Antiaggregant Treatment Research Articles

SMERNICE ZA PREPREČEVANJE IN ZDRAVLJENJE NEŽELENIH UČINKOV NESTEROIDNIH PROTIVNETNIH IN ANTIAGREGACIJSKIH UČINKOVIN NA PREBAVILA

Adverse effects of nonsteroidal antiinflammatory drugs and antiaggregants on gastrointestinal tract can be prevented or reduced by rational prescribing, use of proton pump inhibitors and Helicobacter pylori eradication.Nonsteroidal antiinflammatory drugs should not be used to treat patients with high risk for serious adverse effects on either upper gastrointestinal or cardiovascular system. Proton pump inhibitors in standard oral dosages are used for treatment of dyspepsia or gastric and duodenal erosions and ulcers, caused by nonsteroidal antiinflammatory drug or antiaggregant use. Peptic ulcer hemorrhage is treated with endoscopic hemostasis and proton pump inhibitors (72-hour continuous infusion followed by 4 – 8 week standard dose oral treatment).Patients can be stratified into three groups based on risk for upper gastrointestinal system adverse effects associated with nonsteroidal antiinflammatory drugs or antiaggregants use. Absence of risk factors denotes low-risk patient population, one or two risk factors are associated with medium risk; high-risk patients harbor either three or more risk factors or history of complicated peptic ulcer disease. Helicobacter pylori should be eradicated (if present) in all medium and high-risk patients prior to introduction of nonsteroidal antiinflammatory drugs or antiaggregants and proton pump inhibitors in standard daily dose should be prescribed for the duration of the treatment.Risk of gastrointestinal hemorrhage should be considered when planning invasive cardiovascular procedures or introduction of antiaggregant or anticoagulant treatment. In the context of acute gastrointestinal hemorrhage, antiaggregants should not be discontinued for longer than 7 days and oral anticoagulant therapy should be stopped and converted to low-molecular-weight heparin after complete hemostasis.

Clopidogrel: A multifaceted affair.

Clopidogrel has been the therapy of choice, combined with aspirin, against platelet aggregation in patients at risk of suffering a vascular thrombotic event. Not all patients respond equally to clopidogrel, an observation that has led to searching for a test that, in the clinical setting, could predict patients' "resistance" to therapy. The evidence reveals a complex pharmacokinetic profile for clopidogrel, with multiple players involved, including cytochromes, characteristics of the target tissue, and accompanying clinical conditions. Despite FDA black box warnings recommending CYP2C19 genotyping before clopidogrel use, no robust evidence indicates that CYP2C19 function determines clinical response to the drug, either based on the presence of loss of function alleles or drug interactions with CYP2C19 inhibitors, like omeprazole. A tailored anti-aggregation treatment based on ex vivo platelet reactivity also seems unlikely due to the lack of robustness of most assays. The identification of clinical conditions that are at higher risk of new cardiovascular events, such as diabetes, obesity, coronary artery disease, or specific stenting procedures, seems to be a prudent approach to tailor anti-platelet therapy with more powerful drugs, accompanied by careful counseling to promote patient compliance.

Dynamic parameters of homeostasis under the influence of antiaggregant treatment in patients with atrial fibrillation and metabolic syndrome

The condition of coagulation and platelet hemostasis in 125 patients with atrial fibrillation (AF) and with metabolic syndrome (MS) has been analysed. Сoagulation and platelet hemostasis in 125 patients with AF and MS under treatment with acetylsalicylic acid (ASA) (group 1), omega-3 polyunsaturated fatty acids (omega-3 PUFAs) (group 2) and ASA with L-arginine (3 group) during 2 months were measured. It was established that omega-3 PUFAs are more effective compared with ASA/aspirin with L-arginine and it promotes normalization of fibrinogen, soluble fibrin-monomer complexes (SFMK), D-dimer and improves the platelet aggregative activity (PAA).

Primary Stenting of TASC C and D Femoropopliteal Lesions: Results of the STELLA Register at 30 Months

The 1-year results of the prospective register STELLA suggested that primary stenting of long femoropopliteal (FP) lesions (≥15-cm) was a sure and effective treatment. However, the long-term results of this technique remain unknown. STELLA is a prospective monocentric register of patients treated for FP lesions ≥15-cm (Trans-Atlantic Inter-Society Consensus [TASC] C and D) by direct stenting (Flexstar(®), Bard). The patients with de novo atheromatous lesions were included between November 2008 and October 2009 when the guidewire had crossed the lesion. Restenoses were excluded. The follow-up was coordinated by a clinical research assistant. Clinical and ultrasound evaluation were carried out every 3months for 12months, then every 6months up to 30months. Restenosis was defined by an index of peak systolic velocity >2.4. Among the 58 patients (62 limbs) included, 40.3% presented an effort ischemia and 59.7% a critical ischemia (CI). The mean age was 71±12years. The lesions were classified as TASC D in 37.1% of the cases. The median length of the stenting was 26±18cm. The average follow-up was 26.1months (1-30). At 30months, a complete follow-up was obtained in 55 patients (58 limbs). The rate of survival was 79.6%. Nine of the 11 patients deceased presented initially with CI. Death was in connection with CI in 2 cases. At the date of latest news, 98.3% of the patients were under antiaggregating treatment, 20% received antivitamin K treatment, 75% received statins, and 75% received angiotensin-converting-enzyme inhibitors. The rates of maintenance of the primary and secondary clinical improvement were 68.6±6.0% and 82.6±5.1% at 12months and 65.1±6.2% and 78.4±5.6% at 30months, respectively. The mean Rutherford index was 4.1±1.0 in preoperative, 0.7±1.2 at 12months, and 0.6±1.1 at 30months (P<0.001). Two major amputations were carried out at 9 and 28months for patients initially with CI. The mean systolic pressure index was 0.6±0.1 in preoperative and 1.0±0.2 at 1-year and 0.9±0.3 at 30months (P<0.001). The rates of primary and secondary patency were 66±6.3% and 80.9±9.5% at 12months and 62.2±6.6% and 77.2±5.9% at 30months, respectively. Between 0 and 12months, 12 (19.3%) intrastent restenosis (ISR) were noted. One ISR was observed after 12months. At the same period, we observed 11 and 1 target lesion revascularization, respectively. In the long run, the primary stenting of long FP lesions (≥15-cm) is a safe and durable treatment. A strong clinical and ultrasound monitoring is indicated during the first year to maintain the clinical improvement.

Vliv antikoagulační a antiagregační terapie na rozsah, vývoj a prognózu akutního kraniocerebrálního poranění

Vliv antikoagulační a antiagregační terapie na rozsah, vývoj a prognózu akutního kraniocerebrálního poranění

Pattern of and risk factors for brain microbleeds in neurodegenerative dementia.

A cross-sectional study was conducted to describe the prevalence, locations, and risk factors for brain microbleeds (BMBs) in neurodegenerative dementia. The database of the Alzheimer Center Reina Sofía Foundation was searched, BMBs were described, and the potential associations of BMBs were investigated using univariate statistics. A total of 148 patients (age 81.6 [standard deviation 6.7], 79.1% female) were studied. Prevalence of BMBs was 44.6%. A group of patients with unusually high (ie, ≥4) number of BMBs were identified, which displayed higher number of vascular risk factors and vascular diseases. Brain microbleeds were also associated with ischemic lesions in the basal ganglia (r = .39), clinical diagnosis of Alzheimer's disease (AD) and cerebrovascular disease (r = .33), cortical infarction (r = .20), and antiaggregant or anticoagulant treatment duration (r = .20). Brain microbleeds are associated with vascular burden and AD diagnosis in old patients with neurodegenerative dementia. More research is warranted regarding the mechanisms and potential clinical implications of these results.

Isolated thrombus-like mass in a patient with multiple myeloma

A 55-year-old man was referred to our clinic to investigate the etiology of transient ischemic attack. He had no structural heart disease, atrial fibrillation, stroke, or renal or liver disease. However, he had been treated with thalidomide (200 mg/day) for three months due to multiple myeloma. He had received no antiaggregant or anticoagulant treatment. His physical examination was unremarkable. The electrocardiogram showed normal sinus rhythm. Routine laboratory tests were within the normal ranges. Both transthoracic (Video 1*) and transesophageal (Video 2*) echocardiographic examination demonstrated a pendulous mass suggesting a thrombus (24x12 mm) attached to the wall of the ascending aorta (Figure). The ascending aorta was not dilated, and no aortic dissection was observed. There was no thrombus-like image in the left atrium or left atrial appendage. Other echocardiographic parameters were also normal. No hereditary causes of atherothrombosis, such as factor V Leiden, prothrombin gene mutations, or antithrombin III, protein C and protein S deficiencies were found in the comprehensive hematologic examination. Therefore, the thrombus-like image in the ascending aorta was thought to possibly be due to an adverse effect of thalidomide. Surgical thrombectomy was recommended, but the patient refused this therapy and was lost to followup. The risk of thromboembolic events is increased in patients with multiple myeloma, especially in those treated with thalidomide-based regimens. Although a few cases of arterial thrombosis have been reported in these patients, a thrombus located in the ascending aorta has not been reported previously. Patients with multiple myeloma receiving thalidomide-based regimens with chemotherapy should receive thromboprophylaxis with either aspirin or low molecular weight heparin for lower-risk patients and low molecular weight heparin for higher-risk patients according to the guidelines of the American Society of Clinical Oncology. 413

ROLE OF GENETIC FACTORS IN THE DEVELOPMENT OF CLOPIDOGREL RESISTANCE AMONG PATIENTS REFERRED FOR PERCUTANEOUS CORONARY INTERVENTIONS

Aim. To study the associations between genetic polymorphisms and the development of clopidogrel resistance in patients referred for percutaneous coronary interventions (PCI).Material and methods. The study included 84 patients with coronary heart disease (CHD), who underwent planned PCI. Dynamic assessment of platelet aggregation was performed using light transmission aggregometry method (two-channel laser analyser Biola-230LA). The role in the development of inadequate suppression of platelet aggregation during the standard-dose dual antiplatelet therapy (DAT) was investigated for the following genes and polymorphic alleles: CYP2C19 (rs4244285*2, rs4986893*3, rs28399504*, rs56337013*5, and rs12248560*17); CYP2C9 (rs1057910*3); CYP3A4 (rs2242480); CYP2B6 (rs3211371 (5*); CYP3A5 (rs28365083*2 and rs776746); and CYP1A2 (rs762551).Results. The two study groups demonstrated a statistically significant difference in the prevalence of CYP2C19 rs4244285 (2*) polymorphisms, with an increase in GA and AA genotypes and a reduction in the “wild” GG genotype (Χ2 =11,7; р=0,003). The GA genotype was associated with inadequate suppression of platelet aggregation in patients receiving clopidogrel (75 mg/d) and aspirin (300 mg/d; odds ratio 6,27; 95% confidence interval 1,8–21,69). No significant inter-group differences were observed for other polymorphisms (CYP2C9 (rs1057910*3); CYP3A4 (rs2242480); CYP2B6 (rs3211371 (5*)); CYP3A5 (rs28365083*2, rs776746); and CYP1A2 (rs762551)).Conclusion. The degree of platelet aggregation in patients on DAT is related to their genetic status. The assessment of genetic polymorphisms can facilitate the choice of optimal therapeutic strategies in clopidogrel-resistant patients. Patients with the CYP2C192* polymorphism are in particular need for an additional correction of the antiaggregant treatment scheme.

Discontinuation of anticoagulation or antiaggregation treatment may be safe in patients with primary antiphospholipid syndrome when antiphospholipid antibodies became persistently negative

Recommended treatment for patients with primary antiphospholipid syndrome (APS) after a thrombotic event is long-term anticoagulation. Few patients with APS and previously positive antiphospholipid antibodies (aPL) may become negative over time. It is still not exactly known how to treat these patients when aPL become persistently negative. We described the follow-up of 11 primary APS patients whose aPL become persistently negative and in whom thromboprophylaxis was discontinued. The primary end-point was the recurrence of thrombosis in patients with previous thrombotic event and a first thrombotic event in women with previous obstetric APS. Ten (90%) patients were female. Seven (64%) patients had a history of deep venous thrombosis, two of them with pulmonary embolism, and four (36%) women had recurrent miscarriage. Lupus anticoagulant (LAC) was the aPL most frequently detected (82%). Two patients had both LAC and IgG anticardiolipin antibodies. No new thrombotic episode was observed after a median follow-up period of 20 months. Anticoagulation or antiaggregation could be discontinued in some peculiar patients with low-risk primary APS whose aPL become persistently negative. However, studies including a larger number of patients are required to confirm these results.

Monitoring of antiaggregation therapy effectivity inpatients with acute stemi: Is it really necessary in clinicalpractice?

Antiaggregation therapy is the keystone of acute ST elevation myocardial infarction (STEMI) drug treatment; but effectivity of this therapy is not always sufficient. The aim of the study was to determine wheather laboratory monitoring of antiaggregation therapy helps to improve the management of patients with acute STEMI. A pilot prospective study in patients with acute STEMI treated with direct percutaneous coronary intervention (dPCI) of culprit lession. Optic aggregometry was chosen to assess the effectivity of antiaggregation treatment. Samples were taken prior to coronarography (sample 1) as well as at first day after diagnostic procedure (sample 2). MACE (in-stent trombosis, heart failure, in hospital death, all cases mortality, ventricular arrhytmia, needs of repeat revascularization) were sequently monitored. Study group included 22 patients (average age 66 years, 11 men, 11 women), from whom 14 had recieved clopidogrel loding dose and 8 had recieved prasugrel loding dose. In clopidogrel group 11 patients did not reach effective drug activity in first sample and 3 patients did not reach effective drug activity in second sample. While in prasugrel group ineffective antiaggregation was seen just in 1 patient in first sample. In patients with clopidogrel treatment more MACE developed in followed period (13 vs. 6). Our results show that optic aggregometry seems to be a usefull laboratory method for antiaggregation drugs effectivity assessment. Prasugrel treatment seems to be more effective than clopidogrel administration in patients with acute STEMI and dPCI of culprit lession.

Antiplatelet Therapy in Endovascular Surgery: The RENDOVASC Study

Antiplatelet treatment prevents cardiovascular events and thrombosis during the endovascular surgery procedure. The aim of this study is to analyze the different antiplatelet treatment used in endovascular procedures in Spain. In this investigation we included observational, retrospective, and multicenter study patients who underwent arterial endovascular therapy in 2006 or in the first 3 months of 2007, and follow-up of at least 1 year. The following data were collected: the usual epidemiologic variables, history of cardiovascular disease (coronary, cerebrovascular, or peripheral artery disease), risk factors, endovascular procedure performed, blood pressure, ethiology of arterial disease, the pre-operative antiaggregant treatment, and antiplatelet therapy used at 1 month and 1 year after the procedure. A total of 1,557 patients were evaluated, of whom 84.3% were male. In addition 72.1% were hypertensive, 53.1% dyslipidemic, and 43.3% diabetic. From these patients, 32.6% presented with ischemic cardiomyopathy, 17.9% had a cerebral vascular history, and 35.3% had peripheral arterial disease. The most common etiology was occlusive disease (76.9%), the most commonly treated arterial sector was iliac (33.4%), and the most frequent procedure was stent angioplasty (46.9%). In the preoperative period, 75.1% of the patients were given antiplatelet therapy (89% simple antiplatelet treatment), 62.9% in the perioperative period, and 93.8% at 1 month after surgery (37.3% double antiaggregation). Antiplatelet treatment was administered previously to 86.2% of patients with history of cerebrovascular disease and to 88% of those with coronary disease. In the femoropopliteal sector 76.1% patients were receiving antiaggregation treatment before the procedure (11.1% double). However, 1 month later, double antiaggregation therapy was increased (45.3%), especially in the angioplasty and stent. In the iliac sector, 43.1% of patients with arterial stenosis and 38.2% of patients with complete arterial occlusion treated with angioplasty and stent continued receiving double antiaggregation 1 month after the procedure. In the carotid territory, 65.7% of patients treated with stent were receiving double antiplatelet treatment 1 month after the procedure. We believe it is necessary to create consensus committees to perform clinical practice evidence-based guidelines to formalize antiaggregation treatment in endovascular procedures.

Current Status of Clopidogrel Pharmacogenomics

Antiaggregant therapy with aspirin and clopidogrel has an important role in treatment of patients with acute coronary syndrome (ACS) to reduce the risk of major adverse cardiovascular events (MACE; myocardial infarction, cardiovascular death, stent thrombosis and stroke) [1]. Clopidogrel has a substantial benefit in high-risk patients undergoing percutaneous coronary intervention (PCI) and stent implantation. Despite adequate antiaggregant treatment, MACE occur in these patients. Patients who develop MACE have a high-on-clopidogrel platelet reactivity (HPR), suggesting that inadequate responsiveness to clopidogrel is one of the main causes of thrombotic events [1–3]. Multiple chronic or transient mechanisms are involved in HPR and risk of MACE [4]. Among these mechanisms, genetic polymorphisms play a pivotal role and represent a possible tool for clinicians to improve the management of high-risk vascular patients requiring clopidogrel [4–6]. Since 2006, studies in healthy subjects and in ACS patients undergoing PCI on clopidogrel treatment showed that a CYP2C19*2 polymorphism is an independent predictor of clopidogrel response and occurrence of MACE [4]. Therefore in 2010, owing to the power of the evidence, the US FDA added a boxed warning to the clopidogrel label to alert clinicians to the impact of the CYP2C19 genotype on the drug’s efficiency, thereby leaving the decision to use genetic testing to the discretion of physicians. We believe that a clear definition of usefulness of clopidogrel pharmacogenetics is particularly important in a context in which new alternative drugs with different characteristics and costs are available. Indeed, the generic version of clopidogrel is still available, while the patents for the brand name versions of prasugrel and ticagrelor will

In Vivo Uptake of &amp;beta;-Amyloid by Non-Plaque Associated Microglia

The role of microglia in β-amyloid (Aβ) deposition or clearance in the Alzheimer's disease (AD) brain remains unclear. Previous in vivo studies have focused primarily on the association of microglia with Aβ-positive parenchymal plaques, but have given little consideration to the possible interaction between Aβ and non-plaque associated microglia. Further, it is not known if microglia play a direct role in mediating Aβ uptake following anti-aggregant treatment. We report here the identification of Aβ-positive processes throughout the cortex and hippocampus of TgCRND8 mice expressing the human Swedish (KM670/671NL) and Indiana (V717F) amyloid precursor protein mutations, which localized to ionized calcium binding protein-1-positive resident microglia that were not associated with extracellular plaques. Oral administration of 1-deoxy-1-fluoro-scyllo-inositol, a scyllo-inositol analogue, to TgCRND8 mice improved spatial memory impairments and suppressed amyloid pathology in a dose-dependent manner. Further, treatment with 1-deoxy-1- fluoro-scyllo-inositol significantly increased hippocampal intra-microglial Aβ levels without stimulating microglial proliferation or peripheral macrophage recruitment. These results reveal a novel, beneficial role for non-plaque associated microglia in the regulation of cerebral Aβ levels in a mouse model of AD.

Platelet response to standard aspirin and clopidogrel treatment correlates with long-term outcome in patients with acute ST-elevation myocardial infarction

Platelet activation mediated by multiple signaling pathways and consecutive coronary thrombosis plays a central role in the pathogenesis of acute coronary syndromes [1,2]. Baseline platelet reactivity in these patients is an independent predictor of both successful myocardial reperfusion and the extent of myocardial necrosis after primary angioplasty [3–5]. Dual antiaggregation treatment is the therapeutical mainstay in these patients, but around 15% still develop recurrent thrombotic events [6].

Splenomegaly in Primary Antiphospholipid Syndrome without Accompanying Portal Hypertension or Comorbidity

Objective: To demonstrate the presence of splenomegaly in primary antiphospholipid syndrome (PAPS) patients without accompanying portal hypertension or comorbidity. Methods: Twelve patients (7 women) aged 23–65 years followed upon the diagnosis of PAPS were enrolled in the study. We documented the identified causes of splenomegaly in patients with PAPS, and searched for the potential causes of splenomegaly in patients with spleen enlargement. PAPS patients with or without splenomegaly were evaluated in terms of demographic and clinical findings. Results: Splenomegaly was present in 6 of the 12 patients. In these patients, there were no infections, hematological disorders, portal hypertension or malignancy that might lead to splenomegaly. The long axis of spleen was found to be in the range of 137–155 mm in patients with splenomegaly. Splenomegaly was more frequently determined in female PAPS patients. The splenomegaly group had a longer duration of disease (median 5.5 vs. 0.75 years) and a higher number of thrombotic events (median 3 vs. 1.5). The splenomegaly group was especially composed of patients who never received any anticoagulant and acetylsalicylic acid, or who used these agents irregularly for very short periods. Conclusion: Splenomegaly was observed in association with disease duration, frequency of thrombotic events and irregular antiaggregant or anticoagulant treatment in patients with PAPS, in the absence of comorbidity or portal hypertension.

257 Prevalence of aspirin resistance in stable coronary heart diseased patients and correlation with platelet turn-over

Aspirin resistance has been widely reported but the underlying mechanisms remain unclear. Previous studies have suggested a relationship between accelerated platelet turn-over and aspirin resistance in patients with coronary artery disease. The purpose of this study was to determine whether aspirin resistance could be linked to accelerated platetet turn-over. We performed a prospective monocentric study including 50 consecutive patients with stable coronary artery disease treated by aspirin (75 to 250 mg/day) without any other antiaggregant treatment. Aspirin resistance was characterized 24 hours after aspirin intake by light transmission aggregometry using 0.5 mg/mL arachidonic acid. Aspirin resistance was defined as >20% residual agregation. Platelet turn-over was estimated at the same time by measurement of mean platelet volume, % of reticulated platelets, serum P-selectin, platelet P-selectin and serum thrombopoietin. Among 50 patients (70 ± 11 y.o. mean ± 1,5, 76% male, 52% type 2 diabetes mellitus, 16% active smokers), 18 (36%) were identified as aspirin resistants. Table 1 shows the mean value of markers currently linked to platelet turn-over depending on the presence of aspirin resistance. Serum thrombopoietin was significantly increased in patients with aspirin resistance compared to patients with no aspirin resistance. No statistical difference was demonstrated for mean platelet volume, reticulated platelets, platelet P-selectin and serum P-selectin. Serum thrombopoietin values were not correlated with other platelet turn-over parameters. There was no significant correlation between serum thrombopoietin and inflammatory markers. Serum thrombopoietin is associated with aspirin resistance, but no other parameters currently linked to platelet turn-over. Further studies are needed to determine whether serum thrombopoietin can predict aspirin resistance in a larger cohort. Aspirin sensitive Aspirin resistant p Platelet volume (fl) 8.78 ± 0.26 8.82 ± 0.30 0.92 Reticulated platelet (%) 8.4 ± 0.52 8.6 ± 0.76 0.82 Serup P selectin (ng/ml) 42.6 ± 4.29 42.9 ± 4.75 0.97 Platelet P selectin (%) 11.1 ± 1.0 9.5 ± 1.5 0.35 Serum thrombopoietin (pg/ml) 130.6 ± 11.3 319.9 ± 97.8 0.01

Anterior ischemic optic neuropathy after conventional coronary artery bypass graft surgery – a case report

SummaryBackgroundPerioperative optic neuropathy is a disease which can lead to serious, irreversible damage of vision. This complication could be the result of non-ocular surgery, for example, cardiac or spinal procedures.We present a case of anterior ischemic neuropathy (AION) which occurred following a conventional coronary artery bypass graft procedure.Case ReportA 57-year-old man, 4 days after Conventional Coronary Artery Bypass Graft surgery as result of multi-vessel stabile coronary artery disease and history of anterolateral wall myocardial infarction, was admitted to the Eye Clinic due to significant loss of vision in his right eye. The patient had hypertension and was a heavy smoker. On admission, the slit lamp examination revealed a relative afferent pupillary defect in the right eye. The fundus examination showed optic disc edema with the presence of flame hemorrhages. Best corrected visual acuity (BCVA) was 0.02. The results of eye examination and fluorescein angiography confirmed the diagnosis of AION. Anti-aggregation and antithrombotic treatment was continued with steroids and vasodilators. After 7 days of this treatment we noticed the improvement of BCVA to 0.2. At 6-month follow-up, the vision was stable, and fundus examination revealed optic disc atrophy.ConclusionsAfter cardiac surgical operations, such as coronary artery bypass graft procedures, anterior ischemic optic neuropathy may occur. In those cases, close cooperation between the various specialists is necessary.

Spontaneous branch artery occlusion in idiopathic retinitis, vasculitis, aneurysms, and neuroretinitis syndrome despite panretinal laser photocoagulation of widespread retina nonperfusion

Editor, I diopathic retinal vasculitis, aneurysms, and neuroretinitis (IRVAN) syndrome is an exceptional form of arteries disease. The diagnosis is based on three major criteria (retinal vasculitis, aneurysmal dilatations at arterial bifurcations, and neuroretinitis) and three minor criteria (peripheral capillary nonperfusion, retinal neovascularization, and macular exsudation) (Chang et al. 1995). In most cases, visual loss is because of peripheral neovascular retinopathy with vitreous haemorrhage secondary to peripheral nonperfusion or to exsudative maculopathy with retro-foveal exsudate. One case of branch artery occlusion has been reported after direct laser of the aneurysm. To our knowledge, spontaneous occlusion of first-order artery has not been described. Here, we report a spontaneous branch artery occlusion that occurred after prior peripheral laser photocoagulation as recommended before or shortly after the development of neovascularization. We present a case report describing a young patient affected with idiopathic retinitis, vasculitis, aneurysms, and neuroretinitis syndrome (IRVAN) who developed spontaneously branch artery occlusion after the photocoagulation of the no-perfuse peripheral retinal surface. A 29-year-old woman presented at our department for scotoma and decreased vision in her left eye (LE) (20 ⁄ 50). She presented with a history of sudden visual decrease in the LE 4 days ago. She had no known systemic illnesses. Infectious, autoinflammatory, and vascular causes were eliminated. Preliminary aetiological investigations were negatives. The patient signed a comprehensive consent form, according to Good Clinical Practice guidelines and French legislation, before proceeding any examinations or treatments. Slit-lamp biomicroscopy did not reveal any abnormality. On fundus examination and photographs of both eyes, we observed an extensive peripapillary exudation, arterial narrowing, and aneurysmal dilatations along the arteries. In the LE, the inferotemporal area showed a yellow-white ischemic retina (Fig. 1A). The spectral domain optical coherence tomography (SD-OCT) (SD-OCT, Cirrus; Carl Zeiss Meditec, Dublin, CA, USA) confirmed the presence of exudation translated as focal hyperreflectivity in the plexiform outer layer with any modification of the retinal pigment epithelium (RPE) or cystoid macular oedema (Fig. 1B). Fluorescein angiography of the LE illustrated the macroaneurysmal dilatations along the arterial tree leakage. The left inferotemporal arterial flow stopped after a macroaneurysm and delayed filling of the corresponding vein (Fig. 1C). A retrograde arterial staining was observed along the FA sequence (Fig. 1D). Photocoagulation peripheral retinal scars were also seen in the both eyes. After discussing treatment options, both antiaggregants and steroids were introduced. Two months later, arterial flow was partially restored without extensive photocoagulation on fluorescein angiography (Fig. 2A early stage FA, Fig. 2B late stage FA), but the patient had no visual acuity improve-

Cambios inducidos por la enfermedad renal crónica en los pacientes con diabetes

Diabetic nephropathy affects about 25-40% of diabetic patients and is a marker of morbimortality. Complications related to kidney failure in these patients become even more relevant with decreasing glomerular filtration rate.Cardiovascular disease is the most relevant complication, which include coronary disease, arterial hypertension, left ventricular hypertrophy, congestive cardiac insufficiency, arrhythmias and pericarditis. Other related renal complications will influence the prognosis and evolution of diabetic patients such as anemia, hemorrhagic complications, thrombotic phenomena, alterations of immune response and susceptibility to infections. All these complications, which are present in the patient with diabetic nephropathy, force towards a multifactor approach, which includes firstly the prevention of the appearance/progression of the complications through a control of the risk factors for macro and microangiopathy as glycemic and blood pressure control, proteinuria reduction, avoiding nicotine abuse, keeping closed to the ideal weight, salt intake reduction, antiaggregant treatment and statins therapy, as well as preventing additional renal toxicity.

Prognostic Factors of Stroke: the review of factors related to patient

Cerebrovascular diseases, the most frequently encountered diseases of neurology clinics, are important because they cause high morbidity and mortality rates (1). As well as being important, they are also complex diseases since they are difficult to treat and the prevision of their progression is vague (2). Doctors who are dealing with cerebrovascular diseases need to anticipate the prognosis in order to direct the treatment and to modify the expectations of the patient’s relatives. Inquiries and problems of the patients and their relatives can be guided through sound responses in the future. There are various variables defined to determine the prognosis of cerebrovascular diseases. The variables that will guide the doctor in the determination of the prognosis depending on the patients, the medical clinic, diagnostic methodology and treatment approach. The age, the gender, ethnicity, educational level, family history, elements of risk (atrial fibrillation, hypertension, hyperglycemia, atherosclerosis, vasculitis, fibrinogenemia etc.) of the patient, the family and social support, genetics and biomarkers are the variables depending on the patient. Characteristics of the lesion; localization and its extents are the variables depending on the diseas. Motor deficits, aphasia, anosognosia, dementia, urinary incontinence, presence of sleep disorder, the improvement rate of the symptoms are the variables of clinics of the stroke. Monitoring methods are the variables of diagnostics. Antiaggregant and thrombolytic treatment, cognitive therapy constitutes the variables at the treatment approaches. The rehabilitation therapy is also dealt with this review from its prognostic aspects. The cerebrovascular disease’s prognostic factors which is depending on patients were reviewed in the first episode. The studies on the stroke prognosis are compared and evaluated. Dependent variables of the disease and diagnostic factors were reviewed in the second episode of the paper.