Elsevier

The American Journal of Cardiology

Volume 134, 1 November 2020, Pages 99-107
The American Journal of Cardiology

Effect of Progression of Valvular Calcification on Left Ventricular Structure and Frequency of Incident Heart Failure (from the Multiethnic Study of Atherosclerosis)

https://doi.org/10.1016/j.amjcard.2020.08.017Get rights and content

Highlights

  • Valve calcium progression and heart failure risk was assessed in a diverse cohort.

  • Progression of valve calcification was associated with increased heart failure risk.

  • Association seen for heart failure with preserved but not reduced ejection fraction.

  • This was independent of interim coronary heart disease & atrial fibrillation events.

Heart failure (HF) is a leading cause of morbidity. Strategies for preventing HF are paramount. Prevalent extracoronary calcification is associated with HF risk but less is known about progression of mitral annular (MAC) and aortic valve calcification (AVC) and HF risk. Progression of valvular calcification (VC) [interval change of >0 units/yr] was assessed by 2 cardiac computed tomography scans over a median of 2.4 years. We used Cox regression to determine the risk of adjudicated HF and linear mixed effects models to determine 10-year change in left ventricular (LV) parameters measured by cardiac magnetic resonance imaging associated with VC progression. We studied 5,591 MESA participants free of baseline cardiovascular disease. Mean ± SD age was 62 ± 10 years; 53% women; 83% had no VC progression, 15% progressed at 1 site (AVC or MAC) and 3% at both sites. There were 251 incident HF over 15 years. After adjusting for cardiovascular risk factors, the hazard ratios (95% confidence interval) of HF associated with VC progression at 1 and 2 sites were 1.62 (1.21 to 2.17) and 1.88 (1.14 to 3.09), respectively, compared with no progression (p-for-trend <0.001). Hazard ratios were higher for HFpEF (2.52 [1.63 to 3.90] and 2.49 [1.19 to 5.25]) but nonsignificant for HFrEF. Both AVC (1.61 [1.19 to 2.19]) and MAC (1.50 [1.09 to 2.07]) progression were associated with HF. VC was associated with worsening of some LV parameters over 10 years. In conclusion, VC progression was associated with increased risk of HF and change in LV function. Interventions targeted at reducing VC progression may also impact HF risk, particularly HFpEF.

Section snippets

Methods

The Multiethnic Study of Atherosclerosis (MESA) is an ethnically diverse cohort of 6,814 women and men aged 45-84 years old enrolled between July 2000 and August 2002 from Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore City and Baltimore County, MD; St. Paul, MN; Chicago, IL; and Los Angeles County, CA.12 The study design and methods are available at http://www.mesa-nhlbi.org and have been previously described.12 Participants were free of clinical cardiovascular disease and

Results

We studied 5591 MESA participants with mean (SD) age of 61.8 (10.2) years, 53% were women, and 40% White. At the time of baseline CT scan, 691 (12%) had prevalent AVC and 502 (9%) prevalent MAC. Eighty-three percent of participants had no progression of VC, 15% had progression of VC at only 1 site (AVC or MAC), and 3% at both sites (AVC and MAC) after a median of 2.4 years of follow-up. Table 1 shows the baseline characteristics of study participants stratified by number of sites with

Discussion

Baseline CAC and CAC progression have previously been shown to be associated with incident HF.11,20 In this study, we now show that progression of VC at 1 or both sites after a median of 2.4 years is associated with an increased risk of HF in this multiethnic community-based cohort free from clinical cardiovascular disease at baseline independent of ASCVD risk factors. We also found stronger associations with the incidence of HFpEF, with a greater than twofold risk of HFpEF with VC progression,

Author Contributions

Oluwaseun E. Fashanu: Conceptualization, Methodology, Formal analysis, Writing- Original draft preparation. Sireesha Upadhrasta: Conceptualization, Writing - Review & Editing. Di Zhao: Conceptualization, Validation, Writing - Review & Editing. Matthew J. Budoff: Conceptualization, Writing - Review & Editing, Funding acquisition. Ambarish Pandey: Conceptualization, Writing - Review & Editing. Joao A. C. Lima: Conceptualization, Writing - Review & Editing. Erin D. Michos: Conceptualization,

Disclosures

Dr. Budoff receives grant support from General Electric. The other authors have no disclosures to make. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Acknowledgments

The authors thank the other investigators, the staff, and the MESA participants for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org.

References (23)

Cited by (0)

Financial support: This research was supported by R01 HL071739 and MESA study was supported by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute (NHLBI), and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from NCATS. Drs. Michos and Zhao are additionally funded by the Blumenthal Scholars Award in Preventive Cardiology at Johns Hopkins University.

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