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Is there an entity called “Isolated” systolic pulmonary arterial hypertension ?

May 15, 2020 by dr s venkatesan

What is the incidence of Isolated systolic pulmonary arterial hypertension (ISPAH) and its Implication? We attempted to answer this question and found some interesting answers. It was published in the Indian heart journal  December 2007 Abstract issue. More than a decade gone. I think this issue is still largely misunderstood. Fellows may pursue this. One more parameter that can be explored is pulmonary artery pulse pressure and effect on progressive pulmonary vascular disease and PVR. Mean while  PAH definition and classification has changed many times, ISPAH definitely requires a place in the new scheme of things.

The abstract

ISOLATED SYSTOLIC PULMONARY ARTERIAL HYPERTENSION
S.Venkatesan ,G.Gnanavelu,V.Jaganathan , Madras Medical College. Chennai

Pulmonary circulation is a classical example of a low-pressure low impedance circulation. It is generally presumed high output states generally do not increase the systolic blood pressure in the pulmonary circulation. In systemic circulation, there can be divergence of systolic and diastolic blood pressure depending upon the cardiac output and peripheral vascular resistance. This has resulted in separate clinical entity -Isolated systolic hypertension.(ISH). It has been our observation many of the patients with PAH during echocardiographic and cath study were found to have an elevation of systolic pulmonary artery pressure(PAP) with normal diastolic PAP . In this context, this study was undertaken to specifically identify whether there is an entity of Isolated systolic PAH
( ISPAH ) and it’s the incidence in various clinical situations.
We analyzed the echocardiographic data of patients who were referred to our echo lab retrospectively. A total of 4000 echocardiograms over a period of 6 months were reviewed. Majority of these patients were referred for routine screening echo from our OPD. Data from patients who were assessed to have PAH were thoroughly scrutinised. They constituted shunt lesions, RHD,PPH, COPD, pregnancy, and patients with unexplained dyspnea for evaluation Those Patients who had both TR and PR jet were only considered for analysis .The Systolic PAP was estimated with TR jet and diastolic PAP with End diastolic PR Jet. ISPAH was diagnosed when the calculated systolic PAP was more than 30mmhg. And the diastolic PAP was less than 16mmhg  Antenatal women formed 2 % of the study population. A total 72 patients fulfilled the criteria of ISPAH Among the shunt lesions it was most common in large VSD( 4/10), followed by ASD(14/35) and PDA( 1/3) . In patients with RHD it was observed in 12%(15/110) , COPD 10%(15/150), in pregnancy and general population it was 5%(23/450). None of the patient with PPH had ISPAH.The mean Systolic PAP was 38mmhg(R 32- 74) The mean diastolic PAP was 14mmhg(R 8-15).The highest systolic PAP was 74mmhg recorded in patient with large VSD.
It is often presumed hyperkinetic states elevate systolic PAP and reactive elevates diastolic PAP .But it is clear from our study the rule is not that simple. Surprisingly many of the RHD patients had only the systolic PAP raised.It is important to recognize systolic PAP was very high in some of the shunt lesions. Taking this alone as an index of severe PAH is fraught with the risk of declining corrective surgeries in these patients.
Perhaps the most important observation from the study is the incidence of PAH in apparently healthy individuals, which is very significant as it could be the marker of continuously increasing chronic lung disorders due to the worsening environment of the 21st century.

 

A PowerPoint presentation of the paper is available with the author and may be requested.

Posted in Pulmonary arterial hypertension, Pulmonary circulation, Pulmonary vascular resistance, Thesis/Research topics for cardiology fellows | Tagged , , , , , | Leave a Comment »

Can we mix philosophy with science in medical teaching ?

May 14, 2020 by dr s venkatesan

I think it is an Invalid question. Whether you like it or not , medical science and philosophy are always bonded together and its relationship is eternal. It doesn’t make sense to separate them. I think we have misunderstood the meaning of philosophy. While science is presumed truths, philosophy is trying to believe in unknown truths. Philosophical truths are built-into every decision a medical professional takes.

If the expected natural history of any disease is science, unexpected deviations are philosophy. (RT PCR testing for diagnosing  Corona is science, why 90% of them are not infective and don’t transform disease is philosophy) When something is not seen or quantifiable like human immunity, it is a perfect example of concealed science or manifest philosophy.

Taking about what we think we know is science, Talking about what we really don’t know is philosophy. The term Idiopathic syndrome finds a  proud of the place in every specialty in medicine, Isn’t? 

 What will be your answer when your patient wants an assurance that a stent, you had just implanted will not get occluded in the next 6 months or so.“I don’t know, I cant assure you about that”  will be your most likely answer. (Though, we do it in style, hiding behind  the scientific hyperbole decorated with numbers,  also referred to as statistics) Please realize, this is the expression of medical philosophy in the finest form.

Final message 

My Impression is, philosophical truths should be liberally used in a regular fashion right from the first-year medical school to advanced specialty teaching. This seems essential as science in the current times suffers from too much sanctity. This has spilled over to the doctor population as well, and make them appear invincible. 

If only we realize science often trails behind the philosophical truths at least by a few decades, our patients will not be injured inappropriately and prematurely. Mixing science with philosophy in the right composition ( a perfect academic cocktail ) will bring out the best from the noble profession.   

Postamble

Can anyone guess, why scientists are given a doctorate in Philosophy degree  (PhD ) ?

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Difficult calls in cardiology : Be ready for DC cardioversion during pregnancy !

May 11, 2020 by dr s venkatesan

Fortunately, indications for DC cardioversion in pregnancy is rare. A literature search suggests only about 50 cases are reported. I haven’t shocked electively in pregnancy but occasionally have come closer to it. In this current corona lockdown period, we had a call for a potential shock in pregnant mother with fast AF, which was again avoided by the optional  rate control measures.

Let us see, how often DC cardioversion might be necessary during pregnancy and few tips for its safety.

General principles

We know pregnancy can be pro arrhythmogenic. Most arrhythmias are non-sustained VPDs and APDs.They can be ignored if there is no structural heart disease, or at least postponed till delivery.

Drugs remain the mainstay.

The most common sustained arrhythmia in the young reproductive age group is SVT (AVNRT/AVRT) that can be managed with drugs like  Adenosine and beta-blockers. (Flecainide/Sotalol are found to be safe in pregnancy) . Though IV Verapamil is very effective, it has with some concern for fetus, so better avoided. Please, note many of the SVTs can be reverted with simple vagal maneuvres and oral beta-blocker /Verapamil. IV Digoxin has been widely used in RHD population for AF during pregnancy.

Mind you, even Injections Adenosine, Esmolol do have bradycardic potential and need to be given in monitored setting (No surprise, they are called medical cardioversion with the attendant risk) 

The universal antiarrhythmic drug Amiodarone still might come in handy in any refractory arrhythmia (Including AF) though it comes under the list of contraindication.(Safety of amiodarone in pregnancy) 

One important suggestion to make. Magnesium is a wonder antiarrhythmic drug, a membrane stabilizing agent through its indirect Ca + and K + blocking properties can be a powerful antiarrhythmic agent, especially in VT. This has a unique safety profile in pregnancy.We use it in eclampsia liberally  with the same action to suppress brain convulsions. (Cerebral tachycardia). Please consider IV magnesium  prior to considering  shock in VTs with dysfunctional ventricles as in peripartum cardiomyopathies et(Dose  to 2 g in 10mL of D5W over 1 to 2 minutes)

Consider DC shock only if there is hemodynamic instability.

Hemodynamic instability demands DC version. One practical issue is , what defines hemodynamic instability? In pregnancy, the systolic BP is already in lower normal due to systemic vasodilatory state. An HR>150 makes it further fall to around 90mmhg. This tempts us to label it as unstable. In this situation, we have to rely on patients’ symptoms to define hemodynamic instability. Never try to shock a comfortable pregnant women in whatever tachycardia she is in . (Including some VTs especially from outflow, fascicular, etc  ) Try to use drugs and get an expert opinion. to rule out subsets like cardiomyopathy, documented CAD, LV dysfunction.

When to shift to a cardiac facility?

This question crop up often. It is mainly logistic. May be in peripartum cardiomyopathy /Suspected ACS  with VT require special care.

 DC Shock checklist  & Precautions 

  • Biphasic shocks with energy levels 100 joules ( up to 200). Ideal to give single shock, ok to err on high energy  
  • Pads should be well away from the abdomen. 
  • Synchronized with QRS complex (Machine does this) 
  • In an unusual event of VF and cardiac arrest Defibrillation with 300/320 J (Here unsynchronised) 
  • Check the crash cart ready with essential drugs.
  • Keep cardiologist either on-call (Even a junior resident in labor room give immense confidence) 
  • Rule out  LV dysfunction or significant valve disease by echo (CAD can’t be ruled out though) If echo machine is not available ask the radiology or cardiology fellow to use the abdominal USG probe to document good LV contractility and gross EF% estimate.
  • If intramural thrombus is not convincingly excluded and there is AF and valvular heart disease, better to heparinse  and shock to avoid embolic events.
  • Temporary pacemaker support (Some of the cardioverters has transcutaneous pacing to tide over transient bradycardia that might occur post-shock) 
  • CPR readiness ( Extreme precaution !)
  • Fetal heart monitoring and Emergency cesarian readiness. 
  • Finally, most important consent with patient and family.

Is electrical Insulation of baby necessary or is it possible? 

 It’s not required. Fetus inherently tolerates stress better. Even if,  few joules reach the fetal heart inadvertently it may not mean much. What is, to be worried is maternal hypotension or bradycardia post-DC shock.

Impact on the fetus: Evidence?

The impact on fetal blood flow is not significant. This report from Taiwan  reassures there is no adverse effect by measuring umbilical artery flow (Yu-Chi Wang European Journal of Obstetrics & Gynecology and Reproductive Biology 126 (2006) 268–274)

While we consider DC shock during pregnancy is safe for the fetus, still, shock pads close to the abdomen, amniotic fluid being a good conductor of electricity at least one mother showed a sustained contraction of the uterus and fetal distress. This was possibly attributable to DC shock  Eleanor J. Barnes BJOG 2003 https://doi.org/10.1046/j.1471-0528.2002.02113.

Final message 

Most cardiac arrhythmias in pregnancy are carefully managed by non-electrical means. Of course, emergencies can’t afford to wait. Though two lives are at stake, it’s the mother’s heart that prevails over in drug selection and risk estimation. After all, it is her loving heart, that keeps the fetus alive.

I have seen Obstetrician anxiety (which spills over to attending cardiologist too!) can be extreme in such situations. I must admit, Obstetricians, are truly sincere warriors fighting at odd hours to protect the two delicate lives. After all, taking  responsibility brings the anxiety. Cardiologists must understand this and help them out in their difficult times.(without any super specialty ego !)

Reference

  1. Crijns HJ. Electrical cardioversion in healthy pregnant women: safe yes, but needed?. Neth Heart J. 2011;19(3):105‐106. doi:10.1007/s12471-011-0079-3

 

2.Finlay AY, Edmunds V. D.C. cardioversion in pregnancy. Br J Clin Pract. 1979;3:88–94. 

3.Oktay C, Kesapli M, Altekin E Wide-QRS complex tachycardia during pregnancy: treatment with cardioversion and review. Am J Emerg Med. 2002 Sep;20(5):492-3.

Which drugs are safe?

From BMJ 

Click to access pregnancy_heart_disease_v28_web.pdf

 

Further frontiers 

The DC shock from ICD experience

There have been a good number of women who got ICD for various indications (Commonly HOCM, long QT, ) who subsequently became pregnant, successfully managed during pregnancy.

(One rare study Andrea Natale et ll Circulation. 1997;96:2808–2812 documents at least 10 shock episodes documented in large series of 44 patients without any consequences)

 

 

Posted in cardiology women, Pregnancy and heart, Uncategorized | Tagged , , , , , |

Do I add “real value” to my medical profession ?

May 10, 2020 by dr s venkatesan

 

A throbbing query …for so long

Got into this amazing lecture, that Infuses knowledge and wisdom about values in life, in just 14 minutes .Probably, It has more treaures than what we may get, in our entire life time as we search for truths.

I wonder, such thoughts can come only from God’s special messengers.Devdutt Pattanaik seems to be one. 

 

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Why we ignore LA appendage when measuring LA volume?

May 7, 2020 by dr s venkatesan

LA volume is one of the critical parameters that define (as well as determines the symptoms) both diastolic and systolic LV dysfunction.Still, we are tentative in the true estimates about the normal range of LA volume. (Upper limit 40ml/m²) .We are surprised to note, the difference between MRI derived and Echo measured LA volume showed a disturbing variation nearing 80 %.

How to measure  LA volume?

While the timing of LA volume measurement has not much controversy (end-systole), and the shape errors are largely eliminated by 3D echo, still why this variation?

It is a telltale error, of either including (or excluding ) the pulmonary vein ostium and complete blindness to LAA during LA border tracing. We know, LAA is physiologically, pathologically, and electrically is a critical accessory of LA. Still, we have so for excluded it from routine LA volume calculations. Is that a right-thinking in the overall evaluation of LA volume?

Normal LAA volume

Though the LAA volume is directly related to its size, shape much great confounder, since it precludes in arriving any mathematical calculation of volume from the area. Direct casts ofLAA and 3D echo to a certain extent will help measure LAA volume. MRI may also do the same.The normal LAA volume is calculated to be up to 20 ± 9 ml. Whatever be the  LAA  volume, one estimate suggests it will reach 25 % of total LA volume. This is very important to know. In fact, In significant LV dysfunction, LAA  is expected to stretch, efface, and dilate and contribute more to LA volume. Both static and dynamic LAA volume status also gives us an idea about potential thrombus formation risk.

(Ref : Measurement of Left Atrial Appendage Size by Transesophageal Echocardiography  Kazuko Yoshimoto et al. J Med Ultrason (2001). 2012 Jan.)

Are we justified to Ignore the LAA volume during routine LA function assesment ?

I don’t know. It may be wise to routinely add LAA volume to LA chamber volume to truly assess  1.Overall LA function, 2.Estimate the risk of thrombus formation and  3.Risk of developing AF. Meanwhile, its found LAA appendage volume might even approach that of  LA volume when it’s pathologically enlarged. (Left Atrial Appendage Volume as a New Predictor of Atrial Fibrillation Recurrence After Catheter AblationPedro Pinto Teixeira et al. J Interv Card Electrophysiol. 2017 August) 

LAA volume is Important for one more reason 

We are getting new data about dynamic LAA volume status during LAA closure.In fact , this particular study (JACC: Cardiovascular Interventions Volume 8, Issue 15, December 2015)  documented how LAA appendage balloons out during volume loading of LA.This study suggests we have to be careful about the hidden potential of LAA to expand and if ignored the device is likely to get dislodged with volume overloading. These observations make it clear we can’t isolate LAA volume when calculating LA volume. 

Final message

There is a strong case for measuring  LAA size & volume separately and preferably be added in the net LA volume Index. We can’t simply Ignore this vital and inherent part of LA , just because its called as an appendage. Of course, even a novice will rank LAA first,  as the pathological hot spot within the entire LA.

Reference

Everything about LAA

Giuseppe Patti, Vittorio Pengo, Rossella Marcucci,The left atrial appendage: from embryology to prevention of thromboembolism  European Heart Journal, Volume 38, Issue 12, 21 March 2017, Pages 877–887, https://doi.org/10.1093/eurheartj/ehw159

 

 

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Anatomical paradox: When ventricular outflows crisscross , left main becomes closer to RVOT , than even the LVOT !

April 26, 2020 by dr s venkatesan

Thermox flask Image

If you think coronary artery ostia are exclusively related to LVOT, and they nowhere come closer to RVOT, we are seriously wrong for some hidden anatomical reasons. Though, Its a well recognised anatomical reality , we had to learn it from EP labs during the ablation of RVOT VT. The left main ostium is at equal (If not more ) at risk as we ablate across RVOT.The reason being the complex twist God conferred on the outflow tracts of heart.

The LVOT goes beneath and posteriorly travels from left to right, while the opposite happens for RVOT. This results in the net anatomical conundrum of RVOT and LVOT sharing common wall at some part.

Here is an excellent article that specifically looked into this issue of the relationship between RVOT and the coronary artery.

(VASEGHI, M., CESARIO, D.A., MAHAJAN, A., WIENER, I., BOYLE, N.G., FISHBEIN, M.C., HOROWITZ, B.N. and SHIVKUMAR, K. (2006), Catheter Ablation of Right Ventricular Outflow Tract Tachycardia: Value of Defining Coronary Anatomy. Journal of Cardiovascular Electrophysiology, 17: 632-637. doi:10.1111/j.1540-8167.2006.00483.x)

The following illustration from this paper reinforces this . The left main is just 4mm away from RVOT.(While, the distance from LVOT to left main ostium is much wider)

Final message

Never underestimate the risk of injuring the left coronary ostia when you manipulate catheters and devices across RVOT. This is especially true with RVOT ablations. There has been so many instances of injuring coronary arteries and precipitating ACS. Working within the right heart tends to give a false sense of safety, as if you are away from systemic coronary circulation. After all, both outflow tracts originate from the same embryological source (bulbus cordis) still, intertwined in adult life, not willing to leave its innate anatomical Intimacy that began and ended between 4 th and 8th week of fetal life.

  1. D. Biermann, J. Schonebeck, M. Rebel et al., “Left coronary artery occlusion after percutaneous pulmonary valve implantation,” The Annals of Thoracic Surgery, vol. 94, pp. e7–e9, 2012.View at: Google Scholar

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Aortic valve anatomy : A complete exploration

April 25, 2020 by dr s venkatesan

Found a wonderful anatomy teaching resource. A succinct yet comprehensive lecture on Aortic valve .A must-read for anyone who deals with valvular Interventions. For the cardiology fellows , I can tell you can’t find anything better than this. Thanks to Prof Gregory M Scalia and the structural heart disease Australia. It starts with this one master diagram of Aorta in the center with all surrounding structures and goes on to ensure we watch this 25-minute lecture nonstop.

At the end of the lecture, you should be able to learn about.

  • The complex fusion points of LVOT with Aorta. Understanding them is critical as we deploy Aortic valve percutaneously.
  • Understand the illusion of Aortic annulus.
  • When it is an advantage to keep the aortic valve supra annularly.
  • The Implication of sharing of myocardial cells into the aortic cusp zone, and Aortic tissue into the myocardium.
  • How closely the conduction tissues located beneath the non-coronary cusp making it vulnerable with calcific spur Injury.
  • How pathology of Aortic root with its central location reaches the surrounding tissue.

These are just a few . . . It is a treasure out there.

Over to Prof Gregory Scalia

Please note ,the talk on Aortic valve begins after a brief conference Introduction.If you are not patient enough begin at 2.45mts.

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