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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Uwe Nixdorff,
What is SHAPE? Why do we need to SHAPE up primary prevention? Professor Nixdorff comments on the Satellite Symposium organised by SHAPE during EuroPRevent 2011 in Geneva, Switzerland.
Dr Naghavi, Houston, USA, having inaugurated SHAPE (Society for Heart Attack Prevention and Eradication) introduced this symposium. As chairperson he introduced the first speaker; Dr Falk, Aarhus, Denmark, who explained SHAPE to the auditorium. The key issue is screening for disease, i.e. subclinical athero-sclerosis rather than just for risk factors. The provocative statement is “Do not rely on cholesterol” which was argued by presenting overlapping graphs of different cholesterol levels in patients with vs patients without coronary events. The well-known American Journal of Cardiology (AJC) papers from 2006 transferring the concerns of vulnerable plaque to vulnerable patient (published in 3 parts) as well as 'The 1st SHAPE Guideline' were quoted. Also, the 'Copenhagen City Heart Study' underlines the only weak predictive power of cholesterol, blood pressure and smoking, even if age- and sex-adjusted. Moreover, newer emerging risk factors as highly sensitive C Reactive Protein (CRP) misclassified hard events in > 75% in a work by Ridker (JAMA 2007) and even > 90% in the World Health Survey (WHS). The well-known scores (namely Framingham and ESC SCORE) only give information on risk exposure, but susceptibility is missed. Disease results from exposed risk factors and susceptibility. Thus, the 2010 American College of Cardiology Foundation / American Heart Association (ACCF/AHA) guideline for assessing cardiovascular risk in asymptomatic adults consented evidence classes IIa for carotid intimal medial thickness (CIMT), ankle brachial indices (ABI), as well as coronary artery calcium (CAC). An actual Lancet paper (online 28 March 2011) published by the speaker concludes that preventive measures should “target Rx to those who need it”. Dr Erbel, Essen, Germany, who is the principal investigator of the recently published Heinz Nixdorf Recall (HNR) trial, gave a short overview of this prospective study looking for predictive powers of functional and imaging diagnostic modalities in assumed healthy individuals. CAC evaluated by electron beam computed tomography significantly discriminated coronary risk similar to data by Greenland 2007, the Multi-Ethnic Study of Atherosclerosis (MESA) trial, and the Rotterdam group. Actually, additional value of new biomarkers have to convince by so called net reclassification improvement (NRI) that was 30,6% (p = 0.0004) in the HNR trial in comparison to solely Framingham risk score (FRS). Erbel underlined the significance of findings remembering that actually 60 – 80% of fatal MI happen outside the hospital. He dedicated his lecture to two well reputed European cardiologists having died suddenly of heart attack, Professor Philip Poole Wilson at his office and Professor Helmut Drexler at cycling. Dr Sillesen, Copenhagen, Denmark, again insisted on the aspect of susceptibility, this time in respect of intimal medial thickness (IMT). The prediction of future events is well established; he quoted the CAPS study, further the meta-analysis by Lorenz (European Heart Journal [EHJ] 2010). However, the hazard ratio (HR) of 1.5 – 2.0 is just fair. Also, he mentioned the population-based data information that may be more limited in specific individual assessments and he talked about the methodological problem of scanning which may produce relevant variability. In the Atherosclerosis Risk in Communities (ARIC) trial 23% of patients have been reclassified. The detection of circumscript plaque formation further enhances prediction. Plaques in comparison to CAC do better in prediction, IMT worse. The future will be 3D plaque volumetry. Dr Möhlenkamp, Essen, Germany (working group of Erbel) talked about peripheral artery disease (PAD), a subject often not recognized in systemic atherosclerosis detection. According Criqui there is survival discrimination by Kaplan-Meier curves worsening from no PAD, asymptomatic PAD, and symptomatic PAD to severe symptomatic PAD. The prevalence rate ratio (PRR) within a variety of 10 risk implying parameters (body mass index, age, hypertension a.s.o.) was highest for PAD in men and women (Erbel, Atherosclerosis 2007). Of course, the GetABI (German epidemiological trial on Ankle Brachial Index) was quoted; however, besides principal predictive potential symptomatology did not turn out as a discriminator. PAD is a marker disease as patients do not die from it but from cardiac events. Reasonably, the speaker concluded that PAD for improving risk stratification has finally not been established. In summary, the SHAPE symposium was highly interesting as very well attended due to fast technical medical development data increases showing the valid possibility to directly screen for preclinical atherosclerosis in still asymptomatic individuals. Notably, the 2010 ACCF/AHA guideline for assessing cardiovascular risk in asymptomatic adults already met those concerns. However, the post symposium interview with selected attendees also discerned some skepticism as besides increasing evidence, the lacking reimbursement regulation of such pre-clinical programs on one hand as well as industry sponsorship on the other actually raises the question of a reasonable sort of implementation.
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