Bisoprolol
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Rebound effect following the discontinuation of bisoprolol: case report An 84-year-old man experienced rebound effect (i.e. rebound of myocardial infarction following the discontinuation of bisoprolol) following the discontinuation of bisoprolol [indication not specified]. The man was admitted for a left carotid endarterectomy due to tight 90%–99% stenosis of the left internal carotid artery, diagnosed after an episode of amaurosis fugax. Due to the recent neurological symptomatology and the appearance of the critical carotid stenosis on the CT angiography, heparin was started right after admission to the hospital. His medical history included the following: chronic stable angina pectoris treated with sublingual nitroglycerine on demand, total ostial occlusion of the right coronary artery and nonsignificant stenoses of the other coronary arteries, paroxysmal atrial fibrillation treated with apixaban, hypertension, chronic renal failure), anaemia and peripheral vascular disease manifested as intermittent claudication. He had been receiving valsartan, isosorbide mononitrate, bisoprolol [dosage and route not stated], lercanidipine, apixaban, doxazosin and omeprazole. On the day of admission, he developed postprandial angina that resolved with nitroglycerine. The resting ECG showed first-degree heart block, a complete right bundle branch block and suspected old inferior wall myocardial infarction. The cardiology consultant requested dipyridamole methoxyiso-butyl-isonitrile (MIBI) scan, which showed diffuse filling defects, specifically with severe, partially reversible filling defect of the inferior wall and a moderate, reversible defect of the anterior wall. Consequently, he underwent coronary angiography that showed a complete ostial occlusion of the right coronary artery, a 50%–70% stenosis of the mid left anterior descending artery and a wide open left circumflex coronary artery. After an interdisciplinary discussion, coronary intervention was not performed and a decision was made to continue with his conservative therapy. On the following day, he experienced prolonged typical angina at rest radiating to his left arm. The electrocardograph recorded during chest pain showed deep ST depressions on the anterior leads. Due to severe hypertension (systolic BP higher than 210mm Hg), the daily dose of diazoxide was doubled. It was then discovered that bisoprolol had been discontinued before his MIBI scan and was not resumed. Subsequently, his HR increased to 100–110 beats/min as compared with 60–70 beats/min on admission. Bisoprolol was immediately resumed and diazoxide was given as per the regular dose because of very low diastolic BPs ranging from 40–50mm Hg. Within 24h, his HR retuned to 60–70 beats/min, chest pain resolved, and the ECG changes normalised. Highsensitivity troponin-T obtained shortly after the resolution of the chest pain was 0.749 ng/mL (normal
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