In this issue of Stroke, Marileen Portegies and colleagues seek to determine the theoretical impact of pre-morbid cardiovascular risk factors on mortality after stroke. 

The study population was the well-described prospective, population-based Rotterdam cohort. Each patient with incident stroke was age and sex matched with four stroke-free participants. Poisson regression was used to determine age and sex adjusted mortality rate ratios. Interactive Risk Attributable Program, a method to calculate population attributable risks, was used to determine the population attributable risk for each vascular risk factor and for all risk factors (those independently contributing to mortality) combined. Interaction term analysis evaluated for effect modification by stroke.


For this study, they included 1,237 stroke patients and 4,928 non-stroke participants. The mean age was 80 years, and 60.4% were female. Cardiovascular risk factors were measured for a mean of 3.7 (±3.2) years before stroke.

Mortality rates after stroke were highest in the first 30 days and remained double that of the non-stroke group 1 year onward from inclusion. The increased mortality after stroke was largely due to cardiovascular death.

The population attributable risks for the most important modifiable risk factors were as follows:
  • Smoking: 0.13 (in other words, 13% of post-stroke mortality can be attributed to pre-stroke smoking status)
  • Diabetes: 0.06
  • Atrial fibrillation: 0.06
  • Hypertension: 0.06

The cumulative proportion of mortality of included vascular risk factors was 0.27 (95% confidence interval, 0.14-0.45). This means that 27% of post-stroke mortality can be attributed to pre-existing modifiable risk factors. This was only 8% higher than the attributable risk in patients without stroke.

The authors acknowledge that population attributable risks of certain risk factors were driven by the increased prevalence of these risk factors in patients with stroke.

The authors keenly point out that the main conclusion here is that 73% of post-stroke mortality is not explained by premorbid cardiovascular risk factors. Understanding the “other 73%” may yield stroke-specific actionable targets to reduce post-stroke mortality.