The stretch and strain experienced by the action potential’s left shoulder region is almost similar* in both long and short QT syndromes that trigger a VT.(* Hope this explanation makes some electrical sense !)
*Click over the image for high resolution
Posted in Cardiology - Electrophysiology -Pacemaker, Infrequently asked questions in cardiology (iFAQs), Long and Short QT syndromes | Tagged how short qt syndrome induce vt, long and short qt syndromes, Mechansim of VT in long and short QT syndrome, short qt syndrome | Leave a Comment »
Time is muscle. This quote became sort of ” cardiology sermon” in the last few decades .Cardiologist think they stand on a 100 meters sprint track once a patient with STEMI arrives .This is indeed true , if we agree time is muscle and our urge is to reduce the door to balloon time .Please remember , this rush matters much , only if the patient comes through very early when the muscle is really getting damaged . (No issues . . . even if the fire engine comes in slow motion if the house is burnt fully !)
Time is muscle agreed . . . but muscles are kept alive by factors other than time ! So muscles can defy time if God is willing !
Time is one of the important components of management of STEMI. Other things matter too ! Age , baseline co-morbidity , underlying extent of CAD, collateral support of IRA territory , and finally individual variation in hypoxic damage in myocyte is (Rarely been studied in detail.)Door to balloon time for a patient who lands up within 1 hour window need to be much different from a patient who comes at 10 th hour .The issue is important because we use a procedure which requires delicate decision-making ,(IRA-Non IRA issues etc) the results can be sub optimal , and even be hazardous in low risk STEMI . So , door to balloon time may be a less important component of time window in a patient who comes after 6 hours .This is the reason overall outcomes are not changing in a large cohort of rapidly performed PCI.
The presumed absolute relationship between “Time and muscle” concept is always been a suspect . This is proven by a flawless study from NEJM .
http://www.nejm.org/doi/full/10.1056/NEJMoa1208200
This study should infuse more sense to us , time and again, we are hijacked and sedated by high dose of pseudo scientific concoction .In fact , indiscriminate rapid PCI may not be in the good interest of all patients with STEMI , if it is not properly done .Without realising this fact many developing countries are indulging in extravagance of costly STEMI programs wasting the exchequer.
This landmark NEJM paper convincingly underscores a fact that achieving rapid door to balloon time is not going to be the game changer in conquering the Global STEMI championship . We have to take the coronary care into the streets or to their homes as well .This is where the pre-hospital thrombolysis will emerge in a big way in the future .
A slow and steady thrombolysis beats a fast and furious primary PCI on any given day in all uncomplicated STEMI .This we have proven for over three decades in one of the India’s largest coronary care unit .( Where is the data man ? Genuine experience is data . Why we require , the act of publication to convert an experience into evidence . Often times , I would feel , data is the most unscientific word in medicine . Many Truths lack evidence , false hoods come with plenty ! For all those scientific homo sapiens , please recall 70 % of ACC/AHA class 1 recommendations are backed by level C evidence ie simple opinion from perceived experts! )
Final message
A fast and furious primary PCI may not be the answer in all STEMI population
Thrombolysis can be done with near zero time delay , it does not require special expertise where an ambulance driver can reperfuse a myocardium without much fuss and glamor ! He does not have to split his hair to identify which is the IRA in a complex multivessel STEMI as well ! The streptokinase and TPA will home in to the target site smoothly and swiftly .
If indeed , time is the major factor in STEMI , we have many other ways to tame the time . If muscle is more important than time , pPCI is rarely the answer !
Some India specific thoughts
Is it not a shame , we talk about primary PCI for all our patients who do not even get timely Aspirin* after a STEMI! .It is something akin to what we witness every day , as our country folks wield touch screen Androids . . . conversing in open air toilets !
* While the importance of Aspirin is undermined , It is different story altogether , these patients get sorbitarate promptly whenever they get chest pain (mis-placed and dangerous priority ! ) prescribed by the roaring GPs , who suffer from discontinuous medical education , propelled by the deeply penetrated 1000 crore oral Nitrate market .
And STEMI workshops are conducted by self-proclaimed experts every few months in posh 7 star hotels all over India .
Posted in Cardiology -guidelines, Cardiology -Interventional -PCI, Cardiology -unresolved questions, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), STEMI-Primary PCI, Two line sermons in cardiology | Tagged components of time window, door to balloon time, door to needle time, management issues in stemi, nejm time window, primary PCI vs thrombolysis, stream study stemi, streptokinase vs primary pci, symptom to door time, time windows in STEMI | Leave a Comment »
Anterior mitral leaflet has a classical M shaped motion. Infrequently , M mode echo will record a triphasic pattern .
The exact answer is not known . I guess it is a normal variant.
Often it is recorded when there is a long and redundant AML , especially if the M-mode cut is too close to the tips.
Though it is not common , I have seen in few the triphasic gets converted into classical M shaped pattern if the cursor is moved slightly away from the tip of AML.
Relationship to Heart rate
Some times it appears in slow heart rate and tends to disappear with tachycardia .
Triphasic Doppler filling vs Triphasic M-Mode
We do not know yet , how the triphasic AML motion correlate with triphasic Doppler filling pattern which is considered a fairly good evidence for LV dysfunction.
Posted in Cardiology -unresolved questions, Echo library and gallery, echocardiography, Infrequently asked questions in cardiology (iFAQs) | Tagged aml motion in m mode echo, anterior mitral leaflet motion, m mode echo, M Mode of mitral valve, m sahped m mode echo mitral valve, triphasic aml motion, triphasic mitral valve motion | Leave a Comment »
The pericarditis of acute rheumatic fever is not a true infective pericarditis.It is more of inflammation .It is primarily T cell mediated reaction . Neutrophils rarely take part in this inflammation and hence no significant exudation . Hence , there is less sticky and adhesive molecules inside the pericardial space .The most inflamed layer is epicardium which a nothing but visceral pericardium .This layer lacks the tensile strength to constrict the underlying myocardium.
For constriction to occur the fibrinous ( thick ) layer of pericardium need to be involved . In rheumatic fever even though it is pancarditis , fibrous layer is not involved. Further the inflammatory gradient is thought to spread from within (Unlike tuberculosis )
Note : In chronic tuberculous pericarditis, diffuse inflammatory process invade from the exterior surface . Very often , one can not differentiate layers. In extreme cases even myocardium and pericardium can not be separated .
Summary
The peri-cardial effusion of acute rheumatic fever
Other lingering questions
1.How common is tamponade in acute rheumatic fever ?
2.How important is the mass of the effusion (Viz a Viz Intra pericardial pressure !) in causing tamponade ?
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Posted in acute rheumatic fever, constritctive pericarditis, Infrequently asked questions in cardiology (iFAQs), pericardial disease, rheumatic heart disease | Tagged acute rheumatic fever, fibrinous pericarditis, jones criteria, mechanism of pericarditis in acute rheumatic fever, pan carditis, serous pericarditis, why constriction and tamponade occur rare with rheumatic pericardial effusion, why contrictive pwericarditis is rare in rheumatic fever ? | Leave a Comment »
In this mean world ,most truths exist without evidence . . . and often falsehoods masquerade as truths with overwhelming evidence !
Human biology has always been a mystery and can express in dramatic ways . While , many disorders combine to play havoc on the body , few tend to protect each other. HT and DM can join a deadly coalition to attack the heart .Smoking causes extensive peripheral vascular disease , still thrombo angitis of coronary arteries ( due to smoking ) is virtually unknown. Tuberculosis does not have the courage to attack the heart valves , while it can inflict serious injuries all over the body . Similarly , systemic hypertension and Rheumatic heart disease does not combine well . So , it can be assumed some unique and hidden protective factors are at play among different pathological entities and their target organs.
A brief account of how COPD could be related to CAD ! (* Mostly Imaginary !)
We know , COPD , stresses the right ventricle by pressure overload and in extreme situation affects the LV function because of hypoxia. It rarely impacts the coronary artery disease . This has been our consistent observation. While COPD patients often land up with LV dysfunction , investigations reveal they are more of a dilated cardiomyopathy and their coronary arteries are entirely normal. Diffuse atherosclerotic CAD is a rarity in patients with history of bronchial asthma. Coronary micro circulation is also observed to be largely intact in most people with COPD .
We haven’t got a call from our pulmonology wards in many decades , for a true emergency coronary consult . Mind you ours is a 200 year old Institution , with 3000 beds , largest east of Suez canal !
It’ s very rare for bronchial asthma patients to die of a cardiac event. Thousands of elderly patients throng our ER with acute severe asthma every winter , still extremely rare to precipitate an acute coronary event !
We are yet to see critical triple vessel disease in a patients with documented bronchial asthma and COPD . Even non-critical CAD is far less frequent in COPD vis a vis general population . It is indeed a strange observation , considering both entities are rampant in the community .
What could be mechanism for the perceived disconnect between COPD and CAD ?
Is it a myth ? Does it happen in all geographical zones ? If hypoxia is the sine qua non of COPD , one would rather expect a close association with CAD , isn’t ?
One suggestion that keeps erupting from my cortex . It is the wide swinging intra thoracic pressures in COPD or asthmatic individuals . . . somehow responsible . These wide swings of pressure are transmitted to aortic root . They transform into good coronary perfusion pressure , keep the vessels clean by pressure vacuuming effect .
We have asked our epidemiological unit to analyse the 25 year data from our coronary care unit to decode the mystery .
Counterpoint
Meanwhile, a diagonally opposite question was asked in UK and found a partial proof as well . Our experience do not agree with this study conclusions .
What is your take on the issue ?
http://ije.oxfordjournals.org/content/33/4/743.full.pdf+html
Introspection
How can a opinion (rather an Imaginary essay !) based on personal observation projected as a scientific fact ? We need to observe , analyse and publish the data . This is what the scientific world expects us to do . Unfortunately , the journey form observation into publication has been kept purposefully difficult . In my opinion bulk of the international peer reviewed medical journals with high impact factor can convert any junk data into a scientifically palatable recipe !
Posted in Uncategorized | Tagged COPD and CAD, does copd has a protective effect on CAD | Leave a Comment »
The doctrine of modern medicine goes something like this . . .
For most medical problems , there would be a solution. Keep trying . . . till you get it !
*But , just make sure that problem on hand deserves a solution in the first place !
Modern medicine continues to remind us every day , the much hyped solutions often end up in new problems and many times worse than the original problem !
Oh ! what a great a quote ! When I was boasting myself . . . My wife reminded me , this is just plagiarized version of a 2000 year old Hippocratic thought !
Primum non nocere . . . first do no harm !
But , Hippocrates’ life was not contaminated with drug eluting stents, I pads, and BMWs
If Hippocrates arrives in cath lab today by BMW which sucks 50000 Rs EMI ,Everolimus coated coronary jewellery will definitely tempt him !
You can’t simply compare lives separated by 2000 years
. . . I told my wife !
Posted in Cardiology -guidelines, Cardiology -Interventional -PCI, medical quotes, Two line sermons in cardiology, Uncategorized | Tagged cath lab ethics, ethics in medicine, hippocrates, primum non nocere | Leave a Comment »
Inter atrial septal aneurysm is a benign disorder of IAS where the flap of fossa ovalis bulges on either to right or left atrium. It may be associated with fine fenestration or even a classical ostium secundum ASD.
An unusual buckling motion of IAS aneurysm.
Though the pressure within the atria is one of the determinant of this bulge.The morphology of the flap is such that it more often prolapse into LA than RA. Rarely it can be dynamic and moves 180 degrees , buckling between RA and LA .This unusual motion is real stress to IAS and can trigger atrial ectopic beats. and atrial tachycardia .
Read related article IAS aneurysm
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Posted in cardiac surgery, cardiology -congenital heart disease | Tagged bi directional IAS aneurysm, fossa ovalis aneurysm, ias aneurysm, Inter atrial septal aneurysm, ostium secundum asd and ias aneurysm | Leave a Comment »
Human physiology can dramatically surprise us.Here is a situation regarding K+ ion and cardiac function.
Low potassium level is a well known cause for skeletal muscle weakness and paralysis.While,in cardiac muscle usually the opposite happens.It is the high potassium levels that depresses and cause paralysis.(That’s why,it is used in cardioplegic solutions. )
But,the classical differences between skeletal and cardiac muscle need not apply in critically low levels of K +
What happens when K + is critically low ?
We know, K + is the vital ion that maintain not only the membrane potential ,(Recall Nernst potential ) but also keeps the action potential floating and dipping with every beat.
Imagine the intracellular chaos when these ion levels changes in dramatic fashion . (Of course,God has ensured very tight regulatory controls at various levels within each cell ! )
However , ECG changes are expected 100 % of time with falling K + especially below 3meq.Surprisingly , low K + levels have little mechanical impact.(Or is it our ignorance,considering the fact , cardiac electrical mechanical activities are tightly coupled?)We have to find answer from patients like this .
A 30 year old women came with breathlessness and fatigue and her ECG.
Can we afford to miss a diagnosis of STEMI ? With all our collective wisdom STEMI was diagnosed promptly . . . of course wrongly !
She was adviced streptokinase.A shrewd fellow who reviewed the old records spotted the past history hypokalemia , and Inj streptokinase was put on hold.(Lucky patient . . . she was not shifted to cath lab )
Her K + was 2.3 Meq. The LV function was significantly impaired with global hypokinesia, which improved with correction of K+.
She was later referred for nephrology work up , they had made a possible renal tubular disorder for the Hypokalemia.
Clinical Implication.
When potassium levels are critically low myocardial function may deteriorate.Here is a patient with dramatic STEMI like ECG with extreme hypokalemia.
Our ignorance regarding electrolytes and myocardial function remains unexposed .In critical care units wide swinging metabolic and electrolytic parameters are common.ECG is just a marker for these .Similarly all LV dysfunctions are not primary myocardial disorders (Sepsis, Hypoxia, Extreme acidois , Uremia ,drugs,toxin can lead to myocardial dysfunction.)
Experienced physicians do not form hurried opinion.Wait . . . allow things to settle down and assess again.After all ,there is long list of causes for ST elevation other than STEMI !
Reference
Posted in cardiology -ECG, Cardiology-Electrolytes, Electrolyte and Heart, Electrolytes and heart, Infrequently asked questions in cardiology (iFAQs) | Tagged effect of hypokalemia on ecg, hypokalemia and lv dysfunction, hypokalemia nd myocardial paralysis, hypokalemic periodic myocardial paralysis | 1 Comment »
Takotsubo cardiomyopathy is an unusual response of the left ventricle to extreme emotional stress .The catecholamine surge has a profound stunning effect of LV apex and a paradoxical hypercontractility of basal LV.
The exact mechanism is not clear , Following factors may contribute.
However , the most accepted mechanism is Endogenous catecholamine-induced myocardial stunning and microinfarction
Why is LV apex alone affected ?
Image Source- http://www.radiologyassistant.nl
The adrenergic receptor distribution is high in LV apex .They are exposed to high concentration and gets stunned easily . Basal LV has less adrenergic innervation , so it shows less of catecholamine toxicity , instead it exhibits. hyper-contractile mode. However, this rule is not absolute.
One more suggestion was apical balloons correlated with wrap around LAD.(Báñez B et all 2004)
Image courtesy Circulation December 16/23, 2008 vol. 118 no. 25 2754-2762
*Some consider ACS should never be linked to Takotsubo.But it is not easy to differentiate.(Carrillo JACC 2009) (Kosuge JACC 2010)
Reference from this site
A link to related article -Ischemic Takosubo from this site .
1.Báñez B, Navarro F, Farré J et al. (2004). Tako-tsubo syndrome associated with a long course of the left anterior descending coronary artery along the apical diaphragmatic surface of the left ventricle.]”. Revista española de cardiología (in Spanish; Castilian) 57 (3): 209–16
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Posted in myocardial disease | Tagged takotsubo cardiomyopathy, What is the mechanism of apical ballooning syndrome | Leave a Comment »
Dr.S.Venkatesan MD 