Cardiology

The cardiac output increase during the pregnancy,and modifies the blood flow and could be appear innocent  murmur, that disappear after the childbirth

depending on the echocardiography machine being used. The latest technology is actually emphasizing on the use of tissue Doppler which older machines may not have. The other conventional markers such as E/A ratio, deceleration time, isovolumic relaxation time combined with pulmonary venous and hepatic systolic : diastolic flow must be combined to determine the diastolic parameters using echocardiography.

• http://imperialandglobal.exeter.ac.uk/2014/02/a-beginners-guide-to-writing-a-post-doc-research-proposal/

Also added to the project, https://www.researchgate.net/project/Examining-Porges-Polyvagal-suppositions

Still no evidence for the polyvagal speculations and only very substantial evidence against
 
In this time of "fake news," "alternative facts," "post-truth modernism," "creating one's own reality" (Karl Rove from Suskind, NY Times 2004) and surviving 2017 in Trumplandia, it seems more important than ever to question controversial ideas in "Science" that parade as fact and can have significant impact upon people's lives and pocket books, as well as upon future research directions. Although I have opened up discussion about polyvagal notions a year and a half ago, although probably more than 5000 researchers have viewed the above-mentioned project and/or this question, there has not been a single strand of evidence offered in support of things polyvagal and my colleagues in evolutionary biology and cardiovascular autonomic physiology completely discount the polyvagal suppositions. Evolution of the autonomic nervous system does not seems to work the way the polyvagal assertions claim, nor does the brainstem dorsal motor nucleus appear to play any significant role in regulation of parasympathetic influences upon heart rate. Each of these points is very well substantiated, and each provides--by itself--a source of refutation of the polyvagal speculations. On the other hand, I have personally been at lectures of Steven Porges (the author of things polyvagal) in which he claims the opposite, as though his contentions were fact.
 
Ten years ago, a very prominent expert on the evolution of the autonomic nervous system (Edwin [Ted] Taylor) and I published a multi-tiered refutation of the polyvagal ideas (attached). Cited almost 600 times (Google Scholar), with not one serious critique of our arguments, its publication has done nothing to stem the tide of enthusiasm for polyvagal suppositions. Two years ago, Ted Taylor asked what can we further do to bring some science into this area: my ResearchGate attempts at dialogue result from his and another well known autonomic evolutionary biologist 's (Tobias Wang) frustration with this business. They wanted to write another paper. However, I thought this ResearchGate avenue might actually reach more researchers--young and old—as well as provide a platform for serious discussion, pro and contra, unhampered by biases of conventional journal publications. I figured that if I could support my ideas with accessible literature documentation (see link above), we could have a lively debate about things.

6000 reads later, only several additionally critical comments about the polyvagal (and most of them in private mails to me), but no dialogue: So what is going on in our "science" and "research"? Has our discipline succumbed to the same sociopolitical and economic forces as the rest of our Western institutions? Are proponents of polyvagal ideas merely keeping quiet in the hope that critical discussion may simply fade away? Are they wary of an open discussion? Are they or the opposite school afraid that funding possibilities may be diminished, should they enter the dialogue? Do researchers feel so profoundly insecure in their knowledge of the issues involved that they fear for entering a discussion? Or has this area of polyvagalness become a place where believers can merely exercise their beliefs and provide a plausible (if untrue) metaphor for relations between mind and body? Or maybe there are other reasons for this state of affairs (please tell)?

Anyhow, I continue to find this a fascinating and curious situation, and I will persist to try to stimulate discussion. We will see what happens.

Additional information maybe helpful.

Please see ANMCO/ELAS/SIBioC Consensus Document published in May 2017.

Point 1. There are still some doubts on efficiency, prognostic role, and cost-effectiveness of biomarkers of cardiac remodelling and myocardial fibrosis, even if many studies have been published recently.

Point 2. Considering the wide range of biomarkers of cardiac remodelling and myocardial fibrosis, the clinician should direct his decision remembering the analytical characteristics of the assay, the efficiency and prognostic effectiveness of the biomarker also in relation to patients’ setting, possible confounding variables, co-morbidities and costs.

Point 3. Novel biomarkers and multi-markers models

The search is still open for novel biomarkers useful for prognosis and guide therapy in HF patients. Promising candidate biomarker may be: growth differential factor-15 (GDF-15), carbohydrate antigen-125 (CA-125), C-terminal pro-vasopressin (copectin), mid-regional pro-adrenomedullin (MR-proADM), NEP and orexin. Some of these molecules have been utilized for many years as tumour-markers (CA-125), neuro-hormones (copeptin, MR-proADM) or inflammatory markers (GDF-15) in clinical practice.

Here is a link to the Delta CHES,

http://msdh.ms.gov/msdhsite/_static/44,0,353.html

assessing CVD risk in the Mississippi Delta region

https://login.webofknowledge.com/error/Error?Src=IP&Alias=WOK5&Error=IPError&Params=&PathInfo=%2F&RouterURL=https%3A%2F%2Fwww.webofknowledge.com%2F&Domain=.webofknowledge.com

PV pressure as it has been said above reflects changes in LA pressure (if do you want I have added a book chapter related with this topic, you can see LA pressure changes during cardiac cycle in table 1 and figure 1)  and its interaction with pulmonary venous capacitance-resistance and also importantly changes in Intrathoracic pressures.

Thank you very much for your answer.

Regards,

Anup

Cardiology Department,  Medika Cardiocenter, Saint Petersburg, Russian Federation

Fractional Flow Reserve-FFR ; Fraction of hymodynamic in Stenosed Vessel: Normal Vessel. FFR of 70% reflects a 30% drop in Hemodynamics.

Computed tomography-derived FFR[CT-FFR]

Employs ; Modeling of coronary arteries &  blood flow

Prior Technology had Poor Correlation With Invasive Coronary Angiography[ICA] but Using 3D FFRCT +Heart Flow FFR-CT SoftWare, Results are PRETTY KOOL.

The results showed that Heart Flow FFR-CT was able to correctly identify 84 % of the significant blockages identified by FFR as requiring intervention, and 86 % of blockages identified by FFR as not requiring intervention.

Each method has its Pros & Cons, but with latest advances in Hemodynamic Software, CT-FFR will replace ICA.

https://www.dicardiology.com/product/fda-clears-ffr-ct

Dear Tobias,

We use LUCAS on a regular basis- in and out Hospital - but do not see that often.

In those cases with bleeding complications - Lysis after fulminat PE , renal insufficiency, OAK or therapeutic dosage of heparin  etc. were involved...

I also think that bleeding complications are dependent on your patients characteristics.

Greez

GREAT Case

EKG INTERPRETATION

LBBB +LAEnlargement

PRWProgressionn NOTED, possibility of Ischemia as cause of LBBB

DELTA WAVES[More Marked in aVL] + Short PR intervals noted.==>WPW[Type B]

I have a troponin I  on my wall right now from april 2009 that reach 1593.5

Dear Dr. Paul Peter Lunkenheimer. It was interesting to learn about the original hypotheses of your compatriot as well as the morphofunctional model that is remarkably presented in your article "Models of Ventricular Structure and Function Reviewed for Clinical Cardiologists". Thanks

2:1 HB

My answer is yes. Nebivolol is a modern cardio selective beta 3 blocker. When the heart fails with preservation of systolic function, drugs in this class reduce tachycardia which adversely impacts diastolic function and by reducing tachycardia improve myocardial perfusion. It also causes myocardial hypertrophic regression which improves diastolic compliance and function. By its mechanism of function it is not adverse to systolic function while at the same time improves diastolic function

Thank you Dr. Majumder,

I'm inclined to agree. Consideration should be given to alternative cardiac evaluation options, unless otherwise contraindicated.  

Quite a few factors to consider--including AAA sizes > 6 cm and blood pressure.  I've seen blood pressure responses to Dobutamine range between 60 mmHg and as high as 200 mmHg. For some patients, beta blockers are held prior to Dobutamine stress echo. It is not always easy to predict BP responses.  

yes in patients with severe pain, because you can exclude triple etiology: coronary, aortic or pulmonary embolic chest pain

CMAJ. 2011 Nov 8; 183(16): 1821–1823.
doi:  10.1503/cmaj.111674

This commentary is helpful. This comments on the above article mentioned by Dr. Pesl as well.

That’s the idea behind the Eko Core, a tool that brings the modern stethoscope into the age of the smartphone and cloud computing.

The Core, developed by Berkeley, California-based startup Eko Devices, pairs with a smartphone or tablet over Bluetooth, and records heart sounds. The audio can instantly be shared with a cardiologist anywhere for an expert opinion, or compared to heart sounds in a cloud-based database, to help discern the likelihood of a heart murmur or other serious issue. 

A few stethoscopes already on the market have the ability to record. 3M’s Littmann 3200, for instance, can record and store up to 12 heart readings. But it pairs with a proprietary USB dongle, so is meant to be used with a desktop or laptop computer, not mobile devices, and Apple products are not supported.

Read more: http://www.smithsonianmag.com/innovation/smart-stethoscope-attachment-could-lead-more-accurate-diagnoses-180953912/#5ITc31IkwdupWDAZ.99

Obesity, tachycardia, and extreme stress have all been shown to result in impaired left ventricular function and dilatation. Several of these reversible CMs, including:

• Tachycardia-induced (ECG and ECHO: arrhythmias include atrial fibrillation, atrial flutter, atrial tachycardia, reentrant supraventricular tachycardia, accessory pathway tachycardia, frequent ectopic beats, and ventricular tachycardia. Persistent tachycardia causes elevated ventricular filling pressures, severe biventricular systolic dysfunction, reduced cardiac output, and elevated systemic vascular resistance)
• Takotsubo (contractile function of the mid and apical segments of the LV are depressed and there is hyperkinesis of the basal walls, producing a balloon-like appearance of the distal ventricle with systole)
• Sepsis-induced cardiomyopathy (Increased LVEDP is indicative of diastolic dysfunction in sepsis patients),
• Thyroid Disease–Induced Cardiomyopathy (systemic changes in cardiac function due to reduced peripheral vascular resistance, activation of the renin–angiotensin mechanism, increased LV end-diastolic volume (LVEDV) and increased preload; the increased preload and decreased peripheral vascular resistance leads to a high cardiac output, even at rest, resulting in CM. In contrast to hyperthyroidism, hypothyroidism causes a low cardiac output CM via the same pathways mentioned above, however, by downregulating the previously mentioned receptors/channels causing decreased myocardial excitation and contractility leading to a low-output CM)
• Peripartum CM (by clinical criteria: ( development of heart failure symptoms either during the last month of pregnancy or within the first 5 months after delivery;  no other identifiable causes of HF exist; no evidence of heart disease prior to the last month of pregnancy)
• Inflammatory CM (there are both non-infectious and infectious causes . Non- infectious origins include toxins, alcohol, cytotoxic chemotherapy, and metabolic abnormalities)

Echo is useful for diagnosing structural heart disease. Echodoppler also gives indirect and direct haemodynamic parameter of critically unwell newborn which has got therapeutic relevance. Ecg is useful for diagnosing arrhythmia. However Ecg finding may be adjuncting with echo finding to diagnose certain disease like Pompe's disease. Ecg maybe also helpful for followup of children with family history of certain genetic disease like Damon disease, HCM where Ecg is abnormal but echo may be normal. 

Atrial Tachycardia

www.echobasics.de

https://www.escardio.org/Education/Practice-Tools/EACVI-toolboxes/3D-Echo/Clinical-cases

i share the same opinion than Joseph an Biswajit, about Danon Disease. which is x-linked. the WPW shape is not realy a WPW because the PR interval is not abbreviated.

best

I wonder how much more reliable is stressed nucleotide study and how has global longitudinal stress speckles study improved long term predictive power. The latter, I believe, is a matter of software.

I am not familiar with urethane as an anesthetic agent. I would recomment ketamine intramuscular with Vetranquil and Fluothane as inhalent.

Hi, Rezhna      Endothelial dysfunction in umbilical artery may be an important  predictor of future atherosclerosis. Expression  of NO synthases(eNOS,iNOS,nNOS).pro oxidative enzymes and antioxidative enzymes like supernatural dismutase1-3,glutathione peroxidase1in umbilical arteries may be helpful in detecting Endothelial dysfunction. It has clinical implication. Small and large for gestesional age babies have Endothelial dysfunction in umbilical artery compared to appropriate for gestesional age babies and they are having higher risk of future  development of atherosclerosis. 

Dear Dr. Tatiyana,

 Really, it is beyond any word that can express my sincere gratitude and deep appreciation to you.

Actually, the first and foremost thanks are owed to you, for opening such a valuable wonderful discussion about such an interesting case, engaging colleagues from different scientific backgrounds and it will always be greatly appreciated to you Dr. Tatiyana for keeping us updated in regard to any result.

Indeed, it gives me great pleasure to express my heartfelt thanks and utmost respect to you Dr. Tatiyana.

Respectfully yours.

If you agree that "optimal BP" need for optimal blood flow

Good Morning, my name is Mayela Labarca, I'm an internal Medicine specialist and a non invasive clinical research cardiologist with a  3 years research Master in  Cardiovascular Diseases and 1 additional year training in electrophysiology, I'm looking forward to join the research group

Here is a link showing an advantage of using strain during post-TAVI evaluation of the patient. Basically, LV GLS shall improve >1.5% to be sure that the patient has a good prognosis.

bit.ly/2j5wpmM

I guess it depends indeed more on symptoms, on functional capacity of a patient and maybe on NT-proBNP levels than specific echocardiographic findings. But Sir you are right, at the moment it is still a very subjective decision. 

 Good morning, I'm Mayela Labarca, an internist with 3 years training as a  Máster in research in Cardiovascular Diseases, currently working as a clinical research cardiologist in Maracaibo,, Venezuela, I'm interested in joining the  Cardiovascular Meta-analyses Research Group, could that be possible? 

Thank you so much Deon!!!

I must say, I agree with Dr Wong. Close monitoring is indicated, but, even if the incidence of an asymptomatic pneumoperitoneum were 10%, I would find routine post-procedure CT difficult to justify, considering management is based on the clinical findings. The scenario in oesophageal stenting is much different, where spontaneous resolution is not the norm and one has to look for pneumomediastinum proactively. 

Many publications? - I think we can find 3 or 4.

It is perfectly normal to calculate the delta, as in figures 1C and 1F (representing responses in pulmonary arterial pressure) in the paper below.

Expressing the data in this way can give a better idea of the responses from pre  to post exercise situation. Maybe it is already your intention: why not taking different time points during/after the exercise? You could get pressure values every minute for example, to study its evolution during exercise, and the recovery pattern afterwards. It would give you a kinetic graph with delta values over time.

If the subject is a fully trained stamina athlete such as a long distance runner, he/she may have cardiac hypertrophy that I regard as a pathological condition, but my colleagues above may consider physiological!

Thanks everyone! All of these are much better than anything I could find on my own. RG community is the best! 

Yes, I suppose that is so

I agree with the fact that it is possible to surgically intervene if medical treatment is not controlling the situation. To me the must important point is that patients should be properly diagnosed and thoroughly evaluated prior to the initial surgery and surgeons should have the knowledge, criterion, training and expertise, to perform the correct and complete surgical procedure during the initial operation.

Awesome job Mohammad. Keep it up.

The flap can extend into the its first branch leading to obstruction and non  conduction of  a beat

Dear dr. Kamhman, thank you very much for your mention. Really in papers Holst (Can J Cardiol 2012) , Olesen M (Heart Rhythm 2012) were described this mutation in adult pta with BrS, AF. But in observation of the Hu D. (Heart Rhythm 2012) was  revealed one child 4 month who died from SIDS with the same mutation. I think clinical polymorphism of this mutation not clear complectly at the present time.

During exercise test  (tredmil test) PR interval shortening in one brother and was normal in other.

Thank you another time.  

Does he have Dysphagia? In any case I would start with UGI gastrografin or Barium. This would help to map out esophagus before EGD.  if this is recurrent achalasia, he may have megaesophagus or even epiphrenic diverticulae at risk of perforation.

I would even entertain the possibility of Zenker's with that presentation. UGI study  should be able to show it too.

Heart Failure Risk Calculator
Meta-Analysis Global Group in Chronic Heart Failure
The Heart Failure Risk Calculator presents 1 and 3 year all-cause mortality estimates for people with heart failure, as developed and presented in Pocock et al. "Predicting survival in heart failure: a risk score based on 39372 patients from 30 studies" Eur Heart J 2012 doi:10.1093/eurheartj/ehs337.

The intended audience for the Risk Calculator is health care professionals knowledgeable in cardiology and the management of people with heart failure.

The model was constructed from research data collected from 1980-2006 and may not be indicative of current or future trends in heart failure management. The variability in risk between studies and cohorts is greater than that explained by known risk factors. True risk within any centre may be higher or lower than the stated estimates for 1 and 3 year mortality.

This site and its contents are made available as a research courtesy, with no direct or indirect liability accepted by the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC), or the study sponsors: The University of Auckland, the New Zealand Heart Foundation, the University of Glasgow.

Hi all,

Apologies for the delayed reply. Thanks for all the help. I now have a much better understanding of what I want to do in Kubios. 

In particular, I was not certain about whether to use automatic or some sort of manual editing so clarification on this has been important but so has the elaboration and further detail. 

In my case I do have ECG data and so then, from my understanding, I will want to focus on manual artifact removal. To do this I would simply remove the R wave detection markers only (rather than using the other two option when right clicking on markers such as add and edit I think) and by doing this the RR interval data will change accordingly so that the artifacts will no longer be present. I should end up with better data which neither includes artifacts nor removes real data points as possible with automatic approach. 

This makes better sense now. Thanks again for all the help all.

Hi

This is an interesting piece of work using an animal model which may help to answer your question. Best wishes

Dear Colleagues. Thank you everybody. I agree with you and I think, too, that in the remaining part of the recipient`s atria there is atrial fibrillation/flutter while the donor atrium escaping ectopic inferior-atrial (perhaps nodal) rhythm.

Dear Tony! Dear Vinícius Eduardo! You are absolutely correct that the donor heart is compromised as evidenced by the chronotropic incompetence of the sinus node and the expressed disturbances of repolarization (ST-T).

Best regards

3 Ways to Test the Accuracy of Your Predictive Models
 
by Victoria Garment 
  
 In data mining, data scientists use algorithms to identify previously unrecognized patterns and trends hidden within vast amounts of structured and unstructured information. These patterns are used to create predictive models that try to forecast future behavior.

These models have many practical business applications—they help banks decide which customers to approve for loans, and marketers use them to determine which leads to target with campaigns.

But extracting real meaning from data can be challenging. Bad data, flawed processes and the misinterpretation of results can yield false positives and negatives, which can lead to inaccurate conclusions and ill-advised business decisions.

There are many different tests to determine if the predictive models you create are accurate, meaningful representations that will prove valuable to your organization—but which are best? To find out, we spoke to three top data mining experts. Here, we reveal the tests they use to measure their own results, and what makes each test so effective.

Compare Predictive Model Performance Against Random Results With Lift Charts and Decile Tables
Karl Rexer is the founder of Rexer Analytics, a small consulting firm that provides predictive modeling and other analytic solutions to clients such as Deutsche Bank, CVS, Redbox and ADT Security Services. The measures his firm uses to create predictive models are often binary: people either convert on a website or don’t, bank customers close their accounts or leave them open, etc.

Rexer’s firm creates models that help clients determine how likely people are to complete a binary behavior. These models are created with algorithms that typically use historical data pulled from the client’s data warehouse to characterize behaviors and identify patterns.

To test the strength of these models, Rexer’s firm frequently uses lift charts and decile tables, which measure the performance of the model against random guessing, or what the results would be if you didn’t use any model. It’s a methodology commonly used to increase customer response rates by identifying the most promising targets.

Let’s look at an example. One of Rexer’s clients wanted to create a more focused, cost-effective marketing campaign for the coming year, so he and his team built a predictive model for the client using data from the previous year’s campaign.

In the previous year, the client had sent marketing material to 200,000 total leads, 1,579 of which became customers—a conversion rate of 0.8 percent. For the coming year, the client wanted to know in advance which of their new leads would be more likely to buy their product so they could focus their marketing efforts on this segment. Essentially, they wanted a smaller, cheaper campaign with a higher conversion rate.

Rexer and his team first took the client’s lead data and randomly split it into two groups. Approximately 60 percent was used to build the model, while the other 40 percent was set aside to test it (known as the “hold-out” sample).

Splitting the data “helps ensure that you’re not creating a ‘super’ model that only works on that one set of data and nothing else,” Rexer explains. “You’re essentially building something that works on two different sets of data.”

Rexer and his team used a variety of data mining algorithms to comb through hundreds of data fields to find the best set of predictors that worked in the modeling sample. These predictors were used to identify a highly responsive subset of leads.

This algorithm was then used to score each lead in the hold-out sample on a scale of 1 to 100 based upon the characteristics identified by the algorithm, such as how long the person had been a customer and various socio-demographic information. The closer to 100, the more likely the lead was to convert.

The list of leads in the hold-out sample was then rank ordered by score and split into 10 sections, called deciles. The top 10 percent of scores was decile one, the next 10 percent was decile two, and so forth.

For more plz read at following link.

Regards

As the patient is hemodynamic stable, I agree with the use of low molecular heparin as the best option for this baby. Removing the thrombus could cost a lot, as it is a premature, usually low weight and a premature heart that do not deal well with anemia and volume overload that would happen in procedures for trombectomy. A conservative approach with heparin is more reasonable to me, best regards

At the end of Valsalva manoeuvre, due to increased vagal tone, there is transient higher AV block which may terminate SVTs. But considering the patient with WPW, in case of higher AV block, there will be higher chances of conduction through accessory pathways. Thus, chances of VT, VF increases. Due to the similar mechanism, beta blockers and calcium channel clockers are not advised for wpw patients.  

unfortunately there is no good solution for your problem aside from surgical redo. catheter interventions will likely generate a severe regurgitation in a too small valve.

Dear Daniele,

I can recommend a transfection reagent called Lullaby Stem for your application

You can find more information here:

http://www.ozbiosciences.com/transfection-sirna/25-lullaby-stem-transfection-reagent-stem-cells-silencing.html

If you need a sample, just let me know at tech@ozbiosciences.com

Good Luck

Olivier

Dear colleagues, thank you all for your interest and attention.

Best regards.

Many Thanks, Lets keep looking for..

 Thanks for Dumitru Casian,and i have send a email about this query to seek advice to the Pro caprini and i hope to receive some feedback.

Changes in LV dynamics and mitral regurgitation during , and post, acute heart failure are complex. They can be dependent on aetiology (ischaemic, MI, cardiomyopathy, infiltrative diseases etc.), and if there is any chronic component prior to the acute event. Generally speaking the LVESV and LVEDP will increase and the degree of mitral regurgitation will also be increased (especially if LVEDV and mitral annular size are increased) The consequent increase in LA pressure leads to increasing pulmonary venous pressures which is the driving force for pulmonary oedema.

Takotsubo or any type of cardiomyopathy is not what the question is even referring to. Cardiospasm is synonymous with achalasia which results from a painful esophagus that is dilated and typically leads to reflux and other nasty problems. The use of the prefix 'cardio' in cardiospasm refers to the cardiac sphincter of the stomach.

Despite not addressing Richard Savage's question, you do bring up a highly interesting condition mainly because of the etiology of the condition's name. As you know the condition has been around for a very long time, however, takotsubo is Japanese which was the first country to document the condition and is a extremely collectivistic culture. While it does not seem to have a drastically higher prevalence in Japan than western countries it does seem right that the west would push strongly against a psychosomatic-esque condition until they had to accept it.

This being said, I will not tell the story of a female very dear to me who was having severe panic attacks. These attacks were unquestionably psychological in nature and I am well aware of what would cause them. Sure enough, when the attacks would flare I would see the panic in her eyes and within seconds she would exhibit Levine's sign though she never had any actual cardiovascular issues. These attacks lasted for about 4 months with 1-3 occurring each day. And similar to what the individual  told Mr. Savage, I told her they would resolve within a 1/2 hour to hour,.. fortunately I was right.

To sum up my main point, Yes! I have seen the phenomenon of which you speak of. In canines a condition resembling achalasia results from damage to the vagus nerve. I don't know if you care about that but though I would share.

Wishing you all the best,

Logan Netzer

P.S. Just a few canine studies that I briefly mentioned.

J Neurol Neurosurg Psychiatry. 1982 Jul;45(7):609-19. Abnormalities in the vagus nerve in canine acrylamide neuropathy.Satchell PM, McLeod JG, Harper B, Goodman AH.

J Neurol Neurosurg Psychiatry. 1981 Oct;44(10):906-13. Megaoesophagus due to acrylamide neuropathy. Satchell PM, McLeod JG.

Yes we do but we prefer to use the impedance technique for PWV measurement. It is easy to use, fully automatic and operator-independent.

http://www.ncbi.nlm.nih.gov/pubmed/12558611

https://tampub.uta.fi/bitstream/handle/10024/99556/978-952-03-0124-8.pdf?sequence=1

The question why something is like it is, is a teleological question. Since organs like organisms  have an evolutionary and developmental origin, one has to look into both to get an idea why. The sinuatrial and atrioventricular nodes are the remnants of the linear heart tube, which is the first functional state of this organ. Looping and ballooning positions this myocardium to its locations found in the mature organ. The heart has the ability to generate nodes on both sites of the venous inflow tract, however development of a second sinuatrial node is blocked on the left side by Pitx2. I would consider the atrioventricular node to be central between the atria and ventricles. It is also partly positioned to the right in the atrial floor due to the looping process and remodeling. There are certainly also biophysical and mechanical aspects to the positioning of the conduction tissue. The structure of the mammalian and also the human heart can be followed back to the primitive hearts found in lower chordate hearts, like the heart of Ciona,  however we lack good insight into the evolutionary origins since hearts so not survive fossil formation. In the Heart of tunicates both inflow and outflow trägt are equvalent and Act als pacemaker

The two papers above are good.  Harper's paper is a classic.  Having studied dozens of valves, microscopically, I never saw blood vessels within the substance of the leaflet of NORMAL valves.  It appears that inflammed valves develop neovascularity just as in other "granulation" tissues.

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

I would highly recommend to read my 2 co-authored articles mentioned below. If u need the full manuscript, feel free to write to me.

Phan K, Wang N, Pison L, Kumar N, Hitos K, Thomas SP: Rivaroxaban versus warfarin or dabigatran in patients undergoing catheter ablation for atrial fibrillation: a meta-analysis. International journal of cardiology Int J Cardiol. 2015 Apr 15;185:209-13.DOI: 10.1016/j.ijcard.2015.03.102

Phan K, Wang N, Pison L, Kumar N, Hitos K, Thomas SP: Meta-analysis of dabigatran vs warfarin in patients undergoing catheter ablation for atrial fibrillation. International journal of cardiology 04/2015; DOI:10.1016/j.ijcard.2015.04.072

That's so so called cuff method - it workes, there are several paper out describing this method, e.g. the following:

Interposition Vein Cuff and Intimal Hyperplasia: An Experimental Study
2004     L. Fleurisse

If i m not wrong IgE is mainly meant for allergic reactions triggered by ur immune system. but yes link of it to CVD can be considered

Reversal from Cardiac Arrest:

If its peri-arrest - Spontaneous return of circulation depends on upon various factors (physical conditions)

If it is confirmed arrest:- 

Shockable Rhythm :- High chance of spontaneous return within in 1 minute

Non-Shockable Rhythm - Very poor chance for spontaneous return

Witnessed arrest have higher rate of spontaneous return compare to  un-witnessed arrest.

This is  highly evident in highly specialized care environment  such as Cardiac theatre, Cardiac ICU, Interventional and non interventional CV procedure room, A&E

Regards

Immanuel Victor George

Thanks for the input. this was very useful :)

Thank you.

Guinea pigs

One surgeon used to use 6 mg intraaortic prior to release of cross clamp.  

I did not check my data in the statistical models, because as it is only a description, without physiological foundations. I like the suggestion of Dr  Sven Rupprecht: those who active lives in 80 a priori more healthy, than those who died in 60. Especially in our sample. The vast majority of our cohort are people who have reached retirement age (in Russia 55 years for women and 60 years for men) and continue to work as a teacher at the school. I have some reasons to believe that those who stopped working at thease ages, have several other parameters of HRV.

Nevertheless, it is awesome that our data do not contradict each other. There is a wide field for discussion and planning of new studies.

thank you for your reply Tanja 

yes it is the one that i intend to use but i would like to know is there is another one 

thank you 

In Chronic Kidney Disease, Effusions are not exceptional, some drugs, as Minoxidil, were connected to Pericardial effusions, for malignant effusions, local 5-FU or Thiotepa were used, also Radioactive Coloidal Gold as Brachytherapy. FU is connected to worsening Ischemic Heart Disease. The condition whose exact nature is not fully known is hard to treat and to issue a prognosis. Best for you and your patient. Regards, + Salut 

Sudden  cardiac  Death (  SCD ) is  a  well accepted  entity  that can  occur  in  structurally  normal  heart.  Classical  eg. Brugada  syndrome, Congenital  Long Q-T Syndromes where  the  patient  die  of  Ventricular  Fibrillation  not  responding  to DC  shock. Postmortum Heart :  structurally  normal  but  having  genetic  based  functional  abnormality  not  found  in autopsy.

The clinical  picture  of  Rheumatic  Fever  is  divided  into 

1)  Classical  Major  and  Minor  Criteria

2) Atypical  Manifestation  of  Rheumatic  Fever

Major  Criteria  are i) Migrating non deforming  Major  joints  arthritis ii) Pan Carditis  iii) Sydenham's  Chorea iv) Erythema  Marginatum v) Sub  cutaneous nodules.

Minor  Criteria :  Fever > 38.5 degree C,  olyarthalgia, raised  ESR > 60  mm first  hour, Prolonged  PR  interval > 200 msec, Previous  history  of  Rheumatic  fever, Evidence  of  previous  streptococcal  throat  infection, a  positive  throat  culture for  group A  beta  haemolytic  strptocooci,  A positive rapid group A streptococcal carbohydrate antigen test ,  Raised  ASO  titre > 12, increased  CRP > 3.0 mg/dl.

Atpical  manifestation  incldes  abdominal  pain,  epistaxis,  Jaccoud's athritis.

Reference :  Dr.  Mrs. Padmavathy in  Text  book  of  Paediatrics, New Delhi,  India

American  Journal  of  Cardiology,  May 08, 2015 | David S. Bach, MD, FACC,  

Adenosine and calcium-channel antagonists have both demonstrated efficacy. See attached.

I think it's a sad manifestation of the general trend in all areas, unfortunately :-(

Thank you for information,I'll see .

We did not notice in our practice an improvement in outcome of children with myocarditis receiving corticosteroid. 

Would it perhaps be safer to manage inflammation with ascorbic acid and electrolyzed reduced water than with a statin?

The ductus arteriosus can close prenatally in some cases.  

I'm not sure if it's been studied to ascertain the quickest time from the start of closure until it is no longer physiologically patent, but prenatal closure can lead to RV hypertrophy.  When prostaglandins are used to maintain a PDA in suspected ductal-dependant pulmonary flow, physiological closure can be auscultated sometimes hours after PGE1 is stopped, but I'm guessing that's also dependent on the age of the neonate and the  PaO2 at initiation.

@ Alexander Valdés Martín & Miikue-Yobe Togenu

Thank you very much for your kind interest. 

Due to medical registration aspects we have to limit the geographical area of application of vasometrix to EU.

Best wishes

Lutz 

Whatever the genetic basis in different racial groups, we follow the International Society oh Hypertension guideline Jornal of Clinical Hypertension Vol. 16; No.1; January,2014 )  to give ACEI?ARBs as first line regimen in non-black people and calcium channel bolckers & diuretics in black poeople ahich are derieved from different prospective trials.

I figured out a way to get rid o the unsolveable Proteins: I used the Qiagen Shredder Columns directly after centrifugation, soi had a clear suparnatant after the chloroform addition

Jose, thanks for your feedback! I understand now that the size of a heart (possibly not size of an animal or age) is critical for the perfusion time. Do you weigh a heart before cannulation? I would use some free available "weight-time" tables (but for rats) to choose appropriate time. Also, I do tried trypsin in a few cases but without significant changes in the outcome of the cells. Again, I can see that my total time in collagenase is too short, so I think this is the main step I will check in future.