 Hello, everyone. I'm Dr. Barani Dharan. I'm an observer at Vista Imaging and Specialty Diagnostics Hydrabad. My guide is Dr. Vijay Bhaskar Nori sir. I'll be presenting a pictorial review on cardiac MRA of hypertrophic cardiomyopathy. The aim of this talk is to learn how to diagnose HCM, what to look for and report in case of HCM on cardiac MRA, and finally to review a case example. What do you need to look for on cardiac MRA in a case of HCM? Wall thickness and severity, morphological pattern of wall thickness, obstruction, it can be at the level of left ventricular outflow tract or LV cavity, mitral regurgitation, papillary muscle abnormality, late geranium enhancement, and myocardial mapping. To diagnose the case of HCM, the wall thickness needs to be more than 15 mm on endiastole. There should not be any explainable systemic or cardiac causes like hypertension or infiltrative diseases. In general, the septal involvement is common. Even in cases of concentric hypertrophic cardiomyopathy, there will be asymmetrical involvement of the septal. Whereas in case of other etiologies like severe hypertension or infiltrative diseases, there will be symmetric concentric involvement. To differentiate this, we can use the ratio between septal to infrolateral wall thickness, which should be more than 1.3 in case of hypertrophic cardiomyopathy. There are different morphological pattern. The most common one is septal form. The other common ones are concentric variety, mid ventricular type, epical type. In general, the apex is thinner when compared with basal and midsection. So a 15 mm mark may not be reached in all case of epical HCM. For this, we can use the ratio between epical septal thickness and basal septal thickness. If it is more than 1.3, it favors the diagnosis of epical HCM. In this case, the ratio is 1.36. The septal thickening and hypertrophic can cause dynamic changes. In this case of septal HCM, you can see the LVOT is narrowed because of the septal thickening and systolic anterior movement of mitral leaflet, which is also called SAM. This SAM is due to venturi effect. Because of this LVOT narrowing, you can see a turbulent jet. Because of anterior movement of systolic, anterior systolic movement of mitral valve, the mitral orifice gets opened and there is an eccentric mitral regurgitation as seen by this black jet. In case of mid ventricular cavity type of HCM, there will be cavity obstruction. Here you can see the mid cavity is obstructed and there is a turbulent jet. And there is also a resultant epical ballooning. In case of epical HCM, the epical cavity gets obliterated. Here in this case, a two-chamber view showing obliteration of the epical cavity. This is short axis view at the epical level showing cavity obliteration. There can be associated papillary muscle and mitral valve abnormality as well. There can be elongated mitral valve leaflet. In this case, the anterior papillary muscle is hypertrophied. It is arising more from the apex and it is directly inserting into the mitral leaflet without forming a chordate antennae. The same scene on a two-chamber view. This is a three-chamber view. On short axis view, the septum is mildly thickened. This is at the level of mid cavity. The anterior papillary muscle is much thicker than the postrolateral one. And also instead of being antrometrial, it is more anterior. This is at the basal section. Basal section, you should not be seeing the papillary muscle because it will transform into chordate antennae. But in this case of direct insertion into the mitral leaflet, we can see it in the basal section as well. The reason why we need to look for these abnormalities, this can cause LVOT obstruction and mitral regurgitation. When not addressed and only the septum thickening is addressed by ablation or surgery, there will be persistent LVOT obstruction and SAM. Myocardial fibrosis happens in case of HCM. It is seen as late gadolinium enhancement. The usual pattern is mid myocardial patchy enhancement and RV insertion point enhancement. Other pattern of LGE should raise the suspicion of alternate diagnosis. Even in cases with absent LGE enhancement, like in this patient with a septal form, the T1 values can be elevated, indicating early fibrosis. The main concern in patients with HCM is sudden cardiac death. MRI can predict the sudden cardiac death. Some of the markers are LVOT thickness more than 30 mm, late gadolinium enhancement involving more than 15% of the myocardial mass. LV apical aneurysm and thrombus. The thrombus can pose the risk of cardiac embolic stroke. Ejection fraction less than 50%. Usually, ejection fraction is preserved in HCM cases. If it is less than 50, it indicates birth dot HCM, and these patients are candidate for cardiac transplantation. Let's see a case example, 50-year-old male with concentric LV hypertrophy and preserved ejection fraction on echocardiography. Here are the short access views at multiple levels, spatial, mid and apical, showing asymmetrical thickening of the septum, more than 15 mm, establishing a diagnosis of HCM. It's a concentric type of HCM, as you can see in this four-chamber view. Right ventricle also is mildly thickened in this case. There is incidental erectile right atrial lesion. These are CINY loops, four-chamber view, showing cavity obliteration of the mid and apical region, and apical ballooning. There is also mitral regurgitation in this case. This is two-chamber view, CINY loop, showing mid and apical cavity obliteration, and a part of the apex is ballooned out. And there is also mitral regurgitation. Three-chamber view showing the same cavity obliteration, apical ballooning, and mitral regurgitation. However, there is no LVOT abstraction in this case. These are short access view at multiple levels. Here in the mid-cavity level, you can see the cavity obliteration and an apical region that is part of the cavity is obliterated, and in the true apex and the inferior area, it is thinned out and ballooned. These are late cardinium enhancement images, two-chamber view and four-chamber view, showing severely thinned out apex and inferior part of apical region with transmural enhancement. There is also an incidentally-detected clot. This is in four-chamber view. The right atrial lesion turned out to be a clot. It did not show any enhancement on contrast. Short access view at base-aliment level shows patchy mid-myocardial enhancement and RV insertion point enhancement. Ejection traction was calculated to be 55%, which is above 50%. LV-myocardial fibrosis was approximately 15%. It is calculated using software and of using the LG images. 15% is significant. Through summarize, it's a concentrated biventricular HCM. There was no SAM, LVOT abstraction. It was a moderate MR. MR leads to left atrial dilation, so the patient has a risk of arrhythmias. There is systolic obliteration of the apical and mid-myocardial cavity. The poor prognostic features seen in this case are myocardial fibrosis, more than 15%, and apical balloon dyskinesis and scarring. These two pose a risk of certain cardiac death due to arrhythmias, so this patient can benefit with ICD placement, which is implantable cardioverted defibrillator. There is a small clot in the LV, so there is a risk of cardiac umbilical stroke, so the patient needs anticoagulation. There is right ventricular hypertrophy in this case and clot in the right atrium. These are my references, and thank you.