 Hello, I am Dr. Ajay Asarkar, junior resident at the Department of Radio Diagnosis, Grand Government Medical College, Mumbai. Today I will be talking on the rule of cardiac MRI in evaluation of hypertrophic cardiomyopathy. Cardiomyopathy refers to primary disease of the myocardium that can result in systolic and or diastolic dysfunction and can manifest in congestive heart failure. Types of cardiomyopathies can be hypertrophic, dilated, restrictive, left ventricular non-compaction, and arrhythmic right ventricular. These can either be inherited or sporadic. Hypertrophic cardiomyopathy or HCM is the most common monocytic cardiovascular disorder affecting one of every 500 adults and is characterized by left ventricular hypertrophy in the absence of any other systemic or cardiac disease to account for the changes noted. Although the usual diagnosis of HCM relies on clinical assessment and transphoracic echo, recent studies have demonstrated the increased brutality of cardiac MR imaging and multi-detector CT in diagnosis, therapeutic planning, and prognostication. Our patient, a 34-year-old male, presented with chief complaints of intermittent chest pain since six months without any history of palpitations, dyspnea, without any history of hypertension, diabetes, smoking, or tobacco use. These pointed to a cardiac cause for his complaints. A further workup and echo was planned which revealed asymmetrical septal hypertrophy, mild MR, trivial TR. Subsequently, a cardiac MRI was planned which revealed asymmetrical basal and mid-septal hypertrophy seen on short axis and two chambered views, and fibrosis in the form of late gadolinium enhancement involving basal anterior and septal segments. There was no evidence of systolic anterior motion of the mitral valve leaflet. Neither was there any left ventricular outflow tract obstruction. These findings confirmed a diagnosis of asymmetrical non-obstructive hypertrophic cardiomyopathy. HCM is a genetic disease affecting proteins of myocardial sarcoma and associated myofilaments characterized by LVA hypertrophy without secondary cause. While some patients are asymptomatic, others develop nonspecific symptoms including chest pain, dyspnea, palpitations, syncope, or nearsyncope. Symptoms of heart failure may also develop at any stage. However, the most feared complication is sudden cardiac death. Hyper HCM is a monogenic disorder and myosin heavy chain 7 and myosin binding protein Cg mutations account for most cases. The gross pathology shows a disproportionate ventricular and septal hypertrophy involving basal and mid ventricular region while microscopy shows myocyte hypertrophy and dysarray. Most common diagnostic criteria of HCM on imaging is LV wall thickness more than 15 other although HCM can be present with any degree of hypertrophy. A symmetrical septal hypertrophy is commonly defined by a ratio of wall thickness of septum to non-hypertrophic segment being more than 1.3. X-ray findings are variable and may include enlargement of cardiac silhouette or left bacterial enlargement. ECHO is the first line diagnostic method for differential diagnosis in HCM. The first echocardiographic criteria for diagnosis of LV hypertrophy is LV mass index. However, ECHO is limited by availability of acoustic windows and is a highly operated dependent. Hence, cardiac MR is now emerging as a vital tool in imaging cardiomyopathies. One added advantage of cardiac MR is that it has excellent soft tissue contrast resolution. Many phenotypic forms of HCMR recognized on cardiac MR and are illustrated as below. Following are a series of cases that are presented to our institute showing the various phenotypic expression of hypertrophic cardiomyopathy. This is a case, first is a case of asymmetrical HCM in a 64 year 62 year old male presenting with complaints of great to greatly dyspnea. Asymmetrical septal form is a most common morphological variant and in this the ventricular septum is disproportionately enlarged and with the interseptal myocardium most commonly involved. Concentric HCM is seen in this 34 year old male presenting with complaints of chest discomfort and sweating. It is the second most common phenotype and characterized by diffuse thickening of the LV. The diagnosis, however, should be made in the absence of secondary cause like hypertension, eotix stenosis or the patient being an endurance athlete. A pical HCM is seen in this 64 year old male complaining of exertional breathlessness. This variant is also known as Yamaguchi syndrome and it is characterized by a spade like configuration of LV cavity since most of the hypertrophy is confined to the apical portion of LV. Mass like HCM seen in this 72 year old male complaining of dyspnea and exertion. In this variant there is exuberant focal thickening of the left ventricular cavity simulating a cardiac mass. Dynamic and functional parameters are also assessed via MR. The left ventricular outflow tract obstruction is seen as a gradient of 30 mmHg which is considered obstructive and is an independent predictor of adverse outcomes like sudden cardiac death and potentially lethal arrhythmus. This systolic anterior motion of mitral valve leaflet is also seen here which shows co-aptation of the mitral valve to the basal septum and mitral regurgitation that is detected posteriorly. Myocardial viability is assessed via gadolinium enhancement in dynamic phase. The late gadolinium enhancement shows non-viable myocardium which is seen in the below mentioned two cases. First is the case of a 50 year old male presenting with breathlessness and tachycardia showing endocardial enhancement pattern. Second is a case of a 64 year old male presenting with complaints of dry cough with breathlessness showing mild heterogeneous and myocardial deliad enhancement seen in basal, antroceptile and mid-antroceptile segments. Lately MR has emerged as a gold standard for risk stratification in cases of hypertrophic cardiomyopathy. The LV wall thickness more than 30 mm is a negative prognostic indicator. Gradient across LV OT being more than equal to 30 mmHg is again a negative prognostic indicator. Deliad enhancement shows fibrosis which is again a negative prognostic indicator. Left ventricular rejection fraction may be decreased in HCM in its burnt out phase. Figure 1 shows the gross thickening of the interventricular septum being 30 mm with near complete obj. of the left ventricular cavity in a 30 year old female. The second series of figures shows burnt out HCM characterized by focal thinned out burn, focally thinned out and ballooned LV apex with presence of a small clot in a 72 year old male. The velocity encoding gradient here also shows decreased ejection fraction of 25%. Differential diagnosis of HCM include concentric ventricular hypertrophy due to an underling secondary cause like hypertension or physiological in ethyl which is shown in the above three figures. Cardiac amyloidosis is also a differential which is differentiated on the basis of diffuse endocardial late gadolinium enhancement predominantly in base and mid zone not following in any vascular territory in a 69 year old female who is an already unknown case of cardiac amyloidosis. Management can be conservative and systematic in the form of lifestyle modifications, genetic counseling, screening, pharmacological drugs in while invasive procedures include percutaneous alcohol septal ablation or surgical myotomy. Patients with arrhythmia or survivors of sudden cardiac death are treated with implantable cardiac defibrillator or the end stage treatment is cardiac transplant. In conclusion HCM is the most common monogenic cardiovascular disorder characterized by diverse phenotypic expression. Management is based on a thorough understanding of underlying morphology, pathophysiology and clinical course. Imaging is fundamental for diagnosis, characterization and risk stratification and to guide therapy. Even though ECHO is the initial imaging modality, cardiac MR is emerging as a powerful tool that provides clinically useful information for screening. Furthermore the unique ability of cardiac MR lies in detection and quantification of scar and fibrosis using the delayed enhancement techniques. This is the list of my references which I have used for this talk. Thank you.