Science topic

Vascular Medicine - Science topic

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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The number of papers published every year on medical CFD has increased by 10 times in the last 20 years (see attached figure).
We all know that there are many papers are just out there for the sake of publication or to get points for a funding program. However, CFD has indeed become quite a mature technology for medical simulation applications in many areas such as vascular and respiratory medicine.
What are the genuine drivers power this increase in the number of medical CFD papers?
Would love to read your thoughts.
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Just a personal opinion, based on 60 years experience.
From the 1950s, with analogue computers and calculating machines, there have been attempts at physical modelling of cardiovascular hydrodynamics and to a lesser mathematical extent respiratory fluid dynamics and gas exchange.
These have usually been motivated by inter disciplinary collaborations or in some rare cases by individual medical trained people who were also well educated in mathematics and physics ..
The topics chosen were usually the most amenable to mathematical modelling rather than the most clinically relevant.
With the development of digital computers and easy to use software packages requiring much less mathematical and physical knowledge, modelling has become more doable in medicine and especially in biomedical engineering. This has enabled more relevant problems to be addressed and has attracted a wider class of "mathephysicians", medical biophysicists and medical computing people and created its own academic niche.
However , many of the most important medical research developments have been due to mathematics/physics carried out by non medical people eg CT scanning, MRI, DNA sequencing, PCR, prosthesis design, neural net theory, drug design.
See Nobel prize winners.
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About Mitraclip implantation
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Apologies for not joining this discussion sooner... Did you eventually get what you were looking for?
Did you want to publish an article on this topic? I am assuming this is what you wanted - for this, I would also keep in mind those journal groups - as mentioned by Yoshihiro J Akashi and Rajkumar Doshi - have a specific one for interventions - and we would, of course, consider MitraClip being a type of intervention...
"JACC: Cardiovascular Interventions"
"Circulation: Cardiovascular Interventions"
"EuroIntervention"
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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.
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Yes,I agree with you
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In recent research (pdf attached is below) we found that patients with a low educational level became adapted to the prosthesis less frequently.
This was a cross-sectional study. The patients were identified by primary healthcare teams.
The inclusion criterion was that these should be patients who underwent major lower-limb amputations of any etiology. Associations between sociodemographic and clinical variables and the adaptation to lower-limb prostheses were assessed.
We examined 149 patients. Adaptation to the prosthesis occurred in 40% (60/149) of them, but only 62% (37/60) of these were using it.
Adaptation occurred more often among male patients (P = 0.017) and among those who had a higher educational level (P = 0.013), with a longer time since amputation (P = 0.049) and when the etiology was trauma (P = 0.003).
The result from logistic regression analysis showed that only patients with low education (P = 0.031) were significantly associated with a lower frequency of adaptation to prostheses.
What's your opinion and experience about this?
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As amputations results in a variety of limitations that have emotional consequences for patients, we evaluated non-psychotic disorders and their associated factors in a sample of people with lower limb amputations.
We detected a prevalence of 43% of mental disorders assessed with the SRQ-20 questionnaire.
Patients with associated chronic diseases and lack of independence remained significant showed a higher positivity in relation to psychological morbidity.
Reference
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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). 
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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).
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Acroangiodermatitis of Mali is usualy caused by chronic venous
insufficiency
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Compared to extremely unhealthy recommendations by English doctors in Shakespeare's time (discouraging baths, blood-letting), Ancient Egyptians had an extremely sophisticated understanding of the cardiovascular system, surgery and appropriate herbal medicines still in use and effective today. Why were European doctors so far behind African advancements in medicine?
Ancient African Women's Rights and Lifestyle:
Until recent Suffrage Laws, modern women in American and European cultures had very few rights compared to women in Africa during Europe's Dark Ages. Why is it taking several centuries for Europeans and Americans to accomplish what Africans accomplished thousands of years ago?
The respect accorded to women in ancient Egypt is evident in almost every aspect of the civilization from the religious beliefs to social customs. The gods were both male and female, and each had their own equally important areas of expertise. Women could marry who they wanted and divorce those who no longer suited them, could hold what jobs they liked - within limits - and travel at their whim.
Why is it that European and American scientists still do not know how ancient Africans built the Giza Pyramid?:
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On the East coast there was certainly urban development although Zimbabwe, an important city, was not built until about the 14th century. But in truth, archaeology is lacking for many parts of sub-Saharan Africa as nobody has expected or expects anything. Mali of course was then a rich and influential state. Famously, the Moors arrived in Spain from Morocco and other parts of Northern Africa and built one of the outstanding civilisations of the time.
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When to measure INR _as a follow up monitoring_ following warfarin administration in a patient with VTE? 
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INR should be measured after 3 days of starting warfarin therapy. After that, measurement is variable between institutions. It an be done every week first and if INR is in the therapeutic range continue every 2 weeks and then every 4 weeks. 
There is a guide: Evidence-Based Management of Anticoagulant Therapy
CHEST 2012; 141(2)(Suppl):e152S–e184S
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I've tried to perform both wire injury and carotid artery ligation models of hyperplasia. However i was not able to get transverse section of the carotid artery for histology analysis. Any tips? thanks in advance
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Dear Ignacio,
I recommend you to use a piece of  filter paper around the artery ( like susage) and you have to fixe it for 24 hr in formalin. It woud be easy for you to cut it in a transverse manner. Please embedd the specimen in paraffin personally.
best wishes
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how can we avoid  cerebral  emboli during CABG  in patients with large mural LV  thrombus
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Thrombus should be removed by left ventriculotomy or if possible by left atriostomy ..large mural thrombus are generally associated with LV dysfunction.. And left ventriculotomy may further reduced the LV function. So if possible thrombus removal by left atriostomy may be preferable... 
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I woulod like to know how it was done.
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I have no personal experience. Following article may help you.. Thanks.. 
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The patient with uruptured aneurysm. Planned cardiac surgery for replacement aortic valve. 
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I would recommend Coiling Prior to AVR and one month at least in-between both procedures.
Cardiopulmonary bypass and heparinization as well as pressure fluctuation in the perioperative period may have a deleterious effect on the un-rupturred aneurysm 
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We were not able to detect elevated EDP in mice using miller pressure catheter. But we see a clear increase in EDV in same mice using MRI scanning? What would be a possible explanation for this?  
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why
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Oxygen supply of vascular wall.
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I would like to point out that another factor thought to have a role in vasa vasorum distribution is the lower osmotic pressure in venous vessels, which, in addition with the difference in oxygen content of blood -as explained above by Dr. Itoo- gives reason of the better development of vasa vasorum in venous vessels.
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Genetic marker have some role in predicting risk of stroke in this condition. Spontaneous apoptosis of smooth muscle cell in the atherosclerotic plaque combined with inflammation contribute to thinning of fibrous cap. Polymorphosims of CRP, I L-6,ICMP-1and MMP-3 are studied as a risk factors of stroke in these patients. Genetic Polymorphosims of coagulation factors also have important role. 
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Acetylcholine lacks relaxatory effect in this artery
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Hi, Rezhna      Endothelial dysfunction in umbilical artery may be an important  predictor of future atherosclerosis. Expression  of NO synthases(eNOS,iNOS,nNOS).pro oxidative enzymes and antioxidative enzymes like supernatural dismutase1-3,glutathione peroxidase1in umbilical arteries may be helpful in detecting Endothelial dysfunction. It has clinical implication. Small and large for gestesional age babies have Endothelial dysfunction in umbilical artery compared to appropriate for gestesional age babies and they are having higher risk of future  development of atherosclerosis. 
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Do you have a detailed protocol?
Vascular Wall siRNA delivery
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For the qunatitaive study of atherosclerosis in mice, is gelatin embedding of heart important or can we do snap freeze with isopentane?
My understanding is that, to study atherosclerosis, we need to do Oil Red O staining to study the foam cells and also the journals now ask for cell types present in the atherosclerotic plaque.
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There is a mistake on this question. I am not an author of this article. Sorry about that.
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What are the non invasive methods for carotid stimulation?
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the link above provides enough information, however be AWARE of the conditions you must NOT perform carotid massage. first if your patient has a history of carotid artery plaques indicated by previous ultrasound or previous thromboembolic strokes. secondly always perform this maneuver in a tertiary setting so that if severe side effects such as cardiac arrest happen you will be able to manage them. I recommend using Vagus nerve stimulators prior to using carotid massage; such as drinking ice cold water and invoking gag reflex.
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How manage preoperative time of  the patients with asymptomatic significant aorta stenosis? Should patient wait for the surgery at home or at the hospital? What criteria for select (home, hospital)? The risk stratification of the sudden cardiac death of the asymptomatic AS patient? And what is your own opinion, practice of the management of the preoperative time?
Thank you!
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I guess it depends indeed more on symptoms, on functional capacity of a patient and maybe on NT-proBNP levels than specific echocardiographic findings. But Sir you are right, at the moment it is still a very subjective decision. 
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What could be the best way to remove Baseline drift from PPG signals.
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HIgh pass filter will do. Or you can do a peak / trough detection of systole and diastole and bring all diastole peaks to the same DC level (also known as baseline correction).
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Hello 
I'm trying to collect the left ventricle from a mouse heart and i have zero experience in that. 
i tried to look for videos and publication and i didn't find any useful ones
could any one suggest a good video or a protocol of how to distinguish the mouse left ventricle and what are the tools used to collect it ?
thank you
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Hello, this is not really a protocol, but a basic HowTo...
Left ventricle is the biggest part of the heart, so you can collect it in a "just remove everything else" way. When you have the heart, take small scissors and cut away all the small parts that are "hanging" from the heart (if you can lift it with the tip of your scissors, then it should go away). That way you should get rid of the aorta and both atria and you will get firm egg-shaped thing. One side will be a bit softer and bulging. That's the right ventricle. 
From the where-aorta-was side insert scissors and cut down so the right ventricle will open. Remove that and you have only left ventricle left. 
Small curved scissors are sufficient, if available spring-type micro scissors are better for removing the tiny bits. For basic anatomy-learning purposes, some people found it helpful to leave the heart for several hours in formaldehyde, which makes it stiffer.
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A 76-year old female was admitted in heart failur, with echocardiographic and MRI signs very suspicious of Loffler endocarditis with apical thrombus and restrictive filling pattern (see figure in the attachment). An extensive clinical work up was done but no HES was found. We excluded parasite infection, hematologic (biopsy+cytogenetics neg.) and rheumatologic disorders, allergic and drug reactions, no malignancy was found. No histological verification was done but according to the specific echocardiographic and MRI findings we concluded that Loffler endocarditis without peripheral eosinophilia is most likely. We started the treatment with oral Methylprednisolone 1 mg/kg/day, warfarin and conventional heart failure therapy. After 14 days, there are no changes on the echocardiographic examination. In your experiences, what do you think would be the best treatment strategy for our patient? How long is the treatment with corticosteroids indicated and when we should taper the steroids? Do you think that cardiac surgery in indicated in this case? What abpit left-sided biopsy (risk for thromboembolism/cost-benefit?)
Thank you in advance for you kind answer and any help.
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Thank you. Good luck to you and your patient recovery.
Кind regards
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58 years old female presented with swelling and unhealing wound in left arm (Figure 1).  She  had not  hemodialysis  fistula , chronic renal failure, hypertension and diabetes mellitus. Angiography showed fistula from brachial artery to venous system (Figure 2-3).
What are your diagnosis ??
What  should be treatment option ?
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I am excluding he congenital origin at this age, it could be a posttraumatic AVF, or an intramuscular haemangioma, I had a similar case that was treated successfully by simple multiple ligations.    
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I am looking to sample questionnaire which measure knowledge, attitude and practice to predict risk behavior for cardiovascular diseases.
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Hi,
I agree that the WHO STEPS modules would be simple tools for risk assessment
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plaque classification obejective
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Just contact the people at the BiKE biobank at the karolinska (Ulf Hedin).
Note that most stable lesions are probably FCPs (stabilized lesions) according to the Virmani classification and not stable lesions (LFA, Virmani classification)
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The first complaint of the patient (54 years, male) appeared  as presyncope and palpitations. A year earlier he developed AF paroxysm and was treated by metoprololi; at that time coronary angiography was performed and found that that his arteries were without changes. Presently, as a result by Echo no structural abnormality of the heart was revealed: LVEF 66%, LVEDV-124 ml, LVEDD-51 mm, the right heart chamber are not expanded, RV EF - 57%. However, by HM-ECG were revealed episodes of ST-elevation at night time (prolonged and brady-dependent) and ventricular arrythmyas. HM-ECG strip attached below. What is the next step of diagnosis is required?
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Hi Philip! Your idea is very interesting and original. I was very impressed with it. Unfortunately, Dr. Myron Prinzmetal in original manuscript (Am J Med. 1959 Sep;27:375-88) variant angina pectoris really described: variant angina  was presented with clinical, electrocardiographic and autopsy findings (attacks of chest pain, reciprocal ST depression/elevation, coronary artery stenosis). In his landmark article in 1959, Dr. Myron Prinzmetal described a distinct type of “variant angina,” termed Prinzmetal’s angina. This chest pain tended to occur at rest (i.e. was not associated with increased cardiac work), waxed and waned cyclically, occurred at the same time each day, and could be accompanied by arrhythmias including ventricular ectopy, ventricular tachycardia, ventricular fibrillation, and various forms of AV block. The patient’s ECG during painful episodes typically showed ST segment elevations (occasionally accompanied by reciprocal ST depressions), whereas the ECG obtained after the pain had resolved showed resolution of these ST segment changes. Prinzmetal postulated that this separate clinical entity was due to transient spasm (“increased tonus”) of a large arteriosclerotic artery, causing temporary transmural ischemia in the distribution supplied by that artery.It was subsequently demonstrated that such episodes of coronary artery spasm can occur not only in patients with underlying fixed coronary artery obstruction but also in patients whose coronary arteries are anatomically normal.
But other case reports of the1960's representing the Prinzmetal`s ECG are very similar to BrS, since "reciprocal" depression of the ST segment in leads distant from those showing ST elevation are absent and the clinical picture described of attacks was blurred and nontypical.
Very interesting your opinion on this issue I have conquered.Thanks!
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Every DVT event is the result of an "abnormal" surface, an abnormal "equilibrium" for plasma coagulation proteins and factors and sometime platelet reactivity (yes, even on the venous side). A local slow flow is an aggravating factor. But a generally reduced microcirculatory flow is a tremendous aggravating factor. Bad microcirculatory flow = low conversion of Protein C to Activated Protein C. Lack of APC leads to increase procoagulative state, decrease protection against platelet aggregation, and less profibrinolytic drive. It is only one factor, look to the antithrombin III content, the other inhibitors and factors and the game becomes very very complex. In cancerous states, some abnormal proteins are often exposed and trigger the coagulation processes, illustrating the surface role.
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How does arterial blood pressure signal morphology change during tachycardia and/or bradycardia? Is there any good reference for studying this subject?
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Of course it does, it has been described for fifty years in all good basic cardiology books.
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Are angiography and lymphoscintigraphy necessarily distinguishing methods
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Dear Rafik Karaman. Thanks very much
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In our lab we are trying to isolate proteins from perfusate from Langendorff perfused rat heart. We desalinated perfusates by dialysis and concentrated them in centri-vap, but the protein concentration is very low and HPLC gave no results. Can by problem in storage of perfusates (-25°C)? Are proteins in frozen perfusate sensitive to degradation? 
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It also depends on what you are trying to detect.
-25°C should be good but -80°C would be better.
Testing the samples close to the time of collection is also important.
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Hello, friends.
I am a new researcher in cardiovascular field and looking for a promising research point. Do you have any advice? 
And I am looking forward to sharing my ideas with you. If we can cooperate, it couldn't be better! 
Thanks in advance for your help!
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I believe that we know (maybe) 5% of what it would be useful to know about humans and about  cardiovascular system. Then there are plenty of useful research, "hot" and interesting. There is still much to discover. The important thing is that searches are well designed and well conducted and that researchers are free
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Especially, I would like to know changes of valvular regurgitation with asystole state. I am trying to study degree (LVEDV or LVEDP) of LV distension  after acute HF.
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In cases of  acute HF the degree of regurgitation is underestimated, becouse of rediced CO. On the other hand it depends on the ethyology of the valve lesions and on the mechenism of HF (AMI, PE, CMP and etc)
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Most of the literature refers to increased troponin in serum as a biomarker but I am interested in knowing if decreased levels in the heart indicates disease.
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Dear Rachael i am afraid i havent come across any evidence that is suggestive of Trop reduction in context of DCM. Trop could indeed be significantly raised in a a wide variety of DCM such as Ischemic cardiomyopathy, Hypertrophic CM, Cardiac Sarcoid/Amyloid & Vasculitis with Cardiac Involvement etc as i am sure you must be aware.
very best wishes
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Is there literature-guidelines in this field?
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Based on my previous suggestion, I would again go along by the advice of Dr. Sujay Shad.
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Are there any screening tools for the detection of heart failure at the community level (other than the biomarkers NT-proBNP and BNP)?
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Thank you very much for the reply
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How to avoid Froth in Wire - Myograph upon incubation with catalase? I see many papers using 1200U of catalase which when used produces froth. Are there ways to overcome this?
Thanks
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Look at:
Liu Y et al, 2011 Circ Res, Hydrogen peroxide is the transferable factor mediating flow induced dilation in human coronary arterioles
This is a very well done study that makes full use of PEG-Cat
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Some time in case of extensive PAD and critical ischemia we need to perform the simultaneous reconstruction of aorto-iliac and femoral-popliteal segment. What is your opinion about the optimal site of proximal anastomosis for femoral-poplieal bypass with reversed saphenous vein? Should vein takes-off from the synthetic graft or from the common femoral (femoral) artery? Some surgeons claimed against the anastomosis between synthetic material and vein.
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I favored to anastomose the aorto-femoral graft limb end-to-side to the common femoral artery with a tongue extending for about 1-2 cm in the profunda femoris artery, and the venous bypass (preferentially over non-autologous graft) end-to-side implanted in the graft limb. I used to implant a venous patch in the graft limb for anastomosis with the vein graft in case the vein graft appeared rather small (< 4 mm in diameter). In skinny patients and patients in whom skin healing might be jeopardized (for instance a redo) I would cover the graft and its anastomic area with a sartorial muscle flap over which the skin is closed with an continuous intracutaneous absorbable suture.
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On what basis some patients with hypertension are specifically given either diuretic or vasodilator or both to lower the blood pressure? How to confirm if the hypertension of an individual is as a result of decreased blood vessel diameter or increased blood volume?
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it wuold be advisable to have the patient evaluated by a physician or cardiologist before embarking on this endevour.
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When and why should I use KCl normalization in vascular reactivity studies (contraction curves)?
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To add to Ellinsworth's answer, you should also use it again at the end of the experiment to ensure your tissue is still viable. There is the possibility that the experiment itself (incubations, washes, treatments, time, etc) could damage the tissue and alter results.
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variation in branching of internal iliac artery radiological OR cadaveric?
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Perhaps This?
Indian Journal of Surgery
December 2015, Volume 77, Supplement 2, pp 248-252
Anatomical Study on the Variations in the Branching Pattern of Internal Iliac Artery
Or Perhaps this one
Anatomy Research International
Volume 2014 (2014), Article ID 597103, 6 pages
Variability in the Branching Pattern of the Internal Iliac Artery in Indian Population and Its Clinical Importance
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Which is the standard and accurate method for finding arterial stiffness?
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Pulse Wave Velocity is considered a gold standard.
Ultrasound is also used in some population studies.
A few references below maybe helpful:
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A 34 years old  female presented with cyanosis  and pain of the right hand. Her patient angiography has been shown in Figure 1.
What is your diagnosis ? and  What can we manage this patient ?
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Structurally it appears that the radial artery is occluded sacrificing arterial supply to the thumb, index, and middle finger.  Without more history or more information, etiology may be difficult to ascertain.
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This 18 year old girl was detected to have Takayasu arteritis with hypertension during evaluation for polyarthralgias. MR angiography revealed her to have severe renal artery stenosis left and left subclavian artery stenosis. Recent literature seems to suggest a higher failure rate and restenosis with stenting rather than with plain angioplasty. This goes contrary to what we see in atherosclerotic coronary artery disease stents have a higher success rates. 
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I suggest angioplasty followed by drug coated balloon therapy.  I recently treated a young patient with a variant of pseudoxanthma elastica who developed sma stenosis and  mesenteric ischemia .  Plain balloon therapy lasted 6 months with recurrence.  I initially approached the patient as if it were fibromuscular dysplasia.  But the patient recurred and I did cutting balloon therapy followed by DCB.  She is now nearly 1 year out without recurrence.
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I have a patient who has gross clubbing of fingers and toes, who is smoking cannabis for last 15 years, 10 cigarettes a day. He is underweight with BMI of 22.5. I also noted epigastric mid line hernia.
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Go for the same symptoms as in nicotine smoker, as the volatile, active compound do not play a big role in development of clubbing
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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?
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Something else we used to do was file the forceps to toughen them up a little. This makes them more grippy... Particularly handy when gripping adipose tissue, or adventitia by the very top of the forceps. 
Sorry Dragan... You did also mention holding the tissue by the outer layer away from the smooth muscle. 
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Deterioration of renal function with significant reduction in GFR following treatment with beta blockers have been outlined in clinical practice and experimental research (vide Wilkinson 1982). The beneficial role of dopamine have also been acknowledged, but clinical evidences about the effects of some specific beta blockers are conflicting, i.e., nadolol, propranolol etc. So what's the current guideline of beta blocker usage in patients who have moderate renal impairment?
Epstein M, Oster JR. Beta blockers and renal function: a reappraisal. J Clin Hypertens 1985; 1: 85-99.
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Beta-blockers and renal function.
Wilkinson R.
Abstract
alpha-, beta 1- and beta 2-adrenergic receptors in the kidney mediate vasoconstriction, renin secretion and vasodilatation, respectively. Blockade of beta-receptors may therefore be expected to influence renal blood flow and possibly glomerular filtration rate by intrarenal effects as well as by reducing cardiac output and blood pressure. Since the various beta-adrenergic blocking drugs available differ in the degree to which they block beta 2-receptors (cardioselectivity) and also in their intrinsic sympathomimetic activity, they would be expected to have different effects on renal function. The acute administration of beta-blockers usually results in a reduction in effective renal plasma flow and glomerular filtration rate, whether or not the drug is cardioselective or has intrinsic sympathomimetic activity, with the exceptions of nadolol, which has actually increased effective renal plasma flow in some studies and of tolamolol. With chronic oral administration, the non-cardioselective beta-blockers reduced glomerular filtration rate and effective renal plasma flow. The cardioselective drugs do not usually produce significant reductions in glomerular filtration rate or effective renal plasma flow, although small increases in serum urea during treatment do occur. Interestingly, in contrast to findings with intravenous administration, orally administered nadolol produced a slight reduction in glomerular filtration rate in 1 study, so the effect of this agent on renal function under clinical conditions remains uncertain. It seems likely that beta-blockers reduce renal function predominantly by blocking beta 2-receptors in the kidney. To keep area of discussion in perspective, it is important to realise that although there have been isolated reports of serious deterioration in renal function coinciding with beta-blocker treatment, the great majority of reports are of reduction in glomerular filtration rate which are not of clinical significance, even in patients with pre-existing impairment of renal function. The beta-blockers with low lipid solubility-i.e. atenolol, nadolol and sotalol-are not metabolised, and their dose must be reduced in renal failure. Propranolol has active metabolites and its dose must also be reduced slightly in uraemia.
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I am looking for theory Information about angiotensin II receptors and about their genes, PDF or electronic books. Can you help me?
Thanks
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Hi Alaa here I send  some papers  that could help you
Clin Exp Pharmacol Physiol. 1996 Sep;23 Suppl 3:S67-73. doi: 10.1111/j.1440-1681.1996.tb02816.x.
Human type-1 angiotensin II (AT1) receptor gene structure and function.
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Atheromatous plaques are commonly seen in the coronaries, carotids and aorta. Despite sharing the same risk factors only certain sites are predisposed. Even in the same individual, despite similar blood vessel size, hemodynamic stress and blood flow patterns, plaques are often unilateral and seem to spare vessels sharing similar stress. 
Why this variation?
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Atheroma site specificity correlates strongly with regions of disturbed shear stress, I.e. on the outer wall at a flow divider, e.g. bifurcation - where shear is low, or at regions of vessel curvature, e.g the aortic arch. Also, contrary to popular believe, shear is not uniform across the circulation. In fact, it is considerably higher in small arteries and especially arterioles. Also, between species there is an inverse relation between shear and body mass, e.g. shear is around 15 times higher in the abdominal aorta of a rat than the same region in a human. Coincidence that rats don't spontaneously develop atheroma?? Notably, shear is a powerful inducer and suppressor of the genes pertaining to vasodilation and vascular disease. 
Hope that helps,
Dave
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Which force is needed to make an implant move/grow through soft tissue? There seems to be a threshold to be overcome by stents (or other implants) to make them grow through tissue. Too low means no growing through. Too high would create lesions. The only reported force I know is from bracelets on the teeth (nearly constant 1-2 N for extraction).
Is there anything known for soft tissue? Ideally for stents in atrial walls? Which biological processes enable this kind of "growing through"? How could i foster it?
I'd be thrilled to hear about your input!
Johannes
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Conventional arterial stents are designed not to grow into the intimal, medial or the adventitial layers. The stent is designed to distribute a uniform radial force sufficient to hold it in place reliably. Restenosis is and undesirable consequence that presents as a growth around the stent. If you want a stent to 'migrate' through the artery wall then it must be designed for that purpose. The form factor and profile for each strut should be reconsidered. Other considerations would be the edge effect of outward radial forces and perhaps other means of constricting the artery to provide a reactive force. These can be mechanically or pharmaceuticaly induced.
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Is there any consensus about the duration of anticoagulation in case of DVT? specially provoked, unprovoked & recurrent DVT?  
and when to introduce warfarin, simultaneously or after few days of administration of heparin? 
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Dear Osaid, standard practice is to start heparin and warfarin on day 1, then to stop heparin when INR is 2 or more for two days. Anyway, heparin therapy should last at least 5 days. The initial dose of warfarin is usually 5 mg. However, if the patient has active cancer, it is better to treat him/her with six months of LMWH without warfarin. After six months the patient should be re-evaluated for oral anticoagulant therapy (OAT).
Provoked DVT should be treated for three months, whereas for unprovoked DVT there is no consensus yet. The decision to stop OAT, or to prolong it, should be individualized on the basis of the personal benefit/risk profile and patient preferences. If you decide in favor of extended therapy, the patient should be re-evaluated at least annually. Now, we have some robust literature supporting aspirin or low-dose apixaban (where available) for extended therapy.
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Actually, I am concerned with the association between the use of contrast agents and rupture of thoracic aortic dissection (Stanford A type).
Here is the case I experienced recently. A 57-year-old male with a history of hypertension and atrial fibrillation visited our department with a complaint of chest pain. His consciousness was clear and his systolic blood pressure was 100 mmHg. TTE revealed dilated ascending aorta along with moderate aortic regurgitation. Immediately, contrast-CT was performed. Contrast enhanced CT revealed Stanford A type aortic dissection. There was no retention of pericardial effusion. Within a few minutes after that, he fell into CPA. TEE revealed massive retention of pericardial effusion. PCPS was introduced. However, PCPS did not work efficiently probably because of collapse in the right heart. Immediately, pericardial drainage was performed; drainage was not effective because of coagulated blood.
In this case,
Should we have performed pericardiotomy to save this patient?
May contrast agents trigger the rupture of thoracic aortic dissection (Stanford A type)? Actually, I know several cases that thoracic aortic dissection ruptured immediately after contrast CT. I want a paper discussing this point.  
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1- I doubt it's the contrast media (it can be catheter)   2- In my >50 yrs experience, I know of several cases of rupture of aneurysms in X-ray.   In fact, we long noted that with acute traumatic rupture of the aortic isthmus, the Radiology Department (& transportation) is very dangerous! 3- Acute intrapericardial rupture of a dissection is VERY unlikely to benefit from  pericardiotomy outside the OR. 
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Our lab group currently uses a conscious, unrestrained but tethered 275-350g male Wistar rat model of sepsis. As part of this model invasive blood pressure measurements are taken continuously. Currently this is achieved by cannulating the carotid artery with PE-50 tubing, tunnelling the tubing to the nape of the neck and exteriorising through a swivel attached tether system. A blood pressure transducer measures the blood pressure changes by tracking the fluid dynamics within the tubing.
This surgery required to place this line (and a jugular line to administer fluids) is quite invasive and I would like to reduce the surgical severity if possible. This will likely require choosing more distal cannulation sites where blood vessel diameter is smaller and where the tubing we currently use would be too large. Smaller tubing would therefore be required however I am concerned that smaller tubing will lose patency more easily and/or simply not transmit blood pressure information well enough.
Does anyone have any advice or experience on this - particularly what the lower limits for tubing diameter for successful blood pressure measurement would be.
Many thanks.
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Some years ago, we used similar techniques for intra-arterial BP recording in conscious unrestrained and untethered rats. Details of our technique can be found in the following publications: Am J Physiol Heart Circ Physiol 275:H1290-H1297, 1998 and Am J Physiol Heart Circ Physiol 292:H2506-H2512, 2007. In particular, we constructed polyethylene catheters [a PE-10 (2 cm length, 0.28 mm ID, 0.61 mm OD; Clay Adams, Parsippany, NJ) fused to a PE-50 (15 cm length, 0.58 mm ID, 0.96 mm OD; Guerbet, Louvres, France)] filled with heparinized 0.9% NaCl (50 U/ml). The catheter was inserted into the lower abdominal aorta via the left femoral artery to record distal (peripheral) aortic BP. The catheter was tunneled subcutaneously under the skin of the back to exit between the scapulae and was plugged with a short piece of stainless steel wire. After 24 h of rest, the catheter was attached to another PE-50 (15–20 cm). At least 2 limits must be highlighted: 1) whatever the diameter of the catheter, its tends to be obstructed with coated blood even if its filled with heparinised physiological saline. 2) Catheterisation of femoral artery leads to a heavier surgery than catheterizing carotid artery, as one have to tunnel the catheter through all the length of the back of the rat. Nowadays, the best way to record arterial BP is using telemetry, although this technique is very expensive.
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I would like to perform a little survey as the use of BITA grafting formyocardial revascularization.
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Thank you. Please, test the score in your patients or send me the necessary data (gius.gatti@gmail.com). Next, I will perform the analysis according to the models that I attached. Finally, if you agree, we will write a report.
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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.
Thanks
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No studies of lipid-lowering agents (statins or fibrates) in patients with NS have reported patient-centred outcomes including all-cause mortality, cardiovascular mortality, or non-fatal myocardial infarction; only single studies reported cholesterol (HDL, LDL and total cholesterol), There is no data on second-line agents (incl. ezetimibe) and outcomes in NS. 
There is also little evidence that secondary hyperlipidemia in NS has the same effect on cardiovascular outcomes. Bring the NS into remission and hyperlipidemia will resolve without the need of treating dylipidemia.
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What criteria do you use to surgery? Which embolization technique do you use?
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To my opinion the ovarian/iliac vein embolization/coils is indicated only in symptomatic cases with important pain or dyspareunia. I consider that in varicose veins (recurrent varicose veins) due to PCS the treatment can be limited to local intervention - phlebectomy or sclerotherapy. If symptoms are mild - the course of MPFF (micronized purified flavonoid fraction) can be tried.
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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?
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Dear Roberto,
Thank you for the interesting question.
I have been treating these feeder veins in the last 15 years. At the beginning only exceptionally, but nowadays I try to find them in every spider vein case. To find them Veinlight is used.
I think it is also important to find some hidden varicose stems or perforators. Previously I had some bad experience, and for this reason I now do US examination in every spider vein case.
Best wishes,
Imre
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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?
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Hi Benjamin,
The normal distribution of a complex biological system or process cannot be managed  by a single number or a linear algorithm.
Remember , a randomised controlled clinical trial describes the  ideal management for only the median patient.
However La Places law applies. P= t / r.h. Rate of change with sequential measurement is also important
A 5 cm aneurysm in a 40 year old Marfan's patient should be managed differently to a 7 cm aneurysm in 80 year old with comorbidities.
I have several elderly patients  referred for surgery with 5 cm + ascending aneurysms who are  who have remained stable over many years  with monitoring rather than operation.
Hope this helps
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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)?
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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. 
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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 ?
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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.
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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).
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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.
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I am working on a specific circular instrument for end to side vascular anastomoses and I am eager to know about other efforts made by my colleagues.
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Cardiac Sugeons worked with vein-to-coronary artery-anastomosis by magnet:
Arch Mal Coeur Vaiss. 2005 Apr;98(4):294-9.
[Preliminary clinical experience with the Ventrica automatic distal anastomosis system in coronary surgery].
[Article in French]
Klima U1, Farhat F, Beilner J, Maringka M, Bagaev E, Kirschner S, Haverich A.
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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?
Thanks
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thanks
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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 ?
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Hi
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.
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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!
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hi Li, could the attached review help you?   
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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?
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Nathan: could you please shortly write the complication rate named in my question in this 5-yrs-study?
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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
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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
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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.
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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.
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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.
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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? 
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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 m.mueller@blutspende.de, I will send you his mail address.
Best,
Markus
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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?
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Much of the research was done in the 1940s and 1950s
I have attached an early article
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I am an endothelial cell biologist looking to branch into VSMCs to investigate ACE2 and AngII effects. I was wondering which of the commercially available cell lines (human or rat/mouse) would be a good model system
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One may get comments that phenotypical changes occur with prolonged culture of ASMC. Commercially available A-10 cells would not be appropriate. It may be best to prepare primary cultures of ASMc or us them within three or four passages to confirm responses to extrapolate to in vivo situation. If you are considering effects at the level of arterioles it may be best to pool full mesenteric cascade and generate cells.
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My understanding is, when the myocadium cells lack of blood supply, the cell will be damaged but to some degree, it's still reversible. When the blood flow recovered, the cell can become alive again. When the ischemia is serious to a certain stage, the cell will die completely. Thus even the blood flow recover, the cell cannot gain live again, call irresversible. (if these are not true, please kindly correct me)
And my question is, for a specific patient, how to judge if his ischemia is reversible, irreversible? E.g. by using some imaging machines??
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How to determine if ischemic hearts have irreversible ischemia_And How to treat them? Answer from a Clinical and Physiology investigator
First, assuming that severe ischemia or infarction occur as consequence of coronary obstruction or occlusion (clot) usually shows large number of coronary collateral anastomosis (inter/Intra artery anastomosis) along with precise natural bypass in the site of the major obstruction (Baroldi G et al, Circulation Res. 1956, Cardiovasc. Ultrasound 2005. His book is available from Internet, 2002): Macrovascular CHD. In these patients is better to assume that myocardial in “bypassed artery” has reversible options. In effect, ECG are reversed or returned to normal, under a novel therapeutic approach (Brief discussed at the end).
Second, assuming that severe ischemia or infarction occur in presence of “normal selective coronary arteriogram” (Likoff W et al, NEJM 1967), “a changing Philosophy“(Bugiardini R, Mertz BCN, JAMA 2005) implies that other critical factors, as the microvascular blood flow and O2 delivery are missing: Microvascular CHD.
However, in any scenario the incontrovertible fact is that O2 delivery occurs at the cellular level and involves a critical role of red-cell K-dependent ATP synthesis and release in presence of low pH or low PO2 (Ellsworth ML. Physiology, Bethesda 2009). Therefore, impaired capillary vasodilation instead of blood flow of the conductive coronary arteries) appears to be a major factor in the pathogenesis of CHD (Research Gate: Delgado-Almeida. Am Coll Cardiology Dec 2014, Figure).
This critical role in red-cell K-dependent function includes the K-activation of O2 binding by human hemoglobin (Delgado-Almeida A. FASEB J, 2012), suggesting that an enhanced hemoglobin O2-binding in the lung capillary bed is a required step for anti-anginal effects of nitrates or any other drugs, while explaining the failure of intracoronary administration of nitroglycerin to relieve angina induced by pacing, rapidly reversed by intravenous or sublingual doses (Ganz W, Marcus HS. Circulation 1972).
Third, how to determine if ischemia is irreversible or reversible damage? And How to treat them
a) Clinical and ECG serial evaluations and others as Echoc.
b) BOLD analysis (intra capillary levels of deoxyhemoglobin, MRI) documenting that reduced coronary perfusion in CHD does not always implies deoxygenation, opening a new way to assess myocardial ischemia (Karamitsos TD, Circ. Cardiovasc. Imaging 2010).
c) Improving the inherited effect in Red-Blood-Cell Potassium Content recorded in hypertensive and half of their normotensive offspring, as reported by our laboratory, confirmed to be a critical factor in vascular, renal function and total body water and K content (Delgado-Almeida A. Circulation. Abstract, AHA 2013).
d) Preserving the impaired RBC-K uptake related to drugs, particularly Diuretics and β-blockers (Oski FA et al, Science 1972, Agostoni A et al, Science 1973, both with propranolol) inducing abrupt K-efflux from RBC-K and disturbed oxygen affinity to hemoglobin.
e) Finally, a Physiological and Therapeutic approach addressing the defective RBC-K content and functions in CHD, by a novel composition of Amiloride HCl Dihydrate, allowing to improve Central Aortic BP and systolic pulse waveform reflection (type II-IV), reversing ischemic ECG with normal ECG in half of angina patients (in 6-months) and inducing electrical regeneration in previous areas of old infarcts (Delgado-Almeida A et al. Recent Pat on Cardiovasc Drug Discov.2010 and 2012).
Although these paragraphs might support myocytes regeneration of adult human heart by resident or bone marrow stems cells, the fact is that collateral anastomosis recorded by angiography are clear angiogenesis evidences in ischemic hearts. These peripheral and capillary support in CHD may explain innate regeneration of the heart and isolated living cells surrounded by large infarction (Anversa P, Leri A. Mayo Clin Proc. 2013).
Of note, that the role of stem cells in human biology might be recognized and traced as far as two centuries ago in different tissues and organs: Bones (bone reparation in fractures, cited in NEJM 1800’s), Liver (Donor and receptor of hepatic lobule, leading to almost normal anatomy by MRI and function in 3-4 months), Heart (collateral anastomosis and electrical regeneration of the heart in CHD). References for Bone and Liver Regeneration in PubMed.
FIGURE: Erythrocyte K-dependent ATP Synthesis-Function (See Delgado-Almeida A. β-blockers in Angina. J Am Coll Cardiol. Dec 2004; 64:2710-12).
FIGURE LEGEND: Electron microscopy views at the myocardial capillary net, in which diameters and blood flow is tightly controlled by a RBC-K dependent enzyme (pyruvate kinase activity) required for ATP synthesis and ATP release in the presence of low pH or PO2 (See, References 11-13, 38).
In myocardial cell, RBC release 1 mmol of O2 and 0.7 mmol of K from Oxyhemoglobin, in exchange for protons and CO2 from the myocardium; the reverse of K and O2-binding occurs at the lung capillary beds, as documented in our laboratory by in vitro studies in human venous blood samples (FASEB J 2012, Delgado-Almeida A).
An anatomical aspect is well evident in this picture, the larger RBC diameter (7±0.5 µ) versus 3.5-5.0 µ for most microvascular lumen (purple arrows). However, despite narrower capillary diameters, the flow velocity of these cells in healthy subject is 300-400 µ/sec, critically dependent of RBC-K dependent Pyruvate Kinase activity for ATP synthesis and release, the most powerful regulator of capillary vasodilatation and blood flow. Therefore, impaired vasodilatation and longer RBC transit time, instead of arterial vasoconstriction appears to be the most critical factor in essential hypertension and CHD, and probably represent a novel paradigm in the therapeutic management of these cardiovascular diseases.
See References in RG.net
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Wrist-Type PPG is very popular right now, but I would like to ask what kind of useful information can be extracted from it (except the head rate)?
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Hi Parth,
Thank you very much for your answer
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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.
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you are welcome prof shahid  and i agree lowering the viralload would naturally resolve the etiology as in children the etiology is ifferent from that of adults with obesity or children with FH. and one has to modify treatment according to the aetiology.