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Archive for the ‘Dilated cardiomyopathy’ Category

New ESC 2023 Cardiomyopathy guidelines: Truths trail by 17 years!

Posted in cardiomyopathy, Dilated cardiomyopathy, hypertrophic cardiomyopathy, ischemic cardiomyopathy, Uncategorized, tagged , , , on August 27, 2023|

It was 2006

Allow me to recount an unassuming piece of a PowerPoint presentation from my institute, Madras Medical College, at the annual Cardiological Society meeting in New Delhi. The paper was categorized under miscellaneous sessions. I vividly remember the day. I have to admit, It was a nearly empty hall E, located in the basement of Hotel Ashoka. After the talk, I looked up to find that neither the chairman nor the handful of kind academic souls had any questions or comments to make. Pausing for a few moments, I quietly walked down the podium with an inexplicable silent pain.

The title of the presentation was “Non-dilated cardiomyopathy”

non-dilated-cardiomyopathyDownload

Welcome to ESC Congress Amsterdam August 2023

ESC, has come out with this new update on cardiomyopathy. It is a pleasant surprise to find the term “Non dilated cardiomyopathy” entered the cardiology academia, authenticated by the ESC.

I must confess, it is difficult to conceal the joy and a little bit of self-pride.

Some observations from this document

1. Despite our tremendous knowledge base, we are yet to hang up our boots, in pursuit of an Ideal cardiomyopathy definition. Genotypic or phenotypic ? Phenotype is closer to reality, while genotype is largely imaginary. It looks like, The newer guidelines are moving towards a phenotype-based approach in all aspects except in risk prediction. Fair enough.

2. All cardiomyopathies, whatever way we segregate, ultimately end up in the common clinical syndrome of heart failure. So. it is better to spend some quality time here and concentrate on HF therapeutics.

3. Cardiologists are expected to critically fine-tune their general medical knowledge, which will help recognize and treat systemic disorders like Amyloidosis, and other metabolic infiltrates.

4..Almost all RCMs have non-dilated ventricles, so why a new term NDLVC? Anyone wants to ask this question ?. Further, there can be significant overlap between RCM & NDLVC as well. Definitely, there is a lot to understand beyond this 2023 document.

5. Why do some ventricles refuse to dilate even in the face of adverse hemodynamic and pathological conditions. Is it an advantage or disadvantage? If ventricles are adamantly stiff and decide not to dilate, there is no other option, the atria will proxy dilate, creating more problems in the lung circuits. This also raises a fundamental question Is NDCM a better stress buster (think Laplace law ) than DCM? or vive versa , the accomodative nature of LV passify & blunt the slope of LVEDP at times of exertion.

6. One more reality is, NDLVC is also an Important subset in the now fashionable HF entity HFpEF

Final message

The message to youngsters is this. Discuss, debate, and document your thoughts in whatever forum, that is available. Don’t wait for all those big brother journals and their recognition. If there is truth in your writing, someday it will be revealed to the world.

Reference

1.Robert A Byrne and others, 2023 ESC Guidelines for the management of acute coronary syndromes: Developed by the task force on the management of acute coronary syndromes of the European Society of Cardiology (ESC), European Heart Journal, 2023;, ehad191, https://doi.org/10.1093/eurheartj/ehad191

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Will PCI reverse LV dysfunction in Ischemic cardiomyopathy ?

Posted in CABG for Ischemic DCM, Dilated cardiomyopathy, Uncategorized, tagged , , on December 9, 2020| Leave a Comment »

PCI is effective in relieving angina,  what does it do to LV dysfunction?

This is a fundamental query in the principles of revascularisation of CAD . The term LV dysfunction can convey a bizarre meaning.It can constitute any of the combinations of the following.Cell death, necrosis, scarring, fully dead, partially dead, partially viable, apoptotic cells that are clustered across various myocardial segments. These cells are interwoven with fibrotic interstitium. Microvascular integrity is also altered.

Cells stretch, slip and slide with one another. Contractile architecture is lost. This is referred to as remodeling.In the process, the ventricle gets dilated. Wall stress increases, LVEDP raises. Patient may go for progressive failure.The whole concept of chronic myocyte loss is due to the process called programmed cell death.

Does PCI cancel this pre-planned program?

The answer seems to be a clear ” No” (Of course few studies do show some improvement ) It is becoming clear,  chronic ischemic juggernaut moves on. The mechanical spiral effect on the myocardium will go unabated whether you rectify the small residual ischemia or not), However, tissue engineering, anti-fibrotic drugs, cell repair molecules, stem cell assistance are attractive approaches to prevent or treat ischemic cardiomyopathy in the future.

If PCI can’t do it what about CABG ?

Read the STICH trial in Ref 2

Point of clarification

Revascularisation does have a role in salvaging the myocardium and improves LV function when done before irreversible damage has happened. When does it happen? To be precise, within 24 hrs of IRA occlusion. This is all about knowing the science of myocardial viability. Of course, In (un)real world this 24 h deadline is the least respected time window because cath lab viability directly competes with myocardial.

Reference

1.Buszman P1, Szkróbka I, Gruszka A .Comparison of effectiveness of coronary artery bypass grafting versus percutaneous coronary intervention in patients with ischemic cardiomyopathy.,  Am J Cardiol. 2007 Jan 1;99(1):36-41. (REHEAT study)

2.Eric J. Velazquez, Kerry L. Lee,  for the STICH Investigators Coronary-Artery Bypass Surgery in Patients with Left Ventricular DysfunctionN Engl J Med 2011; 364:1607-1616

3.Hannan EL, Racz MJ, Walford G, et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med 2005;352:2174-2183

 

 

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Friendly Infarcts in ACS : Ischemic mitral regurgitation and the Papillary muscle paradox !

Posted in Dilated cardiomyopathy, Mitral regurgitation, tagged , on July 18, 2018| Leave a Comment »

Ischemic MR is a critical entity in determining the long-term survival in post MI patients as well as dilated cardiomyopathy. (Originally described  by J. H. Philips Ann Intern Med. 1963;59(4):508-520)

The mechanism of MR  can really be complex .We know mitral apparatus consists of  six components.The sub valvular apparatus plays a key role. LV  free wall especially the inferior and lateral segments which subtends the two papillary muscle has a critical role in maintaining the mitral valve competency .

There seems to me a complex mechano -anatomical behavior of subvalvular structures in progressive LV dysfunction especially so in ischemic cardiomyopathy. The LV size, shape eccentricity in attachment of leaflets to papillary muscle is (Simply called altered geometry ) .The intraventricular desynchrony ,disproportionate  LV dysfunction also make MR more likely .

Beware of a striking  physiological irony in ischemic MR.

While infero basal free wall dysfunction occurs commonly with  LCX/RCA Infarct and  is commonly associated with Ischemic of MR .There is something unique happens . . . when the infarct is larger and involves the head of the papillary muscle .Yes, it attenuates the severity of MR.(Friendly Infarct extension!) The mechanism is , papillary muscle dysfunction  tends to prevent apical tensor effect leading to   improved tethering of leaflets .This may appear a blessing in terms of  prevention of acute pulmonary edema. This also explains why some patients are as cool as cucumbers and lie flat comfortably with silent lungs in spite of severe LV dysfunction .The LV is too weak it doesn’t  have contractile energy to generate acute  severe MR.

Here is an illustration  from circulation .Note: The Infarct extends to pap muscle head, the MR is arrested.

Image courtesy : Emmanuel Messas J. Luis Guerrero, Mark D. Handschumacher, et all  Paradoxic Decrease in Ischemic Mitral Regurgitation With Papillary Muscle Dysfunction Insights From Three-Dimensional and Contrast Echocardiography With Strain Rate Measurement Circulation. 2001; 104: 1952-1957

Further debates 

Papillary muscle dysfunction may be protective against progressive MR.Still ,sudden papillary muscle rupture result in flash pulmonary edema and death is imminent . How ? Complete rupture  causes flail free-floating leaflet that prolapse into LA and result in free MR.While simple dysfunction without flail leaflet is less likely to cause MR . The key determinant seems to be the net force that keeps the alignment of mitral,leaflet at annular level.

In this context , we also realise the impact of primary PCI on the  regression of  Ischemic MR is not uniformly positive.Reasons not clear.

Final message

Ischemic MR  due to LV free wall infarct is a near knockout punch , that may determine the ultimate ACS  outcome. However , a simultaneous lesser punch ( by a friendly devil ! ) on the adjacent head of papillary muscle neutralises the effect of Initial Injury. While such non academic scripts are enjoyable , we are still a long way away to understand this anatomical ,hemodynamic conundrum.

Reference

1.

mechanism of ischemic mitral regurgitation papillary muscle dysfunction

2.Leaflet remodelling in functional mitral valve regurgitation: characteristics, determinants, and relation to regurgitation severity Philippe Debonnaire , Ibtihal Al Amri , Darryl P./ehjci/jeu216 290-299 First published online: 3 November 2014
3.Fang Zhu, Yutaka Otsuji, Goichi Yotsumoto Mechanism of Persistent Ischemic Mitral Regurgitation After AnnuloplastyImportance of Augmented Posterior Mitral Leaflet Tethering , Circulation. 2005; 112: I-396-I-401

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How common is angina in Ischemic cardiomyopathy ?

Posted in Dilated cardiomyopathy, tagged , , on March 31, 2015| Leave a Comment »

We generally believe ischemia and it’s clinical counterpart  angina would  go together .It is not true .Most patients with ischemic cardiomyopathy do not have any significant  angina in spite of  having one or more critically  narrowed coronary arteries.

The reasons could be many ,

  1. Little viable tissue to generate Ischemia.
  2. Less contractile elements and less MVO2 consumption.
  3. Severe LV dysfunction makes these patients adopt a very restrictive lifestyle.
  4. Loss of nerve fibers  along with myocyte necrosis and apoptosis.
  5. Post CABG patients often have no angina due to denervation..

The benefits of revascularisation in ischemic DCM is not clear. As the cardiomyopathy  progresses , intensity of angina regresses and dyspnea dominates .Presence of angina makes the decision to  revascularise easy .To consider dyspnea as an anginal equivalent in ischemic DCM and advising revascularisation can not be  justified .

 

 

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ICD secrets : Appropriate shocks are not benign after all !

Posted in cardiac resynchronisation, Cardiology - Electrophysiology -Pacemaker, Cardiology -unresolved questions, Dilated cardiomyopathy, Electro physiology, ICD -Tips and Tricks, Infrequently asked questions in cardiology (iFAQs), Land mark articles in cardiology, Pace maker Tips and tricks, Permanent pacemaker, tagged , , , , , , on October 5, 2014| Leave a Comment »

Inserting an ICD  for  DCM  may a be great therapeutic success  for the physician  as well as the patient . But there is one big truth hidden behind the statistical screen.

Following  study  provides dramatic data from Maanhiem in Germany in about 561 patients who had ICD .The long term patient outcome after appropriate shocks were much worse  than those without    shocks .This was more pronounced in Ischemic DCM .

appropriate and inappropriate shocks ICD

Source : Streitner et al ,University Medical Centre Mannheim, Mannheim, Germany PLoS One. 2013 May 10;8(5):e6391

The fact that these patients continue to throw VT , some thing is wrong in the cellular  milieu or a fresh scar / fibrosis / ischemia is progressing .Further , the VTs and the  subsequent  shocks  set in temporary  hemodynamic instability .We have evidence , EF can be depressed for days  worsening the long-term out come.

While it is easy  to blame it on natural course of DCM , there are  solid reasons to believe  , shock induced myocardial damage is definitely contributing to this  excess mortality.

One important  clinical tip is to screen  all  these so called Idiopathic DCM  patients  who  had appropriate shocks.  They should be monitored for fresh signs of any systemic illness  , like a  connective tissue disorder , chronic granulomatous lesions  like sarcoid etc .To our surprise  some specific  myocardial disease may unmask themselves in the natural history. Identifying them may offer a dramatic cure .

Final message

Some where along our EP mind-set  we are conditioned to think  , as along as there is an ICD in situ and it appropriately  shocks, every thing is bliss ! Blame it  on semantics . The  word “appropriate”  inappropriately  soothes  our nerves.

The fact of the mater is , every appropriate shock is a  grim reminder  that the heart  in question  is restless electrically and VT continue to emanate  from diseased  myocardium  . It could  mean either the LV   is destabilising  , or the original  disease  is   progressing  or a new disease  is evolving .

Mean while, paradoxically , inappropriate shocks give us a quixotic comfort , since the  heart is not really  throwing any dangerous arrhythmia, after all it is  the device related  false alarm   that  could be easily  reprogrammed!

Reference

ICD appropriate and inappropriate shocks

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