SCF ENCYCLOPEDIA ENTRY

HYPERTROPHIC CARDIOMYOPATHY (HCM)

SCF SARCOMERIC HYPERCONTRACTILITY & CARDIAC SYNCHRONIZATION COLLAPSE DOSSIER

I. OFFICIAL DISEASE CLASSIFICATION

Hypertrophic Cardiomyopathy belongs to SCF Clinical Domains C9 (Cardiology), C1 (Genomic Medicine), C2 (Cellular Signaling), C6 (Bioenergetics), and C13 (Systems Homeostasis).

II. CLINICAL DEFINITION

Hypertrophic Cardiomyopathy is a genetic cardiac disorder characterized by:

• Unexplained left ventricular hypertrophy
• Diastolic dysfunction
• Myocardial fibrosis
• Arrhythmias
• Sudden cardiac death risk
• Variable heart failure symptoms

Primary affected systems:

• Cardiac sarcomeres
• Ventricular myocardium
• Cardiac conduction networks
• Coronary microvasculature
• Autonomic regulation systems

Associated conditions:

• Cardiomyopathy
• Sudden cardiac death

III. MAJOR CLASSIFICATIONS

A. Obstructive Hypertrophic Cardiomyopathy (HOCM)

Associated condition:

• Left ventricular outflow tract obstruction

B. Non-Obstructive Hypertrophic Cardiomyopathy

C. Apical Hypertrophic Cardiomyopathy

D. End-Stage (“Burned-Out”) HCM

Associated condition:

• Heart failure

IV. CORE SCF ETIOPATHOGENIC THESIS

Within the Synergistic Compatibility Framework (SCF), Hypertrophic Cardiomyopathy represents a systems-level collapse of:

• Cardiac contractile harmonics
• Sarcomeric force regulation
• Myocardial energy optimization
• Ventricular filling synchronization
• Electromechanical communication networks

SCF interprets HCM as a decentralized cardiac intelligence disorder in which excessive contractile signaling progressively disrupts myocardial architecture, energy balance, and electrical stability.

V. SARCOMERIC FOUNDATION

Normal Sarcomere Function

The cardiac sarcomere coordinates:

• Force generation
• Cardiac contraction
• Mechanical efficiency
• Ventricular ejection
• Electromechanical coupling

Core Pathophysiologic Mechanisms

VI. MAJOR GENETIC CAUSES

Principal Genes

Genetic Characteristics

Associated condition:

• Autosomal dominant disorder

VII. SCF FAULT ARCHITECTURE

VIII. MULTI-OMICS PATHOGENESIS

A. Genomics

Affected pathways:

• Sarcomere assembly
• Contractile regulation
• Mechanotransduction
• Cardiac development

B. Transcriptomics

Dysregulated pathways:

• Hypertrophic signaling
• Fibrosis pathways
• Calcium handling
• Stress adaptation

C. Proteomics

Observed abnormalities:

• Sarcomeric proteins
• Calcium-regulatory proteins
• Fibrotic mediators
• Contractility regulators

D. Metabolomics

Key dysfunction:

• ATP depletion
• Mitochondrial stress
• Oxidative stress
• Energetic inefficiency

E. Cardiomics (SCF)

Observed abnormalities:

• Contractile overactivation
• Synchronization instability
• Ventricular communication impairment
• Mechanical inefficiency

IX. SCF PATHOGENESIS FLOW

Stage 1 — Sarcomeric Mutation

Contractile regulation becomes abnormal.

Stage 2 — Hypercontractility

Cardiac force generation becomes excessive.

Stage 3 — Myocardial Hypertrophy

Myocytes enlarge and remodel.

Stage 4 — Fibrosis & Electrical Instability

Conduction abnormalities emerge.

Stage 5 — Diastolic Dysfunction

Ventricular filling becomes impaired.

Stage 6 — Advanced Cardiac Disease

Heart failure, arrhythmias, or sudden death risk develops.

X. SYSTEMIC CONSEQUENCES

Associated conditions:

• Atrial fibrillation
• Ventricular tachycardia
• Syncope

XI. RHENOVA INTERPRETATION

Project RHENOVA interprets HCM as a cardiac force-amplification destabilization syndrome.

RHENOVA Dynamics

• Contractile amplification loops
• Energy-consumption escalation
• Fibrosis propagation cascades
• Electromechanical uncoupling
• Cardiac synchronization collapse

RHENOVA Biomarkers

XII. DBI INTERPRETATION

The SCF Decentralized Biological Intelligence framework interprets the heart as a distributed biomechanical intelligence network coordinating:

• Force generation
• Electrical conduction
• Perfusion regulation
• Rhythm maintenance
• Systemic circulation

DBI Failure Features

• Contractile over-signaling
• Energetic inefficiency
• Electrical communication disruption
• Mechanical synchronization loss

This transforms a highly coordinated cardiac network into an increasingly unstable electromechanical system.

XIII. CLINICAL MANIFESTATIONS

Cardiovascular Manifestations

• Exertional dyspnea
• Chest pain
• Palpitations
• Syncope
• Exercise intolerance

Associated condition:

• Palpitations

Rhythm Manifestations

• Atrial fibrillation
• Ventricular tachycardia
• Sudden cardiac arrest

Associated condition:

• Cardiac arrest

Structural Manifestations

• Asymmetric septal hypertrophy
• Left ventricular hypertrophy
• Mitral valve abnormalities

Associated condition:

• Left ventricular hypertrophy

XIV. DIAGNOSTICS

Diagnostic Hallmarks

Sarcomeric principle:

$Sarcomeric\ Mutation \Rightarrow Hypercontractility$

Mechanical relationship:

$Hypercontractility \Rightarrow Myocardial\ Hypertrophy$

Clinical consequence:

$Hypertrophy \Rightarrow Arrhythmias\ +\ Diastolic\ Dysfunction$

XV. SCF SYSTEMIC AXIS INVOLVEMENT

XVI. STANDARD OF CARE

Pharmacologic Therapy

Examples:

• Metoprolol
• Verapamil
• Mavacamten

Procedural Therapy

Examples:

• Septal myectomy
• Alcohol septal ablation

Sudden Death Prevention

Example:

• Implantable cardioverter-defibrillator

XVII. SCF-PCR THERAPEUTIC ARCHITECTURE

A. Preventative (PCR-P)

Goals:

• Prevent arrhythmias
• Reduce fibrosis progression
• Preserve ventricular function

B. Curative (PCR-C)

Goals:

• Correct sarcomeric dysfunction
• Normalize contractile regulation
• Restore genetic homeostasis

C. Restorative (PCR-R)

Goals:

• Improve cardiac efficiency
• Restore electromechanical stability
• Reduce energetic stress
• Rebuild myocardial synchronization harmonics

XVIII. ETHNOBIOPROSPECTING TARGETS

Note: These represent exploratory cardioprotective research domains and are not substitutes for evidence-based cardiac management.

Traditional Chinese Medicine

• Salvia miltiorrhiza
• Astragalus membranaceus

Ayurveda

• Terminalia arjuna
• Withania somnifera

Vietnamese Thuốc Nam

• Nelumbo nucifera

XIX. SCF API DISCOVERY TARGETS

High-Priority Molecular Targets

• Sarcomere-modulating therapeutics
• Cardiac myosin regulators
• Fibrosis-reduction technologies
• Mitochondrial optimization platforms
• Electrophysiologic stabilization therapies
• Precision gene-editing approaches for HCM
• Cardiac synchronization restoration systems

XX. SCF LAYMAN’S SUMMARY

Hypertrophic Cardiomyopathy is a genetic heart disease in which the heart muscle becomes abnormally thick, most often due to mutations affecting the proteins responsible for cardiac contraction. The thickened heart can have difficulty relaxing, filling properly, and maintaining normal electrical rhythms. Some individuals remain symptom-free, while others develop shortness of breath, chest pain, fainting episodes, arrhythmias, heart failure, or sudden cardiac death. SCF interprets HCM as a disorder of excessive cardiac contractile signaling that gradually disrupts the heart’s mechanical, electrical, and energetic synchronization systems.

XXI. STRATEGIC RESEARCH PRIORITIES

1. Sarcomere-modulating therapies
2. Cardiac myosin inhibition platforms
3. Anti-fibrotic cardiac therapeutics
4. AI-driven arrhythmia and sudden-death forecasting systems
5. Precision HTT? (correction: HCM-associated sarcomeric gene) editing technologies
6. Mitochondrial optimization strategies
7. Cardiac synchronization restoration platforms

MASTER REGISTRY INDEX

SCF-HCM-0001 — Hypertrophic Cardiomyopathy Master Registry

SCF-HCM-SARCOMERE-0002 — Sarcomeric Hypercontractility Layer

SCF-HCM-FIBROSIS-0003 — Myocardial Remodeling Layer

SCF-HCM-RHENOVA-0004 — Cardiac Force-Amplification Destabilization Layer

SCF-HCM-DBI-0005 — Electromechanical Communication Failure Layer

SCF-HCM-PCR-0006 — Preventative–Curative–Restorative Layer