ABSTRACT
Paradoxical coronary artery embolism is a rare but under-diagnosed cause of acute myocardial infarction (AMI) and requires a high level of clinical suspicion to make an early diagnosis. We describe the case of a young woman who presented with a severe cough and chest pain who was subsequently found to have a paradoxical embolus in the right coronary artery. Echocardiography showed a patent foramen ovale (PFO) and an atrial septal aneurysm (ASA). The patient was found to be a heterozygous carrier of the factor V Leiden mutation that increases the risk for venous-thromboembolism. The association between a PFO and an ASA is a risk factor for systemic embolisation. This is the first reported case of paradoxical coronary artery embolus causing AMI in a non-pregnant patient with factor Leiden thrombophilia. Identification of this clinical phenotype is vital as the risk of future embolic events can be reduced by anticoagulation and closure of anatomical cardiac defects.
Subject(s)
Coronary Artery Disease/complications , Embolism, Paradoxical/complications , Factor V/genetics , Foramen Ovale, Patent/complications , Heart Aneurysm/complications , Myocardial Infarction/etiology , Thrombophilia/complications , Acute Disease , Adult , Coronary Artery Disease/diagnostic imaging , Coronary Artery Disease/genetics , Echocardiography , Embolism, Paradoxical/diagnostic imaging , Embolism, Paradoxical/genetics , Female , Foramen Ovale, Patent/diagnostic imaging , Heart Aneurysm/diagnostic imaging , Heart Septal Defects, Atrial/complications , Heart Septal Defects, Atrial/diagnostic imaging , Heterozygote , Humans , Mutation , Myocardial Infarction/diagnostic imaging , Myocardial Infarction/genetics , Phenotype , Thrombophilia/diagnostic imaging , Thrombophilia/genetics , Venous Thromboembolism/etiology , Venous Thromboembolism/geneticsABSTRACT
AIM: In diabetes, endothelial dysfunction and an altered retinal blood flow have been reported and precede overt macrovascular and microvascular disease. Furthermore, an association between postprandial hyperglycaemia, retinopathy and cardiovascular disease has been observed. METHODS: Endothelial function and retinal vascular reactivity have been measured in baseline conditions in 10 healthy control subjects and 21 patients with Type 2 diabetes. In the patients with Type 2 diabetes, endothelial function and retinal vascular reactivity have been also measured every hour, for 4 h, during an oral glucose tolerance test. Endothelial function has been evaluated by measuring flow-mediated vasodilation of the brachial artery, while retinal vascular reactivity has been measured using a retinal vessel analyser, during a flicker. RESULTS: At 1 and 2 h after glucose ingestion, endothelial function decreased (P<0.05), while retinal vascular reactivity increased, even at 3 h (P<0.05), vs. the baseline values. CONCLUSION: Our data highlight that acute hyperglycaemia impacts on endothelial function simultaneously at both macrovascular and at microvascular levels, inducing functional change, which could contribute towards explaining the clinical evidence of a strong association between postprandial hyperglycaemia, cardiovascular disease and retinopathy.
