Development Of Collateral Vessels Research Articles

Monocyte dysfunction as a previously unrecognized pathophysiological mechanism in ApoE −/− mice contributing to impaired arteriogenesis

Hyperlipidemia (HL) is a major cardiovascular risk factor promoting atherogenesis leading to coronary and peripheral artery disease. Collateral vessel development, a crucial compensatory mechanism in peripheral artery disease, is negatively influenced by HL [1]. Monocytes and tissue-resident macrophages accelerate both atherogenesis and arteriogenesis by supplying growth factors, cytokines and proteolytic enzymes [2]. The decreased monocyte/macrophage accumulation around growing collateral vessels in HL is associated with jeopardized arteriogenesis [1].

COMPUTED TOMOGRAPHIC AND ULTRASONOGRAPHIC CHARACTERISTICS OF CAVERNOUS TRANSFORMATION OF THE OBSTRUCTED PORTAL VEIN IN SMALL ANIMALS.

In humans, the process of development of collateral vessels with hepatopetal flow around the portal vein in order to bypass an obstruction is called "cavernous transformation of the portal vein." The purpose of this retrospective, cross-sectional, multicentric study was to describe presumed cavernous transformation of the portal vein in small animals with portal vein obstruction using ultrasound and multidetector-row computed tomography (MDCT). Databases from three different institutions were searched for patients with an imaging diagnosis of cavernous transformation of the portal vein secondary to portal vein obstruction of any cause. Images were retrieved and reanalyzed. With MDCT-angiography, two main portoportal collateral pathways were identified: short tortuous portoportal veins around/inside the thrombus and long portoportal collaterals bypassing the site of portal obstruction. Three subtypes of the long collaterals, often coexisting, were identified. Branches of the hepatic artery where involved in collateral circulation in nine cases. Concomitant acquired portosystemic shunts were identified in six patients. With ultrasound, cavernous transformation of the portal vein was suspected in three dogs and one cat based on visualization of multiple and tortuous vascular structures corresponding to periportal collaterals. In conclusion, the current study provided descriptive MDCT and ultrasonographic characteristics of presumed cavernous transformation of the portal vein in a sample of small animals. Cavernous transformation of the portal vein could occur as a single condition or could be concurrent with acquired portosystemic shunts.

Diabetes mellitus and female gender are the strongest predictors of poor collateral vessel development in patients with severe coronary artery stenosis.

Coronary collateral vessel development (CVD), i.e., arteriogenesis, is regarded as one of the most important mechanisms—along with angiogenesis—to result in protection of the myocardium. Coronary CVD is associated with a reduction in infarct size, future cardiovascular events and improved survival in patients with occlusive coronary artery disease by enhancing regional perfusion in the chronically ischemic myocardium. In the present study, we aimed to investigate the relation of cardiovascular risk factors and hematological parameters with collateral development in patients with severely stenotic (≥95%) and totally occluded coronary artery disease including at least one major coronary artery. The study population was selected from the patients who underwent coronary angiography between January 2008 and March 2009. Five hundred and two patients who had at least one coronary artery stenosis ≥95% (368 men; mean age 59 ± 10 years) comprised the study population. Of the 502 patients, 228 had total occlusion in at least one major epicardial coronary artery. Collateral artery grading was performed by using Cohen-Rentrop method to the vessel with coronary artery stenosis of ≥95% and patients with chronic total occlusions (CTO). Patients with grade 0-1 collateral development were regarded as the poor collateral group, and patients with grade 2-3 collateral development were regarded as the good collateral group. Two hundred and fifty-eight (51%) of 502 patients had poor collateral development, and 244 (49%) had good collateral development. Logistic regression analysis revealed that DM was independently associated with poor CVD in patients with ≥95% stenosis (p < 0.001). Additionally, female gender and DM were found to be independently associated with poor CVD in patients with CTO (p = 0.005 and p < 0.001, respectively). Monocyte count was found to be independent of CVD neither in patients with ≥95% stenosis nor in patients with CTO. Our data show that DM is an independent factor for poor coronary CVD both in patients with severe coronary artery stenosis and in patients with CTO. Female gender or being in post-menopausal period is another negative risk factor for poor CVD in addition to DM in patients with CTO.

Impact of obstructive sleep apnea in recruitment of coronary collaterality during inaugural acute myocardial infarction

BackgroundObstructive sleep apnea (OSA) may lead to myocardial preconditioning by increasing coronary collateral vessel recruitment in patients with acute coronary occlusion. AimTo determine the relationship between the severity of obstructive sleep apnea and coronary collaterality during acute myocardial infarction. MethodsThis study prospectively included 71 patients with an inaugural myocardial infarction who had undergone a coronary angiography within 24h of onset. All patients underwent an overnight polygraph before discharge and were classified according to the apnea–hypopnea index (AHI). Coronary collaterals were scored by visual analyses and according to the Rentrop grading system. ResultsMean age was 59±11years and 83% of patients were men. All patients had complete or subtotal occlusion of the infarct-related artery. After the sleep study, patients were divided into two groups: 25 were suffering from OSA (AHI>15/h). Patients with OSA showed better collateral vessel development (Rentrop score≥1) compared to non-OSA patients (68 vs. 41%, P=0.032). AHI was significantly higher in patients with developed coronary collaterals (Rentrop≥1) compared to those without collaterality (17.74±13.2 vs. 12.24±10.9, P=0.025). ConclusionCoronary collateral development may be increased in OSA patients who are presenting with a first myocardial infarction.

The degree of spleen stiffness measured on acoustic radiation force impulse elastography predicts the severity of portal hypertension in patients with biliary atresia after portoenterostomy

Background/purposeAcoustic radiation focus impulse (ARFI) elastography is a new method for assessing the degree of tissue stiffness. We herein evaluated the degree of spleen stiffness (SS) using ARFI elastography in patients with biliary atresia (BA) after Kasai portoenterostomy (KPE). MethodsWe retrospectively collected the liver stiffness (LS) and SS values on ARFI elastography from 43 patients undergoing KPE between September 2010 and November 2013. We analyzed the correlations between these values and variables related to the severity of liver dysfunction and portal hypertension (PHT). The data were expressed as the standard deviation score (z-score) relative to the previously reported normal values for the patient’s age. ResultsThe SS value was significantly associated with the spleen diameter and development of collateral vessels, in comparison to the LS value. Interestingly, there was a significant correlation between SS value and the portal vein (PV) diameter. Thirty patients (69.8%) consequently underwent LT; these patients showed higher SS values and smaller PV diameters than the patients monitored without LT. ConclusionsThe degree of SS measured on ARFI elastography can be used to predict the severity of PHT in BA patients after KPE.

Moyamoya disease - A case report from North Western part of India

Moyamoya disease is a chronic, progressive occlusion of the circle of Willis arteries that leads to the development of characteristic collateral vessels seen on imaging, particularly cerebral angiography. The disease may develop in children and adults, but the clinical features differ. Moyamoya disease occurs predominantly in Japanese individuals but has been found in all races with varying age distributions and clinical manifestations. As a result, moyamoya disease has been under-recognized as a cause of ischemic and hemorrhagic strokes in the Indian subcontinent. At this time, there is no known cure, and existing treatment options are controversial. We here describe the case of a 27-year-old Indian presenting as right-sided hemiparesis with accelerated hypertension.

Case Report: Disturbed Sleep in a Patient with Moyamoya Disease

Background: Moyamoya disease is a chronic, progressive occlusion of the circle of Willis arteries that leads to the development of characteristic collateral vessels. The incidence of moyamoya disease is highest in Japan, with 0.35 cases per 100,000 people. At this time, moyamoya disease is believed to be hereditary and the pathogenesis is unknown. Case report: This case report describes an 11-year-old Asian girl diagnosed with idiopathic moyamoya disease. The patients have a history of severe migraines and sleep disturbances and experienced a stroke-like event with balance, coordination, sensory and motor function impairment. She was subsequently treated with three revascularisation surgeries. Prior to her presentation, the patient experienced severe migraines attacks 4-5 times per week, with migraines representing a primary concern since the age of 5. She experienced difficulties falling asleep and maintaining sleep and developed mood-related problems. A full montage electroencephalogram (EEG) showed abnormal background activity and revealed epileptiform changes. Following treatment of her sleep disturbance with Tryptophan, her migraines improved and functional abilities were also enhanced. Her improvement in sleep function was quantified via repeated polysomnographic studies and actigraphy monitoring between 1/2012 and 2/2014. Along with the details of this case, this article provides a review of the literature related to this condition. Conclusion: This case report demonstrates that investigation of sleep-related concerns is able to provide a window into neurologic abnormalities, allowing for enhanced detection of these issues and improved therapeutic outcomes. A review of the literature indicates that little information is available related to the pathogenesis of moyamoya disease and that the presentation of sleep disturbances has not been widely reported. We believe this case report will help to improve understanding of the disease and its presentation.

Adipose-derived stem cell sheet transplantation therapy in a porcine model of chronic heart failure

Adipose-derived stem cells (ASCs) are a promising resource for cell transplantation therapy for damaged heart tissue. Cell death in the graft early after transplantation represents the main cause of unsatisfactory therapeutic efficacy, but tissue-engineered cell sheets grown in temperature-responsive cell culture dishes may enable improved engraftment of transplanted cells. We investigated the therapeutic potential of this method in chronic myocardial ischemia in swine. We created a porcine model of chronic heart failure by implanting an ameroid constrictor around the main trunk of the left anterior descending artery, just distal to the circumflex branch. Simultaneously, ASCs were obtained from a piece of subcutaneous adipose tissue and expanded to form ASC sheets using temperature-responsive dishes. Four weeks after ameroid constrictor placement, triple-layered ASC sheets were transplanted onto the area of the ischemic myocardium (sheet group, n=7). Controls (n=7) received no sheet. Just before and 4weeks after transplantation, left ventriculography (LVG) and coronary angiography (CAG) were performed. LVG revealed a significant improvement in the left ventricular ejection fraction of the sheet group compared with controls (47.6±2.9% vs 41.4±2.8%, P<0.05). Furthermore, development of collateral vessels was only detected in the sheet group with right CAG. Histologic analysis demonstrated that engrafted ASC sheets grew to form a thickened layer that included newly formed vessels. ASC sheet transplantation therapy is an intriguing therapeutic method for ischemic heart failure.

Abstract 17797: Noninvasive Optical Imaging of Response to On-Demand Antioxidant Therapy in a Model of Peripheral Arterial Disease

Peripheral arterial disease is often modeled by surgical induction of hind limb ischemia (HLI) in mice to study collateral vessel development. However, there is a need for methodologies that provide intravital, multifunctional, quantitative data on ischemic recovery for robust evaluation of new therapeutics. Here, we apply hyperspectral imaging and optical coherence tomography (OCT) to longitudinally assess hemoglobin oxygen saturation (SaO 2 ) and vessel morphology in response to a novel therapy. Injectable microspheres loaded with curcumin were synthesized from reactive oxygen species (ROS)-responsive poly(propylene) sulfide (PPS) to provide “on demand”, local release of the antioxidant drug curcumin to reduce tissue-damaging oxidative stress in a mouse model of diabetic HLI. Curcumin-PPS microspheres significantly reduced intracellular ROS in LPS-activated RAW 264.7 macrophages and rescued viability of 3T3 fibroblasts treated with cytotoxic levels of H 2 O 2 in vitro . HLI was induced in FVB mice with streptozotocin-induced diabetes, and curcumin-PPS or blank-PPS microspheres were injected into the ischemic limb. Curcumin-PPS significantly improved recovery of SaO 2 in the ischemic footpad relative to blank-PPS and vehicle (saline) groups over a one week time course evaluated with hyperspectral imaging (n≥8/group, p&lt;0.05). Vessel structure in the gastrocnemius was imaged noninvasively with OCT at day 7 (Figure), revealing trends toward increased vessel area density and vessel length fraction in the curcumin-PPS group (n=5/group). The vessel diameter distribution was also extracted from OCT data. Our collective data indicate that sustained, on demand curcumin delivery has significant therapeutic promise for improving ischemic tissue recovery. Also, the hyperspectral and OCT imaging methods showcased provide quantitative, noninvasive monitoring of vasculature and can accelerate screening of novel therapies.

Current Role of Multi-detector Computed Tomography (MDCT) in Diagnosis of Pulmonary Embolism

Pulmonary embolism (PE) is a common and serious condition, and if not diagnosed timely may lead to the death of the patient. Imaging plays a major role in the diagnosis of the PE. Since the past decade multi-detector computed tomographic pulmonary angiography is playing a major role in the diagnosis of PE due to its high accuracy. PE may be acute or chronic. PE may cause complete or partial obstruction of the pulmonary arteries. In acute PE, complete obstruction of the segmental and subsegmental branches of pulmonary artery causes enlargement of the vessel. Completely obstructed segmental and subsegmental vessels are smaller in size in the chronic PE. Chronic PE may also lead to the poststenotic dilatation of the obstructed vessel and development of the systemic collateral vessels. Multi-detector computed tomographic pulmonary angiography may be used to assess the clot resolution and severity of the PE.

Determination of the severity of underlying lesions in acute myocardial infarction on the basis of collateral vessel development

We aimed to address the conflict over whether the underlying lesion that leads to acute myocardial infarction (AMI) is representative of low-grade or high-grade stenosis. Because the development of collateral vessels is an indication of ischemia, their presence was used as a surrogate marker for the existence of a high-grade lesion. Coronary angiography was used to assess 159 patients, divided into two groups, with (Rentrop 1-3) and without (Rentrop 0) collateral vessels, who had AMI with ST-segment elevation for which they underwent a percutaneous coronary intervention with the implantation of a coronary stent and had baseline thrombolysis in myocardial infarction 0/1 flow. Of the 159 patients recruited, the presence of collateral vessels was detected in 95 (collateral group; 60%), indicating that the causal lesion was representative of a high-grade stenosis. Among these 95 patients, the Rentrop scores were 1, 2, and 3 in 57 (60%), 33 (34.7%), and six (5.3%) patients, respectively. Logistic regression analysis showed that a baseline thrombolysis in myocardial infarction 0 flow (hazard ratio, 4.6; 95% confidence interval, 1.4-14.6; P=0.01) and a culprit right coronary artery (hazard ratio, 3.0; 95% confidence interval, 1.4-6.2; P=0.007) were independent predictors of the development of collateral vessels. The majority of AMI cases can be attributed to a severe stenosis, as demonstrated by the presence of collateral vessels in 60% of the patients in this study.

Experimental retinal vein occlusion, a model of non‐neovascular microvascular remodeling

AbstractThe main cause of visual loss after retinal vein occlusion and diabetes is microvascular remodelling, a spectrum of functional and morphological changes affecting vessels. Some are beneficial, such as collateral vessel development. The other manifestations of microvascular remodelling are usually detrimental such as chronic rupture of the blood‐retinal barrier, capillary closure or macroaneurysms. The processes underlying microvascular remodelling are poorly understood, in part because of the absence of a clinically meaningful animal model. We have been investigating the effet of retinal vein occlusion in rodents using laser photocoagulation, which eanbled us to reproduce many of the features of human microvascular remodelling. Based on our experience, we will discuss issues related to interspecies variability and clinical relevance.

Identifying and overcoming obstacles in angiogenic gene therapy for myocardial ischemia.

Well-developed coronary collateral vessels in patients with symptomatic coronary artery disease were shown to be associated with reduced future cardiovascular morbidity and mortality. However, the majority of patients with coronary artery disease lack adequate functional coronary collateral circulation. Stimulation of collateral vessel development by angiogenic growth factor therapy (therapeutic angiogenesis) has been tested in many clinical trials in the past, but the potential of this new treatment paradigm has not been realized yet in late stage clinical trials. Mechanistic insights into collateral vessel development and the collective clinical experience in the past decade identified specific obstacles that might have impeded the progress in the field. This review identifies some of the key conceptual, technical, and clinical hurdles and recommends strategies to overcome them in future clinical trials.

Combined autologous bone marrow mononuclear cell and gene therapy as the last resort for patients with critical limb ischemia.

IntroductionOur study was designed to investigate the safety and efficacy of combined autologous bone marrow mononuclear cell (MNC) and gene therapy in comparison to conventional drug therapy in patients with critical limb ischemia (CLI).Material and methodsThirty-two patients with CLI persisting for 12–48 months (average time 27.5 months) were randomized into 2 groups, each group consisting of 16 patients. In the first group, administration of autologous bone marrow MNC and vascular endothelial growth factor (VEGF) plasmid was performed. The patients from the second group were treated pharmacologically with pentoxifylline. Ankle-brachial index (ABI) was measured and angiography was performed before and finally 3 months after treatment. The pain was evaluated using the Visual Analog Scale (VAS) before and after 3 months.ResultsAnkle-brachial index improved significantly from 0.29 ±0.21 to 0.52 ±0.23 (p < 0.001) in 12 patients (75.0%) 3 months after the experimental therapy in group 1. In this group angiography showed the development of collateral vessels. Ischemic ulcers healed completely in 11 patients (68.75%). In group 2 the ABI did not improve in any patient; moreover the complete healing of skin ulcers was not found in any of the patients of this group. Amputation was performed in 4 (25.0%) patients in group 1, and in 8 patients (50%) from group 2.ConclusionsThese data after 3-month follow-up indicate that intramuscular injection of MNC combined with gene therapy in patients with chronic CLI is safe, and a more feasible and effective method of treatment than the conventional therapy. However, both therapies are limited by the degree of microcirculation damage.

Neuron-derived Neurotrophic Factor Functions as a Novel Modulator That Enhances Endothelial Cell Function and Revascularization Processes

Strategies to stimulate revascularization are valuable for cardiovascular diseases. Here we identify neuron-derived neurotrophic factor (NDNF)/epidermacan as a secreted molecule that is up-regulated in endothelial cells in ischemic limbs of mice. NDNF was secreted from cultured human endothelial cells, and its secretion was stimulated by hypoxia. NDNF promoted endothelial cell network formation and survival in vitro through activation of Akt/endothelial NOS (eNOS) signaling involving integrin αvβ3. Conversely, siRNA-mediated knockdown of NDNF in endothelial cells led to reduction of cellular responses and basal Akt signaling. Intramuscular overexpression of NDNF led to enhanced blood flow recovery and capillary density in ischemic limbs of mice, which was accompanied by enhanced phosphorylation of Akt and eNOS. The stimulatory actions of NDNF on perfusion recovery in ischemic muscles of mice were abolished by eNOS deficiency or NOS inhibition. Furthermore, siRNA-mediated reduction of NDNF in muscles of mice resulted in reduction of perfusion recovery and phosphorylation of Akt and eNOS in response to ischemia. Our data indicate that NDNF acts as an endogenous modulator that promotes endothelial cell function and ischemia-induced revascularization through eNOS-dependent mechanisms. Thus, NDNF can represent a therapeutic target for the manipulation of ischemic vascular disorders.

Cell and molecular events comprising collateral vessel development and remodeling (19.1)

Although the relevance of coronary collaterals was debated for many years, more recent studies utilizing more acurate methods for measuring collateral flow have shown that collateral flow can minimize infarct size. The development of coronary collateral vessels by pressure gradients (fluid shear stress), involving the recruitment of multiple genes, including VEGF and FGF, is well documented. However, there is also more recent evidence that ischemia, independent of elevated shear stress can also stimulate collateral growth under certain conditions. Collateral growth is a form of arteriogenesis that involves: 1) endothelial deformation, 2) increases in NOS and NO, 3) VEGF activation of MCP‐1, 4) monocyte and T‐cell recruitment and migration and 5) remodeling of the vessel. The remodelinig process requires proliferation of endothelial cells and vascular smooth muscle, which results in an increase in vessel diamter. Important stimuli for collateral growth include brief, repeated, as well as gradual coronary artery occlusions.

Therapeutic site selection is important for the successful development of collateral vessels

Induction of collateral development to improve tissue perfusion is a promising approach for the treatment of arterial occlusive diseases. Several growth factors and cells have been reported to increase collateral circulation; however, the appropriate site for the delivery of these factors and cells is unclear. In this study, we identified the delivery site for growth factor in a rabbit model of limb ischemia and evaluated whether specific delivery of basic fibroblast growth factor (bFGF) to this site enhanced collateral augmentation. The left femoral artery of Japanese white rabbits was excised to induce limb ischemia. Twenty-eight days thereafter, angiograms were obtained to identify the typical pattern of collateral development in this model. Subsequently, bFGF (100 μg) was selectively injected into the left coccygeofemoral muscle (coccygeo group) or adductor muscle (adductor group), major thigh muscles in proximity. Collateral development was evaluated at 28 days after injection, and its mechanism was assessed by immunologic and morphometric analyses of muscle samples. Angiographic evaluation of this model revealed that after femoral artery excision, collateral vessels generally developed in the left coccygeofemoral muscle, whereas few collateral vessels were detected in the left adductor muscle. At 28 days after injection, calf blood pressure ratio, defined as left pressure to right pressure, was significantly higher in the coccygeo group than in the adductor group (0.85 ± 0.05 vs 0.69 ± 0.05, respectively; P < .01). Similar results were observed in blood flow through the internal iliac artery (resting: 24.6 ± 6.1 vs 17.4 ± 8.0 mL/min, P < .01; maximum: 47.4 ± 12.3 vs 33.2 ± 10.7 mL/min, P < .01) and in the angiographic score (0.67 ± 0.13 vs 0.39 ± 0.11; P < .01). Immunologic analyses of the coccygeofemoral muscle at day 3 showed marked expressions of Ki-67, monocyte chemotactic protein 1, and FGF receptor 1 in the coccygeo group compared with the adductor group. Morphometric analyses of the same muscle at day 14 also revealed that collateral vessel density and wall thickness were significantly increased in the coccygeal group compared with the adductor group. These findings demonstrated that selective bFGF delivery to the coccygeofemoral muscle markedly improved collateral development and limb perfusion compared with delivery to the adductor muscle, suggesting that site selection is important in increasing therapeutic efficacy.

Clinical and Angiographic Features and Stroke Types in Adult Moyamoya Disease

This study was conducted to elucidate the association between clinical and angiographic characteristics and stroke types in adult Moyamoya disease that has been rarely evaluated. We analyzed the clinical and radiologic data obtained from a retrospective adult Moyamoya disease cohort with acute strokes, which were classified into 7 categories: large-artery infarct, hemodynamic infarct, perforator infarct, deep intracerebral hemorrhage, lobar intracerebral hemorrhage, intraventricular hemorrhage, and SAH. With conventional angiography, which was performed in the hemispheres with acute strokes, the Suzuki angiographic stage, intracranial aneurysm, major artery occlusion, and collateral vessel development were confirmed within 1 month of stroke onset. This study included 79 patients with acute ischemic stroke and 96 patients with acute hemorrhagic stroke. The angiographic stage had a strong tendency to be more advanced in the hemorrhagic than the ischemic patients (P = .061). Intracranial aneurysms were more frequently found in the hemorrhagic than ischemic or control hemispheres (P = .002). Occlusions of the anterior cerebral artery and development of fetal-type posterior cerebral artery were more frequently observed in the hemorrhagic than the ischemic (P = .001 and .01, respectively) or control hemispheres (P = .011 and .013, respectively). MCA occlusion (P = .039) and collateral flow development, including the ethmoidal Moyamoya vessels (P = .036) and transdural anastomosis of the external carotid artery (P = .022), occurred more often in the hemorrhagic than the ischemic hemispheres. Anterior cerebral artery occlusion occurred more frequently in patients with deep intracerebral hemorrhage or intraventricular hemorrhage than with lobar intracerebral hemorrhage (P = .009). In adult Moyamoya disease, major artery occlusion and collateral compensation occurred more often in the hemorrhagic than in the ischemic hemispheres. Thus, anterior cerebral artery occlusion with or without MCA occlusion and intracranial aneurysms may be the main contributing factors to hemorrhagic stroke in adult patients with Moyamoya disease.

Angiogenesis in Steno-Occlusive Vasculopathies as a Common Pathway for Intracranial Haemorrhage

Vasculopathies, including vasculitis of the central nervous system, can lead to stenosed, cicatrized vessels and the development of arterio-arteriolar collateral vessels. Bleeding due to these vascular changes, although rare, does occur. We describe six patients (all female, age range, 21-52 years; mean age, 42 years) with steno-occlusive lesions of intracranial vessels who presented with an acute intracranial haemorrhage. All had arterial steno-occlusive changes in conjunction with extensive leptomeningeal and arterio-arteriolar collaterals. Within the collaterals, focal dilatations could be identified, which were in close spatial relationship with the intracranial haemorrhage. Cause of bleeding was depicted on CT angiography in four out of six patients. One patient presented in childhood with acute stroke, one patient was diagnosed with Buerger's disease and one with sickle cell disease; the other three patients had no relevant history and the exact cause remained unclear. Outcome was favourable in all patients. Despite focal vascular weaknesses, no recurrent haemorrhage was seen during follow-up, supporting, at least in this small patient group, a conservative wait-and-see policy.

Nicotinic Acid Treatment for Retinal Vein Occlusion

Objectives: To evaluate the effect of nicotinic acid in management of retinal vein occlusions (CRVO or BRVO). Materials and Methods: This prospective nonrandomized pilot study included 20 patients (21 eyes) with CRVO or BRVO that received nicotinic acid (3 g/day) for 3 months. A complete ophthalmologic examination uncorrected visual acuity (UCVA), best spectacle-corrected visual acuity (BSCVA), testing for a relative afferent pupillary defect (RAPD), slit-lamp examination, gonioscopy, intraocular pressure (IOP) measurement, fundoscopy and fundus photography was performed. Results: Four patients did not appear for follow-up and hypersensitivity reaction to nicotinic acid and severe hyperglycemia happened in two patients. Therefore, the results of treatment in 16 eyes of 15 are reported. These patients had a mean age of 59.56 ± 11.12 years. The average length of follow-up was 8.6 ± 2.7 months. The mean BSCVA was 1.56 ± 0.66 before treatment, 1.38 ± 0.72 (p >0.05) at one month and 0.88 ± 0.69 (p<0.01) at three months. The last BSCVA of all 16 eyes averaged 0.97 ± 0.73 (p<0.01). All patients had reduction of hemorrhagic events, cotton wool spots, edema in macula and disc, venous tortuosity, and dilation on basis of fundus photographs 3 months after treatment. Conclusion: Nicotinic acid usage provides enough time for development of collateral vessels, by induction of vasodilatation. Nicotinic acid use is tolerable and is related with mild systemic side effects.