Cardiac MRI .pptxbbbbbbbbbbhhhhhhhhjhjjjjj

Hhjj

1. CARDIAC MRI Dr. Anjali Deshmukh Junior Resident

2. INDICATIONS Heart failure : etiology – ischemic vs non ischemic. Right and left ventricular function and size. Extent and location of infarct. Viability assessment prior to treatment. Cardiac masses. Pericardial diseases. Constrictive pericarditis. Pericardial effusion. Cardiomyopathies: HOCM, dilated cardiomyopathy, ARV cardiomyopathy, restrictive, Myocarditis. Valvular disease. Congenital heart disease. Aortic aneurysm.

3. Respiratory artefact reduction: Breath holding tech- scan taken under expiration. Navigator technique – navigator box detects position of diaphragm during each slice acquisition and imaging occurs only when diaphragm falls within acceptance window.

4. ECG GATING Image acquisition in particular phase of cardiac cycle to avoid image blur and cardiac motion artifacts. Usually R-wave is used to trigger the acquisition after some trigger delay such that data is acquired in diastolic phase

5. Prospective triggering: Most commonly used. Image acquisition is triggered after R peak and in same stage in each R-R interval. Image taken when heart is at mid diastole during rest. Retrospective triggering: Continuous acquisition of data to produce images from all phases of cardiac cycle. ECG data and acquisition timing are then matched during reconstruction to construct images of all the cardiac phases .

6. Imaging Sequences Dark-blood : anatomy Bright-blood techniques : dynamic and angiography Phase contrast: quantify flow Delayed enhancement : infarct / inflammation / infiltration Gadolinium assisted MRA : angiography Tagging: physiology

7. Black blood seq: T1 and T2 WI These are fast or Turbo spin echo tech. Double inversion recovery HASTE Are T2 WI Single shot FSE

8. Bright blood – gradient echo FLASH: Are spoiled gradient echo with unbalanced gradient Signal is influenced by flow velocity True FISP: (True fast imaging with steady state gradient) SSFP with balanced gradients. Uniform signal regardless of flow velocity. Cine FLASH Cine True FISP

9. Gradient Echo tech: Cine- Prospective and retrospective Multiple phases at one slice location per breath hold Single shot- Single phase with multiple slice location per breath hold

10. Gradient Echo tec: Real time- Gated : then only 5 – images per cardiac cycle, all images from one cardiac cycle. Non gated : Allows patient to breath, for tumor invasion

11. Imaging Planes 1. Vertical long-axis plane (two-chamber view)

12. 2. Horizontal long-axis (four-chamber view)

13. 3. Short-axis plane:

14. 4. Five-chamber view All four chambers with aortic root - the fifth chamber. Demonstrates both mitral and aortic valves. 5. RVOT: Plane passing through RV outflow tract.

15. 17 segments

16. Enhancement patterns Administration of Gadolinium - uptake of the contrast agent into both normal and injured myocardium. In normal myocardium - early wash out of contrast. In injured myocardium the wash out is very slow resulting in delayed enhancement after 10 - 15 minutes compared to the normal myocardium. Delayed enhancement in many pathophysiologic scenarios: Retention of contrast material by fibrous tissue Increased extravascular space Inflammation Tumor neovasculature in primary and secondary tumors Contrast dose 0.05 – 0.1mmol/kg Injection rate 3-7ml/sec For ischemia protocol: adenosine is used .

17. Perfusion imaging (first pass images) Are T1 weighted gradient echo sequence. Image acquisition after 3 mins of contrast administration. Hypoenhanced area is myocardial infarction. Viability study ( delayed myocardial enhancement study). Are T1 gradient echo sequence. Image taken after 10 mins of contrast injection.

18. Since all infarctions start subendocardially and may progress to transmural, the subendocardial region is always involved. Ischemic Cardiomyopathy Infarcted myocardium is bright on late-enhancement images. D elayed enhancement in a typical 'CAD' pattern, Both acute and chronic infarctions enhance.

19. Subendocardial infarction Transmural infarction

20. No reflow phenomenon F ailure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed. O n late-enhancement images as a dark core surrounded by an enhancing rim Both acute and chronic infarctions demonstrate delayed-enhancement, but acute infarction : the presence of a 'no reflow' zone and high signal on T2 weighted images. Left: no-reflow phenomenon Right: later there is transmural enhancement indicating a transmural infarction

21. Stunning P ostischemic myocardial dysfunction that persists despite restoration of normal blood flow. Less than 50% enhancement indicates good prognosis

22. Hibernation S ome segments of the myocardium exhibit abnormalities of contractile function at rest  M anifests itself in the setting of chronic ischemia, that is potentially reversible by revascularization.  The reduced coronary blood flow causes the myocytes to enter a low-energy 'sleep mode' to conserve energy. Hibernation of the anterior wall (blue arrow) and old transmural inferior wall infarction (yellow arrow). No enhancement of the hypokinetic anterior wall mostly due to hibernation

23. H eart muscle is structurally and functionally abnormal, in the absence of other causes of heart dysfunction, like coronary artery disease, hypertension, valvular disease and congenital heart disease.

24. Hypertrophic cardiomyopathy H ypertrophied left ventricle as diastolic wall thickness 15mm or more, without any identifiable cause such as hypertension or valvular disease. Asymmetric thickening predominantly involving ventricular septum. In some 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). In these cases the term HOCM or hypertrophic obstructive cardiomyopathy is used. HCM with narrow left ventricular outflow tract (yellow arrow), systolic anterior motion of anterior leaflet of mitral valve (blue arrow) and mitral regurgitation (red arrow)

25. 3 chamber view HOCM with hypertrophic basal septum . 3-chamber late enhancement image before and after alcohol ablation. T ransmural infarction of the basal septum (arrow).

26. Restrictive cardiomyopathy - Amyloidosis M ost 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. entire subendocardial circumference enhancement

27. Constrictive cardiomyopathy Pericardium is usually thickened in constrictive cardiomyopathy Diastolic septal bounce is seen in constrictive, but not in restrictive cardiomyopathy  This differentiates it with restrictive cardiomyopathy Axial and coronal black-blood images of a patient with constrictive pericarditis after CABG. Arrows point to the thickened pericardium.

28. Dilated cardiomyopathy D ilatation with an end diastolic diameter greater than 55mm measured on the left ventricular outflow image and an ejection fraction < 40%. Idiopathi c dilated cardiomyopathy - either no enhancement or linear midmyocardial enhancement ( due to fibrosis). No enhancement Subendocardial enhancement  so this is dilated cardiomyopathy as a result of ischemia

29. Idiopathic dilated cardiomyopathy with midwall septal enhancement, consistent with fibrosis

30. Arrhythmogenic right ventricular cardiomyopathy (ARVC) I nherited cardiomyopathy - fibrofatty replacement of the RV myocardium. Left: fatty infiltration in the myocardium of the anterior wall of the dilated right ventricle (arrows) Right: dilated right ventricular outflow tract with micro-aneurysm (arrow). develop progressive RV failure and present with ventricular arrhythmias R ight ventricle can have regional wall thinning, hypertrophy, dilatation and microaneurysms. RV dysfunction, microaneurysm formation, and focal areas of RV dyskinesia. 

31. There are two variants of ARVC: fatty and 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'

32. Left: axial black-blood image of a patient with fibro-fatty ARVC Right: late enhancement image shows enhancement of the anterior wall of the right ventricle (arrow). MRI shows segmental hypokinesis, dilatation, fatty infiltration in the right ventricular myocardium, small aneurysms and late enhancement of the myocardium Major criteria demonstrated by MRI are: localized aneurysms severe global or segmental dilatation of the right ventricle global systolic dysfunction. Minor criteria shown by MRI include: mild global or segmental dilatation of the right ventricle regional contraction abnormalities global diastolic dysfunction

33. Myocarditis viral infection late enhancement in myocarditis is subepicardially or midmyocardially, and does not originate from the subendocardium Midmyocardial enhancement

34. Tako-Tsubo cardiomyopathy Tako-Tsubo cardiomyopathy or apical ballooning syndrome is a transient cardiomyopathy affecting postmenopausal women after physical or emotional stress. S ymptoms mimicking an acute myocardial infarction. The ECG changes and abnormal laboratory findings may also mimic an infarction. However, coronary angiography is usually normal marked hypokinesia of the apical cardiac segments in left ventricle angiogram  LEFT: Octopus pot RIGHT: left ventricle angiogram in a patient with Tako tsubo cardiomyopathy. There is only contraction of the basal segments (blue arrows) and the mid- and apical segments balloon.

35. The motion abnormalities are transient and return to normal within weeks. no late enhancement The modified Mayo Clinic criteria for diagnosis of takotsubo cardiomyopathy: Transient hypokinesis, dyskinesis or akinesis of the left ventricular mid-segments with or without apical involvement The regional wall motion abnormalities extend beyond a single epicardial vascular distribution A stressful trigger is often present. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture. New electrocardiographic abnormalities either ST-segment elevation and/or T-wave inversion or modest elevation in cardiac troponin level. Absence of pheochromocytoma or myocarditis.

36. THANK YOU