Current guidelines for venous thromboembolism (VTE) primary prophylaxis are based on randomized clinical trials that exclude subjects at a potentially high bleeding risk. Thus no specific recommendation/algorithm for pharmacological prophylaxis in patients with thrombocytopenia and/or platelet dysfunction is available. Because at least 25% of subjects admitted to medical departments exhibit these conditions, information on this subject is provided here to optimize their VTE prophylaxis. Low platelet number/function and clotting abnormalities are common in patients with liver cirrhosis. However, these patients have a high incidence of portal and idiopathic venous thromboses, implying that cirrhotic coagulopathy does not protect against thrombosis. At variance with severe thrombocytopenia (< 50,000/mL), mild/moderate thrombocytopenia (> 50,000/mL) should not interfere with VTE prevention decisions. In severe thrombocytopenia, prophylaxis should be considered on an individual basis, however. In patients with antiphospholipid antibodies and thrombocytopenia, a thrombotic tendency is usually associated rather than a bleeding risk. VTE prophylaxis in high-risk conditions is thus suggested in these patients. Except in cases with contraindications to anticoagulation, antithrombotic prophylaxis should be always considered in hospitalized cancer patients with thrombocytopenia, especially in those with hematologic malignancies and multiple VTE risk factors. Aspirin treatment is not as effective as heparins in lowering the risk of VTE. Studies in stroke suggest that thromboprophylaxis with heparins is safe in patients with ischemic stroke undergoing aspirin treatment. The need for VTE prophylaxis in patients on chronic treatment with aspirin and/or clopidogrel should be evaluated after assessing the individual risk-benefit ratio.

The pathogenesis and treatment of retinal vein occlusions (RVO) are largely unclear. Prevalence of cardiovascular risk factors and of thrombophilic abnormalities was evaluated in 117 patients (61 M, 56 F; mean age 51 +/- 13 years) with a history of RVO (62 central, CRVO; 48 branch, BRVO; 7 both) and in 202 age- and sex-matched control subjects. Cardiovascular outcome after a mean 8.2 year follow-up was recorded for 90 patients. Arterial hypertension was significantly more frequent in patients than in controls (64.9 vs. 28.2%; adjusted OR 4.5 95% CI 2.4-7.9; P < 0.0001), as well diabetes mellitus (17.9 vs. 7.9%; P < 0.05). Antithrombin, Protein C, Protein S and homocysteine levels, lupus anticoagulant, anticardiolipin antibodies, FV G1691A and prothrombin G20210A polymorphisms were comparable in the two groups, nor were different according to RVO localization or to the age at event. BRVO patients were significantly older (55 +/- 9 vs. 47 +/- 15 years; P = 0.002) and had higher prevalence of diabetes, overweight and hypertension (29.2 vs. 8.1%; 83.3 vs. 58.1%, 79.2 vs. 56.5%; P always <0.05). In 58/90 (64%) patients for whom clinical follow-up was available, new vascular events were recorded (coronary/cerebral, n = 38); only 22 patients (24%) received long-term antiplatelet agents (mostly aspirin 100 mg/d), with lower, but not statistically significant, prevalence of overall vascular recurrence (45.4 vs. 70.6%, P = 0.06). High rate of vascular recurrence is shown in patients with previous RVO, in which conventional cardiovascular risk factors play a major role, especially in BRVO and in older patients.

Summary. The public health burden of air pollution has been increasingly recognized over the last decades. Following the first assessed adverse effects on respiratory diseases and lung cancer, a large body of epidemiologic and clinical studies definitely documented an even stronger association of air pollution exposure with cardiovascular mortality and morbidity, particularly related to atherothrombotic (coronary and cerebrovascular) disease. Particulate matter (PM), mainly that with lower aerodynamic diameter (fine and ultrafine PM), is responsible for the most severe effects, due to its capacity to transport toxic substances deep into the lower airways. These effects have been shown to occur not only after short-term exposure to elevated concentrations of pollutants, but even after long-term relatively low levels of exposure. Vulnerable subjects (elderly persons and those with preexisting cardiopulmonary diseases) show the highest impact. Fewer and conflicting data also suggest an association with venous thromboembolism. Although not completely elucidated, a series of mechanisms have been hypothesized and tested in experimental settings. These phenomena, including vasomotor and cardiac autonomic dysfunction, hemostatic unbalance, oxidative stress and inflammatory response, have been shown to change over time and differently contribute to the short-term and long-term adverse effects of pollution exposure. Beyond environmental health policies, crucial for improving air quality and reducing the impact of such an elusive threat to public health, the recognition and assessment of the individual risk, together with specific advice, should be routinely implemented in the strategies of primary and secondary cardiovascular prevention.

Platelets play a central role in the pathophysiology of atherothrombosis, an inappropriate platelet activation leading to acute ischemic complications (acute myocardial infarction, ischemic stroke). In view of this, platelets are a major target for pharmacotherapy. Presently, the main classes of antiplatelet agents approved for the use in such complications are aspirin and fhienopyridines. Although antiplatelet treatment with these two types of drugs, alone or in combination, leads to a significant reduction of non-fatal myocardial infarction (−32%), non-fatal stroke (−25%), and of cardiovascular death (−17%), a residual risk persists.Newer antiplatelet agents have addressed some, but not all, these limitations. Vis-à-vis their net clinical benefit, the higher potency of some of them is associated with a rise in bleeding complications. Moreover, newer fhienopyridines do not show advantages over and above the older ones as to reduction of stroke. A concerted effort that takes into consideration clinical, genetic, and laboratory information is increasingly recognized as a major direction to be pursued in the area. The well-established road signs of clinical epidemiology will provide major information to define newer potentially useful targets for platelet pharmacology.