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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 

Inferior STEMI, and see the first shot in RCA below. The patient was pain-free and hemodynamically stable at the time of the angiogram. (Don’t wonder how this is possible, defying the fundamental rules learned from  animal experiments after acute ligation of the coronary artery)

                

What needs to be done ?
  • Go ahead and do a primary PCI as we do in any other  IRA.
  • Be watchful, just pass on the wire, feel the lesion, and decide thereupon. Consider intracoronary lysis.
  • How about a long stent from proximal to distal RCA?
  • Kissing the lesion with DEB in the tightest segment (Not a funny option )

 

 

What was done? How is the patient?

Nothing was done & nothing happened to the patient as well. Just guidewire was crossed and few minutes of balloon touch-up work. Did the patient improve? Can’t say anything because he was fine even with this total occlusion. 

Lessons to be learned 

  • The art of leaving a lesion left unattended (rather unstented) in IRA without guilt.
  • TIMI zero flow in IRA need not be a death sentence for the distal myocardium, even in STEMI. 
  • Sometimes, a simple guidewire crossing can do the same job as a complex angioplasty in an IRA.(For acute salvage TIMI 2 or even TIMI 1 is good enough) Most IRA accidents happen when trying improve upon this in an ectatic vessel.
  • Risks of stenting in ectatic /Thrombotic segment is real
  • There can be a useful role for  STENTYS self-expanding stents in localized ectasia (Ref 1)
  • Long-term OAC (Soon NOACs) is a perfect remedy for protecting this type of coronary. 

* By the way, who are all bothered to know LAD anatomy in this patient.  Is it surprising the  RCA is sending collaterals to the left side in its hour of crisis? Yes. LAD had chronic sub-total lesion as well.

Reference

1.The Role of Self-expanding Stents in Patients with Atypical Coronary Anatomy | ICR Journal https://www.icrjournal.com/articles/role-self-expanding-stents-patients-atypical-coronary-anatomy

 

2.

 

Yes, it is a triple vessel disease, with one tight lesion and at least two other significant lesions. One of them appears diffuse as well. 

Representative Image: Source courtesy DOI: 10.14740/cr548w LicenseCC BY-NC 4.0

“What to do next?. Is he symptomatic?  Yes. Definitely has significant angina” but LV function is normal.

“Ok then. If you are daring enough, ask this question”.

Which lesion is causing angina?

No easy answer at all. Try looking for some clues right from history, ECG, stress ECHO, meticulous assessment of individual lesions. Realize, even sophisticated imaging like SPECT, PET functional MR, may not help much either.

Oftentimes, we need to use the lean resources of collective common sense and clinical acumen. 

  • If it is post ACS status,  consider residual ischemia in the culprit artery is the cause for angina.
  • Second, consider the tightest lesion as angina-related.
  • Or the complex, eccentric, thrombotic lesion is responsible.
  • Next, consider LAD as default lesion as  angina related artery (Statistically right 75%, prognostically perfect decision) 
  • Watch for ECG changes during chest pain (ST depression usually don’t localize, but experience tell us V5 /V6 ST depression is more likely to be LAD ischemia )
  • Echo wall motion defect either during rest or (more usefully) in stress can really help. (It needs some effort to look for Wall motion mapping with coronary lesion subtending segment)
  • What about balloon inflation test during PTCA ? . Prompt angina when a lesion is occluded may give a direct clue.

Want to get more confused?

  • Ask your colleagues for an opinion either online or offline.
  • Do FFR/QFR/IFR  and OCT and look for intracoronary pressure-flow data and plaque burden. We are entitled to get excited about fibrous cap thickness, and hunt for vulnerable lesions and decide thereupon.  

Finally some easy options. 

Which lesion is causing angina? Never entertain that troubling question at all. (Need not  squeeze your coronary intellect you know ) 

Consider every lesion as important 

  • Get ready to stent all three or more lesions.(Many times forbidden though !)
  • (or) More convenient, refer to CABG. (Surgeons will welcome for sure )

Final message

Which lesion is causing angina? is indeed an important query one should raise. This paves way for selective focussed PCI in deserving lesions alone. However, when dealing with complex lesions subsets. the most pragmatic way as of today is to educate the patient and include them in the decision-making process (Never forget to offer medical management as a permanent option, especially if there is no critical LAD disease, and say thanks to  ISCHEMIA/COURAGE/ BARI 2D.)

Late PCI: This is a tricky topic to discuss on any day. A tight walk on the evidence base and a narrow risk-benefit ratio. The problem starts right from the genesis point of the true-time window, to the host-dependent myocyte response to hypoxia. Finally, we have the ubiquitous open artery hypothesis, that can taunt even the best brain in cardiology.  

 

 

 
 

We know the right ventricle is a weak pump compared to LV. This is evident from the triangular pressure-volume loop of RV. RV not only generates less pressure, its thin wall and its direct connectivity to the extrathoracic compartment make it vulnerable to hemodynamic fluctuations whenever Intrathoracic pressure swings.

Note the lowly lying pressure-volume loop of the right ventricle. RV is a too gentle chamber and needs to be handled with extreme care especially when it is failing acutely.

Patients on ventilators are typically exposed to iatrogenic rise and fall in right heart pressure. If continuous airway pressure is kept high it’s directly add on to RV afterload. The second adverse event is through interrupting venous return (preload). 

 Effect of mechanical ventilation on RV

  • RV preload is reduced (If they drop too low – they are equivalent to be in “Status Valsalva maneuver” ) 
  • RV afterload increases when Inspiratory airway pressure is increased. (
  • If RV is grossly dilated it may encroach LV and interfere with its function (Reversed Bernheim effect )
  • Many of the unexplained hypotension and reduced cardiac index are due to suboptimal ventilator setting
  • Ventilator increases the mean RA pressure, and if there is PFO, it can shunt right to left and aggravate the preexisting systemic hypoxia. 

In some of the situations where RV is already in the fighting mode for survival, imagine its plight when it had to take on the adverse setting of the ventilator as well. This happens in RV infractions. Pulmonary embolism,  dilated cardiomyopathies, Post heart transplant, and in general in many  ARDS patients. Discussing the ventilatory settings and a sound understanding of the prevailing hemodynamics of patients is so important.

Settings need to be optimized (Good to acquire a basic knowledge of from an Intensivist/Anesthetist)

  • .Optimal PEEP (Often dynamic but <18cm H2o) 
  • Tidal volume 
  • Avoid Hypoxic pulmonary vasoconstriction and hypercarbia (<60mmhg)
  • RV dysfunction can be an independent indication Proning the patient (Apart from PaO2/Fio2 ratio) 

Final message

It is a paradox, for patients with LV, failure ventilators instantly help as it unloads the left ventricle and relieves pulmonary congestion on the go. The same can’t be said about RV dysfunction. Ventilators interfere with RV  in multiple complex ways. However, simple settings change can improve blood pressure dramatically. Always aim for an RV protective ventilation strategy. Many times It’s in our hands to let the tired RV free, from fighting its friend (or foe).

Reference

A comprehensive resource

1.Disselkamp M, Adkins D, Pandey S, Coz Yataco AO. Physiologic Approach to Mechanical Ventilation in Right Ventricular Failure. Ann Am Thorac Soc. 2018 Mar;15(3):383-389.

2.krishnan 2015 Download

 

3.A. Paternot, X. Repessé, and A. Vieillard-Baron, “Rationale and description of right ventricle-protective ventilation in ARDS,” Respiratory Care, vol. 61, no. 10, pp. 1391–1396, 2016.

 

Sharing a presentation on lipid control done in 2020. This talks about newer strategies beyond statins.

 

 

 

A 75-year-old male post CABG with severe LV dysfunction and ICD and dual-chamber pacer in situ presented with NSTEMI.

An angiogram revealed something, and he got this form of treatment. ? What is it?

Image and case courtesy Patel R, Ghadiam H, Patel P, et al. (April 05, 2020) Angina Leading to Metal in the Heart: An Interesting Case of Saphenous Vein Graft Coiling. Cureus 12(4): e7546. doi:10.7759/cureus.7546

Features of SVG venous graft aneurysm

Graft aneurysm what are the risks?

  • Thrombosis
  • Recurrent ACS
  • Rupture 

Management 

  • Vascular plug
  • Multiple coils  (Does coil occlusion offer a permanent cure?  I can’t think so )
  • Covered stent
  • None. No Intervention Just OAC & observe, follow up can be a good option and can beat all above three in many patients.

Reference

1.Ramirez FD, Hibbert B, Simard T, Pourdjabbar A, Wilson KR, Hibbert R, Kazmi M, Hawken S, Ruel M, Labinaz M, et al. Natural history and management of aortocoronary saphenous vein graft aneurysms: a systematic review of published cases. Circulation 2012;126:2248–2256.CrossrefMedlineGoogle Schola

2.Dieter RS, Patel AK, Yandow D, Pacanowski JP Jr, Bhattacharya A, Gimelli G, Kosolcharoen P, Russell D. Conservative vs. invasive treatment of aortocoronary saphenous vein graft aneurysms: treatment algorithm based upon a large series. Cardiovasc Surg 2003;11:507–513.CrossrefMedlineGoogle Scholar

3.Nolke L, McGovern E, Wood AE: Saphenous vein graft aneurysms; the true, false and ugly!. Interact Cardiovasc Thorac Surg. 2004, 3:631-633. 10.1016/j.icvts.2004.07.011

TAVR is a game-changing structural interventional procedure that delivers an Aortic valve percutaneously. With hardware and expertise constantly Improving, excellent outcomes are common. However, this video clip reminds us, nothing can be taken for granted in any Intervention. (Sharing a Twitter feed Courtesy Raffaele Piccolo)

Why did this complication happen? Hardware, technique, or a fragile Aorta?  or just bad time  The fatal perforation seems to have occurred near the distal arch, with no visible signs of porcelain Aorta or gothic aortic arch. What could have been done? Could an ultra-fast deployment of a covered stent with ECMO support possible? Extremely difficult task.

Further reading 

Evidence-based medicine (EBM) is being projected as a scientific God’s secret specialty. Physicians who don’t follow EBM are considered unfit non-professionals. Presumably, in pursuit of truth, all those glamorous official bodies in cardiology bring out umpteen number of protocols, guidelines, advisories, and recommendations.

The blueprint for EBM

We have the famous 3 levels of recommendation backed up by different levels of evidence. Many of us trust these as the jury’s final verdict for most illnesses in cardiology. I would like to bring one particular issue about this hugely popular model of EBM. It is about one specific class of Indication referred to as 2b. The other day, there was an intense argument for an ICD in a young HCM patient and CRT in DCM based on this 2b stuff. Kindly request all of you to pause for a moment and introspect. We can realize, class 2b plays a mischievous game in EBM with the English language “may and may not”. It tries to push subconsciously an interventional bias from equipoise, in spite of lack of good evidence and clear divergence of opinion and a possible trend towards harm.

Further, there is widespread reluctance in many cardiac workgroups to refer class 3 recommendations as an absolute (or at least relative contraindication) It was strange to note one of my colleagues argued that,  class 3 is also a fair recommendation, to accept or reject is in our domain. I was initially shocked to hear that but had to agree with him ultimately as we realized a significant chunk of interventions we do, like delayed PCI > 24 hrs, CTOs, and chronic stable belongs to the proud class 3 recommendation. The debate came to a funny end when a senior cardiologist confessed somehow class 3 seemed to be a lesser evil than even class 2B.

Final message

For the sake of our patients, we need to bring an urgent reform in the EBM. Let us merge class 2b with class 3 and put it in a single basket and keep it out of reach to all tempting stakeholders. We shall display only class 1 in our therapeutic showcase.

Counterpoint

(*Dynamic recommendations is the norm in science, as we accumulate evidence with time.. Agreed, let us do this silently in research labs. Don’t bring it to practical guidelines. No, can’t agree. Freedom to indulge with an experimental modality in a no-option patient must always be there as we are able to give the benefit of doubt to these helpless patients. This is a valid argument but we must not forget even in dire situations  good option need not be a compulsive action, it can be in action as well)

 

 

Why ISCHEMIA trial conclusions often make us nervous?

Because, we know we can’t follow the lessons from it with true intent, as many of us are near slaves to Invisible Interventional forces in some form or other.

I would think, ISCHEMIA trial in one sense was a wasted effort. We always knew OMT is superior to any sort of PCI in stable CAD  (Backed up with COURAGE /BARI 2D/and of course the deadly exposure by ORBITA )

Anyway, we did ISCHEMIA for the sake of deniers, with huge public funding to prove the truth as truth.

Still, I am sure ISCHEMIA will be looked down, by most elite Intervenionlists. For the rest, it becomes a tough fight with their conscience. 

A recent review on European cardiology review 

Final message 

I don’t know, how many more trials would be required to tell us the same story all over again. Hope we grow enough COURAGE to follow the ISCHEMIA lessons. Let us (try to ) make a full stop on this issue.