Ms Christina Basso
The 2011 ESC symposium “How to prevent sudden coronary death in the young” has been organized in collaboration with the Association for European Cardiovascular Pathology (AECVP). The main aim was to address the prevalence and types of coronary artery disease (CAD) as identified at autopsy in sudden cardiac death cases occurring at young age (<40 yrs) in order to identify possible diagnostic and therapeutic algorithms for sudden death prevention. Allard van der Wal (AMC, Amsterdam, NL) focused the attention on premature atherosclerosis which is the main cause of sudden death in people aged less than 40 yrs. According to preliminary data coming from a national survey in the Netherlands, about 25% of sudden death in this age group are due to atherosclerotic CAD. Atherosclerotic CAD frequently consists of a single vessel stenosis due to intimal proliferation. When complicated by thrombosis, superficial erosion appears to be the main pathophysiologic mechanism of plaque instability of sudden death young victims. Cocaine and smoking have been identified as the main exogen risk factors, besides familial predisposition and dyslipidemia. Mary Sheppard (Brompton Hospital, London UK) underlined the existence of rare acquired non-atherosclerotic CAD, that can be at risk of myocardial ischemia and life-threatening arrhythmias particularly at young age. Among them, besides arthritis, embolism and vasospasm, the most challenging remains spontaneous coronary artery dissection, both from the pathogenetic viewpoint and from the diagnostic perspective. Hormonal factors should be involved since the disease is almost exclusively targeting women, often in the peripartum or taking oral contraceptives. Cristina Basso (University of Padua, Padua, Italy) then presented the congenital anomalies of the coronary arteries that can be at risk of SD. Among them, she focused the attention on wrong sinus coronary artery anomalies (LCA from right sinus, RCA from left sinus), which predispose to myocardial ischemia particularly during effort. The negativity of provocative tests such as stress test ECG and scintigraphy in many cases suggests the need of a high index of suspicion when dealing with people presenting with alarming symptoms, particularly during effort. The exclusion of an anomalous origin of the coronary arteries by imaging tools is thus warranted in subjects presenting with effort angina or syncope, even though the 12 lead and stress test ECG are normal. More intriguing is the decision tree when an anomalous coronary artery is found in an individual without any symptom or sign of myocardial ischemia. After the 3 “pathology” lectures, Paul Erne (Luzerner Kantonsspital, Swiss) addressed the main clinical issues, i.e. how to detect these life-threatening acquired and congenital CADs and how to prevent sudden death when CAD is diagnosed in asymptomatic patients. He stressed that, while screening for CAD at risk is not affordable in the general population, for cost implication and the problems of both false positive and false negative results, it can be applied in selected population at higher risk, such as people involved in intense physical activity and those with positive family history. Besides the screening for CAD (either indirect, such as ECG, stress test, myocardial scintigraphy or direct, such as angiography, CMR and CT in selected cases with alarming symptoms or signs), blood cholesterol levels as well as life-style modification (smoking, cocaine, etc) should be pursued for primary prevention in these high risk population subgroups.
How to prevent sudden coronary death in the young
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