Hypercholesterolemia

The GBD 2019 estimation of attributable burden followed the general framework established for comparative risk assessment (CRA)14 (link), 15 (link) used in GBD since 2002. Here, we provide a general overview and details on major innovations since GBD 2017. More detailed methods are available in appendix 1. CRA can be divided into six key steps: inclusion of risk–outcome pairs in the analysis; estimation of relative risk as a function of exposure; estimation of exposure levels and distributions; determination of the counterfactual level of exposure, the level of exposure with minimum risk called the theoretical minimum risk exposure level (TMREL); computation of population attributable fractions and attributable burden; and estimation of mediation of different risk factors through other risk factors such as high body-mass index (BMI) and ischaemic heart disease, mediated through elevated systolic blood pressure (SBP), elevated fasting plasma glucose (FPG), and elevated LDL cholesterol, to compute the burden attributable to various combinations of risk factors.¹⁰ (link)

The VIAMI-trial was conducted to investigate the differences in clinical outcome between an invasive and a conservative strategy in patients with demonstrated viability in the infarct-area. The expected event rate in the viability positive group was estimated to be 35 percent. To demonstrate with a power of 80% (α = 0.05, two-sided) that PCI leads to a 50% reduction in event rate in the invasive group compared to the conservative group, 200 patients would be needed in each group.
As a formal stopping rule for the study the following was used: if one of the treatment strategies appeared significantly superior at interim analysis (p ≤ 0.01), the study would be stopped. Interim analysis was performed each time another 100 patients were included.
Baseline descriptive data are presented as a mean ± standard deviations (SD). Differences in clinical and echocardiographic variables are assessed by unpaired Student's t-test. Differences between proportions are assessed by chi-square analysis; a Fisher's exact test is used when appropriate. Event-free survival curves are computed with the Kaplan-Meier method, and the differences between these curves are tested with a log-rank test. The Cox proportional hazards regression analysis was used to estimate the treatment effect as hazard ratio (HR) with 95% confidence intervals. Besides the "crude" effects, adjustments were made for DM, hypertension, hypercholesterolemia, current smoking, family history of CAD (model a), clinical history (angina, myocardial infarction, PCI or CABG) and medication use at baseline (aspirin, beta-blocker, Ca-inhibitor, statins, ACE-I and AT II antagonist) (model b) and for all covariates (model c).
All analyses were performed on an intention-to-treat basis. Outcome per-protocol was also evaluated, since this would reflect the true influence of PCI on clinical outcome. Because after randomization there was a median waiting-time of two days before a revascularization procedure was performed inevitably some events occurred. In the per-protocol analysis these events are excluded from analysis, because they occurred before the by protocol demanded intervention. To make a fair comparison between the two groups in the per-protocol analysis we also excluded the events in the conservative group occurring during the first two days after randomization. All analyses were performed with the use of SPSS software, version 16.0 (SPSS, Inc., Chigago, Illinois).

The IHS teleophthalmology program records patient demographics (age, sex [self-reported]) and known DR risk factors in templates used by the imagers and graders, taking data from the IHS electronic medical record patient summary. Risk factors recorded include glycosylated hemoglobin A_1c (HbA_1c) level, diabetes therapy, duration of diabetes (but not diabetes type), hypertension, cardiovascular disease, hypercholesterolemia, peripheral neuropathy, and nephropathy. The program also records the clinic where the imaging occurred and whether UWFI or NMFP was used. We created measures indicating whether UWFI (vs NMFP) was used at baseline only, follow-up only, both examinations, or never. IHS administrative areas (derived from clinic addresses) are shown to describe the geographical distribution of the cohort.

Blood samples were collected in the morning after an overnight fast before participants received any medical treatment. Serum levels of free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH), antithyroglobulin (TgAb), thyroid peroxidase antibody (TPOAb), TC, TG, high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C), and glucose were assessed. Lipid markers (TC, TG, HDL-C, LDL-C) and glucose were measured on a Cobas E610 (Roche, Basel, Switzerland). Thyroid hormones were assayed on a Roche C6000 Electrochemiluminescence Immunoassay Analyzer (Roche Diagnostics, Indianapolis, IN, USA). Measurements were conducted in the laboratory of the First Hospital, Shanxi Medical University. The nurses measured the patients’ weight, height, and blood pressure. We calculated body mass index (BMI) according to the following formula: BMI = Weight (kg)/Height (m) ².
According to previous studies in the Chinese population (38 (link), 39 (link)), metabolic disturbances and thyroid dysfunction were defined as follows: (1) overweight or obesity: BMI≥24; (2) hyperglycemia: glucose≥6.1mmol/L; (3) hypertension: SBP≥140 mmHg and/or DBP≥90mmHg; (4) hypertriglyceridemia: TG≥2.3 mmol/L; (5) low HDL: HDL-C ≤ 1.0 mmol/L; (6) hypercholesterolemia: TC≥6.2 mmol/L or LDL-C≥4.1 mmol/L; (7)abnormal TgAb: TgAb≥115 IU/L; (8) abnormal TPOAb: TPOAb ≥34 IU/L; (9) subclinical hypothyroidism (SCH): TSH >4.2 mIU/L with normal fT4 concentration (10–23 pmol/L); (10) hyperthyroidism: TSH<0.27 mIU/L and FT4 >23 pmol/L, and (11) hypothyroidism: TSH >4.2 mIU/L with low FT4 concentration (<10 pmol/L).