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Cardiovascular Medicine - Science topic

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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.
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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.
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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.
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Very interesting reflection, indeed.
in addition, the CVD risk approach can help to define the treatment goal, select a combination of drugs and prioritize the level of specialization and the frequency of clinical follow-up. It is a powerful incentive for patients and providers.
Thanks, Mithila
P
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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:
thanks,
John P. Morrow
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We are still accepting manuscripts.
"Antioxidants is covered in the Science Citation Index Expanded in Web of Science and in 2018 received its first Impact Factor of 4.5"
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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). 
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To assess the effect of hypoxia on NAD/NADH in mice heart.
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We have just established a protocol for the quantification of NAD+ and NADH in human plasma in our study group. Please find the protocol and paper attached.
Protocol:
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I'm looking for a durable matrix slicer to make coronal slicers of an adult rat heart in increments of 1 mm. I'm looking currently at Zivic Instruments and Cell Point Scientific, but am not sure if they are reliable.
Thanks!
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hi 
what are the different pressure waveforms inside internal carotide artery?
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After answering this question two years ago I did the calculus for the exponential decay curve which occurs after the systolic peak and before the diastolic trough. If the pressure is plotted as log pressure against time you get a straight line (approximately). The slope of this line can be derived. It is proportional to compliance (C) multiplied by resistance (R) of the blood vessels (RC).
I wrote an app for my iPhone in BASIC which was fun to play with in the ICU. Unfortunately I could not find a way to separate the two components R and C and in disease states hardening of the arteries increases resistance and decreases compliance. This means the two factors tend to cancel each other out, making the calculation of RC less sensitive. But the program can help us understand sepsis cases where resistance drops over time.
Some people use the pulse pressure, which is systolic pressure minus diastolic pressure, but this does not take into account the pulse rate. The slower the heart rate the longer the time between the systolic peak and the diastolic trough. This gives more time for the blood pressure to drop off as blood flows away from the heart. Consequently the diastolic pressure drops as heart rate decreases. But if we calculate RC it takes into account all three factors: Systolic Pressure (PS), Diastolic Pressure (DP) and heart rate (HR).
Perhaps I should write an article about this, but who would publish it?
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using weighted vest i want to analyze the cardiovascular functions in response to aerobic and enaerobic exercise stress.
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I agree with Tatiyana's answar. Treadmill test only  for cardiac function evaluation  . Cardiopulmonary stress testing detect function of heart, lung and muscle. It can find the reserve of the three organs in health and disease. 
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A long standing hypertensive patient with heart failure of reduced ejection fraction. He is in functional class II and recently presented with bradycardia increasing fatigue.
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2:1 HB
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Heart, failure, diastolic, nevibolol 
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According to the European guidelines beta bloquers and specialy nebivolol were able to reduce mortality but only HF hospitalizations in older patients. You can read about that in the following meta analysis.
The phisiological explanation might be the improvement of isovolumetric filling time and improvement of diastolic funtion.
One other recomendacion is the control of risk factors and arrhythmias like hipertension and atrial fibrillation. Here the beta bloquers can help specially in the AF.
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what are the exact mechanism affecting the cholesterol changes in smokers after aerobic exercise?
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I am of the same view as Dr. Aurelio Leone and endorse his comments.
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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
other conditions
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In your question the paradigm of duality incorporated. Physical activity has both beneficial and adverse effects on SCD risk. Most studies, but not all,have found inverse associations between increasing regular physical activity and SCD or sudden cardiac arrest. Results are most consistent for moderate levels of exertion, where the majority of studies have documented favorable associations. Despite the long-term benefits of exercise, it is also well known that SCD occurs with a higher-than-average frequency during or shortly after vigorous exertion.Case-control and case-crossover studies performed among men have demonstrated that vigorous exertion can trigger cardiac arrest and SCD. Regular vigorous exertion diminishes the magnitude of this excess risk; however, the risk remains significantly elevated even in the most habitually active men. The magnitude of the risk associated with exertion appears to be lower among women where exertion-related SCD is much less common. 
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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:
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v
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Dear Laurent,
since 2008 I am working in a Cardiac Rehabilitation Unit linked to the University Hospital of Padua, Italy. Our Unit is located in the Alps (Cortina d'Ampezzo), at an altitude of 1315 m a.s.l.. Such an altitude is generally considered as "low altitude".
We usually receive patients with a combination of risk factors: middle age and elderly persons, with coronary heart disease or recent major clinical events (myocardial infarction, cardiac surgery), that are exposed to exercise-based rehabilitation during a two weeks (average) period. Among more than 2000 patients submitted to residential cardiac rehabilitation in the past few years, no major side-effects have been registered during the daily sessions of structured exercises. It must be said that exercise intensity was based on careful evaluation of patient's status and "monitored" with Borg scale. In patients with recent episodes of heart failure, a preliminari cardiopulmonary exercise test was performed, and exercise intensity was maintained at or around anaerobic threshold.
In this way, we believe that exercise-based cardiac rehabilitation is feasible and safe in this kind of patients also in a mountain resort.
No significant modifications have been observed also of blood pressure, heart rate or other clinical parameters with the rapid ascent from the University Hospital at Padua (12 m a.s.l.) to the level of 1315 m a.s.l. of the Rehabilitation Centre.[i] These results are somehow similar to what is knownin literature for patients with metabolic syndrome, that travelled from Innsbruck (576 m a.s.l) to Obertauern (1700 m a.s.l.), resided there during 3 weeks and went also hiking, taking care that physical effort did not exceed 55-65% of individual maximal heart rate, without major adverse effects.[ii] Furthermore, in literature can be found a paper reporting that patients with stable heart failure have been accompanied to an altitude of 3454 m a.s.l., where they were able to perform moderately vigorous effort, without serious events, demonstrating only a reduced performance that was approximately 22% less than their performance at lower altitudes.[iii]
Thus, we believe that it is possible to perform exercise-based rehabilitation at least at low mountain altitudes, provided that physical effort is maintained approximately below or around individual anaerobic threshold.
Hoping to having been somehow useful, I present my best regards.
Merry Christmas and Happy New Year.
Leonida Compostella, MD
[i] Carraro Umberto. [Effects of ascension to mountain in heart disease patients in subacute phase: an observational study]. Thesis for Graduation in Medicine, University of Padua, AA 2009-2010
[ii] Mair J, Hammerer-Lercher A, Mittermayr M et al. 3-week hiking holidays at moderate altitude do not impair cardiac function in individuals with metabolic syndrome. Int J Cardiol 2008; 123(2):186-188
[iii] Schmid JP, Nobel D, Brugger N et al. Short-term high altitude exposure at 3454 m is well tolerated in patients with stable heart failure. Eur J Heart Fail 2015; 17(2):182-186
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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?
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What I wonder is whether the nitric oxide dosage is feasible to be measured in plasma and it would be different before and in the first minutes of tilt testing in patients with syncope and patients without syncope. Thank you!
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Hello.
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?
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I haven't read the previous comments but fluctuation of the baseline is not normally a problem as you normally normalise responses to a standard response (e.g relaxation as a percentage of the constriction preceding it, contraction as a percentage of a standard contraction to say KCl. for these you measure form the currentl baseline to the peak response, normalising to a % removes the effect of the baseline variation. You could also wash out less frequently every 15 min not necessary.
Only other comment  more for future reference!  is to use an even smaller organ bath if possible (10 ml more than enough) ideally you should be trying to get 4 running at once (again you have to go with what you have). Also the Mouse aorta is quite small, if there is no particular reason to use this species (e.g. going to use a knock out) I suggest using rat as it will be easier to use and more stable. If I use mouse aorta i tend to run the experiment in a wire myograph designed for smaller arteries such as those made by danish myotechnology or living systems - (obviously these are very expensive).
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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
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Many thanks for all your helps. I have readed the papers. I will try other methods to examine the level of apoptosis, such as the LDH assay and TUNEL . 
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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)
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I think you can use ATP Assay Kit (Colorimetric/Fluorometric) (ab83355). Best wishes.
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Hello, friends.
I am a new researcher in cardiovascular field and looking for a promising research point. Do you have any advice? 
And I am looking forward to sharing my ideas with you. If we can cooperate, it couldn't be better! 
Thanks in advance for your help!
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I believe that we know (maybe) 5% of what it would be useful to know about humans and about  cardiovascular system. Then there are plenty of useful research, "hot" and interesting. There is still much to discover. The important thing is that searches are well designed and well conducted and that researchers are free
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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.
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In cases of  acute HF the degree of regurgitation is underestimated, becouse of rediced CO. On the other hand it depends on the ethyology of the valve lesions and on the mechenism of HF (AMI, PE, CMP and etc)
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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. 
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Dear Dr.Boban,
As far as I can see the cited studies have not assessed potassium intake and sodium-potassium balance. There were numerous studies (although mostly the preclinical ones, such as the works of Prof. Dr. S. Yu. Shtrygol’ and co-authors, Eksp Klin Farmakol. 2006 May-Jun;69(3):32-4. PMID: 16878496; Eksp Klin Farmakol. 2002 May-Jun;65(3):22-4, PMID: 16878496; Eksp Klin Farmakol. 2002 Jan-Feb;65(1):37-40, PMID: 12025783 etc.) providing the strong evidence of salt substitutes efficacy and supporting their hypotensive, antiedema, diuretic, hypoglycemic effect, protective activity in the disorders of cerebral blood flow, improvement of trophic processes in tissues and rheological properties of blood as well as such effects as anticonvulsive and antidepressive.
In clinics it has been shown that the patients with IHD and atherosclerotic changes in blood lipoproteins benefit significantly from hypocholesterolemic effect of the salt substitute hyposol (summarized in SYu Shtrygol’. Pharmacological Effects Modulation by Different Salt Regimens, Avista-VLT, Kharkiv, 2007). Unfortunately, the work on salt substitutes is scarce now (although there are some products on the markets) and surely there is a certain opposing of food industry interests.
Regards,
Dr. Olga Tovchiga
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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.
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Dear Rachael i am afraid i havent come across any evidence that is suggestive of Trop reduction in context of DCM. Trop could indeed be significantly raised in a a wide variety of DCM such as Ischemic cardiomyopathy, Hypertrophic CM, Cardiac Sarcoid/Amyloid & Vasculitis with Cardiac Involvement etc as i am sure you must be aware.
very best wishes
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We have cleaned the system thoroughly, prepared new buffers and used the control rats. However, the problem remains the same. 
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We have had similar problem for several months. The main problem was probably in pH of Krebs-Henseleit solutions. Another big issue is temperature, which affects not only the heart itself (contractility), but also pH and amount of oxygen in solution.
You need good nerves to go through this. I wish you good luck!
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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? 
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Agree with Béatrice : both Could be important to consider. It also depends on the setting e.g. elderly individuals tend to have a very stable drug consumption in our cohorts and 6 months and 4 yrs would be similar in most of them. Best Christophe 
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I am specifically interested in publications that dealt with the development, validation and improvement of performance indicators in the cardiovascular or cerebrovascular diseases.
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Australas J Ageing. 2010 Mar;29(1):39-42. doi: 10.1111/j.1741-6612.2010.00411.x.
Performance indicators to measure dementia risk reduction activities in primary care.
Travers C1, Martin-Khan M, Lie D.
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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.  
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Management
The RCP and NICE have produced evidence-based reviews of the management of stroke.[5][8] They recommend that:
  • Alteplase should only be administered within a well-organised stroke service.
  • Staff in such a service should be trained in delivering thrombolysis and in monitoring for any associated complications.
  • Care should be provided by level 1 and 2 nursing staff trained in acute stroke and thrombolysis.
  • There should be immediate access to imaging and re-imaging and staff appropriately trained to interpret the images.
  • Protocols should be instituted for the delivery and management of thrombolysis, including post-thrombolysis complications.
  • Staff in A&E departments, if appropriately trained and supported, can administer alteplase for the treatment of acute ischaemic stroke provided that patients can be managed within an acute stroke service with appropriate neuroradiological and stroke physician support.
  • Every patient treated with alteplase should be started on aspirin 300 mg daily after 48 hours, unless contra-indicated. This should be continued for 14 days.[9] 
The situation is more complex for acute ischaemic stroke than for coronary thrombosis:
  • Only 80% of strokes are ischaemic and giving thrombolysis for a haemorrhagic stroke would be disastrous.
  • Stroke tends to be more gradual in onset and may even start during sleep. Hence, patients tend to present later.
  • The window of opportunity for effective thrombolysis is four and a half hours from the onset of the stroke and, in that time, a firm diagnosis of ischaemic stroke must be made.
  • As a result, only about 1-11% of patients fulfil the criteria.
Cochrane is uncertain as to whether lower doses of thrombolytics are safer or if there is any advantage to intra-arterial over intravenous routes of administration.[10] Intra-arterial treatment tends to be used for posterior stroke but it is still uncertain if it is superior.[11]The important point is early recovery of flow and the vertebrobasilar system appears to take longer to recover.
Clot retrieval is an alternative management method for acute ischaemic stroke.[12] Research is underway looking at the benefits of thrombectomy with thrombolysis.[1] 
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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).
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I am of view a Sinus Capture beat negates the ECG Diagnosis of Fasicular VT - a micro re-entrant tachycardia.
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I am looking for studies showing the benefits of reduced door to balloon times.
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Door-to-balloon time is associated with mortality in patients undergoing primary percutaneous coronary intervention for ST elevation myocardial infarction.Prospective cohort study of patients enrolled in the American College of Cardiology National Cardiovascular Data Registry (43 801 patients with ST elevation myocardial infarction undergoing primary percutaneous coronary intervention)/below file.
Other:  GUSTO-IIb trial
Nallamothu BK, Normand S-LT, Wang Y, et al. Relation between door-to-balloon times and mortality after primary percutaneous coronary intervention over time: a retrospective study. The Lancet 2014. - See more at: https://www.acc.org/latest-in-cardiology/articles/2015/06/03/13/23/is-door-to-balloon-time-a-misleading-metric#sthash.umE2fYE7.dpuf
Wimmer NJ, Cohen DJ, Wasfy JH, Rathore SS, Mauri L, Yeh RW. Delay in reperfusion with transradial percutaneous coronary intervention for ST-elevation myocardial infarction: Might some delays be acceptable? American heart journal 2014;168:103-9. - See more at: https://www.acc.org/latest-in-cardiology/articles/2015/06/03/13/23/is-door-to-balloon-time-a-misleading-metric#sthash.umE2fYE7.dpuf
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How to avoid Froth in Wire - Myograph upon incubation with catalase? I see many papers using 1200U of catalase which when used produces froth. Are there ways to overcome this?
Thanks
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Look at:
Liu Y et al, 2011 Circ Res, Hydrogen peroxide is the transferable factor mediating flow induced dilation in human coronary arterioles
This is a very well done study that makes full use of PEG-Cat
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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?
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IN my opinion, electrophysiological testing will reveal and aberrant A-V pathway that can be ablated to obtain a permanent cure.
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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.
Regards,
Onkar Marway
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Dear Onkar Marway 
FFT and AR are both estimates of the spectrum. Their results depend on how close the assumptions built in the 2 different techniques hold. FFT assumes periodicity. AR assumes that future values can be predicted from a linear combination of previous values (that is, that there will be no discontinuities on the signal and a certain number of derivatives). For the same data length AR has a better spectral resolution than FFT, especially for short data segments. The 'difficulties' associated with AR are that (I) it requires the choice of a 'model order' p and (ii) it is slower than FFT for the same data set. Also AR can only 'see' a maximum of p/2 spectral peaks for a model order p. Fortunately there are several good techniques for finding the 'optimum order' of the AR model. Check the literature. In my experience an order of around p=16 should produce good results. Also beware that AR does not require a sampling frequency which is too high. Oversampling in AR is not a good idea. Just respect Nyquist, (fsam>2*fmax) but don't go to more than 4*fmax, as doing that will not improve your spectral estimation and will demand an artificially higher model order (and consequently longer processing time).
I would not dismiss AR spectral analysis. It is a very interesting approach.
The following 2 publications might be useful:
doi:10.1088/0967-3334/23/2/308 and
doi:10.1016/j.measurement.2012.05.005
Have fun :-)
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When and why should I use KCl normalization in vascular reactivity studies (contraction curves)?
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To add to Ellinsworth's answer, you should also use it again at the end of the experiment to ensure your tissue is still viable. There is the possibility that the experiment itself (incubations, washes, treatments, time, etc) could damage the tissue and alter results.
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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 
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"Certain patients, independent of BP levels, present neither evidence of acute target-organ damage (TOD) nor an immediate threat to life, which obviates the need for antihypertensive therapy in the emergency room. This condition occurs usually in oligosymptomatic or asymptomatic hypertensive patients, whose BPs, although under treatment, are not controlled and are typically elevated. Another group of hypertensive patients may have a transient BP elevation caused by any emotional, painful or uncomfortable event, such as migraine, vertigo or headache of muscleskeletal origin, and manifestations of panic disorder. Such symptoms characterize hypertensive pseudocrisis". 
Sobrinho S, Correia LC, Cruz C, Santiago M, Paim AC, Meireles B, Andrade M, Kerner M, Amoedo P, de Souza CM. Occurence rate and clinical predictors of hypertensive pseudocrisis in emergency room care. Arq Bras Cardiol 2007; 88: 579–584.
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Hi. Iam segmenting  heart vessels. i need ground truth data . Which software is good at obtaining ground truth for the 3D heart vessels?
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Ground truths are usually created by experts, practitioners, and/or radiologists for the image/volume under study not by software. Ground truth are considered as the perfect or perfect most accurate segmentation. Then you use the ground truth to compare the accuracy of  your segmentation with it, mostly using Dice coefficient, Jaccard similarity or Hausdorff distance.
You better use standard dataset or publicly available database to avoid this obstacle as if you tried to make the ground truth is very time consuming and definitely requires a lot of experience which mostly not available for junior researchers.
Good Luck 
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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.
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think about tako tsubo cardiomyopathie - it seem typical and ther is a lot of literature for this item available. In Austria it is also called floridsdorfer frauenherz.
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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?
Thank you. 
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It is known that HRV reflects the level of general health but, more importantly that HRV is an active process that serves as a tool to provide baroreflex functioning. Each heart beat causes the afferent fire from baroreceptors that promotes inhibition process in the brain. HRV provides the continual, bidirectional communication between the heart and brain, which allows the individual to precisely adapt to changes in his/her internal milieu and external environment by integrating neural and cardiovascular reactions. This information is necessary for interpretation of the HRV indices, in particular, HRV total.
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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)
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The following Indapamide Hypertensive Crisis side effect reports were submitted by healthcare professionals and consumers.
This information will help you understand how side effects, such as Hypertensive Crisis, can occur, and what you can do about them.
A side effect could appear soon after you start Indapamide or it might take time to develop.
This Hypertensive Crisis side effect was reported by a consumer or non-health professional from VENEZUELA. A 79-year-old female patient (weight:NA) experienced the following symptoms/conditions: hypertension. The patient was prescribed Indapamide (dosage: NA), which was started on Oct 01, 2010. Concurrently used drugs:
Caduet ([amlodipine Besilate 5 Mg/ Atorvastatin Calcium 40 Mg], 1x/day)
When starting to take Indapamide the consumer reported the following symptoms:
Renal Impairment
Blood Creatinine Increased
Blood Urea Increased
Hypertensive Crisis
These side effects may potentially be related to Indapamide.
For more plz read at folowing link
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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?
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Atheroma site specificity correlates strongly with regions of disturbed shear stress, I.e. on the outer wall at a flow divider, e.g. bifurcation - where shear is low, or at regions of vessel curvature, e.g the aortic arch. Also, contrary to popular believe, shear is not uniform across the circulation. In fact, it is considerably higher in small arteries and especially arterioles. Also, between species there is an inverse relation between shear and body mass, e.g. shear is around 15 times higher in the abdominal aorta of a rat than the same region in a human. Coincidence that rats don't spontaneously develop atheroma?? Notably, shear is a powerful inducer and suppressor of the genes pertaining to vasodilation and vascular disease. 
Hope that helps,
Dave
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IF AF WAS CONVERTED TO SINUS, when to stop warfarin and when to stop amiodarone?
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Dear Dr.
It is advised to continue warfarin for two months then depending on risk factors.
Best regards
Dr. Hyder O. Mirghani
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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
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Hi Herman,
Tthank you very much for reply. Unfortunately I'm interesting in a developing a technique for stent modeling using CAD software. The problem is that I can not find any guide of how to deform a stent to fit a vessel. In all publication they present only a final stent geometry but there is now description of how to do it on practise.
With best regards,
Sergey
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Which is the better, anticoagulant therapy only or combination of anticoagulant therapy and antiplatelet therapy?
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NOAC: as simple as that. Presumably Pradaxa 2x150 mg - superior anticoagulation profile with acceptable bleeding complications.
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Intersting guidelines on prevention of SCD and treatment of ventricular arrhytmias, by means of drugs, electrophysiology/interventions, as well as devices. 
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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.
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Please also the attachment added.
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Hello all
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. 
Thanks
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U-SHAPE: This is called the bath tube function or Teguchi loss function type. It generally is used in failure rate modeling. If your data distribution fallows this characteristic, the modeling test that comes close to it is the Weibull.
POWER: The relationship of sample size are explained in the attached articles---Beta Probability. See attached figure. Power = 1 - beta. The power formula is also given at the link below.
Power and samples size are related. If you select to adopt Weibull as the tool of analysis, the Gou et al. article gives sample size calculation that would meet your power requirement.
The shape of U or non-U is not relevant to beta probability because even if you deal with the loss function U shape, the cumulative probability distribution still follows the bell shape, i.e the bottom of the U (minima) matches the bell's maxima when the two curves are super-imposed (see figure: loss function). The beta probability (testing for power) is the verification of how much does your observed tail intrudes into the (1 - a) region.
REFERENCES: See attached and links.
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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?
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Hi Benjamin,
The normal distribution of a complex biological system or process cannot be managed  by a single number or a linear algorithm.
Remember , a randomised controlled clinical trial describes the  ideal management for only the median patient.
However La Places law applies. P= t / r.h. Rate of change with sequential measurement is also important
A 5 cm aneurysm in a 40 year old Marfan's patient should be managed differently to a 7 cm aneurysm in 80 year old with comorbidities.
I have several elderly patients  referred for surgery with 5 cm + ascending aneurysms who are  who have remained stable over many years  with monitoring rather than operation.
Hope this helps
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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.
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Prasad, The original description of the sIgM -/- mice is described here. The apoE -/- and LDLR -/- background should not directly affect the immune system. You may be observing differences in the mechanism of atherosclerosis development. Have you considered the comparing atherosclerosis in the 2 different apo E -/- mice on a chow diet where the development of atherosclerosis will be slower?    http://www.jimmunol.org/content/160/10/4776.full.pdf+html
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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,
Erik
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Quite the contrary; the THAPCA study had a profound effect size favoring the colder arm, and showed statistical significance in outcome (albeit, this was buried in the appendix, so those that don't read the whole article will miss it).  
From the point estimates, we're looking at a Number Needed to Treat (NNT) of 12.5 (20% vs. 12% to primary outcome of survival at 12 months after cardiac arrest with a VABS-II score of 70 or higher). This is amazingly large. And an overall 1-year survival of 38% in the hypothermia group vs. 29% in the normothermia group gives us an NNT of 11.
This study was underpowered to find the statistical significance, but that shouldn't affect the obvious effect size signal. The goal was 276 patients, the analyzed number was short of that, and the sensitivity analysis (reported only in the Supplementary Appendix), despite being downplayed somewhat, suggests that in fact the results were quite close to crossing into significance had the trial ran a bit longer.
Survival over time was significantly longer with therapeutic hypothermia than with therapeutic normothermia (mean survival, 149±14 days vs. 119±14 days; P = 0.04 for the comparison of survival between the two treatment groups by means of the log-rank test) (Fig. S1 in the Supplementary Appendix). Looking at Figure S1 (way down on page 22 of the Supplementary Appendix), I think it's pretty clear which arm you'd put your loved one in if faced with that decision.
The authors rightly emphasize though that this was not a study against a non-treated arm, but rather was a comparison between two very rigorously treated arms (for out to 120 hours).
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any possible interaction between arrhythmia and heart scan results?
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PVCs are generally not an issue unless they are extremely frequent. Bradycardia is a concern as the sensitivity and positive predictive value of the test is greatly affected by the heart rate attained when the patient is on the treadmill. If the patient is unable to exercise a drug such as dobutamine may be used as it mimics the effects of heart rate  and BP produced by exercise. The arrhythmia that is of most concern is atrial fibrillation as the irregularity of the rhythm results in many beats not being counted or being double counted. Gating is helpful but does not totally solve the problem with atrial fibrillation.
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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!
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hi Li, could the attached review help you?   
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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.
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For indication it's clear that myocardial viability and suitable coronary arteries are needful prerequisites,  along with risks factors just mentioned
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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?
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Your answer surprises me. With a dose of 80 MBq at rest and a normal collimator, ignoring decay / scatter / attenuation / part of patient outside FOV / geometric efficiency / poor algorithmic efficiecy, your 'true' data compromises at most 6E5 events amidst a lot of noise. Given that likely half the photons are scattered, half are attenuated and three quarters will be outside the field of view and that probably the GP will compromise less than 1.5% of the MIBG uptake within the field of view, I am not convinced that it is at all feasable. 
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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?
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See the relevant chapter in my wonderful new book. CARDIORENAL CLINICAL CHALLENGES.  Eds Goldsmith, Covic, Spaak. Published by Springer Jan 2015.
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what are clinical longitudinal, radial and circumferential strain values for ischemic heart diseases? a common strandard range for strain values at ischemic heart diseases!
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The normal range of global longitudinal strain has been a fair topic of debate. It depends on what instrument  and software package you are using. -12% would actually be at least moderately decreased for us. Many consider -17 or -18 GLS (aka GLPS) to be the lower limit of normal for GE software, but that's not sensitive or specific for CAD. See the attached. In CAD vs. non-CAD populations there will be significantly different average GLS's, but that's about it. Following it serially for a decline would likely be better. As far as radial and circumferential strain, many don't use them because they aren't very reproducible. 
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What is the clinical evidence for safety of Arginin and Citrullin administered orally for children
> 6 years of age?
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There is a report on toxicity with subpotent L-citrulline administered. kindly check the link...
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I wanted to ask if there is a score used to assess risk of cardiac events for patients undergoing colonoscopy procedures? 
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This is the current classification
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Hi Gopal, I see no reason why the pharmacological inhibition of CETP may lead to cardiovascular benefit. In fact, major studies to date have provided results that agree with this statement. Admittedly CETP inhibitors increase levels of HDL cholesterol (theoretically beneficial), but probably from HDL2, making it unable to collect more tissue cholesterol and blocking the transfer of cholesterol to other lipoproteins.
The only possibility that this treatment was effective, in my opinion, would be if the HDL2 quickly transferred their excess cholesterol through the SRB1 receptor, thus leading to a stimulation of reverse cholesterol transport, which does not seem to occur
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What is the risk of having hypertension(160/90) + gout(9)?
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Uric acid is a known herald of hypertension...Treatment is indicated once being symptomatic/ problematic and/ or exceeding cut-off of 10mg/dl...Needless to reemphasize that both hyperuricemia and hypertension are independent cardiovascular risk factors and need to be rigorously attended to forestall adverse outcomes at an era of comorbidities and polypharmacy; a lot of confounders are difficult to pinpoint in the arena!!! Again, pros and cons of medications as well as personalization of overall management should be poised by the end of the day...
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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.
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If I understand well, you are talking about a patient who already had PCI+ stenting, and then SAH. This is one of the greatest unanswered clinical problems, which doesn't have just one solution. In my opinion, as Dr Oteh M said, it depends on how serious the SAH was, on how has it been resolved (if possible), and on how much time ago the patient had PCI and stenting. The second anti-platelet drug (tyeno) must be stopped. About Aspirin I have no data in patient at intermediate or high thrombotic risk, whereas I usually decide about withdrawal in low thrombotic risk (e.g. 12 months after DES or 6 months after BMS).
Regards
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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.
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Or Mitral Stenosis! Looking at some recent data, its not about the wholesome Metabolic syndrome as a factor, rather individual component of blood pressure, lipid and glycaemia that are stronger determinants of risk and prognosis
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No Detail Available.
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The maximum tolerated dose for the angiotensin blocker Azilsartan is 80mg both for hypertension and congestive heart failure
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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.
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Most critical for stent sizing/ stent to artery ratio is the vessel diameter proximal and distal to the stent and the the distal distribution area. However, decision making in these cases is complex depending on many other factors like neointima formation, calcification, bifurcation, collaterals, previous stents and stent design.
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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.
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I am not sure we can use this to diagnose deconditining with reasonable certaininty. The change in heart rate in response to orthostatic changes, could be seen in patients with hypovolumeia of any cause and in patients with autonomic neuropathy and in elderly patients with Shy-Dragger's etc.
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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.
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Here are a couple of articles talking about respiratory rate being used as a clinical measure:
Is this what you mean?
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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?
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As concerning my hospital, the main questions asked are: tissue characterization and myocardial anatomy/function.