Clinical Cardiology - Science topic

Dear Lutz Kraushaar

Not sure whether you should call this a scam, but I do know that both the journal and the publisher behind it (Geneft) are not that well-known. I see red flags:

-Google contact info (85 Great Portland Street, First Floor, London, England, W1W7LT) and you end up with a virtual office (why hide the true origin you might wonder)

-The “In-Press” papers are dated in year 2022

-No transparency about APC. What can be found is that they charge a ridiculously high fee for some kind of membership https://geneft.com/membership

-The figure used on their homepage is… well not original (just look them up in Google Lens). The same is true for the cover image of https://geneft.com/neurology-and-neurosurgery-open which they took from https://www.utm.utoronto.ca/main-news/rethinking-psychedelics-how-microdosing-might-help-ease-anxiety-and-sharpen-focus without the mentioning of the proper source

-I see that some of the members of the editorial board have the same role in known predatory publishers (“Baishideng Publishing Group, Science Repository”, “Hilaris”, “Biomed Grid LLC”, “Open Access Journals” which can be checked here https://beallslist.net ). Not sure if all of them are aware of this by the way

Personally, I would avoid this one.

Best regards.

Hello Deborah Darlene Williams

Thank you for setting up this question. It is funny that I did not discover it until five years after you first asked it here! My attitude has oscillated over this time and now I am more agreed with your conclusion. I thank Biswajit Majumder for pointing to an evidence-based response. I wonder if Asif Machhada alsoAsif Machhada has supportive literature as this is somewhat different to my anecodtal experience.

Interesting also that Lexiscan/regadenoson is not available in some parts of the world, still. I presume it applies equally to other vasodilator testing such as with adenosine and dipyridamole.

The following RG link is also very useful:

Thank you for your answers!

I don't have experience with a case like this, but it seems plausible that they could be related with this manifestation. I suggest the following literature:

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- https://www.thelancet.com/action/showPdf?pii=S2352-3964%2820%2930558-2

Best regards

Since Echocardiography do not contributes in decisions making nor does it assess the outcome of the CRT. It is our practice only we look at the routine base line echocardiographic parameters only.

The manual blood pressure is of course the best, but if you do not know how to take a manual blood preassure/or the patient will measure the blood preassure at home it is better with automatic. However the automatic is not that reliable if the patient has atrial fibrillation.

Are asking strictly on the Physio device or others (such as the Zoll model)?

Good question. And that is the beginning of something, I hope you will explore it and offer us some explanation. There is no such possibility for now, which does not mean it will not. Congratulations on an interesting question.

Please share me the best answer might you get...

Regards…

Aortic stenosis followed by mitral regurgitation. However, we observe sometimes in patients with chronic IE a combined aortic vitium (Stenosis & regurgitation)

Undoubtedly systemic hypertension is a major risk factor for both Thoracic and abdominal aortic aneurysms. In the absence of hypertension or cystic median necrosis related to Marfan or other connective tissue disorders, Aortic aneurysms and dissection especially of the Thoracic aorta are uncommon. However, smoking is an equally important etiological factor for abdominal aortic aneurysms. In some studies, smoking is found to have stronger correlation with Abdominal aortic aneurysm than hypertension.

Cardiac tamponade results from an accumulation of pericardial fluid under pressure, leading to impaired cardiac filling and haemodynamic compromise. Prompt diagnosis is the key to reducing the mortality risk for patients with cardiac tamponade. Although cardiac tamponade is a clinical diagnosis, echocardiography provides useful information and is the cornerstone during evaluation (availability, bedside, and treatment). However, cardiac tamponade is associated with a variety of abnormalities that lead to changes on the electrocardiogram (ECG), chest X-ray, and on echocardiography. Abnormalities of tamponade on the ECG are typically low voltage and electrical alternans. However, reduced voltage can also be seen among other conditions such as infiltrative myocardial disease and emphysema, whereas electrical alternans characterised by beat to beat alterations in the QRS complex caused by swinging of the heart is specific, but not sensitive for tamponade. The chest X-ray reveals a normal cardiac silhouette until the effusions are at least moderate in size (~200 mL). In general, an enlarged cardiac silhouette is neither sensitive nor specific for the diagnosis of cardiac tamponade.

Echocardiographic techniques remain the standard non-invasive method to establish the diagnosis and can be used to visualise ventricular and atrial compression abnormalities as blood cycles through the heart.An effusion appears as a transparent separation between the parietal and visceral pericardium during the cardiac cycle. Physiologic pericardial fluid may only be visible during ventricular systole, whereas effusions exceeding 75-100 mL are visualised throughout the cardiac cycle

1. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, Brucato A, Gueret P, Klingel K, Lionis C, Maisch B, Mayosi B, Pavie A.; European Society of Cardiology (ESC). 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015 Nov 7;36(42):2921-64.

2. Ben-Horin S, Shinfeld A, Kachel E, Chetrit A, Livneh A. The composition of normal pericardial fluid and its implications for diagnosing pericardial effusions. Am J Med. 2005 Jun;118(6):636-40.

Administration of sodium bicarbonate increase the concentration of Na+ in the extracellular fluid compartment. High extracellular Na+ concentration leads to its increased cellular uptake via the sodium-proton exchanger. The subsequent movement of Na+ out of the cell creates an electric gradient, forcing K+ into the cell via Na+-K+-ATPase, resulting in net increase in intracellular K+ .

After MI, Fb are activated throughout the LV, presumably through TGF-β1 in response to increased wall stress and/or inflammation. Additional regional specific signaling leads to interstitial fibrosis via collagen cross-linking in MIadjacent. Local LOX activity could be stimulated by higher mechanical load imposed by tethering to the infarct or signals could diffuse from the scar. Identifying specific signaling cues to maintain the mature state of MyoFb phenotype in the scar tissue may open new perspectives in targeting the MyoFb reversibility in interstitial fibrosis without damaging existing scar tissue.

I agree with that. One has to think of a superiorly directed venous flow probably exaggerated due to the hyperkinetic state of pregnancy

I think that this algorythm will be useful to evaluate LV diastolic function.

Thank you dear Paul 

FFR-CT is a novel technology that enables determination of the functional significance of lesions noninvasively, using sophisticated computer algorithms based on computational fluid dynamics applied to coronary CTA . There is evidence from several randomized studies, comparing FFR-CT with invasive FFR (representing the gold standard), that FFR-CT can be helpful in evaluation of hemodynamic significance of stenosis, especially in patients with intermediate severity stenosis.

-B.K. Koo The present and future of fractional flow reserve

Circulation Journal, 78 (2014), pp. 1048–1054

-Noninvasive Fractional Flow Reserve Derived From Coronary CT Angiography Clinical Data and Scientific Principles

James K. Min, Charles A. Taylor, Stephan Achenbach, Bon Kwon Koo, Jonathon Leipsic, Bjarne L. Nørgaard, Nico J. Pijls, Bernard De Bruyne JACC: CARDIOVASCULAR IMAGING, VOL. 8, NO. 10, 2015

Noninvasive Fractional Flow Reserve From CT OCTOBER 2015:1209 – 2 2

-Noninvasive FFR derived from coronary CT angiography in the management of coronary artery disease: Technology and clinical update

Matthew Budoff, Rine Nakansihi, Vascular Health and Risk Management 2016;12:269—278

Of Course professor.

In my country I am focusing specifically in young age, to start a primary prevention program at this early age inside Schools ! Thats why we just focus kids with this metabolic pattern !

Agree with your comment !

Long systolic murmur with thrill in severe TOF  ? I agree with hypothesis of pure pulmonary stenosis without  significant infundibular stenosis.

In addition to increased insulation by effusion or myxedema, generated electrical energy is also reduced.  Thyroid hormon is the energetic gear of whole organs and the heart as well. The decreased contractile performance induced by hyperthyroidism is largely mediated by decreased expression of the calcium adenosine triphosphatase (ATPase) of the sarcoplasmic reticulum  thus the electrical activity. İon channels are also affected and so the meberane potetials

2:1 HB

I believe that the permanent artery ligation model is the most used, not only because the repercussions of acute myocardial infarction, its physiology, its implications and its repercussion on myocardial dynamics can be more definitively observed, since in the ischemia model -reperfusion in which the artery is occluded and open, if the period is less than 20 minutes, we will only have transient alterations (stunning model), which is completely different from the infarct model, so if it is to study the infarct and its consequences the most suitable model is permanent vessel occlusion.

In patients with acute, low-risk chest pain (meaning negative troponin and nonischemic ECG; majority of US chest pain population) there is no evidence that CT angiography improves outcomes compared to the standard pathway of functional stress testing but it does lead to a significant increase in catheterization and revascularization procedures.  The revascularization rate is twice a high and the absolute number of patients needed to test with CCTA to lead to one excess revascularization is only 30-40. This is not beneficial and could be harmful. Furthermore, radiation exposure from CCTA is an unnecessary hazard. While the radiation dose is less than nuclear stress testing, stress echocardiography, which is arguably the best modality, has none. Finally, there is NO evidence that performing ANY diagnostic test in this low-risk population is beneficial and several, large comparative studies suggest it is NOT.  So we should think hard about performing ANY test, since there is no strong evidence to support it. AND, if you insist on performing a test, it should be safe and associated with the least risk of unnecessary downstream invasive procedures, which is stress echo.

In patients with intermediate-risk chest pain (<20% of chest pain population in US), such as those enrolled in the PROSPECT trial, CCTA may be beneficial and I use it in this cohort. I find it especially useful to avoid invasive procedures in those patients admitted to the hospital with abnormal troponin where I have a low index of suspicion for obstructive coronary disease.

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. 

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

the rhythm start with low atrial tachycardia then switched to sinus tachycardia 

that is a common issue in worsening heart failure

I think correction of heart failure and its true precipitation would terminate this compensatory rhythm

Incomplete Heller operation is most often the cause of failure. A complete Heller operation needs i) single cut vertical myotomy of the muscle layer from the constriction limit above to jntra-abdominal area close to the GI junction in a single incision without disturbing the surrounding structures, thus avoiding the risk of GI reflux; ii) the muscle layer has to be separated from the underlying mucosa  for at least half the circumference. A Heller operation done in this manner has never failed. Multiple operation permanently damages the area with fibrosis. Lifting the esophagus from its bed and holding it on finger makes the operation easier.

Thank you so much Deon!!!

Hi Tatiyana

I agree with Hasso. There are good grounds for offering a DDD pacemaker to this young patient, if only on prognostic grounds. There are a few things to consider:

1. Did her P wave rate increase appropriately with stress.

2. If this is congenital conduction disease, and the ventricular rate has always been relatively slow, then LV systolic function and stroke volume might be expected to be supra-normal. If this is the case, then a normal EF  could be considered to be  abnormal.

3. Subjective assessments of symptoms are often an underestimate.

4. Some of the ECGs suggest SVEs with aberrant conduction. Given the slow base heart rate this may be due to diffuse conduction disease (also supported by lack of shortening of the PR interval post dropped beat) rather than a focal abnormality. This may have a worse prognosis.

Interesting case

Tony

Thank you Dr. Alia

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.

Dear Rachael i am afraid i havent come across any evidence that is suggestive of Trop reduction in context of DCM. Trop could indeed be significantly raised in a a wide variety of DCM such as Ischemic cardiomyopathy, Hypertrophic CM, Cardiac Sarcoid/Amyloid & Vasculitis with Cardiac Involvement etc as i am sure you must be aware.

very best wishes

Preexisting risk factors- genetic or epigenitic - would be important in such cases.

Kind regards.

HS Buttar

The cause of Macrovascular complications such as cardiac diseases in T2DM is due to associated Dyslipidemia & hypertension which cause Atherosclerotic cardiovascular disease . This is probably due to polygenic inheritance of DM /  Dyslipidemia & hypertension . Control of DM does not prevent coronary artery disease & there is need for statins to treat dyslipidemia & ACEI/ARB to treat hypertension to prevent CAD . In T1DM  it is microvascular complications ( CKD) which is the cause of morbidity & mortality than CAD .

I think a partial pericardiectomy and biopsy will both help symptomatically and will probably give the diagnosis.  Malignancy should be high in the differential especially sonce the last effusion was bloody. You can also do a mammography and a thorough skin examination. Please let us know of the progress. 

Great, thanks

it is an inverted T-wave before the blue star.

Dear Vladislavs Sokalsky

I think your question lacks some clarity. If you refer to is a clinical trial and seeks to investigate the effect of medicines, then you are looking for, what is your goal?

By the time these dimensions, hoping to enrich the discussion on the problem.

Sincerely

Dr. Jose Luis Garcia Vigil

Dear Dr van Jole:

1-Primary Haemostasis

It is the set of events that leads to platelet plug formation, first step in stopping the bleeding, preventing release of cellular components of blood. During this phase involves two mechanisms: a vascular and other platelet.

• a) vascular spasm. Immediately to the production vessel rupture way, a powerful contraction of muscle fibers of the same occurs. The result is a decreasing vasoconstriction vessel diameter, and even if it is small can reach close, reducing blood loss.

• b) Formation of platelet plug. In the formation of the platelet plug can distinguish the following steps:

1. Accession or platelet adhesion.

2. secretion and platelet aggregation.

1-Accession or platelet adhesion

After the rupture of the vascular endothelium platelets adhere to subendothelial structures, mainly collagen fibers that arise by broken surface will contact and platelets. In this process platelets lose their discoid shape, becoming spherical and emitting spikes through which adhere to surrounding tissue. In the process of joining various platelet membrane glycoproteins are required, the plasma von Willebrand factor and subendothelial collagen and basement membrane. This process lasts very little, about 2-3 seconds.

Normally, the endothelium functions as an inert surface for hemostatic factors that circulate within the vessel. Any change in the endothelial wall, can lead to activation of coagulation and their regulatory systems. Vascular injury can occur directly or indirectly. Initially, when the vascular endothelium is damaged, it responds with a local vasoconstriction induced by platelet released serotonin. The exposure of the underlying collagen fibers subendotelio attract the circulating platelets adhere to collagen trying to close the endothelial defect and experiencing significant metabolic changes that promote continuity of hemostasis.

2-secretion and platelet aggregation

It is called the aggregation process by which platelets are fixed to each other. This process requires Ca ++ and ADP to be released from platelet granules by a process called platelet activation or secretion.

Platelets undergo a profound structural transformation. Membranes dense granules bind with the plasma membrane, releasing their contents to the outside and α granules release their contents. The released substances have very different types of biological activity:

• Stimulate changes estrucuturales own platelets.

• Increase in platelet adhesion and platelet granule secretion more.

• Increase the recruitment and activation of additional platelets.

• favor the aggregation and coagulation.

• Platelets possess on its surface adhesion molecules belonging to integrin family, which serve as receptors for various substances involved in platelet adhesion and aggregation, such as von Willebrand factor (vWF) and fibrinogen (FIB). Either by their adhesion to collagen, in contact with thrombin (TB), or by the action of platelet activating factor (PAF) produced by monocytes / macrophages (MON / MF) and polymorphonuclear (PMN); platelet activating your metabolism producing ADP, serotonin and Ca ++ dense granules, and other pro and anticoagulant substance of their alpha granules. Alongside the path of Phospholipase A2 (FA2) which releases arachidonic acid (ACA) is activated. This AcA, is metabolized by cyclooxygenase resulting in a series of cyclic endoperoxides that form in the endothelium Prostacyclin (PGI) of antiplatelet effect; and platelets by the action of thromboxane synthetase will result in thromboxane A2 (TXA2), potent platelet aggregating local and vasoconstrictor. AcA share equally the lipoxygenase metabolites produced family of leukotrienes, which are activators of PMN and MF .In this activation process, platelets change their discoid shape to a spherical structure with internal extension and contraction pseudopodia his cotráctil actin-myosin system, after the release of Ca ++ and generation of prostaglandins (PG). Thus they served on platelet thrombus.

That is, stimulated platelets in their adherence to subendotelio, TB and PAF, free Ca ++ activates the system actin-myosin coupling. TXA 2 mobilizes and involves other circulating platelets; and these reactions release the contents of dense granules - secreción- initiating similar phenomena in the surrounding chain platelets. Later receivers exposed for FIB and platelet aggregation begin to form the thrombus. This primary plug must be stabilized by fibrin deposition, final product of the coagulation cascades that form the plasma phase

   

This discharge produces more changes in platelets adhered and attracts other platelets, gradually adding to leave. Platelets are held together by bridges link between their membranes and subendothelial tissue. Thus a barrier is established, yet permeable for the free spaces left between platelets, but forming an initial line of defense, platelet plug or thrombus blank for the subsequent performance of the process of coagulation.

3 - Secondary haemostasis or coagulation

It is a process that modifies the liquid state of the blood giving it a gel structure type. It is the transformation of a soluble protein, fibrinogen, into an insoluble protein: fibrin; forming a mesh or net enclosing formed elements (clot), thereby strengthening the bond between platelets in order to permanently prevent bleeding.

Schematically it can be represented as an enzymatic cascade by and plasma proteins.

It has several phases:

1. Formation of prothrombinase or prothrombin activator.

2. Formation of thrombin.

3. Formation of fibrin.

This plasma coagulation phase begins with the activation of the contact system factors: Factor XII (FXII), XI (FXI), IX (FIX). Prekallikrein (PK) and high molecular weight kininogen (HMWK), the latter resulting kallikrein (KK) and kinin (K) respectively. All of these factors are the intrinsic coagulation pathway, because its components are in the plasma. The extrinsic pathway begins with the expression of tissue factor (TF) which activates factor VII (FVII). Both routes lead to the common pathway with activation of factor X (FX) in the presence of Factor V and prothrombin transform Ca ++ (PTB) in TB, and this in turn IFF fibrin monomers and fibrinopeptide A and B. the factor XIII (FXIII), activated TB and FXII, stabilizes the soluble fibrin monomers in polymers and insoluble stable serine protease coagulation are activated with the help of cofactors - FV, Ca ++ and factor VIII by both tract, for cascade mechanism whose final product is the fibrin network, which together with platelets form the final haemostatic .Paralelamente to serine protease members coagulation pathways, a series of inhibitory proteins coagulation try to maintain a stable equilibrium, the final product is the blood flow and maintaining circulation. Thus, for the extrinsic pathway inhibitor of tissue factor (ftpi) produced in the endothelium, that seek to regulate this pathway is known. Endothelium also produce thrombomodulin (TRM), responsible for modulating the action of TB, which activates protein C (PC) which together with its cofactor Protein S (PS), exert anticoagulant and fibrinolytic action. Also described is an endothelial inhibitor PC (IPC) that regulate this anticoagulant mechanism.

   

3-1 prothrombinase Formation

You can follow two paths:

• extrinsic extravascular or exogenous pathway (see diagrams of the presentation in supplementary material).

• Intrinsic, intravascular or endogenous pathway (see diagrams of the presentation supplemental material).

The two-way match for activating the X factor from this point form the final common pathway. This factor along with platelet factor 3, calcium and factor V form an enzyme complex called prothrombinase and prothrombin activator.

3-2 Formation of thrombin

It is performed in a single reaction of prothrombin (Factor II).

3-3 in blood is present an inactive protein, Factor I or fibrinogen.

Thrombin catalyzes the splitting of this molecule to form fibrin monomers, soluble and unstable in the presence of Ca ++ and Factor XIII are polymerized activated; forming an insoluble polymer in the form of three-dimensional mesh network or closes the spaces between the platelets and seals definitively the platelet plug, resulting in the red thrombus or clot

think about tako tsubo cardiomyopathie - it seem typical and ther is a lot of literature for this item available. In Austria it is also called floridsdorfer frauenherz.

Thank you Jan. Definitely I would also appreciate other answers. Let's hope.

In my previous answer about the value of ECG for the non invasive diagnosis of ARVD I forgot to stress the Fontaine Lead System ACCORDING TO THE DENOMINATION of Willis Hurst in Circulation 1998 also reported by the Brazilian group  Gottshalk Barenchuck Lopez-Riera

As already mentioned by Timo Weimar and Christian Zemlin, times have changed since the Initial phase of the MAZE III. Controls have become more strict, especially since the introduction of the event recorders and - not every MAZE IV is really performed completely, as described by J. Cox with the complete lesion set on the left and right side!

I agree with all my colleagues. The most intriguing is consideration of the event what happened indeed. The ordinary (not dangerous) blunt trauma of the chest or actually commotio cordis. Unfortunately, scanty data are available to conclude whether commotio cordis (trauma induced VF with subsequent sudden cardiac death) or a nonthreatening trauma was occured.

Tiit, it's  very interesting and important information for us. You have used CircMon system in your own researches?

Dear Sunil, As you know the NOAC's were all tested with warfarin and there are no direct comparisons of these new drugs. They showed a 10% reduction in all cause mortalityand 50% reduction in ICH..The decision to with drug to choose from will be made by evaluating Kidney function, age and weight. For instance, if one patient has a good renal function (eGFR > 95 mL/min), Edoxaban should not be used. On the other hand if a patient has eGFR < 15 mL/min, you should not use any of the NOAC's and use warfarin instead. Dabigatran is not recommended for patients with chronic gastritis because the pills are coated on acid, and Rivaroxaban is badly tolerated in patients which are lactose intolerant. These are only but a few differences among them.

This is a classical question . 

As it has been recognised, CHA2DS2-VASc is the best scheme to identify those patients at very low risk. These patients will not obtain benefit to be under oral anticoagulation. 

Refer to: J Antimicrob Chemother. 2015 Feb;70(2):325-59. doi: 10.1093/jac/dku383. Epub 2014 Oct 29. Review.

Ms.Azadeh Esfandiary your question:

"Any suggestions for a method for the measurement of prevascular Fibrosis?"

Coronary Perivascular Fibrosis is associated with impairment of coronary blood flow. Suggest calculate  Collagen Volume Fraction (CVF) and Perivascular Ratio (PFR) in biopsy samples taken by endomyocardial biosy. 

It makes sense to start a statin if the patient is not already on one, in order to obtain stability, or hopefully remission, of arterial atherosclerotic lesions.  I am not sure about whether the anti-inflammatory effect will reduce myocardial damage because trials of  anti-inflammatory medication during myocardial infarction (e.g., steroids) have not been convincing enough to establish such treatment.

We had a little (6 cases in 12 months) of Patients treated with IABP undergoing physical therapy. All patients were cannulated via axillary artery, none of those was intubate nor ventilated. We start with a "cyclette" time of 15'/day. Recruitment criteria: only IABP, no inotrope/vasopressor. The endpoints was:

- absence of arrhythmias;

- BP augmentation < 20% from baseline;

- FC augmentation < 30% from baseline.

At this moment we didn't register any kind of accident.

Bye

I agree with all of the above. Other than a coil, you could deploy a covered stent in the LIMA as well, occluding the side branch.

The 30 seconds was determined by consensus to be a reasonable threshold by which most would consider calling that an episode of Afib.  However, it is still unclear how little is still significant.  We have pacemaker patient data saying that both several minutes of Afib per month is enough for increased events and that strokes occur in sinus rhythm in patents with a history of Afib (see ASSERT and IMPACT trials).  The 2014 AHA/ACC/HRS Atrial Fibrillation Guidelines took out the 30 sec comment and left it up to the reader to conclude how long of an episode should count.

PVCs are generally not an issue unless they are extremely frequent. Bradycardia is a concern as the sensitivity and positive predictive value of the test is greatly affected by the heart rate attained when the patient is on the treadmill. If the patient is unable to exercise a drug such as dobutamine may be used as it mimics the effects of heart rate  and BP produced by exercise. The arrhythmia that is of most concern is atrial fibrillation as the irregularity of the rhythm results in many beats not being counted or being double counted. Gating is helpful but does not totally solve the problem with atrial fibrillation.

Just to summarize shortly the options you have in Kubios:

1) You can manually check and correct (if necessary) the artefacts by editing the R-wave detection markers presented in the ECG data axes. This approach is naturally availble only when you have imported ECG data into Kubios.

2) To correct artefacts automatically, you can use the artefact correction tools and set the correction level such that all clear artefacts are corrected, but normal beat intervals are not modified.

If I have the ECG, then I like to go through with first option, and rely on the second option only if necessary (e.g. if the ECG is so noisy for a short interval that you cannot visually observe the correct time instances for R-waves). 

thanks

I will leave a small Pfo only in infant and neonates with severe compromission of the right ventricle. Never in adult with pulmonary stenosis

Fibronectin

Muscarinic (M2) receptor antagonists

miRNA

Fibrillin

MMPs

TIMPs

NAFLD is actually part of the metabolic syndrome to which also belongs ischemic heart disease and DM. This is also the reason why NAFLD has been shown to increase risk of cardiovascular disease. The pathophysiologic mechanism of metabolic syndrome [hypertension, hyperlipidemia, insulin resistance] also underlie the pathogenesis of NAFLD and heart disease like IHD, arrhythmia etc.

I prescribe Inderal (propranolol) in consultation with internists/cardiologists for treatment of lithium tremor and occasionally performance anxiety. Others (e.g., Yudosky and Silver) have published extensively on using high dose propranolol for rage attacks in persons with TBI.  Other than that, I do not prescribe beta blockers.

Stop researching risk factors and get into prevention. If you want to research risk factors, find a disease we haven't already studied to death. 

Hi Theodore,

As indicated in my previous message the formula MAP = DAP + 0.40 PP will have a better yield. Our colleagues (from the engineering department of Patrick Segers) derived it from a population of more than 2500 subjects in which they have both office BP's and tonometric signals. As you know mean and diastolic BP's are the same along the arterial tree, so it is crucial to derive values from a proper calibration. The investigation learned us that both carotid artery SBP and central SBP obtained via a transfer function are highly sensitive to the calibration of the respective carotid artery and radial artery pressure waveforms. Our data suggest that the one-third rule to calculate MAP from brachial cuff BP should be avoided, especially when used to calibrate radial artery pressure waveforms for subsequent application of a pressure transfer function. Until more precise estimation methods become available, it is advisable to use 40% of brachial pulse pressure instead of 33% to assess MAP.

Ref. Mahieu et al. J Hypertens. 2010 Feb;28(2):300-5. 

Best regards,

Thierry

hi

other than increased volume of LA of what ever etiology causing stretch on LA and hence atrial ms fibre stretch and changes in the RMP. The cause of transient A F could  also be explained due to transient increase in LA pressure and increase in LA pressure and so also in the Pulm veins so their ostia ware fully stretched /dilated due to raised LA pressure  thus causing changes in the ms fibres present in the PV sleeve and setting AF and dis appears  as soon stretch is reduced. I m just hypothesizing it.It needs validation also.one can work on this as it holds true for all AF as initially all are  transient before permanent irreversible  changes in the LA occurs .

GOKHROO

Hi Kumar,

If you look at the latest ESC guidelines, which are appended, you will find the precise answer to your question. NT-pro-BNP is a step to diagnosis and helps for the prognosis. It is less well established (and presumably not wise) to use it to guide therapy. Unfortunately the test is not yet reimbursed for these indications in some countries, for budget reasons.  

For prognosis look at the I_PRESERVE prognostic data (Michael Zile Circulation 2011) and the TOPCAT prognostic data (Amil Shah Circ HF 2014). 

Best regards,

Thierry

See the relevant chapter in my wonderful new book. CARDIORENAL CLINICAL CHALLENGES.  Eds Goldsmith, Covic, Spaak. Published by Springer Jan 2015.

I strongly feel that echo training should be part of curriculum for training undergraduate and postgraduate students.This will enhance their practical knowledge and make them good doctors and the community will benefit as whole.

"For non invasive modality such as ECG, ECHO, CT, MRI or PET, how could we differentiate that the atrial remodeling process already occur or not? Any atrial size enlargement was associated with atrial remodeling?"

It is possible to compare the volume of the atria, typically normalized by the body surface area, to various studies that have compared normal versus diseased populations.  However, you raise a significant point about how to differentiate between arrhythmia induced remodeling, and remodeling caused by other comorbidities, such as mitral valve regurgitation, hypertension, etc.  Because of the complex manner in which all of these factors intertwine, I don't think post-hoc attribution of causality is possible for any feature of atrial structural remodeling.  Fortunately, measurement of these features, e.g. fibrosis, or atrial volume, can help determine the best treatment options to pursue.

If you are looking for tools that can help you measure atrial volumes from image data, check out Seg3D.  It is a free image segmentation package that is quite stable and has releases for most major operating systems.  

"For CARTO 3, how could we differentiate between scarred tissue and true atrial remodeling?"

I am not certain what you are looking for here.  If a patient has an atrial arrhythmia (AF), and no prior ablation therapy, I would assume that any abnormal tissue is atrial remodeling.  If the patient has previously undergone an ablation procedure, then there may be a difference between scarred tissue, and remodeled tissues.  If you are interested in trying to classify these tissue types, I would look at work that has been done with voltage mapping.   Marchlinski et al. looked at the amplitude of intracardiac electrograms as a means of classifying different types of cardiac pathology.  Their work has largely focused on ventricular scarring, but I would start there anyway.

Good luck!

BVR -- acute, high flow, traumatic CCF example: http://www.ncbi.nlm.nih.gov/pubmed/24527815

Post MI ventricular septal rupture is generally managed waiting as long as clinically possible to improve the surgical result. The reason is related to the inconsistency of peri-infarcted tissue in the weeks following the acute phase. Post MI papillary rupture is an acute complication due to the massive mitral regurgitation. Post MI free ventricular wall rupture is a generally a final complication with few exception represented by cases with subtile wall fissuration of the necrotic area with thrombus closing the hole. I remember single patients surviving these distinct complications but no one surviving with the three at the same time. A post MI free wall rupture with pericardial tamponade was successfully treated in my Department with surgeons at bed site and immediate starting of cardiac surgery during resuscitation maneuvers.

Let me update the physiology and hemodynamics in Acute Myocardial Infarction (AMI) Cardiogenic Shock (CS), as a Clinical research investigator

a) 1975-76: Our research at William Likoff Cardiovascular Institute (Hahnemann Medical College and Hospital of Philadelphia): First, prospective study of CS in Post-op of coronary bypass surgery, with evidence of intra-operatory evidence of RV-AMI, and post-op CS.

In brief, RV-AMI was involved in all episodes of CS, explaining the absence of pulmonary edema (RV-IAM), and RX-regression of pulmonary edema (RV and LV-AMI) simultaneously with the episode of hypotension. Improved survival 69%.  

Antonio Delgado Almeida. Deborah Young Investigator Award, Deborah Hospital Foundation, NJ, USA, 1976. 

b) 1978-1983: Founder and Director, Intensive Care Unit, Adolfo Prince Lara, MD Hospital, University of Carabobo Medical School. The same approach with some unexplained failures. We developed new method for RBC-K content, monitoring the large cell K fraction, and safety infusion of G-I-K (Sodi-Pallares solution), while new method for ionized calcium, sharply decreased in metabolic acidosis of CS, while reversion of ionized hypocalcemia rapidly improved LV C.O, and shock: Two novel points in the treatment of AMI and CS.

c) 1983-present: Discovery of an inherited defect in RBC-K content in hypertensives and 48% of their normotensive sibling and offspring, and the simultaneous RBC-K and O2 binding by human hemoglobin (2012) change the prevention, diagnosis and treatment of hypertension and related CVD. Since then, the improved of this genetic defect was associated to rapid BP control and ST-T alteration of ischemia.

In brief, treatment of hypertension and coronary heart disease with Amiloride HCl Dihydrate, have simply vanished complication of CHD as CS, hoping to be in the future worldwide!

Sorry, for this extensive response, I was simple immerse on the request from APS Living History Program, invitation for an interview videotape, received at Dec. 05, 2014.

Before play chess you should known the pieces, and I probably help in the basic.

Magnesium ion has an ionized and intracellular fractions, being the 2nd largest intracellular cations in our body, critically important with potassium ions in most cell functions, as enzymes, at times being part of enzymes or protein structures. In fact, RBC magnesium is about 3 times of the plasma fraction. 

In blood, similar to calcium, magnesium is found as bounded, ionized and intracellular fractions (RBC), in which bounded or Mg salt represents the reservoir to maintain ionized Mg, the only functional fraction, except when bounded to enzyme or proteins.

In pharmaceutical form, we usually refers as 100 mg of magnesium oxide or 600 mg of magnesium sulfate. Unfortunately, in 500 mg of Mg sulfate there is only 5 meq (10 mg) of Mg. In other ions as calcium: 1 g of IV calcium gluconate (FDA: 8 mg of calcium), very effective but tiny fraction as compared with calcium chloride.

Therefore, taking 800 mg of Mg sulfate = 6.4 mg (3.2 meq), half of RBC Mg/liter cell, is harmless from pharmacology and physiology aspects. However, 793 mg of oral sulfate after absorption may decrease blood ionized ions, thus cell function, while 793 mg of IV sulfate rapidly bounds ionized calcium leading to hypotension, seizures and bleeding in presence of surgery. 

In brief, don't worry about our metal ions, our body has a lot, take care of the ionized and intracellular fractions (iron in Hb) which maintain us alive!