Case presentation: A case of 45 years old male who had coiling for anterior communicating artery aneurysm 6 weeks prior to his death. He was asymptomatic until a week prior to his death. The decedent had a fever and was treated for urinary tract infection with oral cefuroxime. He had a sudden onset of breathlessness and died …show more content…
He had no history of drug abuse and was asymptomatic until he was admitted for subarachnoid haemorrhage due to cerebral aneurysm which was 6 weeks prior to death. He was hospitalised for 14 days and underwent coiling procedure for anterior communicating artery aneurysm. The coiling procedure was uneventful. Urine and blood culture that were taken during the hospital stay were negative. He had no history of hospital admission previously or in between the procedure and death. The deceased had a fever and was treated for urinary tract infection with tablet cefuroxime as outpatient 1 week prior to death. On the day of his death, he had sudden onset of breathlessness and became unresponsive within minutes. Post mortem examination showed no stigmata of infective endocarditis externally. On the internal examination, his heart weighed 410 grams. The aortic valve was dilated with crumbly mobile vegetation on the left aortic cusp measured 1cm x 1cm x 0.8cm (figure 1A). The left aortic cusp was eroded. Vegetation on other cusps was small. There was part of the vegetation occluded the left ostia extended to the left main stem coronary artery which measured 1cm in length (figure 1B). There was no gross evidence of infarction on the myocardium. The left kidney showed scarred surface and poorly demarcated corticomedullary junction. However, the right kidney and urinary …show more content…
According to the multicentre prospective European study, 34.1% of patients developed embolic phenomena of which 62% had cerebral emboli and 49% had splenic emboli. Only about 1% of patients developed coronary emboli.1 So far, only six cases of coronary embolism from Infective endocarditis (IE) resulting in sudden cardiac death secondary to left main stem occlusion have been reported.4 Sudden cardiac death can occur at the early stages of an acute coronary occlusion either due to ventricular arrhythmias, pulseless electrical activity or asystole causing hemodynamic collapse.5 Strong afferent stimuli from the ischaemic myocardium impair arterial baroreflex causing sympathetic hyperactivity resulting in the genesis of life-threatening ventricular tachyarrhythmias and eventually to haemodynamic instability.6 Studies with a human angioplasty model have shown that the outcome also depends on several factors. Although the site of the occlusion is not a significant determinant of the outcome but the severity of a coronary stenosis, adaptation or ischaemic preconditioning, beta-blockade and gender seemed to affect the autonomic reactions and occurrence of complex ventricular arrhythmias.6 Most embolic events occur at the left anterior descending artery which arise from the mitral valve vegetation and from prosthetic valve.7 The prevalence of the left coronary artery occlusion is higher than right coronary due to