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Questions related to Clinical Cardiology
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At what AAA size would you consider Cardiac Nuclear PET/SPECT with Lexiscan over Dobutamine Stress Echo? (outpatient setting)
How important is the potential for a hypertensive blood pressure response with use of Dobutamine?
How important is the presence or absence of a previously placed graft?
What are other clinical factors on which you would base your decision?
-comments greatly appreciated!
Deborah Williams, NP 
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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.
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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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Hello,
I would like to ask your opinions on an interesting case:
46 yr old female patient had an infection of uppper respiratory system in the beginning of September. Shortly afterwards she developed angina pectoris like symptoms. EKG was without pathological signs. In 24h-EKG only a sinus tachycardia showed, when walking slowly (up to 140-160 beats /minute). Echocardiography was without pathological signs as was lab (CRP, troponin, myoglobin, hemoglobin,...). In a cardio-MRI in November a cardiac microvasculatory dysfunction (endothelialitis? small vessel disease?) was diagnosed.
In a blood test, troponin, creatine kinase, creatine kinase-MB, CRP, c-ANCA, p-ANCA, lupus anticoagulant, anti-cardiolipin antibodies... and so on all were negative.
Only antibodies against endothelium could be shown.
Does anybody here have experience with a case like that? At the moment, we think mainly about an autoinflammatory process (e.g. triggered by auto-antibodies). Is there any way to find evidence pro or con?
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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:
Best regards
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To avoid non- responders to this therapy cardiac imaging has been proposed as a possible solution. But it does not work always...
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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.
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What shall be the choice: manual or automatic? It is clear from research and practice that inaccuracies exist with automatic BP use while manual seem preferable or yet not really? Some claim that automatic exclude bias in measurement.
Inaccurate reads of blood pressure lead to consumption of medications otherwise not needed if blood pressure measurements would be accurate. It affects lives-health. Which BP monitor shall be used? Both? How to resolve this dilemma in our age of automatisation?
I know that much inquiries are made by me but its a life related investigation.
Thank you in advance for contributions.
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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.
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I have recently repeatedly observed pulmonary haemorrhage in association to an appropriate use of the LUCAS device by different team for OHCA CPR. This was very different from haemorrhagic secretions, that can somtimes occur during prolonged CPR.
Any thoughts or experience?
Thanks
Tobias
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Are asking strictly on the Physio device or others (such as the Zoll model)?
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Is there any research on if/how a slightly dilatated thoracic aorta root dilatation (caused by high blood pressure and not Marfan) can be successful reversed? If not, what is the physiological reason that a dilatated aortic root (4cm) (caused specifically by high blood) pressure cannot return back to normal size after aggressive blood pressure control?
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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.
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A 40 days premature neonate reffered other center due to large ra thrombosis.
.he hasn't positive history of cvp catheter .
in examination ,stable hymodynamic , normal saturation , gread 2/6 systolic murmur ,no sign of respiratory distress.
in echo: a large echogenic ,pedinculated ,moveable thrombus protruding to tv ,area about 1.1 cm2 ,mild tr with p.pg= 27 mmhg ,otherwise is normal .
what is your opinion about managment of this neonate?
best regards 
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Please share me the best answer might you get...
Regards…
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58 year man with Achalasia cardia who underwent Trans thoracic Heller"s cardio myotomy in 1962, started c/o of regurgitation of liquids from nose and mouth mostly at night for over one year.Details of the procedure are not available.Requested to have Upper GI scopy,Manometry and 24hr PH.Not a diabetic or Hypertensive.No respiratory symptoms.
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A timed barium study with liquid and bread component plus repeat manometry with ph impedance monitoring
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A - Tricuspid Regurtitation
B - Mitral Regurgitation
C- Aortic Regurgitation
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Aortic stenosis followed by mitral regurgitation. However, we observe sometimes in patients with chronic IE a combined aortic vitium (Stenosis & regurgitation)
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Is Hypertension only risk factor for Abdominal Aortic aneurysm or it can be a risk factor for Thoracic aneurysm as well ?
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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.
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Do we have any best test to run in diagnosing cardiac tamponade , or clinical signs are considered reliable here ?
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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
References
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.
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While managing Patient with hyperkalemia ,we administer sodium bicarbonate !how does it work , or mechanism in action ?
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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+ .
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The fibrotic response after a myocardial infarction (MI) can be classified into two types of fibrosis:
1-Replacement or reparative fibrosis at the infarcted area (scar formation)
2- Reactive fibrosis outside the infarcted area usually after the replacement fibrosis
The replacement fibrosis or fibrosis healing phase (takes 4 to 6 weeks post MI) is a pivotal process to prevent the rupturing of the ventricular wall after an ischemic insult. However, is it wrong if we disrupt this process?
I would be grateful if you could give me anything about this topic.
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Very interesting data...
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.
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This is a left parasternal short axis view at the level of aortic valve and pulmonary artery in a 29 years full term pregnant female, she was asymptomatic, no abnormality detected on auscultation, echo was indicated before CS. 
In your opinion, what this flow stands for ?
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I agree with that. One has to think of a superiorly directed venous flow probably exaggerated due to the hyperkinetic state of pregnancy
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left atrium volume?
tissue doppler myocardial velocities?
pulmonary venous flow?
ratio  E/e LV ?
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I think that this algorythm will be useful to evaluate LV diastolic function.
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We want to know the most common polymorphism of β adrenergic receptor gene associated with bisoprolol therapy in heart failure studies. We want replicate in our population. 
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Thank you dear Paul 
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Can in future combined CT FFR and CT coronary angiography replace invasive coronary angiography for diagnosis of CAD ?
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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
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Is there a different CVD risk profile in Senegal? How has the prevalence of rheumatic heart disease and coronary artery disease changed over time?
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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 !
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Generally systolic thrill is absent in severe TOF.. According to standard book teaching.. We are seeing fair number of patients of severe TOF with systolic thrill... They generally have good size pulmonary artery with pure valvular PS.. Anybody can share personal experiences.. 
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Long systolic murmur with thrill in severe TOF  ? I agree with hypothesis of pure pulmonary stenosis without  significant infundibular stenosis.
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It seems that there are other causes of decreased EKG voltage than pericardial effusion according to publications I have found, but what are they?
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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
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A long standing hypertensive patient with heart failure of reduced ejection fraction. He is in functional class II and recently presented with bradycardia increasing fatigue.
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2:1 HB
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I have been reading about various drugs inducing anti-remodeling effects in animal models (rats) of myocardial infarction. Can someone suggest why ischemia-reperfusion is not preferred in this regards and permanent ligation of the coronary artery is preferred? Is it because of the influence of reperfusion on infarct size, thus "reperfusion" itself may mask the true effect of therapeutic drug?
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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.
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Cardiac CT angiography, aortic dissection, pulmonary embolism, acute chest pain
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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.
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Echo helps in seeing the chambers and  valves at the same time. It seems to be a better option for diagnosing congenital heart diseases. What benefits of ECG have led to this research? 
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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. 
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A mini-case report. History-evolution of the family disease from peripartal CMP to cardiac transplantation:
 - Disease manifested in 35-year-old female to the last trimester of the pregnancy as peripartal cardiomyopathy.  Heredity is burdened by the SCD of her mother at the 29-year age.
- ECG 2015: a high voltage complex, WPW phenomenon. ECHO:  LV EDVol 187 ml;  LV ESVol 135 ml;   LVEF  28%; GLS  -10.4%;
 After 12-18 months post delivery the condition worsened. There were signs of progressive heart failure with  biventricular dilatation and systolic dysfunction.
- ECHO 2017: LV EDVol 290 ml;  LV ESVol 242 ml;   LVEF  17%; GLS  -5.1%;RV EDVol 64 ml;  RV ESVol  43 ml;  RVEF 32%;  GLS  -9.8%; TPSE 12 mm; index of myocardial mass is 135 g / m2,  RV free wall thickness  8 mm, LV free wall thickness 9 mm.
 - ECG 2017 :  Atrial Flutter, atypical LBBB pattern with "pseudo-infarction" signs of Sodi-Polares (QS in I, avL, V5-V6) and Cabrera (V4).
N-terminal proBNP 16766 pg / mmol.
Cardiac MRI revealed  signs of subendocardial linear fibrosis (areas of poor gadolinium uptake that indicate scarring).
ECG and MRI results are in the attached file (mother)
A successful heart transplant (HTx) was performed in the patient.
Since our patient has three children - sons 16,10 and 2 years old, we examined them: Еcho normal, ECG abnormal (see the file attached below).
What cardiomyopathy needs to be differentiated in children under dynamic follow-up? What potential genes should be examined?
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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
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A 52 year old man with DCM, came to the ER with palpitations and worsening  dyspnoea.
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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
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A 22 years old male patient  had achalasia diagnosed  3 years ago by CT chest with oral and iv contrast, barium swallow and manometry  He had endoscopic dilatation 4 times  with temporary relief followed by lap. Heller cardiomyotomy 2 years ago with improvement of dysphagia for 3 months only.  He had open Heller 4 months ago with improvement of dysphagia for 3 months and then he has dysphagia again. Barium swallow repeated 1 week ago showing achalasia. 
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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.
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Hello,
I'm looking for suturability test protocol for cardiac patch ( possibly according to ISO norm).
Thank you very much,
Francesca.
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Thank you so much Deon!!!
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Here are strips HM ECG from 19-year-old asymptomatic girl. However, the maximum  sinus heart rate during daily monitoring was 64 BPM, and  79 BPM when the test with physical exercise was performed (test accompanied by ventricular and supraventricular extrasystoles). Echocardiography revealed mitral valve prolapse (3,5 mm A2 with minimal mitral regurgitation) only.
Is there a need for additional examination and what to do next research step?
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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
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I need suggestion for genetic testing that the Clinician may request in prevention and management of many cardiac diseases
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Thank you Dr. Alia
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what is the evidence of this in humans and its applicability in endocarditis?
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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.
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Most of the literature refers to increased troponin in serum as a biomarker but I am interested in knowing if decreased levels in the heart indicates disease.
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Dear Rachael i am afraid i havent come across any evidence that is suggestive of Trop reduction in context of DCM. Trop could indeed be significantly raised in a a wide variety of DCM such as Ischemic cardiomyopathy, Hypertrophic CM, Cardiac Sarcoid/Amyloid & Vasculitis with Cardiac Involvement etc as i am sure you must be aware.
very best wishes
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Given the recent JAMA Internal Medicine Wang et al article on the role of dietary fat in cardiovascular disease, what should clinical cardiologists be advising highly motivated patients with high (>1,000) coronary calcium scores about diet? Would this vary depending on patients' other risk factors?
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what about strong family history but no other risk factors?
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Is uncontrolled blood sugar raise LDL-C? or there are other factors participate in leading to heart disease?
All the best
Aly
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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 .
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A 84 year old woman with hypertension, 2 type diabetes mellitus and chronic renal failure (GFR 30-50 ml).
2005 NSTEMI: LAD and LCX PCI
2006 angina pectoris: distal RCA PCI. LAD and LCX stents no changes
2014 UA: RCA ISR. 1 BMS implantation. Other stents without ISR 
Echocardiographia all the time showed good systolic ejection fraction with good wall motions. 
In 2014 starts: in ECHO showed a non siginificant pericardial effusion. After coronarographia seen hematuria and anemia. 
An urological examination was negative for tumor, but an pelvis CT was done, whith some negative result.
2014.07 gastroscopia: duodenitis erosiva and chronic erosive gastritis was.
              colonoscopy: negative
2015.08.03-04 was admited with melena.  Gastroscopy and colonoscopy was not showed a point of bleeding. 3 U of blood was transfused.
An echo showed a significant pericardial effusion and a pericardiocentesis was performed. 1200 cc. straw-yellow liquid evacuated. And other day 100 cc.
2015.08.05-12 admited to hospital with anemia for blood transfusion. Colonoscopy was done again.  The source of bleeding was not found. A polyp of the  Bauchin valve was cut of.
The histology result of the colonoscopy sample not confirmed malignancy.
2016.01.05 Admited agin with huge pericardial effusion and symptoms of HF. 1500 cc straw-yellow liquid evacuated. A pleural effusion was this time and a diagnostic thoracocentesis was done.
The results from the pleural fluid showed a sigillocellulare cc. cells
The CA 125 was elevetad.  (95 the normla range upper limit is 35 at our lab)
Pericardial fluid: eosinophil cells, mesothel and lymphoid cells was seen.
An cardiac MR was done with negative result for a  autoimmune disease or primer cardiac malignancy.
An chest CT was done: negative for cc.
An abdominal and pelvis MR was done: at the point of obturator in both side an 6 mm diameter  lymphaticus nodus was detected. In the corpus of uterus an 8 mm myoma detected (T2)
Tuberculosis negative.
The hemoculture results is negative
2016.04.20 was admited with huge pericardial effusion. 1200 cc bloody liquid was evacuated. 
And now 2016.05.31. Again was admited with effort dyspnoe and not a very huge pericardial effusion.
The pericardial effusion sizes was 30-35 mm mostly left side and 25 mm from apex and right side.
The gastroentereologist, onkologist, gynecologist and urologyst do not know the reason of chronic pericardial effusion. Please help, what is the diagnostic option which can use to find the cause of pericardial effusion.
Thank you that you read and help.
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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. 
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Dear friends, 
I would be happy if someone can look on the enclosed paper and  help me to understand the meaning of each of the 3 lines in fig. 1 (also the horizontal dotted line). (The general idea of the figure is clear).
Many thanks, Ran
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Great, thanks
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In the following ECG waveform, I don't know which one to consider as the T-wave: is it what is marked by blue start, or is it an inverted T-wave before the blue star?
#ECG
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it is an inverted T-wave before the blue star.
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Dear all,
I would like to know your experience about filling out medications and the corresponding doses when you conduct a clinical trial that primarily doesn't aim to examine the effect of drugs. However, the drugs might affect the final results. When I see the publications of different clinical trials (particularly, in cardiology), usually they just mention the substance group (ACE-inhibitors, statins, etc.) without further giving information about the dosage or particular substance names.
Therefore, the question is - whether you just fill out the substance group of current medications that patient takes (e.g. beta blockers, ACE-inhibitors, statins) or you write down, for example, metoprolol, ramipril, atorvastatin? What about dosages - how do you note, for example, the dosage of Ivabradin 5mg that needs to be taken twice a day? Do you write down the cumulative daily cumulative dosis (10 mg) or the dosis that needs to be taken each time (5 mg)?
Thank you very much in advance!!
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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?
  • A clinical trial is privileged and ethical way to conduct experiments in humans. The phases of drug research; I, II, III and IV aim to investigate together Efficacy and Safety of Medicines.
  • The designs in clinical trials, involving intervention and should describe all the features of the products used; active ingredient, dosage form (capsule, tablet, injection, cream, ointment, spray), total daily dose administration (g, mg, mcg), frequency of administration in the day (once, twice, three times, etc. ), route of administration (intramuscular, intravenous, subcutaneous, intradermal, intranasal, oral / buccal, etc ...).
  • Statistical factorial designs are recommended, crossed double-blind, comparative (drug vs. drug, drug vs placebo), which you certainly already know, to be their field of expertise and professional skills.
  • All this must be considered and describe in your research protocol, although his speech does not involve the efficacy and safety of drugs,
  • If the intervention is for example a biological treatment, as would be the application of stem cells in any way to consider all the characteristics described above for the medicines they use research subjects. It does not fall into methodological errors and their experiment would not have validity.
  • Moreover, I could not explain whether the variables studied and compared with statistically significant difference (compliance alternative hypothesis "H1"), or the same or similar (compliance null hypothesis "H0") effects.
  • On the other hand, it should be descriptive and not interpretive interventions and do not use abbreviations not previously been clarified in the text of the publication or research protocol.
By the time these dimensions, hoping to enrich the discussion on the problem.
Sincerely
Dr. Jose Luis Garcia Vigil
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The image becomes visible after opening the question. The ensuing discussion provides the interesting bottleneck of this problem though. Any help would be much appreciated.
PS. the last sentence on the image is irrelevant and should have been cropped. 
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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
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There seems to be a lot of websites referring to cardiospasm and achalasia of the oesophagus as an anatomical problem, but little about acute cardiospasm as an emotionally-induced reaction. I remember as a student seeing a man visiting his father in hospital (from an arab country) overcome with grief and doubled-over with intense pain beneath his lower sternum, and this responded to quiet reassurance from the senior physician who reassured me that this was cardiospasm which would clear up within an hour, which it did. Thanks for any insights from others who have seen this.
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think about tako tsubo cardiomyopathie - it seem typical and ther is a lot of literature for this item available. In Austria it is also called floridsdorfer frauenherz.
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A recent meta-analysis on clinical use of PEA (https://goo.gl/k6TKwP) has clearly shown good results. Opinion on the efficacy of this product are anyway conflicting. I would very much appreciate if I could directly correspond with clinical users.
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Thank you Jan. Definitely I would also appreciate other answers. Let's hope.
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When a patient is diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVD), first-degree relatives should undergo screening for ARVD. What is the best/recommended screening protocol for first-degree relatives? How often serial follow-up evaluation in individuals at risk of developing ARVD (first- degree relatives) should be done? As electrical abnormalities precede detectable structural changes in subjects at risk for ARVD, should screening with serial ECG and Holter be enough or you recommend also periodical imaging diagnostic (echo/CMR). Do you have different screening protocol for relatives with the presence of a pathogenic mutation (mutation carriers) or relatives of a mutation-negative proband.
What is your experience and how often do you use signal-averaged ECG as one of the criteria (Task Force criteria) for diagnosis of ARVD?
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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
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Data is conflicting whether the addition of surgical ablation technology achieve the same sinus rhythm restoration as to historic controls of Cox Maze III patients. That might be related to different surgical eras, different types of rhythm assessment during follow-up or the precision to get transmurality lesion set.
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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!
With a complete lesion set as well as a complete transmurality, the results of the two procedures should be comparable. 
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Is collapse from commotio cordis immediate or can the subject still walk around for a bit?  Would the subject collapse onto their back and still be able to get up while in this devastating cardiac arrythmia?
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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.
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There are many articles devoted to the assessment of stroke volume (SV) by the method of impedance cardiography (ICG). There is a description and bioimpedance devices that determine the breathing cycle. But we didn't find studies in which these two characteristics were determined simultaneously.
Thank you.
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Tiit, it's  very interesting and important information for us. You have used CircMon system in your own researches?
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of the available options, which is the preferred NOAC for SPAF
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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.
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Antiagregan therapy in non-valvular atrial fibrillation.
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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. 
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Does anyone use Definity contrast agent as a continuous infusion? We have had to manually continuously rotate the syringe pump during use to keep the solution mixed. Any ideas on a better method of mixing during infusion? Thanks in advance.
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Please also the attachment added.
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Why was left out the therapy of endocarditis on PM electrodes? How you comment it. And how will you treat it? 
Thankx for the answers!
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Refer to: J Antimicrob Chemother. 2015 Feb;70(2):325-59. doi: 10.1093/jac/dku383. Epub 2014 Oct 29. Review.
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Any suggestions for a method for the measurement of prevascular Fibrosis?
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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. 
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Following ST Elevation Myocardial Infarction (STEMI) the myocardial ischemia causes an inflammatory response, which is a predictor of mortality and myocardial remodeling. Treatment with statins have been shown to be able to reduce the area at risk by reducing inflammation in hypercholesterolemic patients with unstable angina. It is unknown whether the anti-inflammatory effect can really reduce the size of myocardial necrosis in STEMI and if this is due to the anti-inflammatory effect of statins. What would be the best way to advance in the anti-inflammatory strategy for treating STEMI?
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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.
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I am looking for clinical experience or studies that deal with intra-aortic ballon pump patients and physical therapy exercise protocols while still on balloon pump. 
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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
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41 years old man who had three vessel CABG (LAD-LIMA, RCA-Ao,Cx-Ao) two years ago.
He had history of recurrent exertional angina, poor exercise tolerance despite maximal medical therapy for the  last six months. Therefore we performed coronary angiography. Angiography showed patent grafts of LAD-LIMA, RCA-Ao, Cx-Ao. However, the  large side branch of LIMA had not been ligated. The side branch can be coronary steal.
What  we  do ?
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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.
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What about patients with less than 30 seconds episodes of AF?
A therapeutic difference is a should, may or must?
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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.
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any possible interaction between arrhythmia and heart scan results?
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PVCs are generally not an issue unless they are extremely frequent. Bradycardia is a concern as the sensitivity and positive predictive value of the test is greatly affected by the heart rate attained when the patient is on the treadmill. If the patient is unable to exercise a drug such as dobutamine may be used as it mimics the effects of heart rate  and BP produced by exercise. The arrhythmia that is of most concern is atrial fibrillation as the irregularity of the rhythm results in many beats not being counted or being double counted. Gating is helpful but does not totally solve the problem with atrial fibrillation.
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Hi,
I am interesting to find the answer to a question related to using Kubios (in particular it would be good to get advice from Mika Tawvainen who created the software but if anyone knows anything about this software I would very much appreciate your help). 
I want to remove artifacts from some collected HRT and HRV data. My other colleagues have suggested that only automatic filters can be applied to parts of the data. However, the User's guide of Kubios seems to suggest you can remove artifacts manually. 
If this is so am I correct in understanding that this can only be done using the ECG data but not the RR interval data displayed on the Kubios data browser?
If this is the case as well, is it right to assume that in order to manually remove artifacts you would want to find data points on the RR interval data browser that seem like artifacts (e.g., they spike up very quickly and suddenly) and then find the corresponding part on the ECG data display and add a marker which would remove the data point so that it is not included as an R wave in the RR interval data browser. By doing this all the artifacts that seems like real R waves will be removed from the data resulting in "clean data" as free from artifacts as it is possible to get it.
If this is all correct then I would assume my colleagues were not aware of a manual function to remove artifacts (i.e., they just used the automatic low, medium and high level artifact corrections) because their data did not have the ECG information which I underestand is required to manual remove artifacts. 
It would be great if corrections can be made to my understanding where required.
Many thanks,
Victor
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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). 
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What about LMWH anticoagulation (3-4 weeks) without TOE control before ECV? Because in guideline only VKA or NOAC has written, but nothing said about LMWH. What is you opinion?
Thanks
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thanks
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I would like to know the experience they have with the closure of the atrial septal defect in adults by interventional catheterization?
In patients previously operated  for pulmonary valve stenosis, it is advisable to close a defect of atrial septation or better leave the default...???
Thank you very much in advance
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I will leave a small Pfo only in infant and neonates with severe compromission of the right ventricle. Never in adult with pulmonary stenosis
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I am trying to understand what biomarkers I can use to predict fibrosis and recurrence of AF in a given patient population.
Does anyone know if others exist besides ST2, Galectin-3, TGF beta and TNF-alpha?
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Fibronectin
Muscarinic (M2) receptor antagonists
miRNA
Fibrillin
MMPs
TIMPs
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DM is known to longer the QT intervals and there is evidence that NAFL also longers the QT intervals. what are the other effects and possible mechanisms?
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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.
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Psychiatric patients usually take many different medications and often they have been already treated with beta-blockers. However, there are several cases in where You should add beta-blockers, because of newly recognized heart failure or even atrial fibrillation. Often psychiatric patients take medications, which included antipsychotics or even worse an antipsychotic polypharmacy or combinations with antidepressants. According to the survival studies We know that treatment with beta-blockers in patients with stable heart failure (EF less than 35 %) is necessary for better surviving.
The third group of cases consists the consequences of psychotropic medications adverse events (e. g. arrhythmias and clozapine or olanzapine) or prolonged QTc and supraventricular arrhythmias (e. g. amisulpride with clozapine combination or ziprasidone use and escitalopram together). In these cases a trial with beta blockers is usually a first step before drug discontinuation.
From EBM we know that combination of clozapine and amisulpride is benefitial in short term trials, however long term use should lead to several complications in this field.
To sum up, DDIs with psychotropics and beta-blockers should be calculated before prescribing beta-blockers. For example, atenolol is not appropriate with several antipsychotics and antidepressants (QTc prolongation). Also story with metoprolol is more or less the same, however metoprolol is very selective for B1 receptors, however there are cases of induced delirium with propranolol. Smart use included pindolol, especially in patients on antidepressants, because of add on efficacy, however we do not have long term trials.  At the end I think cooperation between clinical pharmacist and psychiatrist and cardiologist is the best approach to deal with these patients.
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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.
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The essential logic is to decrease the time of exposure to cardiovascular risk factors with genetic insights providing strong justification for this approach. Lifetime exposure to lower concentrations of cholesterol specifically, plasma levels of low-density lipoprotein (LDL) cholesterol, is shown to be associated with larger reduction in the risk of coronary heart disease. The decrease in risk is related to the genetic variants of receptors that remove cholesterol from the circulation matched with individuals who do not carry such variants. For a known reduction in LDL cholesterol, there was much more impact on reduction in cardiovascular disease risk than that reached with pharmacotherapeutic modulation in late life. Several studies have shown that the adoption of a healthy life , the act of not smoking, weight control and perform regular physical activity , with the reduction of cholesterol levels can be more effective than drug therapy of known effectiveness. How best to link these two strategies and show people that the protection of their coronary health goes beyond the use of drugs ?
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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. 
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Beyond the classic formula [MAP = DAP + 0.33 PP] ;
PP = systolic-diastolic pressure, DAP = diastolic arterial pressure
Can you suggest other formulas or methods for non-invasive estimation of mean arterial BP?
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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
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What about recurrence risk models? score sheets?
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Untreated sleep apnea, due to the amount of LA pressure shifts and also because it points to a deeper peripheral neuropathy. The continued stretch and resulting damage creates the perfect storm of a fibrotic substrate. It is my hypothesis though that the cause effect relationship of the two disorders is only developed when they are treated as such instead of two symptoms of the same peripheral neuropathy.
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Some researchers showed evidence for using BNP as a prognostic indicator for individuals with HFPEF (Van Veldhuisen et al., 2013). Is there any other evidence or anecodotal advice on this matter?  Thank you.
References
Van Veldhuisen D, Linssen G, Hillege H, et al. B-type natriuretic Peptide and prognosis in heart failure patients with preserved and reduced ejection fraction. Journal Of The American College Of Cardiology (JACC) [serial online]. April 9, 2013;61(14):1498-1506.
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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
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Type 2 CRS is defined as renal detoriation due to chronic heart failure. because of chronic fluid overload due to CHF, renal venose pressure is increased. thus glomerular filtration rate is decreased. if we use  of dopamine in 2 mg/kg/min dosage, afferent arteriol would dilated and GFR would be increased. Is it like this indeed? is there anyone who had experience use of dopamine (2 mg/kg/min) in Type 2 Cardio Renal Syndrome?
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See the relevant chapter in my wonderful new book. CARDIORENAL CLINICAL CHALLENGES.  Eds Goldsmith, Covic, Spaak. Published by Springer Jan 2015.
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The incidence of asymptomatic valvular lesions is very high and many of them require management based on echo findings.The positive and negative predictive values of cardiac clinical findings is also very poor.The students of cardiology miss out on diagnosis ,assessment of severity and management decisions in valvular heart disease.,A recent WHO report suggested that more than 50% of Rheumatic heart diseases are missed out even by experienced physicians.A lot of time is invested in teaching findings which have poor agreement and predictive values for UG and PG teaching.
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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.
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atrial remodelling in Atrial tachycardia or atrial flutter or Atrial Fibrillation
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"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!
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Superficial Middle Cerebral Vein OR Basal Vein of Rosenthal both these venous drainages are rare in Carotido-Cavernous Fistula. But which one of these is more dangerous?
Thanks Professors in advance.
A sample link for Beginners here:
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BVR -- acute, high flow, traumatic CCF example: http://www.ncbi.nlm.nih.gov/pubmed/24527815
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Rupture of ventricular septum, Papillary muscle and free ventricular wall after myocardial infarction in the same patient .Did your patient survive? Usually these patients don't survive.
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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.
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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.
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Avastin can affect vascular permeability, normal BBB restrictions on Mg diffusion would thereby be bypassed opening the possibility of excitation and possibly seizures in those prone,
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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! 
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Can anybody explain association of Hypertension with High density lipoprotein, I am doing an analysis and the protective association is coming out between low levels of HDL with presence of hypertension. 
What could be the possible explanation, is there any biological plausibility or any other explanation of this phenomenon.
Note: The sample size is adequate, the study is powered statistically and there is no misclassification. Multivariate analysis has also done appropriately with adjusting for potential confounders.
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Adeel are you finding low HDL is associated with low to normal blood pressure? Since high HDL is considered protective of cardiovascular health, this finding is unusual, when considering control variables. Is it possible that persons put on hypertension medications also had low HDL? I do not think there is a biological explanation for low HDL preventing hypertension.
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If yes, what do they cost? I would like to know how much newer generation DES are in Iran.
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All of newer generation of DES are available in IRAN (e.g. promus element,xience  V prime xpedition resolute bintegrity and also Absorb) and their cost is  about 400 euros'.