The common functional HERG variant 897T may predispose to the development of aldosteronoma.
Several studies have established that increased intimal-media thickness (IMT) is strongly related to coronary artery disease, ischemic stroke, peripheral vascular disease, and hypertension. The formation of neointimal lesions modifies vessel wall geometry, intramural elasticity, areas of the lumen, and viability, and plays a critical role for a transition from quiescent state to proliferating phenotype; it involves vascular smooth muscle cells (VSMC) and the associated proteolytic system (serine and cysteine proteinase, catepsin, MMP-2 and MPP-9), VEGF, PDGF and fibroblastic growth factor. We used B-mode ultrasonography to quantify early atherosclerotic vessels wall change, IMT of the carotid artery (CIMT) ranged from 0.48 mm to 1.82 mm, and of the femoral artery (FIMT) ranged from 0.44 mm to 3.48 mm; intramural elasticity ranged from 7 to 125 KPa in normal subject. Wall shear stress was 26.38 +/− 7.34 dyne/cmq in individual without atherosclerosis, and 14.36 +/− 6.36 dyne/cmq in those with atherosclerosis, PWv (pulse wave velocity) were respectively 8.6 +/− 1.8 m/sec., and 7.8 +/− 1.6m/sec., IMT and peak shear stress were inversely correlated. High expression of IMT (>2.24 mm by the carotid artery and > 3.86 mm by the femoral artery) showed a tight correlation of VEGF levels 148.38 +/− 64.30 pg/ml, and an increased inflammatory biomarkers of atherosclerosis like CRP 9.8 +/− 3.6mg/l, and CD40L 5.4 +/− 2.2mg/l dangerous co-workers of thrombotic damage. We have studied 64 patients (aged from 54 to 68) Patients (32) Control (32) CIMT > 2.24 from 0.48 to 1.82 mm FIMT > 3.86 from 0.44 to 3.48mm VEGF 148.38 +/− 64.30pg/ml 84.36 +/− 24.58pg/ml CRP 9.8 +/− 3.6mg/l <2.8 +/− 0.4mg/l CD40L 5.4 +/− 2..2mg/l 2.2 +/− 0.8mg/l The degree of IMT, the plaque morphology, and the levels of inflammatory markers showed a direct relationship in atherosclerosis being significantly correlated with thrombotic risk. Among our 32 patients with high degree of IMT: 18 patients with high expression of CIMT from 2.24 to 3.22 have CAD compared with 2 controls (p<0.0001); 8 patients of CIMT from 2.24 to 3.48 have ischemic stroke compared with 1 control (p<0.0001); 6 patients with FIMT from 3.86 to 4.28 have PAD compared with 1 control (p<0.0001). The level of CRP plays a key role in CAD, as it increases the risk of CAD by 30% over 5 years; the cut points of high risk is >3.5 mg/l and could be enhanced IMT, the CRP increased IMT to 3.5 by 9.5% in carotid plaque and change plaque component. The high level of CD40L > 3.2 mg/l is intimately linked with a strong risk of CAD >24% and ischemic stroke >18% within 12–16 month. Although our present study is limited it shows a clear difference between the groups studied an demonstrated a strong evidence of direct endothelial cells damage and abnormal plasma levels of inflammatory markers as predictors of adverse outcome, IMT is a measure of the degree of atheroma progression, reflects generalized disease and predicts strokes, PAD, and myocardial infarction, although the relationship to disease severity is still subject to debate.
4185 Aggressive antithrombotic therapy with ASA, thienopyridine, GPIIb/IIIa inhbitors, eparin, and Vit.K antagonist (VKA) is used for unstable angina (UA), myocardial infarction (NSTEMI), acute coronary syndrome (ACS), stent implantation, atrial fibrillation (AF),VTE. The main findings of combination of antithrombotic drugs are their association with serious bleeding not withstanding some respectable benefit, and a great effects against thrombosis. At present the preferred approach for the long term treatment is VKA the dose should be adjusted to maintain a target INR of 2.5 (range: 2.0 to 3.0), the controversy focused in a patients with a high risk of recurrence a high intensity VKA therapy (INR: 3.1 to 4.0) although did not confirm a superiority in terms of thrombotic protection, new opportunities have emerged in the treatment of arterial thrombosis with the combinations of antithrombotic drugs (ASA 325mg every days, plus thienopyridine: ticlopidine 250mg orally twice a day, or clopidogrel / GPIIb-IIIa antagonist/ anticoagulant: VKA, LMWH, fondaparinux) with a significant inhibition of thrombosis but always a remarkable and unacceptable bleeding risk, and a narrow safety window. Question: what are the very primary strong end points (death, PE or symptomatic VTE, Myocardial infarction or stroke, recurrence!), or are the inhibition of platelet functions, of signalling pathways, of atherosclerotic process monitoring. Several trials have evaluated the role of long term anticoagulation therapy, and a high intensity anticoagulation and combination therapy with a marvel issue (by 32% to 48% reduction of the risk of relapse) but a burdensome toll of side effects (bleeding by 4.8% to 8.2%). We have studied 118 patients with a tailored therapy and individual strategies selecting the disease and comorbility, the dose, the timing, the manner, the potential validity and the variance of individual responses with a significant reduction of side effects (bleeding by 0.8% to 2.4%), and a preserved therapeutic benefit (by 34% to 44% reduction of the risk of relapse). Answers: the optimal management of antithrombotic therapy is the reduction of side events, and the mainstay of treatment is to maintain patency of the vessels, but it's not so easy, certainly the main road is to have a drug made to be measured. Disclosures: No relevant conflicts of interest to declare.
Schoenlein Henoch Purpura (SHP) may show a cohort of symptoms such as: a palpable purpuric rash where lesions may be prominent mostly on lower extremities, abdominal pain, arthritis and nephritis. It is an inflammatory disorder characterized by an IgA-mediated vasculitis with immune complexes deposition in smaller veins, capillaries and arterioles which often occur as a response to infections (mycoplasma, streptococcus group A, Campylobacter enteritis, Helycobacter, Herpes virus, Parvovirus B19, Epstein-Barr virus), or to an exposure to allergens, drugs, some particular food, cold, or even insect bites. Symptoms are often dramatic at the onset, and the exitus occurs sadly between 30 – 50% of the patients, despite the therapeutic support, for this reason the diagnosis and the therapy should be precocious. Clinically we can observe multi organ failure, hypotension, flushing, capillary leak haemorrhage secondary to thrombocytopenia, platelet dysfunction, disseminated intravascular coagulation, shock. We have studied a young boy (19 years old) with an urticarial wheals, erythematous maculo-papules, purple spots, and larger petechiae, migrant arthritis and arthralgia, renal disease (low grade hematuria with proteinuria), weakness, necrotic and hemorrhagic plaques, with haematemesis, diarrhoea, abdominal pain, fever (38.5°/39.5° C), and increased blood level of human Parvovirus-B19 NS1-gene component. We performed a skin biopsy of SHP that showed: leukocytoclastic vasculitis, with angiocentric neutrophilic infiltrate, fibrin deposition and focal fibrinoid necrosis. We also evaluated a kidney biopsy which showed: mild increase of mesangial cellularity, with segmental capillary luminal leukocytes and scattered capillary wall fuchsinophilic deposit, while the diagnostic finding is constituted by granular mesangial IgA with C3. The management is based on support therapy, with plenty of haemotrasfusions, and immunosuppressive therapy (prednisone 40 mg os/die, and cyclophosphamide100–200 mg/daily/os for 30–60 days (may decrease inflammation, capillary permeability and suppressing granulocytes activity and migration. The prognosis is usually excellent when the syndrome is self-limited and resolves spontaneously often 4/8 weeks without recurrence. Sometimes the diagnostic investigation may show an elevated level of vascular IgA deposition (direct immunofluorescence), elevated plasma levels of C3 and C4, elevated levels of IgA, ANCA (antineutrophil cytoplasmic antibodies: pANCA anti-MPO, cANCA anti-PR3), CRP, fibrinogen, ICAM-1, and increase of TNF, IL-1, IL-6, TGF-beta that reflect endothelial cell damage and dysfunction.
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