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Cardiovascular - Science topic

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Hi frds,
Looking for a monthly updated database for cardiac, cerebrovascular, and multisystemic events. No success as of yet to find one in Europe.
It should correspond to the monthly data of the CDC Wonder database in the USA:
Cherish your feedback.
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Is a GWAS study of LVH genetic predisposition of 500 samples be considered low powered study? If so how to justify a small sample size ? Is there research conducted with small n size with GWAS ?
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Ideally Power of any study directly linked to sample size . More sample size, more will be the power of study. But sample size calculation , importantly depend on
number of objective parameters ( primary ) of your study ,more no of objective parameters , more will be sample size. Definitely if you choose rare cardiovascular parameter, your sample size will be less. For eg you want to study on Hypertension even 1000 sample will be not even for GWAS
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Hello everyone
I Load apolipoprotein on extracellular vesicles (EVs).
After centrifuging, I have EVs, apolipoprotein, and also loaded apolipoprotein. How I can separate them?
And also confirm that?
Thanks for your suggestions.
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after doing centrifugation collect the solid layer and go with that.
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Hi frds,
What calculation formula and hypotheses do actuaries currently use for the assessment of the impact of Covid and Long Covid on life expectancy in years?
How long does it historically take to integrate new diseases in formulas? 2 years? 5 years? 15 years?
Cherish your feedback.
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Dear Thomas Schuermann,
Different risk categories grew during each wave of the SARS-CoV-2 (Covid-19) coronavirus pandemic. On the other hand, each successive wave of the pandemic generated smaller and smaller escalation scales of many risk categories. In particular, the development of highly effective vaccines against the coronavirus and the introduction of nationwide universal vaccination programs for citizens against Covid-19 has reduced the scales of potential different risk categories.
Kind regards,
Dariusz Prokopowicz
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I recorded the ECG of rats using Adinstrument Powerlab device with 3 electrodes, and started to analyze the recorded ECG manually. I want to identify the abnormality in R wave that seems to be fluctuating with low and high amplitudes alternatively. I suggested that could be a Poor (slow) R Wave Progression but all explanation data regarding this was with 12 lead ECG not 3 leads ECG. is there any suggestions to explain this abnormal change in R wave amplitudes.
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In poor R wave progression, amplitude of R wave in lead 3 will be less than V2 . Actually reverse of normal R wave progression from V1 to V6
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I want to work on the effect of nitrate fertilizer on toad (Bufo bufo)
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Interesting question
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2017 ACDC CMR dataset is widely used in segmentation, classification and other CV studies. And to my knowledge, there were many other open cardiovascular imaging dataset(including ECG, CT, MR) but I can't find their exact name and get access to their website. Can anyone help? thanks!
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Besides the ACDC 2017 dataset we can use LVSC ( Left ventricular segment challenge) 2009 Dataset . it will be usefull Dataset
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Plaques form due to a self-healing mechanism of blood vessels and will increase over time. When entering blood vessels, they block blood flow, lead to hypertension and decrease blood flow to organs such as the heart. To get rid of these plaques, we need to boost the good cholesterol such as HDL or improve health of liver to produce enzymes that move these plaques. So, what other ways to get rid of these plaques without using invasive methods?
Thanks and best regards.
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The following RG link is also very useful:
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I'm wondering if there is less stress on the mom's cardiovascular system during a pre-term delivery than a full-term delivery. This is outside my wheelhouse, but smaller baby = smaller cardiovascular stress is my hypothesis. Anesthesia-free data would be ideal. Thanks in advance!
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There are a lot of factors other than baby size involved here. Preterm deliveries can be, for example, because of pre-eclampsia, and so the whole haemodynamics involved are different. Other causes of preterm delivery likewise – a preterm delivery isn't a normal delivery that happened early, it's a pregnancy that ended unusually.
Heart rate is also only a proxy for what is going on with the haemodynamics. Cardiac output and peripheral resistance are probably more important in pregnancy than heart rate. Less so blood pressure, as the same pressure can be generated by low output + high resistance and by high output + low resistance.
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Has anyone seen any interesting gaps in the literature related to cardiovascular exercise physiology and could suggest any potential topic? Would be greatly appreciated
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I recommend that you identify a topic that both you and your advisor are interested in. If your advisor is interested in your topic, he/she can provide more insightful advice and he/she will be more motivated to help you. I recommend setting up a meeting with your advisor to see if he/she has some research questions that might be of interest to you. Showing interest in your advisor's research is never a bad thing.
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Many Studies have now shown benefit of SGLT2 inhibitors in heart failure. The outcome measures often include composite cardiac outcome measures that include Ischaemic Heart Disease [IHD] outcomes.
Is the benefit limited to Heart failure alone?
Anybody aware of any study that shows true benefit for Ischaemic Heart Disease alone?
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Sodium-glucose co-transporter-2 inhibitor (SGLT2i) therapies have emerged with robust evidence for reducing the risk of adverse CVD outcomes in people with T2DM who have either established CVD or are at risk of developing CVD. https://link.springer.com/article/10.1007/s13300-019-0657-8
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Can SGLT2 inhibitors be safely used in Non-Diabetics, as diuretic therapy?
Do they have other beneficial pleiotropic effects in general, eg in endotheleal function and vascular tone
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Diuretics with a long action act as vasodilators in hypertension. They drive sodium out of the cells both it in the renal tubule and in the smooth muscle cells around the arterioles. By excreting sodium the resting potential is more negative, the distance with the threshold potential is higher making the smooth muscle cells less excitable. Less vasoconstriction = vasodilation.
SGLT 2 inhibitors can work in the same way: by vasodilation they lower BP, decrease the afterload on the heart ( useful in heart failure) and protect the blood vessels.
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Dear Colleagues,
Below I copy a call for help in our meta-analytical work. In brief, if you have any data (published or unpublished) that is not on the list of paper below, please let us know!
Thank you RG community!
Call for meta-analysis data: The Undoing Effect of Positive Emotions.
We looking for unpublished data/manuscripts regarding the undoing effect of positive emotions for the purpose of a meta-analysis. We are a team of researcher from Adam Mickiewicz University, Stanford University, and University of Amsterdam.
Specifically, we are looking for studies with the following characteristics:
- Experimental studies that induced positive emotions vs a neutral control following experimentally induced negative emotions or stress.
- Autonomous Nervous System recovery was measured during elicitation of positive emotions and during the neutral conditions.
If you have any unpublished work on this topic, we would like to include it in our analyses. We would be very grateful if you might either send your study information or data at your earliest convenience (deadline: 15th of October), or contact us with any questions you may have to the following address: macbeh@amu.edu.pl.
Additionally, we are interested if you know of any additional unpublished or ongoing studies (by yourselves or other authors) that might be relevant. We would also appreciate it if you would forward our request to any researchers in your network that may be doing relevant work in these areas.
Please find the list of studies that we identified by the literature search. If you cannot find your papers that can contribute to our meta-analysis on this list, please let us know about your work. There have been relatively few studies published about this phenomenon, thus every contribution is highly appreciated
Best regards,
Maciej Behnke & Łukasz D. Kaczmarek
Adam Mickiewicz University
James J. Gross; Stanford University
Mark Assink; University of Amsterdam
List of identified studies:
*Fredrickson, B. L., & Levenson, R. W. (1998). Positive emotions speed recovery from the cardiovascular sequelae of negative emotions. Cognition & Emotion, 12(2), 191–220. https://doi.org/10.1080/026999398379718.
*Fredrickson, B. L., Mancuso, R. A., Branigan, C., & Tugade, M. M. (2000). The undoing effect of positive emotions. Motivation and Emotion, 24(4), 237–258. https://doi.org/10.1023/A:1010796329158
*Gilbert, K. E., Gruber, J., & Nolen-Hoeksema, S. N. (2016). I don't want to come back down: Undoing versus maintaining of reward recovery in older adolescents. Emotion, 16(2), 214–225. https://doi.org/10.1037/emo0000128.
*Hannesdóttir, D. K. (2007). Reduction of fear arousal in young adults with speech anxiety through elicitation of positive emotions (Doctoral dissertation). Retrieved from, https://vtechworks.lib.vt.edu/bitsteam/handle/10919/28941/dissertation.pdf?sequences=2&isAllowed=y.
*Kaczmarek, K. (2009). Resiliency, stress appraisal, positive affect, and cardiovascular activity. Polish Psychological Bulletin, 40(1), 46–53. https://doi.org/10.2478/s10059-009-0007-1.
*Kaczmarek, L. D., Behnke, M., Kosakowski, M., Enko, J., Dziekan, M., Piskorski, J., ... & Guzik, P. (2019). High-approach and low-approach positive affect influence physiological responses to threat and anger. International Journal of Psychophysiology, 138, 27-37. https://doi.org/10.1016/j.ijpsycho.2019.01.008
*Medvedev, O., Shepherd, D., & Hautua, M. J. (2015). The restorative potential of soundscapes: A physiological perspective. Applied Acoustics, 96, 20–26. https://doi.org/10.1016/j.apacoust.2015.03.004.
*Qin, Y., Lü, W., Hughes, B. M., & Kaczmarek, L. D. (2019). Trait and state approach-motivated positive affects interactively influence stress cardiovascular recovery. International Journal of Psychophysiology, 146, 261-269. https://doi.org/10.1016/j.ijpsycho.2019.08.011
*Radstaak, M., Geurts, S. A., Brosschot, J. F., Cillessen, A. H., & Kompier, M. A. (2011). The role of affect and rumination in cardiovascular recovery from stress. International Journal of Psychophysiology, 81(3), 237-244. https://doi.org/10.1016/j.ijpsycho.2011.06.017
*Soenke, M. (2014). The role of positive emotion eliciting activities at promoting physiological recovery from sadness (Doctoral Dissertation). Retrieved from, http://arizona.openrepository.com/arizona/bitstream/10150/325214/1/azu_etd_13407_sip1_m.pdf.
*Sokhadze, E. M. (2007). Effects of music on the recovery of autonomic and electrocortial activity after stress induced by aversive visual stimuli. Applied Psychophysiology and Biofeedback, 32(1), 31–50. https://doi.org/10.1007/s10484-007-9033-y.
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… , positive emotions, and successful adaptation to stress … - ‎Ong - Citerat av 1721
cal Resilience, Positive Emotions, and Successful Adaptation to Stress in Later Life
Anthony D. Ong and C. S. Bergeman Toni L. Bisconti
University of Notre Dame
University of New Hampshire
Kimberly A. Wallace University of Montana
In 3 studies, the authors investigated the functional role of psychological resilience and positive emotions in the stress process. Studies 1a and 1b explored naturally occurring daily stressors. Study 2 examined data from a sample of recently bereaved widows. Across studies, multilevel random coefficient modeling analyses revealed that the occurrence of daily positive emotions serves to moderate stress reactivity and mediate stress recovery. Findings also indicated that differences in psychological resilience accounted for meaningful variation in daily emotional responses to stress. Higher levels of trait resilience predicted a weaker association between positive and negative emotions, particularly on days characterized by heightened stress. Finally, findings indicated that over time, the experience of positive emotions functions to assist high-resilient individuals in their ability to recover effectively from daily stress. Implications for research into protective factors that serve to inhibit the scope, severity, and diffusion of daily stressors in later adulthood are discussed.
Keywords: adaptation, positive emotion, recovery, resilience
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Dear All,
Hope you are doing well.
How to draw a line in center of the artery fluid volume domain. The problem is that, the line/plane couldn't fall properly at center of artery. When i use the option "LINE command from Location in ANSYS Fluent post processor.
The geometry or model was extracted from patient CT scan data so which is not in a single plane.
Thanking you in anticipation.
&
Regards,
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Faheem Ejaz add line/plane?? Yes, i used same to draw above shown yellow line but my question is about exact center of fluid volume or at mid of axis i want to draw a line. I know ur options , those are also not workout.\ Thanks
Regards,
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I conducted a Mendelian randomisation study for assessing the association between X (exposure) on Y (outcome or case). But, I am not sure whether our outcome (cases) are valid. My question is, how can I check the validity of my outcome using genetic data? For example, is there any reasonable method for checking genetic correlation between our outcome and previously published GWAS including gold standard case ascertainment?
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Machine learning possibly helps in these situations.
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There seems to be a lot of controversy about the validity of HRV as a measure of vagal tone. Specifically, Marmerstein, McCallum, & Durand (2021) published a paper suggesting the lack of correlation between HRV and vagal tone. Are there better, non-invasive ways to clearly and accurately measure vagal tone? So much of the literature over the past few decades focuses entirely on HRV in some way or another. Is this still an accurate way to measure vagal tone?
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It's counter-intuitive and nonproductive to think of vagal "tone" as a static index.
The vagus nerve play a key role in hemostasis, circulation and blood clotting. Vital cardiac activity is both a cause and effect of hemodynamic "relativity" (if you will).
An improved measure of Vagal Regulatory Activity (VRA) and/or Vagal Regulatory Capacity (VRC) would reflect VRA at rest and VRC on challenge (exercise and exercise recovery).
Both VRA and VRC could be ratios of pulse volume and/or pulse velocity against selected (e.g., LF) parasympathetic indices.
At least Vagal Regulatory Capacity (VRC) gives meaning to the term "tone" -- notwithstanding that "capacity" is a clinically more useful term.
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I'm looking for an excel sheet to calculate the STS Score. From the website http://riskcalc.sts.org/stswebriskcalc/calculate. Does anyone have a worksheet to calculate the STS Score?
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I also tried to find the Excel version of STS calculator, but I still didn’t find it. There are more than 60 parameters & it’s convenient to use it on STS site.
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I want use the zebrafish to study heart and vessel development, as well as adult heart regeneration.
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I've heard garlic and high nitrate foods like arugula or beets typically occupy high ranking here. What others do you know of or recommend? What's your top 10 list, based on what research? Thanks.
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When I eat lemon, lower my blood pressure
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As we know,the pulse propagates in wave form and the velocity of wave propagation depends on the propagation medium features. So,Is it possible to use the measurment of velocity of pulse propagation in the body to diagnose cardiovascular problems such as hypertension and hypotension?
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Chronic kidney disease (CKD) is commonly defined as reduction in eGFR value < 90 ml/min/1.73 sq. m. Several studies have reported a significant association between CKD and cardiovascular events. Oxidative stress, inflammation, and endothelial dysfunction are important phenomenons in atherosclerotic CVD. Oxidative stress is also observed in patients with CKD. Thus, it further related to atherosclerosis and CVD events.
While doing a CVD risk assessment, I am curious about using the CKD as a surrogate endpoint of CVD events. Can we do that? Is it possible to use CKD as a surrogate biomarker of CVD and other vascular comorbidities including stroke?
Paper that shows the association between CKD and CVD is available at:
DOI: 10.1056/NEJMoa041031
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First I would recommend being crystal clear in language.
You may have cardiovascular disease (CVD) and cardiovascular events, maybe say CVE. Events are occurrences that happen more or less at once, while a disease is a continuous condition.
Endpoints are usually events. Maybe you can use clear-cut conditions that are correleted with immediate risks, not with long-term risks, to define a substitute endpoint.
It appears that the aspect risk should also be carefully considered. Risks are not endpoints!
Having said this and not being an expert in that field I could imagine that hospitalisation or certain intensive care measures related to renal conditions could be defined as endpoint(s), rather as substitute endpoint(s).
The lab condition you mentioned above I would rather consider as marker of risk.
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What are the functional criteria of the cardiovascular, respiratory and autonomic nervous systems predict the severity of the disease, the presence of complications and mortality?
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Dear Reena. Thanks for the answer.
I think this scale is useful when a well-developed clinical syndrome develops. First of all, I mean indicators which would allow to predict development of the same distress syndrome without the expressed clinical signs.
For example, by the parameters of respiratory variability, synchronization of the cardiorespiratory system, simple respiratory tests, etc.
Sincerely. Alexander Romanchuk
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Any ideas/suggestions related to re-opening of fitness centra and personal training and safety measures and/or risk factors related to covid-19?
What about material?
What about training machines?
Risk of spread with breathing, with higher-intensity training?
What kind of safety measures would you suggest?
Any science about this related to sars-covid from before?
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First of all, you need to consider providing high standards hygiene. As Ashraf mentioned earlier, ensure you have good ventilation system while maintaining regular and ongoing sterilization. Second, since the environmental contamination is likely to accure, you need to limit the number of people per each session while maintaining the social distance. This measure is crucial at this time, and recall your plan according to the situation by following the WHO updates and recommendations. Ensure people are wearing PPE ( masks, gloves , goggles, etc). Regarding the training machines, ensure they are cleaned and sterilized efficiently after each use.
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Over the past two years, our understanding of anti-hyperglycemic medications used to treat patients with type 2 diabetes (T2D) has fundamentally changed. Before the EMPA-REG OUTCOME trial, agents used to lower blood glucose were felt to prevent or delay the development of microvascular complications, but were not known to definitively reduce cardiovascular risk or mortality. Previous studies with then novel sodium-glucose cotransport-2 (SGLT2) inhibitors demonstrated improvements in several cardiovascular and renal risk factors, including HbA1c, blood pressure, weight, renal hyperfiltration, and albuminuria. However, as with other antihyperglycemic drugs, it could not be known if these salutary effects would translate into improved cardiorenal outcomes. In the EMPA-REG OUTCOME trial, SGLT2 inhibition with empagliflozin reduced the primary outcome of major adverse cardiovascular events (MACE), while also reducing mortality, hospitalization for heart failure, and progression of diabetic kidney disease. In the CANVAS Program trials using canagliflozin, the rates of the 3-point MACE endpoint, the risk of heart failure and the renal composite endpoint were also reduced, albeit with an increased risk of lower extremity amputation and fracture. As a result, clinical practice guidelines recommend the consideration of SGLT2 inhibition in high-risk patient subgroups for cardiovascular risk reduction. Ongoing primary renal endpoint trials will inform the cardio-metabolic-renal community about how to optimally treat patients with chronic kidney disease – including those with and without diabetes.
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SGLT2 inhibitors could have an impact in prevention/slowing down progression of nephropathy as it helps to lower the renal tubular threshold for glucose re-absorption, and glucosuria occurs at lower plasma glucose concentration
( Pharmacotherapy handbook).
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Does the accuracy of the cardiac flow analysis vary when analysis is done using 2D Cine -3 directional velocity encoded MRI and when it is done using 4D flow MRI with volumetric coverage and 3 directional velocity encoding?
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From the perspective of cardiovascular fluid mechanics perhaps yes, but from MRI physics perspective no: assessing velocity or flow data from 2D cine 3-directional velocity encoding is not exactly the same as obtaining velocity information from a static reformatted plane from 4D flow MRI, even when you are able to design both sequences with identical parameters (FOV, TE, TR, bandwidth).
Firstly, 2D imaging is not the same as 3D volume acquisition (2D uses a slice select gradient where 3D imaging uses two phase encode gradients).
Secondly, 3D imaging provides more SNR than 2D imaging and 2D represents velocity data over a relatively thick imaging slice with possible partial volume errors in case of angulated flow.
And third, obviously 4D flow acquisition requires more scan time, which makes the data more vulnerable to errors associated with heart rate variation and patient movement.
More importantly, from a practical point of view, a static 2D plane with cine 3-directional velocity data does not allow a retrospective correction of the imaging plane in the same way as 4D flow MRI data does (for instance for misalignment correction or for retrospective valve tracking).
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In the clinical world, GLP1 agonists and SGLT2 inhibitors are not commonly co-prescribed, though given the benefit of weight loss, cardiovascular benefits, and blood glucose control in patients with insulin resistance as well as obesity, should this be more commonly used? Thank you!
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Thank you!
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I have 2D PC MRI velocity data in a square matrix. I want to calculate the pressure differences at different points between the inlet and outlet of left atrium from this data. I have calculated using Bernoulli equation where I could calculate the pressure differences along a particular streamline only. I want to know how can I calculate pressure difference in the whole flow?
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Many years ago I worked on this topic, some of my papers on RG illustrate some details. However, if you have a matrix of the two velocity components on a plane, assuming the flow has a divergent-free velocity field, you could set the solution in terms of the 2D Poisson problem for computing the pressure gradient in the plane.
However, I immagine that you have a slice (say the x,y - plane) of 3D real flow and the condition for the 2D continuity du/dx+dv/dy=0 is not satisfied as you have the dw/dz component.
Using Bernoulli is a wrong approximation for a viscous fluid.
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Research gate is continually sending me research on bio stuff (cardiovascular) I am not interested in. I mark it as not interesting but research gate insists. It is a bit frustrating that in teh era of artificial intelligence nothing better can be done.
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send a message to the administrator and it should be sorted out. You can also check the settings and see if it can be sorted out from there.
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I am doing a review work on the cardiovascular conditions of patients living with diabetes Miletus. I wish to know where to look for very recent resources. Apart from published literatures, will the government hospitals be of help?
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Hi Favour,
The availability may vary depending on the region you are researching, but you could try government run research or statistics institutions. Sometimes governments have centres that collect health data and trends over longer time periods. For example, in Australia the Australian Institute of Health & Welfare (AIHW) and the Australian Bureau of Statistics (ABS) collect this kind of information.
I hope this helps, and all the best with your review.
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What do you think that Noise Pollutant affects you the most?
(A) On Heath
o Effect on hearing
o Other health issues
o Disturb sleep
o Result in deafness
o Mental health disorders
o Any other, please mention
(B) On Life
o Reduce Working Efficiency
o Interfere with communication
o Cause annoyance
o Any other, please mention
(Other health issues may include like High Blood Pressure, Hypertension, cardiovascular effects, Heart Disease, Stress
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Headaches mostly .and occasionally it triggers my dormant anger.
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I have only x and y directional blood flow velocity data obtained from MRI. I have no z-directional velocity data . I have learnt that the vortex detection methods like q-criterion, lambda2 method needs velocity data for all three directions (x,y and z) to identify vortex core locations. Is there any method that i can apply for identifying vortex core locations for my two directional data?
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In a 2D field you can directly compute the vorticity field du/dy-dv/dx and plot the iso-vorticity lines. A vortex tube section in the (x,y) plane can be identified this way (envelope of the vorticity vector over a closed line).
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We are working with an industry partner who has developed screening kiosks for general population assessment of physical and mental health. They are measuring HRV, and I want to know if the objective HRV data at an individual level might add predictive variance over and above self-report measures (e.g., K10) in the prediction of high prevalence mental disorders.
HRV is also a predictor of bad cardiovascular outcomes. As a secondary question, are there holistic models predicting multimorbidity (which might use HRV, blood pressure, self-reported anxiey, etc. as a screen for multimorbidity risk)
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There is large inter/intra-individual variability in HRV. Although certain mental disorders such as depression may be associated with lower HRV, that itself can be due to antidepressant medications, whether HRV can predict development of mental disorder is not well investigated yet. Note that measuring resting state HRV requires standard setup since many factors can influence the measure. The other informative measure is HRV reactivity to psychological/physical stress tests.
Anyway, I doubt that an accurate cut-off can be determined for predicting development of mental disorders in future using just HRV indexes mainly because of several other individual and contextual factors that can influence this measure. It is true that lower resting HRV is associated with higher risk of cardiovascular diseases in future but just having association does not mean that an accurate prediction can be achieved.
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Is there anyone who would like to this literature review with me?
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I will be happy for this veron
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Our experience in cardiovascular ischemic heart disease is very promising using TPA in carotid sonography for very large population!!!! Dont you think to use any cardiovascular subrrogate?
This method is easy, in 2d sonography, with very low variability in inter an intra observer variation!!
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TPA and TPV has been shown to vary with population and aging.First it needs to be validated and to familiar with population variation.People are using IMT especially in diabetics as one of the marker for Atherosclerosis.TPA and TPV definately scores over IMT.
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Dear colleagues
Have a good day!
Is there any relationship between lipid profile parameters and cholesterol in patients treated with MTX?
Regards
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Please have a look at this useful PDF attachment.
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I have some MRI images and 2D phase contrast blood flow velocity data of healthy patients obtained from MRI. I need to obtain the vortex lines of blood flow inside the heart from the data. So to clean the data, I have applied Gaussian and wiener filters of certain radius. Still I think proper vortex lines are not coming. I am really in a fix. Any help or suggestion will be accepted with gratitude.
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This is the type of image which I have
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I want to develop a material for a cardiovascular stent application. Therefore, I want to know about the pressure which a stent will bear in the artery.
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The pressure at which stent is deployed has nothing to do with blood pressure. The nominal pressure for most of the stents as has been pointed out is 8 to 12 bar. But most stents require post dilatation with non compliant balloon at 18 to 20 bar. Some lesions rarely require post dilatation at even higher pressures . If the lesion and vascular bed are properly prepared, very high pressure post dilatation can be avoided, as it carries risk of vascular rupture.
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I have ran a study comparing the Daily Mile and HIIT in children to see which is best for improving cardiovascular endurance (Beep test) and anaerobic power (20m sprint).
Scores on both test were measured before and after the interventions so it is a differences in the change in the mean of the scores post both interventions to see which is greatest.
Which is the correct statistical analysis to run on SPSS? I thought a one-way repeated ANOVA but I am now doubting myself.
Any help is appreciated.
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Hello Joel,
One-way ancova or mancova would likely be best. Intervention type is the factor (between-subjects variable; 2 levels), and post-intervention scores are the dependent variables. Pre-intervention scores would make good covariates. Be sure to check assumptions!
A technical issue in using change/difference/growth/gain scores as outcomes is that, if the individual scores are less than perfectly reliable, difference scores will be less reliable than either of the scores from which they are computed. This is exacerbated as the two scores are more strongly correlated.
Good luck with your work.
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Currently I am working on the formulation and development of microsphere formulation for cardiovascular drug, where i am not getting standard references for estimation of drug from same formulation. So I have decide to develop my own method for the estimation of drug from microsphere formulation.
Since I am not getting any related research articles therefor i am not sure to proceed.Please guide me on this..
Thank you all..
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Either by UV spectrophotometer or by HPLC device after extracting drug from them into the same media intended for release taking into account leaving enough time for release in case of retiredent polymer .. you could get benifit from somication
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Currently, physical exercise programs are being developed for elderly people who perform at home and are offering very advantageous results for the prevention of cardiovascular, rheumatic and musculoskeletal diseases. It is interesting to conduct studies aimed at evaluating the effectiveness of these programs, as well as adherence to them.
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you may find these articles helpful
some researchers also look for proxy measures such as exercise self-efficacy that more easily measure changes associated with adherence
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How significant is OSA in your practice and how aggressively do you manage it?
Apart from CPAP therapy, should weight loss strategies be vigorously followed?- Bariatric surgery/ Liraglutide/other?
CPAP doesnt improve mortality
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The goal in this situation is not only to diminish the apnea/hypopnea index but to avoid systemic comorbidities as carduovascular disease, diabetes or neurocognitive impairment
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Do any physicians, researchers and scientisays among us ever wonder how it is that while researching and standing as proponents of advancing the health of the general population —we often fail to acknowledge our own health — and may even put others’ health before our own personal health?
“Doctor health thy self” may not just be a cute anecdote. Seriously. The path to becoming a doctor and the hours invested in treating others, long and arduous, may be killing us. What say you?
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Health care workers often fail to take care of their own health. Some experience burnout or compassion fatigue periodically especially in the mental health field. Health care workers are at high risk due to their contact with patients who may have various diseases. Thus, not only are hand washing and other protocols important it is imperative that these workers periodically take time off to relax and decompress.
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The objective of the position is to develop a PhD work on the subject “cardiovascular stent design and analysis”. The aim of the work will be to analyze the expansion of the stent and the contact with the artery to simulate thrombectomy technique. The developments will have to be carried out within the Kratos framework.
More info:
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Is this position still vacant? Please let me know email ekram.aust08@gmail.com....thanks in advance
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In an experimental study we tested various breathing exercises and monitored respiratory flow, beat-to-beat blood pressure, and heart rate. We developed MATLAB script for baroreflex analysis based on the sequence method and the result was interesting.
Now, we want to compare breathing exercises regarding the magnitude and phase of transfer between respiration -> blood pressure, respiration -> heart rate, and blood pressure -> heart rate using transfer function analysis.
I appreciate if someone with experience in such analysis can help us with a MATLAB script.
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dear Ali
you can find some suggestions of SAP-HP phase and gain analysis in A. Porta et al, Am. J. Physiol. 300, R378-R386, 2011 and J.C. Milan-Mattos et al, J. Appl. Physiol. 124, 791-804, 2018.
All the best, Alberto
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Statins reduce further deposition of lipid and in some cases with very high dose statin, some marginal reduction in atheroma may be seen.
In patients with substantial atheroma, one wants appreciable reversal and removal of lipid. Statins cannot do this
Initial studies with HDL infusions have shown promising results, but problems exist with immunogenicity .
Can HDL be rendered less immunogenic and is it a potential game changer in the world of cardiovascular disease and death?
Can we one day 'clean out' the atheroma from our arteries with this intervention?
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The point is not just raising HDL, but the efficacy of the oxLDL uptake at the site of atheroma and removal by the liver. That blocking CETP didn't work was logical from this point of view Just putting more garbage collecting trucks on the road while not improving the uptake at home nor delivery at the destruction site just creates traffic jams.
This was most clearly addressed in the apo-I Milano study where a population was found with extremely low HDL levels and still no atherosclerosis. So, better understanding of the reverse LDL transport system is of uttermost importance.
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Nano-contribution for cardiovascular disease is quite vast. So, search for marketable nano-medicine for Cardiovascular treatment.
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yes BMC patented innovative mollecular need developpement and finances.
BMC is very active in HTA ,POTECT CARDIOVASCULAIRE,AND NEURODEGENERESCENCES,... but need finacial partenariat
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I use Lagendorff ischemia-reperfusion for rat hears 30 min ischemia then 90 min reprfusion. Half of the hearts did not come back (died) after ischemia. Any reasons for that?
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Dear Colleagues, we have been collecting data for a meta-analysis regarding positive emotions and responses in peripheral physiology. If you wished to contribute please contact us (mansape@stanford.edu)
Call for meta-analysis data: Autonomic Nervous System Activity in Positive Emotions (MANSAPE). 
A team of researchers from Stanford University and Adam Mickiewicz University is conducting a meta-analysis on autonomic nervous system activity in positive emotions. We are looking for unpublished data/manuscripts.
Specifically, we are looking for studies with the following characteristics:
·  Experimental studies that induce positive emotions.
· ANS measures were assessed during baseline and emotional responding
If you have any unpublished work on this topic, we would like include it in our analyses. Please either send your study information or data at your earliest convenience, or feel free to contact us with any questions you may have to the following address: mansape@stanford.edu
Additionally, we are interested if you know of any additional unpublished or ongoing studies (by yourselves or other authors) that might be relevant. We would also appreciate it if you would forward our request to any researchers in your network that may be doing relevant work in these areas.
You will find a list of already included studies attached.
Thank you!
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Here is the list of articles that we've already reviewed:
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I am looking for antibodies against the protein Puromycin N-acetyltransferase.
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I have found some that work for Western but not for IMF.
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Colleagues,
A bit of a puzzle, I am reviewing the effect of an intervention against coronary heart disease (CHD) in a large population (at least 250 000 subjects drawn from North American (USA and Canada), Western Europe (UK, Germany, Netherlands), Southern Europe / The Mediterranean, India, Taiwan and Japan). The challenge is that some of the studies state RR values while others use OR values. Is there a concise way to convert RR values to OR values?
I ran into an argument that was raised in Grant (2014) Converting an odds ratio to a range of plausible relative risks for better communication of research findings, BMJ, 2014, doi: 10.1136/bmj.f7450. The author argues that one can convert OR values to RR, the converse can be true - one can convert RR values to OR?
RR = OR / (1 - p + (p x OR)) (Grant, 2014)
To use the equation, how can one determine the baseline risk of CHD (p) for each of the populations above (North American (USA and Canada), Western Europe (UK, Germany, Netherlands), Southern Europe / The Mediterranean, India, Taiwan and Japan)? Can we assume that baseline risk of such study populations is zero (0) since the subjects recruited into each study were CHD free (obviously there is always a baseline risk greater than 0!)?
Can someone suggest a way to treat such data (RR / OR)?
Thank you in advance. 
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Yes, if prevalence is low (<10%), as a rule of thumb OR and RR are very similar. However, if prevalence is higher, then OR exaggerates risk/treatment efficacy, so conversion is meaningless.
Zhang J, Yu KF. What's the relative risk? A method of correcting the odds ratio in cohort studies of common outcomes. JAMA. 1998 Nov 18;280(19):1690-1. PMID 9832001
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The carotid shunt is made up of a tube on the extremities of which the balloons are glued during the manufacturing process. Quality control (functionality test) are carried out in order to ensure that the product is conform. It has to be ensured that the balloons suffer no leaks.
What are the possible quality control test (non-destructive) that can be put in place after the assembly process to ensure conformity of the product ?
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I tend to agree with Dr. Garry. During manufacture every 10th product should be tested by a competent technician, inflating the balloons to the recommended volume and seeing that they hold the air for a few hours.
Prior to actual use in surgery, the surgeon should make sure that he/she repeats the testing. Only this time it will only be for a few minutes. And it always pays to have a back-up Pruitt-Inahara shunt in the room.
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GLP-1 agonists improved treatment of DM, mainly due to improvement of the complications rate. Numerous of those are cardiovascular related.
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  • ELIXA study (Evaluation of Lixisenatide in Acute coronary syndrome) was the first safety study carried out on GLP-1 RAs and was published in December 2015 (a total of 6068 patients were included )
  • LEADER (Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results) trial (study published in July 2016 included 9340 patients) showed a significant 12% reduction in the expanded composite outcome comprising the primary endpoint plus coronary revascularizations and hospitalizations for angina and heart failure.
  • SUSTAIN-6 trial (сardiovascular and other long-term outcomes with semaglutide in subjects with type 2 diabetes; it included 3297 patients) was conducted to determine the cardiovascular safety of semaglutide \ placebo, and was published in September 2016.
  • EXSCEL trial (Exenatide Study of Cardiovascular Event Lowering, published in September 2017) was conducted to demonstrate the cardiovascular safety of extended-release exenatide versus placebo (study included the largest number of patients with T2DM more than 14,752 patients, in 687 centres in 35 countries)
Liraglutide and semaglutide showed superiority in cardiovascular benefit compared with placebo, both in the presence of standard treatment. Lixisenatide and extended-release exenatide were neutral, that is, they are safe from a cardiovascular point of view, but for the moment they have not demonstrated to provide any benefit. Although many of the mechanisms by which liraglutide and semaglutide produce a cardiovascular benefit are still unknown (the antiatherosclerotic action hypothesis is prevailing). Another notable finding is that the favorable CV outcome benefit observed in LEADER and SUSTAIN-6 contrasts with the null results seen with other GLP-1 RA, lixisenatide, and ELIXA trial, which enrolled patients within 180 days of acute coronary syndrome or EXSCEL trial. Although the exact reasons are not clear, this discrepancy might be related to differences in pharmacokinetic and pharmacodynamic properties. Another explanation for the contrasting results might be the trial differences in the enrollment of lower-risk versus higher-risk patients and between the time of follow-up.
Other studies:
-FIGHT ( Functional Impact of GLP-1 for Heart Failure treatment) evaluated the use of exenatide in people with type 2 diabetes and diastolic heart failure, incretin-based drugs and the risk of heart failure, effects of exenatide in type 2 diabetic patients with congestive heart failure
-PROCLAIM evaluated effect of AC2592 administered by continuous subcutaneous infusion in subjects with advanced congestive heart failure
-MACE (Major Adverse Cardiovascular Events) In this trial, patients on treatment with liraglutide had a lower risk of presenting the primary outcome and a lower risk of cardiovascular death and death from any cause and microvascular complications; the liraglutide group had a statistically significant lower risk of MACE compared with placebo (HR = 0.87; 95% CI, 0.78–0.97).
Read more: Journal of Diabetes Research Volume 2018, Article ID 4020492, 12 pages https://doi.org/10.1155/2018/4020492
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We have data from Finapress NIBP system recorded through the bitscope easy software for 30 min. We wish to perform an ultra short term blood pressure variability. Could anyone suggest possible tools/methods/literature about the same?
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Hi Apar,
you can use this data for univariat and bivariat analyses. Univariat analyses exploit only the beat-to-beat blood pressure (most often systolic BP). The applied processing schemes resemble very much the analysis strategies that are applied for heart rate variability analysis (see e.g. ; this is just one example with a methodological focus; there are many articles, which calculate blood pressure variability parameters in specific applications). Bivariat analyses refer to baroreceptor sensitivity, i.e. the interdepencency of heart rate and blood pressure variability on short time scales ( ).
Greetings, Sebastian
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There are contradictory data, two references are attached. What would be your decision ? Recommend it or not ?
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Studies show that Enalapril and enalaprilat have been detected in human breast milk; because of potential for serious ADRs in breastfed infant, including hypotension, hyperkalemia and renal impairment, there it is preferred not to use enalapril while breast feeding.
Source: @Medscape
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We have EKG and respiration data recorded using ADinstruments. Could anyone suggest the steps to assess the cardiorespiratory synchronization ratio?
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Hi Apar,
no problem. I do not have personal experience in this field, but I'm quite sure, one of the authors of the linked chapter will help out in case you face any difficulties. They are active on RG, too.
Best of luck!
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Very low sodium diet
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Low sodium diets might increase the risk of the development of insulin resistance. This is because limited sodium intake decreases the content of body water, which is usually compensated by increased epinephrine, renin, and angiotensin levels, all of which inhibit the action of insulin and increase insulin resistance. As you are all aware, insulin resistance is linked to many metabolic diseases, including cardiovascular disorders, type 2 diabetes mellitus, cancer etc. Overall, we just have to be careful with under-consumption of sodium, which I regard at the level of less than 1 g (1000 mg) per day.
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Control of hypertension in first trimester of pregnancy is critical. most of traditional drugs such as betablockers, ACEI. ARB, potassium channel opener and diuretics potentially have teratogenic effects. In addition clinician concern about hypertension crisis result in cardiovascular and brain damages. It claims that methyl-dopa is safe and useful without any potential of fetus malformation. Sometimes the therapeutic effects of this agent is not adequate. management of these patients is a dilemma.
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Hi Gennadiy, I agree with your answar. Hypertensive emergency in pregnancy is an potential life threatening condition which needs prompt treatment. Following drugs can be safely given in pregnancy with Hypertensive emergency.
Iv Labetalol
Iv hydralazine
Nicardepine
Sodium nitroprusside can be used as last resort because of potential thiacyanite toxicity and worsening maternal cerebral oedema. Thanks
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Does stroke volume and diastolic BP have a positive linear correlation?
Given greater pre-load and thus end-diastolic volume is it expected that diastolic BP would be reduced?
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Hi Terun Desai,
Increase or decrease in the stroke volume has some influence in the diastolic blood pressure (DBP). But It is directly proportional the total peripheral resistance (TPR) offered by blood vessels, whereas systolic blood pressure (SBP) is directly proportional to the stroke volume.
If there is increase in the peripheral resistance there will be increase in the DBP as seen in atherosclerosis in which condition there is decrease in the diameter of the blood vessel, will offer more resistance to blood flow. In order to pump adequate amount of blood to the tissues in this condition, there will be increase in the heart rate and stroke volume, therefore increase in the SBP. Hence there will be increase both SBP and DPB (Increase in BP).
Exercise causes increase in the SBP and a slight increase in the DBP. During exercise there will be increased production of metabolic waste product which will dilate the blood vessels. Therefore there will be decreased TPR, which will not allow to increase in the DPB much. At the same time, increase in the sympathetic during activity during exercise will increase the heart rate and stroke volume increases the SBP. Though sympathetic activity has vaso-constriction effect on blood vessels, where increase in TPR is expected, overwhelming activity by metabolic waste product eventually increase the diameter of the blood vessels causes decrease in DBP.
Therefore SBP is directly proportional to stroke volume and DBP is directly proportional to the TPR.
To answer the question asked by Sergey Kozhukhov in the last para, you need to understand the regulatory mechanism of BP. Whenever there is decrease in the heart rate (mostly happens if there is decrease in the sympathetic activity or increase in parasympathetic (vagal) activity), cause decrease in stroke volume (amount of blood pumped out per ventricle per beat(stroke) ~ 70 ml/beat), and cardiac output (amount of blood pumped out in one minute ~ 5L/min), therefore decreases in the SBP. Since there is no vaso-constrictor effect by sympathetic fibers, will cause dilatation/ relaxation of blood vessels. Hence decrease in the DBP. An overall decrease in the BP (SBP & DBP), cause a decrease in the activity of the baro-receptor (a pressure receptor that sense changes in the blood pressure). This will decrease inhibitory effect baro-receptors on the on the vasomotor center (which regulates sympathetic activity) in the brain. This will increase the sympathetic activity eventually will increase the SBP by increasing the hear rate & stroke volume and increase in the DBP by vaso-constrictor effect.
Hope you doubt is cleared. If not, mail me for more explanation
Best
Ramesh
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are there different ways that hba1c is analysed to support its association to cardiovascular complications in diabetic patients?
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Hbac1c is cons
Glycated hemoglobin (hba1c) is considered an advanced glycation end products (AGEs). These are pro-oxidative and pro-inflammatory and largely contribute to the alteration of the functionality of all proteins. It acts in our organism by interacting with the RAGEs receptors and also by the intersections with the intra and extracellular matrix notably with the collagen and the fibronectin causing rigidity of the arterial wall which would be origin of cardiovascular disease in diabetic patient
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Please suggest some relevant articles.
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Generally, cardiovascular refers to the the coronary system and includes accidents - cardiovascular accident - which is called a stroke. So ri sk factors of heart disease and stroke would be then classified as non-modifiable such as age, gender, ethnicity, family history of heart disease and modifiable such as diet, physical activity, tobacco use, sedentary behaviors, perceived and physical stress. Cardiometabolic is generally used to refer to diseases of the system such as insulin resistance, diabetes, hypercholesterolemia, etc. The risk factors for cardiometabolic disease are similar to those for cardiovascular diseases. Cardiovascular adversities are usually social events that contribute to stress and then to heart disease. Here is a link for APA that describes how childhood adversaries such as poverty, abuse, abnormal living conditions, exposure to environmental toxins, etc. can increase risk for cardiovascular diseases in adulthood. This is different from stress over the lifetime. Critical periods where hormonal changes take place in children can have a more profound effect on the risk of heart disease then continuous lifetime stress. For example, social isolation during childhood, may have a greater impact to the development of heart disease then social isolation as an adult.
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As it is seen most of the heart failure is from lack of energy source in the heart muscles, but it is hypothetizing that D-ribose is essential component for energy replenishing instead of glucose, dextrose and other sugar sources, it is practice going on practically for cardiovascular problems. Any proofs available
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Hi Abdul.. Very interesting and relevant question.D Ribose is is very essential molecule for formation of ATP which is very essential for function of myocyte. Majority of failing heart like ischaemic and nonischaemic cardiomyopathy patients have depleted cellular ATP level, so theoretically D Ribose supplementation should have beneficial effect on heart failure patient. However small studies have shown it's beneficial effect in diastolic heart failure or heart failure with preserved EF rather than systolic heart failure patient. It may be because diastole is energy dependent. Studies have shown fatigue of diastolic heart failure may improve after DRibose supplementation. I think some large well designed trial is needed with this molecule in heart failure patient to know it's benefit.. Thanks
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Hi,
I want to create a cardiovascular search engine and I need to download cardio related meta data, where can I get it?
Thanks
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I may not have understood your question very well, but I believe you will find information in the databases available from the American College of Cardiology and the Society of Thoracic Surgeons. Clinical and experimental cardiology journals also have special sections publishing meta-analyzes and systematic reviews that may be useful to you.
I hope I helped you
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I need to evauate if variability of an inipendent variable can partially explain a risk of cardiovascular events.
Since standard deviation and coefficient of variation both are considered to be too closer to mean value, I found that a parameter called VIM is poorly influenced by mean value.
Anyone can suggest me how to calculate it from a pool of data?
Thanks.
Guido
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I have some doubts about the possibility that intravitreal avastin injections are a safe alternative to Eylea in some cases of essudative maculopathy. I'like to know your opinion about its potential role in favouring cardiovascular problems. Thanks.
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Thanks a lot for your answer, Marianne
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I have 300+ participants to analyze in Kubios for heart rate variability. Currently, the only option I know of, is to save each data file one by one, which is very time consuming. Is there a way to run a batch in Kubios, or MATLAB scripts to speed the process up?
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Dear Shai Porat
Well because I don't know about your research. But I think on Matlab you maybe can create a model-builder or some scripts to speed the process up. Anyway, it is a challenge.  Additionally, maybe just my imagination but,
can you use Matlab instead of Kubios for your data process ? Or you can input your raw data together (maybe one excel file is possible) If possible, Matlab can do them all and save each data file automatically and  qucikly.
Hope my answer can help you.
Best wishes.
Kai Liu
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Would anyone know how I can test this question. Patients with Cardiovascular disease complete the DASS - depression scale and also the Cognitive Emotional Regulations Strategies scale which has 9 predictors (strategies). I want to know if Cognitive reappraisal  (CRA) moderates the relationship of depressive symptoms in men and women with Cardiovascular patients? Does anyone know how I would analysis this? Depression is the DV, gender dichtomous variable and CRA continuous IV.
Or should I be saying gender moderate the relationship between CRA and Deperssion?
thank you
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i would recommend PROCESS software for SPSS, it's free. you can test both your hypothesis there
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I am performing a propensity score analysis with weights on different medications.  I'm obtaining a very low misclassification rate based on the fact that these medicines were introduced at different times and, the data seem to say, were most often prescribed right after their introduction to the market.  By including when the patient first got their prescription I'm able to predict with a fairly high degree on certainty what drug she got.
The problem is that other variables pivotal to the clinical outcomes, such as measures of cardiovascular or overall health, are not as predictive and so remain unbalanced after propensity score weighting.
Since it seems to me that the outcomes (stroke and adverse bleeding) are not dependent upon when the drug was prescribed am I right in thinking that I can exclude the date of the first script as a predictor, settle for a much higher misclassification rate and conduct a more rigorous propensity score analysis with only those confounders included that I think will have an effect on the clinical outcomes?
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Thank you Mohamed! You shared a lot of good material.
I think I resolved my own question.  Propensity Score analysis relies on the assumption that all variables which had an effect on the treatment group and the outcome are part of the propensity determination. Any variable which simply had an effect on treatment selection, but not on the outcome, can be excluded from the analysis so that balance is achieved on those variables which did have an effect on the outcome measures.
Achieving misclassification rates of 30% or less is attractive, but if it is done by adding in variables with no effect on the outcome it can be detrimental to the analysis. Essentially, these variables are the same as random variation so far as propensity score analysis is concerned.
Fellow researchers, please feel free to comment if anything I said above is wrong.
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I am not sure if this is possible or not. I am aware that greater than 100 ms is generally considered to be "good" hrv. 
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First, higher HRV does not necessarily mean "good", and second 1000 ms is very unusual for SDNN, and most probably not correct or not in healthy state.
Here is the normative data:
In our study with healthy adult subjects performing slow deep breathing which results in considerable increase in HRV, the highest SDNN that we had was around 300 ms, this is the ceiling effect and I don't expect we could have higher values. This was happened in an athlete with mean HR of 56 (MeanNN of 1069 ms) and RMSSD of 242 during slow breathing. I checked the relevant literature and I couldn't find anything even close.
I wonder if Mohammad Karimi can provide us a reference indicating such case?
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If you are interested to be a part of the Quality and Patient Safety in Cardio Vascular practice specific to Nursing and Allied Health Profession, Kindly let me know. 
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Thanks for the offer. Unfortunately I will not be there
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How could I have information about blood flow restriction training and cardiovascular function adaptations?
katso training
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You are most welcome 
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There are a few papers that discuss what the Compensatory reserve index (CRI) is, and its relevance during simulated hemorrhage. These papers only elude that the CRI is calculated using a unique algorithm. How exactly then, is it calculated. i.e which parameters does one need to calculate (MAP, HR, SV, TRP, etc)? Also, can one calculate the CRI retrospectively?
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Hello Michael,
I have published multiple papers on the CRI, and I work for a leading researcher in this area.  The CRI is a proprietary algorithm that has recently been approved by the FDA for use in clinical settings.  It is sold by a company called Flashback Technologies.  The algorithm uses a proprietary signal processing method whereby hundreds of features of the PPG waveform are extracted from beat-to-beat data obtained from a standard pulse oximeter.  The latest version of the Flashback device connects via bluetooth to a small tablet with a readout of the waveform and the continuous CRI value plotted on the screen with a red/yellow/green gauge.  Unfortunately, at present there is no way to calculate the CRI without a Flashback device.  It is possible to retrospectively calculate CRI values on previously obtained data, but you would have to go through Flashback to request this for research purposes, the continuous PPG waveform is all you need to do this.  We have a lot of research ongoing on this topic, including experimental (LBNP) and clinical studies.  You can contact me if you would like to learn more, and I'd be happy to share our papers with you.
I hope this is helpful,
Jeff 
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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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Hello,
I would recommend a free antibody database available at labome.com. For antibodies to CKM for Western blotting you can check the following link: https://www.labome.com/review/gene/human/CKM-antibody.html. Santa Cruz Biotechnology provides goat polyclonal (N-13, sc-15161) ab suitable for WB on mouse or human samples. Also, Abcam has rabbit polyclonal ab83441 for WB (ref only for WB on human samples: Kitaoka et al., Mol Genet Metab. 2013). You can see the references and the description of the antibodies following the provided links.
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We are seeing some sex-specific differences in cardiovascular variables with aging. These differences might be explained by changes in the concentration of sex steroids with aging.