In Oman, hyperlipidemia is managed by family medicines. Hyperlipidemia is an elevation of one or more circulating lipid fractions — most importantly low-density lipoprotein cholesterol (LDL-C), triglycerides, and lipoprotein(a) — that drives atherosclerotic cardiovascular disease, the leading cause of death worldwide. Roughly 38% of US adults have total cholesterol above 200 mg/dL (NHANES 2017-2020), and 86 million American adults need statin consideration under current AHA/ACC guidelines.
Hyperlipidemia (ICD-10: E78.5 unspecified; E78.0 familial hypercholesterolemia; E78.1 familial hypertriglyceridemia; E78.2 mixed) is an abnormal elevation of plasma lipids and lipoproteins. Cholesterol and triglyceride circulate in apolipoprotein-containing particles: chylomicrons (intestinal fat absorption), VLDL (liver-derived triglyceride transport), IDL, LDL (the major atherogenic particle), HDL (reverse cholesterol transport), and lipoprotein(a). The clinically dominant fractions are LDL cholesterol — directly atherogenic at concentrations above 100 mg/dL — non-HDL cholesterol (total minus HDL), apolipoprotein B (ApoB, particle count), triglycerides (which signal residual cardiovascular risk and pancreatitis at very high levels), and lipoprotein(a) (genetically determined, atherogenic and thrombogenic). Primary forms include familial hypercholesterolemia (LDLR, APOB, PCSK9 mutations causing LDL-C above 190 mg/dL and premature ASCVD), familial combined hyperlipidemia, dysbetalipoproteinemia (APOE2/E2), and familial hypertriglyceridemia.
The key symptoms of Hyperlipidemia are: Most patients are asymptomatic until cardiovascular complications develop — the diagnosis is made on lipid panel screening rather than symptoms., Tendon xanthomas on the Achilles tendons or extensor tendons of the hands — present in 30-50% of untreated heterozygous familial hypercholesterolemia patients by age 30., Xanthelasma palpebrarum — soft yellow plaques on the medial eyelids, present in 4% of FH patients and a non-specific finding in older adults., Corneal arcus — a grey-white ring around the iris that suggests FH when present before age 45, but is non-specific in older adults., Tuboeruptive xanthomas on elbows, knees, and buttocks in dysbetalipoproteinemia or homozygous FH., Palmar crease xanthomas (orange-yellow streaks in the palmar creases) — pathognomonic for dysbetalipoproteinemia., Eruptive xanthomas — crops of small yellow-red papules on extensor surfaces during episodes of severe hypertriglyceridemia..
Diagnosis is by fasting or non-fasting lipid panel: total cholesterol, HDL-C, triglycerides, and LDL-C (calculated by Friedewald equation, Martin/Hopkins equation, or direct measurement). Non-fasting samples are accepted for screening in most patients (2018 AHA/ACC); fasting samples are preferred when triglycerides exceed 400 mg/dL or to recheck after dietary changes. Universal screening is recommended for adults age 20+ at least every 5 years; the US Preventive Services Task Force recommends statin consideration for adults 40-75 with one or more cardiovascular risk factors and a 10-year ASCVD risk ≥ 10% (2022 statement). For risk assessment, the Pooled Cohort Equations or the newer PREVENT calculator estimate 10-year ASCVD risk integrating age, sex, race, blood pressure, smoking, diabetes, and lipid levels. Risk-enhancing factors (family history of premature CAD, metabolic syndrome, chronic kidney disease, chronic inflammatory disease, persistently elevated triglycerides, persistent LDL-C ≥160 mg/dL) refine risk in intermediate-risk patients. Coronary artery calcium (CAC) scoring is the most powerful subclinical atherosclerosis test in patients with intermediate risk: CAC = 0 supports deferral of statin in many cases; CAC ≥100 or ≥75th percentile for age/sex supports statin initiation. ApoB and non-HDL-C provide superior cardiovascular risk discrimination than LDL-C alone in patients with elevated triglycerides, diabetes, or metabolic syndrome. Lp(a) should be measured at least once in adulthood in patients with family history of premature ASCVD or recurrent events despite optimal therapy; values above 50 mg/dL or 125 nmol/L are atherogenic. Familial hypercholesterolemia is diagnosed by the Dutch Lipid Clinic Network or Simon Broome criteria; cascade screening of first-degree relatives identifies new cases at low cost per case found.
Prognosis is excellent with adherent treatment and lifestyle change. Every 39 mg/dL (1 mmol/L) reduction in LDL-C reduces major vascular events by 23%, cardiovascular death by 14%, and all-cause mortality by 10% over 5 years (CTT Lancet 2010). High-intensity statins reduce 10-year ASCVD events by 25-30%, with additional benefits from ezetimibe, PCSK9 inhibitors, and bempedoic acid in high-risk patients. Untreated heterozygous familial hypercholesterolemia carries a 50% risk of fatal or non-fatal coronary event by age 50 in men and 60 in women; treated FH approaches normal life expectancy when LDL-C is reduced by 50% sustained over decades. Statin therapy is well-tolerated long-term in 90-95% of patients; myalgia accounts for most discontinuations but is genuinely statin-caused in only 1-3% on placebo-controlled re-challenge. Severe adverse events (rhabdomyolysis, hepatic failure) are rare (under 1 per 10,000 person-years). Statin-induced diabetes occurs in 1 per 250 patient-years but the cardiovascular benefit overwhelms this risk in eligible groups.
Most hyperlipidemia is managed in primary care. Refer to a lipid specialist, cardiologist, or endocrinologist for: confirmed or suspected familial hypercholesterolemia, statin intolerance, persistently elevated LDL-C despite maximal therapy, severe hypertriglyceridemia, recurrent cardiovascular events on therapy, or for advanced therapies (PCSK9 inhibitor, inclisiran, evinacumab, lipoprotein apheresis). Cardiology partnership is mandatory in established ASCVD for combined secondary prevention.
Find specialists →Statin therapy reduces LDL-C by 80-90% of maximum effect within 4 weeks; lipid panel reassessed at 4-12 weeks after starting or dose changes. Cardiovascular event-reduction benefits accumulate over 1-5 years. PCSK9 inhibitor effect is achieved within 2-4 weeks and sustained as long as therapy continues. Lifestyle effect on LDL-C is measurable within 6-12 weeks of consistent dietary change and exercise.
Aim for 150 minutes per week of moderate-intensity aerobic activity (brisk walking, cycling, swimming) or 75 minutes per week of vigorous activity, plus resistance training of major muscle groups twice weekly. Regular activity reduces LDL-C by 5%, raises HDL-C by 4-7%, lowers triglycerides by 10-15%, and improves insulin sensitivity. Patients with established cardiovascular disease should join a supervised cardiac rehabilitation program initially.
Choose a family medicine physician or internist comfortable with statin initiation, intensification, and side-effect management. For complex cases, choose a lipid clinic with FH cascade screening capacity, access to PCSK9 inhibitors and inclisiran, and coordination with cardiology. Pediatric and adolescent FH is best managed at academic centers with combined pediatric cardiology and lipid expertise. Lp(a)-driven recurrent events benefit from research-active centers with access to clinical trials.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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