Risk of ASCVD gradually increases with increasing SBP levels starting from 90 mmHg

Introduction and methods

Many individuals with low traditional atherosclerotic cardiovascular disease (ASCVD) risk factors have subclinical atherosclerosis. Which is measured by the presence of coronary artery calcium (CAC) [1-3]. Individuals with lower exposure to ASCVD risk factors such as high SBP levels during their lifetime have a lower probable risk for future ASCVD events [4-6]. However, it is still uncertain whether the relationship between SBP level and risk for ASCVD also applies to individuals without hypertension or other ASCVD risk factors. Moreover, it remains unresolved whether risk for incident ASCVD plateaus or increases (eg. A J-point) at low SBP levels [7-10].

The present study evaluated the association between SBP and prevalence of CAC as well as incident ASCVD in individuals with SBP levels between 90 and 129 mmHg. A total of 1457 individuals from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort [11] who had normal SBP levels (90-129 mm Hg), a baseline coronary artery calcium scan and no prior history of ASCVDs were included in the study. Individuals with hypertension (SBP >129 mm Hg) or hypotension (SBP <90 mm Hg), dyslipidemia (LDL-c level ≥160 mg/dL or HDL-c level <40 mg/dL), diabetes, who were smokers, or used prescribed cholesterol-lowering or blood glucose-lowering medication were excluded. Average (SD) follow-up was 14.5 (3.9) years. Participants were categorized into 4 groups based on their baseline SBP levels: 90-99 mmHg (n=208), 100-109 mmHg (n=414), 110-119 mmHg (n=504), 120-129 (n=331) mmHg. CAC was measured and classified as absent or present and diffuse CAC was defined as presence of CAC in 2 or more coronary arteries. Incident ASCVD was defined as fatal or nonfatal incident coronary heart disease, incident stroke, or other incident ASCVD.

Main results

• The proportion of individuals with CAC and diffuse CAC presence increased in a stepwise manner with increasing SBP level from 19.7% of participants in the 90-99 mmHg group up to 40.8% in 120-129 mmHg group (P<0.001 for trend).
• There were 94 incident ASCVD events during follow-up. The median 10-year pooled cohort equations ASCVD risk also increased with increasing SBP level (1.1% [IQR 0.5%-3.0%] in the 90-99 mmHg group, 2.1% [IQR 0.8%-5.0%] in the 100-109 mmHg group, 3.3% [IQR 1.5%-6.7%] in the 110-119 mmHg group and 5.6% [IQR 2.5%-12.5%] in the 120-129 mmHg group; P value for trend <0.001).
• The adjusted HR (aHR) for ASCVD was 1.53 (95%CI: 1.17-1.99) for every 10-mm Hg increase in SBP levels.
• Compared with participants with SBP levels 90 to 99 mm Hg, the aHR for ASCVD risk was 3.00 (95%CI: 1.01-8.88) for SBP levels 100 to 109 mm Hg, 3.10 (95%CI: 1.03- 9.28) for SBP levels 110 to 119 mm Hg, and 4.58 (95%CI: 1.47-14.27) for SBP levels 120 to 129 mm Hg (P value for trend <0.06). This increase in ASCVD risk with increasing SBP levels was also observed when SBP was modeled as a continuous variable.

Conclusion

References

Find this article online at JAMA Cardiol.