Embolic Mechanism Research Articles

30 Study on blood dynamic viscosity in arteries via CFD

Objectives Blood is a typical non-Newtonian fluid, and poor fluidity of blood is key to the pathogenesis of thrombus. The dynamic viscosity (high blood viscosity) of blood is a key factor in blood vessel embolization, especially cardiovascular and cerebrovascular embolisms. Computational fluid dynamics (CFD) is an efficient method for Newtonian or non-Newtonian fluid flow simulation. The finite volume method (FVM) is also an efficient numerical method for fluid dynamics simulation. This study aimed to investigate blood flow characteristics in arteries, and the dynamic viscosity is taken into account via the non-Newtonian fluids and CFD theory. Methods A series of numerical computations are presented to reproduce the process of blood flowing in arteries using the FVM code CFX. Blood flow simulation will be accelerated using the GPU parallel computation scheme with the CUDA-enabled GPU coprocessor. Results The dynamic viscosity and flow field of blood will be computed and shown by the contours. The velocity, shear strain rate and dynamic viscosity of blood can be calculated and monitored for different ages of people. Conclusions The dynamic viscosity and flow characteristics of blood in arteries can be reproduced using CFD and FVM. The mechanism of blood vessel embolization can be analyzed via the non-Newtonian fluids and CFD theory. Thrombus occurs when the rheology of blood is enhanced. Acknowledgements This research was financially supported by Shaanxi Hundred People Plan Foundation (Grant No. 302-253051601).

Watershed Infarct due to Massive Pulmonary Embolism: A Rare Diagnosis at the Emergency Department

Introduction: Watershed infarcts, which involve the hemodynamic risk zones that are the junction of distal fields of nonanastomosing arterial systems, can occur due to hemodynamic mechanisms such as hypotension and hypovolemia.Case Report: We present the case of an 86-year-old woman who complained of syncope, was confused, had a seizure at the emergency service and was diagnosed with watershed infarct of the right hemisphere, which was secondary to massive pulmonary embolism.Conclusion: Watershed infarcts can occur due to embolic or hemodynamic mechanisms. Massive pulmonary emboli can cause watershed infarcts via hemodynamic mechanism by causing resistant hypotension. Watershed infarcts coexist with pulmonary embolism; therefore, embolic patients may present with neurological symptoms. Therefore, watershed infarcts must be considered for patients with high risk factors for embolism

Stroke of undetermined cause: workup and secondary prevention.

The purpose of this review is to update the reader on current concepts of workup and secondary prevention in patients with stroke of undetermined cause. Clinical research in patients with cryptogenic stroke has been hampered by the lack of standardized, widely accepted diagnostic criteria. The new definition of 'Embolic stroke of undetermined etiology' postulates an embolic mechanism of ischemic stroke. It is based on the exclusion of lacunar infarction by brain imaging, arterial stenosis more than 50% or dissection of the respective brain-supplying artery by computed tomography/magnetic resonance-angiography or ultrasound, atrial fibrillation by at least 24 h EKG monitoring, as well as some rare etiologies such as vasculitis, drug abuse, or coagulopathies. However, it still comprises many patients with atherosclerotic etiologies (but <50% stenosis) as well as covert paroxysmal atrial fibrillation which can be detected by repeated Holter EKG or an implantable device. A patent foramen ovale can be found in up to 58% of cryptogenic stroke patients, but causality in an individual patient remains uncertain and can only be statistically inferred. The new concept of embolic stroke of undetermined etiology enabled three ongoing randomized controlled trials which investigate oral anticoagulation versus aspirin for secondary stroke prevention.

Venous oxygen embolism after inadvertent subcutaneous injection of hydrogen peroxide

The hazards of hydrogen peroxide have been known for long time, but it is still widely used in our country for irrigation of wounds. We report a case of oxygen embolism when hydrogen peroxide was accidently infiltrated subcutaneously along with local anesthetic during spine surgery and was successfully managed. We discuss the possible mechanism for embolism and its management. We also want to emphasize on the importance of being vigilant and avoiding such mistakes.

Acute Paraplegia as a Presentation of Aortic Saddle Embolism.

Background. Acute onset paraplegia has a myriad of causes most often of a nonvascular origin. Vascular etiologies are infrequent causes and most often associated with postsurgical complications. Objective. To describe the occurrence and possible mechanism for aortic saddle embolism as a rare cause of acute paraplegia. Case Report. Described is a case of a 46-year-old female who presented with the sudden onset of nontraumatic low back pain with rapidly progressive paraplegia which was subsequently determined to be of vascular origin.

Fat Tissue Embolism Caused by Autologous Fat Transfer

Complications of autologous fat transfer (injection) include fat tissue embolization from injection in the glabellar and nasal regions, with blindness and central nervous system damage. A rare complication is fat tissue embolization to the lung that, so far, has always been fatal. The author reviews the literature on fat tissue embolization. The arterial and venous anatomy is discussed and the mechanisms of embolization are described. Also presented are measures to use to prevent embolizing of fat tissue while injecting.

Left atrial mechanical function and stiffness in patients with atrial septal aneurysm: a speckle tracking study.

Atrial septal aneurysm (ASA) is a risk factor for arterial embolism. Atrial dysfunction and atrial arrhythmia, such as atrial fibrillation, might represent a mechanism for arterial embolism in such patients. Speckle tracking echocardiography (STE) is a novel and promising tool for detecting early changes in left atrial (LA) myocardial dysfunction. The aim of the study was to evaluate LA mechanical function and stiffness in ASA patients by 2-dimensional STE strain parameters. Thirty-four ASA patients (44.2 ± 12.3 years, 15 male) were studied, using a STE, and were compared with 31 age, gender, and left ventricular (LV) mass-matched controls (41.8 ± ± 11.5 years, 14 male). LA volume indices, mitral annular velocities, and global longitudinal LA strain were measured. The ratio of E/e' to LA strain was used as an index of LA stiffness. Patients with ASA showed increased LA volume indices and decreased LA global strain (25.3 ± 5.2 vs. 42.1 ± 8.7, p < 0.001). LA stiffness was increased in patients with ASA compared to the control subjects (0.41 ± 0.15 vs. 0.14 ± 0.05, p < 0.001), and LA strain and stiffness were related with LA volume indices. Patients with ASA have decreased LA global strain and increased stiffness, in comparison with those of the control subjects. LA strain and stiffness were significantly related with LA volume indices. LA stiffness and strain can be used for the assessment of LA function in patients with ASA.

A Novel Hypothesis of Visual Loss Secondary to Cosmetic Facial Filler Injection.

With the current tendency of increasing minimally invasive cosmetic surgeries, some rare but disastrous complications of facial filler injections come into sight, such as visual loss. The study aims to investigate the possible route that the injected droplet accesses the ophthalmic artery to explain and prevent such devastating complications. We searched the National Library of Medicine’s PubMed database for cases of visual loss secondary to cosmetic facial filler injection, and reviewed relevant case reports/surveys, as well as accompanying references. Data obtained were analyzed, with special interest in injected sites and filler material, and clinical features of visual loss. Based on the anatomy of facial vessels, we inferred the possible route of injected droplet migrating from injection sites to ophthalmic artery. Most physicians propose a retrograde embolic mechanism, but the culprit artery when injecting different sites is not determined. We consider accidentally breaking into supraorbital artery or supratrochlear artery may cause occlusion of ophthalmic artery when injecting into glabella or forehead region. Speaking of the nasolabial fold and nasal dorsum region, any injections in the anastomosis of the dorsal nasal artery, angular artery, and lateral nasal artery can lead to retrograde embolism. Similarly, in the temporal region, we believe there is abnormal anastomosis between frontal branch of superficial temporal artery from external carotid artery and supraorbital artery from ophthalmic artery. In our hypothesis, we can explain the accompanying brain infarction after iatrogenic visual loss. If the injecting pressure is forceful enough, it may push the embolic materials into middle cerebral artery. Although iatrogenic ophthalmic artery occlusion is a rare complication after the facial filler injection surgery, it is usually devastating. Both the patient and the surgeon should be aware of the risk of irreversible blindness. Ideally, the injection sites should avoid the small vessels nearby, the injecting force and velocity should be as gentle and slow as possible.

Numerical simulation of RF catheter ablation for the treatment of arterial aneurysm.

Considering the blood coagulation induced by the heating of radio frequency ablation (RFA) and the mechanism of aneurysm embolization, we proposed that RFA may be used to treat arterial aneurysm. But the safety of this method should be investigated. A finite element method (FEM) was used to simulate temperature and pressure distribution in aneurysm with different electrode position, electric field intensity and ablation time. When the electrode is in the middle of the artery aneurysm sac, temperature rose clearly in half side of artery aneurysm, which is not suitable for RFA. Temperature rose in the whole aneurysm when the electrode is under the artery aneurysm orifice, which is suitable for the ablation therapy. And in this way, the highest temperature was 69.585°C when power was 5.0 V/mm with 60 s. It can promote the coagulation and thrombosis generation in the aneurysm sac while the outside tissue temperature rises a little. Meanwhile, the pressure (10 Pa) at the top of aneurysm sac with electrode insertion is less than that (60 Pa) without electrode, so electrode implant may protect the aneurysm from rupture. The results can provide a theoretical basis for interventional treatment of aneurysm with RFA.

Heart beats: not to be beaten.

Heart beats: not to be beaten.

Diagnostic dilemmas in a patient with multivascular embolic stroke.

We describe a patient admitted to the intensive care unit with aphasia, which was due to an embolic ischaemic cerebral stroke associated with a previously unknown patent foramen ovale. Eventually, this finding during echocardiography led us to the diagnosis of pancreatic cancer. The thrombotic complications of pancreatic cancer, in combination with a large, patent foramen ovale, support the mechanism of a paradoxical embolism through the patent foramen ovale as the cause of cerebral ischaemic stroke.

Lethal now or lethal later: The natural history of Grade 4 blunt cerebrovascular injury.

Grade 4 blunt cerebrovascular injury (BCVI4) has a known, significant rate of stroke. However, little is known about the natural history of BCVI4 and the pathophysiology of subsequent stroke formation. A 4-year review of patients with BCVI4 at the R Adams Cowley Shock Trauma Center was performed. Rates of BCVI4-related stroke, stroke-related mortality, and overall mortality were calculated. The relationship of change in vessel characteristics and BCVI4-related stroke was examined, as was the mechanism of stroke formation. There were 82 BCVI4s identified, with 13 carotid artery (ICA) and 69 vertebral artery BCVI4s. BCVI4-related stroke rate was 2.9% in vertebral artery BCVI4 and 70% in ICA BCVI4 patients surviving to reimaging. Stroke mechanisms included embolic strokes, thrombotic strokes, and combined embolic and thrombotic strokes. Peristroke vessel recanalization and an embolic stroke mechanism were seen in 100% of ICA BCVI4-related strokes developing after admission. BCVI4-related stroke occurred within 10 hours of hospital admission in 67% of the patients with strokes. Contraindications to anticoagulation were present in most patients with BCVI4-related stroke developing after admission. Multiple etiologies of stroke formation exist in BCVI4. Early risk-benefit analysis for initiation of anticoagulation or antiplatelet agents should be performed in all patients with BCVI4, and the use of endovascular vessel occlusion should be considered in those with true contraindications to anticoagulation. However, more aggressive medical therapy may be needed to lessen BCVI4-related stroke development. Prognostic study, level IV; therapeutic study, level V.

Role of occlusive devices to prevent thromboembolism among persons with a patent foramen ovale and prior stroke.

Patent foramen ovale (PFO) has been linked to stroke, presumably through the mechanism of paradoxical embolism; however, data is confusing regarding the causal relationship between PFO and embolic stroke. What has come to light in the past decade of research is that PFO closure with devices that achieve a high rate of closure may reduce the risk of recurrent stroke compared with medical therapy, but this benefit has not been shown in the general population with a PFO and cryptogenic stroke. The important question now is which patient will benefit from PFO closure for stroke risk reduction. A validated risk prediction tool is needed to help physicians determine those patients who will derive benefit from closure of PFO to prevent recurrent stroke. It is clear that even in studies with a small number of individuals and a very small number of events, there is some benefit to closure. Furthermore, improvements in closure devices and techniques have made percutaneous device closure both safe and efficacious. As such, it is not necessary to wait for a patient to have two strokes prior to serious consideration of PFO closure. We would advocate that the decision to close a PFO in the setting of a cryptogenic stroke be made at an individual level, on a case-by-case basis. Patients with high-risk features may be more likely to benefit, though who exactly comprises this population is still being elucidated. The most difficult aspect of managing this disease is the substantial number of individuals with incidental PFOs, as well as the prevalence of stroke due to other etiologies. When treating this disease, the physician must be able to weigh the likelihood of benefit versus the risk of the procedure, as well as patient preference.

Central nervous system involvement of hypereosinophilic syndrome: A report of 10 cases and a literature review

BackgroundThe central nervous system (CNS) may be affected in those cases of peripheral eosinophila without a secondary cause (hypereosinophilic syndrome, HES). The pathomechanism of CNS involvement in HES remained uncertain. MethodsWe included those with CNS symptoms and peripheral eosinophilia (>1500/μl) at the time of presentation. Those with identifiable causes of eosinophilia were excluded. In addition to data analysis of our cases, we reviewed the literature using the Medline database. ResultsTen patients were recruited. Half of them presented with altered mental status. None of the patients had significant risk factors such as endomyocardial disease (EMD). Their brain magnetic resonance imaging (MRI) showed multiple ischemic lesions in the border zone (BZ) and other cortical areas. In addition to our 10 cases we included 67 cases from a literature review. The total 77 cases were systemically analyzed. We found that the most common type of CNS involvement was cerebrovascular disease (CVD, 63.6%), multifocal lesions in BZ were the most common feature on MRI (45.5%), many patients presented with altered mental status (40.3%), and direct eosinophil infiltration into brain parenchyma was rare in pathologic studies and not found in the patients with CVD. Furthermore, although EMD was one of the major cardiac abnormalities (26.0%), cardiac workup more frequently showed non-EMD or normal findings. Cardiac abnormalities, altered mental status, and higher eosinophil counts were more common in those with poor outcomes, whereas an isolated CNS manifestation was more frequent in those with favorable outcomes. Finally, the presence of altered mental status was the most significant predictor of poor clinical outcomes, whereas isolated CNS involvement and corticosteroid treatment were significant predictors for favorable outcomes. ConclusionsMultiple lesions on MRI were suggestive of an embolic mechanism, but diagnostic workup failed to find significant risk factors such as EMD in the most cases. Impaired anticoagulation by eosinophilic cationic proteins could be an alternative mechanism. Direct invasion of eosinophils into the CNS was rare and those cases with isolated CNS manifestations showed a better prognosis. The preferential indirect involvement of CNS by eosinophils (“CNS-tropism”) may underlie the neurological manifestations of HES. Early administration of corticosteroid after ruling out secondary causes can be beneficial in HES with CNS manifestation.

William M. Feinberg award for excellence in clinical stroke: hemodynamics and stroke risk in carotid artery occlusion.

Five percent to 15% of patients with carotid territory transient ischemic attacks or cerebral infarctions have complete occlusion of the internal carotid artery.1,2 Their risk of recurrent stroke during the next 2 years while on medical therapy is 5% to 9% per year for all stroke and 2% to 8% per year for ipsilateral ischemic stroke.3–6 Debate on the best means to prevent recurrence has centered on whether embolic or hemodynamic mechanisms are most important. In the late 1970s and early 1980s, embolism of atherothrombotic material from the persisting proximal stump of the occluded internal carotid artery through external carotid artery collaterals was put forward as the most common cause for recurrent cerebral ischemic events.7,8 At this same time, extracranial–intracranial (EC-IC) bypass was increasingly used to prevent recurrent stroke by improving the hemodynamic status of the cerebral circulation distal to the occluded vessel.9,10 From 1977 to 1985, an international, multicenter, randomized trial was conducted to determine the efficacy of EC-IC bypass for the prevention of subsequent stroke. Among 808 randomized patients with symptomatic carotid occlusion, no benefit of surgery was demonstrated.11 Some concluded that the reason for the negative results was that the majority of strokes were because of emboli, whereas others criticized the trial for failing to identify patients with hemodynamic cerebral ischemia because of poor collateral circulation for whom surgical revascularization would be of benefit.12,13 However, the pattern of arteriographic collaterals failed to identify a subgroup who benefitted from surgery.14 At the time of the EC-IC Bypass Study, there was no reliable method for assessing the hemodynamic effects of carotid artery occlusion on cerebral circulation. Although direct measurements of arterial-jugular venous oxygen differences had demonstrated that reductions in whole-brain cerebral blood …

Infarct Patterns, Collaterals and Likely Causative Mechanisms of Stroke in Symptomatic Intracranial Atherosclerosis

Background: There are limited data on the specific mechanisms of stroke in patients with intracranial atherosclerotic stenosis (ICAS). We undertook this study to describe infarct patterns and likely mechanisms of stroke in a large cohort of patients with ICAS, and to evaluate the relationship of these infarct patterns to angiographic features (collaterals, stenosis location and stenosis severity). Methods: We evaluated infarct patterns in the territory of a stenotic intracranial artery on neuroimaging performed at baseline and during follow-up if a recurrent stroke occurred in patients enrolled in the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial. We defined the likely mechanism of stroke (artery-to-artery embolism, perforator occlusion, hypoperfusion or mixed) according to the site of ICAS and based on the infarct patterns on neuroimaging. Collaterals were assessed using American Society of Interventional and Therapeutic Neuroradiology/Society of Interventional Radiology (ASITN/SIR) grades, and stenosis severity using the WASID trial's measurement technique. We evaluated the association of infarct patterns with angiographic features using χ² tests. Results: The likely mechanisms of stroke based on the infarct patterns at baseline in the 136 patients included in the study were artery-to-artery embolism (n = 69; 50.7%), perforator occlusion (n = 34; 25%), hypoperfusion (n = 12; 8.8%) and mixed (n = 21; 15.5%). Perforator-occlusive infarcts were more frequent in the posterior circulation, and mixed patterns were more prevalent in the anterior circulation (both p < 0.01). Most of the mixed patterns in the anterior circulation combined small pial or scattered multiple cortical infarcts with infarcts in border-zone regions, especially the cortical ones. Isolated border-zone infarcts were not significantly associated with a poor grading for collaterals or the severity of stenosis. Among 47 patients with a recurrent infarct during follow-up, the infarct patterns suggested an artery-to-artery embolic mechanism in 29 (61.7%). Conclusions: Artery-to-artery embolism is probably the most common mechanism of stroke in both the anterior and the posterior circulations in patients with ICAS. An extension of intracranial atherosclerosis at the site of stenosis into adjacent perforators also appears to be a common mechanism of stroke, particularly in the posterior circulation, whereas hypoperfusion as the sole mechanism is relatively uncommon. Further research is important to accurately establish the specific mechanisms of stroke in patients with ICAS, since preliminary data suggest that the underlying mechanism of stroke is an important determinant of prognosis.

Cerebellar infarction presenting as inner ear decompression sickness following scuba diving: A case report

IntroductionInner ear decompression sickness following scuba diving is not uncommon and the characteristic features of this disorder are acute peripheral vestibular syndrome, sometimes associated with cochlear signs, requiring urgent hyperbaric oxygen therapy. Cerebellar infarction can also mimic isolated peripheral vestibulopathy. Case reportThe authors report the case of a 47-year-old man in good general health admitted with acute left vestibular dysfunction suggestive of inner ear decompression sickness 6hours after scuba diving. Normal videonystagmography and delayed onset of occipital headache finally led to brain MRI that confirmed the presence of recent ischaemic infarction in the territory of the medial branch of the posterior inferior cerebellar artery. Complementary investigations revealed the presence of a patent foramen ovale with atrial septal aneurysm. No underlying atherosclerotic disease or clotting abnormalities were observed. Discussion/ConclusionCerebellar infarction can present clinically with features of inner ear decompression sickness following scuba diving. An underlying air embolism mechanism cannot be excluded, particularly in patients with a large right-to-left circulatory shunt and no other cardiovascular risk factors.

Blunt traumatic occlusion of the internal carotid and vertebral arteries

The stroke rate, management, and outcome after blunt cerebrovascular occlusion (Biffl Grade IV injury) is not well defined, given the rarity of the disease. Both hemodynamic failure and embolic mechanisms have been implicated in the pathophysiology of subsequent stroke after blunt cerebrovascular occlusion. In this study, the authors evaluated their center's experience with Biffl Grade IV injuries, focusing on elucidating the mechanisms of stroke and their optimal management. A retrospective review identified all internal carotid artery (ICA) or vertebral artery (VA) Biffl Grade IV injuries over a 7-year period at a single institution. Fifty-nine Biffl Grade IV injuries were diagnosed affecting 11 ICAs, 44 unilateral VAs, and 2 bilateral VAs. The stroke rates were 64%, 9%, and 50%, respectively. Of the 11 Biffl Grade IV ICA injuries, 5 presented with stroke while 2 developed delayed stroke. An ipsilateral posterior communicating artery greater than 1 mm on CT angiography was protective against stroke due to hemodynamic failure (p = 0.015). All patients with Biffl Grade IV injuries affecting the ICA who had at least 8 emboli per hour on transcranial Doppler (TCD) ultrasonography developed an embolic pattern of stroke (p = 0.006). Treatment with aspirin versus dual antiplatelet therapy had a similar effect on stroke rate in the ICA group (p = 0.5) and all patients who suffered stroke either died (n = 3) or required a decompressive hemicraniectomy with subsequent poor outcome (n = 4). All 10 strokes associated with Biffl Grade IV VA injuries were embolic and clinically asymptomatic. In VA Biffl Grade IV injury, neither the presence of emboli nor treatment with antiplatelet agents affected stroke rates. At the authors' institution, traumatic ICA occlusion is rare but associated with a high stroke rate. Robust collateral circulation may mitigate its severity. Embolic monitoring with TCD ultrasonography and prophylactic antiplatelet therapy should be used in all ICA Biffl Grade IV injuries. Unilateral VA Biffl Grade IV injury is the most common type of traumatic occlusion and is associated with significantly less morbidity. Embolic monitoring using TCD and prophylactic antiplatelet therapy do not appear to be beneficial in patients with traumatic VA occlusion.

Abstract T P180: Diastolic Dysfunction and Left Atrial Volume Mediates Embolic Stroke in Patients with Atrial Fibrillation

Background: Several risk predictors for stroke in AF patients, specifically the CHADS2 criteria, have been implicated in left ventricular (LV) diastolic dysfunction (DD). It is plausible that DD and subsequent elevation in left ventricular filling pressure (LVFP) mediate stasis within the left atrium leading to thrombus formation and embolic stroke in AF patients. Left atrial volume index (LAVI) is known to correlate with LVFP and AF chronicity. We sought to assess whether LAVI can predict ischemic stroke in patients with AF, independent of clinical risk predictors. Hypothesis: In AF patients, LAVI is associated with ischemic stroke independent of clinical covariates. Methods: We conducted a retrospective case-control study with 203 patients. The case group (n=33) was derived from our institution’s stroke database which was used to identify strokes attributed to an embolic mechanism related to AF as adjudicated by expert neurologist. The control group (n=79) was generated of consecutive AF patients without previous history of stroke. The left atrial dimensions were measured and the left atrial volume (LAVI) was calculated. Binary logistic regression analysis was used to explore whether LAVI predicted stroke independently from CHADS2 score. Results: The mean LAVI in the stroke group was 50.74 s 23.83 in the non-stroke group (p&lt;0.001). Binary logistic regression analysis demonstrated that LAVI was significant as an independent risk factor in addition to the CHADS2 score (OR 1.12, CI: 1.0-1.185 per cc/m2 of volume increment, p&lt;0.001). Subsequently, we developed a novel risk score in which 1 additional point was added to the CHADS2 score for every 5cc increment in the LAVI. The receiver operator characteristics curve analysis showed that the AUC for the novel risk score (LAVI +CHADS2) as a predictor for ischemic stroke to be 0.87 vs 0.74 for the clinical factors alone (p&lt;0.05) Conclusion: Our preliminary data demonstrates that LAVI is an independent risk predictor for embolic stroke in patients with AF. Integrating LAVI with clinical predictors (CHADS2 score) may enhance our ability in predicting stroke and to allow us to better select patients for anticoagulation therapy.

Smoking, Periodontitis and Vascular Disease -Collaboration Study with Dentists and Vascular Surgeons

Weak oral bacteria such as periodontal bacteria have been observed in various arterial and venous lesions with epidemiological data reported prior to the discovery of bacterial invasion into vessels. Rich lymph vessels easily bring the bacteria from the mouth to the neck and the venous angle, which is directly open to the blood vessels. Periodontal bacteria travel within platelets. Periodontal bacteria, especially P. gingivalis aggregates platelets and forms thrombus. At the same time, secretions such as serotonin, various cytokines, and adhesion factors also appear in the blood. The characteristic of the arterial lesions are dependent on the age of the patient and the condition of the endothelial cells. In young patients, infectious incidents occur due to embolic mechanisms in Buerger disease or adhesion to the superficial veins valves in varicose veins. In aged patients, incidents result in adhesion in the proximal aorta, coronary arteries or large arteries. The hypotheses here unify the evidence or vessel lesion development and explain possible discrepancy between vascular diseases. We were able to emphasize the collaboration study in this study with dentists and vascular surgeons.