Science topic

Cardiology - Science topic

Cardiology - serves as a discussion platform for clinicians, clinical researchers or basic scientists interested in cardiovascular diseases. For those of you also interested in cardiac electrophysiology please check out the two complementing groups “Cardiac Electrophysiology” and “Catheter Ablation of Arrhythmias”.
Questions related to Cardiology
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To save life in desminopathy, can the body purposefully reduce muscle mass, for example, due to decreased heart function or for another reason?
It is known that when hypothermia, the body sacrifices limbs for survival. Is it possible with desminopathy a similar phenomenon?
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Dear Mozhgan Norouzi, thank you very much for your reply!
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Given the multiple cardiology meetings that we have now, I would like to know which of the meetings you are attending have the mist impact on you education and practice?
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The ESC meetings are popular. Also, there is a meeting called CinC that is interdisciplinary. I sometimes attend FIMH.
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We're conducting a research design as follow:
  • An observational longitudinal study
  • Time period: 5 years
  • Myocardial infarction (MI) patients without prior heart failure are recruited (we'll name this number of people after 5 years of conducting our study A)
  • Exclusion criteria: Death during MI hospitalization or no data for following up for 3-6 months after discharge.
  • Outcome/endpoint: heart failure post MI (confirmed by an ejection fraction (EF) < 40%)
  • These patients will then be followed up for a period of 3 to maximum 6 months. If their EF during this 3-6 months after discharge is <40% -> they are considered to have heart failure post MI. (we'll name this number of people after 5 years of conducting our study B)
  • Otherwise they are not considered to have the aforementioned outcome/endpoint.
My question is as follow:
  1. What is the A/B best called? Is it cumulative incidence? We're well-aware of similar studies to ours but the one main different is they did not limit the follow up time (i.e: a patient can be considered to have heart failure post MI even 4 years after they were recruited). I wonder if this factor limits the ability to calculate cumulative incidence in our study?
  2. Is there a more appropriate measure to describe what we're looking to measure? How can we calculate incidence in this study?
  3. We also wanted to find associated factors (risk factor?) with heart failure post-MI. We collected some data about the MI's characteristics, the patients' comorbidities during the MI hospitalization (when they were first recruited). Can we use Cox proportional hazards model to calculate the HR of these factors?
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Hi,
The study starts with a Cohort A and on Follow up if Ef<40 then it will be in Group B. This Shift suggests that the survival decreases (Failure to be in Group A) i.e Survival Analysis is applicable. Since factors affecting the survival would be examined, then Cox Proportional Hazards Model is applicable. Survival curves are cumulative curves.
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I want journals related to metabolism cardiology this for experimental studies on animals
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If you want go for closed access journal simply go for BMC journal
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Nuclear medicine physicians and cardiologist have disagreement in time of application of cardiac SPECT and coronarography in cases suspected for coronary disease.
Nuclear physicians consider that cardiac SPECT is one non invasive method with very high efficiency for detection of coronary disease.
Cardiologists consider that cardiac SPECT is not sufficient for detection of coronary disease and prefer coronarography as first diagnostic method   
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Dear Rame Miftari and others
I apologise for not joining the discussion sooner! I agree with the point made by Laurens Swart that the situation depends a lot on pre-test probability. I agree with Teik Hin Tan that both functional and anatomical information is required - and Maurício L. Prudente made a good point that FFR is ideal. In the interval between the start of the discussion to now, I believe IFR is even more popular.
All of these points leads to my observation: access is an important issue. It depends on what is available in which place. I have worked in a number of places that MPI is only available two days each week. Even in larger institution, stress echo waiting list is about 8-12 weeks. Both are big problems. Many interventional cardiologists performing angiography unfortunately, do not also perform FFR. All of these types of issues will influence what “functional” assessment will be most used.
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At what AAA size would you consider Cardiac Nuclear PET/SPECT with Lexiscan over Dobutamine Stress Echo? (outpatient setting)
How important is the potential for a hypertensive blood pressure response with use of Dobutamine?
How important is the presence or absence of a previously placed graft?
What are other clinical factors on which you would base your decision?
-comments greatly appreciated!
Deborah Williams, NP 
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Thank you for setting up this question. It is funny that I did not discover it until five years after you first asked it here! My attitude has oscillated over this time and now I am more agreed with your conclusion. I thank Biswajit Majumder for pointing to an evidence-based response. I wonder if Asif Machhada alsoAsif Machhada has supportive literature as this is somewhat different to my anecodtal experience.
Interesting also that Lexiscan/regadenoson is not available in some parts of the world, still. I presume it applies equally to other vasodilator testing such as with adenosine and dipyridamole.
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Plaques form due to a self-healing mechanism of blood vessels and will increase over time. When entering blood vessels, they block blood flow, lead to hypertension and decrease blood flow to organs such as the heart. To get rid of these plaques, we need to boost the good cholesterol such as HDL or improve health of liver to produce enzymes that move these plaques. So, what other ways to get rid of these plaques without using invasive methods?
Thanks and best regards.
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The following RG link is also very useful:
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Sometimes when I am thinking about visual system, my memory also "connected" to my friend who is cardiologist.
we know that at visual cortex there are area V1 V2 and so on.
In cardiology we also know Lead V1 V2 and so on. Are there any relationship between the visual pathway and the cardiology pathway ? If there are none, how to delete one of them from our memory ?
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There is no relationship between v1 and v2 visual area cortex, which is a functional area of the brain. Leads v1 & v2, those are ECG Leads that are attatched to chest for the purpose of doing ECG. One is a part of Human body located in the brain another is part of instrument for the purpose of investigation of heart in relation to electrical activity. If you are working with human body deletete ECG Lead v1v2.
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Planning to write on Covid-19 associated myocarditis. I am a junior doctor without subspecialty qualification in Cardiology, with a special interest in Cardiology.
Any suggestion on non-predatory journals with a good acceptance rate even for non-specialists? Skipping Cureus for now.
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Indian Heart journal
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There seems to be a lot of controversy about the validity of HRV as a measure of vagal tone. Specifically, Marmerstein, McCallum, & Durand (2021) published a paper suggesting the lack of correlation between HRV and vagal tone. Are there better, non-invasive ways to clearly and accurately measure vagal tone? So much of the literature over the past few decades focuses entirely on HRV in some way or another. Is this still an accurate way to measure vagal tone?
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It's counter-intuitive and nonproductive to think of vagal "tone" as a static index.
The vagus nerve play a key role in hemostasis, circulation and blood clotting. Vital cardiac activity is both a cause and effect of hemodynamic "relativity" (if you will).
An improved measure of Vagal Regulatory Activity (VRA) and/or Vagal Regulatory Capacity (VRC) would reflect VRA at rest and VRC on challenge (exercise and exercise recovery).
Both VRA and VRC could be ratios of pulse volume and/or pulse velocity against selected (e.g., LF) parasympathetic indices.
At least Vagal Regulatory Capacity (VRC) gives meaning to the term "tone" -- notwithstanding that "capacity" is a clinically more useful term.
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As Feigenbaum said, it takes only five minutes to perform a 2D longitudinal strain evaluation in patients who underwent cardiotoxic chemotherapy. Is it part of your routine cardiac ultrasound examination?
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In recent years one the student of our department had his dissertation on use of 2D strain in follow up of patients undergoing chemotherapy.
We found that it was not difficult on his part to perform 2D strain during the follow up.
(In some studies revealed that, in performaning 2D strain :fellows are better than faculty.)
I think every centre can have a dedicated Echocardiographer for this purpose and possibly 2D strain is a must do part of echocardiographic examination for the patients receiving chemotherapy .
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How can a patient safely taper off bisoprolol 2.5 mg who used it once daily? What schedule can he follow to taper off gradually? Any reference/paper/textbook for doing this?
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Dear Seyed Ruhollah Musavinsab. I fully agree with you. But ocassionally patients need to be individualized.Excepting renal failure, I prefer to give drugs at usual interval.
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I'm looking for an excel sheet to calculate the STS Score. From the website http://riskcalc.sts.org/stswebriskcalc/calculate. Does anyone have a worksheet to calculate the STS Score?
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I also tried to find the Excel version of STS calculator, but I still didn’t find it. There are more than 60 parameters & it’s convenient to use it on STS site.
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Need to change Hossam Kandil
picture and affiliation
Hossam Kandil
Professor of Oral maxillofacial radiology, Cairo University
Not Cardiology
This is wrong
Kindly help me correct the error.
Thank you
Shereen Shokry
Main Author
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I know that Hossam Kandil is a professor of Cardiology Cairo University. Is this the information you are looking for.
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I've been grappling with this question for a very long time. There must be a logical reason to explain why almost all humans have one bicuspid mitral valve and 3 tricuspid valves in their hearts.
In the same vein of thought,
  1. Are there any reported cases of people having a tricuspid mitral valve? How would they present in the clinic (if at all)?
  2. Theoretically, what do you think would happen if, during a mitral valve replacement, a prosthetic tricuspid valve was used instead of a bicuspid valve?
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This is an interesting question. 3 leaflets mitral valve is unusual. However, you can have prominent A1 or P1. AV canal can be associated with anomalies of the leaflets number and usually has associated mitral regurgitating.
We can implant tri leaflets biological valve in the mitral position with no hemodynamic effect provided that no LVOT obstruction
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I found some ECG along with PCG from Physionet 2016 challenge dataset with name "a". But, description of ECG is unknown hence i am unable to apply particular algorithm to detect important features. If there are any dataset of ECG along with PCG it will be of great help to my research. Thanks
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In this link, you can find several datasets :
Best regards
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I need its pathophysiology.
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From a cellular perspective, the mechanisms of PVC-induced cardiomyopathy are speculative and based on animal models, from which extrapolation for humans is sometimes limited. It has been postulated that the prolongation and marked beat-to-beat variation in action potential duration, as well as decreased outward and inward (L-type calcium) currents, could result in increased repolarisation heterogeneity. This may be associated with an increased risk of sudden cardiac death due to triggered activity and malignant ventricular arrhythmias. The contractile dysfunction observed in PVC-induced cardiomyopathy could be explained by an altered calcium-induced calcium release from the sarcoplasmic reticulum. In another canine model, it was reported that LVEF impairment could occur within 3 months of induced ventricular ectopy. This suggests that the underlying mechanism is functional rather than structural, given the absence of myocardial fibrosis and changes in apoptosis.
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As we know,the pulse propagates in wave form and the velocity of wave propagation depends on the propagation medium features. So,Is it possible to use the measurment of velocity of pulse propagation in the body to diagnose cardiovascular problems such as hypertension and hypotension?
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Where are the best places/institutes that I may find a PhD program for cardiology?
Which job positions are available for graduates of cardiology PhDs?
What requirements are needed for applying for a PhD program in cardiology?
Any other experiences if you have completed or are taking this PhD program...
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VERY USEFUL IN CLINICAL CARDIOLOGY
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I'm referring to the overlapping sigmoidal curves that are used to describe the gain-of-function mechanisms. I understand the activation curve, but I can't seem to get my head around the inactivation curve. Any help at all would be very much appreciated, whether that is an explanation or pointing to one in the literature. It would also be helpful if you could explain the holding potential, depolarising voltage steps, and pre-pulse vs test pulse. Thank you in advance!
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Did you get a satisfactory answer to this, or do you still need one?
The best explanation I ever found was by Peter Backx on youtube. He goes through both activation and inactivation on his channel. This is the link to his inactivation one. Let me know if you need anything else cleared up.
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My name is Mustafa and I'm currently in my 3rd year of my Biomedical Science major. I decided not to take any courses this spring and summer because I want to invest my time in studying the MCATs and also to help with research. Are there any scientist that want any help with research related to Cardiology or such related topics. I have an extreme interest and background information in Cardiac Pathophysiology and Cardiac rehabilitation and I'm also very good with excel. If you need any volunteer I am here for you. Thank you for taking the time to read this.
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Adil Al-Harthi thank you for that suggestion. Im looking into that website at the moment hopefully ill find something.
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I have recently got my Bachelor's degree in medicine and surgery and I have finished step 1 USMLE recently. I am looking for a research opportunity in cardiology or cardiology-related basic science. I have good research experience. I can help in databases searching, statistic work or manuscript writing.
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For sure, we can collaborate together.
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We are in the middle of a crisis, in the quarantines. Irresponsible behavior has brought us to our current state. We did not learn any lessons learned from viruses that preceded and resembled the COVID-19 virus. Today's topic is not the reason that led us to this situation but commenting on the measures we have taken. The study of (Bishwajit et al., 2017) examined the effects of physical activity on depression. Their study had a representative number of middle- and older-aged subjects (7204). They concluded that a lower frequency of vigorous physical activity was significantly associated with higher rates of depression diagnosed. Depression symptoms and physical inactivity are factors that are closely correlated with obesity (Garimella et al., 2016). The elderly population has a prevalence of anxiety and depression around 10 and 12 %, these findings are caused as a consequence of different factors. Health-related quality of life and physical function play an important role in depression and anxiety (Sousa et al., 2017). The logical conclusion is that physical activity can reduce the levels of depression. Many studies have addressed this topic. Throughout history, our race has evolved. From the beginning of the cognitive, through the agricultural and industrial revolution to the present, we can observe a trend of decline in physical activity. This trend was accompanied by the appearance of metabolic and chronic diseases. Chronic diseases are major killers in the modern era. Physical inactivity is the primary cause of most chronic diseases. (Booth et al., 2011). Physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life.
This brief introduction is just a small overview of the literature that has examined the topics of physical inactivity, depression, and chronic illnesses.
Because we are in quarantine, and our movement is restricted and in some environments disabled we face many difficulties. Speaking personally and listening to people from my surroundings, from a psychological point of view, quarantine has a rather negative impact on people. With this, the media and the internet, which is full of misinformation, make people panic.
The following questions are:
  • Is quarantine an ethical solution?
  • How will this inactivity affect people?
  • How will inactivity affect obesity, chronic diseases, and ultimately, mortality?
Reference:
Bishwajit, G., O’Leary, D. P., Ghosh, S., Yaya, S., Shangfeng, T., & Feng, Z. (2017). Physical inactivity and self-reported depression among middle-and older-aged population in South Asia: World health survey. BMC geriatrics, 17(1), 100.
Booth, Frank W., Christian K. Roberts, and Matthew J. Laye. "Lack of exercise is a major cause of chronic diseases." Comprehensive Physiology 2, no. 2 (2011): 1143-1211.
Garimella, R. S., Sears, S. F., & Gehi, A. K. (2016). Depression and physical inactivity as confounding the effect of obesity on atrial fibrillation. The American journal of cardiology, 117(11), 1760-1764.
Sousa, R. D. D., Rodrigues, A. M., Gregório, M. J., Branco, J. D. C., Gouveia, M. J., Canhão, H., & Dias, S. S. (2017). Anxiety and depression in the Portuguese older adults: prevalence and associated factors. Frontiers in medicine, 4, 196.
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You have touched on an interesting problem of long-term and epidemic-related effects. No one is dealing with them right now because of the current situation but in a few months, we will see a terrifying summary of what happens.
Patients have worse control of chronic diseases due to difficult access to health care and almost not existing private health care sector. Quarantine is associated with a lack of physical activity, social life and developing bad eating habits. It will result in a higher suicide rate, higher chronic diseases mortality.
In my opinion, two weeks of restricted quarantine won't lead to increased obesity. Although the quarantine should last as long as the pandemic will end, and we don't know how long it'll take...
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Topics:
1) Coronary Physiology Assessment for the Diagnosis and Treatment of Coronary Artery Disease
2) Non-coding RNAs in coronary artery disease: new and potential therapeutic targets
3) Refractory angina pectoris: an unsolved problem?
These articles will be part of a Special issue on "Coronary artery disease" that will be published in Cardiology Clinics Journal (IF 2.01).
No Publication Charges
Mandatory Deadline May 1st
Please contact me privately if interested
Sincerely,
Alberto Polimeni
---
March 14th , all papers were already assigned. Thank you for your help and contribution
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I am also interested in topic 3
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I'm looking to get a better sense of whether gait speed is mostly used as a research tool, or if people are using it in medical practice, based on real experiences. My initial research seems to indicate that it's indeed a research tool, but it seems it is also used in cardiology/thoracic surgery to assess post-operative risk.
What have been your experiences with gait speed? How are you currently measuring it? (Any relevant references or links are also greatly appreciated!)
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It is simple, reliable but forgotten method to predict frailty. Just you need to know distance and Stopwatch
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Hi, I could not find any reliable articles about the patients with intracranial traumatic contusion bleeding, with traumatic SAH or subdural hematoma. Cardiologists are pretty strict about giving ASS, Clopidogrel and Heparin despitr the bleeding in the head. Do you guys have some ideas how to achieve a maximal compromise on both sides (neurosurgery and cardiology?
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You have to continue Clipidogrel, and pause ASA. I do not see the reason to give Heparin with DAPT after PCI. If you don't give Clipidogrel, you will have a patent with STEMI along with SAH, and studies have shown that mostly major bleeding with DAPT are from ASA and multiple studies are prooving benefit with Clipidogrel and ASA for 7 days, and than only Clipidogrel. So.. To be short, in no circumstances you can not "pause" Clipidogrel, but ASA you can, and Heparin has no benefit after PCI.
Best regards
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Their is need to understand the safety and efficacy of exercise therapy on cancer treatment–induced cardiovascular toxicity and tumor progression and metastasis in oncology practice, this can be achieved by having a fundamental knowledge of exercise prescription, dosing and personalization with regards to cancer treatment and according to global best practices.
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Is iron ingestion from cooking pots still a problem?
Anyone see Haemosiderosis cases?
And how do they differ from Haemochromatosis?
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Hemochromatosis is a rare disease in which direct deposition of iron takes place in body organs such as liver, spleen, pancreas and skin that cause tissue damage. Hemosiderosis on the other hand side is a disorder characterized by deposition of excess iron within the body tissues that normally do not containing iron.
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The patient should consult which specialty if he wants to know, will he stop aspirin prior to the operation or not? Will he consult the Cardiologist, the surgeon or the anesthesiologist?
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Dear Respected Colleagues ,
Cardiologists, Surgeons and Anesthesiologist All are concerned with this management whether this operation is elective or emergency .... but the main controller for the Pre-operative antiplatelet therapy management is the anesthesiologist with help of the cardiologist ... because the indication for using this antiplatelet theray is mainly for a cardiac problem and rarely for neurological problem ....
Best Regards and Respect
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The European Society of Cardiology guidelines and strategies such as TRAPID AMI aim to stratify patients into low ("rule-out"), intermediate & high risk ("rule-in")  for AMI/ACS based on serial troponins, ECG, risk factors etc.  For obvious reasons a >99% sensitivity is the defacto standard for rule-out.  What then should be the specificity or ppv be? While ppv will vary according to prevalence, it matters to the cardiologists what proportion of patients they are told high risk actually have the disease.  I'd like input, especially from cardiologists, on what they think is an acceptable ppv rate and why?  Thanks.
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Aye Min. Your PPV (and NPV) will depend on the prevalence in your study. If you are reporting, then report the Sensitivity and Specificity if you want to discuss the possible transferability of your method to other cohorts. Your PPV could be improved by changing the test threshold that determines what a test positive and test negative is. However, it is possible that will decrease your Sensitivity.
What is the purpose of the test? If it is to be used to determine who receives a treatment that is expense of dangerous then you want to reduce the False Positives. However, if it is to rule-out the disease, then you want to retain a high sensitivity.
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Is there any epidemiological data/ prevalence of left atrial remodelling (assessed mainly by left atrial volume) in patients with HFrEF AND AF
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Highly nsensitive parameter ti pick up /predict LA dysfunction is by speckled Echocardiography-called global longitudinal strain,for LA its LA strain.I extensive use this assesment in all those cobnditions esponsible for AF and HFrEF.Changes can be picked up well before change in LA volume.
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I have recently repeatedly observed pulmonary haemorrhage in association to an appropriate use of the LUCAS device by different team for OHCA CPR. This was very different from haemorrhagic secretions, that can somtimes occur during prolonged CPR.
Any thoughts or experience?
Thanks
Tobias
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Are asking strictly on the Physio device or others (such as the Zoll model)?
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Dear Colleague,
Sri Lankan Journal of Cardiology- January 2019                                 (Official Publication of Sri Lanka Heart Association) We are pleased to inform you that the above mentioned issue of SLJC has been published. The next issue has to be published in time for the Annual Academic sessions of the Sri Lanka Heart Association, in June 2019. Hence, we earnestly solicit a  contribution from you .It would be greatly Appreciated and extremely valuable. We welcome, Reviews, Therapeutic Reviews, Research, Audits,Critiques of Guidelines, Analysis of important Trials, Milestones in achievements, Tutorials, Case Reports and Updates etc ,as contributions for the next issue of the SLJC.Could you please prepare your manuscripts and submit the same by end of April so that the editorial work could be completed in time (ruvan_nishali.ekanayaka@yahoo.com). The PDF version of this issue is attached herewith.  Thanking you in advance for your kind cooperation. Yours Sincerely, With Best regards,RuvanDr Ruvan EkanayakaMBBS,MD,MRCP(UK),FRCP(Lond),FRCP(Edin),FRCP(Glsg),FCCP, FACC,FESCConsultant Cardiologist / Editor in Chief SLJC
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We welcome, Reviews, Therapeutic Reviews, Research, Audits,Critiques of Guidelines, Analysis of important Trials, Milestones in achievements, Tutorials, Case Reports and Updates etc ,as contributions for the next issue of the SLJC.
Could you please prepare your manuscripts and submit the same by end of April so that the editorial work could be completed in time (ruvan_nishali.ekanayaka@yahoo.com).
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Clopidogrel is often used to keep coronary stents patent
Clopidogrel resistance can be up to 30% of African/Asian populations
Should we be doing more routine testing for the marker of resistance- CYP 19 in these populations? Otherwise we may be giving placebo to our stent patients...
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Clopidogrel resistance has been found in roughly 20% individuals. High risk cases of PCI should be recognised and those individuals should be subjected to genetic testing before prescribing clopidogrel. Anyway, we hardly prescribe clopidogrel to our ACS patients who recieve either Ticagrelor or Pradugrel instead. Clopidogrel is reserved for stable CAD patients who are anyway low risk individuals.
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It seems these particular database is not freely available in a simple Google search. Any help is highly appreciated.
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Dear Anirban, u can get some of ECG along with PCG from PhysioNet2016 dataset a. I hope it can be of some help.
Regards
Sinam Ajitkumar
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Hi. Do we need to ask permission from the related publishers if we want to use tables and figures from journal article or a citation is enough ?
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Since the copyright of an article has to be transferred to the publisher by the author(s) before publication, permission to use a table or a figure has to be requested from the publisher. It must be cited in the legend of the table or figure with reference and "with permission of ...". There is an exception only with public sources, whereby the source must be specified however also exactly.
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As we know, there is five phase of Korotkoff sound that could be heard during blood pressure measurement at patient's upper arm using non-electronic sphygmomanometer and stethoscope. Each phase of Korotkoff sound has a unique characteristics that could be distinghuished based on its acoustic parameters. From these parameters, in some research, we are able to know some physical condition of the vessel (like stiffness, age, etc.). But, could the features of each Korotkoff phases be intepreted directly as a sign of certain cardiovascular disease?
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Thank you for your response, Mr. Emin Grbic , and your article recommendation, Mr. Gennadiy Taradin and Mr. Biswajit Majumder . I wonder whether disease that make some change in the vessel physical properties would make a significant change in Korotkoff sound physical parameters or not. Therefore, I intended to make a research to compare five Korotkoff phases sound parameters between patient with certain vascular disease and healthy subject. I would be pleased if you could give me some advice for this research, thank you very much.
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Is there any research on if/how a slightly dilatated thoracic aorta root dilatation (caused by high blood pressure and not Marfan) can be successful reversed? If not, what is the physiological reason that a dilatated aortic root (4cm) (caused specifically by high blood) pressure cannot return back to normal size after aggressive blood pressure control?
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Good question. And that is the beginning of something, I hope you will explore it and offer us some explanation. There is no such possibility for now, which does not mean it will not. Congratulations on an interesting question.
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A 40 days premature neonate reffered other center due to large ra thrombosis.
.he hasn't positive history of cvp catheter .
in examination ,stable hymodynamic , normal saturation , gread 2/6 systolic murmur ,no sign of respiratory distress.
in echo: a large echogenic ,pedinculated ,moveable thrombus protruding to tv ,area about 1.1 cm2 ,mild tr with p.pg= 27 mmhg ,otherwise is normal .
what is your opinion about managment of this neonate?
best regards 
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Please share me the best answer might you get...
Regards…
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I want to isolate Monocytes from Thrombus, I don't know if it's possible, or if it's suitable to disintegrate the thrombus by aspirating up/down with a pipette then to isolate by Ficoll just like the classical protocol.
Any suggestion is needed :)
Thank you!
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agree with@ Steingrimur Stefansson
regards
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The Integrative Medicine is gaining popularity and acceptance as it consists of many healing therapies to treat many diseases. In mini form it is existing in India as Ayurved doctors always prescribes medicine, diet, yoga, meditation, mantra etc. but the present emerging IM is covering many existing therapies so domain is wider. There is need of a post-graduate course of general integrative medicine open for all medical graduates. As it advances the specialty integrative post graduate course may be introduced like integrative cardiology etc.
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please checkot my web site www.livingbrain.eu
and read about salutogenesis e.i. medicine of health = integrative or holistic medicine
jerzy
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Vasodilators (e.g. ACE-I, BB, nitrates) are generally considered to improve blood flow.
There is some evidence indicating that vasodilators reduce delta P (arterial-venous pressure difference) which would seem logical as arteries can dilate more.
Blood perfusion is expressed as perfusion= deltaP/viscosity*resistance
If we decrease deltaP it would indicate lower organ perfusion?
In other words it seems that if you reduce the vascular resistance the blood will tend to circulate better but would also have a lower chance to leave the capillaries and reach the tissues.
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Please have a look at our paper: Intensive Care Med. 2009 Nov;35(11):1893-9. doi: 10.1007/s00134-009-1591-4. Epub 2009 Jul 29. Dose-dependent benefit of nitroglycerin on microcirculation of patients with severe heart failure.
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For how long? Just 2-4 weeks? And is topical steroid necessary? Or it the patient can be on other medications without fearing complication? I.E does topical steroid prevent any serious complications? Or just treat the symptoms like Erythema?
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Dear Dr. Elsersy.
Long term use of topic steroids is not recommended for stasis dermatitis. It can be used as a short course to reduce the inflamation. Treatment aimed to correct the hemodinamic abnormality in venous system responsable for skin changes is most important. Treatment plan also includes elastic and non-elastic compression and veno-active drugs.
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The most commonly affected valve in rheumatic heart disease is the mitral valve. But why? is there any specific pathomechanism. I haven't found the evidence based answers yet.
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The shear stress on the large mitral leaflets is more than the shear stress on the small aortic cusps and much more on the right sided cusps. The mitral cusps are exposed to pressure of the LV during contraction (Say 120 mmHg) in systole but the aortic cusps are exposed to the aortic diastolic pressure during closure (say 80 mmHg). Years ago we had a study in Egypt, if we diminish heart rate and BP during acute rheumatic fever; we can diminish the mitral injury, explained by diminishing shear stress.
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I am going to induce acute myocardial infarction in rats by LAD ligation. As you know, the mortality rate in this model is usually high. What should I do to reduce the casualties?
I would be very grateful if you could give me some advice.
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Hi, for you to increase survival rate , there should reduced time of ligation and the positioning of the tie along the LAD.
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Hi,
I'm working on organ motion modeling specifically for radiation therapy. We do 4D MR acquisition to extract the characteristics of a subject respiratory motion, which is essential for planning of the therapy.
I'm wondering if the intra-subject variability of the respiratory or cardiac motion is also important for some sort of diagnosis. To the best of my knowledge, current dynamic CT or dynamic MR based methods only reconstruct single average motion cycles.
As I'm not a clinician this question might sound quite naive. However, I'm happy for any hints and answers.
Best
Christoph
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Thank's for your answers Fokko and Galya. As I understand you correctly, for your mentioned applications an average cycle or even for looking only onto the heart rate a simple ECG would be enough. I still wonder, if real time resolved 3D images over several respiratory or cardiac cycles are relevant for diagnosis. Or would that open new diagnostic opportunities?
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58 year man with Achalasia cardia who underwent Trans thoracic Heller"s cardio myotomy in 1962, started c/o of regurgitation of liquids from nose and mouth mostly at night for over one year.Details of the procedure are not available.Requested to have Upper GI scopy,Manometry and 24hr PH.Not a diabetic or Hypertensive.No respiratory symptoms.
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A timed barium study with liquid and bread component plus repeat manometry with ph impedance monitoring
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I see some Healthcare Professionals recommend Coenzyme Q10 supplementation because Beta Blockers deplete it. I tried to find evidence for this, and I didn't find except this paper.
So my Q, as a Pharmacist, do I have to supplement someone who is taking Bisoprolol or not? Because I didn't find also Bisoprolol mentioned in this paper.
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Hi Mostafa,, I totally agreed with answar of Dr Koshy. There are some suggestions that propranolol may reduce level of Co enzyme Q. But supplementation is not required. Bisoprolol is very unlikely to cause Co enzyme Q depletion. Following article might help you... Thanks
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I'm a cardiologist
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Is there stil time to participante?
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what is the highest troponin achieved post myocardian ischaemia?
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Mine were 978 after a Nstemi
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Is it after reaching the steady state concentration (3-5days) or it may take more days to reach the maximum effect for atrial fibrillation control?
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Hi,
After administration of one XL capsule, plasma flecainide concentrations gradually increase after a lag time of 2 to 3 hours to reach a peak between the 21st and 25th hour and remain at plateau levels until after the 30th hour.
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how can a patient be managed having Atrial Fibrillation with rapid ventricular response ?
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Controlling ventricular rate is critical in patients with mitral stenosis. Reduced diastolic filling period significantly increases LA pressure. Combination of beta blockers with Digoxin is required for rate control in many much patients, as has been rightly pointed out. Verapamil and Diltiazem for rate control should be avoided in MS patients with right ventricular systolic dysfunction.
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A - Tricuspid Regurtitation
B - Mitral Regurgitation
C- Aortic Regurgitation
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Aortic stenosis followed by mitral regurgitation. However, we observe sometimes in patients with chronic IE a combined aortic vitium (Stenosis & regurgitation)
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what will be the maximum time when we can do PCI ?
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Thank you Dr.Majumder for posting this question. As you have rightly pointed out, PCI for totally occluded infarct related artery in STEMI beyond 48 hours is a Class III indication. The question is what is the optimal timing to open up the vessel if significant viability can be demonstrated. I think the decision will have to be individualized. Large ecstatic vessel with lot of thrombus should not be attempted early. But if one waits too long, it can interfere with ventricular remodelling and can also lead to recurrent ischemia and even Electrical instability. Moreover, chronic total occlusion will be technically more challenging. I think, 5 to 7 days time will be a reasonable time in most patients to open a totally occluded infarct related artery supplying a viable territory.
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I am going to treat the myocardial infarction rats with spironolactone for 8 weeks/56 days. As you know, there are several ways to administer this drug, such as oral (gavage and mixed in rat chow), intraperitoneal and subcutaneous injection. We currently cannot mix it with rat chow.
Which technique do you think is more prior?
How to make the solution of it? Can we make the solution with physiological serum?
Your advice and suggestions will be much appreciated and welcomed.
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The biomedical industry provide support for medical diagnostics & monitoring, cardiology, audiology, neurology, plus..
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@Eduard;
I am wandering how to visualize “Qi (of Qigong)”, atmosphere or vibration of far fine level, sunbeam may be analyzed by your method, I think. With proper and enough training, as well as warming up, we can recognize and feel that we are in the field in which vibration between doctor and patient are coming and going.
My question is, if there is method with such fine detector system.
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What is the mechanism that reverses this condition ?
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When administered, sodium bicarbonate dissociates into a molecule of sodium and bicarbonate. The molecule of bicarbonate in turn binds hydrogen converting into carbonic acid with its subsequent dissociation into carbon dioxide and water.
The benefit of sodium bicarbonate in the setting of TCA overdose is probably due to both an increase in serum pH and the increase in extracellular sodium.
Alkalization favors the neutral form of the drug and reducing the amount of active cyclic antidepressants. The high sodium load increases the electrochemical gradient across cardiac cell membranes, potentially attenuating the TCA-induced blockade of sodium channels.
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Is Hypertension only risk factor for Abdominal Aortic aneurysm or it can be a risk factor for Thoracic aneurysm as well ?
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Undoubtedly systemic hypertension is a major risk factor for both Thoracic and abdominal aortic aneurysms. In the absence of hypertension or cystic median necrosis related to Marfan or other connective tissue disorders, Aortic aneurysms and dissection especially of the Thoracic aorta are uncommon. However, smoking is an equally important etiological factor for abdominal aortic aneurysms. In some studies, smoking is found to have stronger correlation with Abdominal aortic aneurysm than hypertension.
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Do we have any best test to run in diagnosing cardiac tamponade , or clinical signs are considered reliable here ?
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Cardiac tamponade results from an accumulation of pericardial fluid under pressure, leading to impaired cardiac filling and haemodynamic compromise. Prompt diagnosis is the key to reducing the mortality risk for patients with cardiac tamponade. Although cardiac tamponade is a clinical diagnosis, echocardiography provides useful information and is the cornerstone during evaluation (availability, bedside, and treatment). However, cardiac tamponade is associated with a variety of abnormalities that lead to changes on the electrocardiogram (ECG), chest X-ray, and on echocardiography. Abnormalities of tamponade on the ECG are typically low voltage and electrical alternans. However, reduced voltage can also be seen among other conditions such as infiltrative myocardial disease and emphysema, whereas electrical alternans characterised by beat to beat alterations in the QRS complex caused by swinging of the heart is specific, but not sensitive for tamponade. The chest X-ray reveals a normal cardiac silhouette until the effusions are at least moderate in size (~200 mL). In general, an enlarged cardiac silhouette is neither sensitive nor specific for the diagnosis of cardiac tamponade.
Echocardiographic techniques remain the standard non-invasive method to establish the diagnosis and can be used to visualise ventricular and atrial compression abnormalities as blood cycles through the heart.An effusion appears as a transparent separation between the parietal and visceral pericardium during the cardiac cycle. Physiologic pericardial fluid may only be visible during ventricular systole, whereas effusions exceeding 75-100 mL are visualised throughout the cardiac cycle
References
1. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, Brucato A, Gueret P, Klingel K, Lionis C, Maisch B, Mayosi B, Pavie A.; European Society of Cardiology (ESC). 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015 Nov 7;36(42):2921-64.
2. Ben-Horin S, Shinfeld A, Kachel E, Chetrit A, Livneh A. The composition of normal pericardial fluid and its implications for diagnosing pericardial effusions. Am J Med. 2005 Jun;118(6):636-40.
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Isolated Systolic Hypertension in elders is most likely due to rigidity in arterial walls . What is the reason that rigidity doesn't affect Diastolic Hypertension ?
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Briefly, Isolated Systolic Hypertension is due to increased arterial stiffness of large and medium conductance arteries that loose their "cushioning" properties. In these patients peripheral arterial resistances are usually normal and diastolic pressure is not increased.
You may find useful the article attached.
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Are Collagen (I/III) and TGF-β right and adequate?
I would be grateful if you could give me anything about this topic.
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Adverse post-MI LV remodeling can be evaluated at different levels:
- Anatomical level: LV dilatation (increase in LV end-diastolic volume and LV end-systolic volumes), LV hypertrophy (increase in LV mass), architectural / geometrical remodeling (the LV loses its usual elongated, gullet-like shape and acquires a more spherical configuration, you can use sphericity index for this)
- Neurohormonal level: Sympathetic system overdrive (increase in adrenaline/noradrenaline levels), enhancement of RAAS system (higher levels of angiotensin II or aldosterone), raise in BNP (neurohormone marking LV dilatation)
- Histological level in the remote non-infarcted tissue: Cardiomyocyte hypertrophy (using staining for vinculin or wheat hemagglutinin), interstitial fibrosis (staining for picrosirius red), capillary paucity (staining for CD31 or isolectin)
- Molecular level: Activation (phosphorylation) of Akt/ERK/p38 (which drive cardiomyocyte hypertrophy), molecular markers of fibrosis (collagen I/III, CTGF, TGF-beta)
- Metabolism/energetic levels: Healthy myocardium predominantly consumes free fatty acid to generate ATP. There is a shift, however, in cardiac metabolism in remodeled myocardium towards mainly using glucose instead of free fatty acids
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The fibrotic response after a myocardial infarction (MI) can be classified into two types of fibrosis:
1-Replacement or reparative fibrosis at the infarcted area (scar formation)
2- Reactive fibrosis outside the infarcted area usually after the replacement fibrosis
The replacement fibrosis or fibrosis healing phase (takes 4 to 6 weeks post MI) is a pivotal process to prevent the rupturing of the ventricular wall after an ischemic insult. However, is it wrong if we disrupt this process?
I would be grateful if you could give me anything about this topic.
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Very interesting data...
After MI, Fb are activated throughout the LV, presumably through TGF-β1 in response to increased wall stress and/or inflammation. Additional regional specific signaling leads to interstitial fibrosis via collagen cross-linking in MIadjacent. Local LOX activity could be stimulated by higher mechanical load imposed by tethering to the infarct or signals could diffuse from the scar. Identifying specific signaling cues to maintain the mature state of MyoFb phenotype in the scar tissue may open new perspectives in targeting the MyoFb reversibility in interstitial fibrosis without damaging existing scar tissue.
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Looking for a  validated questionnaire on occupational radiation exposure for interventional radiology/cardiology. Study is on using FISH to assess translocation frequencies of low dose ionizing radiation.  Questionnaire to asses occupational exposure history and other confounding factors of translocation. 
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I would also recommend the paper 'Assessment of radiological protection systems among diagnostic radiology facilities in North East India'.
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I am going to induce acute myocardial infarction in rats by LAD ligation. I want to know what protocol is most suitable for getting to the heart.
Thoracotomy or lateral thoracotomy?
I would be very grateful if you could give me some advice.
The video of your surgeries will also be very helpful.
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The outcome of coronary artery occlusions is age-, species, severity of occlusion, duration, coronary collateral blood flow during ischemia (compared to baseline), operator and drugs used to support and stabilize hemodynamic.
In experimental models, regional ischemia is complicated by the above-mentioned factors and contributes to lack of reproducibility in the same laboratory and in literature.
It is seldom to see authors report complications, arrhythmia, fibrillation and mortality that why young investigators waste time and resources by following prior publications that do not report pitfalls of their studies. Swine model lacks coronary collateral, that is why pigs die with small risk areas (occlusion close to the apex) from arrhythmia and cardiac arrest not from infarction. Investigators treat all groups with lidocaine to attenuate arrhythmia and ventricular fibrillation, yet some more lidocaine and other inotropic drugs are used to minimize mortality.
Unlike regional ischemia, global ischemia and measuring load-independent indices of cardiac performance and correlating that to myocardial bioenergetics, marker enzymes of ischemia and infarction and the end-point of infarct size.
To obtain reproducible studies and results you must design experiments that have clinical relevance and try to minimize variations within same group and amongst other groups and time. GOOD LUCK
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Premise 1: Neurogenic bradycardia and RSA are mediated by different branches of the vagus and need not respond in concert.
Premise 2: Neurogenic bradycardia associated with orienting is a phylogenetic vestigial relic of the reptilian brain and is mediated by the dorsal motor nucleus (DMNX).
Premise 3: Withdrawal of cardiac vagal tone through Nucleus Ambiguus (NA) mechanisms is a mammalian adaptation to select novelty in the environment while coping with the need to maintain metabolic output and continuous social communication.
(From Porges SW (2013) Polvagal Theory. NY: Norton)
The current evolutionary vagal evidence indicates that neither Premises 2 nor 3 are accurate. Also 1) there is a confluence of evidence regarding Premise 1 showing that the DMNX  may only manifest vagal effects upon heart rate under conditions of severe physiological respiratory distress (and even this is not very well documented), 2) Porges provides  merely very indirect findings to support his hypothesis (and his Figure 2.3 of  the time course of putative DMNX-stimulated bradycardia in a single anesthetized rabbit shows much too rapid onset and offset for the heart rate drop to be a response of the unmyelinated DMNX vagal fibers [which should have a much more gradual onset and offset than shown because slow conduction time of these fibers prevent sudden changes]), and 3) no mention is made by Porges of earlier findings that indicate that the DMNX is not implicated in normal vagal control of heart rate.
Nevertheless, perhaps there are strands of direct evidence of which I am unaware? In any case, polvagal conjectures have become very popular in psychology, psychophysiology and therapy literature. It seems, therefore, high time to critically assess the value of Stephen Porges' ideas in this area.
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Dear Emily,
If you mean that myths can affect people's lives, I have no problem with that. I also agree that is probably what has inflated the popularity of the polyvagal speculations. Wampold, in his work, makes a very convincing case that improvements in psychological wellbeing don't rely very much at all upon the method (or, perhaps, ritual would be a better word) chosen: improvement has more to do with having some ritual one believes in, a practitioner of it who seems competent to the client, a joint plan and goals, and maybe most importantly an atmosphere of trust and compassion.
However, my problem is that the ritual becomes conflated with science in this case, and the scientific aspect is used to sell the approach, when all the scientific evidence speaks against the speculations. There are, I hope you will agree, multiple myths that could be invoked to explain the various conditions to which you allude. Why not construct an explanation (myth) more consistent with what we know? That would provide, in my opinion, a much healthier approach for the therapy (i.e. ritual), as well as the societal acceptance of it, in the long run. Right now, what might happen to a client who has gone through a therapy with a polyvagal explanation (and who believes in "science" as the new religion) when they eventually read that in the New York Times that the polyvagal ideas have been thoroughly debunked? What happens to the credibility among scientists of a potentially helpful therapy (ritual) when the underlying scientific premises are thoroughly falsified, as seems to be happening. I don't think that is good for anyone. And I strongly believe one could adjust the vagal myth, employing autonomic explanations that have been around for at least a century before the polyvagal speculations were suggested. That is all I am trying to get at.
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I am trying to measure markers of early fibrosis in heart tissue of spontaneously hypertensive heart failure rats. Echocardiographic data shows that my drug treatment improved diastolic dysfunction, while untreated animal group had a prolonged IVRT (a marker of diastolic dysfunction).
Since one possible contributor to diastolic dysfunction is fibrosis, I will like to probe for markers of fibrosis (preferably early fibrosis) in the treated versus untreated animal groups. I am thinking in the line of Collagen I or III and fibronectin?? Does anyone has other ideas of what could be a great marker of fibrosis or diastolic dysfunction? 
Are there other factors that could contribute to diastolic function that I can probe at the molecular levels?? 
Meanwhile the animals still had normal ejection fraction so they are not yet in the decompensated heart failure stage.
Thank you.
B.
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Big project by F. Zannand.
All about fibrosis in HF patients.
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D-ribose has demonstrated significant enhancing abilities in replenishing deficient cellular energy levels following myocardial ischemia, does the metabolic pathway differ from that of D-glucose? It seems to be more ready for catabolism for the ischemic tissue in the congestive heart failure!!
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Dr. Bader,
It depends what you mean by "replenishing deficient cellular energy levels".
One of the characteristics of ischemia in any tissue (but especially heart) is a net loss of 5'-nucleotides.  To replenish these nucleotides (either by de novo synthesis or by salvage synthesis), the cell needs phosphoribosyl pyrophosphate (PRPP) as one of the staring materials.  Ribose is phosphorylated to ribose-1-phosphate, which is then metabolized to PRPP via PRPP synthetase.  Most tissues (aside from liver) have low levels of PRPP synthetase, so the process is slow; however, addition of ribose will enhance nucleoside salvage synthesis in heart two-fold or even more.
Glucose, on the other hand, uses glycolysis and the Krebs cycle to increase ATP levels (and, by proxy, levels of other 5'-nucleotides) via chemiosmosis and the mitochondrial F1-ATPase.  This increase is dependent on the parent molecules for these nucleotides (ADP, CDP, GDP, UDP, TTP) being present.  Glucose will not enhance the levels of these parent molecules, only see to the addition of the final phosphate (an increase in energy charge, but not total cellular levels).
So, ribose and glucose are really doing different things from a cellular point of view.
Cheers,
T. Geisbuhler
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8-16 mg codeine po q8h and 20 mg IM lidocaine HCl : are they absolutely contraindicated for patients with:
-hypertension
-arrhythmias with pacemaker. 
Or they can be given under medical advice in certain conditions?
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These medications are not absolutely contra-indicated in patients with hypertension or a pacemaker. 
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I am trying to analyze PPG data for HRV. I am curious what software are available for automated cleaning of raw PPG data to then be used in Kubios (or other suggested GUI) for HRV analysis?
thanks
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Hi Shai, with ppg signal you should filter high frequency noise before detecting peak and valley for HRV calculations. Still have low frequency noise like base line and motion artifacts in ppg, please refer to some my articles.
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The AMPLIFY study was built in 2x10 mg Apixaban in the first week and 2x5 mg after it. But what if the patient should receive LMWH or NaHeparin in the first week. Can i start Apixaban in 2x5 mg dose? What your opinion? Thank you.
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In my opinion, yes, you probably can start at the lower standard therapeutic apixaban dose after 1 week of LMWH and feel it is reasonably safe for VTE treatment with a caveat.
Why? That is the approach used by two other DOACs in the approval trials for VTE (dabigatran, exdoxaban) and they were (also) non-inferior to warfarin in terms of efficacy (Blood. 2014 Aug 14;124(7):1020-8). Rivaroxaban and Apixaban choose to use a higher dose initially instead of starting with a standard parenteral anticoagulant. The logic for both of these approaches is to be more aggressive in the highest risk period (I.E. the first week(s) after the VTE) by using either the standard of care (LMWH, at the time trials) or a more aggressive DOAC doses (150-200% of the A.Fib dose for the first 1-3 weeks). 
Having said that, there are some reasons you might not always want to take this approach. When looking at the dose ranging trial for apixaban (Br J Clin Pharmacol. 2013;76(5):776-786.) it is clear the 10mg BID dose has a much higher level of anticoagulation (at day 1 & 7). There is accumulation after a week with steady state in ~3 days after starting/stopping. 
                                           Cmax       Cmin        AUC
5 mg twice daily   (Day 1)  81.9       25.3      600.6 
10 mg twice daily (Day 1) 226.2      72.7      1608.3 
5 mg twice daily   (Day 7)  128.5      49.6      1051.9 
10 mg twice daily (Day 7)  329.8    103.8      2424.9 
So if you usually have a AUC of 2400 after 7 days of 10mg BID from day 7 to 10 you are gradually being reduced to an AUC of 1000 as you reach a new (5mg BID) steady state. When you jump into 5mg BID with the LMWH first approach you are starting with an AUC of 600 and gradually moving up to and AUC of 1000  over days 7-10.  So you less protected from days 7-10. Does this matter? Hard to say. Perhaps for the massive PE patient, perhaps not for the small DVT patient. We can't say for sure with the current data.
In the end we usually feel the the patient is "protected" when LMWH or a DOAC peaks after the first dose (2-3 hrs). That plus the "parenteral-first" DOAC trials having good results gives some measure of assurance it will work for most patients. But in some cases I might suggest giving 10mg BID for 2-5 doses to give an extra measure of protection in the mentioned scenario. 
Dose ranging trial:
Frost C, Nepal S, Wang J, et al. Safety, pharmacokinetics and pharmacodynamics of multiple oral doses of apixaban, a factor Xa inhibitor, in healthy subjects. Br J Clin Pharmacol. 2013;76(5):776-786.
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This is a left parasternal short axis view at the level of aortic valve and pulmonary artery in a 29 years full term pregnant female, she was asymptomatic, no abnormality detected on auscultation, echo was indicated before CS. 
In your opinion, what this flow stands for ?
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I agree with that. One has to think of a superiorly directed venous flow probably exaggerated due to the hyperkinetic state of pregnancy
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At what dose do we see the antiinflammatory effects of statins in CAD? Importantly, how do we monitor this activity? Is the fasting lipid panel an adequate measure?
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left atrium volume?
tissue doppler myocardial velocities?
pulmonary venous flow?
ratio  E/e LV ?
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I think that this algorythm will be useful to evaluate LV diastolic function.
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Pulmonary vein, pressure change, systole, diastole,, disease.. And normal heart.. 
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PV pressure as it has been said above reflects changes in LA pressure (if do you want I have added a book chapter related with this topic, you can see LA pressure changes during cardiac cycle in table 1 and figure 1)  and its interaction with pulmonary venous capacitance-resistance and also importantly changes in Intrathoracic pressures.
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I'm cardiologist in CCU and I'm very interested in performing stress-echo in valvular patients. I hope, it would be very useful for patients to be redirected to hospitals participating in the project. 
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Yes we have dr Angela Zagatina from St Petersburg  and Dr Alla Boshenko from Siberia and Prof Matskeplishlivi from Moscow (the latter two still not recruiting)   . Best personal regards Eugenio Picano 
Zagatina
Simon 
Matskeplishvili
Alla
Boshchenko
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Can in future combined CT FFR and CT coronary angiography replace invasive coronary angiography for diagnosis of CAD ?
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FFR-CT is a novel technology that enables determination of the functional significance of lesions noninvasively, using sophisticated computer algorithms based on computational fluid dynamics applied to coronary CTA . There is evidence from several randomized studies, comparing FFR-CT with invasive FFR (representing the gold standard), that FFR-CT can be helpful in evaluation of hemodynamic significance of stenosis, especially in patients with intermediate severity stenosis.
-B.K. Koo The present and future of fractional flow reserve
Circulation Journal, 78 (2014), pp. 1048–1054
-Noninvasive Fractional Flow Reserve Derived From Coronary CT Angiography Clinical Data and Scientific Principles
James K. Min, Charles A. Taylor, Stephan Achenbach, Bon Kwon Koo, Jonathon Leipsic, Bjarne L. Nørgaard, Nico J. Pijls, Bernard De Bruyne JACC: CARDIOVASCULAR IMAGING, VOL. 8, NO. 10, 2015
Noninvasive Fractional Flow Reserve From CT OCTOBER 2015:1209 – 2 2
-Noninvasive FFR derived from coronary CT angiography in the management of coronary artery disease: Technology and clinical update
Matthew Budoff, Rine Nakansihi, Vascular Health and Risk Management 2016;12:269—278
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A late event In Constrictive ventricular hypertrophy is a sudden dilatation, which clinicians understand to be a critical sign of impending final heart failure. Linzbach, the famous german Cardiopathologist, introduced into literature the term " Gefügedilatation" hence suggesting that the myocardial alignmrent is rearranged such that the heart dilates. Unfortunately, even his pupil famousWaldemar Hort could explain after Linzbach died, how his teacher had conceived  the reallignment might happen.
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Dear Dr. Paul Peter Lunkenheimer. It was interesting to learn about the original hypotheses of your compatriot as well as the morphofunctional model that is remarkably presented in your article "Models of Ventricular Structure and Function Reviewed for Clinical Cardiologists". Thanks
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A long standing hypertensive patient with heart failure of reduced ejection fraction. He is in functional class II and recently presented with bradycardia increasing fatigue.