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Archive for October, 2021

This piece of article by Mr. Arun Maira,(The Pakistan-born British Indian ex-planning commission member) is a real eye-opener in the manner we have understood science. All socially conscious scientists must-read. (If properly appreciated, the 15 minutes  you are going to spend on this is worth the time of one full semester in economics at a top-notch university )

Was the past perfect?  & Will the future be tense?

No is the answer to both questions. Noble prizes are increasingly given for some soul-searching simple researches. Complex research methodology is looked down on, especially in economics. Contributors of simple observational studies bordering on common sense shall be rewarded. Incidentally, this year’s physics prize was also different from other years (Given for finding faultlines in working models of climate change). It is heartening to note the shift in thinking and points to good times for true science. We have finally started to question the genuineness in the foundations of existing research models and epistemological purity of knowledge.Very soon, major global awards are waiting for the Innocuous looking amateurish research that is willing to expose trivia and the flawed understanding of science itself.

High stakes in the noble profession

Now, this has major Implications in the terrain of medical practice, a fragile scientific art that is dangling between facts and fakes, uncertainties of nature & certainty of greedy monetization, social inequalities, and finally the stupidity of half-baked knowledge.

I strongly believe the following two concepts if proven properly deserve the Nobel prize in medicine or economics with a huge Implication for humankind. 

1. In the global health care delivery, nurses and para-medical health workers have a multi-fold positive impact on universal health goals than the highly specialized doctors, who are at best have a minuscule role. There should be intensive restudy of their actual requirements and redefining  doctor vs nurse vs population ratio (What a big revelation,  even a novice can say this, but that is exactly  is the reason which makes it eligible for the Nobel award)

2. Specific treatment modalities are either lacking or trail behind the hyped-up diagnostic methods for a good number of illnesses. They are not only redundant but also malignantly consume the global economic resources without a real purpose. What is the big deal of accurately diagnosing and labeling a disease if there is no treatment? (Typical example in recent times,100s of millions of costly RTPCR tests are Indiscriminately used for an incurable self behaving pandemic).

Who is willing to do the above studies? I wish WHO can sponsor this. Research questions, methods, statistics, and even conclusions are ready with 100% accuracy, I am sure, they will withstand any rigorous scientific scrutiny. Though every Tom, Dick  & Harry can do this research from any academic garage, the chances of it getting noticed by Karolinska institute is low, unless It comes from an Ivy League or an elite European university. When someone receives this coveted award down the lane of time, hope this cranky post gets some credit.

Reference

https://www.thehindu.com/opinion/lead/over-simplified-models-complex-social-systems/article37061493.ece

Nobel Prize economics list

Noble prize in Medicine list 

 

 

 

 

 

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Aortic stenosis evaluation was so simple in our early days. Gradients across the valve were the key. Now, we have more parameters to bother about. Dynamic AVOs, flow state, resting LV function, contractile reserves, GLS, dobutamine response, etc. MRI assessment will soon overtake echocardiography. 

Hemodynamics of flow across LVOT. MRI 4D volumetric model of normal Aortic stenotic flow in the bicuspid valve (On the left). The more we know, the more we tend to miss! Image courtesy: Northwestern Medicine

The current AS algorithms, though scientific, I am afraid, appear much complicated with some frightening terminologies at least for the beginner. One such category is PLF-LG-AG.

Let us first answer this. What is LG-AS?

We diagnose a case of significant Aortic stenosis but desperately missing to pick an adequate gradient across the valve. It is indeed a low gradient, still, you are not convinced, since the 2D look of the valve looks severe. Then you find the culprit. It is the dysfunctional ventricle pulling down the gradient. This is called  LG-AS.(one type )

*What is paradoxical -Low flow-Low gradient Aortic stenosis? (PLF-LG AS)

Now, we have another patient. It is indeed LG-AS, but the LV function and EF are normal. You get confused and label it as PLF-LG-AS. 

PLF-LG AS is known to account for approximately one-third of patients with severe AS and preserved LV EF.PLF-LG severe AS is defined by AVA <1.0 cm2, indexed AVA <0.6 cm2/m2, mean gradient <40 mmHg, LV EF ≥50%, and low transvalvular flow (indexed stroke volume <35 mL/m2).

What is the paradox?

AS is severe, but the gradient is not showing at the valve. Wait, don’t think that is the paradox, since this can happen in any category of LG-AS.  So, the real paradox in PLF-LG-AS denotes to the fact that the gradient is low, in spite of normal LV  function (Rather, normal EF %)

Why the paradox? Why gradient is not showing? (In spite of good Ejection fraction ?) 

  • Reduced stroke volume increased afterload due to associated HT are the major hemodynamic mechanisms of PLF-LG AS.
  • The low-flow state can be related to small LV cavity 
  • Significant diastolic dysfunction (Associated Amyloidosis is a new age problem kid on the block. EF is not the only parameter that can compromise the flow you know !)
  • Atrial fibrillation (Ofcourse some cycles will pick up the high gradients, but are they spuriously low or high is the question  ) 
  • Associated mitral valve disease leaks, as well as blocks, will ration the flow to LVOT.

*Finally, every cardiologist should be aware of the following two subsets that could wrongly enter this PLF-LG-AS conundrum without much fanfare but with lots of implications.

1. Most importantly, technical issues and severely malaligned LV due to gross hypertrophy,  Malaligned  LV with LVOT & the actual AVO is the commonest cause of failure to pick up the gradient. (Never report this PLF-LG-AS stuff without confirming it is not technical). A tip: Never complete AS doppler study without a meticulous search for good doppler signal from the suprasternal window. 

2. This could be termed “Paranoid aortic stenosis”. Once, a  shrewd fellow was reporting a shabby-looking calcific valve as low gradient, severe AS with normal LV function. Later, when it was assessed more scrupulously it turned out to be a true mild aortic stenosis, and none of the decorative echo features he was showing were really pathological. It was an error in aortic valve area calculation that had bizarre calcification and LVOT measurement errors that got mathematically amplified. An important teaching point emerged from this echo lab fiasco. Mind you, any true mild aortic stenosis (If the area calculation is wrong for some reason) will happily fulfill the criteria of PLF-LG-AS. One simple tip: Never diagnose severe Aortic stenosis without significant LVH.

What is the role of Doubtamine stress echo in PLF-LG-AS ?

It does help in both forms of LG-AS. You need to read about the contractile reserve, the response of dobutamine to flow (Cardiac index), gradient, and the valve area.

How to manage PLF-LG-AS ?

Many of them will be argued to end up in TAVR. So,follow guidelines carefully but don’t apply them blindly

Final message 

In the evaluation of Aortic stenosis let’s make things simple. Gradients are indeed important. But, realize Doppler gives only pressure data. Converting them to flow and volume data is always error-prone. Instead, let us believe our eyes too.(Need not always depend on o MDCT vision)  Concentrate more on LV morphology, valve pathology, and careful assessment of LV function, finally take a decision to intervene based on true symptomatology and comorbidity.

Reference 

1. For the most authentic knowledge base

2.An excellent review on the topic 

Guzzetti Ezequiel Frontiers in Cardiovascular Medicine 2020

Further thoughts

Is there High flow-High gradient -True mild AS?

High gradients across the AV  generally do not cause much confusion. If the mean gradient is > 40mmhg Aortic stenosis is always severe. Is that right ?. I think so. Exercise-induced paradoxical high flow high gradient AS as an entity is not reported as such. But, what really can happen in high output states, hyper contractile ventricles with high EF? We have observed doppler gradients overestimate the severity of Aortic stenosis. I think there is some dynamic component even in the so-called fixed valvular AS that alters the gradient in response to flow. Do we have proof for this?  OMG, it’s right there in echo lab every day, we are failing to notice it. Look at the AS gradients during AF. It is changing every beat, right.

 

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Doppler E/A ratio reversal is probably the most reported abnormality in clinical echocardiography. We are also pleased to label it as a grade 1 diastolic dysfunction. Making a significant population who come for regular health checks anxious and worried.

Sharing a presentation from the Annual conference ECHO INDIA 2019, I participated in a symposium on Diastolic dysfunction.

Topic : Issues in diagnosing grade 1 diastolic dysfunction: Pearls and Perils

How did we get into this academic trap? Should we continue this practice?

The current ASE guidelines 2016 have a clear message. It has taken off the E/A ratio from the Initial screening for diastolic dysfunction.

Summary & Final message 

Are we ready for the change? By understanding a simple concept, one can reduce the incidence of indiscriminate diagnosis of grade 1 diastolic dysfunction.

  • E/A ratio apparently has a no role in diagnosing diastolic dysfunction in the normal population who have normal EF %.
  • Hence, never report E/A ratio in Isolation as grade 1 diastolic dysfunction.
  • However, in patients with HFrEF it does help in triaging diastolic dysfunction.
  • Always look for symptoms and 2D features  (Unexplained dyspnea, LA enlargement, LVH ) before considering diastolic dysfunction.

*For advanced readers and researchers grade 1 diastolic dysfunction does have a deep meaning and always continues to puzzle.

Patient corner

For all those anxious patients who ramble around with a report of grade 1 diastolic dysfunction, I can assure you this. Please realize, 9/10 times, this is just a decorative echocardiography abnormality meant to add some spice to the report  does not have any significance.

*Will post a PPT presentation shortly.

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This is not a breaking news story. It’s the same old secret that was exposed in JUPITER  trial with Rosuvostatin 14 years ago. Yes, I am talking about the relationship between the usage of statin and the occurrence of diabetes. Now, we have this huge study on possible diabetes progression with statins. It’s not from a small journal to ignore. 

83 thousand patients data, the world’s largest series on link between statin therapy and diabetes.

 

This study has this to conclude

Diabetogenic statins

Something* happens as the statins antagonize the HMG COA  enzyme that resides within the delicate membranes of the endoplasmic reticulum inside the most specialized cells in our human body, called hepatocytes.

*What is that something?

Image source Umme Aiman et al Journal of Pharmacology and Pharmacotherapeutics 5(3):181-5DOI: 10.4103/0976-500X.136097

How to go about this issue?

With-holding statin in as many as possible is the best thing for such diabetic  (non-diabetic?) patients. But, the more pragmatic option is to ignore these negative studies, and instead intensify diabetes management if it worsens. After all, we can’t afford to lose the prodigious evidence-based cardio-vascular protective effects of statins and earn the wrath of our patients and peers you know!

Further Interest

1.Mansi IA, Chansard M, Lingvay I, Zhang S, Halm EA, Alvarez CA. Association of Statin Therapy Initiation With Diabetes ProgressionA Retrospective Matched-Cohort StudyJAMA Intern Med. Published online October 04, 2021. doi:10.1001/jamainternmed.2021.5714

2.Aiman U, Najmi A, Khan RA. Statin induced diabetes and its clinical implications. J Pharmacol Pharmacother. 2014 Jul;5(3):181-5. doi: 10.4103/0976-500X.136097. PMID: 25210397; PMCID: PMC4156828.

 

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Atrial fibrillation has a direct effect on systemic blood pressure as stroke volume swings from beat to beat because of changing  RR Interval ( preload ). The variation in systolic pressure actually reflects not only the changing stroke volume but also the enhanced contractility of the ventricle to the preload( Frank-Starling principle ). The net effect is reflected in the pulse as an irregularly irregular pulse (Both rate and volume /Amplitude).* However, In dysfunctional ventricles or in acute AF* this variation in systolic  BP can be significant. Also realize, If the preload is changing every beat, there is a considerable dynamism in the afterload as well because of ventricular arterial coupling.

(*Acute effects on BP with the onset of AF : There can be transient hypotension with loss of atrial booster pump.This is not significant in otherwise healthy hearts. Inpatient with baseline LV or RV dysfunction, the onset of AF can be detrimental. The ventricular rate is also a determinant of blood pressure. At fast rates, there can be a fall in BP)

How to record BP during AF ? 

As you record the BP by cuff, the Phase 1 Korotkoff sound floats up and down with each beat. If the variation in RR interval is huge one may get a beat-to-beat variation even up to 40 mmHg.We also know, AF can cause pulse drop /deficit intermittently.

What happens to Korotkoff sound during pulse deficit?

Obviously, there will be a loss of these phase 1 sounds, though the other phases of sound may be heard, which are generated by the previous cardiac cycle. So, measuring blood pressure in AF is not a clinically pleasant task. That’s why we are asked to record 3 times and take an average.

Now, coming to diastolic BP in AF. It’s a real hemodynamic riddle. Traditional teaching is, systolic BP is determined by cardiac output and diastolic BP by peripheral vascular resistance. This is at best a gross understanding of circulatory physiology. Both systole and diastole are coupled together as blood flow across the system of varying resistance. In fact. The preceding systolic pressure head stores the elastic energy in large vessels that are thrown back as diastolic BP.

So what happens to BP during AF? What does the literature say? It doesn’t say much. So we decided to look for ourselves. Here is a tracing of femoral arterial pressure curves during atrial fibrillation. Note: the systolic BP shows considerable variations with changing RR interval with little change in diastolic blood pressure.

 

Final message

In Atrial fibrillation, the systolic blood pressure changes from beat to beat and it impacts the timing of the Korotkoff sounds. The diastolic blood pressure behaves the same, but it’s less in magnitude and difficult to detect by conventional sphygmo-manometry.

Further reading 

Clinical Implication for irregular BP of Atrial fibrillation  :https://drsvenkatesan.com/2021/05/04/cerebral-hemodynamics-in-af-irregularly-irregular-brain-perfusion-and-risk-of-dementia-cordis/

The effect of AF on pulmonary arterial pressure is an unexplored topic .Cardiology fellows please note.

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Is there a solution?

As I understand, we don’t have any. Maybe, we can try this.  No way, I can prevent it from appearing ridiculous for the mainstream scientists.

Truths often lie silently  buried deep (many times intentionally). They definitely deserve an intellectual resuscitation beyond the dirty world of data and evidence. Further, why should experience be considered as enemy of evidence ?

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