Resources

These tools may be used for doctor-patient communication or educational or research purposes.

Clinician resources

U-Prevent is an online platform that aims to provide tools for personalizing cardiovascular disease prevention. These tools may be used for educational or research purposes or to support doctor-patient communication. Naturally, we recommend only using U-Prevent within the scope of the locally applicable guidelines. Please read the terms and conditions before using U-Prevent.

Guidelines

You may use the following links to access international guidelines

European guidelines:
American guidelines:
British guidelines:

Risk scores

Individual risk estimations for (recurrent) major cardiovascular events can be used for patient education. These tools may allow patients to gain more insight into their personal prognosis, thereby increasing their health-motivation and positively impacting adherence to prescribed therapy.

Individual risk estimations can also guide medical decision-making about preventive treatment. High-risk individuals are more likely to benefit from preventive treatment, such as cholesterol-lowering, blood pressure-lowering (BMJ 2011). High-risk patients experience a larger absolute risk reduction (ARR) and subsequently have a lower number needed to treat (NNT) from any type of preventive treatment (Eur Heart J 2014).

U-Prevent provides online calculation tools of the following risk scores:
SMART risk score
The SMART risk score ( Heart 2013) can be used for all individual patients with clinical manifest atherosclerotic vascular disease (ASCVD). These include coronary artery disease, cerebrovascular disease, peripheral artery disease, abdominal aortic aneurysm and polyvascular disease. The SMART risk score estimates individual risk for (recurrent) myocardial infarction, stroke or vascular death in the next 10 years if standard care is provided. It is based on common, easy-to-measure, clinical patient characteristics. The SMART risk score was developed in data from the SMART study cohort and externally validated in 18,436 patients from the TNT (Treating to New Targets), IDEAL (Incremental Decrease in End Points Through Aggressive Lipid Lowering), SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels), and CAPRIE (Clopidogrel Versus Aspirin in Patients at Risk of Ischemic Events) trials ( >Circulation 2016).

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) is indicated for all patients with an ASCVD-history. The SMART risk score calculator estimates the effect of additional treatment options based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). Thus, the resulting hazard ratio for cardiovascular events of current to ex-smoking is 0.60.
  • Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L (39 mg/dL) lowering of LDL-cholesterol ( Lancet 2012) to a target of 1.7 mmol/L (70 mg/dL).
  • Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.77 per 10 mmHg decrease ( Lancet 2016) to an optional target of 130, 140, 150 or 160 mmHg.
  • Antithrombotic treatment: estimated risk is based on the assumption that standard care is provided. Such standard care (HR =1) for cardiovascular patients includes the use of aspirin or equivalent type of antithrombotic treatment. We assume that aspirin cessation is associated with the inverse effect of starting aspirin (i.e. HR 1/0.81 = 1.23; Lancet 2009). Other types of antithrombotic treatment that result in equivalent cardiovascular risk reduction include monotherapy with other platelet aggregation inhibitors, vitamin K antagonists or DOAC’s.
ADVANCE risk score
The ADVANCE risk score (Eur J Cardiovasc Prev Rehabil 2011) can be used for patients with type 2 diabetes mellitus without clinical manifest atherosclerotic vascular disease (ASCVD). The risk score is based on 10 clinical parameters and estimates individual risk for myocardial infarction, stroke or vascular death in the next 4 years. The ADVANCE risk score was developed in data from 7,168 participants of the ADVANCE trial cohort without a history of cardiovascular disease and externally validated in 1,836 patients with type 2 diabetes mellitus and without cardiovascular disease from the DIABHYCAR cohort (Eur J Cardiovasc Prev Rehabil 2011). To facilitate clinical interpretation, the U-Prevent tool extrapolates the 4-year risk as estimated by the ADVANCE risk score to 10-years using the following formula: risk10 years = 1-(1-risk4 years)^10/4.

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) is indicated for all patients with type 2 diabetes mellitus. The ADVANCE risk score calculator estimates the effect of additional treatment options based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). Thus, the resulting hazard ratio for cardiovascular events of current to ex-smoking is 0.60.
  • Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L (39 mg/dl) lowering of LDL-cholesterol (Lancet 2012) to a target of 2.5 mmol/L (100 mg/dl).
  • Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.74 per 10 mmHg decrease (JAMA 2015) to an optional target of 130, 140, 150 or 160 mmHg.
  • Antithrombotic treatment: We assume that the use of aspirin or equivalent type of antithrombotic treatment is associated with a hazard ratio of 0.88 (Lancet 2009). Other types of antithrombotic treatment that result in equivalent cardiovascular risk reduction include monotherapy with other platelet aggregation inhibitors, vitamin K antagonists or DOAC’s.
SCORE chart
The different versions of the HEART SCORE are based on the 2016 European Guidelines on cardiovascular disease prevention in clinical practice (Eur Heart J 2016) and the 2018 Dutch Cardiovascular Risk Management Guidelines. The European version of the HEART SCORE risk estimator can be used to estimate 10-year risk for cardiovascular death in apparently healthy individuals. The low-risk version is recommended for use in Andorra, Austria, Belgium, Cyprus, Denmark, Finland, France, Germany, Greece, Iceland, Ireland, Israel, Italy, Luxembourg, Malta, Monaco, The Netherlands, Norway, Portugal, San Marino, Slovenia, Spain, Sweden, Switzerland and the United Kingdom. The high-risk version is recommended for use in Bosnia and Herzegovina, Croatia, Czech Republic, Estonia, Hungary, Lithuania, Montenegro, Morocco, Poland, Romania, Serbia, Slovakia, Tunisia and Turkey. The Dutch version of the HEART SCORE estimator can be used to estimate 10-year risk for both fatal and non-fatal cardiovascular outcomes in Dutch patients only. Age, cholesterol and blood pressure are rounded to the nearest category of the appropriate HEART SCORE table.

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) is indicated for all people with cardiovascular risk factors. The HEART SCORE calculator estimates the effect of additional treatment options based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). Thus, the resulting hazard ratio for cardiovascular events of current to ex-smoking is 0.60.
  • Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L (39 mg/dl) lowering of LDL-cholesterol (Lancet 2012) to a target of 2.5 mmol/L (100 mg/dl).
  • Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.74 per 10 mmHg decrease (JAMA 2015) to an optional target of 130, 140, 150 or 160 mmHg.
  • Antithrombotic treatment: We assume that the use of aspirin or equivalent type of antithrombotic treatment is associated with a hazard ratio of 0.88 (Lancet 2009). Other types of antithrombotic treatment that result in equivalent cardiovascular risk reduction include monotherapy with other platelet aggregation inhibitors, vitamin K antagonists or DOAC’s.
Pooled cohort ASCVD risk equation
The race- and sex-specific Pooled Cohort ASCVD risk equation is based on the 2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk ( Circulation 2014). It can be used to predict 10-year risk for coronary heart disease death, nonfatal myocardial infarction, and fatal or nonfatal stroke in apparently healthy patients from the United States. The Pooled Cohort ASCVD risk equation was developed in pooled data of NHLBI-sponsored cohort studies, including the ARIC (Atherosclerosis Risk in Communities) study, the Cardiovascular Health Study, and the CARDIA (Coronary Artery Risk Development in Young Adults) study, combined with applicable data from the Framingham Original and Offspring Study cohorts.

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) is indicated for all people with cardiovascular risk factors. The ASCVD calculator estimates the effect of additional treatment options based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). Thus, the resulting hazard ratio for cardiovascular events of current to ex-smoking is 0.60.
  • Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L (39 mg/dl) lowering of LDL-cholesterol ( Lancet 2012) to a target of 2.5 mmol/L (100 mg/dl).
  • Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.74 per 10 mmHg decrease ( JAMA 2015) to an optional target of 130, 140, 150 or 160 mmHg.
  • Antithrombotic treatment: We assume that the use of aspirin or equivalent type of antithrombotic treatment is associated with a hazard ratio of 0.88 ( Lancet 2009). Other types of antithrombotic treatment that result in equivalent cardiovascular risk reduction include monotherapy with other platelet aggregation inhibitors, vitamin K antagonists or DOAC’s.
Elderly risk score
The elderly risk score can be used for patients aged >70 years with or without cardiovascular disease ( Clin Res Cardiol 2017). It estimates individual risk for myocardial infarction, stroke or vascular death in the next 10 years. The elderly risk score was developed in data from the “PROspective Study of Pravastatin in Elderly at Risk" (PROSPER) trial and externally validated in data from elderly patients enrolled in the "Secondary Manifestations of ARTerial disease" (SMART) cohort study (n = 1442) and the "Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm" (ASCOT-LLA) trial (n = 1893). Risk estimates are adjusted for the competing risk of non-vascular mortality. If the option 'other' geographical regions is selected, Northern/Western-European risk estimates are reported as a default.

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) is indicated for all elderly people with cardiovascular risk factors. The elderly risk score calculator estimates the effect of additional treatment options based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). Thus, the resulting hazard ratio for cardiovascular events of current to ex-smoking is 0.60.
  • Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L (39 mg/dl) lowering of LDL-cholesterol ( Lancet 2012) to a target of 2.5 mmol/L (100 mg/dl).
  • Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.74 per 10 mmHg decrease ( JAMA 2015) to an optional target of 130, 140, 150 or 160 mmHg.
  • Antithrombotic treatment: We assume that the use of aspirin or equivalent type of antithrombotic treatment coagulation is associated with a hazard ratio of 0.88 ( Lancet 2009). Other types of antithrombotic treatment that result in equivalent cardiovascular risk reduction include monotherapy with other platelet aggregation inhibitors, vitamin K antagonists or DOAC’s.

Lifetime treatment effect estimators

For shared decision-making on the initiation or withdrawal of cardiovascular preventive therapies, personalized estimates of the effect of treatment may be useful in addition to risk. For this purpose, U-Prevent provides tools to estimate both 10-year and lifetime effects of the most frequently applied preventive interventions, including blood pressure lowering, lipid lowering and platelet aggregation inhibition. The 2016 European Guidelines on cardiovascular disease prevention (Eur Heart J 2016) recommend that lifetime calculators may be used as an educational tool in individuals <50 years of age. We expect, however, that these calculators may also help to improve your patients’ insight in their cardiovascular prognosis and motivation for therapy in patients >50 years of age and, especially, elderly. Notably, lifetime estimations of cardiovascular prognosis and the effect of therapy may be especially useful in certain groups of patients. For example, younger patients often have an inherently low 10-year risk due to their age, even in the presence of important risk-factors such as hypertension. But this low 10-year risk masks a high lifetime risk. Conversely, older patients inherently have a high 10-year risk, but the benefit of preventive treatment may be limited by short life-expectancy.
In BMJ 2016 we explained the methodological principles that the lifetime treatment effect estimators are based on. A video-abstract of this article can be viewed below.
The U-Prevent lifetime scores are described below. All scores were derived from multiple, large, observational population-based cohorts and can be used for estimating risk and cardiovascular event-free life-expectancy. For estimation of individual treatment effect, the lifetime score estimates are combined with hazard ratios from trials or meta-analyses. Below, we also summarize which hazard ratios were applied to each of the scores. The effects of these treatments are assumed to be independent and multiplicative. Estimates of (gain) in cardiovascular-free life-expectancy are based on (differences in) median predicted survival for an individual patient.
SMART-REACH score
The SMART-REACH model ( JAHA 2018 ) can be used for all individual patients with clinical manifest atherosclerotic vascular disease (ASCVD). These include coronary artery disease, cerebrovascular disease, peripheral artery disease, abdominal aortic aneurysm and polyvascular disease. The SMART-REACH model estimates individual 10-year risk and lifetime risk (i.e. risk until age 90 years) for (recurrent) myocardial infarction, stroke or vascular death and (recurrent) event free life-expectancy if standard care is provided. It is based on common, easy-to-measure, clinical patient characteristics. The SMART-REACH model was developed in data from 14,259 cardiovascular patients from Western-Europe enrolled in the REACH registry and externally validated in 19,170 cardiovascular patients from Northern-America enrolled in the REACH registry and 6,959 patients from The Netherlands, enrolled in the SMART study cohort. For all 'other' geographical regions, the Western-European version is used as a default.

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) is indicated for all patients with an ASCVD-history. The SMART-REACH calculator estimates the effect of medications changes compared to current treatment. Treatment estimates are based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). The resulting hazard ratio for cardiovascular events of current to ex-smoking, thus, is 0.60. Also, smoking cessation is assumed to reduce the hazard ratio for non-vascular mortality of current smokers versus never smokers (i.e. 1.83; Arch Intern Med 2012) to that of ex-smokers versus never smokers (i.e. 1.34; Arch Intern Med 2012). The resulting hazard ratio for non-vascular mortality of current to ex-smoking, thus, is 0.73.
  • Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L (39 mg/dl) lowering of LDL-cholesterol (Lancet 2012) without a bottom limit. The anticipated change in LDL-cholesterol is based on the patients’ baseline cholesterol level. The percentage change in LDL-cholesterol was derived from BMJ 2003 for different types and doses of statins. Ezetimibe is assumed to result in an additional 24% decrease in LDL-cholesterol (N Engl J Med 2015) and PCSK9-inhibition therapy is assumed to result in an additional 59% decrease in LDL-cholesterol (N Eng J Med 2017).
  • Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.77 per 10 mmHg decrease (Lancet 2016). Treatment effect is truncated at 130 mmHg, since this is currently the lowest recommended treatment target in guidelines. The calculation tool estimates the effect of reaching this target regardless whether this is achieved by lifestyle or medication.
  • Anticoagulation therapy: estimated risk and (recurrent) event-free life-expectancy are based on the assumption that standard care is provided. Such standard care (HR =1) for cardiovascular patients includes the use of aspirin or equivalent type of anticoagulation therapy, including monotherapy with vitamin K antagonists or DOACs. We assume that aspirin cessation is associated with the inverse effect of starting aspirin (i.e. HR 1/0.81 = 1.23; Lancet 2009). Dual antiplatelet therapy (DAPT) compared to aspirin alone is associated with a HR 0.78 (Eur Heart J 2016). Combined use of aspirin with a low dose DOAC is associated with a HR 0.76 (N Eng J Med 2017).
DIAL model
The DIAL model ( Eur Heart J 2019 ) can be used for all individual patients with type 2 diabetes mellitus (T2DM). The DIAL model estimates individual 10-year risk and lifetime risk (i.e. risk until age 95 years) for myocardial infarction, stroke or vascular death and event free life-expectancy if standard care is provided. It is based on common, easy-to-measure, clinical patient characteristics. The DIAL model was developed in data from 389,366 patients with T2DM from Sweden enrolled in the Swedish National Diabetes Register and externally validated in 197,785 patients with T2DM from Europe, Northern-America, Asia, and Oceania enrolled in the Scottish Care Information (SCI) –Diabetes register, the secondary Manifestation of ARTerial disease (SMART) cohort, the European Prospective Investigation into Cancer-Netherlands (EPIC-NL) cohort, the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, the Action in Diabetes and Vascular disease: preterAx and diamicroN-MR Controlled Evaluation (ADVANCE) trial, the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) trial, and the Lipid Lowering Trial component of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT). The DIAL-model was updated for higher cardiovascular event rates in Scotland (i.e. 17 per 1000 patient-years) compared to Sweden (i.e. 11 per 1000 patient-years). Updating for differences in event rates was not necessary for all other geographical regions. However, it should be noted that there may have been a healthy participant bias, as we used trial data to validate the DIAL-model in these regions. Therefore, the U-Prevent calculator assumes that cardiovascular event rates in Eastern-Europe are as high as in Scotland. Event rates in all other regions (including ‘other’) are assumed to be comparable to the Swedish population.

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) is indicated for all patients with T2DM. The DIAL calculator estimates the effect of medications changes compared to current treatment. Treatment estimates are based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). The resulting hazard ratio for cardiovascular events of current to ex-smoking, thus, is 0.60. Also, smoking cessation is assumed to reduce the hazard ratio for non-vascular mortality of current smokers versus never smokers (i.e. 1.83; Arch Intern Med 2012) to that of ex-smokers versus never smokers (i.e. 1.34; Arch Intern Med 2012). The resulting hazard ratio for non-vascular mortality of current to ex-smoking, thus, is 0.73.
  • >Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L (39 mg/dl) lowering of LDL-cholesterol ( Lancet 2012) without a bottom limit. The anticipated change in LDL-cholesterol is based on the patients’ baseline cholesterol level. The percentage change in LDL-cholesterol was derived from BMJ 2003 for different types and doses of statins. Ezetimibe is assumed to result in an additional 23% decrease in LDL-cholesterol ( N Engl J Med 2015) and PCSK9-inhibition therapy is assumed to result in an additional 59% decrease in LDL-cholesterol ( N Eng J Med 2017).
  • >Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.74 per 10 mmHg decrease ( Lancet 2016). Treatment effect is truncated at 130 mmHg, since this is currently the lowest recommended treatment target in guidelines. The calculation tool estimates the effect of reaching this target regardless whether this is achieved by lifestyle or medication.
  • Antithrombotic treatment: The effect of aspirin or equivalent type of antithrombotic treatment depends on the presence of cardiovascular disease. Patients with T2DM without a history of cardiovascular disease are assumed to have less effect of aspirin treatment with a hazard ratio of 0.88 compared with patients with T2DM with a history of cardiovascular disease, hazard ratio of 0.81 ( Lancet 2009). Other types of anticoagulation that result in equivalent cardiovascular risk reduction include monotherapy with other platelet aggregation inhibitors, vitamin K antagonists or DOAC’s.
  • Glucose lowering: The hazard ratio for lowering HbA1c is assumed to be 0.91 per 10 mmol/mol decrease ( Diabetologia 2009). Treatment effect is truncated at 53 mmol/mol, since this is currently the lowest recommended treatment target in guidelines. The calculation tool estimates the effect of reaching this target of HbA1c regardless whether this is achieved by lifestyle or medication.
  • SGLT2-inhibition and GLP1-analogues: For the treatment effects of SGLT2-inhibitors and GLP1-analogues, we assumed that these effects were independent of HbA1c lowering. The hazard ratio for SGLT2-inhibitors is 0.88 and the hazard ratio for GLP1-analogues is 0.91 ( JAMA 2018 )
LIFE-CVD model
The LIFE-CVD model (report not yet published) has been developed for otherwise healthy people. This is defined as people without known terminal illness or an eGFR < 30 ml/min 1.73 m-2, and without prior cardiovascular disease (defined as a medical history of myocardial infarction, angina, revascularization procedures– coronary or otherwise -, current atrial fibrillation, heart failure, and stroke or transient ischemic attack.

The LIFE-CVD model is capable of estimating 10-year and lifetime CVD-risk (i.e. risk until age 90), and CVD-free life-expectancy for myocardial infarction, stroke or vascular death and event free life-expectancy if standard care is provided. It is based on common, standard, and easy-to-measure, clinical patient characteristics. The LIFE-CVD model was developed in data from 6,715 patients from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort, and validated in the Atherosclerosis Risk in Communities Study (ARIC) the Heinz Nixdorf RECALL (Risk factors, Evaluation of Coronary Calcium and Lifestyle) Study (HNR, 2000-2003) and the European Prospective Investigation into Cancer-Netherlands (EPIC-NL, 1993-1997).

Treatment effect assumptions

Lifestyle optimization (i.e. healthy diet, physical exercise and optimal body weight) can be universally recommended to all apparently healthy individuals. The LIFE-CVD calculator estimates the effect of cholesterol and blood-pressure management, smoking cessation, and antithrombotic therapy based on the following assumptions:
  • Smoking cessation: this option is only applicable to current smokers. Smoking cessation is assumed to reduce the hazard ratio for cardiovascular events of current smokers versus never smokers (i.e. 1.98; BMJ 2015) to that of ex-smokers versus never smokers (i.e. 1.18; BMJ 2015). The resulting hazard ratio for cardiovascular events of current to ex-smoking, thus, is 0.60. Also, smoking cessation is assumed to reduce the hazard ratio for non-vascular mortality of current smokers versus never smokers (i.e. 1.83; Arch Intern Med 2012) to that of ex-smokers versus never smokers (i.e. 1.34; Arch Intern Med 2012). The resulting hazard ratio for non-vascular mortality of current to ex-smoking, thus, is 0.73.
  • Cholesterol lowering: A hazard ratio of 0.78 was assumed per 1.0 mmol/L lowering of LDL-cholesterol ( Lancet 2012) without a bottom limit. The anticipated change in LDL-cholesterol is based on the patients’ baseline cholesterol level. The percentage change in LDL-cholesterol was derived from Lancet 2012 for different types and doses of statins. Ezetimibe is assumed to result in an additional 23% decrease in LDL-cholesterol ( N Engl J Med 2015).
  • Blood pressure lowering: The hazard ratio for lowering of systolic blood pressure is assumed to be 0.74 per 10 mmHg decrease ( Lancet 2016). Treatment effect is truncated at 130 mmHg, since this is currently the lowest recommended treatment target in guidelines. For example, this also means that we assume an increase of systolic blood pressure from 120 to 130mmHg not to result in any detrimental effect on prognosis. The calculation tool estimates the effect of reaching this target regardless whether this is achieved by lifestyle or medication.
  • Antithrombotic treatment: The hazard ratio of associated with the use of aspirin or equivalent type of antithrombotic treatment is 0.88. ( Lancet 2009). Aspirin cessation gives a hazard ratio of 1/0.88 (i.e. 1.13). Other types of antithrombotic treatment that result in equivalent cardiovascular risk reduction include monotherapy with other platelet aggregation inhibitors, vitamin K antagonists or DOAC’s.

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