Japanese cardiovascular society publishes this journal called as “Circulation journal” It has some great articles in every Issue .The Impact factor is consistently rising.
Please do not get confused with AHA’s “Circulation”
Posted in cardiology journal club, cardiology journals | Tagged cadiology journal list, cardiology journals, circualtion, circualtion journal, japanese cadiovascualr society, japanese circualtion journal | Leave a Comment »
There are thousands of forums for medical science.
Most are aimed at research. Few are available to scrutinize research.
“Cardiac safety research consortium “
This one from Duke university , is a great beginning in collaboration with FDA .
Let us welcome , this whole heartedly and wish all success in it’s motto !
Namely , exposing all safety issues in the modern cardiac therapeutics .
Posted in bio ethics, cardiology -Therapeutics, cardiology-ethics, Uncategorized | Tagged cardiac safety research consortium, cardiology, csrc, dcri, drsvenkatesan, duke university, ethics in cardiology, fda | Leave a Comment »
Learning (and of course unlearning! ) is a continuing process in the field of medicine. . We have exclusive medical universities for various specialties . The popularity of radial access for doing coronary interventions is progressing very fast and the femoral puncture technique is expected soon to become extinct !
Here comes a virtual on-line university for mastering radial artery interventions.
I wonder , they issue a Master’s degree on the subject !
Thanks to Terumo for initiating the concept .
Posted in Cardiology -Interventional -PCI | Tagged arrow radial kit, radial angiogram, radial aretery, radial artery spasm, radial force, radial pci, radial primary pci, radial vs femoral, radialptca, ulnar angiogram | Leave a Comment »
This article is in response to the prevalent belief about primary PCI for STEMI endorsed by world cardiology forums. (Caution: A highly personalized version)
Time window in STEMI
- Is the window half-opened or half closed ?
- Is it open at all ?
- Or ,does it open only for primary PCI ,and tend to close down bluntly for thrombolysis
Modern medicine grew faster than our thoughts .We have witnessed the audacity of advising arm-chair treatment for MI till later half of last century . Now we are talking about air dropping of patients over the cath lab roofs for primary PCI.
Still ,we have not conquered the STEMI. While , we have learnt to “defy death” in many patients with cardiogenic shock , we continue to lose patients(“Invite death “) in some innocuous forms of ACS due to procedural complications and inappropriate ( rather ignorant !) case selection.
Note : The ignorance is not in individual physician mind , it is prevalent in the whole cardiology knowledge pool.
The crux of the issue for modern medicine is , how to reduce risk in patients who are at high risk and how not to convert a low risk patient into a high risk patient by the frightening medical gadgets.
In other words , arm chair treatment for STEMI was not (Still it is not !) a dustbin management . It has a potential to save 70 lives out of 100. What many would consider it as , nothing but the natural history of MI .
Medical management of STEMI is ridiculous !
That’s what a section of cardiologists try to project by distorting the already flawed evidence base in cardiology. Some think it is equal to no treatment. Here we fail to realise, even doing none has potential to save 70 lifes out of 100 in STEMI who reach the hospital.
Out of the remaining , 10 lives are saved by aspirin heparin (ISIS 2) and the concept of coronary care . Another 7 lives are saved by thrombolysis (GUSTO,GISSI) . PCI is shown to save saves one more life (PAMI).The remaining 6-7 % will die in CCU irrespective of what we do .
Of course , now medical management has vastly improved since those days . A thrombolysed , heparinsed , aspirinised , stanised with adequately antagonized adrenergic , angiotensin system and a proper coronary care ( That takes care electrical short-circuiting of heart) will score over interventional approach in vast majority of STEMI patients.
Now comes the real challenge . . .
When those 70 patients who are likely to survive , “even a arm-chair treatment“, and the 20 other patients who will do a wonderful recovery with CCU care , enter the cath lab some times in wee hours of morning . . .what happens ?
What are the chances of a patient who would otherwise be saved by an arm-chair treatment be killed by vagaries of cath lab violence ?(With due apologies ,statistics reveal for every competent cath-lab there are at least 10 incompetent ones world over !)
In the parlance of criminology , a hard core criminal may escape from legal or illegal shoot out but an innocent should not die in cross fire , similarly , a cardiogenic shock patient with recurrent VF is afford to lose his life , but it is a major medical crime to lose a simple branch vessel STEMI (PDA,OM,RCA ) to die in the cath lab, whom in all probability would have survived the arm chair treatment.
Why this pessimistic view against primary PCI ?
Yes, because it has potential to save many lives !
Time and again , we have witnessed lose of many lifes in many popular hospitals in India , where a low risk MI was immediately converted to a high risk MI after an primary PCI with number of complications .
I strongly believe I have saved 100s of patients with low risk MIs by not doing for primary PCI in the last two decades.
*The argument that PCI confers better LV function and longterm beneficial effect is also not very convincing for low risk MIs .This will be addressed separately
The demise of comparative efficacy research.
Primary PCI is superior to thrombolysis : It is agreed , it may be fact in academic sense .
Experience has taught us , academics rarely succeeds in the bed side.
“superiority studies can never be equated with comparable efficacy”
Only the questions remain . . .
- Where is comparative efficacy studies in STEMI ?(Read NEJM article )
- Why we have not developed a risk based model when formulating guidelines for primary PCI ?
- Is primary PCI for a PDA /D1/OM infarct worth same as PCI for left main ?
- Is high volume center guarantee best outcomes ?
Who is preventing comparative efficacy studies ?
Primary PCI : Still struggling !
This study from the archives of internal medicine tells us , we are still scratching the tips of iceberg (Iceberg ? or Is it something else ?) of primary PCI
Even a pessimistic approach can be more scientific than a optimistic !
When WHO can be influenzed and make a pseudo emergency pandemic and pharma companies make a quick 10 billion bucks , Realise how easy it is for the smaller , mainstream cardiology literature to be hijacked and contaminated .
Final message
Why we reverently follow the time window for thrombolysis, while we rarely apply it for PCI ? This is triumph of glamor over truth . The open artery hypothesis remains in a hypothetical state with no solid proof for over 2o years since it was proposed.
Apply your mind in every patient , do a conscious decision to either thrombolyse , PCI or none . All the three are equally powerful approaches in tackling a STEMI , depending upon the time they present .Remember , the third modality of therapy comes free of cost !
Never think , just because some one has an access to a sophisticated cath lab 24/7 , has a iberty to overlook the concept of time window !
Remember you can’t resuscitate dead myocytes , however advanced your enthusiasm and interventions are !
Realise , common sense is the most uncommon sense in this hyped up human infested planet.
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized | Tagged acc aha, acs, core cath lab, danami, door to balloon time, door to needle time, nejm, pami, pci for stemi, ptca for stemi, stemi, thombolysis vs primary pci, time window | 1 Comment »
VSD is the leading cause of congential heart disease .
- The natural history is hugely variable spectrum , from totally asymptomatic , incidentally detected in childhood to a fulminant cardiac failure and death in early infancy .
- Many small VSDs get closed by year 10. None of the large VSDs close spontaneously.Few of the moderate sized VSD may get closed.
- The site of the VSD is a major determinant of spontaneous closure. Muscular VSDs are more likely to get closed .Of course many of the membranous VSD have at least a rim formed by a adjoining muscular septum
- Associated defects, RVOT obstruction and late onset AR also has a influence on the natural history.
- Progressive PHT leading onto Eisenmenger syndrome occurs has become a diagnostic curiosity in many countries .
It is natural to expect the VSDs to share a close relationship with the conduction system which fights for “equal rights” to occupy the inter ventricular septum , (In spite of a defective septum ! )
How often we see conduction defect in VSDs ?
It is rather surprising to note conduction defects are not common in VSDs .In fact it can be termed rare . How this is posssible ? VSDs , however large it maybe , usually spares the conduction system . This is simply due to the fact , developmentally the two systems , ventricular septum and the electrical system of the heart comes from different embryological focus and and are simply anchored together.
If the IVS is not formed properly ,the bundle of His and it ‘ s major right and left branches are simply displaced and not are destroyed , they tend to occupy one of the rims of VSD
*Further, a VSD located peripherally and distally towards the apex has little impact on the conduction tissue as it has already fanned out and small little twigs are affected ,while central , proximal, and basal VSDs can have more significance .
Classically , it has major significance for the surgeons than cardiologists , as post operative blocks are more common than the preoperative blocks !
What are the changes to the conduction system in various VSDs ?
Membranous VSD
- Migration of A-V node posteriorly toward crux of heart *
- His bundle courses along the posteroinferior rim of defect
* This makes sure the compact AV node never comes into picture of VSD . It also it explains the rairty of complete heart block due to mechanical damage to the AV node by the VSD jet
How to avoid injury during surgery ?
Sutures are made a few millimeters from postero-inferior rim, Do not penetrate the septum. Suture along RV side of the septum as the His bundle is often located on the LV side of muscular septum.
RV approach to close VSDs, make postoperative RBBB a common issue but generally it has no great clinical significance
Location of conduction defect in various VSDs
- Membranous VSD – Conduction tissue runs along posteroinferior border of defect
Muscular VSD - (Especailly with Inlet extension) – conduction tissue is anterosuperior to defect
- AV canal defects . This is the only type of VSD where serious defects of conduction occur .Interruptions can also occur in the AV node.
Coming soon . . .
Where will the conduction system run in single ventricle where there is no IVS ?
Posted in Uncategorized | Tagged conduction system in vsd, post vsd closure blocks, rbbb after vsd closure, rim of vsd and bundle of his, venticular septal defect, vsd | 2 Comments »
Many believe modern science is pure and uncontaminated.
I wish it to be true , But reality mirror tells a different story !
The following “spheres of knowledge” collectively form the cardiology literature .
How much ? each sphere , contribute is any body’s guess !
The same rule might apply in all medical specialties.
Readers are argued to add more spheres of knowledge.
The seventh sphere may be Eg : “Commerce based cardiology “
Posted in Uncategorized | Tagged cardiology, comon sense based cardiology, ethics in cardiology, evidence based cariology, evidence based medicine, experience based cardiology, ignorance based cardiology, knowledge disease | Leave a Comment »
The funny thing in medicine is , simpler the question , greater the difficulty to answer ! f Clopidogrel is an irreversible blocker of platelet aggregation . It probably , is one of the top cardiovascular drugs used currently .It came into human domain as an aspirin killer and failed miserably , and currently piggy packing on the ageless aspirin for it ‘s action. The concept of dual antiplatelet agent is a classical example . The fact that , Clopidogrel can rarely be used as a successful mono anti platelet agent while aspirin can do this job with flying colors will unmask the secrets of antiplatelet drug industry .
Do you know , this drug which is considered as a great antiplatelet drug , does not even, pass the basic test of prolonging the bleeding time in a consistent fashion ?
Still , we are not clear why it does or does not increase the bleeding time in vitro or vivo in linear fashion.We have confirmed this in simple bedside experiments. (More dogmatic conclusions can be drawn in bed side , than those double-blind studies) . In many patients 300 mg of clopidogrel failed to prolong the bleeding time even by few seconds ! Surgeons who operate on clopdogelised patients differ widely in their experience when they do emergency surgeries on them .
The issue is very vital , Questions raised are critical !
- If clopidgorel has a notoriously unpredictable impact on prolonging bleeding time , Then , is it not dangerous ? , for those millions of patients with DES(Drug eluting stents ) who live at at the mercy of clopidogrel’s erratic behavior.
- Cardiology community never got shocked , even as in this era of evidence based cardiology , a drug which is being used for over 10 years without even a basic monitoring strategy for it’s efficacy.
- Such is the scenario , it is not at all a surprise , to find a huge population of DES patients who dial 911 or 108 with sub-acute sent thrombosis due to clopidogrel failure and resistance.
Read this article published in one of the prestigious cardio thoracic journal and comprehend yourself about clopidogrel’s controversy .
Final message
End of life , is looming large on Clopidogrel , but it has done it’ s intended mission : Increasing the basic cost of cardiovascular care in general population .
A costly and a dubious equivalent to Aspirin wrote a phenomenal success story in the narrow lanes of medical wall street !
No doubt , it will face the same fate as Ticlopidine , Prasugrel has just landed to repeat the same old story !
The easiest job to do in this wold is to fooling around the public
and it is an irony medical professionals and their patients are often
the victims
Read also the herd mentality in medical science
Posted in Uncategorized | Tagged antiplatelet drugs, aspirin vs clopidogrel, aspirin vs ticlopidine, bleeding time and clopidogrel, charisma, charm, clopidogrel, clopidogrel vs prasugrel, cure, cure pci, prasugrel, ticlopidine vs clopidogrel | 1 Comment »
Digoxin is a wonder cardiology drug used for more than a century.We know the pioneering efforts of William withering in detecting the potential of the unknown herb Foxglove.
Mechanism of action
The beneficial effects of Digoxin is attributable to
- Positive inotropic action
- Vagal action
Digoxin blocks the sodium potassium ATPase in the myocyte cell membrane .
This cause accumulation of NA + ions within the cells. The excess Na , then facilitates the Na -Ca exchange port .
This pumps in more calcium into the myocyte.
Increased calcium means more forceful contraction and that is positive inotropism* .
* This is a highly simplified version of Digoxin’s action . It should be remembered simple availability of excess calcium can not guarantee contractility, as it requires adequate number of receptors.
Digoxin is used in which type of cardiac failure ?
Digoxin is used for both for LV and biventricular failure .
Digoxins is still often in isolated RV failure of any cause (Cor pumonale, PPH, Eisenmenger etc)
Digoxin and RV dysfunction
Digoxin has a tendency to hit the atrial muscles at random causing multiple short circuiting (Micro reentry ) forming a perfect nidus for complex atrial arrhythmias including MAT .The coexisting hypoxia (which is all the more common here ) aggravates the problem .
Inotropism of RV : Does it really exist ?
It is often quoted , RV is a passive pump. It does not mean inotrpism is an exclusive property of LV.
RV has to generate about 30mmhg to pump the blood into the lungs.
In cor-pulmonale the RV works against an afterload of around 50-70 mmhg , making RV inotropism much more important concept.
Rate control in atrial fibrillation Digoxin lowers the heart rate by vago mimetic action , primarily in AV node and to a certain extent in SA node .Ventricular rate reduction is the prime requirement in the management atrial fibrillation and this property is still the crowing glory of Digoxin.
Though beta blockers and verapamil can be used as rate controlling agent , lack of negative inotropism makes digoxin prevail over , especially in severely dysfunctional ventricle .
But , one disadvantage of Digoxin is , since it requires a vagal traffic to mediate it ‘ s rate controlling effect , it is less effective , when there is high sympathetic activity as during exercise.
What is the action of digoxin on interventricular septal contraction ?
Digoxin , simply does not know where it acts when administered in cor pulmonale ! We believe in cor-pulmonale the maximum action would be the area of maximum dysfunction .This is purely an assumption. In cor -pulmonale septum shifts it’s loyalty from LV to RV as the later is the distressed chamber.So , logic would be there is a theoretical compromise of LV function in patients with cor -pulmonale. These factors make the inter ventricular interaction and dependence a complex one.
Some believe the improvement of sub clinical LV dysfunction in cor pulmonale may be more important factor in giving relief to the patient’s symptom.
What are the other RV inotropes ?
Doubtamine has some RV inotropy .This again may be due to a spill over effect from LV rather than a primary RV inotropism .
As such , there is no great breakthrough in creating a powerful isolated RV isolated RV inotropic dug.
Probably the best way to give relief to RV is to reduce the pulmonary artery pressure as invariably sever PAH is the predominate accompaniment
(Nitric oxide , Epo prostenol etc)
Final message
- Digoxin , indeed has some useful role in cor- pulmonale .
- But ,the benefits are more pronounced in late stages of RV failure.
- Since the dose required to get an optimal RV inotropy is high the safety margin is reduced.
- Since there is a propensity for complex atrial arrhythmias , it has to be used very cautiously in management of atrial fibrillation due to cor pulmonale .(Than in other forms of AF)
Posted in Cardiology - Clinical, Cardiology-Arrhythmias, Infrequently asked questions in cardiology (iFAQs) | Tagged atrial fibrillation in copd, corpulmonale, dig trial, digoxin, digoxin in cardiac faiure, digoxin in cor pulmonale, lanoxin, mat, rate contrl in af, rv lv inter dependence, vagal action of digoxcin | Leave a Comment »
AV nodal reentrant tachycadia(AVNRT) is the commonest mechanism of SVT. It is divided into slow-fast, fast-slow, slow-slow , representing the two limbs of he circuit.
Slow -Slow circuit is the rarest type of AVNRT. It should be appreciated , the scientific validity of slow-slow circuit is applicable only in relative terms . A virtually similar antegrade and retrograde limbs with identical conduction velocity and refractory properties , can neither initiate nor sustain an AVNRT.
Caveat in the definition of slow -slow AVNRT.
Even though , we call it a slow-slow tachycardia , one of the limbs need to be faster than the other. So , every slow -Slow AVNRT in reality will have two types
- Slow- Slow ( Still , faster than antegrade slow) mimic a slow-fast physiology
- Slow( Faster than retograde slow ) -Slow closely mimic typical fast slow .
Implication for electrophysiologists and points of contention for the ablationist !
- In Slow -Slow AVNRT ablation we do not know exactly , which of the slow pathway is being ablated , unless we specifically analyse the post ablative data.
- Very often it is not done.Every one in the lab is happy , for breaking the tachycardia circuit. Only after the procedure is over , we may realise the tachycardia is not really killed as it finds an alternate highway to complete the short circuiting of heart.
- We need to suspect this type of AVNRT prior to the procedure .Electrophysiologist shall spend little more time and a wide area ablation done , in the vicinity of coronary sinus ostium can be attempted. .
It is not a smart practice to advocate wide area ablation as a routine protocol in all AVNRT
as it directly increase the rate of complication >
Final message
A hurriedly done slow pathway ablation which may temporarily terminate the AVNRT ,only to recur later as the retrograde slow pathway may again form a substrate .The area of slow conduction acts as a turnaround gateway and capture the retrograde fast pathway which could be available in plenty in the anterior aspects of AV node . (Note : The unablated slow pathway now form the antegrade circuit )
Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics | Tagged avnrt, avrt, dual nodal physiology, electro physiology, fast pathway ablation, fast slow avnrt, RF ablation, slow -slow avnrt, slow fast avnrt, slow pathway ablation, svt | 1 Comment »
Regional wall motion defect( WMD) is the hall-mark of myocardial infarction.It can vary between complete akinseia to mild hypokinesia.
The wall motion defect is a gross terminology which is used to describe any abnormal motion of the ventricular segments.Technically, hypo, hyper , dyskinetic , akinetic , even any vigorous movement of LV segments will also come under the general category of wall motion defects. For example in extensive anterior MI the posterior segments show vigorous contraction.Though . this compensatory motion benefits many , it has a potential to adversely stretch the scarred myocardium and promote aneurysm formation
What causes the regional wall motion defect ?
- Infarcted segment
- Ischemic segment
- Adjacent normal segment behavior (Piggy pack effect, )
- Loading conditions
- Heart rate
Finally , and most importantly the timing and arrival electrical signal to these ill-fated segments determine the sequential activation fronts. Wall motion defect is a more complex phenomenon than we would tend to believe.
What are the the classical examples of electrical wall motion defect ?
- LBBB
- Pre excitation
- Some forms of VPD
*LBBB causes a paradoxical septal motion with reference to lateral fee wall contraction.It is still a mystery , this paradoxical motion does not cause any mechanical disadvantage in structurally normal hearts .
WMD in combination of LBBB and STEMI
We know , LBBB due to ischemia or infarct carry a sinister prognosis .
Here , there is “Double wall motion defect” . One electrical and two ischemic . We do not know , how LBBB influences the ischemia/Infarct related wall motion defect and vice versa. . This is the reason , there is a large chunk of poor or non responders for cardiac resynchronisation therapy.
Can peri infarction blocks and other non specific intra ventricular conduction defects alter the sequence of ventricular contraction ?
We do not know .It is distinctly possible.Tissue doppler studeis have indicated this.
What is the influence of heart rate on the of Wall motion defect ?
An otherwise insignificant regional wall motion defect could be amplified with tachycardia . Paradoxically , (as in a biphasic response to dobutamine stress test ) a significant WMD may be attenuated at a particular heart rate. So, the influence of HR on WMD is as simple as it could be ! ! !
Which is the best time to assess LV function after MI ?
Considering these issues , LV function assessed at discharge , may not give us the exact quantum of muscle damage. 4 weeks may a reasonable time frame . This is important in the current era as presence of significant LV dysfunction becomes an indication for revascularisation .We can’t be offered, to err on this vital LV functional parameter.
Final message
WMD is a combination of electrical, mechanical , structural, alteration in response to variety of myocardial insults.It is very hard to assess individual components contributing to the net WMA. The easiest and surest way to quantify WMD due to muscle damage is to do a deferred echocardiography , when all time related WMD ( Ischemic stunning , perinfacion block ) disappear.
Coming soon
Diastolic wall motion defects .Is wall motion defects exclusive phenomenon of ventricular systole ?
No , definitely not. Regional relaxation abnormalities are quiet common .it is poorly recognised .
Posted in Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs) | Tagged wall motion defect | Leave a Comment »
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