Rationale:Acute ST-segment elevation myocardial infarction (STEMI) is a rare complication of acute ischemic stroke (AIS) during thrombolytic therapy. We report a case of STEMI occurring 40 minutes after thrombolytic therapy for AIS and discuss the possible mechanisms and therapeutic approaches.Patient concerns:A 87-year-old woman with a history of arterial hypertension was admitted for acute onset of right-sided limb weakness 2 hours before arrival at the emergency department. Forty minutes after intravenous recombinant tissue plasminogen activator (i.v. rtPA) administration for AIS, STEMI occurred (signaled by a third-degree atrioventricular block).Diagnoses:The diagnoses were AIS and STEMI. Coronary angiography confirmed right coronary artery occlusion.Interventions:Four hours after the onset of STEMI, stenting was performed, normalizing the coronary blood flow.Outcomes:The patient died 2 days thereafter because of persistent cardiogenic shock.Lessons:Our case is remarkable owing to the unusually early (<1 hour) occurrence of STEMI after i.v. rtPA administration. A third-degree atrioventricular block after thrombolysis for AIS could signal a STEMI onset. New and ongoing trials are assessing whether adjunct administration of direct thrombin inhibitors of rtPA in the first 24 hours after thrombolysis for AIS can prevent early recurrent ischemic events.

Left main coronary compression syndrome (LMCS) may complicate pulmonary artery aneurysms (PAA), usually developed in the context of pulmonary arterial hypertension (PAH). We report the case of a 51-year-old female patient with an atrial septal defect (unsuitable for device closure) complicated by a PAA generating a 90% left main stenosis. The significant PAH held us back from immediate surgery. After specific dual PAH-targeted therapy (sildenafil and bosentan), the atrial septal defect could be closed with a unidirectional valved patch; the PAAinduced LMCS was treated by reductive arterioplasty. The postoperative course was uneventful. Follow-up showed clinical improvement, but PAH treatment was still needed. After three months, coronary angiography showed only an insignificant residual left main stenosis, proving that reductive pulmonary arterioplasty was effective in treating LMCS. Any PAA requires further evaluation for LMCS, a dangerous but treatable complication. The "treat-repair-treat" strategy and shunt-closure with a unidirectional valved patch can both improve surgical prospects of LMCS with shunt-related PAH.

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