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Impact of coronary artery calcium on progression of diastolic dysfunction: a cohort study
Ki Hong Choi1, Danbee Kang2,3, Seung Hun Lee4
1Division of Cardiology, Department of Internal Medicine, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-Gu, Seoul, 06351, Republic of Korea.
Insights
High coronary artery calcium (CAC) levels are linked to a higher prevalence and faster progression of diastolic dysfunction (DD). This combination significantly increases mortality risk in the general population.
Area of Science:
- Cardiology
- Preventive Medicine
- Medical Imaging
Background:
- The link between coronary artery calcium (CAC) and diastolic dysfunction (DD) progression is not well understood.
- Investigating the combined impact of CAC and DD on mortality is crucial.
Purpose of the Study:
- To examine the prevalence and progression of DD based on CAC severity.
- To determine the synergistic effect of CAC and DD on all-cause mortality.
Main Methods:
- Population-based cohort study of 15,193 adults with simultaneous echocardiography and CAC scans.
- Defined definite DD (≥3/4 abnormal parameters) and definite or probable DD (≥2/4).
- Assessed all-cause mortality in relation to CAC and DD status.
Main Results:
- Higher CAC scores (≥100) were associated with increased prevalence of definite and probable DD.
- Significant linear association observed between CAC severity and E/e' ratio.
- Elevated CAC (≥100) and DD independently and synergistically increased mortality risk.
- Significant CAC (≥100) predicted accelerated DD progression and faster E/e' elevation over time.
Conclusions:
- A significant relationship exists between CAC and DD prevalence in the general population.
- Both CAC and DD are independent predictors of increased mortality.
- CAC ≥100 significantly drives DD progression, independent of other clinical factors.
Background:
The relationship between coronary artery calcium (CAC) and progression of diastolic dysfunction (DD) during longitudinal follow-up is uncertain. This study aimed to investigate the prevalence and progression of DD according to severity of CAC and understand their synergistic effect on mortality.
Methods:
This was a population-based cohort study. All 15,193 adults who underwent a health screening exam with simultaneous echocardiography and CAC scan were enrolled. Definite DD (≥ 3/4 abnormal parameters for DD [e', E/e', tricuspid regurgitation velocity, and left atrial volume index]) and definite or probable DD (≥ 2/4) were defined. All-cause mortality was assessed based on the CAC and DD.
Results:
Among the population, 7995 participants (52.6%) had CAC = 0; 4661 (30.7%) had 0 < CAC < 100; and 2537 (16.7%) had CAC ≥ 100. The prevalence ratios for definite (adjusted ratio: 1.72, 95% CI: 1.23-2.22) and definite or probable DD (adjusted ratio: 1.83, 95% CI: 1.31-2.36) were significantly higher in individuals with CAC ≥ 100 than in those with CAC = 0. There was significant linear association of CAC with E/e' (adjusted p for linearity = 0.001). Compared with CAC < 100 without definite DD, the adjusted HRs with 95% CI for mortality of CAC ≥ 100 without definite DD, CAC < 100 with definite DD, and CAC ≥ 100 with definite DD were 2.56 (95% CI: 1.67-3.94), 3.08 (95% CI: 1.28-7.39), and 3.91 (95% CI: 1.68-9.10). Among participants without DD at CAC measurement who had at least two echocardiographic measurements, the presence of significant CAC (≥ 100) was significantly associated with accelerated progression in definite DD over time (adjusted HR: 1.46, 95% CI: 1.13-1.88), with more rapid elevation of E/e' during follow-up (difference: 0.06, 95% CI: 0.02-0.10, p = 0.003).
Conclusions:
In the general population, there was a significant relationship between CAC and prevalence of DD, and both subclinical parameters were associated with increased mortality. Moreover, CAC ≥ 100 significantly affects the progression of DD independently of other clinical factors.
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