SMART REACH model

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).
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