Lowering the raised LA mean pressure is a major therapeutic goal in any severely symptomatic left heart disease, whether it is valvular or myocardial disease. It is prudent to understand, that even in systolic LV failure; it is the raised LVEDP that causes the symptoms and marks the limits of exercise capacity. Drugs like inotropes, pre-load , afterload modulators like diuretics and vasodilators can take care to a certain extent.
When symptoms are refractory and the underlying condition has no primary correction , we need to intervene with some extreme procedures. We know a small ASD decompresses mitral stenosis, and the combination of ASD and MS, Lutembacher, is a well-known syndrome called Lutembacher. The concept of LA flow regulator or decompressor came from this .
When the left ventricle is stiffened and restrictive, and LA mean pressure is prohibitively high,we have a viable option now. This is to create a small regulatory orifice in the IAS ( A complicated term for a small ASD) to decompress the LA and reduce pulmonary congestive symptoms. Curious minds might ask, can’t we decompress LV it self by creating a small VSD. Probably in the thin membranous area. May be, it will come soon in the innovative lanes of cardiology.
The study finds the device can be beneficial without compromising much on RV side function.
Animation Courtesy: Corvia website; The procedure looks simple when compared with other procedures inside the LA .The device looks like an octopus, and sits on either side of IAS, like a stapler and maintains the orifice.
Here is an audio podcast from the primary author published in JAMA network.
Interview with Sanjiv J. Shah, author of Atrial Shunt Device Effects on Cardiac Structure and Function in Heart Failure With Preserved Ejection Fraction: The REDUCE LAP-HF II Randomized Clinical Trial. Hosted by James E. Udelson,
Final message
This device’s core concept lies in requesting the right ventricle to help its bigger brother LV at its difficult times. You can call this an artificially created interventricular dependence. Though it might help, we need to watch the right heart’s dynamics closely. Maybe, if RV is experiencing difficulty, we can have external control over the IAS orifice and flow as and when required. (This is not new, a remote-controlled switch regulation was done for pulmonary banding in children with congenital heart disease who needed regulation of pulmonary flow by a device FloWatch-R-PAB (Ref 2)
It is logical to expect the same device would be useful to decompress RA at high pressures as in severe primary pulmonary hypertension. If you think backwards, it looks the same as a life-saving, reverse Rashkind procedure variant in adult
Primary PCI of IRA , continues to be a clinically popular & statistically validated (In spite of some critical ifs & buts) coronary reperfusion strategy.
What to do, if we happen to detect, a significant or borderline lesion in the Non- IRA territory during pPCI ?
There are too many guidelines scattered across cardiology literature to “help or confuse” us on this issue. They argue for either immediate intervention or defer transiently, postpone or just ignore , based on clinical ,hemodynamic*, Individual, institutional , or some other non academic factors. (Permanently deferred PCI is other wise called medical management, is practiced by some inferior cardiologists or GPs who never refer such patients to higher centers after a stand alone thrombolysis)
* The FFR, iFR RFR, related stuff
What if if we are completely blinded to the status of Non IRA vessel ?
What do you mean ?
I mean , can we be, “not- aware” of contra-lateral lesion status ?
Yes, “Simply don’t do a non IRA angiogram , that’s it. If its RCA PCI , don’t shoot Left main, and vice versa for LAD. Do a PCI without doing a completed CAG. I mean IRA PCI alone, by guessing it by ECG .
What a crazy Idea ?
This week’s JAMA has something* relatable to this idea. The aim was to do PCI before complete CAG , to document any advantage. (It is important to note, CAG was done in all patients)
Did this study really happen ? Seem to have many ethical issues . That too, published in JAMA net work. Yes, it was done, I guess , with a legal protection . Apparently, It was done without an informed consent even.
Was there any advantage of proceeding directly to IRA PCI ?
Yes. Reperfusion times were significantly shorter as expected.
Any other advantage ?
I think there are definitely few more, that can’t be reported by many of us, for either unscientific or ethical reasons.
Any disadvantage?
Proceeding to do PCI without knowing contralateral coronary status is unprofessional act and potential to end up in low quality reperfusion.
Final message
Incidentally, this study raises lots of interesting possibilities. Why should we know , the status of non IRA at all, if IRA is opened and flowing well ?( Missing a critical lesion in non IRA is a crime , is it not ?) I agree. but, don’t use big words. Wish some one does a study with totally blinded about non IRA status, however unethical and unscientific it may be. After all, globally 90% of all successful myocardial reperfusion is done by the humble streptokinase or the more glamorous TNK -TPA . Both these agents never bother to know, which coronary arterial thrombosis its going to work .
As a learnt cardiologist, we must realize most of the STEMIs can be managed successfully* without even knowing which is the IRA, forget about the non-IRA. Tackling non IRA lesion is never considered as an emergency procedure , in fact it carries a fair chance of precipitating one.
*Post-amble
Beware, the conclusions of this study, and the core suggestion in this post may-not be related , if any one finds , it is at their own cost of “whims or wisdom“
A 76-year-old woman with a history of double valve replacement (Aortic and mitral valves) for rheumatic heart disease, presented with acute dyspnea after a switch from Warfarin to LMWH before a planned bone marrow biopsy.
The investigations revealed a stuck aortic prosthetic valve ,that showed a prohibitive gradient of more than 50 mmhg. Since, she refused further surgery, a rare and risky effort was made to balloon dilate the prosthetic valve leaflet, though it is not a standard approved modality. It was decided to dilate the supero-lateral orifice and the central orifices by simultaneous kissing balloon. The results were dramatic.
The images and video are reproduced with courtesy of Dr. David Smith, Dr. Ayush Khurana, Department of Cardiology & Cardiac Surgery, Morriston Cardiac Centre, Swansea Bay University Health Board, Swansea, United Kingdom
The stuck valve
Twin balloon dilatation of bi-leaflet valve in between the superior and central orifice
There are few important lessons from this rare case report.
The innovative double balloon catheter Inflation across the the mechanical prosthetic valve is possible. This technique is likely to emerge more useful in the post TAVI population as well.(JSCCAI 2023)
Some times, a simple maneuvers like tapping , pushing or releasing stuck leaflet will solve the issue in few lucky patients. The reason is a clot less than 2mm can strategically sit on the hinge point and interfere with its motion. Dislodging a 2mm clot in all likely hood cause a benign TIA , or just vanish in the aortic stream down the hill,
However , the risk of thromboembolism is genuine in those a clear thrombus is visualised. Hence distal protection by an Aortic sentinel device or its equivalent (FilterWire EZ, Tri-guard) is a must. If Aortic protection device is not available, proceeding with patient & family consent is not forbidden if circumstances demand.(In India ,we do PTMC with mini LA clots without any protection) A video on Sentinel aortic filter
4.It is to be noted if the obstruction is due to pannus , risk of thrombosis is almost nil and safety of prosthetic balloon valvuloplasty is almost ensured.(Of course with risk of device leaflet damage )
5.As on today, differentiating pannus from thrombus remains continues to be a learnt clinical guess game. CT and MRI can give more crucial inputs. To make things more difficult , a raw area over pannus could be the nidus for the thrombus.
6.Probably , the major learning point (rather a sort of mistake) is the decision to switch over to LMWH in lieu of OAC. Time and again we have seen LMWH is a weak anticoagulant, with erratic correlation of Anti X-a activity and efficacy.
7.I believe, in the above case. this complication might not have occurred if she had continued on OAC , if that was not possible , a switch to regular un-fractioned Heparin as a bridge during the surgery could have been the right choice. Generally, overestimation risk of bleeding viz a viz with life threatening thrombosis is quiet common especially in patients with prosthetic valve.
Current approach for prosthetic valve obstruction
A comprehensive review and surprise inclusion of leaflet release as an option.(Ref3)
The well known pro-coagulant state of pregnancy is an evolutionary protective process to make blood clot quicker, to save fetal loss in early pregnancy and mitigate postpartum bleeding. Still, in many women, this natural adaptive process confers an enhanced thrombotic risk. The molecular mechanisms for this pro-coagulant state are, there is increased factor VII, fibrinogen, reduced protein S. It is interesting to note, while plasminogen levels are elevated, D-dimer is also increased, indicating an ongoing fight between pro & anticoagulant forces, converting the physiological maternal- placental bed a mini harmless DIC equivalent zone.
There are several important systemic, placental, (Fetal) and cardiac indications for anticoagulants and antiplatelet agents in pregnancy. The list is increasing in a steady fashion. (Most IVF pregnancies seem to need it for some unknown reason)
Finally most importantly prosthetic heart valves & other Intra cardiac devices.
We have few options
Warfarin (Molecular weight 300 Daltons) is used in dose of 2- 10mg
Un-fractioned regular Heparin , (40000 Daltons) -Not practical for long term. Used at peripartum phase , just before labor to take control over possible PPH.
LMWH (Molecular weight 5000 Daltons)
NOACs are not an option as of now
Aspirin alone might give partial or near complete protection in some of the above mentioned indication.
General rules
Warfarin is safe for mother, Heparin is safe for fetus .(both Un-fractioned heparin & LMWH )
Just because heparin is safe, we cant choose t, it must be equally efficacious too. (Till date no study on LMWH has come to show its efficacy any where closer to Warfarin efficacy, (forget about beating it) in protecting mechanical valve events)
The concept of bridging till 12 weeks is not mandatory in all
Switching to regular heparin at term is applicable for both
Any anti-coagulant usage in pregnancy is like playing with fire .They have narrow safety window. Further, we must have have a quick antidote in case of dose excess. Warfarin, a powerful VKA, is the time tested key drug despite the well known teratogenic effect. Now we have an alternative LMWH ,which has gained considerable popularity.
The risk of Teratogenicity in warfarin is absolute or is it dose dependent ?
Yes it is dose dependent. (Warfarin causes two phases of side effects one is embryopathy, it also affects later half of pregnancy ie fetopathy with neurological bleeding etc
The Italian connect
Answer to this question came from oldest Romanian city built by the Greeks, Naples, Italy . Dr.Vitale , from the department of Cardiac Surgery, Monaldi Hospital, did this landmark study, way back in 1999 , and convincingly proved , the dreaded embryological side effects are dose dependent. It was done with a meager 58 pregnant women . The conclusions of the study changed the way we used to worry about this drug. It said, warfarin is safe at low doses even in the first trimester , if used <5mg, in terms of embryo and fetal issues. Isn’t it curious that a dreaded drug was made pregnancy friendly by simple study from smart surgeon . It is a real surprise that the conclusion of this study is still can’t be disputed by another big one. Almost all current guidelines use this 25-year-old study to form the core algorithm of current anticoagulant protocol in pregnancy.
Warfarin vs LMWH debate
Teratogen or No-teratogen, coumadin still rules supreme in most high risk situations, especially in women with mechanical valves, (Despite the ease with which this molecule crosses the placental filter , because of low molecular weight -300)
Heparin one of miraculous drug of last century , remains a life saving anticoagulant for various medical conditions. However, its refined version LMWH, though made it more palatable & user friendly, it un-apologetically took the sting out of regular heparin, made it less efficacious (more glamorous though) LMWH usage is in CAD widespread , it has suspect value* in true ongoing ischemia in any active ACS situation. It is strange anti X-a is never monitored in CAD protocol , while in pregnancy we insist on intensive monitoring i. What does it imply ? Monitoring is primarily done to ensure adequacy of anticoagulant activity , rather than risk of bleeding .
In my 30 years I am yet o see a patient have fatal bleed to poorly monitored Enoxaparin. This is the reason the mid trimester LMWH heparin bridge to collapse in many pregnancy anti-coagulant protocols. Now ,we can understand why the veteran VKAs continues to be a flag bearing drug in pregnancy .Of course, INR-guided OAC therapy, though can be tricky, most of us are used to that, unlike the frightful anti X-a troughs and peaks.
*I am sure most Interventional cardiologists will hesitate to disagree with this observation.
2022 update on LMWH : More trouble for LMWH in pregnancy. There considerable concern , that twice a day sub-cutaneous injection may not maintain target anti -X a trough .6-.8U/ml and peak 1 to 1.2 U/ml and currently many centers advice LMWH three times a day ( Bai C, Wu . Medicine (Baltimore). 2022 Dec 30;101(52):e32550.)
Final message
So far, the traditional dictum has been, Warfarin is safe for mother & heparin is safe for fetus. One has to decide accordingly with patient ,spouse & family. I think, its time to tweak this rule, little bit. Warfarin is safe for both mother & fetus* in most patients till 36 weeks in low doses , while LMWH may be more safe , but lags far behind in efficacy, especially in high risk indication. (*Including first trimester but with a lesser proof though)
Postamble
Even in these era of shared decision making, it’s our duty to impress upon our patients (or even enforce) to choose warfarin over LMWH in appropriate times. Don’t simply leave this critical decision to patients.
I think we need another study ,5, 8 and 10 Warfarin vs LMWH with a prosthetic valve and analyze the fetal bleeding risk in mechanical valves. It may not be a surprise if the cut off of 5mg could move further up.
I don’t know, whether it is a good trend, to note more and more biological vales are implanted at an young age to avoid OAC .These valves have short life span demanding redo surgeries within 10-15 years which may not be not a righteous approach.
A 32-year-old high-profile businessman was advised Holter monitoring for a few ectopic beats during routine screening ECG. The 72-hour extended Holter monitoring picked up a single short pause with a blocked P wave and reported as doubtful Mobitz type 2 AV block.
The cardiologist in-charge, told the patient that findings are significant, and he would need further investigation. He was referred to their associate center for an EP study. After hearing about the procedure ,the patient was freighted about inserting multiple catheters inside his heart.
This was the time he consulted me with Holter report. It was indeed a missed QRS after a well inscribed p wave , recorded at 4.57 AM, It is a 2nd degree AV block, may be Mobitz type 2, . What if ? It could still be be blocked atrial ectopic. (Pseudo AV block) Both preceding and following PR intervals seemed to be non varying . The following QRS was narrow. I don’t know, whether a single blocked P could by any way a concealed Wenke -Bach. I didn’t have calipers to measure the PR accurately though. The baseline heart rate was around a vago-genic 60/mt, that was comforting . He had his echocardiogram done already and was normal.
What does the guidelines say ?
Guidelines are short of evidence , it was as vague as my thought process . It suggested EP study in selected patents with asymptomatic second degree AV block . My fellows tell, it is just 2B indication (To-be frank, 2-B indications should be called as a junk recommendation ) which would mean if you wish you can do a “potential harm”
I asked the patient two questions.
1.Does he have any symptoms like dizziness or syncope ?
Absolutely nil.
2.What is his functional capacity?
Excellent.
That’s great. Within a minute or so , I could confidently confirm, the non-seriousness of the Holter tracing. I asked him to forget everything, and sent him home, with reassurance, taking on myself a miniscule risk of missing a true AV block and its consequences. He thanked me profusely with so much gratitude. Every thing was hunky-dory , then , this thing happened. When he was above to leave the office, he came back. “Doctor, I forgot to tell, my father died suddenly at the age of 48 apparently by a heart attack” .I must admit, I was taken aback the moment he told this.
What an important past history, I failed to elicit earlier. As he left my room, I called my secretary to give a Suo-moto appointment to him 2 weeks later with a plan of TMT and possible CT -angiogram. Till late in the evening, this patient’s Holter recording ran in my mind. What was that reason for original VPDs that invited a Holter test and the subsequent documentation of Innocent appearing AV block ? Are they interconnected or inherited ? or Is it really Ischemic ones, that took his dad’s life?
That was enough for me to make a compelling call to my EP colleague, for a quick chat about this unique patient. We discussed for 15 minutes, right from Padua University paper to all the Brugada variants.(Ref 3) In the end, the basic doubts remained as before. However, the patient was advised for an EP study primarily to know the HV interval and the possibility of diffuse distal disease. The possible need for a MRI study to rule out silent arrhythmogenic intramural granulomas was also discussed. My EP friend poked me with more academic toxemia. He said a screening test called cardiac-arrhythmic genome analysis is available in certain European centers. Ref: Isbister, J.C., Semsarian, C. The role of the molecular autopsy in sudden cardiac death in young individuals. Nat Rev Cardiol21, 215–216 (2024).
I said enough is enough , and requested for hanging up the chat.
Final message
AV blocks, even Mobitz type 2, can occur at normal times of heightened vagal tone.(Massie Block-Ref 1) But, if there is something unusual in the clinical history, be ready to investigate until the arrhythmia, or at least the anxiety disappears.
Opening a CTO, for reasons other than angina (i.e. for relief of dyspnea or improving functional capacity) is largely conjectural and based on randomly accrued data backed by poor interpretation. The role of collateral circulation in CTO that can compensate even during exercise is well known at patient level data. This has become a difficult area of research because it involves spending more time with the patient, and hence not studied much. We are in the era of artificial intelligence ,virtual patients and statistical extrapolations that can steer the Kaplan Meyer curves in the desired direction.
Pure academicians shall follow the current guidelines. Surprise… surprise !, There is some good news. The normally aggressive American guidelines exercise much caution with a 2B punch. Still , even today it is weird to see hours of academic time is consumed in CTO Interventions in any interventional cardiology meets. (May be , they could get a breakthrough benefit , which I couldn’t appreciate)
.
CTO-PCI follow up
The incidence of MACE including ACS varies between 12-28% depending on LV function.(Ref 2) How about Conferring 12% risk of ACS in a person who has normal LV by doing CTO-PCI ? Still it continue to be a smart move for many of us ? This is exactly the reason experts are struggling to come to term with truths behind negativity of most published CTO trials.
Now, answer to the title question. What is the future risk of ACS in opening CTO related artery ?
Asymptomatic CTOs, with fair excercise capacity, should probably never be opened for the simple reason, a closed artery is naturally protected, against a future ACS at least in its territory
Final message
Currently, in the science of cardiac revascularization there is only evidence and it’s Interpretations, little patient level facts.
Living with a single coronary artery, is potentially a frightening scenario for the patient* which has to supply its own area and also, need to donate the occluded coronary artery . What will happen if a single donor (RCA/LCX) gets closed? One more remote risk in CTO is, acute collateral shutdown causing STEMI/NSTEMI. These statistically minuscule risks are well exploited by coronary caretakers. Meanwhile, there is little talk about the chances of CTO getting closed by itself after an apparently successful PCI. The consequences of anatomic and hemodynamic collapse of hitherto well flowing collaterals , after a CTO PCI will require a separate discussion.
*It is wiser to recall , left coronary artery is also single before bifurcating. Surviving an entire life span with a single10-20 mm tunnel called left main, rarely elicit the same fear in us.
It is a120-year challenge. Can anyone replace Rontgen’s X-ray discovered in 1895 for medical imaging? The Nobel winning Invention redefined the way we looked at our body and management of diseases for over a century. However, the fact remained it is an invasive and injuring investigation. What is the alternative for the X-radiation ?
CT scan was a great invention, but it turned out to be a gigantic 360-degree clone of X-ray machine. Today’s cath lab, however sophisticated , is like spending hours together inside a hot Chernobyl coffee shop. MRI was a true game changer. With zero radiation, MRI came close in the fight with innocuous proton imaging. But for live cardiac interventions, MRI was not practical. Meanwhile, over the years, ultrasound moved up from the pelvis, abdomen, right into coronary arteries and heart. Intravascular ultrasound-based interventions are being done in coronary artery, in a few cases to avoid contrast in patients with CKD. (We call it zero-contrast IVUS-guided PCI). But, it is cumbersome and has some technical issues. Transesophageal echo (TEE) & Intracardiac echocardiography (ICE) do help us immensely in certain interventions.
Now is the era of Optics
If a torch light can illuminate and give us vision in absolute darkness ,how about acquiring a deep vision with scattered light ie photons. (Jnana-Chakshush ,third eye of Hindu God Shiva ?) The concept of Optical coherence imaging came (OCT) came in .It has limited use in deep vision of coronary wall anatomy and histology. As of now it has no role to play in catheter guidance.
Here comes the real Innovation . Fibro-Optic real shape( FORS) technology , which reconstructs image from optical data, and beam live fluro- like images, in 3 dimension. May be, we may soon, say good bye to electrons, protons, and welcome these harmless photons.
This video clip shows real time Intervention using FORS in Aortic endovascular stenting
One may Imagine FORS to Electro-physiologist’s electro- anatomic mapping made with a the GPS like pad attached beneath the cath table and reconstructing anatomical Images from the dynamic signals points generated from the catheter tip.
Final message
Now, we are looking at various different modalities to image without radiation injury to the patients, and more importantly the cardiologists .
Intra cardiac Echocardiography (ICE)
Proton imaging (MRI)
Electrical navigation (CARTO)
Fibro-Optic real shape (FORS)
FORS , is the new arrival. Let us hope it stands the test of time.
Hi, welcome Mr George, I just reviewed your records. You have three blocks in your arteries supplying the heart.
Are they serious Doctor ?
Not really, but one of them appear tight
What should I do Doctor ? But, I am comfortable Doctor.
You may be. But I am not .You need to undergo some re-vascularisation procedure .
What do you mean by that Doctor ?
It means either a percutaneous coronary intervention with a stent or CABG.
Can I get my heart re-vascularised by drugs alone Doctor ?
No we can’t . Hmmm , wait, we do have something called OMT/GDMT. Can you put on hold for some time Mr George, you have asked a real tough question.Let me recollect something from my forgotten basics clinical lessons.
The Illusion of myocardial re-vascularisation
PTCA is sort of repair work done over the blocked area that restores the traffic(blood) flow. while CABG, diverts flow from the congestion or road closure, along a by- pass road, which rejoin the main road later. These are called re-vascularisation procedures. Please note, both of them, never bother to find the status of micro-vascular integrity which form 95% of net coronary vascular surface area.
Hiding behind the technicalities
PCI demands reduction in percentage stenosis , resulting in pre-defined minimal luminal area (MLA), maximizing net luminal gain, & restoration of TIMI 3 flow in all three coronary arteries .These are the popular scientific parameters. For CABG we aim at good and complete, uninterrupted short and long term distal flow.
However ,we have some effective clinical and pathological markers too, for effective re-vascularisation They are clinical well being and good functional capacity , relief from chest-pain, reduction of plaque volume, plaque stabilisation, maintenance of collaterals , microvascular patency , reduction of recurrent events .The irony in CAD management is in many patients who are on only drugs , clinical endpoints can be achieved without the above mentioned technical end points ! ( As we have learnt from the OAT, COURAGE trials which dramatically showed arterial patency is nothing or little to do with major clinical end points )
Final message
Scientific minds can not accept certain things which are less glamorous and unassuming. Simply swallowing few drugs can never make us(both physicians and patients) believe it can be an equivalent to PCI/CABG .
Intentionally or unintentionally , we have made PCI and CABG appear invincible and conferred the sole-rights to be referred to as re-vascularsation procedures , Realistically looking medical therapy also provide good revascualrisation (re-or neo) especially where it is needed ie in the coronary micro circulation.
Hence forth, in the overall interest of CAD community , and with good scientific basis “It is good to emphasise to our patients optimal medical management of CAD is also one form of re-vascularization This will help us to neutralise the unfair” Semantic advantage” the PCI and CABG enjoys.
Reference : Apart from the heavily quoted classics of COURAGE, BARI-2D, ISCHEMIA, ORBITA 1 etc. (Please note ORBITA -2 is not an antidote to ORBITA-1) ,Read this 1.AVERT study :Atorvastatin equals PCI .2.Regular exercise equivalent to PCI (ESC 2009) .Will try to get the link for this soon.
Recently , I received two e-mail invite for two major conferences one in India other in Europe.
Once upon a time, in 1990s we as fellows used to attend these conference for Rs 1000 (15 Euros/Dollors). Now it is 50-75 thousands (5000-7500 % increase) Even few years ago it was affordable. I don’t know how many of us can think to attend such conferences. Definitely not me. What prevents these guys to keep the cost nominal. Certainly, inflation is not the reason. Air tickets and hotel room tariffs has just raised 50-100%.over the same period
if you look closely into the above menu card, Indian tariffs would tell a crazy story .When global purchasing power parity ratio is applied, Rs50000 will be equal to approximately 6000 Euros (*Factor of 8 for each Dollar). Which in realty, fix this Indian conference cost, at a true equivalence of 4.8 Lakhs.
Final message
My professor used to say, teaching and learning should be spontaneous, and never be a commodity. Can you guess who is fixing these conference fees beyond the reach of a lay student & doctor ? Some of you might know the true reason. The regulatory bodies are just helpless. There is a direct link between a MBBS seat costing 1 crore in our country , to these jacked up conference costs. The moment greed enters, we become a party to un-professional scheme of things, however good is our expertise and knowledge .
There is a joke going on in India, if you can find one cardiologist who pays the registration fees from his pocket, he shall be awarded highest professional award . I am sure, there will be few eligible souls who defy the rule of the current academic landscape.Let these conferences, be dedicated to them.
We wish, our understanding about cardiac contractile physiology is deep and nearly complete. Heart is an irreversibly coupled electro-mechanical organ , right from the fetal days until the final heart beat. In myocardial pathology, the genesis and sustainability of ventricular arrhythmia are intricately related to the degree of LV dysfunction of any cause.
SCD is the leading cause of mortality in heart failure. Tackling SCD was in God’s domain, until the brilliance of Dr. Michel Mirowski shrunk the defibrillator and implanted it under the chest in 1980. (Dr. MM’s s a unique and inspiring story, from Poland amidst the holocaust times, right up to his invention at Johns Hopkins)
Why ICD for SCD ?
Beta blockers and Amiodarone remain good options for mitigating SCD. (Of course, Amiodarone has a huge baggage of side effects.) But, as you know machines always beat drugs. After multiple RCTs, we found any severe LV dysfunction (EF <30%) requires an ICD to reduce SCD. Though MADIT trial required an inducibility of VT, MADIT-2 told us that just the presence of LV dysfunction is sufficient.
Since then, ICDs have proliferated globally, of course with multiple collateral issues. As we navigated the cardiac EP terrain further, we found that all is not well. ICDs faced some foundational questions regarding its utility value vs. risk . ICD explanation epidemic in the past was a true story. Still, Mirowski”s electrical kid survived the test of time and evolved with great technological innovations from companies like Medtronic, Guidant, Abbot etc. It has, now grown into 45 year old wonder device, that can wake up the heart from death . (Wish ,the Nobel committee has Dr Mirowski’s name in their podetial posthumous prize list)
ICD usage with reference to DCM sub types
One factor frequently debated about ICD is its efficacy with reference to the etiology of LV dysfunction. Many studies indicated this factor could tilt the balance of risk to benefit of ICD in a critical way. ICDs are more useful in Ischemic DCM than non ischemic DCM is a recently observed penomenon ,though we are not sure yet . SCD-HeFT trial (NEJM 2005) did show some benefits in N-DCM, but it was only in class 2 stage. Then came the DANISH study, which made us strongly believe ICDs in Non-Ischemic DCM are not a really useful intervention. (N Engl J Med 2016; 375:1221-1230)
Why ICD doesn’t work well in NDCM ?
Since IDCM patient had more SCD events , ICD is more likely to be useful in ischemic DCM than non ischemic is a distinct possibility (Higgins AY, . Am J Cardiol. 2020)
The un-disputable fact is ischemic DCM has a target to treat, though it is termed as cardiomyopathy. While most of non-ischemic DCM are truly global muscle disease with primary or secondary with known or unknown disease process, unless we are able to correct the etiological factor, these patients are not going to do well in spite of ICD.
The differentiation between DCM and NDCM itself is not a simple task. Overlaps do occur. (An important clue is NDCM involves both ventricles equally and subendocardial sparing almost always suggests NDCM)
Final message
It seems to be a fact, ICD are less useful in NDCM. The simple reason could be we can address the ischemia a potential arrhythmic target by some form of revascularization in IDCM. The second reason is, NDCM is a progressive primary muscle disease.
Still, our understanding is largely incomplete. ICDs don’t exhibit partiality. By default, they try to give a new lease of life to any episode of pulseless VT/VF whether it is from IDCM or NDCM. (Please remember we don’t deny an ICD for a sarcoid cardiomyopathy or end-stage HCM just because they are non-ischemic. in origin )
Post-amble
An unfriendly fight between CRT & ICD
The science of LV dysfunction and the need for ICD got complicated when CRT entered the scene a decade ago. CRT is indicated when a LV is dilated with poorly coordinating contractions due to conduction system malfunction, that stretch the QRS complex either LBBB or monophasic RBBB or combination both BBBs(Masquerading)
Since, the indication between ICD and CRT overlapped, industry guys taught us some cardiology lessons, They offered the option of fusing the two together and called it CRT-D & CRT- P. Please note CRT-P is nothing but the glorified version of plain old CRT (The P could mean either the dual /BV or the mono ventricular (RV) default back up pacing.)
The choice between CRT -P and D has taken more curious turns. Since we are not clear whether the incidence of SCD is reduced by CRT or ICD. This paper from Egypt address this issue in an exemplary manner. (Ref 4).
Now, there are more than handful of papers that show CRT-P per se can reduce the SCD events significantly by reverse re modeling of LV and improvement of LV function. Currently, we have started to believe CRT-D may not be indicated in many and could in fact add more electrical side effects.
It is ironical, currently the issue of in-appropriate ICD/CRT-D implantation appears more important than the well known adversary of inappropriate shocks. Both of them needs some meaningful attention. It is worthwhile to to note ,If we address the former the later issue cease to exist. Let the global EP think tank introspect and to refine and redefine the Indications of CRT-D.
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The author acknowledges all the queries posted by the readers and wishes to answer them .Due to logistic reasons only few could be responded. Inconvenience caused is regretted.
Dr.S.Venkatesan MD 