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Archive for the ‘Pregnancy and heart’ Category

Pregnancy in Hypertrophic cardiomyopathy : LSCS or vaginal delivery ?

Posted in Pregnancy and heart, pregnancy and heart disease, Uncategorized, tagged , , , , , , on August 27, 2021|

Background

Yesterday, my fellow informed me about a frantic call for cardiac fitness for an emergency cesarian section in 24-year-old woman with hypertrophic cardiomyopathy, who is asymptomatic and has a 20mmhg gradient across LVOT.

“Was she in labor”?

“No, she is 36 weeks term.

“Why LSCS? Why emergency”?

“I don’t know sir. Let me discuss and come again”.

 HCM in pregnancy: An approach

Hypertrophic cardiomyopathy is a specific genetic disorder of myocyte (myosin and others) within the sarcomere. Though uncommon in pregnancy it raises considerable anxiety to the patient, family, and the obstetrician. 

Hemodynamics

Though we tend to worry more about dynamic LVOT obstruction, it is actually the restrictive physiology of LV myocardium that might cause more concern. Three key variables operate in this entity namely preload, afterload, and contractility that determine the cardiac hemodynamics and possibly the symptoms. We know the classical consequence of pregnancy is a fall in systemic vascular resistance( SVR) ie afterload.

In pregnancy, there is a complex interaction between these three parameters along with heart rate. Fortunately, the net effect ends up favorable for LV performance. This is made possible because a major compensation occurs by a 50% increase in blood volume that effectively counters the deleterious effect of fall in SVR on LVOT gradient. (If mitral regurgitation is significant, the fall in SVR actually may help reduce regurgitant fraction especially if its intrinsic defect )

Maternal outcome 

Is good (if not excellent). Maternal mortality reported in the literature, is gradually coming down (0 to .5% in various series)  However, about 15 % of HCM patients with gross LVH or obstruction, may develop pulmonary congestion in the third trimester. In some patients, VPDs, nonsustained VT, even AF can lead to some tense cardiac consultations but are usually innocuous. I am not sure about the sudden death in pregnancy. I guess it should be negligible, unlike the non-pregnant HCM. 

A mystery learning point

It is surprising  both fetal and maternal outcome is little related to the severity of LVOT gradient (Ref 2) 

Indication  for cesarian 

  • Most mothers can deliver per vaginalis without much hemodynamic challenge. 
  • Vey rarely cardiac indication for LSCS need to happen. (However, in the real world many land up in LSCS , since true indication can be blurred due to  cardio-obstetrical anxiety)
  • Spinal anesthesia to be avoided as hypotension is poorly tolerated 
  • Beta-blockers to be continued during pregnancy labor.(Need not start however if already not taking)

Fetal outcome

Premature birth, stillbirths, low weight are little more common than normal pregnancies. Fetal bradycardia due to beta-blockers has been noted but not troublesome.

What is the role of cardiologist?

The precise answer is “minuscule role”. I can vouch for this from a personal level. ( Consults are meant only for bringing some comfort to the obstetrical team). Active cardiac interventions are rarely required or rather desired. (Of course, patients who have significant symptoms, operated for HC, on OAC for AF, the rare ones with ICD needs expert care)

Final message 

  • Women with  HCM can safely become pregnant and deliver.
  • Best outcome is likely for both mother, and baby if basic precautions are taken.
  • LSCS is rarely required*.
  • Counseling about the condition needs to be gentle and just adequate. Dwelling deep into the pathology, hemodynamics, and statistics in totally asymptotic patients invites trouble to all stakeholders. 

*It is worthwhile to note other forms of severe  LVOT obstruction like valvular, supra valvular stenosis, and Aortic pathologies like Marfan, coarctation aorta are serious entities that deserve prompt cesarian sections.

Reference

1.Thaman R, Varnava A, Hamid MS, Firoozi S, Sachdev B, Condon M, Gimeno JR, Murphy R, Elliott PM, McKenna WJ. Pregnancy related complications in women with hypertrophic cardiomyopathy. Heart. 2003 Jul;89(7):752-6. doi: 10.1136/heart.89.7.752. PMID: 12807849; PMCID: PMC1767741.

2.

https://academic.oup.com/eurheartj/article/38/35/2683/3811991

 

3. ESC 2018 pregnancy heart disease guidelines 

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Heart disease in pregnancy: Overview & management

Posted in cardiology -pregnancy, Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions, Pregnancy and heart, pregnancy and heart disease, tagged , , , , , , , , , , , , on April 2, 2021|

Some of the questions  addressed  in this presentation

1.What happens to fetal blood pressure during maternal hypotension how good is fetal autoregulation?

2.Why is LSCS increasingly preferred mode of delivery in heart disease complicating pregnancy challenging the traditional scientific concept?

3.What is likely hood of patients with moderate mitral stenosis developing pulmonary edema during prolonged 2nd stage of labor?

3.What is the missing link between PIH and PPCM? How prepartum cardiomyopathy differs from postpartum?

4.Is Eisenemneger really an absolute contraindication for pregnancy?

5. How can we continue VKAs warfarin or Acitrom throughout pregnancy? What are the potential problems of double switching one at 6th week from VKA to Heparin and again from heparin to VKA  at  12th week?

Hope, the man-made hematological bridge in pregnancy has been finally liberated from confusion (Who is saying not yet?)

 

6. On what evidence base the safety margin of 5mg cutoff for Warfarin and 3mg for Acitorm was decided?

7. Who is insisting on us to do Anti-Xa monitoring for LMWH in pregnancy? Is it really needed? What does the American society of hematology say?  (ASH guidelines for VTE in pregancy 2018) Why we don’t insist on Xa estimation in acute coronary syndrome?

8. What is the inflection point of at which risk of termination is almost at equipoise with continuing pregnancy in various heart diseases.

A GIF run-through of the presentation.

PDF & video version will be posted

 

The ultimate reference 

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D-dimer levels in normal pregnancy : Learnt something Important recently !

Posted in Pregnancy and heart, pregnancy and heart disease, tagged , , on March 5, 2021|

Have we ever wondered how six liters of blood in our body flows like a live stream, maintaining the fluidity life long, in spite of an active coagulation system in situ, ready to freeze at the slightest provocation (Invisible vascular wear & tear!) This housekeeping job, within the vast network of the human vascular tree, is silently accomplished by a less apparent system called fibrinolytic system. D-dimer is a physiological breakdown product of this system . D-dimer comes from fibrin monomer. The D in D-dimer stands for the domain. (See below) The ability to detect the D-dimer in the bedside has given us a good opportunity to monitor intravascular thrombus formation and subsequent dissolution in health and disease.

 

 

Formation of D-dimer from fully formed fibrin clot with the help of factor X111a and plasmin

Learning from a false alarm of pulmonary embolism

Recently I came across a pregnant woman in the third trimester with sudden onset dyspnea. Ongoing panic and a  hyper response  ER protocol ended up in D-dimer estimation. It was 2600μg/ml, which created a false alarm among obstetricians. She was started on heparin by then. Though her saturation was 95%, ECG was normal.An emergency bedside echo revealed normal right atrium and ventricle, no pulmonary HT. The diagnosis of PE was now rejected confidently. The much-dreaded dyspnea turned out to be some patient anxiety. Unnecessary exposure of a fragile pregnant lady to heparin was reverted with much difficulty as no one was willing to discount jacked-up D-dimer still. (Such is the power of sophisticated biomarkers and numbers! I asked them to report the elevated D-dimer as false-positive in bold letters in the case sheet and applied the break to bring the high voltage obstetrical -cardiac consult to a halt ) 

What is the normal D-dimer levels in blood?

In the strict sense, D- dimer can’t  have normality. It is flushed-out molecular debris from clots, levles of which fluctuates depending upon the fibrinolytic load on a given day. It is further limited by lab standardization issues and methodology. (ELISA vs latex ) Currently, a level of <500μg/ml is considered diagnostically useful to rule out DVT/PVE (Good sensitivity /low specificity)

What happens to D-dimer levels in pregnancy?

D-dimer levels are nornally high in pregnancy, and  can reach very high levels as well. 

What is this source of D-Dimer In pregnancy? 

  • Pregnancy is a procoagulant condition. (Estrogen Induced effect on fibrinogen and other clotting factors especially factor 2  & 7 ) We presume it is due to more  microthrombus activity in materno placental capillary circulation. When there is a pro-coagulant activity, fibrinolytic activity is also high hence elevating FDP and D dimers. 
  • Pregnancy-associated with diabetes /PIH/preeclampsia elevate it further due to subclinical  endothelial dysfunction 
  • Placental source for D-dimer is documented. (Might be a marker for partial abruption as well)
  • The role of the fetus in generating or triggering maternal procoagulant activity is possible with a reverse breach in the placental maternal barrier. (Many of stillbirth, Intrauterine deaths / DIC in mother could reflect  pathological faces of hypercoagulation states) 

Normality redefined in pregnancy 

This paper has something important. Didn’t  knew this till now. In the third trimester, D-Dimer can reach up to 4400 in diabetic mothers. It is also worthwhile to note the other common causes for high D- dimers sepsis,  autoimmune disorders* and occult malignancy,

*In fact, every normal pregnancy can be termed as a relative autoimmune disorder, as it is impossible for the mother to go through the pregnancy without  immunological modification of the host (by fetus or host itself)  

 

 

Final message 

Never rely on elevated D-dimer in isolation to diagnose DVT/Pulmonary embolism. This is especially true in pregnancy where even very high levels are physiological. The commonest cause for dyspnea in pregnancy will continue to be anxiety, anemia, PIH & physical deconditioning, and weight gain  (not the mitral valve stenosis /PE/or peripartum cardiomyopathy). Yes, It may appear rewarding to think  like a specialist, but please realize if we diagnose rare entities, we are “rarely likely” to be correct and the consequences of that are not always pleasant.   

Reference 

1.Siennicka A, Kłysz M, Chełstowski K, et al. Reference Values of D-Dimers and Fibrinogen in the Course of Physiological Pregnancy: the Potential Impact of Selected Risk Factors-A Pilot Study. Biomed Res Int. 2020;2020:3192350.

2.Gutiérrez García I, Pérez Cañadas P, Martínez Uriarte J, García Izquierdo O, Angeles Jódar Pérez M, García de Guadiana Romualdo L. D-dimer during pregnancy: establishing trimester-specific reference intervals. Scand J Clin Lab Invest. 2018 Oct;78(6):439-442. 

 

 

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

Posted in cardiology women, Pregnancy and heart, Uncategorized, tagged , , , , , on May 11, 2020|

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)

 

 

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