Posted in echocardiography, tagged 2d echocardiography, best site for echocardiography, drsvenkatesan, echo video, echocardiography, echoincontext, jase, madras medcial college on February 4, 2010| Leave a Comment »
Cheers to duke university for sharing ! www.echoincontext.com
Posted in Cardiology - Clinical, cardiology -ECG, tagged athelete heart, athlete's heart, concentric lvh, ECG, echocardiography, pathological lvh, resting heart rate, sinus bradycardia, vagal tone on January 15, 2010| Leave a Comment »
ECG of an athlete is many times difficult to interpret. The influence of autonomic tone in athlete’s heart is an complex one.Contrary to our expectations the parasympathetic tone is higher in well trained athletes. The resting heart rate can be as low as 30/mt which is 99.9 times pathological in non athletes.This happens due to a concept called accentuated antagonism.The athletes who have episodic surge of high catecholamines keep stimulating the para sympathetic neurones in a constant fashion.
LVH is the most common feature.Here there is simple myocyte hypertrophy, without pathological fibrosis.This differentiates athlete’s, heart from HOCM .
Many ECG abnormalities are reported in athletes.
Excerpts from the ACC recommendation
1. Electrocardiographic findings that are common and training-related and that do not require additional evaluation are sinus bradycardia, 1° atrioventricular block (AVB), incomplete right bundle branch block (BBB), early repolarization, and isolated voltage criteria for left ventricular hypertrophy (LVH).
2. Uncommon and training unrelated electrocardiographic findings that mandate further evaluation include T-wave inversion, ST-segment depression, pathological Q waves, atrial enlargement, a hemiblock, right ventricular hypertrophy, a BBB, or a Brugada-pattern of ST-segment elevation.
3. Training-related electrocardiographic findings are more common in men than women, athletes of African descent, and high-endurance athletes such as cyclists.
4. Sinus rates <30 bpm and sinus pauses >2 seconds are common in highly trained athletes, particularly during sleep.
5. A normal chronotropic response to exertion and the absence of bradycardia-related symptoms distinguishes training-related sinus bradycardia from sinus node dysfunction.
6. 1° AVB and Mobitz I 2° AVB are common, but Mobitz II 2° AVB or 3° AVB should not be assumed to be training-related and require evaluation.
7. Early repolarization in Caucasian athletes most commonly consists of upwardly concave ST-segments and tall and peaked T waves; in black athletes, there often is convex ST-segment elevation and negative T waves, mimicking a Brugada pattern.
8. In the presence of voltage criteria for LVH, pathological hypertrophy should be suspected if there is left atrial enlargement, left-axis deviation, repolarization abnormalities, or pathological Q waves.
9. T-wave inversion ≥2 mm in ≥2 adjacent leads should prompt evaluation for structural heart disease.
10. Electrophysiological testing for risk stratification with possible catheter ablation is appropriate in athletes with ventricular pre-excitation.
Source : Fred Morady, M.D., F.A.C.C.
http://www.ncbi.nlm.nih.gov/pubmed/19933514?dopt=Abstract
For an excellent article on the topic click here
Posted in cardiac surgery, Cardiology - Clinical, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), tagged bi leaflet valve pannus, echocardiography, left atrail mass, mass in echo, medtronic hall pannus, pannus, pannus in prosthetic mitral valve, st jude pannus, starr edwards pannus, streptokinase, tee, thrombolysis for prosthetic valve, thrombosis, trans esophagela echo, urokinase, vediodensity, what is paanus ? on March 20, 2009| Leave a Comment »
Prosthetic valve obstruction is an important complication of artificial valves.The incidence of prosthetic valve obstruction is estimated to be 4% per year.
Data from Deviri (J Am Coll Cardiol, 1998; 32:1410-1417 )
*Note statistically you are going to be right 3 times out of 4 if you diagnose thrombus over pannus
Pannus literally means a hanging flap of tissue. It is is a membrane of granulation tissue as an response to healing.It can occur anywhere in the body. When it occurs in the prosthetic valve tissue interface it has important consequences.It is same as excessive scarring , ( something similar to keloid formation ) .
Prosthetic valve thrombosis is usually a acute or sub acute event as thrombus formation rapidly deteriorates the clinical situation.Pannus brings a patient with the complaints of chronic progressive dyspnea.(This rule is very subjective but . . .)
Time is the major determinant. minimum period required is 12 months. It is a avascular mass.It should be noted a injured pannus can predispose a thrombotic process and a chronic thrombus can trigger intravascular growth factors that promotes pannus growth.
The pannus grows , usually in the tissue valve interface.It tracks and creeps along the suture lines .Generally this does not encroach the valve orifice or chamber sapce , but occasionally the hanging edges can hit upon a leaflet.This is more common with tilting disc on the side of minor orifice. When excessive it can make a valve leaflet almost standstill.
Is relatively uncommon as the dynamic ball periodically interrupts the process of pannus in growth within the orifice.
Why is recognition of pannus important ?
Prosthetic valve thrombois is amenable to thrombolysis and it should be proptly differentiated for pannus.This is many times a difficult excercise, but the above observation will be helpful.
Further reading
Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology- coronary care, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), tagged akinetic myocardium, cabg, dead myocardium, echocardiography, fdg glucose myocardial, left ventricualr dysfunction, myocardial viability, pci, pet scan for myocardial viability, post infarct angina, post infarct follow up, revascularisation, stress echo dobutamine stress echo, stunned myocardium what is myocardail viability, viability studies on March 15, 2009| Leave a Comment »
Post myocardial infarction revascularistation either by PCI or CABG forms the bulk of the coronary interventions world wide.There has been considerable controversy in selecting the patients for the procedure.
Certain basic rules are to be applied.
This dilemma is due to a simple fact
coronary revascularisation has a great impact in relieving angina but has less impact in reversing
left ventricular dysfunction
One of the rules written by the cardiology community over the past few decades has been
We must document viable myocardium before doing a revascularisation procedures on them.
This rule was self imposed , to prevent inappropriate revascularisation in post MI population.
So , a gamut of investigations (Both invasive and non invasive came into vogue) to identify viable myocardium in post MI population. Stress echo, Thallium-sesta MIBI, PET to name a few .
Even after liberal usage of these invesitgations , we realised , the confusion in the optimal selection of candidates for revascularisation has not settled.
In fact, the correlation between viabilty and subsequent interventional benefit is inconsistent .Not withstanding this issue ,cardiologists inspite of the negative results of OAT and TOAT trials , started opening or by passing any occluded vessel irrespective of viability status.
1.Why viable myocardium is viable even in the adverse compromised vascular environment ?
It is viable for the simple reason it has some capacity to be alive . By it’s inherent survival capacity (Survival of the fittest ) or it somehow gets the nutrients by cell to cell perfusion.
2. It is viable allright , why it is not contracting ?
Because , it is biochemically and metabolically alive (Can be documented by FDG PET scan mismatch ) but it can not synthesise adequate ATPs to make the muscle contractile.
3.”Viable myocardium is viable ” what more you want from it ?
Simple viability is not suffice . How to make it mechanically active and contractile ?
4.Is viable myocardium synonymous with ischemic myocardium ?.
No, it is not (Contrary to the popular perception ) .
5. Is it not common to find dysfunctional segments with good TIMI 3 flow ?. So what is the purpose to document viability ?
It is not suffice to simply document viable myocardium but it is an absolute necessity to prove this viable segment is also critically ischemic .
7.If angina is a sign of viabilty why most of viable myocardium is painless ?
This again confirms the fact , much of the viable myocardium in the post MI phase is not ischemic but” still dysfunctional” waiting for healing time. This concept was introduced with great fanfare* as stunned myocardium , 20 years ago , which was subsequently rejected my mainstream cardiologists , as this concept tend to restrict the freedom of interventionists. * Even though ,the concept was genuine and proven scientifically !
6.Are we certain , the viable , non contractile myocardium (Which we painstakingly document ) will get back the contractility once the segment is revascularised?
Absolutely not. (With lot of PET study doumentation ) This, we can not guarantee even in ischemic, viable segments , while in the non ischemic, viable segment it is all the more unlikely.
7. What are the chances of these viable but non contractile myocardium regain the contractility by natural course ?
Very significant chances .In fact every patient recover some LV function spontaneously over time .
Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology-ethics, Hemodynamics, Top ten in cardiology, tagged breaking news in cardiology, cardiology, cardiology breakthrough, cardiology of 2oth century, cardiology top ten, echocardiography, frusemide, great cardiology drugs, gruentzig, heparin, lasix, pci, prosthetic valves, ptca, statins, ten great inventions in cardiology on December 24, 2008| 1 Comment »
Selected on the basis of , impact on survival , relief of human suffering index and also innovation
10.Percuateneous interventions
9. Electrocardiography
8 . Hemodynamics of cardiovascular system
7.Fruesemide
6.Thrombolysis
5.Pacemakers
4.Defibrillation
3.Heparin
2.Prosthetic valves
1.Coronary care units
Concept of vascular biology
Statins
RF ablation
Nitric oxide
Total Artifitial heart
Echocardiography
Ten least important concepts and inventions in cardiology
Selected based on duplication of research, futile scientific concepts and of course impact on survival
10.Low molecular weight heparins
9.Cardiac resynchronisation
8.Rotablator
7.Multi chamber pacing
6.Newer ARBs
5.C reactive protein
4.Three dimensional echocardiography
3.
Comments welcome and please contibute
Posted in Cardiology - Electrophysiology -Pacemaker, Cardiology -Interventional -PCI, cardiology -Therapeutics, tagged bmj, cardiac failure, cardiac resynchronisation therapy, care hf, circulation, combo device, CORONARY SINUS, coronary veins, cpmanion, CRT, desynchronisation, echocardiography, electrophysiology, ICD, jama, lancet, lv epicardial pacing, madras medical college, medtronic, miracle, nejm, prospect, resynchronisation, rethinq, st jude, tissue tracking on October 27, 2008| Leave a Comment »
CRT , cardiac resynchronisation therapy is being projected as a revolutionary treatment for cardiac failure , where a failing heart is rewired electrically through multiple leads and make it contract more effectively.The success rate of CRT was highly variable.The basic question here is, there should be a significant documentation of desynchronisation prior to CRT , for resynchronisation to be effective. Further , the sites of myocardial stimulation ( Coronary sinus/LV epicardial) , dose of electricity and the sequence of stimulation and the electrical delay are very critical. Achieving this into perfection is not a simple job and is real rocket science ! ( If we can achieve 5 % of what the normal purkinje network do within the LV we can term it a huge success.) Let us hope we catch up with nature . Finally , it is ironical the sites of LV pacing , electrophysiologists select currently is infact not selected by them but pre selected by the patients coronary venous anatomy ! .So as on date , one can imagine how scientific this treatment could be !
Initially it was adviced for patients with only wide qrs later for even normal qrs patients.When people started using it indiscriminately insurance companies started to rethink and thus came the RETHINQ study in NEJM and brought a full stop to CRT in normal qrs CHF.
It is a million dollar question. So millions of dollars were spent to identify the correct tool to identify the true responders to CRT.Echo cardiography with sophisticated methods tissue doppler, tissue tracking and , 3 D echo ,velocity vector imaging were done .These methods are not only costly but also time consuming and hugely expertise driven.
This simple question was addressed in PROSPECT study in circulation
Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), tagged cardiac failure, cardiology, diastolic dysfunction, dyspnea, echocardiography, orthopnea, pnd, postural diastolic dysfunction on August 1, 2008| 2 Comments »
Orthopnea is a classical sign of established CHF.
While paroxysmal nocturnal dyspnea is an early sign of cardiac failure,orthopnea is a late manifestation of cardiac failure .This symptom was mainly attributed to volume displacement from systemic venous to pulmonary circulation when the patient goes to recumbent posture.The exact mechanism of this has been speculative. Now with liberal usage of bedside echocardiography, we have found out there is postural variation in the diastolic function of the failing left venticle.
Many patients develop a restrictive ventricular filling pattern in recumbent posture (Grade 3 diastolic dysfunction). While sitting up some of them revert to normal or downgrade to grade 1 diastolic dysfunctionThis observation proves another fact that every patient with severe systolic dysfunction also has significant diastolic dysfunction at some point in their course of illness.
Dr.S.Venkatesan MD 