Hypertrophic cardiomyopathy: case report

Introduction :Hypertrophic cardiomyopathy is one of leading death among young athletes and affected ۱ in ۵۰۰ people with genetic disorder cause sarcomere or non-sarcomere mutation. Complications spectrum from hypertension, Dyspnea, various ventricular and supraventricular arrhythmia, ischemia and non-ischemic pump failure to sudden cardiac death. Due to abnormal hypertrophied muscle bulk and less developed microvasculature and endothelial dysfunction, supply demand mismatch happened and cause chest pain. Main treatment for patient without heart failure focused of prevention of sudden cardiac death and Rate reduction cause reduce left ventricular outflow obstruction. Non vasodilating Beta blockers and non dihydropyridine calcium channel blockers are the fundamental treatment in HOCM patients.Report Patient: ۴۹-year’s old female with no previous heart disease and history of uncontrolled hypertension admitted to emergency room with typical chest pain. Chest painbegin two weeks earlier but intensified last night. Retrosternal chest pain radiates to neck and left shoulder, worsen with exertion and better with sublingual trinitro glycerin. First Vital sign in ER was BP:۱۸۰/۱۲۰, HR:۵۰, O۲ saturation ۹۸ %. ECG was obtained less than ۱۰ minutes and showed no ST segment elevation but Deep widespread T inversion in precordial leads suspected us to WELLENS pattern which means stenosis of Proximal Left anterior descending coronary artery and need emergent evaluation. Optimum Acute coronary care started and patient transfer to cardiac care unit. Beta blockers cause severe symptomatic bradycardia.so we forced to cessation of one important treatment. Blood pressure controlled with ARB. Echocardiography demonstrate severely asymmetric hypertrophied Left ventricular septum and Apex with no LVOT obstruction and no valvular disease. Two set of negative troponin and continued chest pain guide us to invasive evolution of coronary anatomy. Coronary artery angiogram showed no Obstructive lesion and patient transfer to ward. After optimum blood pressure control with ARB and Amlodipine patient was pain free. Next day discharge on stable vital sign and recommended CMR for evaluation of Hypertrophic cardiomyopathy.Conclusion: ECG demonstrate deep widespread T inversion could be one of non-specific sign of hypertrophied LV or pattern of important ischemia in LAD territory. Two set of Negative troponin and Echocardiography showed reduce sized left ventricle with normal systolic function. Moderate diastolic dysfunction and Hypertrophied LV apex and septum cause reduce normal opening of LV chamber. No Valvular disease detected and other parameter was normal. Coronary angiography revealed patent coronary arteries.

کلیدواژه ها:

Hypertrophic cardiomyopathy ، case report ، HCM