria is attributable to increases in major cardiovascular risk factors. Treatments for CHD were able to prevent about a quarter of excess CHD deaths, despite suboptimal implementation. These findings stress the importance of population-based primary prevention strategies targeting major risk factors for CHD, as well as policies aimed at improving access and adherence to modern treatments of CHD.

Finland has witnessed a rapid decline in coronary heart disease (CHD) mortality among working-age men and women since the end of the 1960s. Among men aged 35–64, age-standardized CHD mortality declined by 50% from 1971–1972 to 1990–1991. The trend has been similar among women. Concomitant with the declining mortality, there have been improvements in the levels of CHD risk factors. In the provinces of North Karelia and Kuopio, risk-factor surveys have been carried out among independent random samples of the middle-aged population every 5 years since 1972. In these surveys, improvements have been observed in mean serum total cholesterol concentration, diastolic blood pressure, and smoking. Although overall changes have been favorable, relative differences in CHD mortality between educational groups have widened, especially in the 1980s in Finland. In risk factors, the decline in serum cholesterol and in the proportion of hypertensives among both sexes, and in smoking among men, has been similar in all educational groups. However, trends in body mass index have diverged between educational groups, and among women, smoking has changed from a habit of the more educated to a habit of the less educated.

The sustained increase in longevity initiated during the second half of the 20th Century poses huge challenges upon the public and private healthcare and pensions9 systems. Current theories do not explain the observed phenomenon, what precludes predictions of its future trends. The authors goal was to go back to Omram9s original project—to develop an epidemiologic theory of the demographic change—but looking for an explanation alternative to the epidemiologic transition proposed by him. The study expands upon a previous one, that showed, for the first time, a cohort association between the mortality burden of 1918 Influenza Pandemic and the 20th Century rise in CHD mortality. Based on an age-period-cohort analysis of USA and UK mortality (and natality) data (1933–2005) and on the epidemiology of influenza as we know it, it is shown that, overall, temporal changes in mortality and natality accompany the recycling of influenza A viruses, that is, the re-exposure of human populations, from time to time, to influenza A subtypes that circulated in the past. Mortality (and natality) and main causes of death change as birth cohorts (whole population and maternal) primed at early life with one (period-specific) influenza A sub-type, course through subsequent influenza A environments over time.1 The implications of this new theory to demography and to the epidemiology of several diseases are revolutionary.

Source Citation Cice G, Di Benedetto A, D’Isa S, et al. Effects of telmisartan added to angiotensin-converting enzyme inhibitors on mortality and morbidity in hemodialysis patients with chronic hea...

Low mortality from coronary heart disease (CH D) among Eskimos has been attributed to less atherosclerosis in the coronary arteries because of a high dietary intake of omega-3 fatty acids. Other investigators attribute this low mortality to the fact that Eskimos have a high mortality from other causes before middle age, when CH D is common. However, most studies have been epidemiological, either by death-certificate review or risk-factor evaluation. We evaluated the extent of atherosclerotic lesions in the coronary arteries and aortas from Alaska Natives. Standardised comparisons between samples from 103 Native and 101 non-native residents show that the extent of raised lesions increases with age in both groups, but the prevalence of raised lesions in native specimens was consistently lower than in those from non-natives. This difference was statistically significant. The data suggest that the differences in CHD mortality between Alaska Natives and non-natives are, at least in part, the result of less atherosclerosis in natives.

Background Coronary heart disease (CHD) mortality has steadily declined since the early 1970s in The Netherlands. Recent work suggests that in some Western countries the rate of decline in some groups has begun to decrease and may be starting to plateau or even reverse. These changes may be a result of changes in the pattern for major cardiovascular risk factor trends. Methods Data for all deaths between 1972 and 2007 in The Netherlands were grouped by year, sex, age at death and contemporaneous ICD code for CHD as cause of death. Per age-sex-group a joinpoint regression was fitted to detect points in time at which significant changes in the trends occur. For every period the linear slope of the trend, p-value, observed number of deaths (min-max) and observed CHD mortality rates (min-max) were tabulated. Furthermore we calculated the change in observed CHD mortality rate per period. Results Between 1972 and 2007, the age-adjusted CHD mortality rates decreased overall by 75.6% in men and by 75.7% in women. In men aged 35–54 the decline in CHD mortality rate attenuated in the period 1993–1999 (change in CHD mortality rate in period 1980–1993: −0.53 and in period 1993–1999: −0.16). In women aged 35 to 54 the decline in CHD mortality rate attenuated in the period 1989–2000 (change in CHD mortality rate in period 1979–1989: −0.58 and in period 1989–2000: −0.02). After 1999–2000 CHD mortality rate further declined in both gender (in men change in CHD mortality rate in period 1999–2007 was −0.46, in women change in CHD mortality rate in period 2000–2007 was −0.38). Conclusions Evidence from several Western countries suggests some levelling out of CHD mortality rates among younger men and women and warn that CHD mortality rates in these groups may be starting to increase. In the present study attenuation of the decline in CHD mortality among men and women aged 35–54 years has been observed starting in the mid 90s. Furthermore, we observed that after a period where the decline in CHD mortality was attenuated, an increase in the pace of decline was observed. In order to explain these recent changes in CHD mortality rates, a detailed analysis of recent changes in cardiovascular risk factors is urgently required.

The incidence of coronary heart disease (CHD) can be reduced by preventive measures. We know what it costs to treat CHD, but lack even the most rudimentary estimates of what it might cost to reduce the incidence by means of population wide strategies of prevention. American and Australian experience shows that such strategies achieve results. Even in Britain, where official spending on prevention is relatively small, health publicity has succeeded in bringing about marked reductions In the household consumption of animal fats and In cigarette smoking. Yet we know virtually nothing about the cost of bringing about a given reduction in CHD mortality by preventive measures. Estimates of such costs would be useful In persuading public authorities to spend more on prevention.

The question whether there is a level of diastolic pressure during treatment below which further reduction of pressure may be harmful rather than beneficial is of great interest. If, as the proponents of this hypothesis maintain, death from CHD among treated hypertensives becomes more rather than less common at very low diastolic pressure, this might explain at least in part why most primary prevention trials of hypertension have failed to show a reduction in CHD mortality. However, as the sceptics have pointed out, the evidence that drug induced lowering of blood pressure is harmful is not of the highest quality, and alternative explanations for excess cardiovascular mortality at low diastolic pressure exist. In the following review of this hotly contested debate it is concluded that both proponents and sceptics may be correct, but that the presence of a J curve should not divert attention from the main benefit of treating hypertension which is a reduction in the risk of fatal and non fatal stroke.

Most explanations of falls in coronary heart disease (CHD) mortality limit themselves to event based metrics (such as fewer deaths). However, time based metrics (such as life-years gained (LYG)) promise to capture more of the social value attached to the deaths averted. We have assessed the sensitivity of conclusions about the relative contributions of treatments and risk factor changes to the choice of metric. Using a validated CHD mortality model (IMPACT), we integrated data on the number …

Coronary heart disease (CHD) is almost certainly a nutritional disorder related to the quality and quantity of dietary fats and mediated by blood and tissue lipid concentrations. There is current controversy as to when the underlying process of atherosclerosis is initiated and whether the critical susceptibility to CHD may be established in utero or infancy. Blood pressure and hypertension may also be nutritionally based, and the age at which the rate of rise in blood pressure with age is determined is also controversial. The British Regional Heart Study (BRHS) involves 7,735 middle-aged men from 24 towns in England, Wales and Scotland and reveals that average blood cholesterol levels in these towns show no relationship to CHD mortality but all are high by international standards. Blood pressure levels vary markedly between the 24 towns and relate strongly to CHD mortality patterns, which are highest in Scotland and lowest in the South of England. The hypothesis relating adult blood pressures and CHD mortality to foetal and infant life circumstances has been examined using the data on birthplace and place of examination of the BRHS men. Regardless of where they were born, men living and examined in the South had lower mean blood pressures than men living in Scotland. The highest mean blood pressures were observed in Scotland, irrespective of where the men had been born. For CHD, regardless of their place of birth, men living in the South had a lower risk of CHD than men living elsewhere. The geographic zone of examination appeared to be more important than the zone of birth in determining the risk of CHD and the level of blood pressure. While patterns of nutrition during pregnancy, in infancy and childhood may be of importance for some outcomes, such as height, it seems that exposure to risk factors during adult life predominantly determine the outcome in cardiovascular disease.

Summary The etiology of coronary heart disease (CHD) has been debated over the last 60 years. There exists an alternative explanation to the rise in CHD mortality, consonant with knowledge about the role of inflammation. It is proposed that a cohort association existed between rates of vulnerability to influenza deaths in 1918 and CHD mortality among survivors from those vulnerable birth cohorts. According to this hypothesis, hypercholesterolemia may have been a marker of the 1918 immune-priming, with CHD deaths resulting from bursts of endothelial inflammation and thrombosis associated with influenza re-infections during the following decades. We propose a reconsideration of the way we model atherogenesis, from “initiation” and “promotion” to “vulnerable substrate(s)” and “trigger(s)”. Also suggested, based on this hypothesis, is a possible shared condition between vulnerable substrates, which upon triggering, is associated with evolution to acute events, through an imbalance between COX and LOX products. This paradigm has implications for global prevention policies.

More than a decade ago, randomized placebo-controlled trials proved that reducing elevated cholesterol levels in middle-aged men reduced their risk of coronary heart disease (CHD). 1,2 Whether a similar relationship exists between elevated cholesterol and increased risk of CHD events (defined as hospitalization or death due to CHD) in elderly individuals has remained unclear. 3,4 Data from a cohort of subjects reported by Krumholz and colleagues 5 and an accompanying Editorial 6 published in JAMA last year concluded that by at least the age of 80 years, elevated cholesterol no longer confers an increased risk for CHD events. See also p 539. In this issue ofThe Journal, Corti and colleagues 7 report an association between elevated cholesterol levels and CHD mortality in elderly women but not in elderly men. To JAMA readers, the methods and results of the study by Corti et al will appear similar to those of Krumholz et

To the Editor. —In an article in the November 2,1994, issue ofThe Journal, Dr Krumholz and colleagues 1 prospectively followed 997 elderly subjects and reported no significant relationship between total cholesterol or high-density lipoprotein cholesterol (HDL-C) and cardiac events. Because the wide confidence intervals (CIs) included values greater than 1.0, this cannot be considered a negative study. In fact, the upper limit of their CI for adjusted CHD mortality for men and women (1.98) is a similar risk ratio to that reported previously in middle-aged men. 2 Part of the reason for the wide CIs is likely the size of the study and short duration of follow-up. Studies establishing the relationship between hypercholesterolemia and CHD in middle-aged individuals evaluated many more subjects for greater lengths of time. For example, the Multiple Risk Factor Intervention Trial 3 (MRFIT) followed 356222 subjects over a 6-year period, and the Lipid Research Clinics

In his editorial, 1 Castelli makes the rather striking claim that Seventh-Day Adventists experience only one seventh the risk of heart attack as other Americans, thereby suggesting that the reported data 2 may have only limited application to the wider population. We can only assume that, in the context of the editorial, Castelli was playing on a repetition of the word seven , and did not intend any factual basis. Unfortunately, the misstatement was included in press releases and led to some confusion with journalists and the reading public. Contrary to the above statement by Castelli, previous comparisons of coronary heart disease (CHD) mortality suggest that California male Adventists have 50% to 70% of the CHD mortality risk, and female Adventists have 50% to 90% of the CHD mortality risk (depending on length of follow-up) of non-Adventist Californians. The non-Adventist comparison group were participants in a contemporaneous study that used similar

To the Editor. —The article "What If Americans Ate Less Fat?" by Browner et al 1 addressed an interesting and important topic. However, the authors may have substantially underestimated the reductions in mortality rates that may follow a reduction in fat intakes to 30% of energy by overlooking the effects of random error in serum cholesterol measurement, and especially in dietary fat measurement, in projecting corresponding CHD and cancer RR estimates. Specifically, their CHD RR estimates (Table 1, p3287) for a 20 mg/dL increase in serum cholesterol levels used data from Multiple Risk Factor Intervention Trial screenees. The random measurement error associated with a single serum cholesterol measurement is such that corresponding log RR estimates are likely to be underestimated by a factor of about 1.5 (Richard Peto, Oxford University, oral communication, June 1986). This correction increases the projected impact of fat reduction on CHD mortality by more than 50%.

It has been shown that, among white males and females, recent declines in mortality from coronary heart disease (CHD) have not been uniform by region or state. Some clustering has emerged. To describe trends for the black population by states, we compared CHD death rates for persons aged 35 to 74 years for the years 1968–1972 in combination with rates for 1978. Reported mortality from 34 states with reasonably large black populations was described. Not all of the recent geographic shifts for white CHD mortality rates were apparent for blacks. Yet there were similarities, chief of which were the slower decline, and therefore worsening, of relative CHD mortality in certain states in Appalachia.

The mortality from coronary heart disease (CHD) in Finland is remarkably high; according to the vital statistics released by the World Health Organization it has for many years been the highest in the world. This, however, concerns only the male sex; in the females the mortality figures, though also relatively high, do not very markedly differ from those of many other populations. It is also noteworthy that the CHD mortality in the eastern provinces of Finland is higher than in the western provinces.

This paper is concerned with the question of whether elderly people (ages 65-84) are more likely to develop coronary heart disease (CHD) if they continue or stop cigarette smoking. Age-standardized CHD rates and mortality ratios have been computed from data available in four major prospective cohort investigations of smoking and health. The data examined gave consistent results. For elderly men, there were no appreciable excess risks of CHD mortality or morbidity among cigarette smokers compared to ex-cigarette smokers and non-cigarette smokers. For elderly women, the CHD rates seemed lower in continuing cigarette smokers than in ex-cigarette smokers. These results obtained from cohort data are concordant with previous analyses of secular data. Among elderly people, the risk of CHD is essentially the same with persistence of cigarette smoking than with its cessation.

It has been observed that among men of Japanese ancestry, there is a gradient in CHD mortality increasing from Japan to Hawaii to California. A study of 11,900 Japanese men in Hiroshima and Nagasaki, Japan, Honolulu, Hawaii, and the San Francisco Bay Area of California has been conducted to investigate this disease difference. This paper describes the selection of the study populations and their age distributions, and outlines the study methods. This paper also introduces and briefly summarizes four papers that give the results for mortality comparisons, biochemical and blood pressure distributions and results for heart disease prevalence among the three cohorts.

Cardiovascular disease risk factor and mortality data collected since the 1978 Conference on the Decline in Coronary Heart Disease Mortality were reviewed. Risk factor and disease trends were generally parallel and compatible with current hypotheses of cause and prevention. A few discrepancies between risk factors and disease change were noted and discussed. Models were presented for estimating effects of risk factor and medical care changes on disease trends. Their usefulness and limitations were considered. An ongoing need was elaborated for systematic and innovative surveillance research to expand and improve the capability to measure, explain, and predict disease trends. Rational public health policy depends on competent and sustained surveillance.

Coronary heart disease (CHD) mortality declined by about 20 per cent between 1965 and 1976. During the same period there were substantial decreases in the proportion of adults who smoked based on data from the National Health Interview Survey (HIS). This study examines the extent to which changes in smoking can account for the decrease in CHD mortality for men and women aged 35-64 years. By applying US smoking levels (estimated from HIS) to data from four epidemiologic studies on the relative risk of CHD death by amount smoked, we obtain estimates of the portion of the decline in CHD mortality attributable to changes in smoking. Smoking changes among women were not generally consistent with declines in CHD mortality. For men, the estimated impact of smoking on CHD mortality varied considerably depending upon which study was used to estimate the relative risk by amount smoked.