While our brain perceives whatever option we choose is the best for the patient , in reality it is rarely true !
The only comment I wish to make, there is nothing called standard guidelines for complex and unusual problems .We need not be obsessed with protocols !
Please remember , If you apply standard guidelines in non-standard situations 9/10 times we are going to err !
So my choice would be, to go with your gut feeling , of course your gut should be alive , up to date and periodically maintained !
If you don’t have the guts . . . don’t worry you have plenty of other options !
A 40 year old women came with acute dyspnea who had a prosthetic mitral valve implanted 2 years ago for RHD .
An emergency echo showed a peak gradient of 35mmhg across the valve .She was on warfarin regularly and her last INR was 2.2.Heart rate was 138/minute, lungs showed congestion .LA,LV were dilated. LV function appeared mildly compromised but could not be accurately quantified as the patient was in distress.
The fellow on duty had no hesitation in diagnosing prosthetic valve thrombus .He Initiated Inj streptokinse bolus followed by infusion along with diuretics . After few hours the gradient regressed .Patient felt better .Every one was happy . The consultant congratulated the fellow for the good job done .To recognize prosthetic valve obstruction early and successfully lysing it too ! The fellow felt gratified .
Since I was hanging around the CCU , watching the proceedings , I Initiated a debate which was curious to the team that handled the patient !
Was it really thrombotic obstruction that caused his symptoms ?
No one has visualized the thrombus
TEE was not done
Fluroscopic evaluation of disk motion was not performed
There was no documentation of raising FDP that would Indicate clot lysis.
All we have is an unexplained tachycardia with raised trans prosthetic gradient . . .
Why we are tuned to think raised gradients to be synonymous with thrombus ?
There has been lot of assumption here . Subsequent analysis of history and clinical presentation revealed the patient had a febrile illness which triggered an atrial tachycardia that possibly resulted in transient LV dilatation and dysfunction.
Once the failure is controlled the gradient has come down , I argued !
Of course, this again could be a guess work , How can you still rule out a thrombus ? They wondered !
I told them , question here is not ruling in or ruling out prosthetic valve thrombus.
It is an important lesson to learn , raised prosthetic gradient is not equal to thrombus in many acute hemodynamic situations* .
Many factors other than prosthetic valve obstruction can elevate the gradient.
After all , prosthetic valve orifice is inherently stenosed .(MVO is never >2.5sqcm in any prosthetic mitral valve) . So at times of tachycardia the gradient is bound to be elevated .
Other factors that can elevate trans – mitral gradient includes
LV dysfunction
Acute diastolic dysfunction
Acute peri-valvular MR
Loss of LA compliance
*One of the commonest (yet not recognised) cause for elevation of trans mitral prosthetic gradient is acute left ventricular failure due to any cause.It can be either acute diastolic dysfunction or a sudden raise in blood pressure that result in after load mismatch.
Final message
Please remember flow across prosthetic valve is governed by delicate local hemodynamic rules .The gradient is critically dependent on heart rate, LA size and compliance , LVEDP and after-load mismatch if any !
Transient raise can occur at times of tachycardia and falling LV function (Mitral valve has to push hard, in the process elevating the gradient)
Simple raise in trans-valvular gradient should be carefully interpreted. Since visualising thrombus in routine TTE is difficult in an acutely dyspnic patient many of us have taken this granted !
Nothing wrong in playing guess games in medicine . . . but we need to acknowledge it!
*Note:Other causes for chronically elevated gradients like pannus formation, mechanical defects of valve, degenerated prosthesis should be addressed separately.
Brugada syndrome has three distinct type of ECG pattern.ST segment in V1 to V3 shows the maximal changes .All manifest as subtle forms of ST elevation .
This is an ECG of a young male who was suspected to have CAD with an abnormal ECG .(Which was Infact Brugada . )
He was adviced EST by a physician .Compare the leads V1 to V3 pre and post exercise
Prompt normalization indicate correction of repolarization heterogeneity and suggest relative immunity for development of ventricular arrhythmia at fast rates.
In contrary , new appearance or worsening of Brugada pattern would help us identify high risk subsets of Brugada.
Message : We have sophisticated genetic and EP studies available EST is a simple test to risk stratify these individuals.( Not a perfect screening test though !)
Can we close an ASD in a 25 year old women severe pulmonary hypertension ?
Volumes of literature has been written on the subject.Dedicated cath studies have been done with multiple parameters .
Still , there is a lingering doubt !
Here is a 3 minute practical* solution based on 5 easily available parameters. (*Also referred to as unscientific in medical parlance !)
1. O2 saturation
2. Pulmonary artery diastolic and pulse pressure
3. RV function,
4 .Systemic pressure
5. Functional class
If O2 saturation is > 90 % consistently there is likely to be significant left to right shunt .Closure is to strongly considered
If 02 saturation is near 95 % there is absolutely no contraindication at any level of PVR.
Systolic pulmonary artery pressure derived by TR jet is least useful index.Pulmonary artery diastolic pressure reflects true vascular reactivity of the pulmonary circulation.A wide swinging pulmonary arterial pulse indicates dynamism in circulation and hence operablity.
If pulmonary artery pulse pressure is wide (>50) , or PA diastolic BP is < 30 one can safely presume irreversible damage to pulmonary vasculature has not occurred and these patients would benefit from surgical closure .
RV function should be assessed carefully in every patient.This is as important as PVR .Significant RV dysfunction is an absolute contraindication.
Never close the shunt in patients who is in class 4 symptoms.
Never close a shunt if the systemic blood pressure is low( 90mmhg)
Some believe PDA may be closed at any given PVR , while worst outcomes occur with ASD as supra-systemic pulmonary pressure is possible.
Always monitor these patients meticulously especially in the initial days following surgery for deterioration .Most patients will do well if they cross the first 30 days. The RV learns to adopts with new pulmonary hemodynamics !
Many readers of this site might have wondered , about a series of biased articles pulling down the superiority of pPCI in STEMI.
This French study (FAST-MI) throws stunning data from the real world. Initial Fibrinolysis* defeated pPCI in all aspects of coronary reperfusion !
*When we say fibrinolysis arm it means Pharmaco -Invasive approach .Today our brain is irreversibly conditioned to believe standalone fibrinolysis is forbidden in STEMI . (Which I strongly disagree!) I am sure, very soon another stunning study will unmask the truth about standalone fibrinolysis as well !
Final message
The truth is , pPCI is really a superior modality in some of the complicated subsets of STEMI that too if performed fast.
In all other situations Initial fibrinolysis will rule supreme !
pPCI is not an Innovation for mass consumption!
Hence, “the roof top call” for pPCI for every STEMI is nether desirable nor feasible.
Now, we have this evidence from France (Which was well known to us a decade ago) As always , truth takes time to arrive , while falsehood can come instantly !
In 2014 , after two decades of celebration of pPCI the flagship Circulation journal throws this Editorial !
Unfortunately, there is a strong bias towards raw basic science when it is given in the filed of medicine.Do you know ,there is no Nobel prize exclusive for medical science ? It shares with human physiology the only field included for Nobel prize in medicine.
Evolution of human history reveals it is not the stunning scientific discoveries that impact the mankind . It is largely dependent on how we use them . It is true and natural ,invention of sub atomic particles , decoding quantum mechanics and trans-cellular signals always generate great interest than others.
In medical science, time and again we have seen problems arise in applying fruits of scientific research into practical usage in the patient domain in the bedside.
What is use of rewarding inventor of nitric oxide with a Nobel prize , when billion-dollar nitrate industry is thriving on a non existing life long indication of stable angina .
It is surprising to note , Nobel committee does give credit to wisdom & intellect while awarding prize in peace, literary or economic sciences. For some reason it lacks such a vision when it comes to medical sciences !
We have seen Nobel prize being awarded to organization that strive for peace and welfare of society and community like UN ,EU etc.The world health organization is the premier power supposed to provide and regulate the health in this planet.I do not recall any time WHO was close to considered for the Noble prize in medicine !
Nobel Ironies
Nobel committee rewards economists who point out lacunae in vital world macro and micro economics theories.
Dubious men(Heads of state ) are decorated with Noble peace prizes for preventing a war in one geographical area while doing exactly the opposite elsewhere !
In this modern millennium where scientific pursuits are contaminated and many of the research questions are misdirected or irrelevant , Nobel committee needs a through rejig in the manner in which medical Nobel prize is being awarded. We know ,Noble’s death wish was to award the brightest mind with highest scientific breakthroughs in those world . . . but
I guess Alfred Nobel if alive would have changed his rules .He wouldn’t have imagined modern science would systematically devalue common sense and reinventing it would also deserve an award equivalent to Nobel !
Some of the medical discoveries that deserve noble medical prize
States which excel in school health nutrition and other basic health programs for the downtrodden
Doctors who promote bed side clinical skills
Tobacco eradication networks
Organisations like medicine san-frontiers which strives for basic life saving medication for all
Journal houses that specialise on Medical ethics and clinical sciences
Medical professionals and institutions provide value education
Medical economists who expose the wasted financial resources that widen the gap between sick and rich
How about Nobel prize in cardiology for preventive cardiologist who successfully terminates a million statin prescription and restoring natural exercise directed lipid regulation in them ?
How about Noble prize for a noble physician sitting in corporate hospital infested with all commercial ingredients who could resist and argue successfully against inappropriate tonsillectomies and appendectomies ?
I am sure , such a man will be a laughing stock for most of us !
An appeal to Nobel committee
It is a wish , Noble prize in medicine is to be included for people who do yeomen services in preventive and clinical care and professional who carry forward the legacy of caring for the sick with clinical application of available scientific wisdom !
In this scientifically obsessed world , It will be a new beginning in the way future medical research will be directed and nurtured ! Only then the true power of Noble prize in medicine will be realised !
In whatever way I look at it ,It keeps both physicians and their patient population guessing in a confused sate regarding their cholesterol levels the treatment modalities !
It seems to revolve around a single point agenda, how to fit a single drug called statin in the scheme of things !
What if , a new drug comes and statin is proved not an angel in our fight against the evil of atheroscerosis !
Summary as I interpreted
“All healthy and unhealthy human beings should ask only one question
whether they can some how benefit from taking statins ? “
If your answer is yes , administer the statin not in low dose but in moderately high dose ! (It appears there is little role for low intensity statins )
There is generally no need to to monitor the lipid levels as long as patient is comfortable.
Disclaimer : *Sorry , the Intention is not to hurt the hard work of a elite panel who toiled for years to bring this much awaited guidelines on lipids and atherosclerosis! but to express my view , biased though !)
A mini research
To confirm my assumption I did a curious word search in this 85 page document .
For words statin , diet and exercise
Statin appeared 814 times
Diet appeared 8 times
and exercise just once in the entire document !
The importance of diet and body activity which are the primary determinant of serum lipid levels is mentioned in a cursory fashion in this global guideline meant to control the total cholesterol load and atherosclerosis of our population .
Meanwhile . a drug which acts in a physiological cell servicing metabolic path way in a complex fashion is glorified 814 times !Do you still think this post is is biased ?
Tree of life : When professional morality suffers a mortality . . . human health becomes a causality !
Greatest threat to the future of human health is . . .
Not from exotic infectious agents , bird flu or mosquito fevers
Not from epidemic of cardio vascular disease
Not from thousands of published diseases in ICD code
Not from aging population and failing vital organs
Not from lack of availability of life saving drugs and devices
Not from lack of hospital beds.
Not from good sanitation
Not from hunger and poverty
Not from lack of para medical workers
Not from lack of health awareness and education
But from . . .
The way health care is administered in this planet .
The way noble professionals are created .
The way trivial health issues prevail over major health crises that wallop the health budgets.
The way by which medical morality is systematically destroyed
The way “concept of health” is sold as a buyable commodity by insurance companies.
The way medical journals churns out junk articles in the name of research.
The way corporates indulge in delirious pursuit to increase bed occupancy rate of their patient ware houses (Also called Hospitals)
The way greedy drug companies aim to increase the per capita drug consumption of ill informed homo-sapiens by discovering pseudo drugs for pseudo illness
The way health insurance policies are misused
The way rich spend billions for reconstructive cosmetic surgery while the poor die for want of basic medicines !
What happens to diastolic blood pressure in severe Aortic stenosis ?
Traditional answer: The diastolic BP remain unchanged. Only systolic BP falls as it is related to LV stroke volume .(What we refer to as systolic decapitation of BP )
Reasoning :Diastolic BP is related to peripheral vascular resistance , hence aortic stenosis has little impact on diastolic BP .
Further analysis
If we assume only the systolic blood pressure is bound to decrease in AS , at one critical point of time* systolic BP should approach the diastolic pressure and pulse pressure should approach zero .This can not happen , hence at that point diastolic pressure will also fall.
*What is that point ?
No one really knows !
Correct answer
In severe aortic stenosis both systolic and diastolic pressure falls , but the fall in systolic BP is more striking .
* Though it is customary for clinicians to discuss them in isolation both systolic and diastolic blood pressure are closely coupled parameters..In the absence of peripheral run off one of the strong determinant of diastolic BP is . . . systolic BP !
Complex concepts
1. What happens in combined aortic stenosis and regurgitation ?
In combined AS and AR we get pulsus bisferiens. implying AR will elevate the systolic blood pressure in spite of obstruction.
2.What happens in associated systemic Hypertension and aortic stenosis . (Which is very common combo in elderly )
Since HT will increase the aortic pressure , the LV-Aorta gradient tend to fall.
However ,this does not happen always as if the original cause for HT was dependent more on the stroke volume rather than peripheral mechanisms .
3. Aortic stenosis with aortic atherosclerosis .
A stiff aorta augments the percussion wave amplifying the symbolic BP and blunting the classical anacrotic pulse of AS.
4.What happens to BP during exercise in severe AS ?
Exercise demands raise in systolic BP and temporary reduction in diastolic BP due to peripheral vaso dilatation in exercising muscles.
If a fixed crtical AS does not allow the systolic BP to raise as required , diastolic continue to fall pulse pressure should still become wide .
Excercise testing is a tricky business in AS. Some have attempted it to assess the functional capacity.(Read below)
A 76 year old man with history of recent stroke presented with acute chest pain and his ECG showed ,
It was diagnosed as Anterior STEMI .Since he had co-exciting renal dysfunction also he was not considered for thrombolysis (Primary PCI not feasible !)
IV Heparin bolus followed by infusion was started. Patient had a comfortable night stay. The ECG taken on the morning looked like this.
Do you call this aborted STEMI or a simply an Ischemic RBBB ?
Transient RBBB due to Ischemia in LAD territory(with septal compromise ) is very much possible during ACS. But , it is a rarely discussed entity unlike ischemic LBBB .
We know qRBBB complicating anterior STEMI is much commoner than LBBB , still transient ischemic RBBB in non STEMI setting seems to be uncommon .Is it possible propensity for Ischemic RBBB is different from necrotic RBBB ?
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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 