Dr.S.Venkatesan MD

Cardiac Holography : Lets get ready to welcome, in our cath lab soon !

July 7, 2022 by dr s venkatesan

Medical science has evolved over 2000 years and moved far away, from the spiritual cure times at the temple of health at Kos islands to the Imaginations of Davicini. We are now in an era, where we can, not-only take stunning live photographs of individual organs but also go inside, assisted by  X RAYs, Ultrasound, CT  MRI, and Optical fiber. Now, a new kid is entering ie Holography. (We may expect haptics very soon).

 

How about a cardiologist operating with a virtual  3D beating heart hanging in front of him?

Yes, it is possible in a scientific fiction movie . No. it’s real. True view, an innovative medical Imaging company from Israel doesn’t think it is a fiction story. The immediate clinical use comes  in electrophysiology labs

Senti-AR command EP system is cleared for clinical use. 

 

Final message

Breaking new frontiers in medicine is becoming the norm, especially in digital imaging. No doubt, we have entered a  new medical world. However, we should be able to realize, that all the excitement is justified, if and only it makes a positive impact on humankind. Even as we are deeply immersed in medical technology, let us remind ourselves, how a tiny virus is teaching all of us, some hard lessons in basic principles and practice of medicine.

Reference

Jennifer N. Avari Silva, Michael K.Southworth, Walter M.Blume, et al. First-In-Human Use of a Mixed Reality Display During Cardiac Ablation Procedures. JACC: Clinical Electrophysiology. Volume 6, Issue 8, August 2020, Pages 1023-1025. https://doi.org/10.1016/j.jacep.2020.04.036.

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Posted in Multimodality Imaging, Newer cardiac Imaging | Tagged acc aha esc scai guidelines, agumented reality in heart, artificial intelligence, cardaic 3d printing, Cardaic mri, cardiac holography, carto ep, future of cardiology, medical Imaging, senti AR COMMAND EP system, virtual cardiology |

Duroziez’s murmur : A simple bedside marker of diastolic descending Aortic flow reversal & VTI

June 14, 2022 by dr s venkatesan

Murmurs are audible noises from within the Heart or vascular tree when blood flow loses its laminar flow and becomes turbulent. There are many factors responsible for it (Recall Reynold’s number ).It is obvious, that when there is hyperdynamic circulation, even in physiology one may hear a murmur. Pregnancy is a classical example and Innocent (still murmur) in children is another one.

Duroziez murmur: A brief history 

In this post let us dwell on something about a classical murmur that occurs in the peripheral circulation away from the action-packed organ heart. It was originally described by French physician  Dr Duroziez  two centuries ago. (In his own words it was called a double crural murmur ). This happened shortly after Lennec’s new era of auscultation began. When everyone was concentrating on the heart Dr. Duroziez was curiously auscultating the legs and found this crural murmur. For this out-of-the-box thinking, he is still being remembered.

In significant aortic regurgitation, we know a substantial amount of blood regurgitates back into LV. This backflow though happens in the chest and into the LV,  it is reflected all over the vascular tree. It so happens, the entire aortic forward flow for a moment slows in end-systole or even reverses at the end-systole and early diastole when the Aortic valve leaks. Almost all peripheral signs of AR are due to this. It is critical to remember, that these signs are heavily modified by arterial distensibility, associates obstruction, LV  contractility, and peripheral vascular resistance.

Is there real reflux of blood back towards the heart* ? 

Duroziez’s murmur remained controversial both for its mechanism and intriguing questions about, whether the blood really travels back in early diastole in the limbs or is just an acoustic illusion from a  pressure wave. The debate was so intense it demanded a curious animal study. The femoral artery of Dogs with induced AR was injected with contrast and retrograde blood reflux was documented up to the iliac artery and Aorta.(NEJM 1965 Ref 1) 

* While retrograde reflux of blood in the femoral artery is real, which manifests as EDM, we must understand antegrade diastolic flow murmurs or even continuous murmurs are common in hyperdynamic circulation over narrowed peripheral arteries and veins (venous hum)

**For Advanced readers: Some of the issues are not clear. Whether Duroziez murmur is truly decrescendo (Like its EDM counterpart in the Aortic area) or Is it mixed with antegrade diastolic flow murmur over the femoral artery due to hyperdynamic circulation.

Echocardiographic correlates of Duroziex murmur 

Now, we are able to document bizarre hemodynamics that happens the entire length of the vascular tree that is responsible for this murmur.(A related post 😦 In AR the run-off is central or periphery ?_)

Image courtesy: medmastery https://www.youtube.com/watch?v=eVhEXCO13ys 

 

 

Phoncardiography with ECG correlation, help us to  time the murmur exactly and also demonstrates reversal of flow in femoral artery  by color flow doppler.

Importance of Duroziez’s murmur & A research proposal 

Though it’s of historical interest, it is still discussed in exams. It may be amusing for the busy clinical cardiologist to auscultate over the legs, when they may be contemplating a  TAVI for leaky Aortic valve  (Arias EA,  Interv Cardiol. 2019). But, for students, it is a different story. If anyone wants to beat the acumen and curiosity of Duroziez, they may assess the length of this murmur and correlate it with descending aortic flow reversal, aortic ERO, and regurgitant fraction. The fate of Duroziez’s murmur after Aortic valve replacement may also be studied.

Final message 

Duroziex murmur is not just a vintage cardiac auscultatory sign meant for exam halls. Looking deep into it, we may get more insights into the behavior of the peripheral circulatory system in normal physiology as well as in patients with AR.  

Reference

1.Duroziez PL. Du double souffle intermittent crural, comme signe de l’insuffisance aortique. Arch Gen Méd 1861; 17: 417–443,588–605.

2. N Engl J Med 1965; 272:1207-1210

3.Jama.1933.Blumgart and Ernstene

 

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Posted in Aortic regurgitation, Uncategorized | Tagged cardiology research topic, cardiology thesis topic, classification of murmur, double crural murmur, mechanisim of Duroziez murmur, peripheral signs of aortic regurgitation |

Nocturnal hypertension : Something Important is being cooked in the hypertensive world !

June 12, 2022 by dr s venkatesan

Some physics: Why is blood under pressure? 

In perfect vascular climatic conditions, the human circulatory system is comparable to a smooth flowing river irrigating 100 trillion cells, traversing many kilometers of the capillary network, to the far away tissue bed. One major difference in the river analogy is, that in human biology, the entire blood has to return back to the heart in about 30 seconds. (The fact that the venous system does this in style with near-zero pressure head is the greatest wonder in circulatory physiology)

The force per unit area, that drives the blood is the blood pressure. It is expressed in kilo pascals. (16/10 Kpa one Kpa is 7.5 mmHg. It has two components streaming pressure as well the lateral pressure. What we measure by conventional BP apparatus is the lateral pressure on the vessel, which is what we are worried about most times. But, the forward driving head is equally important because the branch points bear the brunt of this pressure head. Sudden surges and spikes attack the grade separators more. This is one of the reasons, the arterial branch points are more prone to atherosclerosis. Though we believe onward pressure head does all the damage, it is also worth knowing the velocity of blood flow can also be defining factor in vascular Injury. The flow velocity is surprisingly low in physiological conditions, about 4-6km/h something similar to our walking speed. 

What is normal blood pressure?

We don’t know. The search is going on. But, what is important is the net lifetime BP harming effect on blood vessels. Of course, BP is not a mono player, it interacts with other risk factors like lipids, diabetes, and smoking, along with genetic susceptibility, and epigenetic vulnerability, making cardiovascular events perfectly polygenic.  

How do we define and grade systemic HT?

A dozen different societies keep defining this (ACC/AHA. ESC, ISH, British, whatever be the normal,  one set of numbers is permanently etched in our mind ie 120/80 as the cut-off. 

A more philosophical definition would be, that high BP is defined as the BP at which our blood vessels feel the stress and strain and begin to wear out. We may never ever know that in a given patient. Now, we are adding more twists to this already confusing normality data. Namely nocturnal BP.

Why 24 hr /Nocturnal BP important?

If the average human lived for 75 years, he or she will be spending  25 years in sleep. What does our circulatory system do in those 25 years? We don’t know. We believe if the brain sleeps the vascular tree takes rest as well. How can it be?  The reticular activating system should go off mode, still the vasomotor centers should be vigilant enough to keep vital organ perfusion. Ironically, sleep can be stressful for some. During recumbent posture the fluid compartment redistributes and ECF expands especially in patients with renal and cardiac compromise. (Recall the mechanism of PND) .Add on to this, the ever-fluctuating sympathetic tone with REM/NREM sleep phases. One of the offshoots of widespread use of ambulatory BP monitoring is (ABPM)is the new term nocturnal hypertension. 

Defintion of nocturnal HT

The definition of nocturnal hypertension is, night-time BP ≥120/70 mm Hg (Now it is more stringently defined as >110/65 mm Hg by the 2017ACC/AHA guidelines. I am not sure, but I think this is applicable to anyone with or without HT irrespective of treatment.

Two more entities exist to confuse us. Just don’t bother. (Fellows can’t escape from this though). A Clinic and morning home BP of <130/80 mm Hg is defined either as masked nocturnal hypertension or masked uncontrolled nocturnal hypertension if they are already on drugs.

Night time BP patterns

Normally we expect 10 -20% dip in BP is expected.

The following are four nocturnal BP patterns defined:

1. Dipper: 10-20 %;
2. Extreme dipper, more than 20%;  
3. Non-dipper: less than 10%, 
4. Riser: 0%.or + side  (I think, this is the same as the reverse dipper )

 

An Important resource from HOPE Asia net work on ABPM Kazuomi Kario Journal of clinical hypertension.https://doi.org/10.1111/jch.13652 While everything looks ok, that blue line amuses us the most. These guys are also called reverse dippers.

Nocturnal dipping: Is it systolic, diastolic, both or mean?

Most studies documented as systolic dippers. Dipping is expected to Impact both systolic and diastolic BP similarly. But, we know it need not be. systolic BP is more volume-dependent, while diastolic BP is resistance is related. I think the concept of diastolic vs systolic non-dipper is yet to be evaluated.

How to measure? How many readings? 

• Ambulatory BP monitoring equipment is the key. Few companies have defined and have patented software (Omran HEM series is the leader, Micro life is another one )
• The night-time BP is calculated as the average of night-time BPs (from going to bed to arising) measured by ABPM The number of night-times BP measurements required may be ≥6.
• The methodology is getting standardized. Errors in measurement are considerable. Posture, temperature, and inflation triggered awakening all matters. 
• Substantial technology is still evolving. Remote wireless monitoring is possible (Apple and Google are keenly watching the global BP market potential !)

Management issues

Though there are 4 subsets in nocturnal BP patterns,  currently, Identifying non-dippers is the key target that will help diagnose more resistant HT. 

How to convert non-dippers into dippers?

• Night-time dose of antihypertensive drugs to be encouraged.
• Salt restriction in the evening diet 

How to prevent excessive dipper (>20%)

The reverse of the above advice is true in this subset. 

Isolated nocturnal  hypertension

I think it is an overzealous concept in sleep medicine. Let us wait and observe. Stojanovic, M., Deljanin-Ilic, M., Ilic, S. et al. Isolated nocturnal hypertension: an unsolved problem—when to start treatment and how low should we go?. J Hum Hypertens 34, 739–740 (2020).

Is there a J curve phenomenon  among dippers ?

We cant generalize,  pro-dipping forces are good & non-dipping forces are bad. Should we consider labeling excessive dippers as nocturnal hypotension? Considering the fact both non-dippers and excessive dippers carry more CVD risk. Like any other biological variables with dynamic safety margins, we are clueless about what is ideal dipping .(A nocturnal J curve)

Clinical trials on nocturnal hypertension 

• JHOP study Kario K, Hoshide S, J Clin Hypertens 2015 from Japan is a very popular one on this topic.
• While this elegantly done Finish study  (J.Hypertension 2004 ) stressed the importance of home BP monitoring. 

What is new in nocturnal HT management?

Melatonin, administered as circadian hormone therapy is expected to play a useful role as a night watchman in BP control (Frank et al Hypertension 2004)

Final message

Nocturnal hypertension is trying to emerge as a new cardiovascular risk factor. Understanding this condition and intervening seems to be important, considering the well-known fact, that cardiovascular events are clustered in the early morning hours.

Still, routine ABPM to know the status of nighttime BP in all hypertensive individuals is not warranted. However, people who had an event or who have secondary hypertension may need to do so. The simple truth is if you have a peaceful day and a perfect sleep, your BP is bound to dip naturally. So, the message to all those active and energetic men and women who are carrying a tag of hypertension need not worry about this dipping and non-dipping stuff. Instead, maintain a healthy lifestyle. There is a thin line separating awareness and anxiety.

Reference 

1.Yano, Y., Kario, K. Nocturnal blood pressure and cardiovascular disease: a review of recent advances. Hypertens Res 35, 695–701 (2012). https://doi.org/10.1038/hr.2012.26

2,Cuspidi, C, Sala, C, Tadic, M, et al. Clinical and prognostic significance of a reverse dipping pattern on ambulatory monitoring: An updated review. J Clin Hypertens. 2017; 19: 713– 721. https://doi.org/10.1111/jch.13023

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Posted in Hypertension, systemic hypertension | Tagged acc aha esc hypertension guidelines, dippers non dippers, hypertension guidelines, melatonin for nocturnal hypertension, night time bp, nocturnal hypertension, reverse dipper |

Is there Intracellular edema in congestive heart failure ?

May 31, 2022 by dr s venkatesan

I am unable to answer this question confidently even after spending 25 years in the specialty of cardiology. I thought, the answer was yes. Reality is definitely different. Such is the complexity in the biology of the fluid and circulatory systems. The heart’s function doesn’t seem to end with just pumping 6 liters of blood every minute, ultimately, it has to handle a huge load of water as well with delicate coordination with the kidney. (ANP,& RASS feedback). It is fascinating to note, that the heart transforms into a powerful endocrine organ as and when it is necessary.

Read further, with a caution: (There is no specific physiological /molecular answer attempted)

About 28 of the 42 liters of fluid in the body are inside the 100 trillion cells and are collectively called the intracellular fluid. Thus, the intracellular fluid constitutes about 40 percent of the total body weight in an “average” person. Still, cells are somehow protected from the edema creating hemodynamic force until the very late stages. Fortunately, the Interstitium is the place all excess fluid stagnates. This is a great biological adoption. The simplest explanation is (Na /K+pump never sleeps  ) Bi-directional osmotic forces keep the cell dry even in adverse cellular milieu. Can’t imagine the implications, if every cell begins to swell in early heart failure. Still, it does happen to some degree I guess. We never quantified this.( Andrew Boyle,et al  Myocellular and Interstitial Edema and Circulating Volume Expansion as a Cause of Morbidity and Mortality in Heart Failure)

 

What happens to massive Intra cellular compartment size in HF? If renal perfusion is compromised (As one would expect in any significant heart failure) How does it affect this fluid distribution over that of heart failure? If the lymphatics’ final destination is the right heart how does this interfere with interstitial space clearance?

Practical implications

Though local factors operate, edema* in heart failure is a reflection of a more serious systemic plumbing issue. Even, subclinical fluid collection can interfere with cell function and contribute to unexplained fatigue which is an early sign of heart failure. No doubt, NYHA  gave much importance to this non-specific symptom in heart failure. Further, Individual organ functions may react in a different fashion with respect to water logging.Hepatic, portal splanchnic congestion directly affect GI function and intermediate energy metabolism.

.(*HF with zero edema so-called dry CHF  is a bigger mystery, is discussed elsewhere on this site)

When does the cardiac failure become a disorder of sodium & water metabolism 

Though the heart is a mechanistic pump when it fails it soon becomes a neuro-metabolic-endocrine problem. We are not clear whether heart failure retains sodium and water equally?  In renal failure-free water, accumulation is less than sodium. What happens in cardio-renal syndrome. These have practical implications as both hyponatremia and hypernatremia can be a feature with water content modulating it.(Now the term dysnatermia is more often used)

If RASS is activated net gain in sodium is expected. It doesn’t really happen. (Even with secondary hyperaldosteronism  sodium knows how to escape from the kidney). Vasopressin antagonist was considered a new innovation for hyponatremia associated with HF. To know the current role of V2 receptor antagonists Tolvapan, read here. 

Can we get rid of this excess water by any other means 

We do have powerful diuretics. It can unload the heart rapidly but can be harmful due to intracellular dehydration and electrolyte imbalance. When I asked an experienced Nephrology colleague  “Does excessive diuretics deplete ICF or ECF space? and how to quantify? , he was honest enough to accept, that it is primarily guesswork in a given patient and clinical assessment is supreme.

It is understood now, that there is a role for ultrafiltration of pure water in refractory hydrophilia. Bart B.A  (RAPID-CHF) trial. J Am Coll Cardiol. 2005; 46: 2043-2046

Imaging subclinical edema in heart failure 

How to catch Heart failure early before clinical edema ? NT pro-BNP is a good option (>400pg/l) but physiologists armed with new generation imaging are working on how and where the fluid is accumulating in early heart failure. Nailfold video capillaroscopy (NVC) and confocal laser scanning microscopy (CLSM).  Wish, these modalities are really useful and do not end up as fancy tools and hike up the heart failure treatment costs. 

 

Yakimov BP, . Pericapillary Edema Assessment by Means of the Nailfold Capillaroscopy and Laser Scanning Microscopy. Diagnostics (Basel). 2020 Dec 18;10(12):1107. doi: 10.3390/diagnostics10121107. PMID: 33353241; PMCID: PMC7766602.

 

Future of Cardiac Hydraulics management.

1. Afterload reduction, 2. Preload optimization, and 3.Inotropics. We have been playing with these three famous principles in heart failure treatment for quite some time. We must admit, nothing really worked to our expectations. “Total body water management” is a new hope. It will revolve around a mechanical fluid management system as this overview from circulation tantalizingly discuss. DRI₂P₂S  (Circulation heart failure 2020)

Final message 

Edema in HF is primarily extracellular and interstitial until the end stage. Fortunately, the ionic and osmotic forces along with capillary hemodynamic forces keep the excess fluid within a safer interstitial compartment. However, we must realize each organ swells in a different manner depending upon cell membrane responsiveness to neural and humoral factors. The mechanism and content of edema fluids are different in heart vs kidney failure. It is also true, that every cardiac failure patient has a renal component and vice versa.

That’s it. I know it was a superficial attempt to understand water distribution in HF. Someone needs to break the complete truth about H2O metabolism in cardiac failure.

Postamble & a Non-academic trail

 Should we really bother to know where does fluid accumulate in HF ?  In a pragmatic sense the answer is “No” Let it accumulate anywhere, just push inj. Lasix, or if refractory add Metolazone and Torsemide, (I need to rush to the cath lab for the next angioplasty for that angina-free RCA stenosis, you know !)

Reference

This 37-page landmark review about fluid dynamics will help you find many queries raised here. (Tough read though)

wp-1652850634527Download

 

 

 

 

 

 

 

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Posted in cardiac failure | Tagged edema in heart failure, heart failure |

When to revascularise in stable CAD: A Single slide presentation

April 2, 2022 by dr s venkatesan

This graph is a rare treasure in CAD therapeutics (fished out from a huge, often conflicting chronic CAD literature) that elegantly shows us the complexities involved in the revascularization of ischemic hearts with risks and benefits criss-cross each other. Our job is to identify, that critical point in a given patient’s CAD timeline for optimal management. To make things difficult, this point is a moving target and makes this delicate clinical exercise truly complicated.

http://assets.escardio.org/assets/presentations/OTHER2013/Coronary-physiology/213-PIJLS.pdf

It conveys a simple message in strong terms. It says the inflection point is around 10-15%. When the total ischemic areas are beyond this the benefits increase and when it is less there is sure shot harm.

Now comes the tough part. How best we can identify and quantify the true area of ischemia?

There is no such thing called coronary mathematics. Even if we try to make out one, vascular biology will giggle at us. Still, we have no other option but to go for sophisticated imaging modalities. Stress Echo, Nuclear Imaging, Scar imaging, MRI, PET, quantify total ischemic burden, plot it with corresponding coronary anatomical zones for a potential correction.

What this curve does not convey is the complex interplay between Ischemia vs symptoms. Ischemic myocytes have so many invisible tricks to adopt themselves. Should I go after the burden of Ischemia (Often Imaginary) or the burden of symptoms? Despite the lack of benefit in most trials on CTO in hard endpoints, it is yet to rectify the thinking patterns of many elite evidence-based cardiologists.

Final message

However, It will be an unpardonable act of omission if we miss or fail to offer the benefit of opening a critical LAD disease that has troublesome symptoms.

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Posted in Uncategorized | Tagged medical vs pci vs surgery in cad, revascularisation in cad, wisdom slides in cardiology | 3 Comments »

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