An ECG showing HOCM A diagnosis of hypertrophic cardiomyopathy is based upon a number of features of the disease process. While there is use of echocardiography, cardiac catheterization, or cardiac MRI in the diagnosis of the disease, other important considerations include ECG, genetic testing (although not primarily used for diagnosis), and any family history of HCM or unexplained sudden death in otherwise healthy individuals. In about 60 to 70% of the cases, cardiac MRI shows thickening of more than 15 mm of the lower part of the ventricular septum. T1-weighted imaging may identify scarring of cardiac tissues while T2-weighted imaging may identify oedema and inflammation of cardiac tissue which is associated with acute clinical signs of chest pain and fainting episodes. Pulsus bisferiens may occasional be found during examination. Variants Depending on whether the distortion of normal heart anatomy causes an obstruction of the outflow of blood from the left ventricle of the heart, HCM can be classified as obstructive or non-obstructive. The obstructive variant of HCM is hypertrophic obstructive cardiomyopathy (HOCM), also historically known as idiopathic hypertrophic subaortic stenosis(IHSS) or asymmetric septal hypertrophy (ASH). Another, non-obstructive variant of HCM is apical hypertrophic cardiomyopathy (AHC), also called Yamaguchi syndrome. It was first described in individuals of Japanese descent. Cardiac catheterization QRS complex, the ventricle has more time to fill. Since there is more time to fill, the left ventricle will have more volume at the end of diastole (increased preload). Due to the Frank–Starling law of the heart, the contraction of the left ventricle (and pressure generated by the left ventricle) will be greater on the subsequent beat (beat #4 in this picture). Because of the dynamic nature of the outflow obstruction in HCM, the obstruction increases more than the left ventricular pressure increase. This causes a fall in the aortic pressure as the left ventricular pressure rises (seen as the yellow shaded area in the picture). Upon cardiac catheterization, catheters can be placed in the left ventricle and the ascending aorta, to measure the pressure difference between these structures. In normal individuals, during ventricular systole, the pressure in the ascending aorta and the left ventricle will equalize, and the aortic valve is open. In individuals with aortic stenosis or with HCM with an outflow tract gradient, there will be a pressure gradient (difference) between the left ventricle and the aorta, with the left ventricular pressure higher than the aortic pressure. This gradient represents the degree of obstruction that has to be overcome in order to eject blood from the left ventricle. The Brockenbrough–Braunwald–Morrow sign is observed in individuals with HCM with outflow tract gradient. This sign can be used to differentiate HCM from aortic stenosis. In individuals with aortic stenosis, after a premature ventricular contraction (PVC), the following ventricular contraction will be more forceful, and the pressure generated in the left ventricle will be higher. Because of the fixed obstruction that the stenotic aortic valve represents, the post-PVC ascending aortic pressure will increase as well. In individuals with HCM, however, the degree of obstruction will increase more than the force of contraction will increase in the post-PVC beat. The result of this is that the left ventricular pressure increases and the ascending aortic pressure decreases, with an increase in the LVOT gradient. While the Brockenbrough–Braunwald–Morrow sign is most dramatically demonstrated using simultaneous intra-cardiac and intra-aortic catheters, it can be seen on routine physical examination as a decrease in the pulse pressure in the post-PVC beat in individuals with HCM.
medical cause of Cardiomegaly
medical cause of Heart failure
medical cause of Chest pain
types of Cardiomegaly
medical cause of Cardiac tamponade
symptoms of Bird fancier's lung
symptom of Pulmonary heart disease
symptom of Pulmonary embolism