This document describes the components of the initial (new patient) assessment at The Sandusky Dyslipidemia Model clinic. The initial visit is 40 minutes and follows the structure outlined in 01 — Clinic Overview, Section 4.1.
2.0 History Components
2.1 Lipid History
Age at first known dyslipidemia diagnosis
Prior lipid panels (request trends if available)
Prior lipid-lowering therapies: agents, doses, duration, response, and reason for discontinuation
History of statin intolerance: specific statin(s), symptoms, timing, CK levels if checked
History of myalgia from other causes
2.2 Cardiovascular History
Known ASCVD: myocardial infarction, stroke/TIA, peripheral arterial disease, coronary revascularization (PCI or CABG), carotid endarterectomy
Date and type of most recent cardiovascular event (if any)
First-degree relatives with premature ASCVD (males < 55 years, females < 65 years)
Family history of severe hypercholesterolemia or known FH
Family history of elevated Lp(a) (if known)
Family history of sudden cardiac death
2.4 Comorbidities Relevant to CV Risk
The following conditions are not managed by this clinic but are documented as they modify cardiovascular risk assessment and may affect medication eligibility:
Comorbidity
Relevance
Diabetes mellitus (type 1 or 2)
Major ASCVD risk factor; affects PREVENT calculation; may alter LDL-C targets [1]
Chronic kidney disease
ASCVD risk enhancer; affects PREVENT calculation (eGFR input); may alter drug dosing
Note: The specific laboratory panel is at the provider’s discretion. The following represents guidance, not a prescriptive protocol. The provider selects tests based on clinical context, available prior results, and the reason for referral.
3.1 Standard Lipid Assessment
Test
Clinical Utility
Total cholesterol
Baseline lipid characterization
LDL-C (direct or calculated)
Primary treatment target per 2026 ACC/AHA guidelines [1]
HDL-C
Risk assessment; component of non-HDL-C calculation
Renal function; PREVENT calculator input; drug dosing
3.4 Fasting vs. Non-Fasting
Per the 2026 ACC/AHA guidelines [1], non-fasting lipid panels are acceptable for screening and most clinical decisions. Fasting specimens (9–12 hours) are preferred when:
Triglycerides are ≥ 400 mg/dL on a non-fasting sample
Accurate LDL-C calculation is needed (Friedewald or Martin-Hopkins equation)
Baseline assessment where triglyceride level will influence treatment decisions
4.0 Physical Examination
4.1 Focused Cardiovascular Examination
Component
What to Assess
Blood pressure
Both arms at initial visit; hypertension documentation
Heart auscultation
Murmurs, S3/S4, rhythm
Carotid auscultation
Bruits suggesting carotid stenosis
Peripheral pulses
Diminished pulses suggesting PAD
Extremities
Edema, xanthomas (tendon xanthomas at Achilles, extensor tendons of hands)
4.2 Signs Suggestive of FH
Finding
Significance
Tendon xanthomas (Achilles, hand extensors, patellar)
Highly specific for FH [8]
Xanthelasma (periorbital yellow plaques)
Suggestive but not specific
Corneal arcus (in patients < 45 years)
Suggestive of FH [8]
Tuberous xanthomas
Severe hypercholesterolemia
5.0 Risk Factor Documentation
At the conclusion of the initial assessment, the provider documents the following for risk stratification (see 04 — Risk Stratification):
5.1 PREVENT Calculator Inputs
Input
Source
Age
Patient history
Sex
Patient history
Race/ethnicity
Patient self-report (optional for PREVENT; used in select model coefficients)
Systolic blood pressure
Clinic measurement
Total cholesterol
Laboratory
HDL-C
Laboratory
LDL-C
Laboratory
Current smoking status
Patient history
Diabetes status
History or HbA1c
eGFR
Laboratory
BMI
Clinic measurement
Antihypertensive medication use
Medication review
Statin use
Medication review
HbA1c (optional)
Laboratory
UACR (optional)
Laboratory
5.2 Risk Enhancers Checklist
Document presence or absence of each risk enhancer per the 2026 ACC/AHA guidelines [1]:
Family history of premature ASCVD (male first-degree relative < 55 years; female < 65 years)
2026 ACC/AHA/Multisociety Guideline on the Management of Dyslipidemia. J Am Coll Cardiol. 2026.
Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease (CANTOS). N Engl J Med. 2017;377(12):1119–1131.
Sniderman AD, Thanassoulis G, Glavinovic T, et al. Apolipoprotein B particles and cardiovascular disease: a narrative review. JAMA Cardiol. 2019;4(12):1287–1295.
Mora S, Buring JE, Ridker PM. Discordance of low-density lipoprotein (LDL) cholesterol with alternative LDL-related measures and future coronary events. Circulation. 2014;129(5):553–561.
Otvos JD, Mora S, Shalaurova I, et al. Clinical implications of discordance between low-density lipoprotein cholesterol and particle number. J Clin Lipidol. 2011;5(2):105–113.
Kronenberg F, Mora S, Stroes ESG, et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43(39):3925–3946.
Tsimikas S, Fazio S, Ferdinand KC, et al. NHLBI Working Group recommendations to reduce lipoprotein(a)-mediated risk of cardiovascular disease and aortic stenosis. J Am Coll Cardiol. 2018;71(2):177–192.
Defesche JC, Gidding SS, Harada-Shiba M, et al. Familial hypercholesterolaemia. Nat Rev Dis Primers. 2017;3:17093.