Cardiac MRI can be used to evaluate ischemic heart disease in several ways: 1. Perfusion imaging with contrast can identify areas of reduced blood flow to the heart muscle during stress testing to detect blockages. 2. Late gadolinium enhancement reveals areas of injured or dead heart muscle through enhanced areas on imaging. This can help assess viability after heart attacks. 3. Functional imaging sequences like cine can evaluate the heart's structure, motion, and pumping ability to see effects of heart disease like reduced ejection fraction or wall thinning.

1. Cardiac MRI for ischemic heart
disease
Dr.Abhijeet Bhambure
Junior Resident
Radio-diagnosis dept.
KIMS, Karad.

2. • INTRODUCTION: Leading cause of mortality and morbidity in developed
counteries. Estimated will be leading cause of death till end of this decade.
First attack> high risk of death d/t complication related.
• Emerging imaging modalities CCT and CMR for IHD and coronary heart ds.
• PATHOPHYSIOLOGY:
- CAD (A.plaque) mcc >IHD
- Chronic stable : slow plaque obcstruction
- If plaque ruptures > thrombus > acute coronary syndrome (fig)
- Therapeutic current: PCI and thrombolysis t/t
- Myocardial infarctions are usually classified by (a)location (anterior, inferior,
lateral), (b) size (focal necrosis,small (<10%), moderate (10–30%) and large
(>30%of LV myocardium) and (c) temporally as evolving (<6 h),acute (6 h–7
days), healing (7–28 days) and healed (>28days).
- healing process can result to thinning of the wall resulting to remodelling and
finally causing dilated type cardiomyopathy.
- Stunned vs hibernating myocardium? > acute reperfusion injury (generally
occurs within hours of reperfusion) causing contractility dysfunction which
takes days to become normal – stunned. Takes years (chronic form) to regain
normal function – hibernating m.

6. CORONARY ANGIOGRAPHY
• Coronary MR angiography is at present still not
incorporated in daily clinical care, mainly
because of long acquisition times, unreliable
image quality and the availability and ease of
use of CCT. However, clinically interesting
indications for coronary MR angiography are
imaging of congenital anomalies of the coronary
arteries, coronary artery imaging in
(postoperative) patients with congenital heart
disease and diagnosis (and follow-up) of patients
with coronary aneurysms in Kawasaki’s disease

9. FUNCTIONAL IMAGING
- imp for the IHD workup
esp. for post MI with
remodelling changes.
Includes: echo, CMRI, CCT,
nuclear study, SPECT and
angiographic studies.

10. White blood Imaging
• gradient echo sequences and steady-state free precession MRI (SSFP).
• The main advantage of white blood imaging is its fast acquisition. It can obtain movement
sequences and allows studying cardiac function and movement. CINE can find volumes in
chambers.
PERFUSION STUDY:
- Using contrast like gadolinium. perfusion across the myocardium is studied. (STRESS TEST can be
usde in perfusion detection where adenosine <beta agonist> is given for the stress on myocardium). Its
first pass contrast.
LGE is late gadolinium enhancement. done after 10-25min of the contrast administration.
• Dark blood Imaging- on spin echo or steady-state free precession sequences -These can be
T1, T2, or proton density weighted sequences - T1 weighted sequences achieve better
anatomic definition and T2 and PD weighted sequences reach better tissue characterization
MYOCARDIAL INFARCTION IMAGING
CASES:

11. 73/F Cine stress MRI shows perfusion defect along anterolateral myocardial wall predominantly in
subendocardial region. On cartherization 70% stenosis was noted then PCI was done.
Importance of stress MRI which
find out the perfusion defect
region suggesting chronic stable
CAD.
microvascular obstruction (MVO) –
lack of tissue perfusions (its seen
inearly post contrast) as contrast not
diffused.

12. rest can be normal, here on stress MRI showing persisent myodcardial perfusion defect. it was post
CABG case in 70m post x increasing chest pain non relieved on medicines. surgical intervention was
planned.

13. T2 SA HLA bright – edema
(excess water content or in
short myocardium at risk). T
with STIR is commonly done
to find out the edema
LGE corresponds to edema
suggests irreversible damage
to the tissue. (non salvagable)
Lcx branch.

14. T2 edema-bright LGE infarction with pericardial inflammation.

15. LGE is not reliable indicator of necrosis in acute setting.

16. T2 shows bright-edema
with central dark core.
first pass contrast shows
main microvascular
obstruction (MVO) – lack
of tissue perfusions (its
seen inearly post
contrast) as contrast not
diffused.
on early and late contrast
the darker area appear
reduced suggesting the
diffusion of GD into the
necrotic part.
on cine (end diastolic and
end systolic) shows
inferolateral wall shows
impaired contraction.
additional now T2 dark
could reflect the
hemorrhage. Cine even
shows bright signal
pericardium s/o effusion/
inflammation. the blood in
T2 will be heterogenous
ie peripheral hyperintense
rim

17. MYOCARDIAL VIABILITY IMAGING
Post contrast enhancement with occlusion. CINE end systolic early and late (6month) shows mardked
thinning of the myocardium.
following such remodelling revascularition can help. but revascularition would only help in viable, stunned
and hybernated myocardium and not necrotic/scarred myocardium. here comes role of CMR to find out the
viable myocardium

18. Viability imaging in 57-year-
old patient presenting
ischaemic cardiomyopathy
and increasing dyspnoea
CINE showing increased
volume, reduced EF, severe
thinning. LGE shows
transmural enhancment
suggesting healed
myocardial infarction (non
viable)
thinning of <6mm even has
low chances of reversibility
(done in end diaslolic)
transmural enhancement in
the inferolateral wall
reflecting a healed
extensive
inferolateral myocardial
infarction - irreversible
damage

19. CINE image shows posterior
myocardial wall shows
thinning with reduced EF
and increased chamber
volume.
On LGE shows transmural
enhancement suggesting
MI. on confirmation by
angiography shows RCA
occlusion.

20. POST MI COMPLICATIONS
- Ventricular thrombus common complication associated with ischemic dilated cardimyopathy. common
after anterior wall MI.
- actually contrast study for CMR is bonus thing as we do it for the detection of MI so can incidentally find i
- to differentiate between the myocardial occlusion and intraluminal - for intramyocardial there will be no
reflow on late contrast images.
- CMR also shows incidentally the presence of pericardial inflammation (this are common association
with transmural type of infarction) as we seen in earlier cases could be pericardiatis or pericardial
effusion.
- aneurysms

21. first pass post contrast
(inversioin images)
shows transmuaral non
enhancement. but on
LGE shows endocardial
non late enhancement
with altered signal and
looking at VLA view
shows altered signal
suggesting presence of
mural thrombus in
presence of MI

22. CINE - myocardial hypo and thinnin. on early and late contrast shows transmural enhancement and hypointense
thrombus with apex aneurysm

23. CMR at 1 wk and after 4months – shows edema them thinning. Subendocardial no reflow and transmural
enhancment. Papillary muscles shows no reflow.

24. DIFFERENTIAL SIMILAR TO MI on imaging
T2 edema. post contrast in all view shows epicardial and subepicardial enhancement suggesting acute
pericarditis. this was case of 17 F with retrosternal pain on BX pericardium lyphohistiocytic infiltrates were noted.

25. T2 WI shows edema in left lateral wall. On LGE enhancement noted mainly in subepicardial region. Its acute
myocarditis in 18yr female.
CINE and T1 shows hyperintense mass. on LGE shows non enhancing mass with myocardial wall enhancement
hyper on T1 and hypo LGE suggests myocaradial hematoma with scarring of the adjacent myocardium - case of
post traum to chest in 71m

26. THANK YOU!