Archive for May, 2021

This 90-second video clip is a “perfect provocation”

Allan Savory  is a renowned ecologist from Africa. He is a global leader in environment and eco protection. He is making this famous comment, during one of his interviews from the deep forests of Zimbabwe, after years of ground-level work in the field of desertification and climate change. I can understand his feelings, as we also encounter similar situations at ground zero of the health care delivery system. (I wonder if there is anything called peer-reviewed bedside caring)

We realize wide gaps between academia, patient care, and research are the norm, not an exception. One reason for this is, even well-learned medical professionals find it difficult to comprehend, that the practice of medicine is essentially an art, administered with love, care, service-mindedness. A cost-effective infrastructure with an immense amount of teamwork is critical ( Of course, guided by a fair amount of knowledge, expertise based on good scientific principles)  

Final message 

As Savory says, let us hope, the future looks bright, that welcomes young researchers from the fringes of the scientific community. Let them be conferred with all courage and resources to course-correct medical science from its frequent aberrant and awkward turns.


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The concept of Fractional flow reserve ( FFR) has dominated the coronary interventional field for over a decade. It gave us a (false) sense of security and pride that we have been advocating physiology-based appropriate stenting.

The much-expected FlOWER-MI trial was presented in ACC & NEJM a week ago. (May 16th  Issue 2021)

FFR, though physiologically an attractive concept, has many well-known confounders right from the technical factors, lesion-related errors in physics, mirage of true hyperemia induction with Adenosine, finally & most importantly microvascular dynamism. The value of FFR in the ACS setting was always a suspect. So, no surprises with the FLOWER trial conclusion. It has concluded FFR guided interventions in the non-IRA vessels following STEMI had no use in terms of the hard endpoint. Lesson: We can’t really expect true coronary physiology rules to be alive when severe pathology has set in)

Wait, there can be quixotic ways to Interpret this study be as well.

FLOWER trial reveals the number of stents used with FFR guidance was 50% less (mean 1.01 vs 1.5 stents). Though there was no difference in deaths, the incidence of nonfatal myocardial infarction was more in FFR group 18 (3.1%)  than the non-FFR group (1.7% ). Similarly, unplanned hospitalization leading to urgent revascularization was more in FFR  (2.6%)  than non-FFR (1.9%). Though all were not stat significant, FFR has helped reduce the number of stents in non-culprit lesions. Still,  recurrent non-fatal MI and urgent revascularisation were high in the FFR group. So, is it possible FFR related procedural hazards are real? Who can (& how) quantify that? or Is it Inappropriate non-stenting due to FFR misguidance responsible for this trend?

There is one more risk with the potential demise of FFR as a concept. Extreme scientists, might ditch physiology to the backyard and go for free for all stenting again. (Back to shadow physiology & oculocardiac reflex) 

Final message

There is an extrapolated lesson to be learned from DEFER*/ FLOWER trial combo. FFR or no FFR, never touch the non-IRA lesions in stable STEMI* however tempting it may be. (*This rule applies even in some unstable STEMIs (Please recall Culprit shock trial ) 

*DEFER 15 year follow up EHJ 2015 ( Note : DEFER contain significant non ACS population)

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Next to the atmospheric pressure, the most curious pressure to understand is stored within the human circulatory system. Yes, it is the “blood pressure” fondly referred to as BP by both physicians and patients. (When worried men & women visit us and say, that they are suffering from BP, please make it a point to clarify, BP is a sign of existence of life, rather than a dreaded pathology ) 

Why should blood have pressure?

BP is lateral pressure exerted by flowing blood on the vessel wall (or is it the propelling pressure head ? It is to be noted, cuff pressure doesn’t measure this !) BP is generated by the heart in systole and sustained by the vascular system in both systole and diastole. BP is measured as mmHg. It can also be expressed as PSI(Pounds /sq Inch)  or Pascals or ATMs. If you allow me to spoil with some physics. Pressure is force per unit area ie Newton/m². So, pressure is essentially a force. Force is mass times the acceleration. Mass is weight independent of gravity, while the acceleration of blood is essentially the force of gravity added to the velocity of blood flow. If you think gravitational waves and planetary positions might influence the mass of blood (and hence the BP)  you may not be insane. (Environmental & astrological influence of BP and cardiovascular events need not a be mythology) (Oomman A,  J Indian Med Assoc. 2003 )     (Robert D Brook Cardiac clinic 2017)

How is it regulated?

Physics uttered at the bedside is sure to appear as nonsense for practicing physicians. Forget It. BP is not only a continuous variable, the neural, hormonal, cardiac control mechanisms are also in a dynamic flux. What we need to bother is, how to sustain a mean BP of around 90 mmHg within the human circulation, with robust autoregulation. (For the fellows in cardiology, it is a dangerously simplified teaching & belief  that cardiac stroke volume determines systolic BP and PVR determines diastolic BP) In fact, It is the systolic pressure that confers the energy required for diastolic BP. Regulation of BP is all about large vessel stiffness,  neuro-humoral tone of small vessels, water and sodium metabolism. This makes the kidney a central organ for long-term control of BP. It must also be emphasized BP is regulated in a regional and organ-specific manner. (Ex -The cuff brachial artery pressure may tell little about what is happening at the glomerular perfusion pressure )

Who are the guardians of BP?

Though general Physicians , Neurologists, Nephrologists even Endocrinologsts  have more geograhcial rights  cardiologists have largely taken siege over the entity of SHT because the heart happens to be a glamorous victim organ. We are witnessing an almost intoxicating number of cardiovascular trials on hypertension, right from Framingham’s days of 1970s to just released BP LLTC in 2021, trying to bring down cardiovascular risk. Based on the accrued evidence, the guardians of human  BP in various global institutions bring out strategies to reduce the risk of vascular injury. Have we succeeded in this  Intravascular number game.? I think we are. At what cost?

Two repeatedly asked two trivial questions 

  1. What is normal BP  &  When to start treatment?
  2. How much lower is best for our body?

Probably, we have got an answer for the first question from this Impactful publication. 


I think this study is trying to tell us, there is no normality for blood pressure in terms of risk reduction in cardiovascular disease. (Please recall, one JNC -Joint national committee  was dissolved after  including a controversial term pre-hypertension in healthy public  few years back) What will be the implication for this study? Its core conclusion is about 5 mmHg BP reduction across any subset of adult population will reduce CVD risk considerably. I am sure this study is so intense and powerful it will take at least a decade for its conclusion to fade away. So, can we make these funny conclusions? Hereafter we need not measure BP before starting treatment. Just administer drugs to any live adult who has blood & pressure. (J or U curve need a big debate later)

Mind you, sustained  5mmhg reduction* can be brought by any of the following habits. A salt moderated fruit-rich diet, reasonable physical activity, good sleep, a stroll in the park, yoga, a deep breath, having a pet, watching a movie in a quiet evening, having a loving  family, and so on so forth (Of course, 5mg Amlodipine, 40 mg of Telmisartan, or a  paradise device can do the same, with an add on pride)

*There is a big catch in this landmark paper. Read the title again. The important take-home point is that this 5mmhg lowering should strictly come by pharmacological means, not by any other means. (Correct me if I am not correct)

Final message 

We got the final answer from this marvelously done meta-analysis for the toughest question in cardiology. Hereafter  It’s going to be a celebration time for mankind, who struggle in a hypertensive world.


True, sustained high BP is a major risk factor for stroke, heart failure, and CVD. However, it is also true BP can’t* do much damage to the coronary artery without the help from its naughty cousins DM & dyslipidemia. All three parameters must be optimized in unison. May I propose a rough rule? It may be called DFL index for the collective CVD target.  Diastolic BP, fasting blood sugar and LDL all should converge around a unitless number of 70 to 80. 

*HT is a powerful risk factor for stroke and HFpEF. 



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No doubt, the heart is a biological wonder with its non-stop pump function. Still, it cannot function as a continuous rotary pump like the electrical motors do. It has no other option but to contract in a pulsatile manner. However, the mean pressure in circulation is fairly constant, flow is kept continuous, and fairly laminar. This is made possible by the built-in elastic pressure in the aorta and the poorly understood but vitally important parameter vascular tone. Aging widens the pulse pressure due to dissipation of vascular tone. Atrial fibrillation adds new bizarre dynamism to this pulsatility and challenges the aortic wall’s competence and compliance further. This is the basic mechanism behind the classical description of an irregularly irregular pulse in AF. The pulse can be  so unpredictable, it was originally referred to as acute confusional status of heart (Delirium cordis)

What is the effect of AF on systolic, diastolic, and mean blood pressure?

In AF systolic BP varies considerably from beat to beat. Diastolic BP does show some changes but less obvious. So far mean pressure fluctuations in AF have not been given much significance.  

Clinical significance of AF on the brain: Thinking beyond stroke 

From a stroke perspective rate and rhythm control did not show much difference. The prime reason for AFFIRM  trial not showing benefit with rhythm control was embolic stroke was much more common from sources other than left atrium proper and hence the usage of oral anticoagulants was more important than rhythm control in overall stroke control. 

Now, an important study trying to look at this hitherto ignored aspect( Andrea Saglietto,  EP Europace, 2021). It raises concern about the impact of AF on long-term cerebral function. Should we restart the debate in favor of rhythm control? No doubt, the pulmonary venous electrophysiologists will be too glad to welcome this concept.

Now, we have new evidence based on near-infrared spectroscopy AF does cause unpredictable beat-to-beat changes in cerebral microcirculation that leads to neurocognitive dysfunction. It is possible there can be a breach in cerebral autoregulation limits in a significant number of post-long RR  beats. We may soon look forward to a new entity of “dementia cordis“as a sequel to chronic AF.  



1.Andrea Saglietto, Stefania Scarsoglio, Daniela Canova, et al Increased beat-to-beat variability of cerebral microcirculatory perfusion during atrial fibrillation: a near-infrared spectroscopy study, EP Europace, 2021;, euab070, 



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Here is an uncommon story of a patient with palpitation,SVT , Troponin +ve, and suspected ACS.

Palpitation in ER ⇒ {Tachycardia +Troponin positive ≠ ACS}

Mechanism of troponin elevation following any SVT

  • At high heart rates (>200) myocardium is subjected to non-Ischemic mechanical strain & squeeze. Minute amounts of Troponin is let out like a myocardial juice into the circulation (Like atrial natriuretic peptide release which causes polyuria during AVNRT)
  • Tropinin releases have been shown to correlate with both heart rate and duration of ST depression (Subendocardial strain /AVRT left lateral pathways)
  • Short diastole induced low coronary perfusion pressure and a true transient (but insignificant) Ischemia
  • Finally, SVT (especially in the elderly) is a natural “exercise stress test” equivalent, ST depression with Troponin positivity is a true marker of significant epicardial CAD


False alarm of ACS is the most important issue. (Except one study which showed a different conclusion Chow GV, Prognostic significance of cardiac troponin I level in hospitalized patients presenting with supraventricular tachycardia. Medicine (Baltimore) 2010;89:141–148. doi: 10.1097/MD.0b013e3181dddb3b. [PubMed]

Note: If AVNRT occurs with aberrancy, or AVRT presents as antidromic tachycardia with a wide qrs tachycardia the confounding effect is perfect as it can no way be differentiated from true Ischemic VT or atrial fibrillation.

Final message

It is no ER room secret that a single spot Troponin value has lost its credibility considerably in segregating ACS from non-ACS conditions. It is falsely elevated in a long list of cardiac and noncardiac conditions. It is a worthy point of learning, among the cardiac conditions, the commonest cause for false elevation is during any tachycardia. This should be kept in mind. Because a patient with chest pain who present with benign palpitation due to prior SVT (Arrival ECG could be normal) a false raise can trigger a chain of inappropriate reaction that may land the spot even in the cath lab.


In spite of these limitations, non-diagnostic ECGs, we expect Troponin and CPK to guide us in chest pain screening. We now have added one more marker, high sensitivity Troponin Assays. Let us believe, it doesn’t add to more confusion. I think the main purpose of these biomarkers in the future, would be to arrest the habit of using cath lab as triaging place for chest pain instead of ER room. (A brief review from ACC https://www.acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians)


1.Troponin elevation in supraventricular tachycardia: primary dependence on heart rate. Ben Yedder N, Roux JF, Paredes FA Can J Cardiol. 2011 Jan-Feb; 27(1):105-9. [PubMed] [Ref list]

2.Kanjwal K, Imran N, Grubb B, Kanjwal Y. Troponin elevation in patients with various tachycardias and normal epicardial coronaries. Indian Pacing Electrophysiol J. 2008;8(3):172-174. Published 2008 Aug 1.
3.Carlberg DJ, Tsuchitani S, Barlotta KS, Brady WJ. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: outcome after ED care. Am J Emerg Med. 2011;29:545–548. doi: 10.1016/j.ajem.2010.01.041. [PubMed] [CrossRef] []

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