Questions related to Cardiovascular Medicine
In most of the communities especially are owned by lower socioeconomic status.Diet contains more of carbohydrate than protein and fat. More carbohydrate after catabolism produce more saturated fatty acids. This may disturb the level of LDL( high ) lead to atherosclerosis.
Hypertension control is cost-effective and feasible its control should be a public health priority. For many, the total CVD risk approach must be a mandatory step to initiate the treatment of hypertension. For many others, is unclear how well currently available risk scores predict CVD risk in LMIC.
Happy New Year! Along with Sam Dudley Jr. and Jin O-Uchi, I am a guest editor for the journal Antioxidants (impact Factor: 4.5) for a special theme issue:
"Antioxidant Therapy in Cardiovascular Medicine: Bench to Bedside.”
If you are working on something relevant I hope you will consider contributing an original research article or a review article.
If you are unable to contribute yourself, feel free to pass this on to a colleague who might be interested.
Please see this website for more details:
John P. Morrow
Could it be that the glycated cells are under such force in the arterial vessels of the heart that plaque builds up quickly in the damaged lumens more rapidly than other arterial vessel locations? It seems to me that a red blood cell that is highly glycated can cause a lot of damage when accelerated at such close proximity of the pressure wave of the left ventricle. A glycated cell cannot slip in between tissues in a normal function and maybe it scratches the lumens along the path to distal locations that have slower circulatory surges (speed in the vessels of circulation).
using weighted vest i want to analyze the cardiovascular functions in response to aerobic and enaerobic exercise stress.
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.
Which are more risk at sudden cardiac death(SCD); sedentary people or active people?
in general population
in specific high risk population, such as people with DM & hypertension, family history in SCD
Can overemphasize on high intensity intermittent exercise (HIIT) in a training protocol lead to micro trauma to the cardiac muscle due to the micro-ischemia caused by intense exercise over a longer period of time (5-10 years)?
Some researchers from Russia (Victor Seluyanov) have proposed that the lack of inclusion of steady-state long duration continuous exercise for improving eccentric hypertrophy of the heart and overemphasize on HIIT training methods for improving aerobic power could lead to micro damages to the heart muscle over a longer period of time and therefore cause sudden cardiac failure or heart attack in healthy physically active asymptomatic population.
Victor Seluyanov, Russian professor in sports biochemistry states that:
a) Heart training is important to deliver enough O2 to muscles
b) Training with pulse higher than 180 bpm promotes D-type heart growth. Eventually, it results in myocardial degradation (dystrophy) and is one of the major causes of death and debilitation in high ranking endurance athletes. Prolonged training with 120-150bpm promotes L-type growth which is healthy and safe.
For those who understand Russian I'd recommend this video regarding sambo training: https://youtu.be/n7c352NSDUk
Other references on Victor Seluyanov's work:
The vasovagal syncope can be triggered during the tilt test. Nitric oxide has a vasodilating effect.
Will be there diference in its dosage before and during the tilt test?
I am currently using a mouse aortic ring model. However, these rings require low passive tension which just barely stretches the suture to which they are connected to the force transducer (thus, the suture can wiggle a lot in the bath). Thus, every time we wash these rings the baseline reading of force changes, which makes observations frustrating and difficult. Any recommendations to limit this variation?
I found that the cell with more activated caspase 3 showed less aopotosis indicated by flow cytometric assays of annexin/PI, although with a concern that the FCA failed to seperated into two clear populations: the Annex+ PI- and Annex- PI-. Do you meet this problem? It is possible that the timing for the treatment : too long or less, or something due to the staining
I need to perform the measurement of ATP in cardiac extracellular milieu without disaggregating the organ to prevent not to release intracellular ATP. How can I perfuse it?
(ATP colorimetric/fluorometric assay kit- Sigma Aldrich)
I am a new researcher in cardiovascular field and looking for a promising research point. Do you have any advice?
And I am looking forward to sharing my ideas with you. If we can cooperate, it couldn't be better!
Thanks in advance for your help!
Especially, I would like to know changes of valvular regurgitation with asystole state. I am trying to study degree (LVEDV or LVEDP) of LV distension after acute HF.
In general, dietary salt intake was found to be in correlation with arterial hypertension and increased prevalence of cardiovascular diseases, which is endorsed in guidelines of cardiovascular societies and WHO.
On the other hand, decrease of salt intake in patients with heart failure, especially those with hyponatremia was found to increase the mortality, and lower quality of life.
Are there any studies (controlled would be the most desirable), reporting on the effects of sodium diet uptake depending on age, existence of renal disease, COPD, liver failure, diabetes, obesity, or others.
What if you double the water intake, would it not decrease sodium concentration.
Could there be a "salt paradox" similarly to the obesity paradox.
Most of the literature refers to increased troponin in serum as a biomarker but I am interested in knowing if decreased levels in the heart indicates disease.
We have cleaned the system thoroughly, prepared new buffers and used the control rats. However, the problem remains the same.
PACIC is short for Patient Assessment of Chronic Illness Care. The questions in the PACIC ask about the chronic illness care received by the patients over the past 6 months. Conceptually thinking, which one is more likely to affect a patient’s blood pressure: chronic care received during the past 6 months or chronic care received 4 years ago? How much can the chronic illness care received during the past 6 months affect a patient’s blood pressure measured about 4 years later?
I am specifically interested in publications that dealt with the development, validation and improvement of performance indicators in the cardiovascular or cerebrovascular diseases.
Unlike Patients with Acute STEMI, Patients with Ischaemic Stroke eligible for thrombolysis are not being thrombolysed even though they present within the thrombolytic time window. Benefit is not easily documented, Intracerebral haemorrhage is more frequent and very expensive as only r-TPA is being recommended.
There was an opinion about sinus capture of the Ventricles with a Fasicular VT. I am unable to capture the Mechanism of Sinus Capture which obviously should terminate the Fasicular VT. ( Mechanism being a re-entrant tachycardia).
How to avoid Froth in Wire - Myograph upon incubation with catalase? I see many papers using 1200U of catalase which when used produces froth. Are there ways to overcome this?
I have posted the ECG of the ventricular arrhythmia that I am trying to work out. The subject is young and has normal MRI, SAECG, ETT, adrenaline and ajmaline tests are negative.
Can anyone explain what is really going on?
Working Paper Idiopathic ventricular storm
I'm trying to figure out what the difference is between FFT and autoregressive frequency domain methods of HRV analysis. I'm particularly interested in looking at base-line V.S. task differences in HF-HRV and the HRV analysis software that I have (Kubios) outputs HF-HRV using both of these methods. I'm unsure which one to use and why I would use one over the other. I also have measures of respiratory rate and intend to correct HF-HRV outputs with it later. Any help in understanding the difference between the two methods and which one may be better would be greatly appreciated.
Is headache in patients with hypertensive crisis considered as a sign of target organ damage (TOD)?
Hypertension, Medical emergency, Acute medicine, Cardiovascular diseases, Cardiology, Cardiovascular medicine, A&E
Hi. Iam segmenting heart vessels. i need ground truth data . Which software is good at obtaining ground truth for the 3D heart vessels?
There seems to be a lot of websites referring to cardiospasm and achalasia of the oesophagus as an anatomical problem, but little about acute cardiospasm as an emotionally-induced reaction. I remember as a student seeing a man visiting his father in hospital (from an arab country) overcome with grief and doubled-over with intense pain beneath his lower sternum, and this responded to quiet reassurance from the senior physician who reassured me that this was cardiospasm which would clear up within an hour, which it did. Thanks for any insights from others who have seen this.
Total power HRV reflects overall autonomic activity. But I rarely see it being used in clinical investigations that involve HRV as an outcome. What conclusions can be drawn from a high/low total power HRV (in comparison to the other frequency domain measures)?
Is total power indicative of an increased blood flow?
Indapamide is used to control hypertension in patients who have CHF with overt signs of oedema. A serious side-effect of this drugs is hypokalaemia, as with other loop and thiazide diuretics. There have been several reports of indapamide-induced hypertensive crisis which further limits its use. What's the pathophysiological mechanism behind this? How can an antihypertensive agent induce hypertensive crisis?
Between January 2004 and October 2012, 13 individuals taking indapamide reported hypertensive crisis to the FDA. (source FactMed)
Atheromatous plaques are commonly seen in the coronaries, carotids and aorta. Despite sharing the same risk factors only certain sites are predisposed. Even in the same individual, despite similar blood vessel size, hemodynamic stress and blood flow patterns, plaques are often unilateral and seem to spare vessels sharing similar stress.
Why this variation?
Does anybody know how to implant stent model into virtual vessel vessel model for CFD studies ? Maybe someone know special software or method how to deform a straight pipe model of a stent to fit a vessel geometry. I need to deform it something like the image in attachements
Which is the better, anticoagulant therapy only or combination of anticoagulant therapy and antiplatelet therapy?
Intersting guidelines on prevention of SCD and treatment of ventricular arrhytmias, by means of drugs, electrophysiology/interventions, as well as devices.
Does anyone use Definity contrast agent as a continuous infusion? We have had to manually continuously rotate the syringe pump during use to keep the solution mixed. Any ideas on a better method of mixing during infusion? Thanks in advance.
I am evaluating whether the ankle-brachial index (ABI) is associated with adverse cardiovascular events and hypothesize a U shaped association (high risk at extremes of ABI). Is there a method to perform power calculation for this? I have a fixed N and previously had only calculated the power per SD change, but was told this is not accurate since I hypothesize the association to be U shaped.
There is no powerful evidence to support any specific threshold. The study reported by the Yale group reported an increase in complications at sizes of 70mm (Davies 2002), but most consensus guidelines suggested repairing them at 55mm. Given the lack of natural history data, what are the arguments for and against this aggressive threshold?
In atherosclerosis disease, secretory IgM (sIgM) is important for protection. Atherosclerosis levels were significantly increased in sIgM-/-LDLR-/- mice than sIgM+/+LDLR-/- after 12 weeks WD feeding. However, there is no significant difference in atherosclerosis after 12 weeks WD feeding in sIgM-/-ApoE-/- mice when compared with its control group sIgM+/+ApoE-/- mice.
Last I heard, this trial (https://www.thapca.org/) was completed, and results were about to be published, however have not seen anything yet. Anyone have any updates or knowledge?
Thanks in advance,
Hi, dear all, can you please help me with the follow questions: How to define preclinical carotid atherosclerosis? and what is the marker of it? If carotid intima-media thickness >1mm, may I say this patient already have carotid atherosclerosis, or I should say the patient is in the status of preclinical carotid atherosclerosis?
Thank you all very much!
Viability scan, assessment of angina and dyspnea and fractional flow reserve are some of the tools. A very important paper by John Elefteriades (Circulation 1999) says that revascularizing even scarred myocardium benefits the patients in terms of symptomatic and survival improvement.
Gangionic plexus (GP) have an associated with initiation and maintenance of AF. Is there a way to accurately locate them with out high intensity frequency (HIF) such as nuclear imaging - MIBG?
If there is a accurate method of locating GP then what methods are currently being employed in the clinical setting which are reproducible and accurate at the same time?
Type 2 CRS is defined as renal detoriation due to chronic heart failure. because of chronic fluid overload due to CHF, renal venose pressure is increased. thus glomerular filtration rate is decreased. if we use of dopamine in 2 mg/kg/min dosage, afferent arteriol would dilated and GFR would be increased. Is it like this indeed? is there anyone who had experience use of dopamine (2 mg/kg/min) in Type 2 Cardio Renal Syndrome?
what are clinical longitudinal, radial and circumferential strain values for ischemic heart diseases? a common strandard range for strain values at ischemic heart diseases!
What is the clinical evidence for safety of Arginin and Citrullin administered orally for children
> 6 years of age?
I wanted to ask if there is a score used to assess risk of cardiac events for patients undergoing colonoscopy procedures?
Subarachnoid hemorrhage in a post-PCI patient on antiplates is a double jeopardy. Antiplatelet drug(s) is essential in a patient undergoing PTCA with stenting. On the other hand, intracranial hemorrhage is a contraindication to use of such drugs. Commonly antiplatelet drugs are stopped, and restarted 6 weeks or more after stabilization. Clipping of the culprit vessel may have an important role.
In acute coronary syndrome (ACS) patients, those with MS were more likely to be female, have a history of percutaneous coronary intervention, and have a lower left ventricular ejection fraction and higher Thrombolysis in Myocardial Infarction (TIMI) score. Since the MS has a negative long-term impact on cardiovascular mortality and reinfarction in patients with ACS, it can be used as a marker of cardiovascular mortality in patients with ACS and aggressively targeted.
This calculation can be done before and after stenting, but what about an already-stented artery without any knowledge of pre-stenting status? Obviously the size of artery is not the same in the proximal and distal side of a single stent. It is also tapering before and after stent tips and the ratio depends on that.
Many patients who are mainly deconditioned undergo a significant number of tests to rule out ischemia, etc., when they are simply deconditioned. A simple and reliable test to clearly assess physical deconditioning would save the healthcare system tons of resources.
There are only a few simple measures of physical status (temperature, nutritional status, heart rate, blood pressure and respiratory rate), However, some of them are missing in a plea of EBM studies.Considering respiration as important physiological and pathphysiological feature ("dum spiramus, speramus"), one should be surprised that simple bedside-measured variable is usually ignored.
There are published data on the indications for referring patients to a CMR study. However, almost all these data have Ben primarily acquired in cardiology environments. So, what are radiologists asked for and what do they think is a valuable question?