Who said this non-sensible statement? ( I guess ,this would be the first response from many cardiologists !) If you feel the same, then this post might not be for you.
Relationship between Ischemia and arrhythmia
While the relationship between Ischemia and VT is really complex, the term “Ischemic VT” itself adds more twists. Its all about timing, intensity of Ischemia , associated factors and finally the baseline arrhythmic risk that includes the mystery defects in myocyte gap junctions and ion channels.
Following are some of the observations.
Primary VT
This is the true Ischemic VT. Even here, it is the associated factors, like hypoxia or acidosis are the triggers which of course are resultant of Ischemia. There are further problems . Even critical Ischemia, as in high grade unstable angina, rarely Initiate a VT, while STEMI seems to have the exclusive rights to trigger it , by its ability to produce acute transmural ischemia . (Note: Whether primary VT occurs before or after myocardial necrosis is not clear) There is evidence to prove, susceptibility to VT at times of Ischemia is in the genetic make-up of ion channels, as pointed out by famous French electrophysiologist Haïssaguerre. (NEJM 2008)
Post Infarct VT : (24 hrs to 2 weeks ,an empirical criteria we use)
This can be called as Ischemic, still we ‘wouldn’t know whether the arrhythmia is originating from dead or live tissue. It can even be combined Ischemic-Scar VT
Late Ischemic VT
These are the typical scar – substrate -mediated ,micro/macro reentry VT .The strip of tissue on the border zones of conflict (between viability and non viability is always restless (Gaza strip of VT?) This is rarely amenable to revascularization, unless some one is able make that area 0% Ischemic , which is a highly improbable scenario. The alternate option is diagonally opposite .EP guys are empowered with a deadly solution, and authorized to shoot down focus (or isolate) instead of the futility of revascularisation. (Please note, this doesn’t work and should not be attempted in early ischemic VT, though few case reports of RF ablations during VT storm li- Juan Qu et al AMJS 2924 )
Final message
The relationship between Ischemia and VT is poorly understood, (rather than to say complex.) It is true ,acute Ischemic VTs has more closer relation with Ischemia, often settles down with prompt revascularization.
In chronic VT , shooting down the ischemic focus by ablation is more likely to extinguish the arrhythmia ,rather than revascularization. This is because partial revascularization irritates the viable myocardium and keep the ischemic focus active. ( Class C evidence) ICD though a revolutionary technology to prevent a SCD in these circumstance it makes a poor choice to reduce the arrhythmic burden .At best , it is just a back up device to tackle the escaped VTs in spite of RF ablation and drugs.
If you understand the pericardial anatomy fully, you can call yourself real master of clinical anatomy. (Ref 3,4) We know, it is a complex protective cover over the heart , that has three layers with a unique relation with one another. The outer one is tough conical bag .It has an embryologically distinct origin .It develops from septum transversum and sits over the diaphragm tightly, to which it shares the same embryological origin. While the inner serosal layer (rather cavity) splits into two layers and encloses the heart .Though this serosal layers develop from a different mesenchymal tissue , it is biological wonder both fuse in perfect harmony. , The developing heart bends, folds and loops within the serosal cavity.
The inner one embraces the heart fully forming epicardium (otherwise called visceral pericardium) and reflects back after covering great vessels .While reflecting back it is firmly attached to inner surface of fibrous pericardium forming the pericardial cavity . Never confuse parietal layer of serous pericardium with the thick outer fibrous pericardium, though both are gelled together. Since heart is not a strict globular organ, the hug of visceral pericardium over the heart is not uniform and complete , especially over the great vessels enter or leave the heart (Hilum of the heart). Hence it folds , and forms two sinuses and recesses.
What happens with pericardial Inflammation ?
Inflammatory pericarditis can occur in differential fashion. For example, the most common chronic pericarditis tuberculosis affects the fibrinous layer. Post MI pericarditis involves the epicardium. It is vital to understand epicardium is thin and transparent sheet of tissue , one may not split it from the heart. It is also important to know coronary arteries run under this thin visceral pericardium( ie sub epicardial) So anatomically , In constrictive pericarditis , the immediate target would appear to be the coronary artery , than the myocardium . But, what really happens ? Let us Introspect on this.
In CP which layer exerts the force of constriction ?
Macroscopically ,It would be a dramatic sight to see the heart caged within hard shell of pericardial mass. To be frank, we can never make a distinction between the three layers once its thickened. Which layer is the triggering force, that promotes adhesion and compression is also not clear. We presume, the thick fibrous layer is villain de chief. (This we learnt , by observing rheumatic heart disease pathology ,wherein pericarditis , never evolve into constriction as it doesn’t affect the thick fibrous layer) .The inflamed exudative pericardial fluid doubling up as a glue to stick all three layers is a true possibility.
Whatever happens, once the inflammation become chronic, it goes on steadily and begin to compress (rather restrict in diastole). At this stage, anti- inflammatory drugs like NSAIDS, colchicine or specific anti-tuberculous drugs along with a bit of steroids can arrest or slow down the pathological process and prevent this deadly disease. The phenomenon of transient constriction with normal thickness pericardium is also reported.
The normal and the pathologically thickened constrictive pericardium
The quantum of constrictive force widely varies in different areas of the heart. Obviously, the thickened pericardium hurts the heart in diastole . Right side of the heart is more vulnerable because of its thin wall and the low pressure beneath . However the constriction process continues over, anterior, lateral , posterior and even the AV groves The sinus the recesses can also become obliterated .
Does the coronary artery gets compressed ?
When the whole heart become as hard as a cricket ball , what do you expect the fate of coronary artery would be ? Fortunately, it escapes in many . But, the threat of compression or calcific (ice-berg) injury is always there. There has been many reports of patients with angina in CP (Ref 1). Here is case report from India , where a calcific pericardium exerts a vice like tightening over LCX. (Ref 2)
This is not surprising, when we know, at late stages the pericardium can even infiltrate the myocardium.
One important reason is , unlike myocardial bridge here the artery gets compressed in diastole , with a passive distending pressure from LV cavity rather than active constrictive force.(See the above video) The diastolic coronary arterial pressure rarely goes below intrapericardial space pressure , which in fact is obliterated. Still, the point to be noted is, mass effect can still result in non hemodynamic compression.
Final message
Fortunately, coronary arteries often escape from serious pressure effects of constriction but the threat is real especially in late stages .It can happen either by the calcific spurs in the pericardium or diffuse pressure effect or tight ring like localized constriction. While de-nova coronary Involvement is far less common, the operating surgeon needs to take extreme care to avoid it during surgery . Surgical pericardiectomy is either partial or total caries considerable mortality even today. Total pericardiectomy is myth at best. Few pieces of adherent pericardium are left over especially in the posterior aspect.
A set of attitudes, habits, or possessions associated with a particular person or group. and such attitudes, etc, are regarded as fashionable or desirable.
Final message
Communicable disease need not be an Infectious disease like covid. The word “Communicable” shall soon convey a new meaning, to the enlightened. Adverse life styles ,disseminated into the community that vigorously propagate CVD, has every reason to be referred to as a ‘Neo non-infectious pandemic”
Postamble
In the strict sense, CVD is not a communicable disease ,rather the risk factors are …but technically it is.
1.What is the response of RV to pressure overload ?
A. Dilatation
B. Hypertrophy
C Both occur together
D. Hypertrophy is the Initial response, followed by dilatation
Answer :
Since we believe RV’s behavior is generally opposite to that of LV , many would tick, dilatation as the first response. This may be correct when there is acute raise in RV after load, as in PE. However, It is surprising even in chronic pulmonary hypertension , the degree of RVH is not constant and homogenous .This is because , different parts of RV chamber has different wall thickness .Further, the pressure distribution from PA to RV is uneven. The co-existing TR confounds the loading conditions. It is not yet clear, how the RV would respond to raised PA pressure. In the bed side, we are seeing both flight(dilate) ot fight (RVH) reactions from RV (more often the former than the later) It is possible RV behavior is be pre-programed and built into the genes of the contractile proteins.
It is worthwhile to note, RVH is constant feature in non pulmonary hypertension related “after-load” conditions as in valvular or sub valvular PS. This is more to do failure of regression of RV mass early after birth, rather than the actual effect of high after load. Another point is purely technical. RVH is measured in RV free wall, in subcostal view in diastole and inspiratory phase.(upper limit is 4mm) Many of us could miss RVH in routine echocardiography unless specifically looked for.
2.Which is the first echocardiographic parameter to get impaired when RV fails ?
A. RV FAC (Fractional area change)
B.TAPSE
C. RV Ejection fraction
D.RV longitudinal strain
E. RV S‘
Answer : I am not very sure about the right answer , but TAPSE is last to get Impaired .(Still, we celebrate it like anything is a different story) Many believe transverse functional Indices like FAC is impaired early. and is less influenzed by the spurious spill over of Left ventricular contractile force in transannular plane (Which augments longitudinal functional Index like TAPSE),
The following illustration (From Ref 2 ) summarizes all RV functional parameter in a succinct fashion. Fellows must be familiar with at-least half of them.( RIMP is less practical and error prone can be ignored)
Though foundational and prodigious, moving beyond De-bakey ,Stanford is a necessity in the management of Aortic dissections in current times. The first step is to understand the perfect 3 dimensional anatomy of entire Aorta from its origin to bifurcation and even beyond. (The 11 or12 segment demarcation of aorta is well established and gained acceptance.)
This labeling tells us instantly about whether the dissection is A, B, or Indeterminate .It also reveal the origin of dissection, extent of dissection and the exit point, if available.
Naming & coding of Aortic dissection
Aortic dissection : Management cues
The above scheme is just a part of Initial work up with the help of MR angiogram or spiral CT. There are more critical factors like, clinical stability, time since dissection, false vs true lumen identification, its volume ,rate of propagation, branch involvement, mal-perfusion , etc need to be counted.
The curious Irony about this dreaded entity lies in the fact that in type A dissection, the surgical team need to be alerted well before they embark on this most complex cardiovascular emergency, usually in a state of the art CTVS unit. Meanwhile, most uncomplicated type B dissection demands total inactivity on the part of surgeon(as well as some cardiologists !) while the patients can be casually shifted to the intensive care ward, essentially for monitoring , bed rest and few drugs to reduce BP and shearing stress on aortic wall. The dissection can heal themselves.
The role of Interventional cardiology in Aortic dissection is evolving rapidly , still at best supportive or can buy time to bridge to surgery in some late presenting type A dissection. There has been lot of experience in some centers, where type B dissections are exclusively managed by scaffolding. But, the concern is, catheter based Interventions in low risk subsets of dissection is always a tricky decision.
Medical strategies should never be looked down upon as enemy of endovascular Interventions. So, one of the live and debatable issue is, how & where can we fit-in the hyper-talented endovascular Interventionists in the complex vascular arena of aortic dissection.
The contents of the this blog is being published as Kindle E book , as per the request of many of the readers. Every article will continue to be open source in this site. Again I shall reiterate the book format is not aimed at any commercial intent. It is only to facilitate learning in a single book format Here is the link to book https://amzn.in/d/euhL5vu
Click below to see who is watching this website live !
This site will never aim for profit. Still ,this donation link is added at the request of few visitors who wanted to contribute and of-course that will help make it sustainable .
Please Note
The author acknowledges all the queries posted by the readers and wishes to answer them .Due to logistic reasons only few could be responded. Inconvenience caused is regretted.
Dr.S.Venkatesan MD 