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 moleculesinside 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 .
The peri-cardial effusion of acute rheumatic fever
Is transient ,non infective and resolving (Unlike valvular inflammation !)
Less of neutrophil activation (Less adhesion)
It does not involve the thick , tensile fibrous layer of pericardium hence lacks the contractile force .
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 ?
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 .
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 .
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 !
Platelets are humble blood cells that roam in clusters and guard against any bleeding in internal organs. Though it has natural powers to regulate itself against aggregation at inappropriate sites , certain high risk individuals need to take these drugs to prevent cardiac event. Patients who harbor intra-coronary foreign bodies like stents need more intense antiplatelet regimens.
We have variety of antiplatlet drugs. Aspirin does it by blocking COX. It is irreversible .Clopidgrel does this differently by inhibiting P2 Y12 receptors .Clopidogrel has been used extensively in India. Some brands of it are many folds costly as well !
A curious encounter
A certain patient with a stable CAD, from higher strata of society was offended when I replaced his long term prescription of Plavix(Clopidogrel) with Aspirin.His major humiliation was this new drug costs just 50 paise ! He suggested to me , it is huge insult to him as his driver also takes the same medication !
What does pride do in platelet inhibition I tried to explain him ?
He was amused !
I asked him to go elsewhere , to any star-rated , upscale health suit nearby to fulfill his wishes !
The above event happened few years ago . I am just posting it from by diary .
In this unequal world , prestige comes to play even in illness and the drugs they take ! I wonder, how prevalent, is the issue of pride in our patient’s mind that decide the treatment modality in modern day medial care !
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 .
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.
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 !