Table 3.
Propensity score matched models estimating the association between statin use vs. non-use and 10-year change in CMR parameters of left ventricular structure/function
| Estimate | 95% CI* | p-value* |
|---|---|---|
| Δ LVMI (percent predicted by height, weight, and gender) | ||
| −2.35 | (−4.24, −0.47) | 0.01 |
| Δ LVM unindexed (grams) | ||
| −2.03 | (−4.67, 0.61) | 0.13 |
| Δ LVM-BSA indexed (grams/BSA) | ||
| −1.58 | (−2.96, −0.19) | 0.03 |
| Δ MVR (no units) | ||
| −0.03 | (−0.07, −0.00) | 0.02 |
| Δ EDV (mL) | ||
| −1.35 | (−4.32, 1.63) | 0.38 |
| Δ LVEF (percent) | ||
| 0.57 | (−0.45, 1.60) | 0.27 |
The PSM models used nearest-neighbor matching within 0.025 caliper with replacement to estimate the average treatment effect in the treated. Propensity scores for statin initiation were derived from a logistic regression using the following at baseline: age, gender, race, smoking status (former, never, current), BMI, diabetes status (normal, impaired fasting glucose, untreated diabetes, treated diabetes), waist circumference, antihypertensive agent use (yes/no for diuretics, calcium channel blockers, beta-blockers, ace-inhibitors, and angiotensin type 2 antagonists), systolic and diastolic blood pressure, HDL cholesterol, triglycerides, total cholesterol, intentional exercise defined as moderate and vigorous physical activity total (met-min per week), health insurance status (yes/no), and the Agatston CAC Score as the ln(score + 1).
Normal-based confidence intervals were bootstrapped with 1000 repetitions.