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Keywords:

  • coronary artery disease;
  • epidemiology;
  • mortality;
  • prevention;
  • treatments

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices

Abstract.  Björck L, Capewell S, Bennett K, Lappas G, Rosengren A (Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden; University of Liverpool, Liverpool, United Kingdom; Trinity College and St. James’s Hospital, Dublin, Ireland). Increasing evidence-based treatments to reduce coronary heart disease mortality in Sweden: quantifying the potential gains. J Intern Med 2011; 269: 452–467.

Objectives.  Between 1986 and 2002, coronary heart disease (CHD) mortality in Sweden fell by more than 50%. Approximately one-third (4800 fewer deaths) of this decline in age-adjusted CHD mortality could be attributed to treatments in patients with CHD and primary prevention medications. High treatment levels were achieved in some cases, but in others, only 50–80% of eligible patients received appropriate therapy. We therefore examined to what extent increasing the use of specific treatments in eligible patients might have reduced CHD mortality rates in Sweden.

Design and methods.  We used the previously validated IMPACT CHD model to combine data on CHD patient numbers, medical and surgical uptake levels and treatment effectiveness. We estimated the number of deaths prevented or postponed for 2002 (baseline scenario) and for an alternative scenario (if at least 60% of eligible patients were treated).

Results.  If treatments were increased to consistently cover at least 60% of eligible patients, approximately 8900 deaths could have been postponed or prevented, representing a potential gain of approximately 4100 fewer deaths than actually occurred in 2002. Approximately 45% of the 4100 gain would have come from primary prevention with statins, 23% from acute coronary syndrome treatments, 15% from secondary prevention therapies and 15% from treatments for heart failure.

Conclusion.  Increasing the proportion of eligible patients with CHD who receive evidence-based treatment could have resulted in approximately 4100 fewer deaths in 2002, almost doubling the actual mortality reduction. These findings further emphasize the importance of aggressively identifying and treating patients with CHD and high-risk individuals.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices

Since the 1980s, coronary heart disease (CHD) mortality rates in Sweden have halved in both men and women [1]. We recently investigated the decline in CHD mortality between 1986 and 2002 using the previously validated IMPACT CHD mortality model [2, 3]. In addition, we investigated how much of the decrease in age-adjusted CHD mortality rates could be attributed to changes in risk factors in the population or to specific medical and surgical therapies during the same period. [4]

Between 1986 and 2002, the age-adjusted CHD death rates decreased by 53.4% in men and 52.0% in women aged 25–84 years, resulting in 13 180 fewer CHD deaths in 2002 according to the International Classification of Diseases, 10th revision (codes I20–I25). The Swedish IMPACT model explained approximately 11 985 of this decline (91%). Changes in risk factors (cholesterol and smoking) explained approximately 55% (7200 fewer deaths) of the decline in CHD mortality. The agreement between the number of estimated deaths and the number of observed deaths was generally good across all age groups [4].

Medical and/or surgical treatments in 2002 accounted for approximately 36% of the decrease, or 4790 CHD deaths prevented or postponed (minimum estimate 2850 and maximum estimate 10 290). The largest reduction came from the use of secondary prevention medications or rehabilitation after myocardial infarction (MI) (1175) or after revascularization (420), initial treatment of acute MI (745) and unstable angina pectoris (225), hospital and community treatments for heart failure (915) and treatment for chronic stable angina by coronary artery bypass graft (CABG) surgery or medical treatment (535). Primary prevention of hypertension accounted for 575 deaths prevented or postponed whereas lipid-lowering drugs for hypercholesterolaemia (e.g. statins) accounted for 200 fewer deaths [4].

In 2002, Sweden already had high rates of treatment in CHD patients compared with other countries [3, 5]. However, treatment levels varied in different patient groups. High treatment levels were achieved in some cases (e.g. aspirin and beta-blockers in acute MI) but were as low as 50–80% in many others (secondary prevention, hypertension, heart failure and statins in primary prevention), and a large proportion of eligible patients were not receiving appropriate treatments. In this study, we examined how a more aggressive approach to identify eligible patients together with increasing use of specific medical and surgical treatment would further reduce the CHD mortality rates in Sweden.

Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices

The Excel-based IMPACT CHD mortality model previously used in the United Kingdom, Europe, North America and elsewhere has previously been described in detail [3–6]. The model is comprehensive and includes all standard evidence-based medical and surgical treatments that were in use for CHD in 2002. It also includes the major population risk factors: smoking, total cholesterol, systolic blood pressure, body mass index, diabetes and physical activity (Appendix 1). Briefly, CHD patient numbers are included for specific medical and surgical treatments and the effectiveness of these treatments estimated from randomized controlled trials and meta-analyses (Appendix 2). The number of CHD deaths prevented or postponed by each specific intervention and also by a change in each of the major CHD risk factors was calculated for Sweden for the base year 1986, and again for the year 2002 (Appendix 1). Only the treatment effects were analysed in this study.

Total population and age distribution data for Sweden for 1986 and 2002 were obtained from the National Board of Health and Welfare. The number of CHD deaths by age and sex in 1986 and 2002 was obtained from the Cause of Death Register. The number of patients with different categories of CHD was obtained from the Swedish Hospital Discharge Register, and case fatality rates were then calculated by linking this information to the Swedish Cause of Death Register [4].

We calculated the number of CHD deaths prevented or postponed by each specific intervention stratified by age and gender for 2002. The reduction in CHD deaths attributable to each treatment was calculated based on (i) the number of patients in a specific disease group, (ii) the relative mortality reduction reported in published meta-analyses and trials, (iii) the uptake of the intervention and (iv) the age- and sex-specific case fatality rates stratified by diagnosis. For all treatments, a survival benefit for ≥1 year was required [4].

We identified and incorporated data for men and women aged 25–84 years in the total Swedish population in defined patient groups (Table 1) of those with (i) acute MI, (ii) unstable angina, (iii) previous MI, (iv) heart failure because of CHD, in hospital and in the community, (v) chronic stable angina, (vi) hypertension, but no CHD, (vii) total cholesterol concentration ≥5.2 mmol L−1 (200 mg dL−1), but no CHD, and (viii) those who had undergone CABG surgery or percutaneous coronary intervention (PCI). Adjustments for potential overlaps between patient groups, such as those with angina and with previous MI, were determined from the data from the Hospital Discharge Register, administered by the National Board of Health and Welfare (Appendix 3).

Table 1.   Coronary heart disease (CHD) mortality reduction in Sweden in 2002 if treatment levels increased to 60% of eligible patients
InterventionTotal patients eligible (n)Treatment uptake level in 2002 (%)RRR (%)Deaths prevented/postponed
Baseline scenario 2002If treatment uptake increased to 60%
Total deaths prevented (n)Total gain (%)
  1. ACE, angiotensin-converting enzyme; CPR, cardiopulmonary resuscitation; CABG, coronary artery bypass grafting; gpIIb/IIIa, glycoprotein IIb/IIIa; MI, myocardial infarction; NA, not applicable; PCI, percutaneous coronary intervention; RRR, relative risk reduction.

  2. aTreatments in 1986 subtracted. bAssumed no increase in uptake. cBoth unfractionated and low-molecular-weight heparins. d20% maximum uptake assumed for warfarin. eIncreased uptake modelled by increasing number of operations in 2002 in patient group with chronic angina by 60%.

Acute MI20 955  745a134513.0
 Community CPR 395701050.9
 Hospital CPR 10032230 
 Thrombolysisb 182270 
 Aspirinb 8115260 
 Beta-blockersb 85475 
 ACE inhibitors 51780950.4
 Primary PCI 831402805.9
 Primary CABG 02002305.8
Unstable angina17 290  22563010.1
 Aspirin and heparinsc 56331651750.3
 Aspirin alone 351545 
 gpIIB/IIIA antagonists 1095400.9
 CABG 14302205.4
 PCI 432101503.5
Secondary prevention after acute MI99 815  1175164511.6
 Aspirinb 7715270 
 Beta-blockers 56233303550.6
 ACE inhibitors 37202203603.4
 Statins 49222453151.8
 Warfarind 722401151.9
 Rehabilitation 1826702304.0
Secondary prevention after revascularization41 950  420a5603.2
 Aspirinb 7815110 
 Beta-blockersb 662390 
 ACE inhibitors 432060850.6
 Statins 58221051100.1
 Warfarind 82210801.7
 Rehabilitation 372655850.8
 Chronic angina revascularization132 215  535a6451.9
 CABG surgery76 790NAe223904150.7
 Chronic angina medical treatment23 740  1802301.2
 Aspirin in community158 530271540901.2
 Statins in communityb158 53074221400
Heart failure, hospital7030  3656406.8
 ACE inhibitors 48201001300.6
 Beta-blockers 49351151801.6
Spironolactone 1030251603.4
Aspirin 511570800.3
Statins 352255900.9
Heart failure, community46 095  5508908.5
 ACE inhibitors 48201201601.0
 Beta-blockers 49352102751.6
 Spironolactone 1030251503.1
 Aspirin 51151301500.6
 Statins 3522651552.3
Hypertension treatment1 488 90059135755800.1
Statins for primary prevention3 922 480630200200544.8
Total treatment effects   47908940100

Treatment efficacy, defined as the relative risk reduction for CHD death, was determined from the most recent meta-analyses or largest randomized controlled trials (Appendix 2). The absolute mortality reduction in each patient group, stratified by age and gender, was then calculated by multiplying the trial-based relative risk reduction by age-specific case fatality rate reported for patients from the Cause of Death Register. The survival benefit for a minimum period of 1 year was calculated for treatments in all patient groups in hospital and in the community. Combination therapy is common for patients with CHD. Therefore, the cumulative benefit was estimated using the formula of Mant and Hicks [7]: relative benefit = 1 − (1 − treatment a) × (1 − treatment b) × (1 − treatment c)… etc.

Adherence (compliance), defined as the proportion of patients taking therapeutically effective levels of treatment, was assumed to be 100% whilst in hospital, 70% in symptomatic patients with angina pectoris or heart failure, and 50% in asymptomatic individuals with hypertension or with elevated cholesterol levels [8, 9].

For the purpose of this study, uptake level was defined as the prescription rate multiplied by adherence. The best available data on the uptake of specific treatments in each group of patients were used to calculate the baseline benefits. All existing values contained within the model for 2002 were left unchanged (numbers of eligible patients, treatment compliance and effectiveness) [4].

The potential mortality benefit if the treatment levels were increased to 60% of eligible patients was then estimated. For practical and clinical purposes, this was considered to be a realistic and achievable level of uptake. However, in some treatment categories, the uptake level was already higher than 60% (aspirin and beta-blockers for acute MI), and in those cases, the level was left unchanged. We assumed that elective procedures involving CABG surgery increased by 60% compared to 1986. We estimated the numbers of deaths postponed by multiplying the patient numbers, relative mortality reduction and case fatality rate. We also assumed no mortality benefit for PCI compared with medical treatment for chronic angina pectoris [10], as in the earlier model [4].

The mortality effects were stratified by age and gender. Multi-way sensitivity analyses were then performed using the analysis-of-extremes method [11]. Minimum and maximum mortality data were generated using 95% confidence intervals from meta-analyses for treatment efficacy, multiplied by the minimum and maximum plausible values for patient numbers, treatment uptake and adherence. Examples and full details of the data sources are available from the authors.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices

In 2002, treatment levels in Sweden varied between patient groups. High treatment levels were achieved in some cases, such as aspirin (81%) and beta-blockers (85%) in patients with acute MI. However, in others, only 50–80% of eligible patients received appropriate therapy. For example, although the largest mortality reduction came from the use of secondary prevention medications or rehabilitation after MI, only 50% of patients received lipid-lowering treatment (e.g. statins) and only 37% were taking angiotensin-converting enzyme (ACE) inhibitors after MI, with a minority of patients participating in any rehabilitation programme. Likewise, in patients with heart failure, average treatment levels were generally poor: 48% for ACE inhibitors, 49% for beta-blockers and 10% for spironolactone (Table 1).

If treatment levels were increased to include at least 60% of eligible patients, there would have been approximately 8940 fewer deaths (minimum estimate 5090 and maximum estimate 18 730). This would represent a potential gain of approximately 4100 fewer deaths than actually occurred in 2002 (approximately 4800). The largest reduction, 44.8% of the 4100 deaths prevented or postponed, would have come from lipid-lowering drugs in primary prevention, followed by 23.1% from better initial treatment for acute coronary syndrome (ACS; including primary PCI and thrombolysis), 14.8% from optimizing secondary prevention therapies after acute MI or revascularization and 15.3% from improved heart failure treatments. A small proportion of the potential gain would have come from increases in uptake of aspirin and statins for patients with chronic angina treated in the community (1.2%) and hypertension treatments (<1%) (Table 1). Figure 1 summarizes the proportional contribution of each of the specific interventions to CHD mortality if the treatment uptake was increased to reach 60% of eligible patients.

image

Figure 1.  Estimated reduction in coronary heart disease mortality in 2002 if medical treatments and interventions reached 60% of eligible patients.

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With an increase to 60% in treatment uptake, 40% of the 4100 deaths prevented or postponed would have been in women compared to 60% in men. The largest mortality reduction in absolute numbers (Fig. 2) would have occurred amongst those aged above 55 years (7.9%, 22.5% and 26.8% in men and 4.9%, 9.9% and 23.2% in women aged 55–64, 65–74 and 75–84, respectively). Half of the total mortality reduction would have been in men aged 65–74 and 75–84 years, compared to 33% amongst women in the same age groups. The difference between men and women was reduced amongst individuals aged 75–84 years, with little gender difference in deaths prevented or postponed. In absolute numbers, there would have been only a minor reduction in mortality amongst individuals aged <55 years with little or no difference between men and women.

image

Figure 2.  Age and gender distribution of reduction in coronary heart disease mortality in 2002 if medical treatments and interventions reached 60% of eligible patients.

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The sensitivity analysis using the extreme-values approach shows that the proportional contribution from each of the modern cardiology interventions remained relatively consistent, irrespective of whether the best, minimum or maximum estimates were used. The largest potential mortality reductions would have come from primary prevention with lipid-lowering drugs (best estimate 2005), from improved treatment in ACS (acute MI and unstable angina) (1980) and from secondary prevention post-acute MI and revascularization (2205) (Fig. 3).

image

Figure 3.  Sensitivity analysis showing best estimates for coronary heart disease mortality reductions in 2002 if specific treatments reached 60% of eligible patients. Diamonds, best estimates; bars, maximum and minimum estimates.

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Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices

During recent decades, the mortality rate for CHD has decreased dramatically, with the rate decreasing by more than half between 1986 and 2002 [4]. During the same period, cardiology treatments developed rapidly but CHD remains the single most common cause of death in both men and women [1]. However, treatment effects could explain only a third of the decline in Swedish CHD mortality in 2002. In other industrialized countries, medical therapies have accounted for a higher proportion of the decrease in mortality, compared to Sweden [2, 3, 5], suggesting that increasing use of specific coronary medications and interventions in a larger group of eligible patients would have been beneficial.

Even though Sweden has high treatment levels in patients with CHD compared to other countries, a large proportion are still not receiving appropriate therapy. If 60% of eligible patients had received appropriate medical treatment, the mortality benefits might have almost doubled (4100 fewer CHD deaths, in addition to the baseline decrease of 4800). These findings are consistent with other studies in European countries and the USA [12–14].

The largest mortality reduction could come from lipid-lowering treatment in primary prevention. In 2002, treatment levels for statins were low in Sweden; therefore, an increase in treatment levels to 60% would have had a large impact on mortality reduction explaining almost half of the potential mortality reduction, or 2000 of the 4100 extra deaths prevented or postponed. Hence, treating 60% of all individuals with hypercholesterolaemia (defined as total serum cholesterol ≥5.2 mmol L−1) in the population may be too optimistic. During recent years, there has been a large increase in the use of statins, and by 2008, about 12% of all men and women aged 45–64 years as well as about 30% of those above 65 years of age were on lipid-lowering treatment (http://www.socialstyrelsen.se/publikationer2010/2010-3-14/Documents/2010-3-28Lkemedel). However, we recently showed that two of three men aged 50 years have a total serum cholesterol level at or above 5.0 mmol L−1 (195 mg dL−1) indicating that there is probably still substantial undertreatment [15]. Nevertheless, we recognize the continuing uncertainties around statin effectiveness in primary prevention [16] and acknowledge that the true potential benefit may be smaller.

The second largest additional treatment benefit, approximately 23% of the total gain, would have come from initial treatment in ACS (acute MI and unstable angina). In 2002, Sweden had high medical treatment rates in ACS (aspirin and beta-blockers) but comparatively low rates of thrombolysis and revascularization (PCI and CABG surgery). Hence, an increase in PCI and CABG surgery to 60% of eligible patients would have accounted for more than half of the potential additional mortality reduction in ACS (PCI 5.9% and CABG 5.8%).

The third largest additional treatment benefit, approximately 15%, would have come from heart failure treatment (in hospital and in the community). During the last 30 years, long-term mortality in patients with heart failure has decreased dramatically in Sweden (more for ischaemic than nonischaemic heart failure). Even so, case fatality rates are still high, and around 20% of younger patients (35–64) and 40% of patients aged 65–84 die within 3 years after discharge. Moreover, no decrease in long-term case fatality has been observed since 2001 [17]. An increase in the use of effective medical treatment to 60% in heart failure patients would have resulted in more than 1500 fewer deaths. Given this, the potential gain in deaths prevented or postponed with increased treatment levels in heart failure patients is large and could be even larger if treatment levels were increased above 60%. In addition, increased initial treatments in acute MI would not only result in fewer deaths but also potentially prevent the development of heart failure in patients with this condition.

Only a small proportion of deaths prevented or postponed would have come from hypertension treatment in this population, which could be explained by the high treatment levels already achieved by 2002. However, as Sweden has a high prevalence of hypertension [18], higher treatment levels could possibly reduce the mortality rates even further.

Study limitations

Modelling studies have a number of potential strengths. The best models can transparently integrate and simultaneously consider huge amounts of data from many sources. Explicit assumptions can then be tested by sensitivity analysis. However, modelling studies also have limitations. First, there might be an overestimation when applying the treatment efficacy seen in randomized controlled trial to effectiveness in ordinary clinical practice [19, 20]. Second, over the last two decades, there has been a shift in case severity with milder and fewer fatal MIs, with less ST-segment elevation MIs and more non-ST-elevation MIs and unstable angina [21]. This might partly be explained by increasing medical treatment before MI onset in patients with hypertension, angina and hypercholesterolaemia [22]. As a consequence, there could be a potential overestimation of the mortality reduction effect in the model. In addition, cholesterol levels in the general population are decreasing [23], which could influence the use of statins in primary prevention. Accordingly, potential future gains from statin treatment (after 2002) should be interpreted with caution.

Sweden has a long-standing tradition of administrative registries, a public health system with national coverage, and individual personal identification numbers for all citizens. This provides the possibility of linking data of good quality and excellent precision from various registries. The present analysis suggests that improved implementation of evidence-based treatments could prevent a substantial number of CHD deaths. This has potentially important implications for population health.

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices

Increasing the proportion of eligible patients with CHD who receive evidence-based treatment could have resulted in approximately 4100 fewer deaths in 2002, almost doubling the mortality reduction actually achieved. This finding emphasizes the importance of aggressively identifying and treating all eligible patients with CHD as well as of using evidence-based treatments in high-risk individuals.

Acknowledgements

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices

This work was supported by EpiLife (Göteborg Center for Epidemiologic Studies on Mental and Physical Health Interacting over the Lifecourse), by the Swedish Council for Working Life and Social Research and by grants from the Swedish Heart and Lung Foundation and the Swedish Research Council.

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  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices
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Appendices

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Conflict of interest
  9. Acknowledgements
  10. References
  11. Appendices
Table Appendix1.   Main data sources for the parameters used in the Swedish IMPACT model 1986 and 2002
 19862002
Population, deaths, CHD mortality Number of patients admitted yearly: MI, AP, HFThe National Board of Health and Welfare The Hospital Discharge RegisterThe National Board of Health and Welfare The Hospital Discharge Register
Number of patients treated with CABGThe Hospital Discharge RegisterSwedish Quality Registry for General Thoracic Surgery, the Hospital Discharge Register
PCIThe Hospital Discharge RegisterThe Hospital Discharge Register, SCAAR
Cardiopulmonary resuscitation in the communityAssume zeroSwedish Cardiac Arrest Registry
AMI, UAPAssume zeroRIKS-HIA
Secondary prevention following AMIAssume zeroEUROASPIRE [26], RIKS-HIA
Secondary prevention following CABG or PCIAssume zeroEUROASPIRE [26]
Congestive Heart FailureAssume zeroIMPROVEMENT [26],OBS-CHF [27]
Treatment for chronic anginaAssume zeroEUROASPIRE [26]
Community angina pectoris: totalMONICA WHO Got and Northern SwedenINTERGENE Study 2001–2004
Community chronic heart failureAssume same 1986 as 2002 [24]The Hospital Discharge Register 2003
Prevalence medication (ACE inhibitors, Beta-blockers, SpironolactoneAssume zeroIMPROVEMENT [28]
Medication (aspirin, statins)Assume zeroOBS-CHF [27]
Hypertension prevalence treated (%)MONICA GOT and Northern SwedenINTERGENE Study
 MONICA WHO GOT and Northern SwedenINTERGENE Study and MONICA WHO Northern Sweden
Statins for primary preventionAssume zeroINTERGENE Study
Population risk factor prevalence  
Current smoking, Physical activity, Obesity (BMI), DiabetesULF, the Official Statistics of SwedenULF, the Official Statistics of Sweden
Systolic blood pressureMONICA GOT and Northern SwedenMONICA Northern Sweden and INTERGENE, the Prospective Population Study of Women in Goteborg
CholesterolThe AMORIS Study [25]MONICA GOT and Northern Sweden, INTERGENE Study
Table Appendix2.   Clinical efficacy of interventions: relative risk reductions obtained from meta-analyses and randomized controlled trialsa
TreatmentsRelative risk reduction (95% CI)CommentsSource paper: first author (year), notes
Acute myocardial infarction
 Thrombolysis31% (95% CI: 14, 45)<55 years: OR = 0.692; RRR = 30.8 (95% CI: 14–45)Estess (2002) [29], [updated FTT] [29]
55–64 years: OR = 0.736; RRR = 26.4 (95% CI: 17–40)
65–74 years: OR = 0.752; RRR = 24.8 (95% CI: 15–37)
>75 years: OR = 0.844; RRR = 15.6 (95% CI: 4–30)
 Aspirin15% (95% CI: 11, 19)OR = 0.85 (95% CI: 0.81, 0.89). RRR 15% (95% CI: 11, 19) p. 75: outcome is vascular and nonvascular deathsAntithrombotic Trialists’ Collaboration (2002) [30]
 Primary angioplasty STEMI32% (95% CI: 5, 50)OR 0.68 (95% CI: 0.50, 0.95). RRR 32% (95% CI: 5, 50) outcome compares primary angioplasty to thrombolytics, not specific to STEMI, in results on p. 3Cucherat (2003) [31]
 Primary PCI non-STEMI32% (95% CI: 5, 51)OR 0.65 (95% CI: 0.49, 0.95). RRR 32% (95% CI: 5, 51) for cardiovascular death on p. 917 [RRR for cardiovascular death or MI was 26 (95% CI: 3, 44) and was 24 (95% CI: 0, 42) for any death]RITA 3 (Fox 2005) [32]
 Beta-blockers4% (95% CI: −8, 15)OR 0.96 (95% CI: 0.85, 1.08), RR 4% (95% CI: −8, 15) on p. 1732Freemantle (1999) [33]
 ACE inhibitors7% (95% CI: 2, 11)OR 0.93, (0.89, 0.98), RR 7% (2, 11) for 30 day mortality in MIACE Inhibitor Myocardial Infarction Collaborative Group 1998 [34]
Cardiopulmonary resuscitation (CPR)
 Community Sweden5% (95% CI: 4, 15.3)Nichol study reports overall median survival to discharge at 7.4% in this multi-country/site review, p. 520Nichol (1999) [35]
The Model focuses on 30/7 survival. Discharge survival will therefore provide an overestimate, which we have explicitly addressed by assuming 5% at 30/7Rea (2001) [36]
Rea looks at odds of bystander dispatcher assisted CPR and bystander CPR without dispatch assistance and compares to No bystander CPR. 7265 out-of-hospital arrests attended. OR 0.59–0.69 for these two groups which would give RRRs of 41% and 31%. [Consider as crude equivalent of CPR to no CPR comparison.] 15.3% survival to discharge in King-county, WA; consider as maximum value. Use Nichol (1999)35 5% as USA average
Graham et al. 1999 meta-analysis of papers 1973–1996 report 6.4% at discharge. Assume better in 2000, thus 6.4% at 30/7 OPALS RCT reports only 5.2%
Data from Swedish cardiac arrest register, and consistent with data with Nichol [35] and Rea [36]Holmberg (1998) [37]
 Hospital CPR Sweden33% (95% CI: 10, 36)AMI accounted for 35% of adult total cases. Adult survival to discharge 36% post-VF or VT (majority of post-AMI cases, only 10.6% post-asystole, adult survival to discharge 18% overall, but this reflected ALL Medical arrests in hospital) (varied from 10% to 36% depending on type of initial rhythm) (Tables 4 and 5 p. 55)Nadkarni (2006) [38]
Review of 36 000 adults with cardiac arrests in the 253 US/Canadian Hospitals National Registry of CPR. Nadkarni, JAMA 2006; 295 (1): 50–57Tunstall-Pedoe (1992) [39]
Older article from Tunstall-Pedoe on p. 1350 shows survival at 24 h to be 32%, discharge to home at 21%, and 1-year survival to be 15% overall. (16% and 8% in general wards, 31% and 16% in coronary care unit (p. 1349), etc.
Corroboration: model assumes that approximately 2% AMI admissions have primary VF (Olmsted County study). This is consistent with RIKS-HIA, suggesting approximately 2.5%. AMI admissions have primary VF/VTRIKS-HIA
Secondary prevention in patients with CHD
 Aspirin15% (95% CI: 11, 19)OR 0.85 (95% CI: 0.49, 0.95), RR 15% (95% CI: 11, 19) outcome is vascular and nonvascular deaths on p. 75. This data seem to be appropriate to this outcome in patients with CHDAntithrombotic Trialists’ Collaboration (2002) [30]
 Beta-blockers23% (95% CI: 15, 31)OR 0.77 (95% CI: 0.85, 0.69), 23% (95% CI: 15, 31) on p. 1734. Odds of death in long-term trialsFreemantle (1999) [33]
 ACE inhibitors20% (95% CI: 13, 26)OR 0.80 (95% CI: 0.74, 0.87), 20% (95% CI: 13, 26) on p. 1577, death up to 4 years [endpoint of study looking at those with heart failure or LV dysfunction]Flather (2000) [40]
 Statins22% (95% CI: 10, 26)OR = 0.78 (95% CI: 0.74—0.84). RRR = 22% (95% CI: 10, 26)Cholesterol Treatment Trialists’ Collaborators (2005) [41]
RR = 0.77 (95% CI: 0.68—0.87). RRR = 23% (95% CI: 13, 30) in those with other CHD
OR = 0.77 (95% CI: 0.71–0.83). RRR = 23% (95% CI: 17, 29)Wilt (2004) [42]
Wilt (2004) Section CHD mortality, p. 1430
Warfarin22% (95% CI: 13, 31)OR = 0.78 (95% CI: 0.67–0.90), RRR = 22% (95% CI: 10, 33)Anand and Yusuf (1999) [43]
Meta-analysis looking at oral anticoagulant therapy in coronary artery disease (31 trials about 18 000 patients) by intensity of INR control: high intensity (INR > 2.8) warfarin versus control for outcome of death had OR of 0.78 (95% CI: 0.69–0.87) corresponding to a RRR of 22% (95% CI: 13, 31); Moderate intensity warfarin (INR 2–3.0) versus control had OR of 0.82 (95% CI: 0.23–2.33) not significant but corresponding RRR of 18% (95% CI: −133, 77)Lau (1992) [44]. Table 1, p. 253 (anticoagulants)
 Rehabilitation26% (95% CI: 10, 39)OR = 0.74 (95% CI: 0.61–0.90), RRR = 26% (95% CI: 10, 39) in Fig. 1, p. 685 Taylor reference.Taylor (2004) [45]
Chronic angina
 CABG surgery years 0–539% (95% CI: 23, 52)OR = 0.61 (95% CI : 0.48–0.77), RR 39% (95% CI: 23, 52) on p. 565, 5-year mortalityYusuf (1994) [46]
 CABG surgery years 6–1032% (95% CI: 2, 30)OR = 0.83 (95% CI: 0.70–0.98), RR 17 (95% CI: 2, 30) on p. 565, 10-year mortalityYusuf (1994) [46]
OR = 0.68 (95% CI : 0.56–0.83), RR 32 (95% CI: 17, 44) on p. 565, 7-year mortality
CABG compared to medical treatment
 Angioplasty in chronic angina, with stents13% (95% CI: 0, 16)OR = 0.87 (95% CI: 0.52–1.45), RRR = 13% (95% CI: −45, 48)BASKET RCT (Lancet 2005; 366: 921) [47]: Comparison of drug eluting stents versus bare metal stents. Folland (1997) [48] Table 3, all deaths, 60-month follow-up
Maximum benefit, assume equivalent to CABG surgery for two vessel disease CABG, OR 0.84, (RR 16% 2, 30) 5-year survival 88% in controlsYusuf (1994) [46] Pocock (1995) [49]: no difference between PTCA and CABG as initial revasc procedure
Minimum assumption: NIL benefitDitto Bucher (2000) [50]
 Aspirin15% (95% CI: 11, 19)OR = 0.85 (95% CI: 0.81–0.89), RR 15% (95% CI: 11, 19) outcome is vascular and nonvascular deaths on p. 75Antithrombotic Trialists’ Collaboration (2002) [30]
 Statins22% (95% CI: 10–26)RR = 0.78 (95% CI: 0.74–0.84). RRR = 22% (95% CI: 10, 26)Cholesterol Treatment Trialists’ Collaborators (2005) [41]
RR = 0.77 (95% CI: 0.68–0.87). RRR = 23% (95% CI: 13, 30) in those with other CHD
Unstable angina
 Aspirin alone15% (95% CI: 11, 19)OR = 0.85 (95% CI: 0.81–0.89), RR 15% (95% CI: 11, 19) outcome is vascular and nonvascular deaths on p. 75. Assume appropriate for unstable angina patientsAntithrombotic Trialists’ Collaboration (2002) [30]
 Aspirin and Heparin33% (95% CI: −2, 56)OR 0.67 (95% CI: 0.48, 1.02) RR 33% (95% CI: −2, 56) in Table 3. The study outcome is composite MI death and nonfatal MI, compares those on ASA + Hep to ASA onlyOler (1996) [51]
 Platelet glycoprotein IIB/IIIA inhibitors9% (95% CI: 2, 16)RR 0.91 (95% CI: 0.84, 0.98) RR 9% (95% CI: 2, 16) study looked at acute coronary syndrome without persistent ST elevationBoersma (2002) [52]
Primary PTCA non-STEMI32% (95% CI: 5–51)OR 0.68 (95% CI: 0.49, 0.95). RRR 32% (95% CI: 5, 51) forRITA 3 (Fox 2005) [32] Cardiovascular deaths, Table 3
 Primary CABG surgery43% (95% CI: 19, 60)OR 0.57 (95% CI: 0.40, 0.81). RR 43% (95% CI: 19, 60) reduction in mortality at 5 years in those with class III/IV angina, Table 4, p. 566Yusuf (1994) [46]
Heart failure in patients requiring hospitalization
 ACE inhibitors20% (95% CI: 13, 26)OR 0.80 (95% CI: 0.74, 0.87). RR 20% (95% CI: 13, 26) on p. 1577, [death up to 4 years was study endpoint for those with heart failure or LV dysfunction]Flather (2000) [40]
 Beta-blockers35% (95% CI: 26, 43)OR 0.65 (95% CI: 0.57, 0.74). RR 35% (95% CI: 26, 43): all cause mortalityShibata (2001) [53]
 Spironolactone30% (95% CI: 18, 41)OR 0.70 (95% CI: 0.59, 0.82). RR 30% (95% CI: 18, 41) in those that had at least one cardiac related hospitalization [31% (95% CI: 18–42) in entire study population of those with CHF, p. 711]Pitt (1999) [54]
 Aspirin15% (95% CI: 11, 19)OR = 0.85 (95% CI: 0.81, 0.89), RR 15% (95% CI: 11, 19) outcome is vascular and nonvascular deaths on p. 75Antithrombotic Trialists’ Collaboration (2002) [30]
 Statins22% (95% CI: 10–26%)OR = 0.78 (95% CI: 0.74, 0.84). RRR = 22% (95% CI: 10–26), post-AMICholesterol Treatment Trialists’ Collaborators (2005) [41]
OR = 0.77 (95% CI: 0.68, 0.87). RRR = 23% (95% CI: 13, 30) in those with other CHD
  1. aRelative risk reduction calculated as 1- odds ratio.

Heart failure in the community
 ACE inhibitors20% (95% CI: 13, 26)OR 0.80 (95% CI: 0.74, 0.87). RR 20% (95% CI: 13, 26) on p. 1577, death up to 4 years [in those with heart failure or LV dysfunction]Flather (2000) [40]
 Beta-blockers35% (95% CI: 26, 43)OR 0.65 (95% CI: 0.57, 0.74). RR 35 (95% CI: 26, 43). Section 3.3 p. 353Shibata (2001) [53]
 Spironolactone31% (95% CI: 18, 42)OR 0.69 (95% CI: 0.58, 0.82). RR 31% (95% CI: 18–42) in entire study population consisting of those with CHF, p. 711 [30 (95% CI: 18, 41) in those with a cardiac related hospitalization]Pitt (1999) [54]
 Aspirin15% (95% CI: 11, 19)OR = 0.85 (0.81, 0.89), RR 15% (11, 19) outcome is vascular and nonvascular deaths on p. 75. Assume appropriate for patients with CHF owing to CHDAntithrombotic Trialists’ Collaboration (2002) [30]
 Statins22% (95% CI: 10–26%)OR = 0.78 (95% CI: 0.74, 0.84). RRR = 22% (95% CI: 10–26)Cholesterol Treatment Trialists’ Collaborators (2005) [41]
OR = 0.77 (95% CI: 0.68, 0.87). RRR = 23% (95% CI: 13, 30) in those with other CHD
Hypertension treatment
 13% (95% CI: 6, 19)OR 0.87 (95% CI: 0.81, 0.94). RRR 13% (95% CI: 6, 19) in those with high blood pressure without disease at entry [RRR 29% (95% CI: 17, 37) those with average blood pressure and CHD, treated with ACEI]Law (2003) [55]
Therapies for primary prevention of raised cholesterol
 Statins35% (95% CI: 11, 52)OR 0.65 (95% CI: 0.48, 0.89). 35% (95% CI: 11, 52) for CHD mortality (only trials using statins), Fig. 3 on p. 4Pignone (2000) [56]
 Gemfibrozil7% (95% CI: −8, 19)OR 0.93 (95% CI: 0.81, 1.08); RRR 7% (95% CI: −8, 19)Studer (2005) [57]
 Niacin5% (95% CI: −10, 18)OR 0.95 (95% CI: 0.82, 1.10); RRR 5% (95% CI: −10, 0.18)Studer (2005) [57]
Table Appendix3.   Main assumptions and overlap adjustments used in the Swedish IMPACT model
  1. AMI denotes acute myocardial infarction, CABG coronary artery bypass graft surgery, CHD coronary heart disease and DPPs deaths prevented or postponed. EPC the Centre for Epidemiology at the National Board of Health and Welfare and SBU denotes the Swedish Council on Technology Assessment in Health Care. aPrevalence of angina according to Rose’ questionnaire was established. Validation of the cases reduced the prevalence by half. ▮

Treatment categoryAssumptions and overlap adjustments 
Efficacy of PCI in anginaAssumed equivalent to CABG surgery for two vessel disease (maximum estimate), or equal to medical therapy (minimum estimate)Sculpher (1994) [58] Folland (1997) [48] Yusuf (1994) [46]
Angina in the communityStart with the total patient numbers with angina in the community, based on INTERGENE prevalencea Then deduct patients counted elsewhere  Patients already treated for unstable angina in hospital  50% of those receiving CABG for angina  50% of those receiving secondary prevention post-AMI/post-CABG/post-AngioplastyHagman (1977) [59] Capewell (2000) [60]
Hypertension treatment: overlaps with other CHD patient groupsTotal hypertensive patient numbers in community calculated, then deduct  50% of post-AMI patients  50% of community angina patients  50% of community heart failure patientsMONICA WHO INTERGENE Study, SBU
Fall in population blood pressureEstimate the number of DPPs by hypertension treatment  Then subtract this from the total DPPs attributed to the secular fall in population BPCapewell (1999) [61] Capewell (2000) [60]