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Specific findings
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Right ventricle
- Complex, geometrical shape
- More (coarse) trabeculation and thinner walls (3-5 mm compacted myocardium) than LV
- RV ejection is determined by longitudinal rather than circumferential contraction
- Ventricular interdependence
- mediated by septum
- RV is more sensitive than LV to volume and pressure loading
- RV volume overload → diastolic D-shaping*
- RV pressure overload → systolic D-shaping*
*Overlapping features possible
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RV volume overload
General
- RV diastolic volumes ↑
- RV function may be impaired
- Normal RV free wall thickness
- Diastolic D-shaping / bounce of the septum due to rapid filling of the RV in diastole (diastolic pressure ↑)
- Fibrosis at RV insertion points possible
Severe tricuspid regurgitation
- Often secondary due to annulus dilation (RV and/or RA dilatation)
- Always check for Ebstein´s anomaly
- Severe TR jet is laminar and difficult to visualise
- Dilated inferior vena cava / Coronary Sinus
- Valve assessment – see specific chapter
Severe pulmonary regurgitation
- Rare, but frequently after post-Fallot repair or pulmonary valvotomy
- Dilated RV / RVOT / MPA / PAs (Ao > MPA diameter in healthy subjects)
- Severe PR jet is laminar and difficult to visualise
- Valve assessment – see specific chapter
Severe left / right shunt (ASD and/or PAPVD)
- Always check for Ebstein´s anomaly (frequently associated)
- Dilated RA, RV, MPA, and PAs (usually Ao > MPA diameter)
- Dilated inferior vena cava / Coronary sinus
- Percutaneous closure – check for sufficient rim surrounding most of the defect to lodge the device, particular inferiorly
- Red flags:
- Significant RV dilatation and / or dysfunction
- Qp : Qs > 1.8
- Pulmonary hypertension
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RV pressure overload
General
- RV dilation and dysfunction in progressive disease
- Hypertrophy of the RV free wall (>5 mm) and of the interventricular septum
- Systolic D-shaping if severe pressure overload
- Fibrosis at RV and RV insertion points
Severe pulmonary hypertension
- Dilated MPA, and PAs (Ao > MPA diameter in healthy subjects)
- Classification
- PH due to left heart disease (systolic and/or diastolic LV dysfunction, valvular disease, etc.)
- Chronic thromboembolic PH
- Lung disease and/or hypoxia
- PAHT
- Other causes
Severe pulmonary stenosis
- Valvular, sub-valvular, supra-valvula
- Congenital stenosis (mainly Fallot’s tetralogy)
→ Typically mobile leaflets with fused tips (Prussian helmet sign)
- Rarely: rheumatic and carcinoid
→ Thickened valve with restricted movement
- Often post-stenotic dilatation of MPA and PAs with preferential dilatation of the LPA (vs. RPA): LPA with in-line orientation; RPA takes a more right angle course from the MPA
- Valve assessment – see specific chapter
RV Infarction
- Up to 50% of inferior MI (proximal to acute marginal RCA branches) also involve the RV; isolated RV infarction is extremely rar
- RV infarction not limited to RCA MI but also occurs in LAD and CX MI and rarely in the absence of coronary disease in substantial RV hypertrophy
- RV RWMA, impaired RV function
- Myocardial oedema on T2w imaging for acute RV infarction
- Check for RV thrombus with subsequent PE
- LGE: coronary LGE pattern of RV +/- RCA territory of LV
<Non-ischemic CMP
- Various non-ischemic CMP may cause RV dilatation, please see specific chapters
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