Ischemic heart disease and myocardial infarction
Ischemic heart disease and myocardial infarction can affect regional contraction, global systolic function, strain, relaxation, chamber remodeling, and tissue signal. CardiacNexus provides quantitative descriptors that should be interpreted with symptoms, ECG, perfusion, scar, and clinical history.
- Modality
- Cine short-axis, strain, native T1
- Pipeline step
- Clinical interpretation
- Outputs
- Function, wall thickening, strain, and tissue phenotypes
- Maturity
- Clinician review draft
What clinicians look for
Clinicians usually inspect EF, EDV/ESV, regional wall thickening, strain, post-systolic or diastolic strain features, and tissue markers. EF can be preserved despite regional dysfunction; strain and wall-thickening measures can be more sensitive to regional mechanics [1].
Relevant CardiacNexus phenotypes
| Phenotype page | Measurements to inspect | Interpretation role |
|---|---|---|
| Ventricular function | EF, SV, CO | Global systolic consequence |
| Myocardial mass and wall thickness | Segmental thickness and thickening | Regional contraction and remodeling |
| Ventricular mechanics and strain | Strain, SI-DI, strain rate | Ischemic mechanics and delayed relaxation context |
| Myocardial tissue characterization | Native T1 and corrected T1 | Edema, acute injury, or diffuse tissue context |
| Cross-chamber phenotypes | AVPD and atrial contribution | Longitudinal pumping and filling context |
Interpretation patterns
Reduced EF after infarction is prognostically important, but regional wall motion, strain, post-systolic shortening, and diastolic strain indices may add context in patients with preserved EF or subtle ischemic memory [2].
Limitations
CardiacNexus does not include late gadolinium enhancement, perfusion, coronary anatomy, or troponin. Native T1 and strain findings are supportive context, not proof of infarction or obstructive coronary disease.
Source audit
- Draft primer checked against promoted ventricular function, myocardial mass/wall-thickness, ventricular mechanics, tissue-characterization, and cross-chamber pages.
- The primer explicitly excludes coronary anatomy, perfusion, scar, troponin, and diagnostic MI classification from CardiacNexus outputs.
- Disease-badge routing must not treat
I63stroke/cerebrovascular context as ischemic heart disease or myocardial infarction. docs/data/reference_sources.ymlexists and is the current registry for strain, tissue, and output-contract sources.- Textbook context boundary: broad Braunwald/Hurst ischemic-heart-disease background was treated only as clinical context; page-specific phenotype and method sources are sufficient for this draft.
- Textbook routes checked: Braunwald Coronary Blood Flow and Myocardial Ischemia pages 1-27, STEMI clinical features pages 39-62, NSTEMI pages 130-161, and Stable Ischemic Heart Disease pages 162-221. These routes are not used as diagnostic criteria because CardiacNexus lacks coronary anatomy, perfusion, troponin, and LGE outputs.
References
- Hoit BD. Strain and Strain Rate Echocardiography and Coronary Artery Disease. Circulation: Cardiovascular Imaging. 2011;4(2):179-190.
- Kimura K, Takenaka K, Pan XF, Ebihara A, Uno K, Fukuda N, Kohro T, Morita H, Yatomi Y, Nagai R. Prediction of Coronary Artery Stenosis Using Strain Imaging Diastolic Index at Rest in Patients with Preserved Ejection Fraction. Journal of Cardiology. 2011;57(3):311-315.
- Chew DS, Huikuri H, Schmidt G, Kavanagh KM, Dommasch M, Bloch Thomsen PE, Sinnecker D, Raatikainen P, Exner DV. Change in Left Ventricular Ejection Fraction Following First Myocardial Infarction and Outcome. JACC: Clinical Electrophysiology. 2018;4(5):672-682.