Φ
Read This First
Philosophy & Framing
"Lower is better. Lowest is best."
— Dr. Rasch, DO · Practice Guiding Principle
This practice takes an aggressive, proactive stance on LDL management. The tolerance for an LDL above 100 mg/dL is essentially zero — it is an actionable finding that requires a treatment response today, not a "watch and wait" situation.
We draw on both ACC/AHA and ESC/EAS frameworks. ESC/EAS provides our treat-to-target numbers (which align better with how Dr. Rasch practices). ACC/AHA provides the shared decision-making tools useful for patient conversations. When they diverge — default to the more aggressive target.
Plaque Behavior by LDL Level — The Science Behind "Lowest is Best"
| LDL Level | What Happens to Arterial Plaque | Key Evidence |
|---|---|---|
| > 80 mg/dL | Plaque continues to progress | — |
| 70–80 mg/dL | Plaque progression halts | IVUS meta-analysis · 31 studies · ~5,000 patients |
| < 70 mg/dL | Plaque regression becomes possible | Multiple IVUS analyses |
| < 60 mg/dL | Plaque regression becomes likely | ASTEROID trial: 2/3 of patients regressed at mean LDL 60.8 mg/dL |
| ~37 mg/dL | Significant regression demonstrated | GLAGOV trial — PCSK9 inhibitor + statin |
| ~20–40 mg/dL | Maximum regression zone — no floor effect found | GLAGOV post-hoc: continuous linear relationship to ~20 mg/dL |
Use This Data in Patient Conversations
When a patient understands that their plaque can actually shrink — and that the lower the LDL, the more it shrinks — the conversation changes completely. Frame it: "We're not just trying to stop things from getting worse. At these LDL levels, we can actually start to reverse the damage."
⚠ On HDL — No Longer a Therapeutic Target
The concept that a high HDL "cancels out" a bad LDL has been largely disproven. Raising HDL pharmacologically has not demonstrated cardiovascular benefit in trials. Never reassure a patient with elevated LDL on the basis of a high HDL. Document HDL for risk stratification only — it does not offset LDL-driven risk.
Our Patient Population — Encinitas
This practice sees a high volume of statin-hesitant and statin-refusing patients, driven by local culture and social media. Do not debate it or dismiss it. The strategies in Step 4b are designed to meet this population where they are and still achieve meaningful LDL reduction.
Def
Before You Begin
Risk Categories & LDL Targets
Establish risk category before touching the lipid panel. This determines the LDL target — everything else follows from it.
Risk Classification & LDL Targets (Dr. Rasch's Practice)
| Risk Category | Who Qualifies | LDL Target |
|---|---|---|
| Very High Risk | Established ASCVD (prior MI, ACS, stroke, revascularization, symptomatic PAD) — or any incidental ASCVD finding (carotid plaque, coronary/aortic calcifications on CT or CXR, subclinical PAD) | < 55 mg/dL preferredMinimum <70 mg/dL |
| High Risk | Diabetes + age ≥40 · CKD stages 3–4 · 10-year ASCVD risk ≥20% · FH · Severely elevated single risk factor | < 70 mg/dL |
| Intermediate Risk | 10-year ASCVD risk 7.5–19.9% | < 70 mg/dLGuidelines say <100; we treat to lower — aim for plaque regression territory |
| Low Risk | 10-year ASCVD risk <7.5%; no diabetes, CKD, or ASCVD | < 100 mg/dLLifestyle first; treat if not achieved |
| Elevated Lp(a) | Any patient with Lp(a) ≥50 mg/dL or ≥125 nmol/L, at any baseline risk level | As low as absolutely possibleNo ceiling — see Lp(a) section |
Incidental ASCVD Is Still ASCVD
Carotid plaque on ultrasound, calcifications found on a CT chest or abdominal scan, a low ABI — any of these reclassify the patient as very high risk and lower the LDL target to minimum <70 mg/dL, with <55 mg/dL preferred. Flag these findings immediately and act on them.
Practice Standard — No Untreated LDL > 100 mg/dL
No patient in this practice should have an untreated LDL above 100 mg/dL. If you see it, a treatment response is required at that visit. Document it, address it, follow up on it.
1
Step 1
Obtain a Fasting Lipid Panel
Order All of the Following
| Lab | Notes & Clinical Importance |
|---|---|
| Total Cholesterol | — |
| LDL-C | Direct LDL preferred if TG >400 mg/dL — calculated LDL is unreliable above this threshold |
| HDL-C | For risk stratification only — not a therapeutic target. High HDL does not offset elevated LDL. Do not reassure on this basis. |
| Triglycerides | Fasting preferred; TG >500 = pancreatitis risk — address separately before starting a statin |
| Non-HDL Cholesterol | Total cholesterol minus HDL; secondary target; more reliable than LDL when TG is elevated |
| ApoB | Order in metabolic syndrome, insulin resistance, or discordant LDL/non-HDL — better reflects atherogenic particle burden |
| hsCRP | Useful in intermediate-risk patients — hsCRP ≥2.0 mg/L upgrades risk and supports statin initiation |
| Lp(a) — screen once | Order at least once in every patient. Elevated Lp(a) fundamentally changes the treatment approach. See dedicated section. |
| TSH | Always order — hypothyroidism causes secondary hyperlipidemia and increases myopathy risk on statins |
Follow-Up Timing
Recheck fasting lipid panel 6 weeks after any medication initiation or dose change.
Lp(a)
Special Topic — Screen Every Patient
Lp(a) — "LDL's Evil Twin Cousin"
Lipoprotein(a) — LDL's Evil Twin Cousin
Genetically determined · Largely unresponsive to lifestyle · Independently atherogenic
5–6×
More Atherogenic Than LDL Per Particle
Equimolar comparison · Range 3.8–6.6× depending on study population and methodology
Standard LDL
- Dietary and lifestyle modifiable
- Responds to statins, ezetimibe, PCSK9i
- Primary target of conventional therapy
- Atherogenicity well-characterized
Lp(a) — The Evil Twin
- ~90% genetically determined
- Not meaningfully reduced by diet or statins
- 5–6× more atherogenic per particle than LDL
- Also prothrombotic and pro-inflammatory
- No FDA-approved specific therapy yet
How to Frame Lp(a) with Patients
Patient Script
"Think of Lp(a) as LDL's evil twin cousin. They're related, but Lp(a) is significantly more dangerous — roughly 5 to 6 times more damaging to your arteries per particle. And unlike regular LDL, it's almost entirely determined by your genetics. You didn't eat your way into this. Your body was wired to make it. The way we manage it is by being especially aggressive about lowering everything else we can control — particularly your LDL — as far down as we possibly can."
Lp(a) Protocol — What to Do in This Practice
| Action | Details |
|---|---|
| Screen every patient once | Not optional. Threshold: Lp(a) ≥50 mg/dL or ≥125 nmol/L = elevated |
| If elevated — LDL target changes | Goal becomes "as low as absolutely possible" — no ceiling, no floor. Reassign to maximum therapy pathway regardless of baseline risk category. |
| Screen first-degree relatives | Lp(a) is ~90% heritable. An elevated result is a family finding. Counsel: "Your parents, siblings, and children should all be tested." |
| Low threshold for PCSK9i | PCSK9 inhibitors anecdotally lower Lp(a) by ~20–30% as a secondary effect. Document Lp(a) elevation as part of the PCSK9i indication in the chart note. You do not need to wait for Dr. Rasch. |
| Monitor emerging therapies | Novel RNA-based agents (pelacarsen, olpasiran) in late-stage trials. Not yet available outside research. Watch this space. |
Counseling Script for Elevated Lp(a)
"Your Lp(a) is elevated. This is almost entirely genetic — you didn't cause this with your diet or lifestyle, and diet or exercise alone won't fix it. What it means is that your arteries are under more stress than your regular cholesterol numbers suggest. We manage it by being especially aggressive about lowering everything else we can control. We also need to test your close family members — this gets passed down."
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Step 2
Calculate 10-Year ASCVD Risk
Use the ACC/AHA Pooled Cohort Equation (MDCalc or ACC app) for patients without established ASCVD, ages 40–75.
Risk Score → Action
| 10-Year Score | Risk Category | Action |
|---|---|---|
| < 5% | Low | Lifestyle counseling; treat if LDL >100 or risk-enhancers present |
| 5–7.4% | Borderline | Assess risk-enhancing factors; lean toward treating if LDL >100 |
| 7.5–19.9% | Intermediate | Statin indicated; consider CAC score if decision uncertain |
| ≥ 20% | High | High-intensity statin; aggressive targets; do not delay |
Risk-Enhancing Factors — Use to Upgrade Borderline Patients
Family history of premature ASCVD (male <55, female <65) · LDL persistently ≥160 · Metabolic syndrome · CKD · Inflammatory conditions (RA, psoriasis, HIV) · Preeclampsia history · Premature menopause · hsCRP ≥2.0 mg/L · Lp(a) ≥50 mg/dL · ABI <0.9
Coronary Artery Calcium (CAC) Scoring — Critical Nuance
| CAC Score | What It Means | Action in This Practice |
|---|---|---|
| 0 | No calcified plaque. Soft/non-calcified plaque may still be present — calcification is a late-stage finding. Does not mean "clean arteries." | Reasonable to defer statin in low-risk patients; do not promise clean arteries; repeat in 3–5 years; continue lifestyle |
| 1–99 | Early calcified plaque present. Actual ASCVD disease burden is likely greater. | Initiate treatment. LDL target <70 mg/dL. |
| ≥ 100 | Significant calcified plaque burden. | Treat as high/very high risk. LDL <70 mg/dL; <55 preferred. |
| Any > 0 | Calcified ASCVD is present — this is not early or borderline disease. | LDL target <70 mg/dL minimum in Dr. Rasch's practice. |
CAC as a Patient Motivator
Even a modest CAC score (10, 25, 50) is a powerful motivator for hesitant patients. "This is real plaque in your arteries that showed up on a scan. The good news is we caught it. The plan now is to get your LDL low enough that we can actually start to reverse it."
3
Step 3 — Always First, Always Ongoing
Lifestyle Counseling
Lifestyle Interventions & Expected LDL Impact
| Intervention | Recommendation | Expected LDL Reduction |
|---|---|---|
| Saturated fat reduction | <6% of total calories; eliminate trans fats | 5–10% |
| Soluble fiber | 10–25 g/day (oats, beans, psyllium husk) | 5–10% |
| Plant stanols/sterols | 2 g/day (fortified foods or supplements) | 5–15% |
| Weight reduction | Per 10 lbs lost, LDL drops ~5–8 mg/dL | Variable |
| Aerobic exercise | 150 min/week moderate-intensity | 3–6% |
| Smoking cessation | Raises HDL, reduces ASCVD risk independently | Indirect benefit |
| Alcohol reduction | Primarily impacts triglycerides | Primarily TG ↓ |
Timing Rule
Low/borderline risk: Minimum 3-month lifestyle trial before initiating medication.High/very high risk: Start medication now alongside lifestyle — never delay pharmacotherapy in high-risk patients waiting for lifestyle results.
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Step 4
Statin Selection
⚠ Practice Rule — Rosuvastatin Maximum Dose is 20 mg
Do not initiate or escalate rosuvastatin to 40 mg in this practice. If a patient transfers in on rosuvastatin 40 mg and is tolerating it well — continue it. But we do not start or up-titrate to that dose ourselves.
Rosuvastatin (Crestor) — Preferred Statin in This Practice
| Intensity | Dose | LDL Reduction | Notes |
|---|---|---|---|
| High-intensity | 20 mg QD | ~50–55% | Maximum dose in this practice. Hydrophilic — lower myopathy risk, no CYP3A4 interactions. |
| Moderate-intensity | 5–10 mg QD | 30–40% | Intermediate-risk; or if high-intensity not tolerated |
Atorvastatin (Lipitor) — Strong Alternative
| Intensity | Dose | LDL Reduction | Notes |
|---|---|---|---|
| High-intensity | 40–80 mg QD | ~45–55% | No dose ceiling restriction in this practice |
| Moderate-intensity | 10–20 mg QD | 30–40% | — |
Statin Intensity by Risk Category
| Risk | Intensity | First Choice |
|---|---|---|
| Very High / High | High-intensity | Rosuvastatin 20 mg or Atorvastatin 40–80 mg |
| Intermediate | Moderate-intensity | Rosuvastatin 5–10 mg or Atorvastatin 10–20 mg |
| Low / Frail Elderly | Low-to-moderate | Pravastatin 40 mg or Rosuvastatin 5 mg |
Dosing Tip
Dose statins in the evening when possible — hepatic cholesterol synthesis peaks overnight, maximizing drug effect.
4b
Step 4b — Encinitas-Specific
Navigating Statin Hesitancy
Don't debate social media. Don't lecture. Redirect, offer alternatives, and find the path the patient will actually walk. Most hesitant patients are not opposed to the goal — they're opposed to the drug. Separate those two things early.
Lead with the Plaque Data First
Opening Script for Hesitant Patients
"I hear you on the statin. Let's set that aside for a second. The reason we're pushing on your LDL is that below a certain level, the plaque in your arteries doesn't just stop growing — it actually shrinks. That's what we're aiming for. Now let's talk about how to get there in a way you're comfortable with."
1
Pitavastatin (Livalo) 4 mg QD Dr. Rasch Default
Dr. Rasch almost always starts at 4 mg — the maximum approved dose — to maximize LDL reduction at the 6-week recheck and demonstrate meaningful results early.
Key patient talking points: Developed in Japan through an Eastern pharmaceutical tradition — a distinct chemical lineage from the Western statins patients have read about. Does not raise blood glucose. Minimal CYP450 interactions. Does not meaningfully deplete CoQ10. Genuinely different cellular uptake profile.
~$30/month cash price with GoodRx for a 90-day supply — no insurance friction.
Frame it: "This isn't the statin you read about. This is a different drug, developed through a completely different tradition."
Key patient talking points: Developed in Japan through an Eastern pharmaceutical tradition — a distinct chemical lineage from the Western statins patients have read about. Does not raise blood glucose. Minimal CYP450 interactions. Does not meaningfully deplete CoQ10. Genuinely different cellular uptake profile.
~$30/month cash price with GoodRx for a 90-day supply — no insurance friction.
Frame it: "This isn't the statin you read about. This is a different drug, developed through a completely different tradition."
2
Nexlizet (bempedoic acid 180 mg + ezetimibe 10 mg)
If pitavastatin is refused or not tolerated — go here immediately. The bar for initiating Nexlizet is intentionally low in this practice.
Not a statin. Does not enter muscle tissue. Does not cause myopathy. Two complementary non-statin mechanisms: hepatic ATP-citrate lyase inhibition (upstream of the statin pathway) + intestinal cholesterol absorption blockade. 28–38% LDL reduction as monotherapy.
Start as monotherapy in statin-refusing patients without hesitation. If access is denied: Nexletol (bempedoic acid alone) + separate ezetimibe 10 mg is functionally equivalent.
Not a statin. Does not enter muscle tissue. Does not cause myopathy. Two complementary non-statin mechanisms: hepatic ATP-citrate lyase inhibition (upstream of the statin pathway) + intestinal cholesterol absorption blockade. 28–38% LDL reduction as monotherapy.
Start as monotherapy in statin-refusing patients without hesitation. If access is denied: Nexletol (bempedoic acid alone) + separate ezetimibe 10 mg is functionally equivalent.
3
Ezetimibe 10 mg QD (standalone if above not accessible)
15–25% LDL reduction. Generic, inexpensive, well-tolerated. Not a statin. Useful bridge or addition in any patient. Often already included if using Nexlizet — but available separately as a low-friction option.
4
PCSK9 Inhibition — Earlier Than You Think Act Independently
For statin-refusing patients who are Medicare beneficiaries — Leqvio is a legitimate first-line or early option, particularly with the 2025 monotherapy indication. Do not wait for every step above to fail first. See Step 7.
Pitavastatin Dosing Reference
| Dose | LDL Reduction | Notes |
|---|---|---|
| 1 mg QD | ~30% | Rarely used in this practice |
| 2 mg QD | ~36% | Occasional step-up if tolerability concerns |
| 4 mg QD | ~43% | Dr. Rasch's default starting dose for hesitant patients |
5
Step 5
Monitoring & Side Effect Management
Baseline before starting any statin:
- Lipid panel (done in Step 1)
- CMP — baseline LFTs and creatinine
- CK — only if baseline muscle symptoms or high myopathy risk; not routine
- HbA1c or fasting glucose — document baseline; statins carry a small diabetes risk
- TSH — already ordered; treat hypothyroidism first if found
Statin-Associated Muscle Symptoms (SAMS) — Response Guide
| Severity | Presentation | Action |
|---|---|---|
| Mild myalgia | Aches, no CK elevation | Hold 2–4 weeks; rechallenge at lower dose or switch to pitavastatin or rosuvastatin |
| Moderate | Significant pain or weakness; CK 3–10× ULN | Hold statin; recheck CK in 2 weeks; consider CoQ10 supplementation |
| Severe / Rhabdomyolysis | CK >10× ULN; myoglobinuria; dark urine | Stop immediately · Aggressive IV hydration · Escalate to Dr. Rasch urgently |
True Statin Intolerance Is Rare
Most patients reporting muscle symptoms tolerate a different agent. Pitavastatin and rosuvastatin (both hydrophilic) are better tolerated in myalgia-prone patients. Alternate-day rosuvastatin is evidence-based. Exhaust all options before declaring true intolerance.
6
Step 6
Add-On Therapy — When LDL Goal Not Met
Confirm Before Escalating
Patient is on maximum tolerated statin (rosuvastatin 20 mg or atorvastatin 40–80 mg) · Adherence confirmed — ask directly; non-adherence is the most common cause of failure · Lifestyle in place · Secondary causes ruled out (see Step 8)
1st
Ezetimibe 10 mg QD
15–25% additional LDL reduction · Generic · Inexpensive · Well-tolerated · Should be on board before escalating further. (Already included if patient is on Nexlizet.)
2nd
Nexlizet (bempedoic acid + ezetimibe)
If ezetimibe alone is insufficient, switch to Nexlizet to add the bempedoic acid component. Also the first move in statin-intolerant patients.
3rd
PCSK9 Inhibition — Initiate Early, Independently
See Step 7. Midlevels act on this independently. Particularly low threshold in elevated Lp(a) patients. Do not wait for everything else to fail first in high-risk patients.
7
Step 7 — Act Independently
PCSK9 Inhibition
✓ Midlevels Are Empowered to Initiate PCSK9 Therapy Independently
You do not need to wait for Dr. Rasch. If a patient meets criteria — move forward. PCSK9 inhibition, especially Leqvio in Medicare patients, should be proactive and early, not a last resort. Particularly low threshold in elevated Lp(a) patients.
How Dr. Rasch Frames PCSK9 for Patients — Use This Language
PCSK9 is a naturally occurring protein — a "toxin" — that binds to and destroys the liver's LDL receptors (the body's natural LDL "garbage disposals"). When PCSK9 is overactive, receptors get disabled and LDL builds up because nothing is clearing it.
PCSK9 inhibitors are not traditional cholesterol-lowering drugs. They are a detoxifying therapy — they neutralize PCSK9 and restore the liver's own receptors, so the body naturally clears LDL. Side effects are minimal because nothing is being forced on the body. An interference is simply being removed.
Patient Script — Use Consistently
"This isn't a drug that lowers your cholesterol. It removes a toxin that was blocking your body's own natural LDL cleanup system. Once we remove that toxin, your liver can do what it was always designed to do — and it clears the LDL on its own. That's why side effects are so minimal."
This framing resonates powerfully with health-conscious, supplement-oriented, statin-hesitant patients. "Removing a toxin" fits their existing worldview far better than "lowering cholesterol." Use it consistently.
Leqvio (Inclisiran) — Preferred Agent
siRNA therapy · 2× per year · Infusion center
Mechanism
siRNA — silences the gene that produces PCSK9, rather than blocking the protein directly. Fundamentally different from evolocumab/alirocumab.
Key Patient Point
"The medication is completely out of your system within 72 hours. It doesn't sit in your body — it simply turns off the factory that makes the toxin for 6 months. Your own body then clears the LDL naturally."
Dosing
284 mg SQ — Day 1, Month 3, then every 6 months
LDL Reduction
~50% additional on top of statin therapy · Additional ~20–30% Lp(a) reduction (secondary benefit)
Where We Refer
Livewell Infusion Center, Del Mar — not patient self-administered
Medicare + Supp.
Sweet Spot — Act Early Covered as a service/procedure, not a drug benefit. Most patients pay near $0 out of pocket. This is the population to identify and treat proactively.
Private Insurance
Nearly universally denied — not a practical option at this time.
2025 FDA Update
Approved as monotherapy for primary prevention — no prior statin or step-through required. Statin combination still preferred when achievable, but do not withhold from patients who won't take a statin.
Initiate Leqvio Independently in These Patients — No Dr. Rasch Sign-Off Needed
Medicare + supplement with LDL not at goal · Statin-intolerant or statin-refusing Medicare patient · Any high/very high risk Medicare patient needing more aggressive LDL reduction · Elevated Lp(a) — document as part of the indication. Loop Dr. Rasch in at next convenient opportunity — informational only, not a gate.
Injectable PCSK9 Inhibitors — Non-Medicare or Leqvio-Ineligible
| Agent | Dose | Notes |
|---|---|---|
| Evolocumab (Repatha) | 140 mg SQ q2 weeks or 420 mg SQ monthly | Patient self-administered autoinjector · 50–60% LDL reduction · Prior auth required |
| Alirocumab (Praluent) | 75–150 mg SQ q2 weeks | Patient self-administered · Prior auth required · Document statin + ezetimibe trial for approval |
Prior Authorization Documentation Tips
Always document: (1) maximum tolerated statin dose and duration, (2) ezetimibe trial, (3) Lp(a) elevation if present — this substantially strengthens the prior auth case for both injectables and Leqvio in private insurance patients.
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Step 8
Secondary Causes — Always Rule Out
Secondary Causes of Hyperlipidemia
| Cause | Effect on Lipids | Screen With |
|---|---|---|
| Hypothyroidism | ↑ LDL, ↑ TG | TSH — always order at baseline |
| Diabetes / Insulin Resistance | ↑ TG, ↓ HDL, small dense LDL | HbA1c |
| Nephrotic Syndrome | ↑ LDL, ↑ TG | Urine protein/creatinine ratio |
| CKD | ↑ TG, dyslipidemia | Creatinine, eGFR |
| Obesity | ↑ TG, ↓ HDL | BMI, waist circumference |
| Alcohol excess | ↑↑ TG | History |
| Medications | Variable | Review: thiazides, beta-blockers, steroids, antiretrovirals, isotretinoin, cyclosporine |
| Liver disease | ↓ LDL — can mask dyslipidemia | LFTs |
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Step 9
Special Populations
Triglycerides >500 mg/dL — Pancreatitis Risk, Address First
| Action | Details |
|---|---|
| Dietary intervention | Eliminate alcohol and simple carbohydrates aggressively — primary intervention |
| Fenofibrate 145 mg QD | First-line pharmacotherapy for severe hypertriglyceridemia |
| Icosapent ethyl (Vascepa) 4 g/day | Effective for TG reduction; ASCVD benefit in REDUCE-IT. Use judiciously — at least one trial has raised a signal for increased AFib risk. Discuss with Dr. Rasch before initiating in any patient with AFib history or elevated AFib risk. |
| LDL calculation | Do not calculate LDL from a panel with TG >400 — order direct LDL |
⚠ Vascepa and AFib Risk — Use Sparingly in This Practice
We are a cardiology practice managing AFib. While REDUCE-IT demonstrated ASCVD benefit with Vascepa, subsequent trial data has raised a signal for increased atrial fibrillation risk with high-dose omega-3 therapy. Use sparingly and thoughtfully. When in doubt about a patient with AFib history or risk factors — discuss with Dr. Rasch first.
Triglycerides 200–499 mg/dL
| Strategy | Notes |
|---|---|
| Lifestyle first | Alcohol reduction, refined carbs, weight loss, glycemic control — primary intervention |
| Non-HDL as primary target | Goal: non-HDL < LDL target + 30 mg/dL |
| Vascepa consideration | Same AFib caution applies — use sparingly and with intention |
Familial Hypercholesterolemia (FH)
| Action | Details |
|---|---|
| When to suspect | LDL >190 mg/dL · Tendon xanthomas · Family history of early MI (male <55, female <65) |
| Start high-intensity statin immediately | Do not wait for risk score calculation — treat now |
| If LDL remains >100 on max statin | Add ezetimibe; initiate PCSK9 inhibitor if still not at goal — you do not need Dr. Rasch's sign-off |
| Family screening | Screen all first-degree relatives |
Elderly ≥75
| Scenario | Approach |
|---|---|
| Established ASCVD | Continue statin — ongoing benefit is clear; do not discontinue for age alone |
| Primary prevention | Individualize based on life expectancy, frailty, polypharmacy, and patient values |
| Frail patients | Moderate-intensity preferred over high-intensity to reduce side effect burden |
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Step 10
Follow-Up Schedule
6 Weeks Post-Start or Dose Change
Fasting Lipid Panel + CMP
Confirm LDL goal met. Assess tolerability and any muscle complaints. Adjust therapy if needed. This is the standard recheck interval for all medication changes.
3–6 Months
At-Goal Check
If at goal: reinforce adherence and lifestyle. Repeat labs. Confirm Lp(a) family counseling has been addressed if applicable.
Annually
Maintenance Review
Fasting lipid panel · HbA1c · Reassess risk category (can change with aging, new diagnoses, new imaging findings) · Drug interactions review · Reinforce lifestyle · Lp(a) family screening follow-up.
Any New ASCVD Event
Immediate Escalation
Escalate to high-intensity statin + add-on therapy regardless of current LDL. Any new incidental ASCVD finding on imaging also triggers this — reclassify risk and adjust targets at that visit.
Patient Education — Reinforce Every Visit
"Lower is better. Lowest is best." · At LDL below 60, your plaque isn't just stable — it's shrinking · Never stop medication without calling the office first — alternatives almost always exist · Consistent daily dosing matters; intermittent use significantly reduces benefit · If elevated Lp(a): remind patient to share result with first-degree relatives
11
Step 11
Escalate to Dr. Rasch If…
When in doubt — always better to ask.
Suspected rhabdomyolysis — urgent. Stop statin immediately and call.
TG >1000 mg/dL — urgent pancreatitis risk
LDL >190 mg/dL at baseline — possible familial hypercholesterolemia
Vascepa consideration in a patient with AFib history or elevated AFib risk — discuss first
True statin intolerance after multiple agents and genuine rechallenge attempts with no viable path forward
Complex polypharmacy with significant statin drug interactions
Any incidental ASCVD finding on imaging — confirm risk reclassification and target adjustment
Elevated Lp(a) with complex management questions or unclear path to LDL goal
Leqvio or PCSK9 inhibitor initiated — loop Dr. Rasch in at next convenient opportunity (informational, not a gate)
Any scenario where you are uncertain — always better to ask than to proceed alone.