Dilated & Restrictive Cardiomyopathy

RDCS Adult Echocardiography AE

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1 Introduction & Exam Overview

The RDCS AE Exam, SPI Requirement & Logistics Content Outline, Domain Weights & How to Study

2 Cardiac Anatomy

Chambers, Walls, Myocardial Layers & the 17-Segment Model Cardiac Valves & Subvalvular Apparatus Great Vessels, Pericardium, Coronary & Venous Anatomy

3 Cardiac Physiology & Hemodynamics

Cardiac Cycle, Phases & Pressure-Volume Relationships Normal Systolic & Diastolic Function Hemodynamic Principles & Response to Stress

4 Echo Modalities, Instrumentation & Contrast

2D (B-Mode) and M-Mode Imaging Spectral, Color, and Tissue Doppler Modalities Image Optimization, Artifacts, and Contrast Echocardiography

5 Standard Views, Windows & Protocol

Parasternal Long- & Short-Axis Views Apical Views Subcostal & Suprasternal-Notch Views Exam Protocol, Patient Positioning & Provocative Maneuvers

6 Quantification & Doppler Hemodynamic Calculations

Chamber Quantification: LV, LA, RA, and RV Size, Mass, and Volumes Systolic Function: Ejection Fraction Methods, Fractional Shortening & Strain Diastolic Function Grading (ASE/EACVI 2016) Core Doppler Math: Modified Bernoulli, VTI, Stroke Volume & the Continuity Equation Advanced Hemodynamics: PISA/EROA, Pressure Half-Time, dP/dt, Qp/Qs & RVSP

7 Aortic & Mitral Valve Disease

Aortic Stenosis Aortic Regurgitation Mitral Stenosis Mitral Regurgitation

8 Right-Sided, Prosthetic & Infective Valve Disease

Tricuspid & Pulmonic Valve Disease and Pulmonary Hypertension Assessment Infective Endocarditis and Vegetations Prosthetic Valves and Postoperative Evaluation

9 Ischemic Disease & Cardiomyopathies

Coronary Anatomy, Ischemic Heart Disease & Wall-Motion Abnormalities Stress Echocardiography & Myocardial Viability Mechanical Complications of Myocardial Infarction Dilated & Restrictive Cardiomyopathy Hypertrophic Cardiomyopathy, SAM & LVOT Obstruction

10 Pericardial Disease, Masses & Aorta

Pericardial Effusion & Cardiac Tamponade Constrictive Pericarditis vs. Restrictive Physiology Cardiac Masses, Tumors & Thrombi Aortic Disease: Aneurysm, Dissection & Atheroma

11 Congenital Heart Disease & Shunts

Septal Defects & Shunt Quantification Common Adult Congenital Lesions

12 Clinical Care & Safety

Patient Care, Clinical-Data Integration & Exam Protocols Bioeffects, ALARA, Infection Control & Ergonomics

Dilated & Restrictive Cardiomyopathy

Key Takeaways Explain This Topic AI

Dilated cardiomyopathy shows LV dilation with global hypokinesis and an ejection fraction typically below 40%, often 15-30% in advanced disease.

Functional mitral regurgitation in DCM results from annular dilation and leaflet tethering from LV remodeling, not primary leaflet disease.

Restrictive cardiomyopathy preserves normal LV cavity size and ejection fraction while producing marked biatrial enlargement.

Cardiac amyloidosis, a common infiltrative cause of restrictive cardiomyopathy, produces increased LV wall thickness with a granular 'speckled/sparkling' myocardial texture.

Restrictive mitral inflow shows E/A ratio >2 and deceleration time <150 ms, reflecting a stiff, noncompliant ventricle that fills almost entirely in early diastole.

Last updated: July 2026

Dilated Cardiomyopathy (DCM)

Dilated cardiomyopathy is the most common cardiomyopathy encountered in general echo labs and is characterized by left ventricular (and often biventricular) dilation with global systolic dysfunction that is disproportionate to any abnormal loading condition or coronary artery disease. Etiologies span idiopathic, familial/genetic, viral/post-myocarditis, peripartum, toxin-related (alcohol, anthracycline chemotherapy), and tachycardia-induced forms; regardless of cause, the echocardiographic phenotype converges on a common pattern.

Key 2D/M-mode and Doppler findings

LV cavity enlargement — LV end-diastolic diameter typically exceeds the upper limit of normal (commonly >58-60 mm, or an LVEDD index >3.2 cm/m²).

Global hypokinesis — reduced endocardial excursion and wall thickening affecting essentially all segments equally, in contrast to the regional pattern seen with ischemic disease.

Reduced ejection fraction — EF is usually well below 40%, often in the 15-30% range in advanced disease; this is the defining functional abnormality of heart failure with reduced ejection fraction (HFrEF).

Increased sphericity — the normally elliptical LV remodels toward a more spherical shape; the sphericity index (LV short-axis diameter divided by long-axis length) rises toward 1, and apical rounding is common.

Functional (secondary) mitral regurgitation — the MV leaflets are structurally normal, but annular dilation plus symmetric or asymmetric leaflet tethering from papillary muscle displacement prevents coaptation, producing a central-to-posterior MR jet. Severity tracks the degree of LV remodeling rather than intrinsic valve pathology.

Diminished tissue Doppler and stroke volume indices — reduced mitral annular s′ and e′ velocities, reduced LVOT VTI/stroke volume, and frequently a restrictive or pseudonormal diastolic filling pattern superimposed on the systolic dysfunction.

Apical thrombus risk — apical flow stasis from severely reduced EF and spherical remodeling predisposes to LV apical thrombus; every study on a low-EF ventricle should specifically screen the apex (contrast or harmonics if endocardial definition is poor).

Dyssynchrony clues — a widened QRS with septal-to-posterior wall motion delay on M-mode can flag mechanical dyssynchrony relevant to cardiac resynchronization therapy candidacy, though it is not a primary diagnostic criterion for DCM itself.

Restrictive Cardiomyopathy (RCM)

Restrictive cardiomyopathy is the least common of the three classic cardiomyopathy phenotypes (dilated, hypertrophic, restrictive) but is critical to recognize because its echocardiographic signature is nearly the mirror image of DCM.

Key findings

Normal or near-normal LV cavity size with preserved, or only mildly reduced, EF — systolic function is often deceptively normal despite severe symptoms, because the disease primarily impairs diastolic compliance rather than contractility.

Marked biatrial enlargement — both atria dilate significantly (often described as a 'cherry on a stick' appearance against a normal-sized ventricle) because chronically elevated filling pressures are transmitted backward into the atria.

Restrictive diastolic filling pattern — mitral inflow shows a tall E wave, a blunted A wave, an E/A ratio >2, and a short deceleration time (DT), classically <150 ms, reflecting a stiff ventricle that fills almost entirely in early diastole with minimal atrial contribution.

Elevated filling pressures — E/e′ is typically elevated and left atrial volume index (LAVi) is increased, both consistent with chronically high left atrial pressure.

Etiology-specific wall findings — infiltrative causes such as cardiac amyloidosis classically produce increased LV wall thickness with a granular, 'speckled/sparkling' myocardial texture , often paired with a disproportionately low-voltage ECG relative to the degree of wall thickening (a useful clinical discordance clue). Other infiltrative/storage etiologies include cardiac sarcoidosis and hemochromatosis; idiopathic disease and endomyocardial fibrosis are non-infiltrative causes.

RCM vs. constrictive pericarditis

Because both conditions produce a 'restrictive' clinical and Doppler picture, differentiating restrictive cardiomyopathy (myocardial disease) from constrictive pericarditis (pericardial disease) is a frequently tested discrimination:

• Feature Restrictive Cardiomyopathy Constrictive Pericarditis
• Pericardium Normal Thickened/calcified
• Septal motion Normal Respirophasic 'septal bounce'
• Respiratory mitral inflow variation Minimal (<10-15%) Exaggerated (>25%)
• Medial e′ (tissue Doppler) Reduced Often preserved, sometimes exceeding lateral e′ ('annulus reversus')
• Atrial size Markedly enlarged (both atria) Usually only mildly enlarged
• Hepatic vein diastolic flow reversal Accentuated with inspiration Accentuated with expiration

The 'annulus reversus' pattern (medial e′ ≥ lateral e′) is a particularly useful clue for constriction, because in most other cardiac conditions — including RCM — lateral e′ normally exceeds medial e′ due to tethering effects near the septum.

Strain imaging and secondary clues

Speckle-tracking longitudinal strain adds a further discriminator in suspected amyloid RCM: a 'relative apical sparing' pattern — markedly reduced basal and mid-ventricular longitudinal strain with relatively preserved apical strain — appears on the polar (bullseye) map and is characteristic of infiltrative amyloid infiltration, which preferentially affects the base. Secondary findings supporting RCM over other causes of dyspnea include a thickened, hyperrefractile interatrial septum and valve leaflets (amyloid infiltration), a small or normal-sized pericardial effusion, and elevated estimated pulmonary artery pressure from chronically elevated left-sided filling pressures transmitted backward through the pulmonary vasculature.

Sonographic role

Quickly recognizing these two patterns on a limited or bedside study, then triaging toward the correct confirmatory workup (cardiac MRI with late gadolinium enhancement or biopsy/scintigraphy for RCM/amyloid subtyping; CT for pericardial thickening or calcification in constriction), is a core AE clinical-integration skill and a recurring exam scenario.