Hypertrophic cardiomyopathy: case report

Background and aim: Hypertrophic cardiomyopathy is one of the leading death among young athletes and affected ۱ in ۵۰۰ people with genetic disorders that 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. The main treatment for patients without heart failure focused on the prevention of sudden cardiac death and Rate reduction caused by reduce left ventricular outflow obstruction. Non-vasodilating Beta-blockers and non-dihydropyridine calcium channel blockers are the fundamental treatment in HOCM patients. Report Patient A ۴۹-year’s old female with no previous heart disease and a history of uncontrolled hypertension was admitted to the emergency room with typical chest pain. Chest pain begin two weeks earlier but intensified last night. Retrosternal chest pain radiates to the neck and left shoulder, worsens with exertion, and is better with sublingual trinitro glycerin. The 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 the cardiac care unit. Beta-blockers cause severe symptomatic bradycardia. so we were forced to the cessation of one important treatment. Blood pressure controlled with ARB. Echocardiography demonstrates severely asymmetric hypertrophied Left ventricular septum and Apex with no LVOT obstruction and no valvular disease. Two sets of negative troponin and continued chest pain guide us to the invasive evolution of coronary anatomy. Coronary artery angiogram showed no Obstructive lesion and patient transfer toward. After optimum blood pressure control with ARB and Amlodipine patient was pain-free. Next-day discharge on a stable vital sign and recommended CMR for evaluation of Hypertrophic cardiomyopathy.Conclusion: ECG demonstrates deep widespread T inversion could be of the non-specific sign of hypertrophied LV or a pattern of important ischemia in LAD territory. Two sets of Negative troponin and Echocardiography showed reduced sized left ventricle with normal systolic function. Moderate diastolic dysfunction and Hypertrophied LV apex and septum cause reduce the normal opening of the LV chamber. No Valvular disease was detected and another parameter was normal. Coronary angiography revealed patent coronary arteries

کلیدواژه ها:

Hypertrophic cardiomyopathy ، case report ، HCM