The acute coronary syndrome (ACS) is subdivided into ST segment elevation myocardial infarction (STEMI), non-ST segment elevation acute coronary syndrome (NSTE-ACS) and unstable angina pectoris. It poses a particular challenge in terms of diagnostics and treatment, especially in the elderly. Starting with the possibly difficult anamnesis, through the laboratory chemical findings up to special features in the electrocardiogram (ECG), echocardiography and angiography, these patients should be considered in some ways different to the younger population. Because of the mortality and morbidity after ACS, especially in old age, it is important to adhere to evident strategies in diagnostics and treatment and to employ specially trained personnel for people with acute chest pain in order to improve the prognosis and quality of life. A first important step is to provide certified chest pain units which ensure smooth diagnostics and treatment and thus positively influence the clinical decision-making processes.

This review tries to answer the following 15 questions: Is atherosclerosis a systemic or a regional disease? Is atherosclerosis in any particular region focal or diffuse? What is the quantity of atherosclerotic plaques in endarterectomy specimens of the right coronary artery in patients undergoing coronary artery bypass grafting (CABG) compared to that in the right coronary artery in patients with fatal coronary artery disease? How do the units used for measuring arterial narrowing by angiography compare to the units used for measuring arterial narrowing at necropsy? What do atherosclerotic plaques consist of in coronary arteries in patients with fatal coronary disease? What is the quantity of atherosclerotic plaque in bypassed -vs- non-bypassed native coronary arteries in patients dying early (<60 days) or late (>60 days) after coronary artery bypass grafting? What is the frequency of acute coronary lesions and multi-luminal channels at necropsy in patients with unstable angina pectoris, sudden coronary death, and acute myocardial infarction? What is the mechanism of luminal widening by angioplasty in the coronary arteries? What observations suggest that atherosclerotic plaques are the result at least in part of organization of thrombi? Is atherosclerosis a multifactoral or a unifactoral disease? What characteristics distinguish carnivores and herbivores? What are reasonable guidelines for whom to treat with lipid-altering agents? What is the rule of 5 and the rule of 7 in statin therapy? What is the effect of lipid lowering drug therapy on coronary luminal narrowing? What are some requisites for a healthy life?

Background Coronary computed tomography angiography (CCTA) is increasingly used to detect coronary artery disease (CAD), but long-term follow-up studies are still scarce. Purpose To evaluate the prognostic value of CCTA in patients with suspected CAD. Material and Methods A total of 1205 consecutive CCTA patients with chest pain were classified as normal coronary arteries, non-obstructive CAD, or obstructive CAD. The primary outcome was major adverse cardiac event (MACE), defined as a composite outcome including cardiac death, myocardial infarction, unstable angina pectoris, or late revascularization (after >90 days). Results Over 7.5 years follow-up (median = 3.1 years), Kaplan-Meier estimates demonstrated a MACE in 1.0%, 4.6%, and 20.7% in normal coronary arteries, non-obstructive CAD, and obstructive CAD, respectively. Log rank test for pairwise comparisons showed significant differences between non-obstructive CAD and normal coronary arteries ( P = 0.023) and between obstructive CAD and normal coronary arteries ( P < 0.001). In a multivariable analysis, adjusting for classical risk factors, non-obstructive CAD and obstructive CAD were independent predictors of MACE, with hazard ratios (HR) of 3.22 ( P = 0.041) and 25.18 ( P < 0.001), respectively. Conclusion Patients with normal coronary arteries have excellent long-term prognosis, but the risk for MACE increases with non-obstructive and obstructive CAD. Both non-obstructive and obstructive CAD are independently associated with future ischemic events.