Infiltrative and inflammatory cardiomyopathy

Infiltrative and inflammatory cardiomyopathies can change native T1, wall thickness, mass, strain, and ventricular or atrial function. CardiacNexus currently provides native T1 and corrected T1 context, but not contrast-enhanced scar or ECV outputs as mature pipeline measurements.

Modality
Native T1 mapping, cine, strain
Pipeline step
Clinical interpretation
Outputs
Native T1, corrected T1, mass, wall thickness, and strain phenotypes
Maturity
Clinician review draft

What clinicians look for

Readers usually inspect native T1, corrected native T1, LV mass, wall thickness, strain, EF, and atrial remodeling. Elevated native T1 has been reported in edema, myocarditis, infarction, amyloidosis, diffuse fibrosis, and some hypertrophy contexts; reduced native T1 can occur in Fabry disease [1].

Relevant CardiacNexus phenotypes

Phenotype pageMeasurements to inspectInterpretation role
Myocardial tissue characterizationNative myocardial T1, corrected T1, blood-pool T1Tissue signal context
Myocardial mass and wall thicknessLV mass and segmental thicknessHypertrophy or infiltration burden
Ventricular mechanics and strainStrain, strain rate, torsionMechanics affected by tissue disease
Ventricular functionEF, SV, COGlobal pump consequence
Atrial structureLA/RA volumeFilling pressure and chronic remodeling context

Interpretation patterns

Native T1 is valuable because it does not require contrast, but it is not disease-specific. Interpretation should consider field strength, ShMOLLI or mapping sequence, scanner, segmentation, blood correction, and the phenotype being compared.

Limitations

CardiacNexus does not currently provide mature ECV, late gadolinium enhancement, hematocrit-adjusted fibrosis burden, or disease classification. ECV-related figures and notes should remain labelled as planned or literature context unless implementation changes.

Source audit

  • Draft primer checked against promoted myocardial tissue, myocardial mass/wall-thickness, ventricular mechanics, ventricular function, and atrial structure pages.
  • Infiltrative/inflammatory wording is limited to T1 and remodeling context; CardiacNexus does not diagnose amyloidosis, Fabry disease, myocarditis, infarction, or inflammatory cardiomyopathy.
  • docs/data/reference_sources.yml exists and is the current registry for native T1, blood correction, ShMOLLI, and tissue-characterization sources.
  • Textbook context boundary: broad Braunwald/Hurst infiltrative and inflammatory cardiomyopathy background was treated only as clinical context; T1-specific and phenotype-specific references are sufficient for draft rollout.
  • Textbook routes checked: Braunwald Myocarditis pages 185-200 and related cardiomyopathy chapters. These routes are used only to bound broad disease context; public T1 interpretation remains scanner-, sequence-, and source-paper dependent.

References

  1. Taylor AJ, Salerno M, Dharmakumar R, Jerosch-Herold M. T1 Mapping: Basic Techniques and Clinical Applications. JACC: Cardiovascular Imaging. 2016;9(1):67-81.
  2. Karamitsos TD, Piechnik SK, Banypersad SM, Fontana M, Ntusi NB, Ferreira VM, Whelan CJ, Myerson SG, Robson MD, Hawkins PN, Neubauer S, Moon JC. Noncontrast T1 Mapping for the Diagnosis of Cardiac Amyloidosis. JACC: Cardiovascular Imaging. 2013;6(4):488-497.
  3. Sado DM, White SK, Piechnik SK, Banypersad SM, Treibel T, Captur G, Fontana M, Maestrini V, Flett AS, Robson MD, Lachmann RH, Murphy E, Mehta A, Hughes D, Neubauer S, Elliott PM, Moon JC. Identification and Assessment of Anderson-Fabry Disease by Cardiovascular Magnetic Resonance Noncontrast Myocardial T1 Mapping. Circulation: Cardiovascular Imaging. 2013;6(3):392-398.