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.
A 40 year old women with palpitation found to have complex multiple VPDs and elevated thyroid hormones.
The GP has refered for further management to a cardiologist, frightened by the morphology and frequency of VPDs.
The cardiologist has sent him to a EP guy .I guess he was not briefed well about the patient, and he decided to do , what he is best at .He tried to fix and shoot down the VPDs. The apparemt inappropriate procedure went on, as per the demand of patients and science . Now, let us question the basics .
The question is,
Where will be the focus of VPD in hyperthyroidism?
A. LV apex or septum
B. RVOT
C.Papillary muslce of LV or Intra -cavity
D. It is an invisble microrentry , or automaticity. Focus can be anywhere and can not be loclaised.
E. Technically there can not be a focus, it is simply enhanced adrenergic drive by free T 3 & T 4
Answer
There has to be a focus for every arrhythmia.It is my thinking. Some of my EP colleagues, say once circuit is established the focus looses it value . In systemic causes of cardiac arrhythmia , there need not have a visible focus. Make a Pardon , as of now , I can only frame a question, not the answer.
Final message.
Leave alone the answer to this question, I am sure every physician knows the correct treatment. Treat the cause, forget the manifestation. If some one is adamant he can do a RF ablation …not in the heart , but in thyroid gland.
Postamble
Even though , it is hyperthyroidism, we have a responsibility to rule out any tissue level substrate because, not every hyperthyroid patient throws this much of VPDs. It is highly possible, thyroid hormomes can un-mask a hitherto non -arryhthmogenic myocardial focus.
One of the foundational lessons in echocardiography is, How to measure the cardiac output ?
Echo formula for estimating cardiac output is
(HR X LVOT area X LVOT-VTI*)
* VTI (Velocity time Integral -a Link ) is complex sounding, but a simple parameter. It is expressed in CMs .In simple terms, it tells how many cm, the blood will move per second ? with a single ventricular contraction.
Such a simple calculation, why is it not popular among cardiologists. ? (Many ER physicians still use it effectively )
I guess being a humble and simple, works against it. It is surprising, the awareness about EF% is all to pervasive (which is a crude and load dependent parameter) while the info about stroke volume per beat finds difficult to enter bed side cardiology. Generally, we tend to trust complex things and ready to spend ( waste) lots of time with equations, such as in PISA, EROs , DVIs , PAPIs, , stroke work etc . Mind you the probability of error increase directly with number of factors you take in a calculation
The potential bed side usage of stroke volume data
1.Cardiac Index is one of defining criteria for cardiogenic shock. I rarely see my fellows documenting LV stroke volume in any major STEMI, that can detect an impending cardiogenic shock.
2. It will help assess the efficacy of inotropes .Find, objectively how much the Dobutamine really worked in LVF ? and correlate it with clinical assessment of S3, rales and BP. (Mind you BP is very poor surrogate marker. for stroke volume. )
3. More Importantly, Similar to LV stroke volume, we can measure RV stroke volume by RVOT area x VTI x HR. This can be of critical value in the management of RV infarct, where two ventricular stroke volumes often mis-match often. Once RV stroke volume equals the LV , we can presume recovery.
4.The enigma of high output cardiac failure can be studied with this simple formula.
5.In any mechanical assisted circulation LV, stroke volume is going to give important prognostic info.
6.Finally, assessing stroke volume will aid in fluid therapy in ER with any cause of systemic hypotension.
.Final message
Its time, we concentrate & fine tune the echo derived stroke volume as a definitive circulatory volume data in day to day practice.
A request to all ER physicians and cardiology fellows, try measuring the cardiac output whenever you see patient in shock and hypotension .Make it a habit to measure the stroke volume. You need just two minutes. It is cheap, you can repeat as many times as you want in follow up. It can totally change the way you understand hemodynamics of cardiac failure and shock.
There is one more methodology, called EIT electrical Impedance tomography, that can provide live online stroke volume , comes inbuilt in ECMO and other MCS systems
I don’t want to do this …but EBM compels me to do it
The word “Evidence” is the most powerful in the world of science and enjoys disproportionate bias towards positivity (of course in any walk of life). But, the fact of the matter is, it can result in either monumental breakthroughs or mindless havoc to mankind in equal quantities.
EBM is not a sacred movement. It came into the medical domain in the early 1970s and grew at an unprecedented pace, invading the medical practice and literally robbing the charm & goodness in clinical medicine.In fact, many point out ,EBM is in direct conflict with Individual-based holistic medicine. If you rely only on EBM without Individual patient data, it might take you to the doorsteps of department of clinical negligence.
But, unfortunately, EBM in an unpure form has grown to gargantuan proportions and penetrated deep into medical academics. Armed with a possible legal authenticity, ignoring it, could easily push us into clutches of criminal negligence. (In fact, the opposite may be true)
Final message
Does trusting EBM too much imply a reduced wisdom?
If you offer a free pass to EBM*, to enter into all your decision-making process, then wisdom will quietly leave through the back door. Taking evidence, at its face value is going to be the biggest intellectual insufficiency or inefficiency for the future world, especially in medical science.
*I know, It is unwise to blame EBM in such a disparaging manner, rather we need to cleanseand eliminate thelimitations of the EBM .That would be a more correct approach, but is it possible ? , since both appear to be built into it.
*This post may not be meant for cardiology fellows but for young students of medicine
Have you ever thought about how a Giraffe’s heart can pump blood to the summit of a lengthy neck and perfuse the brain?
Unlike a blue whale which has a huge heart, a Giraffe’s heart is not as big as one would Imagine, A Giraffe’s heart weighs .5 to . 6 % of total body mass. If the average weight of a Giraffe is 650kg, the heart would be around 3 kg.It is almost in similar proportion to the human heart.( In a 70 kg man heart weighs about 350 grams). However, it generates more power and pressure, up to 300mmhg BP.
Lessons from Giraffe heart
1. Although the heart is not big, the walls are thicker many times times. In simple terms it mimics a heart of Hypertrophic cardiomyopathy, which we know has brisk ejection. The combination of thick wall and a small cavity attenuates the wall stress significantly .This enables the heart to pump a good stroke volume, high into the brain located more than 5 to 8 feet above the heart. What a remarkable phenomenon.(Laplace law executed in the best manner in biology) *Laplace law states , the wall stress is directly proportional to the cavity diameter, indirectly related to the thickness of the wall
2.We can also understand the principles of the management of cardiomyopathy from a Giraffe’s heart. If the ventricles assume a tubular morphology, optimal energy and cardiac power can be accrued. This forms the basis behind the ventricular reduction and reconstruction surgery for Ischemic dilated cardiomyopathy.(Batisda procedure etc)
3.The innovators and engineers of new-age mechanical assist systems could learn a few crucial insights from these unique and humble animal beings. (Shall we think about,axial pumps in ascending Aorta in series with LV. An Aortic Impella device, that is distal to the aortic valve and devoid of LV-related issues. )
With each systole, blood has to travel a maximum of up to 8 feet up, with enough power at the same time not to injure the vessel wall
When bending the opposite happens, and the valves in both arterial and venous systems come to protect by dampening the flow and avoiding congestion.
An alternate hypothesis: Siphon effect in cranial circulation
Some believe the heart is assisted by an alternate mechanism in the Giraffes. The carotid artery could act like a siphon from the heart. Siphons can defy gravity. Is it a reality in living beings? How is this possible? I am not clear. If so, that can be tried in human experiments on cerebral insufficiency.
Final message
Every living and (even non-living things) surrounding us, keep sending some silent scientific messages. The hemodynamic of the Giraffe’s vascular system is a good physiologic model of circulation, that defy gravity. It reinforces a basic, but important learning point* that a tubular & cylindrical heart can generate more power than a large globular one.
It is an acceptable diagnosis, if you thought an anomalous LCA, a LAD CTO or a single coronary artery. But, the true diagnosis is different. It is left main atresia .(Which can also be called a single coronary artery, if RCA gives origin to LCA)
How common are coronary artery anomalies?
It is about 1 to 2%. It can be in the origin, course, and termination. The common ones are the wrong sinus origin. Right arising from the left sinus is much more commoner than left arising from the right. This topic of anomalous origin needs a separate discussion. (Prachi P. Agarwal ,et al Radiographics 2017 )
Left main Atresia: Is it a sub-set of the anomalous origin of LCA from the right sinus ?
Technically yes, since the left coronary ostium is absent in its designated place in both conditions. But, the entity of true Left main atresia is rare and distinctly different.The difference is, that anomalous LCA often doesn’t travel in the pre-designated path of true LAD and LCX (Ie Intraventricular and Left AV groove). In true atresia, only the origin is sealed. Rest of the LCA is anatomically intact , which gets filled from one of three familiar Inter arterial collateral (Vieussens, Kugel, and retro-conal coronary ring)
Apart from angiographic surprises, these anomalous coronary arteries may under-perfuse the ventricle and present as unexplained cardiomyopathy , until we realize the anatomical errors in coronary anatomy.
Some unanswered queries
1. Is the atresia confined to the ostium alone, or does it extend to variable lengths of the left main?
2. How do the fetal and subsequent neonatal LV mass outgrow RV , when the LCA is atretic?
Treatment of left main atresia
Surgery with graft makes logical correction. If absolutely asymptomatic, and the stress test is negative, leaving it, as it is, is not a forbidden option, in spite of the fact, that the patient would have a single coronary arterial supply.
3.Ostial Athero-sclerosis( Rare, but status of other areas of coronary artery will usually reveal evidence for atherosclerosis)
True confirmation, is possible only during surgery , ie visulaing the absence of left coronary ostia.
Final message
Coronary arterial anomaly is a less discussed topic nowadays, unless & until, it intrudes an interventional cardiologist in his daily routine life, of delivering stents. In reality, there could be thousands of asymptomatic ones in the public domain. it can result in both risky as well as protective events. One theoretical and realistic possibility can be extrapolated. We know, how adverse is the outcome of Left main STEMI. But, It might also be true in a few lucky souls, one of the above rings can open up instantly and change the destiny.
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
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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 