The full read

One body system, read in full.

What follows is a real Cardiovascular surface from a real anonymized panel. Score, narrative, 19 biomarkers, plan, follow-up testing, and questions to ask your physician. Every system Merlin reads gets this depth.

Cardiovascular surface

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Cardiovascular is one of eleven systems read against your whole body.

Each system sits at its home on the body, lit by how it's doing. Lab-scored systems carry a score; the rest open straight into their deeper portals.

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Your Body Systems — eleven body systems visualized at their anatomical home with scores. Cardiovascular at 58, Immune at 72, Vitamins & Minerals at 90, Liver at 93, Metabolic at 95, Kidney at 94, Endocrine at 84, Blood at 93. Neuropsychiatric, Gastrointestinal, and Musculoskeletal open into their deeper portals.

First read

A score built from a whole-system read.

Cardiovascular at 58 — Fair, by Merlin's reckoning. The number sits on top of a paragraph of narrative that names what's driving it, what's protecting it, and what's still uncertain. Below is the actual surface from a real anonymized panel.

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Cardiovascular Health

A detailed look at the factors influencing your Cardiovascular score.

Cardiovascular

Fair

58/ 100

The headline sits in the Lipoprotein Profile axis, and it is unambiguous: ApoB 117 mg/dL (reference <90), LDL-P 2181 nmol/L (reference <1138), LDL-C 195 mg/dL, and total cholesterol 281 mg/dL together clear the familial hypercholesterolemia screening threshold - LDL-P at or above 2100, LDL-C at or above 190, ApoB at or above 110 - all three tripped at once. ApoB is the primary lipoprotein risk marker here, and 117 mg/dL means the number of atherogenic particles in circulation is high, not just the cholesterol they carry. LDL-P is an NMR-derived estimate from lipid signals rather than a direct protein count, and it agrees with ApoB - concordant, both high, which removes the usual escape hatch of a discordant read. Now the part that changes the trajectory: your particle morphology is Pattern A, peak size 222.9 Angstrom, triglycerides 69 mg/dL, HDL-C 69 mg/dL, and measured HDL efflux capacity (PCEC) 11.9% - a functioning reverse-transport machine, not just a quantity. High particle count carried in large buoyant Pattern A particles in an insulin-sensitive, low-triglyceride milieu is a categorically different picture than the same count in small dense Pattern B. It is still a lot of particles. The Inflammation axis is largely quiet - hs-CRP 0.4 mg/L is protective, MPO 306 pmol/L and fibrinogen 273 mg/dL in range - but OxLDL 63 U/L and Lp-PLA2 145 nmol/min/mL both sit just over their cutoffs, and your omega-3 index (OmegaCheck 5.4%) is below 5.5% - thin pro-resolving substrate against a high particle load. Your ApoE 3/4 genotype amplifies the LDL and cognitive stakes. The Endothelial axis is clean: homocysteine 7.7 umol/L, TMAO 2.9 uM. Particle number is the finding. Morphology is the reprieve.

The breakdown

Five threads that drove the 58.

The high-particle picture, the protective morphology, the wall-engagement pivot, the upstream physiology, and the low-cost levers. With Merlin's reasoning on why the 58 settled where it did, and the parsimonious root-cause hypotheses underneath.

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Score Breakdown

The key factors influencing your score.

ApoB 117 mg/dL, LDL-P 2181 nmol/L, and LDL-C 195 mg/dL all cross the threshold where familial hypercholesterolemia becomes a clinical consideration worth ruling in or out - not a diagnosis, but a question that warrants a physician conversation given the convergence on all three markers.
The morphology data softens the picture meaningfully: Pattern A, peak size 222.9 Angstrom, triglycerides 69, HDL efflux capacity intact at 11.9% - the particles are large and buoyant, the platform underneath them is metabolically clean, and reverse cholesterol transport is working. High particle count with Pattern A morphology and low triglycerides is a categorically different risk picture than the same count with Pattern B and TG above 150.
OxLDL at 63 U/L and Lp-PLA2 activity at 145 nmol/min/mL together indicate that some fraction of these circulating particles is being oxidized and that vascular-wall enzyme activity is engaged at the endothelial interface. This is the mechanistic pivot from circulating risk to wall-resident risk - and where glycocalyx integrity becomes the deciding variable.
ApoE 3/4 carrier status with Apo C1 elevated at 59.71 nmol/L tells you something about the upstream physiology: dietary cholesterol absorption is amplified, hepatic LDL receptor activity is somewhat blunted, and remnant lipoprotein clearance is slower than average. The high LDL-C in this context is a substrate-and-clearance story, not just an output story.
Vitamin D 30 ng/mL is at the lab floor and well under the 50-70 ng/mL functional cardiovascular target. Omega-3 index 5.4% is just below the 5.5% threshold and far below the 8%+ target where outcome data starts to favor the supplemented state. Both are low-cost levers.

Why this score

Threshold position lands in the 50-59 band - LDL-P, LDL-C, ApoB, OxLDL, and Lp-PLA2 are all out of standard range, with three of those crossing FH thresholds. Layer 4 protective credits applied for triglycerides, hsCRP, HDL quantity, and low Lp(a). The ApoE4 carrier status and elevated Apo C1 modify trajectory unfavorably, while Pattern A morphology and intact HDL efflux capacity (PCEC 11.9) prevent the score from sliding lower. Net: 58.

Possible root causes

ApoE 3/4-driven dietary cholesterol hyper-absorption combined with reduced hepatic LDL receptor turnover - this is the most parsimonious explanation for ApoB 117 and LDL-C 195 in someone whose triglycerides are 69 and metabolic platform is clean. The genotype amplifies what dietary saturated fat and cholesterol contribute, and the standard 'eat less saturated fat' advice has roughly twice the effect size in E4 carriers as in E3/E3 individuals.
Possible heterozygous familial hypercholesterolemia - the convergence of LDL-P ≥2100, LDL-C ≥190, and ApoB ≥110 on a metabolically healthy platform meets the threshold where genetic lipid testing or formal FH screening (Dutch Lipid Clinic Network criteria, family history review) becomes a reasonable next step. The phenotype isn't diagnostic on its own, but it crosses the line where the question gets asked.
Insufficient pro-resolving substrate alongside engaged wall-level oxidation - omega-3 index at 5.4% means the SPM precursor pool is thin, and OxLDL plus Lp-PLA2 indicate that the oxidative-inflammatory machinery is already running at the endothelial interface. This is where glycocalyx protection becomes the leverage point.

Before the appointment

Specific questions about specific results.

FH screening, imaging and plaque assessment, lipid-lowering decision framework — drafted in your voice, ready to send to your physician. Plus the questions worth sitting with on your own.

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Questions about your specific results

Familial hypercholesterolemia screening

Given that my ApoB is 117, LDL-C is 195, and LDL-P is 2181 - all crossing the FH consideration thresholds - is formal FH screening warranted? This could include Dutch Lipid Clinic Network scoring, family history review, and possibly genetic testing for LDLR, APOB, and PCSK9 variants.
How does my ApoE 3/4 genotype factor into your interpretation of these lipid numbers, and does it change the threshold at which you'd consider pharmacological intervention?

Imaging and plaque assessment

Can we order a coronary artery calcium (CAC) scan? Given the ApoB burden and my ApoE4 status, knowing whether plaque has actually begun depositing - versus circulating risk only - would meaningfully change the urgency and approach to intervention.
Would CT coronary angiography or carotid intima-media thickness imaging add useful information beyond CAC in my specific picture?

Pharmacological lipid lowering

If a 12-week nutraceutical and dietary trial doesn't move ApoB meaningfully below 90 mg/dL, what's your threshold for starting pharmacological lipid-lowering therapy? Given the ApoE4 status and the FH-threshold values, I'd like to understand the decision framework before we get there.
Are there any additional markers worth running before that decision - ADMA/SDMA, additional oxidized lipid panels, or repeat Lp-PLA2 to track trajectory?

Questions to sit with

When you look at your typical week of eating, where is the saturated fat actually coming from - and is the pattern something you've consciously chosen, or something that's defaulted into place around your schedule? The ApoE 3/4 genotype makes this a higher-leverage question than it would be for someone else.
The phenotype context flagged sleep that doesn't restore even at 6+ hours, and a perceived drop in concentration. Sleep is one of the most underappreciated inputs to vascular inflammation and glycocalyx integrity - what does the runway into sleep actually look like for you, and is there a specific friction point (caffeine timing, light exposure, evening cognitive load) you already know is in the way?
ASCVD risk numbers can produce two distinct psychological responses - dismissal or catastrophizing - and the locus-of-control question affects outcomes independent of any specific intervention. When you read this panel, which direction does your mind want to go, and what would a third option look like?

Across four layers

How the 58 breaks down.

Lipoprotein profile at 58 carries the score down. Inflammation at 93, Endothelial function at 100, Genetics at 100 hold it up. Every marker, every value, every status — visible in context.

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Journey Through Your Cardiovascular System

Your cardiovascular health is analyzed across four critical domains.

Lipoprotein Profile

The lipid particles circulating in your bloodstream

Score

14 Optimal10 Need Attention

Apolipoprotein A1
157 mg/dL
Normal
Apolipoprotein B
117 mg/dL
High
Apolipoprotein B/A1 Ratio
0.75
Normal
AALP Apo A1
222.08 nmol/L
Normal
AALP Apo C1
59.71 nmol/L
High
AALP Apo C2
14.02 nmol/L
Normal
AALP Apo C3
21.47 nmol/L
Normal
AALP Apo C4
0.73 nmol/L
Normal
HDLfx PCEC
11.9 % efflux/4hr
Normal
HDLfx PCAD Score
3
Normal
OxLDL
63 U/L
High
Cholesterol, Total
281 mg/dL
High
HDL Cholesterol
69 mg/dL
Normal
Triglycerides
69 mg/dL
Normal
LDL-Cholesterol
195 mg/dL
High
Chol/HDLC Ratio
4.1
Normal
Non HDL Cholesterol
212 mg/dL
High
Lipoprotein (a)
17 nmol/L
Normal
LDL-P (NMR)
2181 nmol/L
High
LDL Small
249 nmol/L
High
LDL Medium
497 nmol/L
High
HDL Large
6692 nmol/L
Low
LDL Pattern
A
Normal
LDL Peak Size
222.9 Angstrom
Normal

Inflammation

Systemic inflammatory markers affecting cardiovascular health

Score

13 Optimal1 Need Attention

Fibrinogen Antigen
273 mg/dL
Normal
Myeloperoxidase
306 pmol/L
Normal
Ferritin
98 ng/mL
Normal
hs-CRP
0.4 mg/L
Normal
Vitamin D, 25-OH, Total, IA
30 ng/mL
Normal
OmegaCheck (EPA+DPA+DHA)
5.4 % by wt
Low
Arachidonic Acid/EPA Ratio
22.3
Normal
Omega-6/Omega-3 Ratio
7.9
Normal
Omega-3 Total
5.4 % by wt
Normal
EPA
0.6 % by wt
Normal
DHA
3.8 % by wt
Normal
Omega-6 Total
42.5 % by wt
Normal
Arachidonic Acid
13.7 % by wt
Normal
Linoleic Acid
24.9 % by wt
Normal

Endothelial Function

The health of your blood vessel lining

100

Score

2 Optimal

TMAO (Trimethylamine N-oxide)
2.9 uM
Normal
Homocysteine
7.7 umol/L
Normal

Genetics

Cardiovascular genetic risk factors and polymorphisms

100

Score

6 Optimal

LPA Aspirin Genotype
Ile/Ile (Homozygous noncarrier)
Normal
9p21 Genotype rs1
aa
Normal
9p21 Genotype rs1333
gg
Normal
4q25 AF Risk Genotype rs22
ct
Normal
4q25 AF Risk Genotype rs1
gt
Normal
ApoE Genotype
3/4 (Apo E4 Carrier)
Normal

Working plan

Lifestyle, supplements, and the questions for your provider.

The highest-leverage moves that don't come in a bottle - blood pressure, Zone 2, sleep. Supplements activated by your specific markers - Citrus Bergamot triggered by ApoB 117, D-Evail by vitamin D at 30. The CAC scan to consider, the discussion prompts for your provider, and the 3-month retest tags to track.

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Lifestyle

The highest-leverage moves that don't come in a bottle.

Get blood pressure measured professionally
primary
Hypertension is one of the most powerful glycocalyx degraders and one of the most modifiable. There is no reason not to know this number.
Cardio Zone 2 protocol
secondary
Sustained sub-aerobic-threshold work improves endothelial function, mitochondrial density, and metabolic flexibility - all upstream of ASCVD risk.
Address sleep architecture
secondary
Poor sleep elevates cortisol, impairs glucose handling, and degrades the inflammatory resolution capacity that downstream supplements rely on.

These are educational starting points, not a treatment plan. If your data shows elevated cardiovascular risk markers, schedule a conversation with your physician before changing anything in your regimen.

Supplements

Bundled as “ASCVD Complete” — every supplement below is in the plan.

Disclosure: Merlin's parent company maintains a Fullscript dispensary relationship; orders placed through this plan generate practitioner-side commissions. Pricing on Fullscript matches retail; the relationship doesn't change what you pay.

Activated for your specific markers
This supplement activated because your lab values match its clinical trigger.
Citrus Bergamot
Jarrow Formulas· 2 capsules dailyYour ApoB: 117 mg/dL
Polyphenol formulation (bruteridine and melitidine) with HMG-CoA reductase inhibition + AMPK activation + PCSK9 modulation. Useful for early-to-moderate particle burden where pharma is not yet indicated.
Triggered by your ApoB: 117 mg/dL
Arterosil HP
Calroy Health Sciences· 2 capsules daily
Glycocalyx-specific intervention. Sulfated polysaccharide derived from Rhamnan sulfate that directly mimics the heparan sulfate proteoglycans constituting the glycocalyx structure.
SPM Supreme
Designs for Health· 2-4 softgels daily
Specialized Pro-Resolving Mediators (18-HEPE, 17-HDHA, 14-HDHA + EPA/DHA). Active resolution signaling - not anti-inflammatory in the suppressive sense, but the off-switch that terminates inflammation properly.
Discuss with your prescribing physician if on anticoagulant therapy
D-Evail Supreme
Designs for Health· 1 capsule daily
Vitamin D3 + K2 (MK-7) + vitamin A in a fat-soluble base. Targets serum 25-OH-D of 50-70 ng/mL.
OmegAvail TG1000
Designs for Health· 2-4 capsules daily (3-4 for therapeutic CV dosing)
EPA + DHA in triglyceride form, ~70% better absorbed than ethyl esters. Substrate for SPM synthesis; reduces triglycerides and shifts LDL toward larger, more buoyant particles at therapeutic doses.
Discuss with your prescribing physician if on anticoagulant therapy

Imaging to consider

External imaging studies — one-time tests ordered by a clinician.

Coronary artery calcium (CAC) scan

Get testedimportant

Score of zero is meaningful reassurance. Score above zero is a meaningful signal of established plaque worth acting on.

Discussion prompts for your provider

1.Is a coronary calcium score appropriate to order for me now?
2.Given my lipid/lipoprotein profile, are lipid-lowering pharmaceuticals worth considering now, or would a 3-month protocol-only trial be reasonable first?
3.Is my blood pressure pattern (including white-coat variability) something we should track at home?

Retest at 3 months: Three months is the minimum honest evaluation window. Retest the markers that were abnormal at baseline - not just the ones already normal. If the protocol has not moved them, the most likely explanations are dietary pattern, sleep and stress drivers, or pharmaceutical-tier severity.

ApoBhs-CRPHomocysteineTriglyceride-to-HDL ratio

Above: an actual Merlin Cardiovascular surface from a real anonymized panel. Your read will be built on your panels, not a template.

This is what one upload becomes - every number read against your history, your symptoms, and the rest of your panel. Your first full read is free.

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