Sumatriptan
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Sumatriptan Coronary artery vasospasm induced acute myocardial infraction: case report
A 55-year-old man developed coronary artery vasospasm induced acute myocardial infarctions (AMI) during treatment with sumatriptan for headache [times to reactions onsets not stated]. The man presented to the emergency department with a dull aching pain around the epigastrium and lower sternal areas. He had a medical history of hiatus hernia, 2 previous deep venous thrombosis, migraine headaches and asthma. He developed a headache around 04:00, and he took two oral sumatriptan 50mg tablets before going to sleep. He woke up around 06:30 with the dull chest ache, which described as an ’internal pressure’. It ranked as a 2/10 in terms of pain severity. Later, the pain radiated to his left hand and wrist. There was associated diaphoresis. His pain lasted 30 minutes. He was apyrexial, and his vitals signs showed the following: BP 145/105mm Hg, respiratory rate 17 breaths per minute, pulse rated 72 beats per minute, oxygen saturation 98% on room air. The troponin-I levels were increased at 245 ng/L. Repeat troponin-I levels were markedly elevated at 2666 ng/L. Laboratory investigations showed the following: D-dimer levels less than 150 ng/mL., random glucose 5.7 mmol/L, total cholesterol 5.50 and triglyceride 1.60 [units not stated]. An ECG was largely unremarkable except small drug reactions T-wave inversions in V4–V6. Following these investigation, he was thought to have a non-ST elevated myocardial infarctions. Subsequently, he was transferred to the coronary care unit. A repeat ECG was conducted 2 hours following the admission, and it demonstrated deepening T-waves across V2–V5. From day 2 onwards following his admission, the ECG reveled further prominent T-wave inversions in leads I, II, III, aVL and aVF. During day 3, an echocardiogram demonstrated that the basal-inferior and infero-lateral wall segments were hypokinetic, and the left ventricular systolic function was not impaired. The man received glyceryl trinitrate. A coronary angiography on the same day showed a dominant right coronary artery. Further, it was noted that his AMI was a result of coronary vasospasm secondary to sumatriptan. After the presentation, when the troponin-I levels and ECG changes were known, he was treated with unspecified dual antiplatelet therapy (DAPT) and fondaparinux sodium [fondaparinux]. Once his cause of the AMI was known following the angiography, he started on unspecified DAPT, unspecified ACE inhibitors and unspecified beta-blockers for 6 months. He was reviewed in the cardiology clinic 4 months later. A repeat echocardiogram demonstrated good left ventricular systolic function. There were no regional wall motion abnormalities. A repeat ECG reveled a sinus rhythm with a first degree atrioventricular block. T-wave inversions in lead III was noted. Subsequently, aspirin was stopped; as he reported dyspepsia. He was continued on rivaroxaban and later, discharged. Okonkwo K, et al. Vasospasm induced myocardial ischaemia secondary to sumatr
