BridgeCare LA · SYNC-PREVENT™

Biology changes before symptoms begin.

SYNC-PREVENT™ is an 11-layer biomarker and device-based Clinical Status Monitoring platform for patients 50 years and older with two or more chronic conditions — built to close the gap standard care leaves open.

11 integrated clinical layersCMS-aligned biomarker frameworkFDA-cleared device diagnosticsAI-driven clinical interpretationTEFCA / Carequality interoperabilityPhysician-led at every step

Executive Summary

A Clinical Status Monitoring system — not an RPM program.

SYNC-PREVENT™ — Proactive Risk Evaluation, Vital Early Notification Tracking — is a continuously operating clinical framework built to identify disease before it becomes symptomatic, before it drives a hospitalization, and before it becomes expensive to reverse. It is not a remote patient monitoring program or a chronic care management service, though it uses both.

Designed for patients aged 50 and older, the platform combines eleven clinical detection layers — spanning biomarkers, device-based diagnostics, AI-driven interpretation, and behavioral intervention — into a single, continuously updated picture of each patient's physiologic status.

Synchronize Health, LLC built SYNC-PREVENT™ on the foundation of the American Heart Association's cardiovascular risk model and expanded it substantially. Where the AHA model estimates future cardiometabolic risk from traditional factors at a single point in time, SYNC-PREVENT™ is designed to track actual physiologic change longitudinally, across multiple organ systems, in real time. BridgeCare Louisiana, LLC is the exclusive licensee for Louisiana.

The Detection Window

A typical patient's timeline

SYNC-PREVENT™ monitors here

50 years

First hospitalization

The Governing Principle — Non-Negotiable

The physician retains full clinical authority at every step. BridgeCare LA supports, informs, and executes — it never directs care. Every alert, every escalation, every clinical insight exists solely to give the physician a more complete and timely picture, so their decisions are better informed, not made for them.

Program Objectives

What SYNC-PREVENT™ is built to accomplish.

These objectives define how the platform is designed to create clinical and operational value for physicians, patients, payers, and care teams.

Earlier Detection Across Multiple Organ Systems

Identify cardiovascular, renal, metabolic, neurologic, and endocrine conditions before symptoms emerge — ahead of what score-only or symptom-based models allow.

More Precise Risk Stratification

Extend beyond the AHA model by incorporating longitudinal biomarker trends, device data, renal-adjusted interpretation, and cross-organ analysis.

CMS-Reimbursable Diagnostic Structure

Every core clinical layer is designed around existing CMS billing pathways and integrated with RPM and CCM workflows, so advanced care does not create unfunded services.

Improved HEDIS / STARs Performance

Structured detection of CKD, diabetes, hypertension, heart failure, and diabetic eye disease is designed to close care gaps that affect quality scores and value-based contract performance.

Fewer Avoidable Hospitalizations

Early risk alerts and structured escalation pathways are designed to let physicians intervene before acute events occur, rather than after a patient reaches the ED.

Unified Patient-Centric HIE

Primary care, specialists, and hospitals work from the same current clinical record through TEFCA/Carequality connectivity, closing care-transition gaps.

Biomarker Architecture

Eleven layers yield one continuous picture.

Each layer detects a specific category of physiologic risk. Biomarkers are never interpreted in isolation — they are evaluated longitudinally, adjusted for renal physiology where applicable, and cross-referenced across layers by AI-driven reasoning engines.

Layers 1 through 8 are CMS-aligned and built around reimbursable laboratory and device testing. Layers 9 through 11 are addressed separately, with appropriate clinical context.

CMS-aligned core layersEmerging / specialized layers

Layer One

Atherosclerotic Risk & Plaque Biology

Detect early arterial disease before clinical events occur.

Core Biomarkers

ApoB — atherogenic particle burden, more precise than LDL-C alone
Lp(a) — genetically driven plaque amplification; tested once in a lifetime
hs-CRP — vascular inflammation, which the AHA model does not include
Lipid panel — LDL-C, HDL-C, triglycerides
Remnant cholesterol — triglyceride-rich atherogenic remnants missed by standard panels

What This Layer Detects

Active plaque formation and oxidative plaque instability
Residual inflammatory cardiovascular risk
Inherited lipid risk that standard LDL-C calculations miss

FrequencyAnnual testing; every 6 months for high-risk patients. Lp(a) is a one-time baseline, repeated only if clinically indicated.

Layer Two

Cardiorenal, Hemodynamic & Mineral Stress

Identify early heart failure, renal stress, fluid imbalance, and mineral-driven cardiac risk — including PTH-mediated pathways particularly relevant in women over 50.

Core Biomarkers

NT-proBNP — subclinical heart failure and myocardial wall stress
High-sensitivity troponin (T or I) — microscopic myocardial injury
Cystatin-C — early CKD, independent of muscle mass
eGFR — global renal filtration capacity
Albumin:creatinine ratio (ACR) — renal microvascular injury
Aldosterone–renin ratio (ARR) — RAAS neurohormonal activation
PTH — cardiac fibrosis risk, RAAS activation, and diastolic dysfunction driver
Vitamin D (25-OH) — PTH regulatory status and cardiovascular risk modifier
Serum calcium — mineral homeostasis, read alongside PTH and vitamin D

What This Layer Detects

Subclinical heart failure, before symptoms are present
Early renal decline missed by creatinine alone
Neurohormonal activation driving fluid retention and cardiac remodeling
PTH-mediated myocardial fibrosis and diastolic dysfunction — a mechanism that operates independently of calcium levels
Vitamin D deficiency amplifying cardiovascular and renal risk trajectories

FrequencyAnnual; every 6 months for heart-failure-risk patients. Troponin quarterly for two cycles after an instability trigger, then every 6 months if stable. PTH, vitamin D, and serum calcium are ordered together as a mineral panel — annually, or when clinically indicated.

Layer Three

Metabolic Dysfunction & Instability

Detect insulin resistance and glycemic instability before clinical diabetes is established.

Core Biomarkers

HbA1c — glycemic burden and trajectory over time
Fasting glucose — current glycemic status
Fasting insulin — early insulin resistance, which the AHA model does not include
HOMA-IR — computed insulin resistance index derived from glucose and insulin
Uric acid — metabolic and endothelial stress marker

What This Layer Detects

Pre-diabetes and early diabetes progression
Metabolic syndrome — a driver of cardiovascular and renal disease
Insulin resistance years before glucose levels become abnormal

FrequencyHbA1c every 3–6 months; metabolic panel annually. HOMA-IR is derived from existing labs — no additional test required.

Insulin-dependent patients in the Moderate and Complex care tiers are provisioned a Dexcom G7 continuous glucose monitor for real-time glycemic surveillance between visits, feeding directly into this layer's glycemic-trend interpretation. Stable-tier insulin-dependent patients continue on standard fingerstick and HbA1c monitoring unless the treating physician directs otherwise.

Layer Four

Hepatic & Cardiometabolic Injury

Identify fatty liver disease and metabolic-driven inflammation — a risk the AHA model does not address.

Core Biomarkers

ALT — hepatic steatosis and metabolic liver stress
AST — hepatic injury signal
GGT — oxidative stress and MASLD/MASH risk
FIB-4 index — fibrosis risk score computed from existing labs

What This Layer Detects

Metabolic dysfunction-associated steatotic liver disease (MASLD/MASH), formerly NAFLD/NASH
Hepatic fibrosis progression — a silent driver of cardiovascular risk
Cardiometabolic liver interactions missed by traditional cardiac models

FrequencyAnnual; every 6 months where MASLD/MASH is suspected. FIB-4 is a computed output — no additional labs required.

Supported by the Sonic Incytes Velacur device for non-invasive liver elastography (CPT 76981) where deeper hepatic assessment is clinically indicated.

Layer Five

Oxidative Stress & Systemic Inflammation

Detect the chronic inflammatory burden driving multi-organ disease progression.

Core Biomarkers

hs-CRP — vascular and systemic inflammatory activity
Ferritin — systemic inflammatory and metabolic load
Serum albumin — nutritional reserve, hepatic synthetic function, and physiologic resilience; low albumin is independently associated with hospitalization and poor procedural outcomes across cardiovascular, renal, and post-surgical populations

What This Layer Detects

Chronic low-grade inflammation — a root driver of atherosclerosis, diabetes, and renal disease
Oxidative stress load contributing to endothelial injury
Inflammatory signals that amplify risk across other layers
Nutritional depletion and systemic physiologic vulnerability, which precede clinical deterioration
RPAL composite score — derived from CRP, serum albumin, and lymphocyte count; no additional testing required

FrequencyAnnual; more frequently where inflammatory burden is elevated or active.

Layer Six

Hematologic & Oxygen Delivery Capacity

Ensure adequate oxygen transport and detect anemia-related clinical risk.

Core Biomarkers

CBC — hemoglobin, hematocrit, red cell distribution width (RDW), and lymphocyte count

What This Layer Detects

Anemia — a commonly under-recognized contributor to cardiac and cognitive decline
Impaired oxygen delivery that worsens heart failure and frailty
RDW elevation as an early marker of nutritional deficiency and chronic disease burden
Immune competence and lymphopenia — a frailty marker and predictor of infection vulnerability in patients 50 and older
Lymphocyte count as the third component of the RPAL composite index

FrequencyAnnual CBC; more frequently if anemia is identified or clinical status changes.

Layer Seven

Autonomic Nervous System & Physiologic Regulation

Identify dysautonomia and physiologic instability, particularly in diabetic and cardiac populations.

Device-Based Testing

Heart rate variability (HRV) — autonomic balance
Sudomotor function — small-fiber nerve integrity
Parasympathetic / sympathetic balance — cardiovascular autonomic regulation

CPT 95921 / 95923ANS testing · VitalScan ANS+

What This Layer Detects

Autonomic dysfunction — a key risk factor for sudden cardiac events
Early diabetic neuropathy before the patient reports symptoms
Cardiovascular instability not visible in standard vital signs

FrequencyAnnual; incorporated into standard visit workflows.

Layer Eight

Peripheral Vascular & Microvascular Disease

Detect peripheral artery disease and microvascular compromise before limb-threatening events.

Device-Based Testing

ABI (ankle-brachial index) — peripheral arterial patency
TBI (toe-brachial index) — distal microvascular status, especially in diabetics

CPT 93922 / 93923ABI/TBI · MESI mTABLET

What This Layer Detects

Peripheral artery disease before limb ischemia develops
Diabetic vascular complications, including early signals of foot ulcer risk
Arterial stiffness as a systemic cardiovascular risk marker

FrequencyAnnual; every 6–12 months in diabetic patients or those with known vascular disease.

Layer Nine — Clinically Emerging

Neurodegenerative & Neuroaxonal Injury

Detect silent brain injury and early cognitive decline risk before symptoms are apparent.

Emerging Biomarkers

Serum neurofilament light chain (NfL) — neuroaxonal injury signal; blood-based and non-invasive
GFAP (glial fibrillary acidic protein) — astrocyte activation marker
pTau217 — Alzheimer's-associated tau phosphorylation

What This Layer Detects

Early neurodegeneration before cognitive symptoms emerge
Silent ischemic brain injury linked to vascular disease
Cognitive decline risk intersecting with diabetes, CKD, and inflammation

FrequencyOrdered only where the treating physician determines testing is clinically necessary.

Layer Ten — Functional Performance

Functional & Frailty Assessment

Detect early functional decline, gait instability, and frailty risk before a fall or hospitalization forces the issue.

Device-Based Testing

Motion-based gait analysis — stride variability, balance, and instability signatures
Functional performance scoring — composite frailty index derived from movement data

CPT 97750KinetikOS · annual

What This Layer Detects

Fall risk before a fall occurs — a leading driver of hospitalization and loss of independence in patients 65 and older
Early functional decline that predates formal frailty diagnosis
Gait instability linked to autonomic dysfunction, diabetic neuropathy, or musculoskeletal decline
Frailty signals feeding into the bone turnover extension and cross-layer risk-tier scoring

FrequencyAnnual; more frequently for patients 65 and older, post-fall, or flagged as frail by other layers.

Layer Eleven — Cognitive Assessment

Digital Cognitive Performance Testing

Measure cognitive decline objectively, complementing Layer 9's blood-based biomarkers with functional performance data.

Device-Based Testing

Digital cognitive battery — memory, attention, processing speed, and executive function
Longitudinal cognitive trend tracking across visits

CPT 96116Creyos · annual

What This Layer Detects

Objective, quantified cognitive performance, replacing subjective impression with measured data
Early cognitive decline before it is apparent in routine clinical conversation
Cognitive trajectory changes that corroborate or contextualize Layer 9 findings

FrequencyAnnual; more frequently when Layer 9 biomarkers are elevated or trending, or where the physician identifies clinical concern.

Clinical note — women aged 50 and older

Declining estrogen after menopause disrupts calcium metabolism and reduces PTH suppression, causing PTH to rise even without primary hyperparathyroidism. Elevated PTH — even within the high-normal range — promotes myocardial fibrosis, impairs ventricular relaxation, and activates the RAAS, all of which raise the risk of heart failure with preserved ejection fraction. This mechanism is often clinically silent and is not captured by standard cardiac risk models. Layer 2 addresses the gap by linking PTH, vitamin D, and serum calcium as a single mineral panel, interpreted in the context of renal function, menopausal status, and cardiac trajectory. The treating physician determines whether and when the panel is ordered.

Clinical note on Layer 9 — reimbursement and renal effects

Neurodegenerative biomarkers are not yet universally reimbursed by CMS. Layer 9 testing is included only where the treating physician determines it is clinically necessary, with education and supporting documentation — including cross-layer findings from other layers — provided to help build a defensible clinical record. Reimbursement pathways are evolving and CMS guidance is monitored. Kidney function must always be considered when interpreting these results, since reduced eGFR independently elevates NfL, GFAP, and pTau217 regardless of neurologic disease.

Specialized Protocol Extensions

Four extensions that activate only on clinical trigger.

These extensions are not applied to every patient. Each is triggered by findings within the core layers, keeping testing targeted rather than universal.

Bone Turnover & Fragility Risk

In older patients, osteoporosis and fragility fractures are not simply orthopedic events — they accelerate loss of independence, trigger hospitalizations, and worsen cardiometabolic trajectories through immobility and deconditioning. This extension adds biologically responsive bone-turnover monitoring to help physicians detect high-turnover bone loss earlier, confirm treatment response sooner than DXA imaging can show, and manage CKD-related mineral metabolism accurately.

Biomarker	What It Detects	Added Value Over Standard Care	Frequency
Intact P1NP	Bone formation rate; early biologic response to osteoporosis therapy	Confirms therapy adherence and response 3–6 months before DXA can show change	Baseline, then 3–6 months after therapy change; every 6–12 months if stable
Bone-specific ALP (bALP)	Bone formation; CKD-related mineral metabolism classification	Differentiates the bone contribution to elevated ALP; critical in CKD-MBD	Baseline; every 6–12 months for CKD-MBD risk; 3–6 months after therapy change in high-risk cases

Trigger conditions

Activated when any of the following are present in the patient record: a known osteoporosis or osteopenia diagnosis; a prior fragility fracture; a frailty flag from Layer 7 or Layer 10 gait analysis; CKD stage 3 or higher (eGFR under 60) from Layer 2; an active or recent corticosteroid prescription; or BMI below 18.5. Renal adjustment applies here as well — in reduced kidney function, bone turnover markers can be distorted by clearance changes and secondary hyperparathyroidism, so results are integrated with eGFR, calcium, phosphate, and vitamin D status.

Familial Hypercholesterolemia (FH) Genetic Testing

FH genetic testing is ordered only when the result is expected to change how the patient is managed — to support therapy escalation, justify biologic agents such as PCSK9 inhibitors, or enable cascade testing of family members. It is not a routine screen.

Severe hypercholesterolemia

LDL-C ≥ 190 mg/dL at baseline
Secondary causes have been addressed

Persistent elevation despite therapy

High-intensity statin ± ezetimibe for 8–12 weeks
LDL-C remains ≥ 160 mg/dL, or under 50% reduction from baseline
ApoB above the patient's risk-tier target

Premature ASCVD or family history

MI, stroke, PAD, or revascularization in men under 55 or women under 65
First-degree relative with premature ASCVD or LDL-C ≥ 190 mg/dL

Discordant or residual risk pattern

ApoB disproportionately elevated relative to LDL-C
Elevated Lp(a) with family history of premature ASCVD
An ASCVD event despite acceptable LDL-C

Do not order rule

FH genetic testing is not triggered when LDL-C is already at target without a premature ASCVD history, when the patient is not a candidate for therapy escalation, or when a secondary cause explains the hypercholesterolemia and has not yet been corrected. The trigger is suppressed automatically when any of these conditions apply.

Inflammatory Bowel Disease Activity Layer

This extension activates only for patients with a confirmed IBD diagnosis — Crohn's disease or ulcerative colitis — rather than across the general population. It tracks disease activity between gastroenterology encounters using a panel of inflammatory ratios calculated from labs the patient is already giving, so no additional specimen collection is required.

Six ratios are calculated: NLR (neutrophil-lymphocyte), PLR (platelet-lymphocyte), SII (systemic immune-inflammation index), LMR (lymphocyte-monocyte), and LHR (lymphocyte-hemoglobin) come from the CBC; NPAR (neutrophil-platelet-albumin) also draws on serum albumin from the metabolic panel. All six are computed automatically at every draw — typically every 3 to 6 months, and more often during an active flare. The physician is flagged whenever a ratio crosses its threshold or trends toward one.

Oncology & Silent Malignancy Screening

Cancer screening is not a core layer. It is a conditional, physician-directed extension that activates based on age, gender, and clinical risk factors surfaced elsewhere in the protocol — keeping oncologic screening targeted and evidence-based rather than applied uniformly.

Lung cancer screening

Low-dose CT for qualifying patients — CMS-covered
Cross-referenced with inflammatory and metabolic findings in Layers 1, 5, and 6

Colorectal cancer screening

FIT / Cologuard — CMS-covered
Standard age- and risk-based screening intervals apply

Prostate screening (men 50+)

PSA ordered per physician determination and current USPSTF guidance
Elevated PSA routed through the escalation pathway rather than immediate specialist referral

Gynecologic risk awareness (women)

CA-125 awareness panel for family history of ovarian or breast cancer, BRCA carrier status, or persistent pelvic symptoms
Not a routine screen — physician-directed only

Trigger conditions

Low-dose CT and FIT/Cologuard follow standard CMS age- and risk-based screening eligibility. PSA and CA-125 are never triggered automatically — they are ordered strictly by physician direction, informed by age, gender, family history, and findings surfaced elsewhere in the protocol. Findings feed into the cross-layer interpretation engine for context alongside the patient's broader risk profile.

RPAL composite — a cross-layer derived score

The RPAL composite is computed automatically whenever CRP and serum albumin (Layer 5) and lymphocyte count (Layer 6) are all present in the current draw. It is surfaced to the physician — rather than simply logged — when the patient is flagged as post-procedural within 90 days of a TAVR or major cardiac or surgical intervention; when serum albumin falls below 3.5 g/dL; when CRP trends upward across two consecutive draws; when lymphocyte count falls below 1.0 × 10⁹/L; or when the care tier includes a frailty or high-infection-risk designation. No additional testing is required at any point.

Cross-Cutting Clinical Modifier

Kidney function modifies how every other layer is read.

Kidney function is not treated as a secondary finding. It is an active physiologic modifier that adjusts interpretation across every clinical layer. Reduced kidney function alters the circulating levels of inflammatory markers, vascular injury signals, and neurodegenerative biomarkers in ways that lead to misclassification if renal physiology is ignored.

Failing to account for it creates real clinical risk: overestimation of neurodegenerative risk, premature specialist referral, inappropriate therapy escalation, and unnecessary cost without benefit to the patient. Renal adjustment is embedded directly in the interpretation logic.

Biomarker Pattern	Kidney Function Context	SYNC-PREVENT™ Interpretation
Elevated neurodegenerative biomarkers	Preserved eGFR	Higher likelihood of actual neurodegenerative pathology — proceed with clinical evaluation
Elevated neurodegenerative biomarkers	Reduced eGFR	Renal clearance effect is likely contributing — prioritize longitudinal trending before escalation
Stable biomarkers	Reduced eGFR	Lower near-term neurodegenerative risk — monitor physiologic contributors to kidney decline
Rising biomarkers over time	Stable or declining eGFR	Adjust slope interpretation; correlate with cognition, function, and device data before escalating

Why this matters clinically

A single elevated biomarker reading in a patient with CKD does not mean the same thing as the same reading in a patient with normal kidney function. Biomarkers are never interpreted in isolation. Renal-adjusted trend analysis differentiates stable renal-related elevation from true pathologic progression, so the physician receives a more accurate signal rather than a false alarm.

Device-Based Diagnostics

FDA-cleared diagnostics, operated in the physician's clinic.

The protocol is built around FDA-cleared diagnostic devices operated on-site under physician supervision, with results transmitted to the physician within minutes of testing — enabling immediate clinical decision-making without disrupting clinic workflow or adding staff burden.

Each device integrates with the platform's clinical workflows and operates under existing CMS billing pathways. Device findings feed directly into the relevant biomarker layer.

Cardiology

Heart Failure Hemodynamic Assessment

Ventric Health — Vivio (non-invasive LVEDP)

Measures left ventricular end-diastolic pressure non-invasively. Detects early heart failure physiology — including HFpEF — before symptoms develop, providing hemodynamic data unavailable from standard clinical examination.

Physician-directed billingAnnual; every 6 months for HF-risk patients

Ophthalmology / Diabetes

Diabetic Retinopathy Screening

AEYE-DS — autonomous AI retinal imaging

Screens for diabetic retinopathy from a single retinal image, returning a referral decision in about a minute. Closes the HEDIS diabetic eye exam care gap without a separate specialist visit.

CPT 92229Annual

Vascular

Peripheral Artery Disease Detection

MESI mTABLET — ABI/TBI

Automated measurement of ankle-brachial and toe-brachial index. Identifies peripheral arterial disease, arterial stiffness, and limb ischemia risk before symptoms become limiting.

CPT 93922 / 93923Annual; every 6–12 months in diabetics

Neurology / Cardiology

Autonomic Nervous System Testing

VitalScan ANS+

Assesses heart rate variability, sudomotor function, and parasympathetic/sympathetic balance — detecting autonomic dysfunction, an early marker of diabetic neuropathy and cardiovascular instability.

CPT 95921 / 95923Annual

Hepatology

Fatty Liver Disease — MASLD / MASH

Sonic Incytes — Velacur (ultrasound elastography)

Non-invasive liver elastography quantifying hepatic stiffness and steatosis for staging of fibrosis and MASLD/MASH. Ordered on physician direction where clinical indicators are present, including elevated FIB-4 or abnormal Layer 4 biomarkers. CMS medical necessity criteria apply.

CPT 76981Physician-directed; disease-specific indication required

Cardiology / Arrhythmia

AI Digital Stethoscope & ECG

Eko Core 500

Amplifies heart and lung sounds, cancels background noise, and applies AI to detect AFib, murmurs, and early heart failure signals during routine examination — turning every visit into a screening opportunity.

CPT 93000Each patient exam

Endocrinology

Continuous Glucose Monitoring

Dexcom G7

Real-time continuous glucose monitoring for insulin-dependent patients in the Moderate or Complex care tier, giving the physician continuous glycemic trend data between visits rather than a single point-in-time reading. Feeds Layer 3 interpretation.

DME benefitContinuous, for qualifying tiers

Additional specialized devices

Device	Manufacturer	What It Detects	Frequency
Bluedrop OneStep	Bluedrop Medical	Plantar temperature asymmetry, identifying diabetic foot ulcer risk 2–4 weeks before visible breakdown, ahead of ulceration, infection, and amputation.	Daily (high risk); weekly (moderate risk)
Wesper At-Home Sleep Study	Wesper	OSA severity, respiratory instability, sleep stages, and oxygen desaturation — identifying sleep apnea contributing to AFib, HFpEF, hypertension, and CKD progression.	Annual, or when symptomatic
Digital cognitive testing	Creyos	Cognitive performance assessment for early decline detection. Formalized as Layer 11; corroborates Layer 9 blood-based biomarkers.	CPT 96116 — annual
Frailty & gait analysis	KinetikOS	Motion-based gait instability and frailty assessment. Formalized as Layer 10; identifies fall risk and functional decline, particularly in patients 65 and older.	CPT 97750 — annual
Continuous glucose monitoring	Dexcom G7	Real-time glycemic trend data for insulin-dependent patients, supporting Layer 3 interpretation between visits.	Moderate/Complex tier — continuous

AI-Driven Interpretation

Raw values don't tell a physician what to do. Context does.

Clinical meaning emerges from context — the patient's full history, medication list, comorbidities, trends over time, and the interaction between findings across organ systems. SYNC-PREVENT™ applies language-model-powered clinical reasoning engines to assemble that context and deliver it to the physician in a clear, actionable form.

These models are trained on validated medical research and produce fact-based, evidence-aligned clinical context. They do not generate opinions and do not override physician judgment. Every output is a tool for the physician, not a substitute for clinical decision-making.

Interpretation Engine

PALMMED / GPT-4 Clinical Layer

What it interprets

The complete patient profile — labs, vitals, medications, comorbidities, EHR notes, RPM data, and longitudinal trajectories across all eleven layers.

What it produces

Cross-organ clinical reasoning that identifies interactions between biomarkers, explains risk trajectories, and surfaces findings the physician can act on. Updated every 30–90 days, aligned with CCM/RPM cycles.

Risk Prediction Engine

Bravo4Health

What it interprets

All biomarkers, device data, medications, EHR history, and RPM trends in real time, with dynamic reclassification as new data arrives.

What it produces

Short-term multi-organ instability prediction, care gap identification, and escalation need scoring. Updated at least monthly, with a full reassessment every 90 days in line with CMS requirements.

Hepatic Risk Model

FIB-4 (model-interpreted)

What it interprets

Age, AST, ALT, and platelets, placed in the context of metabolic, cardiac, and renal comorbidities. No additional labs required.

What it produces

Fibrosis risk classification and MASLD/MASH progression assessment, with hepatic-cardiac-metabolic interaction context. Updated every 6–12 months alongside ALT/AST testing.

Clinical Execution

RPM and CCM are embedded execution components, not the foundation.

Remote Patient Monitoring and Chronic Care Management are the operational infrastructure that carries SYNC-PREVENT™ findings to patients and care teams between physician visits. They enable personalized engagement, medication adherence support, tiered alerting, and the longitudinal follow-through that turns a clinical insight into a measurable outcome.

Clinically Oriented Staff — Not a Call Center

Enrolled patients are supported by BridgeCare LA coordinators who understand conditions, medications, symptoms, and escalation pathways. Every signal delivered to a physician is filtered, clinically relevant, and free of noise.

Tiered Alert Notification Pathway

Structured escalation pathways are designed so that status changes are communicated promptly and at the right level — the right person receiving the right alert at the right time.

Medication Adherence and Reconciliation

Adherence verification and medication reconciliation through TEFCA/Carequality data, aimed at reducing medication-driven readmissions and care gaps.

Streamlined Documentation

Ready-to-sign reports aligned with CMS requirements, designed to reduce administrative burden without adding staff workload.

Behavioral Adherence (COM-B Framework)

Missed readings, non-compliance, and engagement gaps are treated as clinical variables addressed through structured behavioral intervention, not simple reminders.

Interoperability Built In

TEFCA/Carequality integration gives clinicians the complete picture of the patient — not just device readings — with full data security and HIPAA compliance.

Patient-Centric HIE

One patient. One clinical record. Every clinician. In real time.

SYNC-PREVENT™ establishes a patient-centric Health Information Exchange that dynamically links every professional involved in a patient's care — primary care, specialists, hospitals, ancillary services, and care management teams — into a single, continuously updated clinical network.

Through TEFCA/Carequality connectivity, event-based messaging, and real-time clinical alerts, meaningful changes are shared across the care team as they happen: hospital admissions and discharges, ED visits, abnormal laboratory results, device-detected physiologic deterioration, and biomarker-based risk escalation.

Because every clinician works from the same current record, care gaps during transitions are closed, duplicative testing is reduced, and conflicting treatment decisions become visible before harm occurs.

How the Two Models Differ

SYNC-PREVENT™ compared to the AHA risk model.

SYNC-PREVENT™ is built on the foundation of the American Heart Association's cardiovascular risk model and expands it across every dimension. The two are distinct: the AHA model is a published risk equation; SYNC-PREVENT™ is a monitoring platform licensed from Synchronize Health, LLC.

Clinical Dimension	AHA Risk Model	SYNC-PREVENT™
Risk assessment timing	Static — a single point in time	Longitudinal, continuously updated
Organ system coverage	Cardiometabolic only	Cardiac, renal, metabolic, hepatic, neurologic, vascular, hematologic, autonomic, functional/frailty, cognitive, oncologic
Biomarker interpretation	Fixed threshold values	Renal-adjusted, cross-layer, trend-based interpretation
Data sources	Traditional labs and clinical data	Labs, devices, RPM, EHR, medications, behavioral data, TEFCA/Carequality feeds
Kidney function role	Treated as a downstream diagnosis	Embedded as an active physiologic modifier across all layers
Escalation pathway	Clinician-initiated at next visit	Tiered and real-time, with physician notification and structured follow-up
Physician support	Risk score delivery only	Full clinical context, cross-organ reasoning, and workflow-integrated escalation support
CMS / value-based alignment	Partial	CMS-reimbursable structure, HEDIS/STARs gap closure, RPM/CCM integration

How It Works

Detect. Interpret. Act.

Detect

FDA-cleared devices and longitudinal biomarkers surface physiologic change while it's still silent — across cardiac, renal, metabolic, and neurologic systems.

Interpret

AI-driven reasoning engines cross-reference findings across all eleven layers, adjust for renal physiology, and assemble the clinical context a physician needs.

Act

The treating physician — and only the treating physician — decides. SYNC-PREVENT™ delivers the picture; it never delivers the decision.

SYNC-PREVENT™ does not monitor one disease. It monitors the entire trajectory of human deterioration — before symptoms begin, before hospitalization occurs, before outcomes become difficult to reverse.

Summary

A living clinical framework, not a static protocol.

As new diagnostic technologies are validated, as additional FDA-cleared devices are integrated, and as CMS coverage evolves, SYNC-PREVENT™ expands accordingly. That commitment to ongoing refinement is what keeps the protocol current, clinically meaningful, and trustworthy.

Every element is designed around one governing principle: the physician is at the center of every clinical decision. The platform's role is to ensure that physician has the most complete, most accurate, and most timely clinical picture available — so that when they act, they act with confidence.

“Biology changes before symptoms begin. SYNC-PREVENT™ detects it — giving every physician the complete picture they need, at the moment it matters most.”

This page describes the design of the SYNC-PREVENT™ clinical protocol. It is provided for informational purposes only and is not medical advice, a diagnosis, or a treatment recommendation. All testing, device use, referral, and escalation described here occurs at the direction and discretion of the treating physician. CPT codes are listed to identify the category of service and do not constitute a representation that any service will be covered or reimbursed in a given case. Biomarker frequencies reflect protocol design and may differ for an individual patient. SYNC-PREVENT™ is a trademark of Synchronize Health, LLC.

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