Radiology Assistant: Cardiovascular (Ischemic Vs Non-ischemic)

ischemic and non-ischemic

In acute infarctions the contrast enters the damaged myocardial cells due to myocyte membrane disruption.
In chronic infarctions the late enhancement is a result of retention of contrast material in the large interstitial space between the collagen fibers in the fibrotic tissue

No reflow phenomenon is the failure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed.
No reflow zones are identified on late-enhancement images as a dark core surrounded by an enhancing rim.
This finding indicates the presence of damaged microvasculature in the core of an area of infarction
The presence of a 'no reflow' zone is associated with worse functional outcome, larger infarcts and adverse clinical outcome [8,9].

Both acute and chronic infarctions demonstrate delayed-enhancement, but an acute infarction can often be distinguished by the presence of a 'no reflow' zone and high signal on T2 weighted images.

following acute myocardial infarction

in the setting of chronic ischemic disease

Stunning is defined as postischemic myocardial dysfunction that persists despite restoration of normal blood flow.
Over time there can be a gradual return of contractile function depending on the transmurality of the ischemia

If the degree of transmurality as seen on the delayed enhancement images is less than 50%, the myocardial function is likely to recover

Hibernation is a state in which some segments of the myocardium exhibit abnormalities of contractile function at rest [10].

This phenomenon is highly significant clinically because it usually manifests itself in the setting of chronic ischemia, that is potentially reversible by revascularization

There is an inverse relationship between the transmural extent of hyperenhancement, and the likelihood of wall motion recovery following revascularization.
If the transmural extent of late enhancement is less than 50% the function is likely to improve after revascularization

Hypertrophic cardiomyopathy (HCM) is characterized by a hypertrophied left ventricle, defined as diastolic wall thickness 15mm or more, without any identifiable cause such as hypertension or valvular disease

In about 25% of patients there is obstruction of the left ventricular outflow tract (LVOT) due to hypertrophy of the basal septum and a systolic anterior motion of the mitral valve (SAM).

Jet in the narrowed left ventricular outflow tract
Systolic anterior motion of the anterior leaflet of the mitral valve
Mitral regurgitation

The therapy of HOCM is pharmacological, surgical myotomy or alcohol ablation

The most common cause of restrictive cardiomyopathy is amyloidosis

Amyloid deposits in the myocardium cause abnormal diastolic function with biatrial enlargement, concentric thickening of the left ventricle and reduced systolic function of usually both ventricles

Cardiac involvement in systemic amyloidosis occurs in up to 50% and has a poor prognosis with a median survival of 6 months

restrictive

The most important differential diagnosis of restrictive cardiomyopathy is constrictive cardiomyopathy.

MRI can differentiate between those two diagnoses

Pericardium is usually thickened in constrictive cardiomyopathy
Diastolic septal bounce is seen in constrictive, but not in restrictive cardiomyopathy

Dilated cardiomyopathy is defined as dilatation with an end diastolic diameter greater than 55mm measured on the left ventricular outflow image and an ejection fraction < 45%

Patients with idiopathic dilated cardiomyopathy show either no enhancement or linear midmyocardial enhancement

The differentiation between idiopathic dilated cardiomyopathy and ischemic dilated cardiomyopathy is important, as ischemic cardiomyopathy might be treated with revascularization and idiopathic disease not.

Late enhancement MRI will show subendocardial enhancement in patients with ischemic cardiomyopathy.

there is an indication for an automated implantable cardioverter-defibrillator (AICD) if:
ejection fraction < 35% in symptomatic patients with ischemic cardiomyopathy or < 30% in asymptomatic patients more than 40 days after an infarction
ejection fraction < 35% in patients with idiopathic dilated cardiomyopathy.

Idiopathic dilated cardiomyopathy with midwall septal enhancement, consistent with fibrosis

15%

Morphologically the right ventricle can have regional wall thinning, hypertrophy, dilatation and microaneurysms.

Functionally cine images are evaluated for RV dysfunction, microaneurysm formation, and focal areas of RV dyskinesia

MR scans may be overinterpreted since the RV has substantial normal variations including variable trabeculation and small outward bulges near the insertion of the moderator band.

fatty
fibro-fatty

The fatty form is characterized by fatty replacement of the myocardium without thinning of the ventricular wall.

The fibro-fatty form is associated with significant thinning of the right ventricular wall.

The sites of involvement are mostly found in the subtricuspid area, the right ventricular apex, and the infundibulum, the 'triangle of dysplasia'

yes

fatty

yes

very small

no

yes

localized aneurysms
severe global or segmental dilatation of the right ventricle
global systolic dysfunction.

mild global or segmental dilatation of the right ventricle
regional contraction abnormalities
global diastolic dysfunction

viral infection

yes

yes

The late enhancement images are key, as the late enhancement in myocarditis is subepicardially or midmyocardially located, and does not originate from the subendocardium

lateral wall

yes

Tako-Tsubo cardiomyopathy or apical ballooning syndrome is a transient cardiomyopathy affecting postmenopausal women after physical or emotional stress

Patients present with symptoms mimicking an acute myocardial infarction.
The ECG changes and abnormal laboratory findings may also mimic an infarction.

marked hypokinesia of the apical cardiac segments is noted

The motion abnormalities are transient and return to normal within weeks.

no