Vascular Medicine

Vascular Medicine

  • Varshil Mehta added an answer:
    Do glycated red blood cells cause vascular tissue damage that leads to atherosclerosis of the heart arteries?

    Could it be that the glycated cells are under such force in the arterial vessels of the heart that plaque builds up quickly in the damaged lumens more rapidly than other arterial vessel locations? It seems to me that a red blood cell that is highly glycated can cause a lot of damage when accelerated at such close proximity of the pressure wave of the left ventricle. A glycated cell cannot slip in between tissues in a normal function and maybe it scratches the lumens along the path to distal locations that have slower circulatory surges (speed in the vessels of circulation). 

    Varshil Mehta

    I agree with Dr. Antonio

  • Giuseppe Gatti asked a question:
    What is the rate of bilateral internal thoracic artery (BITA) used at your institution?

    I would like to perform a little survey as the use of BITA grafting formyocardial revascularization.

  • Demian Arturo Herrera Morban added an answer:
    What is a recommended dyslipidemia treatment on a Nephrotic syndrome?

    HMG-CoA inhibitors dont really diminish cholesterol on N-S, and hypertrigliceridemia i havent found proper management of it on N-S, but searching for more information i found ideas of PPAR stimulation and potentiation of HMG-Coa Inhibitors, diminish lipid profile and better outcomes, and using ezetimibe and atorvastatine its better for cholesterol management and atorvastatine with a glitazone improves outcome, also that glitazone tend to protect the kidney, but i havent found studies using ezetimibe plus atorvastatine or simvastatine plus glitazone to try and improve outcome of dyslipidemia on N-S.
    So can the triple therapy of glitazone plus ezetimibe plus atorvastatine or simvastine be used in N-S and would or can improve the outcome of dyslipidemia in N-S.

    Can someone provide additional information, or ideas regarding the hypothetical treatment or some guidelines with information of dyslipidemias on N-S, preventing Cerebral Vascular Diseases.


    Demian Arturo Herrera Morban

    Thanks Pablo, but what happens when the patient has a poor response to the NS treatment, no response to steroids and poor response to inmune suppressors? do we believe that events such as stroke cannot be prevented with management of dyslipidemia and use of profilactic aspirin; so complications cannot be prevented on patients with poor response to NS treatment?

  • Sergey Gavrilov added an answer:
    When and how do you treat Pelvic Congestion Syndrome? Pelvic Varices?

    What criteria do you use to surgery? Which embolization technique do you use?

    Sergey Gavrilov

    The indication for surgery PCS is symptoms of PCS and expansion and reflux of blood through the gonadal veins. However, up to the end not clear whether it is necessary to do surgery for asymptomatic pelvic varicose veins.

    Embolization gonadal veins - not a reference treatment for PCS. Resection of gonadal veins produces better results at lower cost.

  • Pradeep Kumar asked a question:
    What are the non invasive methods for carotid stimulation?

    What are the non invasive methods for carotid stimulation?

  • Richard Crane added an answer:
    Do you agree that high carbohydrate diet may cause heart problem (cardiovascular disease) ?

    In most of the communities especially are owned by lower socioeconomic status.Diet contains more of carbohydrate than protein and fat. More carbohydrate after catabolism produce more saturated fatty acids. This may disturb the level of LDL( high ) lead to atherosclerosis.

    Richard Crane

    Im Sid, you a right that, for most people, dietary saturated fat, but not cholesterol, affects levels of total cholesterol and LDL. However, certain individuals are "egg sensitive" and experience significantly higher blood cholesterol levels with increased intake of dietary cholesterol. 

  • Roberto Kasuo Miyake added an answer:
    Resilient Telangiectasias: do you search (and treat) the feeder veins?

    We've been removing feeder veins to treat telangiectasis since the 70's. From 2005 on, we've been finding those veins by augmented reality and treating them with CLaCS (a combination of transdermal laser, skin cooling and Dextrose75%).

    The prevalence of those feeder veins is significantly higher in a patient with telangiectasias comparing to a patient with no aesthetic concern on the leg (no visible telangiectasias or small varicosities)

    What is your opinion/experience?

    Roberto Kasuo Miyake

    True Imre Bihari, 

    It is rare to have a simple telangiectasia, disconnected to feeder veins.

    Duplex ultrasound helps to find them.

    VeinLight illumination helps as well but augmented reality (VeinViewer) is the ideal way to diagnose and guide the treatment. 

    Hope to see you in Brazil at IMAP2016! 

    the website is ready

    Best regards


  • Jeremy P T Ward added an answer:
    What lines of pulmonary artery smooth muscle cells have given you good cGMP levels in responses sGC activation?

    I am studying pulmonary vascular function and I would like to use cGMP as my readout of NO signaling. My lab is very experienced in doing this in systemic vessels (aortics for example), but I am new to the lab and studying pulmonary biology. When I've tested rat and one line of human PASMC I have gotten poor, barely detectable results. Of note, I am using a commercially available cGMP ELISA Kit from Cell Signaling. As an alternative readout, I will also use pVASP to assess PKG responses. 

    Jeremy P T Ward

    I am afraid that it is unlikely you will improve your results using another cell line! Measurement of cGMP is common in pulmonary artery preparations, whether intact or in cells (because of the key importance of  cGMP modifying agents in therapy of pulmonary hypertension, e.g. sildenafil). So there are many papers out there that do this (this is but one: Liu J, Liu H, Li Y, Xu X, Chen Z, Liu L, Yu X, Gao Y, Dou D. Cross regulation between cGMP-dependent protein kinase and Akt in vasodilatation of porcine pulmonary artery. J Cardiovasc Pharmacol. 2014 Nov;64(5):452-9.) The major problem tends to be lack of sufficient tissue mass to start with, as the amount of cGMP is small, and/or being too slow to snap freeze the tissue/cells. cGMP is degraded fairly fast, which is why most assays include PDE inhibitors. So it is likely to be primarily a methodological problem that you have. I would try using a larger tissue mass and as a positive control treatment with sildenafil (or other specific PDE 5 inhibitor), and speed up all preparative processes. 

  • Cristina Rodriguez asked a question:
    Has anyone used pluronic gel for in-vivo siRNA delivery in the vascular wall?

    Do you have a detailed protocol?

    Vascular Wall siRNA delivery

  • Jean Noel Fabiani added an answer:
    What size would you consider repairing a descending thoracic aortic aneurysm and why?

    There is no powerful evidence to support any specific threshold. The study reported by the Yale group reported an increase in complications at sizes of 70mm (Davies 2002), but most consensus guidelines suggested repairing them at 55mm. Given the lack of natural history data, what are the arguments for and against this aggressive threshold?

    Jean Noel Fabiani

    It's a difficult question and the answes depends of etiology. In case of Marfan syndrom, I perform on the direct operation (use of stentgraft is forbidden in this pathology)  at 55mm, in case of atherosclerotic aneurysm between 55 and 60 mm, depending of the evoloution. In case of dissecting Aneuvrysm after a diameter of 60mm.Regards.

  • Adeola Michael Gbadebo added an answer:
    Hw can a drug increase left ventricular end-diastolic and end-systolic volumes without reducing ejection fraction

    Does anyone have a rational explanation for how a drug might increase left ventricular end-diastolic and end-systolic volumes without reducing ejection fraction (and without an increase in natriuretic peptides)?

    Adeola Michael Gbadebo

    It could be that the drug has some lusitropic effect while at the same time reducing contractility a little or not changing the contractility at all.

    Please, I need comments on this view I have expressed. 

  • Gabor T Gyenes added an answer:
    Coronary steal due to the large side branch of LIMA; What can we do ?

    41 years old man who had three vessel CABG (LAD-LIMA, RCA-Ao,Cx-Ao) two years ago.

    He had history of recurrent exertional angina, poor exercise tolerance despite maximal medical therapy for the  last six months. Therefore we performed coronary angiography. Angiography showed patent grafts of LAD-LIMA, RCA-Ao, Cx-Ao. However, the  large side branch of LIMA had not been ligated. The side branch can be coronary steal.

    What  we  do ?

    + 4 more attachments

    Gabor T Gyenes

    I agree with all of the above. Other than a coil, you could deploy a covered stent in the LIMA as well, occluding the side branch.

  • Marco Marano added an answer:
    Where can I find references on the alveolar-arterial gradient?

    The Alveolar–arterial gradient (A-aO2, or A–a gradient), is a measure of the difference between the alveolar concentration (A) and the arterial (a) partial pressure of oxygen. It seems an useful and interesting parameter in the topic of pulmonary imbibition, but I failed to find published research in last years.

    Can you help me?

    Marco Marano

    Dear Francesco,

    Many thanks for the paper. I take it just a quick look. 

    I have not yet  the answer to my question. However within the french paper there are some interesting points to read carefully. 

  • Closed account added an answer:
    Should mice die after middle cerebral artery occlusion (MCAO)?

    I'm doing MCAO on mice 22-26 grams using doccol filaments and find that a number of my mice seem to be dying overnight, often the ones that don't die after 24 hours look as if they would not make it to a 2 week time point. I'm not sure why this is. My mice get 1ml of saline IP'ed and are kept in a heating pad at 37 degrees after surgery and get gel and food on the cage floor.

    It seems like I started having problems when I began using laser doppler so maybe I'm causing alot of trauma when placing the probe (I do need to make a fairly large hole in the muscle to get the probe attatched) or it's causing some kind of infection? I want to say there's some connection to when I began using laser doppler but I might be reaching for answers. I've been told my surgery (in terms of inserting the filament) doesn't cause very much trauma.

    Any ideas?


    Thanks, maybe anesthesia is the issue, when I started using laser doppler it takes me a bit to get the probe attached so my surgery is being noticeably prolonged. I'm going to try to lower anesthesia and work on being faster attaching the probe. Hopefully this works.

  • Alessandro Durante added an answer:
    How do you solve this medical problem ?

    Subclavian  Artery  Dissection;  A  Rare Complication of  Transradial  Angiography

    A 52-year-old female patient presenting with typical angina pectoris was admitted to the cardiac catheterization laboratory with evidence of inferior left ventricular wall ischemia detected by myocardial perfusion scintigraphy spect. A short, 6  Fr  sheath was inserted into the right radial artery and a 5 Fr radial diagnostic catheter (Optitorque; Terumo Corporation) and 0.035˝  260 cm 260 cm “J” tip wire were used for diagnostic coronary angiography. While the guidewire was advanced to reach the ascending aorta, there was resistance on the  right subclavian artery. The guidewire was withdrawn and selective right subclavian angiogram was performed that demonstrated the dissection of subclavian artery  (Figure 1).

    Alessandro Durante

    In absence of symptoms I would perform a close monitoring with US and CT. If any worsening is seen I would implant one or more stents to close dissection.

  • Mostafa Samak added an answer:
    Has any one tried to induce Hypertrophy in mouse neonatal cardiomyocytes and measure increase in cell area?

    I have been using primary cultures mouse neonatal cardiomyocytes (NCM) to study hypertrophy. However, the conventional ways of hypertrophy induction (e.g. by catecholamines, Angiotensin II or Endothelin-1) were previously shown to have very subtle effects in mouse compared to rat NCMs (Deng et al., Circ Res. 2000;87:781–788.). I have personally noticed this, and the best results I got were when I used angiotensin, but yet in very high doses (10 -50 micro M) for 48-72 hours. Increase in cell size, being a widely accepted marker, was not more than 10-15%. Moreover, it was shown that mouse NCMs undergo spontaneous hypertrophy without an inducer. Nevertheless, unlike the cited paper, some papers have published better results of up to 1.5 times increase in cell size. I was wondering if there are some tricks that I can utilize to get a more prominent effect.

    Mostafa Samak

    Thank you Nai-Kei for the valuable information.

  • Roberto Flore added an answer:
    What is preclinical carotid atherosclerosis, how is it defined and what is the marker for it?

    Hi, dear all, can you please help me with the follow questions: How to define preclinical carotid atherosclerosis? and what is the marker of it? If carotid intima-media thickness >1mm, may I say this patient already have carotid atherosclerosis, or I should say the patient is in the status of preclinical carotid atherosclerosis?

    Thank you all very much!

    Roberto Flore

    hi Li, could the attached review help you?   

  • Vittorio Dorrucci added an answer:
    Graft İn stent carotid artery restenosis;What are your opinion with this case?

    We had  reported  the case of a 57-year-old male patient with a history of acute amaurosis fugax. Carotid angiography was performed as blood pressure differed between his left and right arms and there was a pan-systolic murmur on the left common carotid artery. Total occlusion of the proximal right brachiocephalic artery and a thrombus occluding 90–99% of the left internal carotid artery were detected by carotid angiogram. We decided to place a graft-covered stent through the lesion first, and contain the plaque and thrombus between the stent and the lumen. Therefore, a graft covered stent (5×13, Direct) was implanted with 12 atm pressure. After removing the distal blockingbased protection system, we opened the selfexpanding stent (7×10×30, Cristallo) (figure 3) and dilated the stent using a post-dilatation balloon5×20, Tarcomgrande).

    A self-expanding graft-covered stent was successfully implanted and there were no complications. This case  published in BMJ Case Journal “ Covered stents may provide extra protection during carotid artery stenting in high risk patients with an excessive thrombus burden”, Tatli E, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-010258.

     However , the patient presented transient  ischemic attacks after three years. DSA angiography show 99% instent restenosis in the  overleap segment of   the both stent.

    What are your opinion with  this case ?

    + 1 more attachment

    Vittorio Dorrucci


    if I well understand the restenosis was in the overlaping zone where there are two different materials in contact and a different radial force. It's very likely that these two factors have favored the neointimal iperplasia.

  • Dietrich Klueber added an answer:
    What are the complication rates for intravascular placed heart valves?

    Above method is quite new and due to the high insurance pay happily accepted by heart surgeons. Are there studies, that describe the most important complications rates like: malplacement, secondary displacement, cerebral infarct, other kind of embolism?

    Dietrich Klueber

    Nathan: could you please shortly write the complication rate named in my question in this 5-yrs-study?

  • David C. Ellinsworth added an answer:
    Has anyone observed an ability of catalase to attenuate responses to NO donors?

    Apparently catalase can bind NO, but every other publication I've seen where this protocol has been used (usually as a negative control for endothelial dysfunction studies) shows negative results, yet mine were very conclusive

    David C. Ellinsworth

    I did consider using my colleague's chemiluminescence system to see if NO was consumed by catalase but I was at the end of my studies and simply didn't have the time

  • Jonathan Skillings added an answer:
    What is the impact of physical activity, screen time, diet drinks and weather on CV disease?
    Jonathan Skillings

    Data from population studies dating back from the Framingham study/substudies among others demonstrated quite clearly that a sedate lifestyle and a diet high in calories were risk factors for the development of atherosclerosis. I am not aware of any studies looking specifically at "screen time" which I assume you mean computer screen time but any such activity, whether watching TV, playing video games or what have you that limit physical activity will have the same effect of classically measured low activity lifestyles. I am not aware of a US study on the effects of weather but the Scandinavians may have conducted a few.

  • Leong chen Onn added an answer:
    Do you know of any left ventricle or heart localization method for tagged MRI?

    I'm currently researching on left ventricle motion quantification. Can anyone suggest me any heart or left ventricle localization method in tagged cardiac MRI images? Appreciate if you can provide me references too. Thanks.

    Leong chen Onn

    Thanks all. I'm looking for an automated method to define the ROI (left ventricle) for tagged MR images.

    To Aymeric Histace, I think the paper you recommended me is useful to me. I'm interested with the mean-std image method which I have personally tried to apply. But I ran into some problem. I've attached the image of the mean-std image below. The mean-std image i generated does not show a a significant contrast between the cavity and the left ventricle wall. I think I'm doing it wrong or missing some steps.

    Here are the steps I have taken using Matlab to process the image.
    1) compute local mean image using 'conv2' with kernel size N=11
    2) compute local std image using 'stdfilt' with kernel size N=11
    3) compute uendomap(i,j)=wm.mN(i,j) - wo.ON(i,j) with wm=1/3 and wo=2/3 where wm+wo=1 and wo/wo=2.

    Any help is appreciated as I might adopt this method to localize my tagged MR images for my coming paper. Thanks.

  • Hubert Dabire added an answer:
    At what percentage of relaxation of acetylcholine to norepinephrine the endothelium of a rat aorta may be considered intact in vitro?

    Recently, someone asked here how to remove the endothelium in a rat aorta. I do agree with all answers. My question now is how to check that the endothelium is correctly removed. In other words, at what percentage of relaxation to norepinephrine or other vasoconstrictors (what concentration?) induced by acetylcholine (also what concentration?) one can consider that the endothelium is correctly removed? Conversely, at what percentage of relaxation one can consider that the endothelium is present or intact?

    Hubert Dabire

    It will be a pleasure to meet you to discuss this subject. How can i contact you?

  • Norbi Gabor added an answer:
    Can LMWH anticoagulation be used before ECV?

    What about LMWH anticoagulation (3-4 weeks) without TOE control before ECV? Because in guideline only VKA or NOAC has written, but nothing said about LMWH. What is you opinion?


    Norbi Gabor


  • David Gross added an answer:
    What factors may be related to the adaptation of prosthesis in patients with major lower limb amputations?
    We observed that the prevalence of adaptation to lower limb prostheses was 38%. And patients with a low level of education were the least frequently adapted to the prosthesis.
    David Gross

    Thanks,  Dee for  a  very  thoughtful  and  enlightening  post.

  • Mohammad Faramarzi added an answer:
    What is the most common cause of Acroangiodermatitis of Mali?

    Acroangiodermatitis has been described in amputees (especially in those with poorly fitting suction-type devices), in patients with paralyzed legs, in patients undergoing hemodialysis (from arteriovenous shunts distally), and in association with hepatitis C. It has been documented in chronic venous insufficiency and in vascular malformations (eg, Klippel-Trenaunay syndrome, Stewart-Bluefarb syndrome, Prader-Labhart-Willi syndrome).

    Mohammad Faramarzi

    Severe chronic venous stasis and failure of the calf muscle pump could have resulted in the elevated capillary pressure causing reactive vascular proliferation and clinically presenting as lesions of acroangiodermatitis.

  • Markus M. Mueller added an answer:
    Is there any information about haemophilia and ageing?

    Congratulations, you discussed a very interesting issue. I agree with the individualized therapeutic approach, especially in the patients with mild haemophilia phenotype. I would like to discuss the management of elderly haemophilia patients with atherosclerosis, obesity, smokers who have undergone an episode of arterial thrombosis. What do you think about the combination of replacement and antiplatelet therapy? How many haemophilic patients with diabetes and other conditions such as cancer do you have? 

    • Source
      [Show abstract] [Hide abstract]
      ABSTRACT: Owing to the heterogeneity in the clinical phenotype of haemophilia A and B, it is now recognized that disease severity (based on factor VIII/IX activity) may no longer be the most appropriate guide for treatment and that a 'one-size-fits-all' approach is unlikely to achieve optimal therapy. Based on the present literature and consensus views of a group of experts in the field, this article highlights key gaps in the understanding of the diverse relationships between bleeding phenotype and factors such as joint health, genetic susceptibility, laboratory parameters, quality of life and management of pain. Early prophylaxis is a potential 'gold standard' therapy and issues surrounding inhibitor development, variations in its clinical use and long-term outcomes are discussed. Comprehensive treatment should be individualized for all patients (including those with mild or moderate haemophilia and carriers). Wherever possible all patients should be given prophylaxis. However, adult patients with a milder haemophilia phenotype may be candidates for ceasing prophylaxis and switching to on-demand treatment. Regardless, all treatment (on-demand and prophylaxis) should be tailored towards both the patient's personal needs and their clinical profile. In addition, as the associations between risk factors (psychosocial, condition-related and treatment-related) and clinical features are unique to each patient, an individualized approach is required to enable patients to alter their behaviour in response to them. The practical methodologies needed to reach this goal of individualized haemophilia care, and the health economic implications of this strategy, are ongoing topics for discussion.
      Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 11/2014; DOI:10.1097/MBC.0000000000000225
    Markus M. Mueller

    Dear Peter,

    an expert in your field of interest would be Dr. Wolfgang Miesbach, head of the hemophilia clinic at the university clinics of the Goethe University in Frankfurt/Main, Germany.

    If you can send an email directly to, I will send you his mail address.



  • Khaled Saad added an answer:
    What is the maximum dose of statins in children with hypercholesterolemia?

    Use of statins for treatment of familial homozygous hypercholesterolemia: What is the earliest age for initiating statin therapy and what is the maximum dose used in young children.

    Khaled Saad

    Lea S. Eiland, and Paige K. Luttrell,  Use of Statins for Dyslipidemia in the Pediatric Population.J Pediatr Pharmacol Ther. 2010 Jul-Sep; 15(3): 160–172.
    PMCID: PMC3018249

  • Christos P Loizou added an answer:
    Can anyone help me to find the Database of CCA Ultrasound Video and its ground Truth?

    for Atherosclerotic Plaque Segmentation

    Christos P Loizou

    Dear Emimal, We have a database such the one you are describing, but it is not yet available to download. We have however some other image databases with ultrasound images of the CCA with their Ground Truth available. Have a look at See under downloads.

About Vascular Medicine

Vascular medicine (angiology) is the medical specialty which studies the diseases of circulatory system and of the lymphatic system, i.e., arteries, veins and lymphatic vases, and its diseases.

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