Though all of us are aware, the incidence of heart failure is increasing exponentially and is the leading cause of global disease mortality, what we fail to understand is, we still lack a good definition cardiac failure.
Defining HF based on EF% is convenient but adds more complexity, and is less scientific too. Still, as of now, we have adopted this. I think, one of the important factors that apparently increased the incidence of HF is the creation of an entity called HFpEF. (Formerly diastolic heart failure)
Thanks to ESC, we have a consensus document, which has defined HFpEF based on functional, morphological, and biochemical features. This is a more refined model from the original Mayo clinic H2FpEF score.
Both are given below.
Can we diagnose clinically significant HFpEF, without pulmonary hypertension?
In my understanding, the answer is No.
Looking at the two schemes (Mayo & ESC) one thing is clear. Pulmonary hypertension is the key hemodynamic expression of HFpEF. It could be either resting and persistent or exertional and transient.t is obvious the PH in HFpEF is post-capillary. (The modern term for pulmonary venous HT). Mind you, while PVH is mandatory to diagnose HFpEF, PAH (precapillary ) is also observed in most patients with significant HFpEF. This is the reason TR jet velocity is included as one of the criteria. (To make things simple, we may need to create a new classification of HFpEF, ie resting vs exertional HFpEF.This is what the diastolic stress testing is all about.)
Final message
It is back to basics & time to dig into the fundamentals, of what exactly we mean by heart failure. Is the elevation of LV filling pressure alone sufficient? Should it happen at rest or at exertion, and whether neuroendocrine activation is necessary? Is RASS activation similar in both HFrEF and HFpEF? Try to find the answer to this. How often does HFpEF fulfill Framingham’s criteria of HF.? ( Löfström et al ESC Heart Fail. 2019)
Trying to understand the nuances of HFpEF, I think, we can make a statement,- HFpEF can not be diagnosed without pulmonary hypertension. It makes a lot of sense the P in the H2FpEF scoring system denotes PH, however, It is assigned only a single point, which needs revision. In fact, there is a strong case to argue and make it an essential criterion.
Paradoxically & curiously HF with reduced ejection fraction (which is the most common form of HF) doesn’t require the presence of PAH to diagnose it. This issue may also be examined.
Reference
Posted in Uncategorized | Tagged criteria for hfpef, esc guidelines on hfpef, HFpEF |
Does the Aortic root contract or relax during ventricular systole? Some time back, I asked this question in one of my classes for the fellows and found no takers. Not even a guess? I realized later, it was indeed a tough question. The heart is not the only dynamic organ, as we generally believe. The entire aorta which is an extension of the left ventricle has to be dynamic according to the physics of ventricular-arterial coupling and the momentum of blood flow.
What happens to the aortic dimension with systole?
Even prior to systole, there is evidence, the aorta gets ready to receive the blood from the LV. So, the Aortic root must be larger at the onset of systole. (Ref 2 ) It is been generally agreed now, that the systolic dimension is slightly more by a few mm. That is why aortic dimensions are measured in peak systole as per the American society of echocardiography.
There has been an opposite argument as well. The diastolic aortic dimension could be larger, as the aortic valve is in the closed position and the aortic root distended, & becomes a reservoir of blood that’s meant to be distributed during diastole. What determines the aortic dimension on a moment-to-moment basis? Is it the, LV contractility, pressure, or volume, or the compliance of the aortic wall that determines the aortic dimension and pulsatility? How does a prosthetic valve alter this?
So, what exactly happens to the aortic dimension during the cardiac cycle ?
A wonderfully done study from University Medical Center Utrecht, The Netherlands throws some important facts with their analysis of ECG-gated CT scans in 108 Aortas.(Ref 1)
Clinical implication of aortic pulsatility
The implication of knowing (or not knowing )the dynamism of the aorta can be huge.
- Age-related stiffening and onset of systolic hypertension
- Aortic diameter, pulsatility, and shear stress are the key parameters in initiating dissection and its propagation
- Choosing the right sized valve for AVR
- Current interventional heart-throb TAVI involves just a passive placement of the valve in the aortic root. Imagine what will happen, if the foundations are excessively dynamic and shaky
It is surprising, even after decades of vascular research, we lack clarity on what exactly happens to aortic root during various phases of the cardiac cycle. (Currently, paravalvular leak, & migration of TAVI remains a major worry, which has a direct relationship with pulsatility of the aortic root ) One thing is obvious,.Young cardiologists have a lot of work to do in this arena.
Final message
Though the aorta is a direct extension of LVOT, its vaso-motion doesn’t seem to be in complete sync with the cardiac cycle. It tends to have an independent behavior, out of phase with the heart.
As per available evidence, the aortic root dimension can either increase, decrease, or be static in response to LV contractility.
Reference
2. Pang DC, Choo SJ, Luo HH, et al. Significant increase of aortic root volume and commissural occurs prior to aortic valve opening. J Heart Valve Dis. 2000;9:9–15. [PubMed] [Google Scholar]
3. Vesely I. Aortic root dilation prior to valve opening is explained by passive hemodynamics. J Heart Valve Dis. 2000;9:16–20. [PubMed] [Google Scholar]
Posted in Anatomy of heart, Uncategorized | Tagged aortic root dynamism, cardiology research topic |
Welcome to Kuna island. The Kuna Indians are really unique people. living off Panama, right in the isthmus connecting North and south America, The Kunas reside in the San Blas archipelago comprising about 360 islands, of which about 60 are populated by them. They have lived on these islands for centuries, but their exact origin is not completely understood.
These innocent tribes have taught an important lesson in human blood pressure regulation, vascular biology, and salt sensitivity. We know, that high blood pressure, is a maximally researched entity in medical science in terms of etiology, vascular effects, and its control. Still, we don’t know, what are the limits of normal BP for human beings. The debate will not end until we are clear about, whether human beings evolved from monkeys or emerged as de-nova organisms. Recent studies have revealed a remarkably low level of mitochondrial gene diversity in monkeys, suggesting that there has been remarkably little genetic admixture. (Ref 2)
What we know from 3000-years-old human history is, blood pressure is directly related to the physical work done by us and the diet we eat. While salt is considered pro hypertension, physical activity is a much more important determinant in bringing it down. Normal BP in a pre-civilized world was low compared to a civilized population. They also enjoyed better vascular health. Where is the evidence? It comes from the life cycle of Kuna Indians. Here is a very unique paper published in the Hypertension journal.(Ref 1) Three cheers to the authors for confirming this long pending speculation with meticulous data collection. (See the Image)
What was special in Kuna’s diet that prevented cardiovascular events? It is been shown in the study by Hollenberg, their diet contained rich in cocoa and flavonoids that made the difference.(The salt consumption was still high though)
As Kuna’s moved out from their primitive lifestyle to first, the Kuna Nega,(a suburb) and subsequently to a fast-paced Panama city. See the impact on their systole and diastolic stress on the heart. The loss of protective effect of the native diet is obvious.
Final message
Lifestyle is the buzzword today. It is a by-product of the new civilized world that will define human health. The human vascular tree tries to sync with a new lifestyle pushing the BP curve to the north. The true normal BP for denova-human beings may still be very much lower than what we believe. A crazy suggestion was made, that human BP should match that of non-sedentary monkeys. I Hope, we get more evidence later for such hyperboles. As of now, we have to accept, hypertension is largely due to disorder in human civilization, development, and prosperity.
How about embracing the styleless lives of native Kunas to take control of our vascular health.
Reference
BROWN (S.), ATKINS (C.), BAGLEY (R.), CARR (A.), COWGILL, DAVIDSON (M.), EGNER (B.), ELLIOTT (J.), HENIK (R.), LABATO
(M.), LITTMAN (M.), POLZIN (D.), ROSS (L.), SNYDER (P.), STEPIEN (R.) – Guidelines for the Identification, Evaluation, and
Management of Systemic Hypertension in Dogs and Cats. J Vet Inern Med, 2007, 21: 542-558
Posted in Uncategorized | Tagged kuna Indians and hypertension |
This is the story of PCI to LAD from the customary bifurcation workshop for the budding experts, which ended up with a compulsive final OCT run-through, triggering a debate on what to do with the side branch.
- Just balloon dilate the distal strut
- Would consider a second stent. Maybe a TAP depending upon LCX morphology
- At this stage, I would like to know the FFR or iFR across LCX Jail.
- Get rid of this OCT, Let me have look at regular CAG. I bet I can make a better decision.
- Leave it alone if the clinical status & profile is good
Leave it alone? Is it not an incomplete Job?
Definitely incomplete. Please realize, No job is complete in interventional cardiology. If we believe so, it exposes our Ignorance ( & some arrogance). Intentional side branch jailing is an integral part of PCI techniques. Are we not ignoring day in and day out.
Someone in the audience asked Why did you do OCT at all?
The chief operator quipped “You can’t ask this silly question in a scientific workshop. We bought the OCT kit to improve the quality of PCI. We are proud of it. Really feel blessed to use it and I am sure my patients will benefit from it”. We have to agree with him. These new Imaging techniques though give us extra high-definition, but it comes with troubling revelations with their new vision. If you are pathologically honest and believe in empowering patients, it is absolutely necessary to convey the following facts in the discharge record as well. It would be something like this, “There was a 120-micron strut crossing the LCX ostium, that might continuously impede a chunk of platelets & RBCs every beat, for the rest of your life and might enhance the risk for thrombosis. (Of course, DAPT will take care of it and ask the patient not to worry)”
OCT: One-minute review
OCT is Indeed a stunning Innovation. It can be useful in all 3 phases of PCI. 1. Assessment and preparation of lesion bed. 2. during stent deployment and optimization. ,3. Post-stenting follow up. The technology has grown so fast, now angiographic co-registration and longitudinal frame reconstruction comes inbuilt. It required 3 versions of LUMEN study and a 4 th one (LUMEN 4 ) is yet to come, expected in 2022 to prove the worthiness (or worthlessness) of OCT.
One attractively named DOCTORS study asked the specific question directly (Does Optical Coherence Tomography Optimize Results of Stenting)” This is from NSTEMI patients .read yourself for the conclusion. It is not convincing to me. DOCTORS study (Does Optical Coherence Tomography Optimize Results of Stenting)”. Circulation 2016; 134: 906.
Mind you, OCT is not only an expertise-dependent procedure, it also has important imaging limitations. It has low penetration max 2mm, can not differentiate lipids from calcium, shadowing behind red thrombus is an issue and most importantly it may miss the external elastic lamina (EEL) and measurement errors are real.
Cost-effectiveness
If an imaging technique to assess a stent *(*Still waiting to prove its worthiness) could cost more than the device itself, realize how good our economic intellect is. Just because your lab has an OCT console, it need not transform into a technically perfect PCI. There are at least half a dozen factors other than Imaging that matters.
Final message
OCT is a breakthrough technology that needs to be used judiciously and it definitely helps us understand the nuances of coronary stenting, especially in complex lesion subsets, and its mechanical and histological contents. However, let us not propagate a false message, that without OCT we can’t perform a perfect PCI. Give due respect to all those sharp-eyed interventional cardiologists with good techniques, who can do a better job, beating the HD vision of OCT, with their native blindness.
Reference
Post-amble
Can you guess how many PCIs are done with OCT guidance globally?
It is less than 5 %. In India, it must be, I guess it is < 2% So, we are living in a terrifying world of coronary interventions, where 98 % of PCI is happening blindly, sub-optimally, and unscientifically., Data from CLI-OPCI registry adds more panic: Centro per la Lotta Contro l’Infarto – Optimisation of Percutaneous Coronary Intervention (CLI-OPCI) registry: It says device-oriented cardiovascular event (DOSE) is high with OCT detected sub-optimal PCI.
So, what are we going to tell our patients who will undergo PCI (undergone) without OCT guidance in the past, present, and future?
Simply ask them to forget this OCT stuff. Just reassure them. Nothing will happen.
Posted in Uncategorized | Tagged coronary Imaging, ILUMEN study, oct, opitical coherence tomography |
It brings a unique sense of greatness and gratitude to hear the voice of the father of Interventional cardiology decades after his demise.
The invention he made has evolved so much. Though, Dr. Gruentzig didn’t live to see any of them, the genius in him predicted most of them. This Interview was recorded a year before his small plane, which he loved next only to his pet balloons, crashed on the Atlantic coast along with his wife. That is history.
This is how the news was reported across US media on October 29th, 1985. (Reconstructed, click over the pic for high resolution)
It was a fact, that he defied the warning and flew in the adverse weather, what many of us were unaware of was, that he wanted to rush to Emory, only to see a patient whom he had done a PTCA, a few days earlier, developed some complication. This makes his death all the more poignant (Ref Dr. H.V. Anderson )
Here is a good account of the life history of Dr Gruentzig. Link to the article
Posted in history of cardiology, Histroy of medicine | Tagged Dr Gruentzig, history of cardiology |
Why didn’t you do it … for this patient?
“I thought, he was not the right patient for the procedure. I believe, what I did was the correct decision. Why all this fuzz? after all, the patient is doing so well without that procedure,.. are you worried about that?
“No, I need an explanation, we have a fully functional cath lab in our center. The patient came in the right window period. Still, you haven’t offered the best mode of treatment”.
“I can reiterate it again sir. Just because a lab is available 24/7, it doesn’t make all patients eligible for a PCI. I think I didn’t commit a professional misdemeanor when I decided in favor of fibrinolysis. In fact, I would be guilty had I rushed him to the cath lab, just to satisfy the misplaced scientific position we have decided to adopt. If you think, I am culpable for successfully treating a patient without taking the patient to the cath lab, you may proceed with the penal action.
Before that, I would request you to please read the current edition of this book we all revere. (Which continues to mentor physicians all over the globe for the past 50 years)
The current edition of Harrison 2022 is just out. I thought, there is something great learning point in Cardiology chapter, specifically about the reperfusion strategies in STEMI
My hearty thanks to the editors of the chapter for the crystal clear expression about this much-debated procedure* and specifically choosing the word “PCI appears* to be more effective ” (even) if it is done in experienced persons in dedicated centers. The choice of the word used by the authors is Intentional and must be applauded. This message must be propagated to all our fellow physicians. What a way to convey an important truth pertaining to the management of the most common cardiac emergency, while many in the elite specialty are so dogmatic in their assertion without verifying the reality.
* The verdict is still under the jury even after 3 decades, since the PAMI days of the early 1990s. Thank you, Harrison. What a gentle, but a righteous way to express an opinion about a procedure that is apparently enjoying a larger-than-life image based on a handful of studies and a flawed meta-analysis.
Final message
Primary PCI is just an alternate form of treatment to fibrinolysis in STEMI. Both are equipoise in the majority of patients. Extreme care and diligence are required to harvest the small benefit the PCI seems to provide. There are lots of ” if and buts” that decide the success of this procedure. Get trained, and do it selectively for those who really need it.
Postamble
You may call yourself a super-specialist. But, please realize, If you have any doubt about key management strategies, never feel shy to take a cue from Internal medicine books. The greatness of these warrior books is that, it comes devoid of all those scientific clutters backed by premature evidence.
Posted in acute coroanry syndrome, Cardiology -guidelines, Cardiology -Therapeutic dilemma, Cardiology -unresolved questions, cardiology-ethics, Primary -PCI, Thrombolysis, Thrombolysis -Tips | Tagged euro pcr, Harrison principles of internal medicine, management issues in cad, Primary PCI vs Fibrinolysis, scai acc aha esc guideliens, stemi secrets, tct md, tips and tricks in priamry pci, tips in acs |
AF is not only the most common cardiac arrhythmia,it is also an extensively researched entity in cardiology literature. We are trying to rein in, this arrhythmia for the past three decades with multiple strategies. Drugs, pacemakers, ICDs devices, surgical cuts, RF catheters, and the latest technique is trying to frostbite the atrial electrical circuits with ICE. ( Karl-Heinz Kuck,N Engl J Med 2016 )
It is believed that up 60% of AF originate from pulmonary veins. What does it mean? So, when we blindly suggest PV Isolation routinely for all PAF, there is 40% futility straightaway! Apart from the hugely variable anatomy of the pulmonary veins, there are prohibitive levels of recurrence due to PV reconnections. Maybe, will find new technical solutions as we are now moving in 2nd or third generation cryo balloons, 4D imaging, contact force sensing, etc. But let us not forget there are other sources of focal electrical activity too
Importance of non-PV ectopic beats initiating AF(Ref 1,2)
- Superior vena cava (SVC),
- left atrial posterior free wall (LPFW),
- LA appendage
- crista terminalis (CT),
- coronary sinus ostium (CSO),
- Ligament of Marshall
- Interatrial septum (IAS)
Ablation or no ablation, we need to reflect on two things in the management of AF.
1. AF can be triggered by totally different mechanisms like intermittent hypoxia, adverse electrolytic flux, diffuse atrial interstitial pathology or amyloid, etc. Before calling the appointment desk of the EP guy’s office please rule out all the systemic causes. This could be your last (lost) chance to save the atria from pulmonary burns.
2. This one is more important. Read carefully. It is not a divine protocol that demands us to restore sinus rhythm in all patients with AF. There is an excellent knowledge base, backed up by wonderfully done studies. (Need not mention the trial name, I think) that should effectively neutralize our compulsive & misplaced urge to bring back sinus rhythm in all chronic AF.
With respect to the overall outcome, It hardly matters whether you treat the AF by rate control or rhythm control. While there is major technological leap in our fight with AF.It is heartening to know simple measures like regular exercise can control or reverse AF by atrial fatty mass regression.
Final message
We have played with fire for quite some time within the innocent lesser chambers of the heart (RF ablation) and burnt our reputation considerably. Now, silently we have decided to fall for a more friendly weapon ICE. But we must remember our obsession with the pulmonary vein as the only source of initiation of AF is essentially flawed. Further, all these hyper-technology-based combat of AF is indicated only in a fraction of our patients (Maybe 5-10%)
Reference
Postamble
If you think this write-up is too biased, please read the CABANA trial fully before ditching this post into the dustbin.
Posted in Atrial fibrillation, Uncategorized | Tagged affirm trial, atrial fibrillation, CABANA trial, fire and ice study atrial fibrillation, pulmonary vein isolation, race trial, rate vs rhythm control in af, RF ablation for af, right atrial focus in atrial fibrillation, svc focus in af |
1908, Going back on the time machine, more than 100 years ago, world war I was all set to begin, and the great Titanic was being built in the Belfast shipyard. A parallel histroy is being created in cardiology.
This is a brief story of Dr. James Mackenzie, a general practitioner from a remote Scottish village who ended up with the title of the father of British cardiology. Dr. Harvey might have invented circulation, but it was Mackenzie who taught the science of arterial pulse and wrote a classic on the topic to the new medical world. He was able to decode the secrets of the jugular venous pulse as well and diagnosed various arrhythmias including atrial fibrillation at the bedside. He used the polygraph to record his vast observations in pulse and JVP waveforms which were popularised later by Dr. Paulwood. ECG was just beginning to enter the scene in the 1920s. This makes his work all the more significant, as his treatise on pulse and JVP were based purely on clinical acumen.
Sir James Mackenzie, 1853-1925
Apart from his stupendously successful academic life, it was through his death, that he sent out an extraordinary message to the scientific community. His deep desire to know the truths about coronary atherosclerosis was astonishing. Since he himself was suffering from angina and possibly Infarct, he became his own subject of study. He became case number 28 in his own book on cardiology. When he was on his death bed, as a last wish he Insisted his colleagues do a learning post-mortem and keep his heart in the same hospital he worked. When he died in the early morning of January 25th, 1925, as per his wish, his students Dr. Parkinson,(WPW fame) and another pioneer Dr.Thomas Lewis did an autopsy on his heart.
It is tragic to know about the final days of Dr. Mackenzie’s life and how their beloved students performed the postmortem on their teacher and later published their findings in the British Heart Journal. (BHJ link )It is one of the poignant moments ever recorded in the history of cardiology, a doctor wishing to teach cardiology lessons to the generation next with his dead heart.No surprise, he is being conferred the title of father of British cardiology.
Final message
How could an unassuming GP practicing in a remote rural place reach the pinnacle of scientific glory?
Yes, it is possible. Today’s young (super) specialists must realize, that true scientific minds don’t require exotic research labs, tools, or conflict-ridded funds from Industry for the growth of science. All we require is a passion to teach, and the curiosity to learn. The rest of the things will follow… I think that was the message in the great life of Sir James Mackenzie.
Further reading
http://www.dundee.ac.uk/museum/exhibitions/medical/cardiology/cardiology1/
Posted in history of cardiology, Uncategorized | Tagged Dr James Mackenzie, father of british cardiology, history of cardiology, land mark article in cardiology, wisdom papers in cardiology | Leave a Comment »
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