[Myocardial and cerebral infarction as initial presentation of antiphospholipid syndrome]. / Infarto miocardico e cerebrale come presentazione iniziale di una sindrome da anticorpi antifosfolipidi.

The antiphospholipid antibody syndrome is the most common acquired thrombophilia; it is a systemic autoimmune disease characterized by recurrent arterial and venous thrombosis and/or pregnancy loss, in association with circulating antiphospholipid antibodies. The pathogenic mechanisms in antiphospholipid antibody syndrome that lead to in vivo injury are incompletely understood. Like other autoimmune diseases, a combination of genetic and environmental factors is involved. We report the case of a 50-year-old woman suffering from an antero-lateral non-ST-elevation myocardial infarction. After few days, coronary angiography showed a severe occlusive arterial disease, involving anterior descending, circumflex e right coronary arteries. Percutaneous coronary intervention was performed with the implantation of a drug-eluting stent in the proximal segment of the anterior descending coronary artery. One day after discharge (10 days after the first hospitalization) the patient experienced dizziness, nausea, vomiting, swelling in absence of any electrocardiographic abnormalities or myocardial enzyme elevation; then she was hospitalized in the neurology department. Because of a similar episode, urgent cerebral computed tomography scan was performed 5 days later; it revealed two different acute ischemic areas, parietal in the right hemisphere and cerebellar in the left hemisphere. The diagnosis of antiphospholipid antibody syndrome was confirmed by high anticardiolipin antibody titers, also present in medium titer at 5 and 17 weeks apart. She was discharged without any sequelae, on warfarin and double antiplatelet therapy (aspirin and clopidogrel for 6 months), then warfarin and aspirin.

C-reactive protein: interaction with the vascular endothelium and possible role in human atherosclerosis.

C-reactive protein (CRP) is the first acute phase protein that has been described in the literature. It is phylogenetically ancient and - with serum amyloid P - belongs to proteins named as "pentraxin". After being considered a marker of acute inflammation for several decades and fruitfully used in clinical practice, CRP has been recently considered as a potential contributor to inflammatory diseases including atherosclerosis as well as a marker of cardiovascular risk. With regard to the first topic, inflammation is now believed to represent the underlying mechanism leading to the formation of human atheroma and favouring both the destabilization of vulnerable plaques and the formation of occlusive thrombi. In this regard, numerous studies indicated that modest changes in circulating CRP levels, as detected by highly sensitive methods, can be extremely useful in predicting cardiovascular and perhaps cerebrovascular diseases in apparently healthy individuals as well as in patients affected by atherosclerosis. Subjects manifesting with identical low density cholesterol and/or blood pressure levels have different rates of cardiovascular accidents on the basis of different circulating CRP concentrations. In addition, women with identical cardiovascular risk profiles developed more type 2 diabetes in the presence of higher circulating CRP levels and thereby are expected to display divergent cardiovascular prognosis. Therefore, even slight changes in circulating CRP concentrations - assuming that blood is collected appropriately and CRP is measured with correct methods - could help clinicians in defining individual cardiovascular risk. In this review, we have firstly described the current understanding of the structure of CRP, its function, and interaction with the vascular endothelial cell. Then, we have discussed how to measure circulating CRP and the more recent findings on the suggested role of circulating CRP as a novel cardiovascular risk factor.