Noninvasive Testing for Diagnosis of Stable Coronary Artery Disease in the Elderly.

Efficient diagnostic approaches to detect coronary artery disease (CAD) in elderly patients are necessary to ensure optimal and timely treatment. The population of suspected CAD patients older than 70 years is especially vulnerable and constantly growing. Finding the optimal diagnostic approach is challenging due to certain features of this population, such as high prevalence of comorbidities, existing contraindications to exercise tests or cognitive decline, which hinders correct assessment of the patient's situation. Moreover, some symptoms of CAD can have variable significance in the elderly compared to younger adult groups. In this review, we present current recommendations of the United States (US) and European cardiologists' associations and discuss their applicability for diagnostics in the elderly population. Exercise electrocardiogram (ECG) and exercise stress echocardiography (SE) tests are not feasible for a substantial proportion of elderly patients. Coronary computed tomography angiography (CTA) appears to be an attractive alternative for such patients, but is not universally applicable; for instance, it is problematic in patients with significant calcification of the vessels. Moreover, more studies are needed to compare the results delivered by CTA to those of other diagnostic methods. Future efforts should be focused on comparative studies to better understand the limits and advantages of different diagnostic methods and their combinations. It is possible that some of the currently used diagnostic criteria could be improved to better accommodate the needs of the elderly population.

Current Position on the Role of Monomeric C-reactive Protein in Vascular Pathology and Atherothrombosis.

C-reactive Protein (CRP) is an acute phase reactant, belonging to the pentraxin family of proteins. Its level rises up to 1000-fold in response to acute inflammation. High sensitivity CRP level is utilized as an independent biomarker of inflammation and cardiovascular disease. The accumulating data suggests that CRP has two distinct forms. It is predominantly produced in the liver in a native pentameric form (nCRP). At sites of local inflammation and tissue injury it may bind to phosphocholine-rich membranes of activated and apoptotic cells and their microparticles, undergoing irreversible dissociation to five monomeric subunits, termed monomeric CRP (mCRP). Through dissociation, CRP deposits into tissues and acquires distinct proinflammatory properties. It activates both classic and alternative complement pathways, binding complement component C1q and factor H. mCRP actively participates in the development of endothelial dysfunction. It activates leukocytes, inducing cytokine release and monocyte recruitment. It may also play a role in the polarization of monocytes and T cells into proinflammatory phenotypes. It may be involved in low-density lipoproteins (LDL) opsonization and uptake by macrophages. mCRP deposits were detected in samples of atherosclerotic lesions from human aorta, carotid, coronary and femoral arteries. mCRP may also induce platelet aggregation and thrombus formation, thus contributing in multiple ways in the development of atherosclerosis and atherothrombosis. In this mini-review, we will provide an insight into the process of conformational rearrangement of nCRP, leading to dissociation, and describe known effects of mCRP. We will provide a rationalization for mCRP involvement in the development of atherosclerosis and atherothrombosis.

Polymorphonuclear blood leukocytes and restenosis after intracoronary implantation of drug-eluting stents.

Peripheral blood contents of osteonectin-positive progenitor cells and polymorphonuclear granulocytes were examined by flow cytometry in 38 patients after myocardial revascularisation with drug-eluting stents. Repeat coronary angiography performed 6-12 months after stent implantation revealed in-stent restenosis in 15 patients and its absence in 23 patients. The plasma levels of osteonectin-positive progenitor cells, neutrophils, and basophils did not differ in patients with and without restenosis. Eosinophil blood levels in patients with and without restenosis were 262+/-68 and 124+/-67 cells/microL (mean+/-SD, p<0.001), respectively. Only one of 19 patients (5%) with eosinophil content lower than the distribution median for the entire group developed restenosis, whereas in the group with eosinophil contents higher than the median (n=19) restenosis occurred in 14 patients (74%, p<0.001). Our findings suggest that the frequency of restenoses after stenting is related to high peripheral blood eosinophil content.