Estimated Life Expectancy Without Recurrent Cardiovascular Events in Patients With Vascular Disease: The SMART-REACH Model

Abstract

Background In patients with vascular disease, risk models may support decision making on novel risk reducing interventions, such as proprotein convertase subtilisin/kexin type 9 inhibitors or anti-inflammatory agents. We developed and validated an innovative model to estimate life expectancy without recurrent cardiovascular events for individuals with coronary, cerebrovascular, and/or peripheral artery disease that enables estimation of preventive treatment effect in lifetime gained. Methods and Results Study participants originated from prospective cohort studies: the SMART (Secondary Manifestations of Arterial Disease) cohort and REACH (Reduction of Atherothrombosis for Continued Health) cohorts of 14 259 ( REACH Western Europe), 19 170 ( REACH North America) and 6959 ( SMART , The Netherlands) patients with cardiovascular disease. The SMART-REACH model to estimate life expectancy without recurrent events was developed in REACH Western Europe as a Fine and Gray competing risk model incorporating cardiovascular risk factors. Validation was performed in REACH North America and SMART . Outcomes were (1) cardiovascular events (myocardial infarction, stroke, cardiovascular death) and (2) noncardiovascular death. Predictors were sex, smoking, diabetes mellitus, systolic blood pressure, total cholesterol, creatinine, number of cardiovascular disease locations, atrial fibrillation, and heart failure. Calibration plots showed high agreement between estimated and observed prognosis in SMART and REACH North America. C-statistics were 0.68 (95% confidence interval, 0.67-0.70) in SMART and 0.67 (95% confidence interval, 0.66-0.68) in REACH North America. Performance of the SMART-REACH model was better compared with existing risk scores and adds the possibility of estimating lifetime gained by novel therapies. Conclusions The externally validated SMART-REACH model could be used for estimation of anticipated improvements in life expectancy without recurrent cardiovascular events in individual patients with cardiovascular disease in Western Europe and North America.

Keywords: life expectancy; prognosis; risk stratification; secondary prevention; treatment effect.

Figure 1

External calibration of estimated survival with the SMART‐REACH model. A, Estimated vs observed 10‐year survival without recurrent cardiovascular events in the SMART population (after correction for geographic differences in event rates). B, Estimated vs observed 2‐year survival without recurrent cardiovascular events in North American REACH (after correction for geographic differences in event rates). MI indicates myocardial infarction; REACH, Reduction of Atherothrombosis for Continued Health; SMART, Secondary Manifestations of Arterial Disease.

Figure 2

Patient examples. Patient A is a 55‐year‐old woman. She is a current smoker and has no diabetes mellitus. Her systolic blood pressure is 145 mm Hg. Her laboratory values are total cholesterol, 6.0 mmol/L (LDL‐c 4.0 mmol/L); and creatinine, 70 μmol/L. She has a history of 1 location of cardiovascular disease as well as atrial fibrillation, and she has no congestive heart failure. As lipid‐lowering treatment, patient A currently takes atorvastatin 10 mg. The clinician considers raising the atorvastatin dose to 80 mg. Patient A wants to know what her expected benefit is from this change in therapy. The estimated 10‐year risk for patient A is 26.7%. Her life expectancy free from recurrent cardiovascular disease is 70.0 years. When she would take atorvastatin 80 mg instead of 10 mg, this would reduce her 10‐year risk to 20.9% (−5.8%, or 10‐year NNT, 17). The change in therapy would increase her estimated cerebrovascular disease–free life expectancy with 2.0 years to 72.0. Patient B is a 75‐year old male who does not smoke and has no diabetes mellitus. His systolic blood pressure is 140 mm Hg. His total cholesterol is 5.0 mmol/L and creatinine 80 μmol/L. He has a history of 1 location of cardiovascular disease, no atrial fibrillation, and no congestive heart failure. As lipid‐lowering treatment, patient B currently takes atorvastatin 10 mg. The clinician considers raising the atorvastatin dose to 80 mg. Patient B wants to know his expected benefit from this change in therapy. The estimated 10‐year risk for patient B is 32.8%. His life expectancy free from recurrent cardiovascular disease is 84.3 years. When he would take atorvastatin 80 mg instead of 10 mg, this would reduce his 10‐year risk to 26.8% (−6.0%, or 10‐year NNT, 17). The change in therapy would increase his estimated cerebrovascular disease–free life expectancy with 0.9 years to 85.2. CVD indicates cardiovascular disease; NNT, number needed to treat.