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The Country of mine with 140 crore population, is under complete lockdown mode. We are anxiously tense in one aspect, but enjoying the free time due to the peculiar “Corona effect” on cardiac emergencies.

Unable to understand you . . . please go away

What happened to our 24/7 busy CCU ? Does it happen only in my hospital? Can’t be. Let me check it right now. I called my fellow, who has since become a leading cardiologist in the nearby town.

guidelines

I have since called many of my close contacts. In both Government and private hospitals. The pooled data were analyzed in a virtual cloud memory. I am fairly convinced, our observation was indeed true.

The following can be considered as near facts.

  • There have been at least 50% minimum dip of Overall ACS cases. It even went down to 80%reduction in a few places
  • Even UA/NSTEMI showed a significant drop.
  • There was general hesitancy to do primary PCI even if it’s technically Indicated.
  • All most all STEMI were lysed. Heparin was liberally used.
  • Many patients preferred telephonic consultations.ECGs were reported over mobile platforms
  • None of the back pains & gastric pains were admitted as atypical chest pain.
  • Most cardiologists closed down their regular OPD
  • For the first time, Govt institutions were considered worthy to refer.

Why ACS Incidence nose dived?

  1. Under recognition?
  2. Under-reported ?
  3. Low Incidence?
  4. Low rate of referral?

STEMI that goes under-recognized and unreported? The consensus was, it’s less important factor as currently, very few are unaware of the Importance of chest pain and widespread availability of emergency services 108/911

Does that mean real incidence has Indeed come down?

The global atherosclerotic burden,(the substrate for STEMI) in the society is nearly constant. Still, the incidence of ACS has declined dramatically in the lockdown period. This conveys an important message and compels a search (research)

The plaques that are waiting to rupture in the population somehow getting a reprieve. Mind you, the presence of a risky plaque in LAD alone won’t cause a STEMI. It needs a trigger. The day to day physical stress, spikes of catecholamine, emotional swings, traffic pollution etc. The only plausible explanation appears to be the vulnerable patients along with their plaques are also locked up inside its Intimo-medial home. (Armchairs and bed rests can not only treat STEMI , they can prevent it too !)

Why the incidence of NSTEMI /UA has also come down?

Again, the same factors might operate. But, more likely self-stabilizing pseudo / Low-risk ACS is a distinct possibility.

A significant chunk of UA /?CSA/suspected NSTEMI patients come from referrals by GPs.The biggest pool of cases for cath labs comes from this group of noncardiac/Atypical chest pain syndromes*. Which shows some Incidental (In)significant lesions that subsequently becomes a cardiac emergency.

Since they have reduced their consultations the numbers have quite significantly reduced.

*Chronic CAD masquerading as ACS is not a forbidden concept

Final message

We are taught some important lifetime lessons in cardiac practice by this 20 nm, lifeless RNA particles.

1. The bulk of the ACS in the society is triggered by the day to day stress of the fast and furious “Just do it” world. The mitigating effect of social lockdown on physical and emotional stress on plaque dynamics on the incidence of ACS will be a big research subject in the coming months.

2. More importantly, It has exposed the existence of one more hidden epidemic in the community “manufactured coronary emergencies” propagated by a resistant cardio tropic virus that has disseminated deep into evidence-based cardiology. Let us cleanse this virus too after finishing off the Corona.

Postamble

It’s just a crazy opinion from a scribbling, blogger. However, I am sure, It’s only a matter of time, great journals like NEJM, JAMA, and Lancet will be screaming the same truths in a more palatable evidence-based manner.

Meanwhile, I can see early signs of restlessness(withdrawal) among us waiting for early release from the lock-up and resume the customary mode of evidence-based cardiology practice.

As I complete this write up . . . .surprised to find this report from TCT MD. Similarities if found, could only be coincidental.

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One of my well-educated patients asked me, how ready is our state health services. How many ventilators do we have, he asked? I told him, we have enough but short of it only technically. I had great difficulty in explaining to him that ventilators are not the antidote for coronavirus.

I continued, even if we have an unlimited number of ventilator and other gadgets, the major determinant of the outcome is going to be the overall viral load, severity of lung Injury and other system involvement. Finally, it is the patient’s ultimate fighting power along with the forbidden word in medicine, ie fate.

In fact, need for ventilator is the strongest predictor of adverse outcome.However, judiously timed, non invasive assisted breathing (CPAP etc) might have a major role , since it could avoid pushing mild cases in to ventilators.

This pyramid tries to explain there are many other ways, by which, we can successfully tackle this pandemic other than critical care.

Corona management strategies prevention

(Please, take this in proper perspective. It is not intended to undermine the importance of critical care.)

Emerging trend In India

Things look positive .The virulence of covid here seems to be less pronounced.(About 2000 cases with 50 deaths). As of now , it appears, the take off slope from phase 2 to 3 struggles to sustain.It could still be an assumption but would love to see it as a fact.

Indian Government is on the right tract and we should all be glad about the steps taken, inspite of the collateral social suffering of the lock down.

Looking forward to celebrate the summer folks !


Now, look at this article that comes 3 weeks after I posted the above.

 


 

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Even in the best of non-Corona times 90 -95% of STEMI population in our country (the rich and famous included) are discriminated by denying life-saving primary PCI. Instead, they are subjected to an inferior and near-forbidden therapeutic modality called coronary thrombolysis or its slightly less inferior cousin pharmaco-invasive strategy. Now, thanks to corona, for some time it’s going to be near 100% discrimination. 

Fortunately, “Corona” or “No -Corona” this discrimination has never harmed in true sense in the real world.

 My feeling is, there is going to be little overall impact on ACS /CCS  outcomes with current “Acute cath lab distancing” protocols. If at all,  it might accrue some invisible benefits. Of course, few random lives could be saved in heroic cath lab maneuver in complex STEMI and NSTEMIs (which are not possible due to prevailing situations)

Final message 

Things will settle down. Cardiologists need to introspect with the large pool of outcome data,  emanating from the underused cath labs. It is a natural cross control study available free of cost and effort.

I wish, I can say loudly, many of the IRAs and the myocardium in distress will definitely welcome this sudden turn of events. Let us continue to keep a watch on our ‘distance with the cath lab’ even after Corona settles down.  

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Presentation

A 38-year-old women,with episodic chest discomfort, mild dyspnea, and occasional non-productive cough. She was investigated in a non-emergent fashion. After an abnormal X-ray chest, A CT scan was requested. (*X-ray chest is Intentionally not posted here to add some curiosity factor)

This is probably one of the most curious Images in cardiology I have stumbled upon. At the first look, it seemed a baseball has replaced a heart. Is it not?

Most curious Image in cardiology

Posted with Creative Commons Attribution License CC-BY 3.0. Afzal et al. Dept of Internal Medicine, Florida Hospital, Orlando, USA.Cureus 10(11): e3566.

When you see such a large round shadow occupying an area exclusive meant for the heart what will you think? The following thoughts came in.

  • A Hydatid cyst of heart ?
  • An Aneurysm from a chamber of the heart?
  • Pericardial mass
  • A granulomatous cardiac mass
  • Aortic aneurysm?
  • A mediastinal mass (Teratoma, Lymphoma)
  • A foreign body?

Answer: It turned out to be none of the above. The best part is this woman was diagnosed, undergone surgery and cured of the condition.

Find out from the link and read yourself about this curious case report from online journal Cureus, . Hats off to this journal, doing a great job of dissemination of knowledge without much restriction as other peer-reviewed ones do.

Acknowledgment

Original source of Image : Afzal A, Mobin S, Sharbatji M, et al. (November 09, 2018) Rare Case of Giant Asymptomatic Left Coronary Artery Aneurysm of 10 cm Associated with Coronary Cameral Fistula. Cureus 10(11): e3566.

Reference

A review of giant coronary artery aneurysm

1.Crawley PD, Mahlow WJ, Huntsinger DR, Afiniwala S, Wortham DC: Giant coronary artery aneurysms: review and update. Tex Heart Inst J. 2014, 41:603-608. 10.14503/THIJ-13-3896

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As human life enters an extraordinary new phase ,”Digital distancing” is also critical for Corona(fear)control.Let us make all mobiles into “non-smart mode” for the next 30 days at least . Use TV time judiciously. Just listen to radio for official Govt.Communication.No panic buying. Help the needy. Let the economy shrink considerably and get rid of all the wasted expenditure.

Meanwhile, let us use this lockdown period to find a  “fresh purpose” for a meaningful life. “God will definitely bless us”

The anger of Corona is sure to settle down very soon and will start living with us in complete harmony, like billions of other organisms do.

How far we are from a vaccine? 

It is estimated it may take at least a year. Might happen earlier too. There are at least 12 companies working on creating a vaccine. Let us hope breakthrough happens at the earliest 

vaccine tracker

 

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Viruses are essentially lifeless molecules (A nucleic acid RNA/DNA) .In the case of CoRoNA, it is the inbuilt RNA that acts as a commander in mischief. Ironically, it gets to life only when it attaches to the host cell. How a small bit of nucleic acid with a lipid cap infects a cell and becomes a deadly factory of new viruses and spread through the body remains a deep biological mystery.

Someone asked me , “Can we kill the Corona en masse”? The answer is frighteningly simple, we can’t kill them really, because they don’t have life in the first place. At best, we can deactivate or make it dormant and reduce its spread.

I just got contaminated with coronavirus . . .Is it a death sentence?

Even if you forcibly feed COvid 19 at random to 100 persons 80 % will be near normal or with a mild respiratory infection. You may wonder how can so many people are positive for Covid 19, and comfortable. We are still far away from understanding the complexity of how this virus will behave in a given human body.

This is because we are not clear what is the exact port of entry and how the first cell reacts to it.The way the body deals with it is entirely different if it attacks the respiratory tract through aerosol or it enters gastric tract (Imminent death with acidic PH ? we don’t know )

The mysterious interaction of genetic susceptibility, response to initial entry, epigenetic memory and subsequent immunological activation, will determine whether one is going to get simply infected and completely decimated.

Healthy humans enriched with good protein diet are expected to have good immunity. However, it can never be foolproof. It is obvious, there is something more than a host stress response readiness.(The fighting power and the fitness of your Immune cells T,B ,K,NK cells, infinite number of Interstitial scavenger cells and molecules)

When you are stressed the Immune system is activated or deactivated?

As expected the answer can be both. Then, how does the body will fight it over? Cells start synthesizing defense molecules. Unfortunately and paradoxically, cortisol is a major hormone released at times of emotional stress, that can severely compromise the immunity. Steroids are firefighters but cause collateral damage.

So its easy to conclude, positive emotions have positive immunity and negative emotions like fear, anger, distress can pull our immunity down.

Fear is a thought virus

Technically and biochemically, every human thought is a neurotransmitter. A neurotransmitter is nothing but a chain of amino acids synthesized in response to DNA/RNA codecs. So, straight away there is an obvious link between thoughts we harbor and the fighting power of the body. Why depression and anxiety affect the infection rate ?
The effect of various emotions on the Immune system is a big emerging topic. Fear-mongering about Corona and the manic digital dissemination of the virus of fear could turn out to be a great Immune system dampener.

One of my wonderfully healthy friends wanted to estimate the fighting power of his body’s immune system in case he is affected by Corona. He asked, whether his blood can be mapped and give a reassuring report?

I said no, it is not possible. Just take all the precautions. Reassure yourself that you have all the Immunity to fight. That’s it.

This following article elegantly explores the link between emotions and Immune response.

Final message

Can viruses befriend “fear” that reduces host Immunity and help self propagate? No one can be sure. But, I wish “unrestricted courage” acts as a vaccine to Corona, which can ooze from the brain free of cost.

Postample: What will happen to this pandemic?

It will (and should) settle down taking its toll. Preventive measures are gratifying. We need to learn from China, how they blunted the steep ascending curve of propagation.(Of course it started from there)

Who is responsible for such global pandemics?

I am sure, this is the toughest question, probably with no answer. Is it man-made or God made ? If you strongly believe, God will never punish human beings without a reason, then the answer is simple. Now, the world is under freeze. Its one way of arresting the mad growth of artificial,materialistic, biased economy. Corona could be a whipping force on mankind and let us use it to heal and unite fellow human beings.

Now, some positive news from CoVid 19 positive population

The false positive results are too high with currently done active screening tests.

This study from China says positive predictive value of a positive test is just 19% .It would mean 80% error rate. So, don’t really get unnerved with a positive test.

https://www.ncbi.nlm.nih.gov/m/pubmed/32133832/

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Professional medical practice demands to put always the patient’s interest first. Unfortunately, current practicing methods threaten doctors to yield to patient’s whims & wishes which are influenced by significant non-academic forces. The principle of Informed consent is gradually losing its true meaning. Who is informing what ? and to whom?  is becoming a hazy conundrum in complex two-way confabulation based on severely battered evidence-based medicine.

pateint empowerment

Some of the conversations not heard in silent corridors of big hospitals

Why did you stent his LAD ? , He had triple vessel disease Is’int CABG Ideal?

“Yes , I agree. What  can I do , the patient  chose to get stented”

Why did you replace his keen joint, it was not that bad isn’t ?

“Yes, I agree but the patient chose it.”

Why did you do the cesarian madam? the pelvis was fine, she was contracting well  Isn’t?

“Yes, I agree, what to do. The patient decided it”

Why did you do the endoscopy, you are sure it was simple dyspepsia right? 

“I agree. What to do? The patient wanted it”

Final message 

We all agree patient empowerment is a critical component of health care delivery and management. I am afraid it can very easily go wrong and take a bizarre direction. Many times I felt it has seriously Interfered with professional decision making.

Still, I am not able to come to terms with this awkward situation. “How can  patients  (or their health care provider) enforce me to do a procedure on them , which I feel is Inappropriate or Injurious to them !

Missing you Dr.Hippocrates

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Bernoulli equation is the most critical equation on which the foundation of clinical Doppler echocardiography is built. Bernoulli equation tells about fluid mechanics. Bernoulli’s principle states that the sum of potential and kinetic energy of fluid per unit volume flowing through a tube is constant.

A more detailed explanation regarding Bernoulli equation is linked in this video

Applying Bernoulli in Echocardiography

So, if we can somehow measure the velocity gained across a point inside the heart we can deduce the pressure gradient. Here comes the Doppler principle that helps us calculate the velocity. Doppler is based on the reflection of sound and the Doppler shift. With the Doppler shift, we can arrive difference in velocity across a valve, or conduit. When fluid flows across a narrowed orifice (Valve /Outflow) it accelerates and builds up velocity. This gain in velocity is equal to the pressure lost ie as given by the Bernoulli equation. Since potential energy is related to height and gravity same intracardiac zones it cancels out on either side. Hence, essentially the Bernoulli pressure gradient is equal to the difference between the kinetic energy on either side.

Let us see how this 1/2 of mass becomes 4. We have to convert density of blood which is 1.060 to mass.

mass to density

Note : Mass = ρV . Density is mass per unit volume. So the “m” in the equation is some times referred to synonymously with the density of blood.

modified simplified bernouli equation doppler pressure gradient mass density velocity drsvenkatesan madras medical college echocardiography 2 tr jet lvot gradient

Application in clinical echocardiography

There has been pioneering work from Holen, Hatle and Angleson who proved the value of this equation in the clinical situation in the late 1970s. Of course, Gorlin and Gorlin worked on this similar concept in the cath lab derived pressure gradients

Reference

1.Gorlin R, Gorlin SJ. The hydraulic formula for calculation of the area of the stenotic mitral valve, other cardiac valves, and circulatory shunts. I. Am Heart J 1951:41:1-29.

2.Holen J, Aaslfd R, Landmark K, Sknonsen S, Ostrem 1. Determination of effective orifice area in mitral stenosis from noninvasive ultrasound Doppler data and mitral flow rate. Acta Med Stand 1977;201:83-88.

3.Hatle L. Noninvasive assessment and differentiation of left ventricular outflow obstruction with Doppler ultrasound. Circulation 1981;84:381-
4.Hatle L. Brubakk A. Tromsdal A. Angelsen B. Noninvasive assessment of pressure drop p in. mitral stenosis by Doppler ultrasound. Br Heart J 1978:40:131-140.

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Here is a 3-minute algorithm for the management of acute pulmonary embolism. Just need to ask 3 questions.

Caution: User discretion is advised. Tainted with reasonably acceptable levels of non-scientific content.

Click over the image for a high-resolution slide

Some more critical  questions need to be answered.

What is hemodynamic stability?

It is purely based on clinical signs and judgment.(One need to be doubly sure to rule out hypovolemia and sepsis-related hypotension)

Is RV dysfunction equivalent to hemodynamic stability?

No, it is not. Clinical instability must be associated.( The dogma is,  if the patient is stable even if there is significant RV dysfunction by echo , that RV dysfunction is not attributable to the current episode of PE)

Can we diagnose and proceed with lysis without CT pulmonary angiogram confirmation?

Yes, you can, provided your suspicion is too strong or you have the extraordinary talent to argue/defend even a fatal bleed ( with your boss or in medical audit ) in a patient who was subsequently proven not to suffer from PE .

How to switch over to Lysis from Heparin alone protocol?

Occasionally one may require to do it. There is an added risk of bleeding here. It can’t be avoided in some situations as Initially, it appear as low-risk PE later on becoming more Intense. Generally, high-risk unstable patients should receive lysis straightaway.

Is 60/60 sign is really useful in deciding lysis?

60 /60 sign tell us if Pulmonary artery acceleration time (PAT) and the TR jet both are less than 60 the likely hood of PE is high in a patient with suspected PE.

  • This sign recently got popular not because of its utility, rather because of its simplicity and attractive caption.
  • It may be very specific but least sensitive (<20%) So it can never be used as a screening test.
  • It also fails to differentiate chronic RV dysfunction from acute RV dysfunction.
  • The PAT is strongly influenced by RV dysfunction (It pulls it down below 60 as PAT is dependent on RV Dp/Dt and falsely diagnosing PE
  • 60/60 sign adds up to the value of  Mconllels sign and can confirm PE with almost 100% specificity.

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Pulmonary atresia with VSD is one of the complex CHD subsets that requires a meticulous understanding of anatomy, physiology of pulmonary circulation. It can be termed as TAPAC -Total anomalous pulmonary arterial connection in extreme cases. Should we attempt to reverse this total chaotic pulmonary blood supply is the question?

It demands a highly focused cath study(hands & brain) and CT Imaging which might actually throw more light. Post-study Interaction with surgeon and team of cardiologist are vital. The decision to take up the challenge of surgery or abandoning poses equal intellectual stress. Continuous and critical decisions need to be taken. Repeat surgeries and cath based Interventions are often a rule.  Very few centers have mastered this surgery.

A single slide presentation

 

pulmonary atresia 4

In spite of all technological developments in pediatric cardiac surgery, there is considerable variations and expectation of the surgical outcome. The major surprise is the original Melbourne group(Ref 1 )  that advocated the uni-focalization as a  concept has almost abandoned this. Stanford and other groups still continue to use this technique more often as a single-stage procedure to improve the outcome.

Let us hope these children get the best of the right mix of technology and natural survival power and more importantly we must ensure the former do not interfere with the later

Reference 

1

Post ample

Surgery has definitely  revolutionized the outcome in neonates and children in less severe forms of PA with good central pulmonary arteries ( Most of the Barbero Marcial Type A and many type B) The perceived negativity in this post regarding the outcome of surgery is primarily belong to some of the  Barbero Type B and many of  C.

gr1

Barbero-Marcial M , Jatene A Semin Thorac Cardiovasc Surg. Surgical management of the anomalies of the pulmonary arteries in the tetralogy of Fallot with pulmonary atresia.1990 Jan;2(1):93-107. 

 

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