The distinct relationships of carotid plaque disease and carotid intima-media thickness with left ventricular function.
BACKGROUND
Subclinical carotid atherosclerosis has been associated with impaired left ventricular (LV) function and the development of heart failure. Whether impaired LV function is related primarily to increased intima-media thickness (IMT) or burden of plaque disease or both remains to be determined.


METHODS
A total of 2,279 subjects without clinical cardiovascular disease recruited from the London Life Sciences Prospective Population cohort study were studied. Carotid ultrasonography and transthoracic echocardiography were performed on all subjects. Carotid IMT and plaque scores were measured, and their relationships with LV volumes, LV ejection fraction, myocardial LV longitudinal function (Sa and Ea velocities), and LV filling pressure (E/Ea ratio) were assessed before and after adjustment for covariates.


RESULTS
Compared with those without carotid artery disease, subjects with either increased IMT and/or presence of plaque disease had identical Sa velocities (both 9.0 cm/sec), lower Ea velocities (8.7 vs 9.9 cm/sec, P < .001) and higher E/Ea ratios (8.4 vs 7.6, P < .001). After multiple linear regression analysis, increasing IMT remained independently related to reduced Ea velocity (P < .001) but not LV ejection fraction, Sa velocity, or E/Ea ratio. In a separate adjusted analysis, subjects with severe burdens of carotid plaque disease (more than five plaques) had reduced LV ejection fractions (β = -2.9; 95% confidence interval [CI], 1.0 to 4.8, P = .003), attenuated Sa velocities (β = -0.79; 95% CI, -1.2 to -0.3, P = .003), attenuated Ea velocities 2 (β = -0.79; 95% CI, -1.3 to -0.2, P = .007), and increased E/Ea ratios (β = 0.84; 95% CI, 0.2 to 1.5, P = .009) compared to individuals without carotid plaques.


CONCLUSIONS
These findings demonstrate that subclinical carotid plaque disease rather than IMT is more closely related to LV systolic function and LV filling pressure. These data support the application of carotid ultrasonography beyond cardiovascular disease risk prediction, while providing insight into potential mechanisms underlying the development of subclinical LV dysfunction.
Chahal
Navtej S
NS
Department of Cardiovascular Medicine, Northwick Park Hospital, Harrow, UK.
Lim
Tiong K
TK
Jain
Piyush
P
Chambers
John C
JC
Kooner
Jaspal S
JS
Senior
Roxy
R
D000328:Adult; D000368:Aged; D002306:Cardiac Volume / Q000502:physiology; D002339:Carotid Arteries / Q000000981:diagnostic imaging* / Q000503:physiopathology; D016893:Carotid Stenosis / Q000000981:diagnostic imaging* / Q000503:physiopathology; D003971:Diastole / Q000502:physiology; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008297:Male; D008403:Mass Screening; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology; D011446:Prospective Studies; D012307:Risk Factors; D012984:Software; D013223:Statistics as Topic; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology; D017539:Tunica Intima / Q000000981:diagnostic imaging* / Q000503:physiopathology; D017540:Tunica Media / Q000000981:diagnostic imaging* / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000503:physiopathology