Science topics: MedicineVascular Medicine
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.
Questions related to Vascular Medicine
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.

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.
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?
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).
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).
, Africa
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?:
When to measure INR _as a follow up monitoring_ following warfarin administration in a patient with VTE?
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
how can we avoid cerebral emboli during CABG in patients with large mural LV thrombus
I woulod like to know how it was done.
The patient with uruptured aneurysm. Planned cardiac surgery for replacement aortic valve.
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?
Acetylcholine lacks relaxatory effect in this artery
Do you have a detailed protocol?
Vascular Wall siRNA delivery
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.
What are the non invasive methods for carotid stimulation?
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!
What could be the best way to remove Baseline drift from PPG signals.
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
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.
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 ?
I am looking to sample questionnaire which measure knowledge, attitude and practice to predict risk behavior for cardiovascular diseases.
plaque classification obejective
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?
How does arterial blood pressure signal morphology change during tachycardia and/or bradycardia? Is there any good reference for studying this subject?
Are angiography and lymphoscintigraphy necessarily distinguishing methods
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?
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!
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.
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.
Is there literature-guidelines in this field?
Are there any screening tools for the detection of heart failure at the community level (other than the biomarkers NT-proBNP and BNP)?
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
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.
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?
When and why should I use KCl normalization in vascular reactivity studies (contraction curves)?
variation in branching of internal iliac artery radiological OR cadaveric?
Which is the standard and accurate method for finding arterial stiffness?
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 ?

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.
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.
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?
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.
I am looking for theory Information about angiotensin II receptors and about their genes, PDF or electronic books. Can you help me?
Thanks
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?
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
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?
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.

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.
I would like to perform a little survey as the use of BITA grafting formyocardial revascularization.
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
What criteria do you use to surgery? Which embolization technique do you use?
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?
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?
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)?
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 ?




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).

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.
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
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 ?


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!
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?
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
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.
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?
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?
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
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??
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)?
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.