Although previous investigations reported on the associations of lipid concentrations with left ventricular remodeling in specific subpopulations, few data exist on these associations in a community-based sample of subjects without cardiovascular disease. In this study, 3,554 Framingham Heart Study participants (mean age 47 years, 53% women) without preexisting clinical cardiovascular disease were examined, and no meaningful associations of high-density lipoprotein cholesterol or non–high-density lipoprotein cholesterol with echocardiographic indexes of left ventricular structure were observed. In conclusion, these data do not support an independent association between lipid concentrations and left ventricular structure.
Dyslipidemia is a key risk factor for coronary artery disease and cardiovascular death. Several lines of experimental and clinical observations also associate abnormal lipid concentrations with systolic and diastolic left ventricular (LV) function, peripheral vascular resistance, aortic stiffness, and LV remodeling after myocardial infarction. These observations raise the possibility of dyslipidemia-induced LV remodeling. Such an association, however, has not been systematically investigated in subjects without prevalent coronary artery disease. We therefore evaluated the cross-sectional associations of blood lipid concentrations to echocardiographic indexes of LV structure. We hypothesized that increasing concentrations of non–high-density lipoprotein (HDL) cholesterol are associated with increasing LV mass (LVM), LV end-diastolic dimension (LVDD), LV end-systolic dimension (LVSD), and LV wall thickness (LVWT). We also posited that HDL cholesterol concentrations have opposite associations (relative to non-HDL cholesterol) to these echocardiographic measures.
Methods
The details of the Framingham Heart Study original and offspring cohorts have been published previously. Attendees at examination cycle 16 (1979 to 1982, n = 2,351) of the original cohort and at examination cycle 2 (1979 to 1983, n = 3,863) of the offspring cohort were eligible for the present investigation. We excluded participants with the following conditions at these examinations: myocardial infarction (n = 111), heart failure (n = 69), valvular heart disease (n = 152), estimated glomerular filtration rate <60 ml/min/1.73 m 2 (n = 609), current use of antihypertensive (n = 936) or lipid-modifying (n = 34) therapy, and missing covariate or echocardiographic data (n = 749). A total of 3,558 participants (1,666 men, 1,888 women) formed the sample for this investigation. All participants provided written informed consent, and the study protocol was approved by the institutional review board of Boston University Medical Center.
Plasma samples for lipid measurement were collected in 0.1% ethylenediaminetetraacetic acid, and lipid concentrations were measured on freshly drawn plasma before freezing. Total cholesterol was measured by the Abell and Kendall method. HDL cholesterol was measured after heparin-manganese chloride precipitation. HDL cholesterol was subtracted from total cholesterol to calculate non-HDL cholesterol.
We measured LVDD, LVSD, and the end-diastolic thicknesses of the interventricular septum (IVS) and LV posterior wall (LVPW) from 2-dimensionally guided M-mode echocardiograms (which were performed at the examinations at which lipids and covariates were assessed) according to American Society of Echocardiography recommendations. LVM and LVWT were calculated as LVM (g) = 0.8{1.04[(LVDD + IVS + LVPW) − LVDD ]} + 0.6 and LVWT (cm) = IVS + LVPW, respectively.
We related non-HDL cholesterol and HDL cholesterol concentrations separately to each echocardiographic measure individually in gender-specific multivariate-adjusted general linear models that included the following covariates: age, body mass index, systolic blood pressure, diabetes, and current smoking. A 2-sided p value <0.05 denoted statistical significance.
Results
The clinical, lipid, and echocardiographic characteristics of the study sample are listed in Table 1 . In women, we observed small inverse relations of non-HDL cholesterol concentrations to LVDD and LVSD ( Table 2 ); non-HDL cholesterol was not associated with any other echocardiographic variables. In men, we observed small inverse relations of non-HDL cholesterol concentrations to LVM, LVWT, and LVDD, but not to LVSD ( Table 2 ). We observed no statistically significant associations between HDL cholesterol and any of the LV measures in men or women ( Table 2 ).
| Variable | Men (n = 1,666) | Women (n = 1,888) |
|---|---|---|
| Age (years) | 47 ± 13 | 47 ± 14 |
| Body mass index (kg/m 2 ) | 26.3 ± 3.5 | 24.5 ± 4.4 |
| Systolic blood pressure (mm Hg) | 126 ± 16 | 120 ± 18 |
| Diabetes mellitus | 4% | 2% |
| Smokers | 35% | 36% |
| HDL cholesterol (mg/dl) | 42 (36–50) | 53 (45–63) |
| Non-HDL cholesterol (mg/dl) | 159 (133–185) | 146 (121–176) |
| Echocardiographic traits | ||
| LV mass (gm) | 186 ± 42 | 128 ± 29 |
| LV wall thickness (cm) | 1.9 ± 0.3 | 1.7 ± 0.2 |
| LV end-diastolic dimension (cm) | 5.1 ± 0.4 | 4.6 ± 0.4 |
| LV end-systolic dimension (cm) | 3.3 ± 0.4 | 2.9 ± 0.3 |
| Variable | Men (n = 1,666) | Women (n = 1,888) | ||
|---|---|---|---|---|
| β (SE) | p Value | β (SE) | p Value | |
| Relations of HDL cholesterol to echocardiographic traits | ||||
| Left ventricular mass (g) | 1.25 (1.00) | 0.21 | −0.22 (0.60) | 0.72 |
| Left ventricular wall thickness (cm) | 0.001 (0.01) | 0.81 | −0.01 (0.01) | 0.052 |
| Left ventricular end-diastolic dimension (cm) | 0.01 (0.01) | 0.16 | 0.01 (0.01) | 0.11 |
| Left ventricular end-systolic dimension (cm) | 0.01 (0.01) | 0.38 | 0.01 (0.01) | 0.33 |
| Relations of non-HDL cholesterol to echocardiographic traits | ||||
| Left ventricular mass (g) | −3.76 (1.01) | 0.0002 | −0.03 (0.02) | 0.08 |
| Left ventricular wall thickness (cm) | −0.01 (0.01) | 0.02 | 0.00 (0.00) | 0.83 |
| Left ventricular end-diastolic dimension (cm) | −0.03 (0.01) | 0.005 | −0.0006 (0.0002) | 0.003 |
| Left ventricular end-systolic dimension (cm) | −0.02 (0.01) | 0.08 | −0.0004 (0.0002) | 0.02 |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
