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Review

Real-world Analyses of Patients With Elevated Atherosclerotic Cardiovascular Disease Risk From the Optum Research Database

Peter P Toth1 CGH Medical Center SterlingIL61081USA;2 Cicarrone Center for the Prevention of Cardiovascular Disease Johns Hopkins University School of MedicineBaltimoreMD21205USACorrespondence[email protected]

https://orcid.org/0000-0001-5810-5460

,

Michael Hull3 Optum Eden PrairieMN55344USA

,

Craig Granowitz4 Amarin Pharma Inc. BridgewaterNJ08807USA

&

Sephy Philip4 Amarin Pharma Inc. BridgewaterNJ08807USA

https://orcid.org/0000-0002-5329-8125

Figures & data

Figure 1. Elevated triglyceride-rich lipoproteins and atherosclerotic plaque initiation, plaque progression and plaque rupture causing myocardial infarction or ischemic stroke.

These images depict a nonfasting or postprandial state with lipoprotein in plasma of both intestinal (chylomicrons and chylomicron remnants) and hepatic origin (VLDL, VLDL remnants = intermediate-density lipoproteins) and LDL. LDLs and remnants cross the endothelial layer of intima in a process dependent on blood pressure, lipoprotein size and lipoprotein concentration, possibly involving transcytosis.

Modified with permission from [Citation10].

Figure 1. Elevated triglyceride-rich lipoproteins and atherosclerotic plaque initiation, plaque progression and plaque rupture causing myocardial infarction or ischemic stroke.These images depict a nonfasting or postprandial state with lipoprotein in plasma of both intestinal (chylomicrons and chylomicron remnants) and hepatic origin (VLDL, VLDL remnants = intermediate-density lipoproteins) and LDL. LDLs and remnants cross the endothelial layer of intima in a process dependent on blood pressure, lipoprotein size and lipoprotein concentration, possibly involving transcytosis.Modified with permission from [Citation10].

Table 1. Patient demographics, characteristics and baseline comorbidities.

Download CSV Display Table

Figure 2. Identification of cohorts used for analyses.

(A) Elevated TG cohort and comparator. (B) High-TG cohort and comparator.

^†Population used for patient characteristics and other analyses.

^‡Population used for multivariate analyses.

HDL-C: High-density lipoprotein cholesterol; TG: Triglycerides.

Reproduced with permission from [Citation21].

Figure 2. Identification of cohorts used for analyses. (A) Elevated TG cohort and comparator. (B) High-TG cohort and comparator. †Population used for patient characteristics and other analyses. ‡Population used for multivariate analyses.HDL-C: High-density lipoprotein cholesterol; TG: Triglycerides.Reproduced with permission from [Citation21].

Figure 3. Multivariate analysis of effect of elevated (≥150 mg/dl) and high (200–499 mg/dl) triglyceride levels on the composite end point and individual major cardiovascular events compared with prematched population with triglyceride levels <150 mg/dl.

Covariates included TG cohort, age, sex, insurance coverage type, geographic region of enrollment, baseline clinical characteristics and baseline medication use. The composite end point included nonfatal MI, nonfatal stroke, coronary revascularization, unstable angina and CV-related death during the follow-up period.

CV: Cardiovascular; MI: Myocardial infarction; TG: Triglyceride.

Figure 3. Multivariate analysis of effect of elevated (≥150 mg/dl) and high (200–499 mg/dl) triglyceride levels on the composite end point and individual major cardiovascular events compared with prematched population with triglyceride levels <150 mg/dl.Covariates included TG cohort, age, sex, insurance coverage type, geographic region of enrollment, baseline clinical characteristics and baseline medication use. The composite end point included nonfatal MI, nonfatal stroke, coronary revascularization, unstable angina and CV-related death during the follow-up period.CV: Cardiovascular; MI: Myocardial infarction; TG: Triglyceride.

Figure 4. Multivariate analysis of effect of elevated (≥150 mg/dl) and high (200–499 mg/dl) triglyceride levels on total direct healthcare costs and probability of initial inpatient hospital stay.

Covariates included TG cohort, age, sex, insurance coverage type, geographic region of enrollment, baseline clinical characteristics and baseline medication use. The composite end point included nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, unstable angina and cardiovascular-related death during the follow-up period. The cost ratio is the relative healthcare cost in one group versus another.

ASCVD: Atherosclerotic cardiovascular disease; TG: Triglyceride.

Figure 4. Multivariate analysis of effect of elevated (≥150 mg/dl) and high (200–499 mg/dl) triglyceride levels on total direct healthcare costs and probability of initial inpatient hospital stay.Covariates included TG cohort, age, sex, insurance coverage type, geographic region of enrollment, baseline clinical characteristics and baseline medication use. The composite end point included nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, unstable angina and cardiovascular-related death during the follow-up period. The cost ratio is the relative healthcare cost in one group versus another.ASCVD: Atherosclerotic cardiovascular disease; TG: Triglyceride.

Figure 5. REDUCE-IT results.

(A) Cumulative incidence of cardiovascular events in REDUCE-IT. Kaplan–Meier event curves for the primary efficacy composite end point of CV death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina in the icosapent ethyl group and the placebo group, in a time-to-event analysis of the REDUCE-IT study. (B) Distribution of first and subsequent primary composite events in the reduced dataset for patients randomized 1:1 to icosapent ethyl versus placebo in REDUCE-IT. HRs and 95% CIs for between-treatment group comparisons were generated using Li-Lagakos-modified Wei-Lin-Weissfeld method for the first, second and third event categories. RR and 95% CI for between-group comparisons used a negative binomial model for additional events beyond first, second and third occurrences (i.e., fourth event or more) and overall treatment comparison. Analyses are based on a reduced dataset accounting for statistical handling of multiple end points occurring in a single calendar day by counting as a single event.

CV: Cardiovascular; HR: Hazard ratio; MI: Myocardial infarction; RR: Rate ratio.

(A) Reprinted with permission from [Citation16] © Massachusetts Medical Society (2019).

(B) Reproduced with permission from [Citation37].

Figure 5. REDUCE-IT results. (A) Cumulative incidence of cardiovascular events in REDUCE-IT. Kaplan–Meier event curves for the primary efficacy composite end point of CV death, nonfatal MI, nonfatal stroke, coronary revascularization, or unstable angina in the icosapent ethyl group and the placebo group, in a time-to-event analysis of the REDUCE-IT study. (B) Distribution of first and subsequent primary composite events in the reduced dataset for patients randomized 1:1 to icosapent ethyl versus placebo in REDUCE-IT. HRs and 95% CIs for between-treatment group comparisons were generated using Li-Lagakos-modified Wei-Lin-Weissfeld method for the first, second and third event categories. RR and 95% CI for between-group comparisons used a negative binomial model for additional events beyond first, second and third occurrences (i.e., fourth event or more) and overall treatment comparison. Analyses are based on a reduced dataset accounting for statistical handling of multiple end points occurring in a single calendar day by counting as a single event.CV: Cardiovascular; HR: Hazard ratio; MI: Myocardial infarction; RR: Rate ratio. (A) Reprinted with permission from [Citation16] © Massachusetts Medical Society (2019). (B) Reproduced with permission from [Citation37].