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The differential diagnosis of coronary embolism, acknowledged to be relevant to the aetiopathogenesis of myocardial infarction in the young,1 would be incomplete without mention of paradoxical coronary embolism, especially in the context of a diagnosis of nephrotic syndrome. As the authors themselves pointed out, severe hypoalbuminaemia is a risk factor for venous thrombosis, and the latter may, in turn, be complicated by embolic manifestations involving either the pulmonary or the systemic vascular bed. The latter, aptly entitled “paradoxical” embolism, may be more difficult to recognise when it occurs in the absence of concurrent pulmonary embolism, as in the 66 year old with patent foramen ovale, reported by Wiecking in 1971.2 In the 24 year old reported by Jungbluth et al, the communication between the cardiac chambers was an atrial septal defect.3 According to the literature review undertaken by these authors, it is the association of pulmonary embolism (giving rise to an increase in right atrial pressure), and an interatrial communication which most commonly provides the pathophysiological “substrate” for this syndrome.3 Diagnostic difficulty may, however, be compounded by the fact that, even in the presence of clinically overt deep vein thrombosis, pulmonary embolism may, itself, be subclinical,4 with the possibility that the only clinically manifest embolic episode may be the one involving the coronary circulation.
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