Recent clinical trials have suggested that intensive versus standard lipid-lowering therapy provides for additional benefit. Electron-beam computed tomography provides the opportunity to quantify the progression of coronary artery calcification (CAC) in serial measurements.In a multicenter, randomized, double-blind trial, 471 patients (age 61+/-8 years) who had no history of coronary artery disease and no evidence of high-grade coronary stenoses (>50% diameter reduction) were randomized if they had > or =2 cardiovascular risk factors and moderate calcified coronary atherosclerosis as evidenced by a CAC score > or =30. Patients were assigned to receive 80 mg or 10 mg of atorvastatin per day over 12 months. Progression of CAC volume scores could be analyzed in 366 patients. After pretreatment with 10 mg of atorvastatin for 4 weeks, 12 months of study medication reduced LDL cholesterol from 106+/-22 to 87+/-33 mg/dL in the group randomized to receive 80 mg of atorvastatin (P<0.001), whereas levels remained stable in the group randomized to receive 10 mg (108+/-23 at baseline, 109+/-28 mg/dL at the end of the study, P=NS). The mean progression of CAC volume scores, corrected for the baseline CAC volume score, was 27% (95% CI 20.8% to 33.1%) in the 80-mg atorvastatin group and 25% (95% CI 19.1% to 30.8%) in the 10-mg atorvastatin group (P=0.65). CAC progression showed no relationship with on-treatment LDL cholesterol levels.We did not observe a relationship between on-treatment LDL cholesterol levels and the progression of calcified coronary atherosclerosis. Over a period of 12 months, intensive atorvastatin therapy was unable to attenuate CAC progression compared with standard atorvastatin therapy. The possibility remains that the time window was too short to demonstrate an effect.
Despite the decrease in overall mortality from coronary artery disease, the number of out-ofhospital deaths from myocardial infarction is in the range of 60% of all infarct related case fatalities. 1 In patients with known risk of sudden cardiac death (SCD), such as survived resuscitation, left ventricular aneurysm or low left ventricular ejection fraction, the incidence of SCD is in the region of 30% per year.In the general population, it is only 0.5% per year. 2 However, the absolute number in this group is 10 times higher than in the patient population with known SCD risk, reaching more than 300 000 case fatalities per year in the USA. 2 Even renowned cardiologists such as Ronald W Campbell w1 and Jeffry M Isner w2 , who were experts on the topic of arrhythmias and myocardial infarction, suffered SCD.The MONICA (Monitoring trends and determinants in Cardiovascular disease) study reported that of all coronary heart disease (CHD) patients who die within 28 days after onset of chest pain, two thirds die before reaching the hospital.w3 Accordingly, the main task has been to strengthen primary and secondary prevention.w3 This strategy brings about a major challenge: how can we define who is at risk?In 1978, Mason Sones, the father of coronary angiography, asked for ''a way of recognizing these people before they drop dead''.He noted, ''We are still living in a world, where almost one third of the patients die before we are aware that these people were ill or that their lives were in jeopardy''.w4 For identifying people at risk the Framingham risk score, 3 the Prospective Cardiovascular Mu ¨nster (PROCAM) Score, 4 the Systemic Coronary Risk Evaluation (SCORE) of the European Society of Cardiology, 5 as well as other more specific scores like the Reynold's Risk Score for women, w5 have been proposed.In young adults in particular, risk prediction based on such global risk scores provides for only limited prognostic accuracy, as has been analysed in patients with myocardial infarction under the age of 55 years.w6 Indeed, improved risk prediction may be obtained by detecting signs of subclinical atherosclerosis.The Third National Cholesterol Education Program Adult Treatment Program (NCEP ATP III) as well as the Third Joint Task Force of European and other Societies of Cardiovascular Disease Prevention in Clinical Practice (European Society of Cardiology (ESC) guidelines) have suggested the use of additional imaging and non-imaging tests in order to detect signs of subclinical atherosclerosis or inflammation for further risk stratification. 3 5-11w7 w8 CORONARY ARTERY DISEASE RISK ASSESSMENT ALGORITHMS cFor individual risk assessment current recommendations suggest the use of algorithms provided by international and national societies as a first step.The most widely used algorithm is based on the Framingham study and is incorporated into the NCEP ATP III. 6 Recently, an update was provided which used four categories of 10 year absolute event risk. 7c I. High risk: .20% 10 year risk for hard cardiac events (cardiac death or non-fatal myocardial infarction) resulting from CHD (history of myocardial infarction, unstable angina, stable angina, coronary artery revascularisation) or from cardiac risk equivalents (peripheral artery disease, aortic aneurysms, carotid artery disease (transient ischaemic attacks, stroke or .50%carotid stenosis)) or diabetes or >2 major risk factors (smoking, hypertension, hypercholesterolaemia, low high density lipoprotein (HDL cholesterol ,40 mg/dl, 1.0 mmol/l), family history of premature CHD (men ,55 years, women ,65 years)) with 10 year risk .20%.c II. Moderately high risk (also called ''intermediate risk''): >2 major risk factors with 10-20% 10 year risk for hard cardiac events.c III. Moderate risk: >2 major risk factors with ,10% 10 year risk of hard cardiac events.c IV. Lower risk: no or 1 risk factor (usually ,10% risk of hard cardiac events).An ESC task force has developed the SCORE risk model, 12 which estimates the 10 year risk of a cardiovascular death based on age, sex, blood pressure, cholesterol, and smoking.The cut off value c Follow up data in Germany demonstrate a constant decrease of cardiac mortality, but still 60% of all acute myocardial infarction related deaths occur out of the hospital.2
A 51-year-old woman, presenting with increasing dyspnoea on exertion was admitted for surgery of a right sided partial anomalous pulmonary venous return. Contrast enhanced electron-beam tomography (EBT) presented a hypoplastic right lower lobe and confirmed the diagnosis of a so-called scimitar syndrome. Surgery consisted of creation of an atrial septal defect, transposition of the anomalous vein and reocclusion of the artificial septal defect with a Dacron patch. One year after surgery, the patient's physical strength increased to a normal level without dyspnoea, while three-dimensional imaging reconstructed from EBT demonstrated an intact operative situs.
