Objectives Speckle-tracking echocardiography enables detection of abnormalities in cardiac mechanics with higher sensitivity than conventional measures of left ventricular (LV) dysfunction and may provide insight into the pathogenesis of coronary heart disease (CHD). We investigated the relationship of LV longitudinal strain, LV early diastolic strain rate (SR) and left atrial (LA) reservoir strain with long-term CHD incidence in community-dwelling older adults.
Methods The association of all three strain measures with incidence of non-fatal and fatal CHD (primary outcome of revascularisation, non-fatal and fatal myocardial infarction) was examined in the population-based Cardiovascular Health Study using multivariable Cox proportional hazards models. Follow-up was truncated at 10 years.
Results We included 3313 participants (mean (SD) age 72.6 (5.5) years). During a median follow-up of 10.0 (25th–75th percentile 7.7–10.0) years, 439 CHD events occurred. LV longitudinal strain (HR=1.25 per SD decrement, 95% CI 1.09 to 1.43) and LV early diastolic SR (HR=1.31 per SD decrement, 95% CI 1.14 to 1.50) were associated with a significantly greater risk of incident CHD after adjustment for potential confounders. By contrast, LA reservoir strain was not associated with incident CHD (HR=1.06 per SD decrement, 95% CI 0.94 to 1.19). Additional adjustment for biochemical and echocardiographic measures of myocardial stress, dysfunction and remodelling did not meaningfully alter these associations.
Conclusion We found an association between echocardiographic measures of subclinically altered LV mechanics and incident CHD. These findings inform the underlying biology of subclinical LV dysfunction and CHD. Early detection of asymptomatic myocardial dysfunction may offer an opportunity for prevention and early intervention.
- coronary artery disease
Data availability statement
Cardiovascular Health Study data are available upon request (https://biolincc.nhlbi.nih.gov/studies/chs/).
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Twitter @danmassera, @HFpEF
Contributors Conception, design, analysis and interpretation of data: DM, MH, JAD, TB, BMP, JSG, JRK and SJS. All authors participated in drafting of the manuscript or revising it critically for important intellectual content. Final approval of the manuscript submitted was granted by all authors.
Funding This study was funded by R01 HL107577 from the National Heart, Lung, and Blood Institute (NHLBI) to SJS. This research was also supported by contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086 and 75N92021D00006, and grants U01HL080295 and U01HL130114, from NHLBI, with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided by R01AG023629 from the National Institute on Aging (NIA). A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org. JRK was supported by K24HL135413 from NHLBI.
Competing interests DM has received consulting fees from Bristol Myers Squibb. JRK reports stock ownership in Bristol Myers Squibb, Johnson & Johnson, Medtronic, Merck and Pfizer. SJS has received research grants from Actelion, AstraZeneca, Corvia, Novartis and Pfizer; and has received consulting fees from Abbott, Actelion, AstraZeneca, Amgen, Axon Therapies, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cardiora, CVRx, Cytokinetics, Eidos, Eisai, GSK, Ionis, Ironwood, Lilly, Merck, MyoKardia, Novartis, Novo Nordisk, Pfizer, Prothena, Sanofi, Shifamed, Tenax and United Therapeutics. All other authors declare that they have no conflicts of interest.
Provenance and peer review Not commissioned; externally peer reviewed.
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