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”.
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I am a senior medical student in Zagazig University faculty of medicine (Egypt) with a strong interest in neurology, cardiology, and hematology/oncology, and I am eager to expand my research experience in these fields. I have foundational knowledge in medical research methods such as SRMA and have participated in clinical and laboratory-based projects during my studies.
I would like to inquire if there are any ongoing research projects or collaborations within these specialties where I could contribute, either through data analysis, literature reviews, or hands-on assistance in clinical studies. I am also open to participating in interdisciplinary projects related to general medicine.
Any advice or suggestions for getting involved in current research initiatives or learning opportunities in these areas would be greatly appreciated.
Thank you!
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hey, Dr Joseph, Yes I've tried and sadly they reject.
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Hello, I’m a second-year medical student eager to develop my research skills, particularly in cardiology and the surgical field. I’m looking for guidance on how to start exploring research opportunities in these areas. Does anyone have any idea where to get started?
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I would agree with Dr Osvaldo Valdés Dupeyrón to start by looking fpor opportunities at yur own organisation/university/hospital. Maybe you've done that already (?) - helpful?
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How can people effectively integrate data from genomics, metabolomics and microbiomics in individualized treatment of cardiovascular disease to achieve more accurate disease prediction and treatment plans ?
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This is just a personal opinion:
Direct multiomics integration for "people" is very difficult. But "AI" has a good potential to do it effectively. What "people" can do is to train AI more efficiently. For this we need to significantly improve the quality of the data we acquire and feed to AI. It is particularly important for metabolomics data, but also there is room for improvement in genomics as well. We also need to have much larger sample size, longitudinal studies, and overall better designed experiments that will be more coordinated between multiple research groups. Realistically speaking it is a great challenge when working with people.
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In the identified case of familial desminopathy (T341P DES mutation in heterozygous state), the son has bradycardia, but the father did not have bradycardia. How can this fact be explained?
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Because of some autosomal dominant & others can be autosomal recessive
"Desminopathy is one of the most common intermediate filament human disorders associated with mutations in closely interacting proteins, desmin and alphaB-crystallin. The inheritance pattern in familial desminopathy is characterized as autosomal dominant or autosomal recessive, but many cases have no family history."
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Hello everyone,
I am a new PhD student starting a project on microRNAs (miRNAs) in myocardial infarction (MI) patients. I would greatly appreciate any guidance on the following points to ensure proper sample collection, storage, and analysis:
  1. Blood Collection Tubes:Which type of blood collection tubes are best suited for miRNA isolation? Should I use EDTA, heparin, or another type of tube?
  2. Sample Handling:What are the best practices for handling blood samples immediately after collection? How soon should the blood be processed after collection to ensure miRNA stability?
  3. Storage Conditions:How should the blood samples be stored before processing for miRNA isolation? If immediate processing is not possible, what are the recommended storage temperatures and durations for whole blood, plasma, or serum?
  4. miRNA Isolation:What are the recommended protocols or kits for miRNA isolation from blood samples? Are there specific steps or considerations to prevent RNA degradation during isolation?
  5. Concurrent Biomarker Analysis:Can the same blood samples be used for other biomarker assays such as BNP and collagen turnover markers? If so, how should I aliquot the samples to ensure there is enough material for multiple assays?
  6. Storage of Processed Samples:How should isolated miRNA be stored until analysis? Are there specific conditions (e.g., -80°C) and storage buffers required for long-term storage?
  7. Biomarker Measurement Protocols:What are the best practices for measuring BNP and collagen turnover markers in blood samples? Are there any specific ELISA kits or assays recommended for these biomarkers?
  8. Data Integration:How can I effectively integrate miRNA data with biomarker measurements and clinical data (e.g., ECG, echocardiograms)? Are there any statistical tools or software that you recommend for this type of multi-dimensional data analysis?
  9. Literature and Resources:Can you suggest any key papers, protocols, or online resources that could help me understand and implement these techniques effectively? Are there any specific training courses or workshops you recommend for a beginner in this field?
Your guidance will be instrumental in helping me get started on my PhD project.
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1. EDTA Tube would be good for price wise, Tempus (Thermo) or RNA Shield (Zymo Research) for better stability
2. EDTA, not more than 4 hours after collection and storage in 4C, Tempus (Claimed 5 days in 4C) and RNA Shield(Claimed 1 month in ambient temp)
3. Recommended storage is -80C, but if you want to isolate it from different part of the blood, separate it first before freezing
5. Yes you can, for how you should aliquot, need to determine first how much is needed for each of the test then calculate the rest by your self and aliquot accordingly
6. Yes -80 is a must, the buffer is Citrate/TE or commercially available RNA storage buffer
7. -
8. -
9. -
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I can not find this journal in the SCOPUS list from february 2023. Thank you for your help.
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The publisher behind this journal “Cardiology and Cardiovascular Medicine" is “Fortune journals” a publisher mentioned in the updated version of the Beall’s list (https://beallslist.net/#update). This is a red flag that you are dealing with a potential predatory publisher (and consequently journal). There are more red flags:
-Contact info (https://www.fortunejournals.com/) 11355 Richmond Ave #507, Houston, TX 77082, USA is fake or at best a virtual office. The same is true for the Delaware address (frequently used by predatory publishers for misleadingly suggesting an US origin while they are not)
-Same Delaware address is used by https://inter-publishing.com/index.php/ijbdepublished by Academic Journal INC a predatory publisher for sure numerous so-called misleading metrics are prominently mentioned on their website (https://beallslist.net/misleading-metrics/)
-Looking at http://www.fortunejournals.com/cardiology-and-cardiovascular-medicine-home-ccm.php I see a prominently mentioned impact factor, which is false and misleading since this journal is not indexed in Clarivate’s SCIE (you can check here https://mjl.clarivate.com/home ) and DRJI a notorious misleading metric often used by predatory journals
-Mentioning PubMed is also misleading since ALL papers published by author’s with a NIH grant are indexed in PubMed irrespective of the journal where the paper is published in. This has nothing to do with being a PubMed indexed journal (which they are not)
-APC (https://www.fortunejournals.com/article-processing-charges.php) is ridiculously high for an essentially non-indexed journal
Overall I would say avoid this one.
Best regards.
PS. Indeed they are not indexed in Scopus (which they do not claim by the way).
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looking for researchers that are willing to work on discussion part and risk of bias of a systematic review, for more details pls leave a message
Thanks!
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I have sent you as message Arvind Kunadi
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I red a paper on an important journal of cardiology. In this work they found that 8 miRNAs were dysregulated in plasma samples of a study cohor of 1710 participants (Controls + patientes affected by Heart failure). I evaluated these 8 miRNAs in plasma samples in a study-cohort of 129 subjects (Controls + Heart failure patients) and I found that only 2 miRNAs were dysregulated according to the work I red. Because I have to explain thi data in "Discussion" I don't know how to explain this difference. Why could be the main reason of these different results? Maybe the size samples or other? Thank you
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The number of participants and their demographics could be a factor. Race and differences in cardiometabolic issues might be influencing the differences miRNA expression. Try look at the DEGs associated with the miRNAs that didn't match up, this will give you more insight into what's happening. It could be technical differences like choice of housekeeping genes, normalization process.
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Please visit:
Heart Attack Deaths Drop Over Past Two Decades - American College of Cardiology (acc.org). It says "Researchers found the overall rate of death from heart attack, adjusted for age, fell from about 87 deaths per 100,000 people in 1999 to about 38 deaths per 100,000 people in 2020".
The reduction may be the result of awareness, better preventive care, obesity reduction, etc.
My question is about a simple step in health care. Has any research been done about the value of a six-monthly blood pressure check and related consultation in reducing heart attacks? A related question is a similar reduction in strokes.
Obviously, this healthcare is not available to the average resident of most developing countries.
Should it not be?
Srinivasan Ramani
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A very simple step to reduce the incidence of Heart attack is life style modification.
Explanation: Cut off unhealthy food like junk food, fast food, oily curry and fat diet from your life. Maintain Balance between protein, cards and fat.. Low fat and high Carbohydrate diet with adequate protein diet is highly recommended. Along with take fiber diet like fruits etc. If you smoke then quit smoking even if it is active or passive smoking. Furthermore, do regular exercise cardio for 1 to 1.5 hours and walking in the morning! If you have previous incident of heart attack then keep follow up with you Cardiologist! Preventive medication plus Life style modification is the best way to reduce the episodes of Heart attack!
Thank you!
Dr. Umer Iqbal.
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Have you ever wished that there was a platform that could help students and researchers learn and grow? A place where you could find mentors, educational resources, and opportunities to publish in international journals?
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The platform we are launching will be a game-changer in the world of academia. We are already working on this platform now. The content is really interactive, unique and really valuable. The community and environment will be very competitive. Researchers and students will be able to find the opportunities to enroll in with supervision and review.
And so, thanks to the dedication and hard work of a few passionate individuals, the world will become a better place, one researcher at a time. If you're looking to make a difference in the world of academia, I highly recommend donating in this amazing platform.
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I want to do a good and worthy research in field of cardiology (DM Cardiology), suggestions for a topic , ideas are most welcome. Thanks in advance.
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Until now unknown genetic amino acid sequence associations of as many as possible important cardivascular diseases. Of course this research must be done as teamwork by professionals...
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ECGs from patients with normal sinus rhythm, sinus arrhythmia and paced beats in the time domain might look very similar for a person without any cardiological skills. However, when looking at the same ECGs in the frequency domain I think most people see that paced beats look really different. The paced beats have a perfect U-shaped pattern, while the sinus and sinus arrhythmia rhythms are characterized by a more noisy pattern. I feel pretty sure that the perfect U-shaped pattern is caused by the regularity of the paced beats, but I don't have a scientific explanation of why this happens.
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Hi Bjorn,
You are right when you discuss the Harmonic frequencies. In FFT you are taking time domain data and converting it into frequency domain data. You are assuming the FFT time domain continuing indefinitely. If you separate the ECG signal into points (you will arrive to certain number of samples) and the FFT assumes that these samples are infinitely repeated. All FFT have a frequency resolution that is equal to the sampling frequency divided by the number of samples. You will have certain sampling rate/ number of samples which would determine your frequency resolution. When you are using pacemaker, you are examining (pacemaker analyzes) frequency components of physiological signals and detect concealed properties to identify physical anomalies. Please read this paper PMID: 32051675 which would explain spectrum analysis algorithms such as Fast Fourier Transform (FFT), which are crucial for pattern detection. You have also listed common abnormal (path-physio ECG recordings) in Table 1. Values from these conditions indicate that in most common cases of pacemaker usage, the sample values encountered by the system will hold a high probability of being repeated over the course of time, hence you are able to find their main harmonic frequency and set up pacing such that it is recognized and reversed to your normal harmonics e.g. (Table 1).
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Searching for a formula to convert into excel for my student's research. Found:
Risk_Factors = (ln(Age) * 3.06117) + (ln(Total_cholesterol) * 1.12370) - (ln(HDL_cholesterol) * 0.93263) + (ln(Systolic_blood_pressure) * On_blood_pressure_medication) + Cigarette_smoker + Diabetes_present - 23.9802Risk = 100 * (1 - 0.88936e(Risk_Factors))
Not sure how to convert it for one and it doesn't make provisions for BMI! Can probably figure out how to do the conversion for the original with time, but then I am still missing the ingredient for the special sauce of this research! Why not just ask my international peers for help? Pretty please.
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One option would be the QRISK3 calculator. This includes all the parameters you mention above plus a couple more. It is well vaildated, and the publications supporting it are available on their website https://qrisk.org/three/.
The site includes a full description of the algorithm used to generate the score . The page for the algorithm is https://qrisk.org/three/src.php. The maths may be a little more complicated than the example you give above and it may not be easy to write it as a formula. Rather than writing it as a formula you might want to use Visual Basic for Applications which is built into Excel.
Good luck!
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I want journals related to metabolism cardiology this for experimental studies on animals
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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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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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Yes.
  • Myopathy is a general term referring to any disease that affects the muscles that control voluntary movement in the body. Patients experience muscle weakness due to a dysfunction of the muscle fibers. Some myopathies are genetic and can be passed from parent to child.
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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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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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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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statin use,low risk cardiovascular patient,mortality benifit,
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Please kindly go through the following PDF attachment, one of the recent update regarding Statins published in European Journal of Pharmacology.
Best,
Niloufar
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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. Gennady 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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Primary Angioplasty for STEMI can be performed up to 48 hours from the onset of chest pain even in asymptomatic stable patients. In those with continuing chest pain, hemodynamic instability or arrhythmias, primary PCI may be considered even beyond this time window.However, routine PCI beyond 48 hours is not recommended in asymptomatic stable patients especially if a totally occluded infarct related coronary artery is seen on coronary angiogram. Benefits of reperfusion strategies are certainly more when the total ischemic time is less than 3 hours. But for those with delayed presentation, primary angioplasty is more beneficial than thrombolytic therapy.
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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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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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High blood pressure is not suitable for human being.
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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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Ventricular renodeling mainly refers to geometrical changes in the LV (dilation, sphericity, etc) and functio. Therefore the gold standard is cardiac magentic resonanc Due to costs, echocardiography is the most used method.
For cardiac function (both dyastolic and systoli) the LvEDP ans P-V loop are also use (Millar catheter).
TGF-b and collagen contribute to remodeling but are not surrogants for ventricular remodelin.
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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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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 t