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
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?
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?
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:
- 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?
- Is there a more appropriate measure to describe what we're looking to measure? How can we calculate incidence in this study?
- 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?
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
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
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.
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 ?
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.
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?
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?
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?
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,
- Are there any reported cases of people having a tricuspid mitral valve? How would they present in the clinic (if at all)?
- Theoretically, what do you think would happen if, during a mitral valve replacement, a prosthetic tricuspid valve was used instead of a bicuspid valve?
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
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?
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...
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!
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.
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.
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?
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.
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
March 14th , all papers were already assigned. Thank you for your help and contribution
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!)
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?
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.
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?
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.
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?
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 (email@example.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
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...
It seems these particular database is not freely available in a simple Google search. Any help is highly appreciated.
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?
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?
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?
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 :)
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.
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.
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?
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.
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.
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.
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.
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.
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?
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.
The biomedical industry provide support for medical diagnostics & monitoring, cardiology, audiology, neurology, plus..
Is Hypertension only risk factor for Abdominal Aortic aneurysm or it can be a risk factor for Thoracic aneurysm as well ?
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 ?
Are Collagen (I/III) and TGF-β right and adequate?
I would be grateful if you could give me anything about this topic.
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.
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.
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.
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.
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.
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!!
8-16 mg codeine po q8h and 20 mg IM lidocaine HCl : are they absolutely contraindicated for patients with:
-arrhythmias with pacemaker.
Or they can be given under medical advice in certain conditions?
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.
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 ?
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?
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.
Can in future combined CT FFR and CT coronary angiography replace invasive coronary angiography for diagnosis of CAD ?
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.
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.