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Posts Tagged ‘cardiology research topic’

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)

It is surprising, to note the aortic root behaves independently. It either contracts or relaxes with a range of 4 mm swing on either side of the systole and diastole. Another stunning fact is, it remains static in a significant number. (One possible explanation is the true aortic annulus is less dynamic because it is bordered by the fibrous skeleton, while the rest of the aortic root only can distend or shrink )

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

1.de Heer LM, Budde RP, Mali WP, de Vos AM, van Herwerden LA, Kluin J. Aortic root dimension changes during systole and diastole: evaluation with ECG-gated multidetector row computed tomography. Int J Cardiovasc Imaging. 2011 Dec;27(8):1195-204.

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]

 

 

 

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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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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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In CKD, LVH is a near-constant feature with echo showing thick, bright echoes from IVS. The LV mass increases, partly due to physiological hypertrophy ,also contributed by deposits of uremic middle molecules and fluid collection in the interstitium as myocardial edema.This, is recognised as T 2 weighted MRI signals. Chronic fluid stasis may progress to myocardial fibrosis. (Kidney Blood Press Res 2018;43:134–142 )  

Effect of Frusemide on myocardial edema 

We know, loop diuretics cause aggressive depletion of ECF volume and to a lesser extent Interstitial fluid. The effect of diuretic on myocardial water content is a poorly studied parameter.(Still more visible to a shrewd echocardiographer)

Effect of dialysis

While the effect of diuretics on myocardial edema is not consistent, however, we have observed definite regression of myocardial thickness, mass, and rigidity following dialysis. This transforms into a better LV systolic and diastolic function. At least in one patient, we have observed  the E velocity shrunk more than 50% the next day following dialysis pushing them to lower grades of HFpEF( A potential study topic.)

Final message 

The Improvement of the functional class of CKD patients immediately after dialysis is not only attributable to the removal of excess fluid and toxic uremic molecules, regression of myocardial edema plays an important role.

Further reading

Trinh E, Chan C, T: Intensive Home Hemodialysis Results in Regression of Left Ventricular Hypertrophy and Better Clinical Outcomes. Am J Nephrol 2016;44:300-307.

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