Feeds:
Posts
Comments

An unpalatable medical quote

January 11, 2023 by dr s venkatesan

Posted in Ethics in Medicine, medical quotes | Tagged , , , , , , |

Missing links in IHD : What is the relationship between Ischemia & cardiac arrhythmias ?

January 5, 2023 by dr s venkatesan

The term Ischemic heart disease (IHD) was once very popular, but many abandoned it as it became an academic cliche.  CAD & CAHD are the other terms that are equally popular and prevalent. Stable IHD was in vogue till recently, which was again replaced by “chronic coronary syndrome’ now. Honestly, I feel the original term IHD to be restored however outdated it may look. it encompasses the entire spectrum of clinical cardiac disorders.

Manifestation of Ischemia heart disease 

  1. Angina
  2. Infarction
  3. Cardiac failure
  4. Arrhythmias 
  5. Silent ischemia
  6. Sudden cardiac death

 The purpose of this post is to share some thoughts on the link between Ischemia and cardiac arrhythmia. 

 

 

What is the relation between  Ischemia and cardiac arrhythmia (especially VT)

A.Strong relation

B.Weak relation 

C.No relation 

D. Recurrent ischemia protects against arrhythmia.

The fact that. acute Ischemia triggers primary VT and VF and is the leading cause of electrical death is sufficient to fix the answer without any doubt. But, the  truth is, the link between Ischemia and cardiac arrhythmia is more complex  

If we could agree ischemia is a powerful trigger of ventricular arrhythmia, will every patient with chronic stable angina be at risk of  VT after walking a certain distance?  

So, where does cardiac arrhythmia fall in the Ischemic cascade of events? the fact that chronic ischemia on exertion rarely precipitates an arrhythmia conveys a strong hidden message. 

Coming back to, STEMI where the arrhythmic risk is powerful, still, if the same acute ischemia, presents as UA/NSTEMI, with severe compromise of resting blood flow, it doesn’t trigger a VT usually. This fact should baffle us and question why even acute ischemia carries low arrhythmic risk except when it happens with STEMI.

The potential mechanisms of lack of VT in UA* (No evidence /Class C evidence) 

  • In UA, ischemia is primarily subendocardial, and the neuronal innervation which is more in the epicardial plexus fails to get stimulated. This is in contrast to what happens in STEMI. Here It is transmural ischemia and the sub-epicardial is always involved.
  • In this context, the high prevalence of VT in Prinzmeal angina where there is subepicardial injury is a point to be noted. In young NSTEMI/STEMI crossover entities like Wallens and De-winters, there is a high adrenergic drive, which triggers the VT rather than ischemia per-se.
  • Finally, even in STEMI, only a minority of 15-20 % of myocardium become arrhythmogenic and face fatal complications. What protects the rest of the 75 %? is genetics, epigenetics, or fate.? 

The practical implication of this question

  1. The VT in ischemic cardiomyopathy is related more, to the scar burden, strategically placed islands of dead and live tissues, and the overall severity of LV dysfunction. This makes the Ischemic VT, as a term,  could be a misnomer.  In fact, it is the viable ischemic tissue that is a powerful trigger.
  2. If baseline chronic ischemia is less likely to trigger any VT, revascularisation in chronic CAD (PCI/CABG) is unlikely to give relief from it as well.

Anti-arrhythmic adaptation in chronic Ischemia 

We know about ischemic preconditioning and angina relief. It may apply to arrhythmic preconditions as well. Recurrent ischemia, while we expect to elevate the arrhythmic risk, it is a curious and exciting possibility it might work as an “anti-arrhythmia vaccination” at the molecular level. 

Final message 

So, what is the true relation between ischemia and cardiac arrhythmia?  

It is not as strong as one would believe it to be( Except in the early hours of STEMI and a very small subset of NSTEMI.

Curiously, in certain lucky beings, recurrent baseline ischemia may protect against future arrhythmias.

Reference 

1.A V Ghuran, A J Camm, Ischaemic heart disease presenting as arrhythmias, British Medical Bulletin, Volume 59, Issue 1, October 2001, Pages 193–210, https://doi.org/10.1093/bmb/59.1.193

2.Janse MJ, Wit AL. Electrophysiological mechanisms of ventricular arrhythmias resulting from myocardial ischemia and infarction. Physiol Rev 1989:  69 ; 1049 –169

Few more questions worth pondering 

Why do certain VTs struggle to become sustained?

Will discuss this later (Will need to talk about the diameter of the primary Rotor, the Curvature of rotors and source-sink mismatch, etc. )

How often  Ischemia triggers AF?

I haven’t heard of Ischemic SVT, or ischemic AF much. Trying to accumulate more Info on this.

Posted in Cardiology -unresolved questions, Cardiology-Arrhythmias | Tagged |

Reviewing top 10 Interventional papers of 2022 : A good lesson on NSTEMI management

January 3, 2023 by dr s venkatesan

EHJ has listed the top 10 papers in cardiology in the year 2022 in its current issue. 

Kindly go through this when free. While each of the 10 has its own importance, one meta-analysis, I thought was a  real bright spot. Though the message it conveys is nothing new,  it reaffirms an important management principle in ACS. Getting curious? Before going into the paper, a mini pretest

What is your take on these 4 statements on ACS?  True or False

1. STEMI is an emergency, NSTE-ACS* is not an emergency

2. Both are true emergencies.

3. STEMI is definite, yes, but  NSTE-ACS may or may not be (Mind the GRACE score dude !)

4. Even STEMI can be a non-emergency if the patient reports after 24 -48 hours.

(Remind you, NSTEACS = UA+NSTEMI , still often used interchangeably)

Hope we don’t have difficulty in identifying the wrong response. Whatever the answer to this somewhat insulting question to our intellect, forget it. Now, read this paper, which is listed as one of the most read last year. It is about the impact of early invasive strategy in NSTE-ACS.

Kite TA, Kurmani SA, Bountziouka . Timing of invasive strategy in non-ST-elevation acute coronary syndrome: a meta-analysis of randomized controlled trials. Eur Heart J. 2022 Sep 1;43(33):3148-3161.

Conclusion is pasted for the busy guys.

Post-test

  1. What is overall NSTEMI in-hospital mortality? (Everyone knows for STEMI it is around 4-8 %, no one seems to be sure about NSTEMI. I think it can’t be estimated accurately, guess it is 1 -2% )
  2. Is there a primary PCI equivalent situation in NSTEMI?  What are they? (Left main UA with AVR ST elevation comes first on the list)
  3. Based on the urgency to treat how does the ultimate outcome change? (This is what this meta-analysis by Kite et all proved.It is not a new revelation though . Recall the landmark ICTUS study  of 2010 which was largely kept in the dark )

Final message

One lay definition of STEMI is, It is a mass of myocardium under fire. True UA/NSTEMI is, a mass of myocardium, that is threatening to go on fire. When firefighters are able to reach a smoky building before the onset of a fire, no doubt, it looks like a great & awesome response, Isn’t it? Unfortunately, the myocardial landscape is different and NSTEACS is such a heterogenous entity that doesn’t welcome unsolicited aggressive, emergency rescue missions. That’s one of the messages we get (at least I got )from this top-read paper in 2022. 

Reference

1.Emanuele Barbato, Margaret McEntegart, Tommaso Gori, The year in cardiovascular medicine 2022: the top 10 papers in interventional cardiology, European Heart Journal, 2023;, ehac778, https://doi.org/10.1093/eurheartj/ehac778

2.Kite TA, Kurmani SA, Bountziouka V, Cooper NJ, Lock ST, Gale CP, Flather M, Curzen N, Banning AP, McCann GP, Ladwiniec A. Timing of invasive strategy in non-ST-elevation acute coronary syndrome: a meta-analysis of randomized controlled trials. Eur Heart J. 2022 Sep 1;43(33):3148-3161.

3.Damman P, Hirsch A, Windhausen F, et al. 5-Year Clinical Outcomes in the ICTUS (Invasive versus Conservative Treatment in Unstable coronary Syndromes) Trial. J Am Coll Cardiol. 2010 Mar, 55 (9) 858–864.https://doi.org/10.1016/j.jacc.2009.11.026

Posted in Uncategorized | Tagged |

Happy new year & memories of 2022 !

January 1, 2023 by dr s venkatesan

Wishing every one of you an Enlightening New year. As we begin a new journey around the sun, yet another time, let us re-dedicate ourself, to use science, for the welfare of our planet & people.

Thank you , for visiting this site and make all its worth.

Just one memory of 2022, lingers ! Retired and left Madras medical college,Chennai after 3 decades, which grew me up as a Cardiologist.

Posted in Uncategorized |

Who can answer this unusual query in mitral stenosis?

December 20, 2022 by dr s venkatesan

I will go with the last response. As for as I understand, we have never quantified Atrial muscle mass properly even in normality. One may be tempted to think there is no purpose to measure it, other than academic reasons. The fact that the incidence of atrial fibrillation in mitral stenosis is not linearly correlating with LA size makes us think, LA mass (Virtual LAH) may have a say in triggering AF.

This post is meant for cardiology fellows. Maybe someone can do a study on this by measuring LA mass pre and post-PTMC, we might get an idea about regression as well. Meanwhile, we are well versed with infiltrative diseases like atria like amyloidosis that can mimic LAH. Currently, we realize fatty infiltration of LA is the common trigger for AF in varied populations.

By the way, readers are welcome to post any specific formula to measure LA mass if they come across .

Reference

A good review of LA anatomy.

Posted in Atrial fibrillation, Mitral stenosis, Uncategorized | Tagged , , , , |

Department of artifact : Normal “wall motion defect” in echocardiography

December 14, 2022 by dr s venkatesan

(This post is about some basics in echocardiography meant for fellows, and echocardiographers. Others can skip please ) 

This is a 27-year-old woman who was referred for routine* cardiac evaluation. What do you see?

What is the diagnosis?

This echo clip is from a woman who is 8 months pregnant. What you are seeing is perfectly physiologically and normal. On lying down there is a mechanical push of the diaphragm altering the LV shape and contraction. In the short axis, the left ventricle is contracting well, but the shape is not spherical in systole implying some desynchrony. Further, the  IVS arena is contracting vigorously, which makes, the other segments appear to be poorly contracting. (Someone could report it as a wall motion defect in antero- lateral segments inviting temporary panic)

It is worthwhile to go through this list of non-ischemic WMA and find the pregnancy at the bottom of the list.

Few more conditions, that can be added to this list

  • Though LBBB is the classical cause for WMA, we have seen even LAFB showing the bumpy motion of IVS and the anterior wall.
  • Some patients with ERS and some patients with Brugada show wall motion defects due to repolarisation heterogeneity. 
  • Regioanl pericarditis
  • Intracardiac scars. Localized fibrosis.
  • Extracardiac tumors 

iFAQ on this topic 

Is this wall motion defect in pregnancy, really an artifact or real? 

They are true artifacts in the sense, the heart is an innocent bystander in this pulsating fight between intra-thoracic vs intrabdominal pressures. A similar situation happens in ascites. 

Any other mechanism other than mechanical push?

WMA due to RV volume overload of pregnancy may also contribute. 

Does this WMA affect cardiac hemodynamics?

Logically it should, but it doesn’t. The normal heart has enormous resilience, it just ignores these subtle pushes from below and keeps working normally. Still, enormous distension of the abdomen especially in twin pregnancies, in small body habitus, can make some women breathless, or orthopenic. I am sure, one of the mechanisms could be this geo-mechanical encroachment.

Final message

Wall motion defects are not synonymous with CAD. There is an important list of non-ischemic conditions that can cause WMA. Cardiology fellows and echo technicians are encouraged to go through the above list one more time. While this knowledge can prevent false alarms, at the same time it is always wise to ask for the ECG before doing echocardiography, and not to miss the omnipotent CAD.

Postamble 

*DIscerned readers might wonder why a routine echo was done in a normal pregnancy. I am surprised to note there is an ongoing fad in this part of the world, to do echocardiographic screening on every pregnant mother to rule out cardiovascular disease. (A luxury even the world’s richest country can’t afford) I am told, this echo is meant to rule out peripartum cardiomyopathy for legal purposes. A spot echo at term can never be going to either predict as an event that is mainly going to happen postpartum. This newfound epidemic of anxiety among obstetricians is unwarranted. 

Reference  

A well-written focused review specifically on this topic 

Yavagal ST, Baliga VB. Non-Ischemic regional wall motion abnormality. J Indian Acad Echocardiogr Cardiovasc Imaging
2019;3:7-11.

 

 

Posted in Cardiology -Hemodynamics, Echocardiography -Normal measurement, Echocardiography-hemodynamics, Teaching points | Tagged , , , , , , |

What are the mechanisms of beneficial action of alcohol in moderate amounts ?

December 8, 2022 by dr s venkatesan

Putative mechanisms 

Forget about the mechanisms. Is it really beneficial?

Very valid question. No simple answers are available. But, some truths try to emanate from this big epidemiological study by INTERHEART that found the beneficial effect of minimal amounts of alcohol with a wide geographical variation.(Mind you INTERHEART can be Interpreted totally differently if type and amount of alcohol are counted)

How much alcohol is acceptable asper ADA recommendation?

The ADA recommends no more than one alcoholic drink per day for women • no more than two drinks per day for men. One drink is defined as 12 ounces of beer • 5 ounces of wine • 1 ½ ounces of liquor.

Does this apply to the Indian population?

No, it doesn’t apply for behavioral and possibly genetic reasons.  (A. Roy, et al Impact of alcohol on coronary heart disease in Indian men, Atherosclerosis, Volume 210, Issue 2, 2010, Pages 531-535,) 

                                            One of the daily scenes In India, at an Alcohol-human Interaction site 

Final message

It is true, disciplined alcohol intake seems to do good if the person takes care of his other lifestyles and potential risk factors. The beneficial effect of moderate alcohol on lipids, and vascular endothelium is based on a weak evidence base, but still good enough to create a recommendation. These (flimsy ?) advantages of alcohol are lost if it exceeds 2 units per day. Meanwhile. let us be aware, alcohol enhances the global burden of disease by many folds and  it should never be tried as the therapeutic drug is a logical and popular opinion (Lancet 2016)

Further research question

All of us would agree, regular alcohol intake, in any amount will end up in danger for native Indians. Now, can an NRI or resident Indian, blessed with so-called western drinking discipline accrue the true benefits of moderate alcohol intake? is a  big research/common sense question.

Reference 

1.Conner H, Marks V: Alcohol and diabetes: a position paper prepared by the Nutrition Subcommittee of the British Diabetic Association’s Medical Advisory Committee.  Diabet Med 2: 413–416, 1985

2.https://www.cdc.gov/alcohol/fact-sheets/moderate-drinking.htm

3.Vu KN, Ballantyne CM, Hoogeveen RC, Nambi V, Volcik KA, Boerwinkle E, et al. (2016) Causal Role of Alcohol Consumption in an Improved Lipid Profile: The Atherosclerosis Risk in Communities (ARIC) Study. PLoS ONE 11(2): e0148765. https://doi.org/10.1371/journal.pone.0148765

4.Leong DP, Smyth A, Teo ; INTERHEART Investigators. Patterns of alcohol consumption and myocardial infarction risk: observations from 52 countries in the INTERHEART case-control study. Circulation. 2014 Jul 29;130(5):390-8. 

 

* ELI -Evidenceless Imagination (Closely associated with class C evidence)

 

Posted in Alcohol and heart disease | Tagged , , , , , , , |

“Professional etiquette” need not be misplaced

November 29, 2022 by dr s venkatesan

 

 

Posted in Uncategorized |

Anemia in cardiac failure : Needs little more attention

November 19, 2022 by dr s venkatesan

HF is the inability (or reduced ability) to supply oxygen and other nutrients to fulfill the body’s demands. In the process, the heart either fights or flights, and results in symptoms due to hemodynamic alterations, or adversities of neuro-hormonal activation.

Now, what is Anemia? Anemia is a condition with reduced or dysfunctional RBCs. that directly interferes with oxygen delivery to tissues. It is not at all a coincidence, the core functions of the heart and blood are strikingly similar and intertwined. While the heart is the powerhouse of the circulatory system, without good-quality blood, the greatness of this vital organ becomes redundant.

 

A failing heart & compromised blood, throws up a double challenge, to the fundamental function of the circulatory system and results in impaired cellular oxygen delivery.

 

Fortunately, RBC and Hemoglobin have an adequate reserve, and real metabolic issues happen only after a 30 %  reduction in hemoglobin. During this time the heart works more to compensate by maintaining high output. When HB falls less than 6 to 7 grams the heart itself suffers from hypoxia and goes for intrinsic failure. So, when anemia coexists with cardiomyopathy imagine the tissue’s plight.

Anemia in Heart failure 

 

While there are many links between anemia and heart failure few things are worth emphasizing. It can be discussed in 4 categories.

  1. Primary anemia that results in heart failure is a separate topic and comes under high-output HF.
  2. Anemia as a part of the same disease process as heart failure. (Anemia of chronic illness) 
  3. Nutritional anemia associated with common forms of heart failure (Ischemic and non-ischemic DCM) 
  4. Anemia of CKD and coexisting heart failure 

*Category 2 is often missed, while category 3 is often ignored

Prevalence of anemia in HF.. Up to 30%. (Iron deficiency anemia is the most common)

Diagnosis: Criteria Ferritin less than100 or 100-299 μg/L with transferrin saturation <20%). 

What is the optimal Hb %?  Should be 13 grams

Iron deficiency is much more than anemia 

It is worthwhile to go back to the basics, anemia is just one aspect of iron deficiency. Humans live their life, essentially inside the breathing chambers of mitochondria in each of the 12 trillion cells.  Without an adequate iron supply, the citric acid cycle will come to a creeping halt. It is now recognized, altered mitochondrial function is one of the key peripheral defects in HF. (Ref 1) Iron deficiency could be an Incidental marker for a more important tissue deficit elsewhere. 

What do the trials say about the role of routine Iron supplements in HF?

As usual, trials blink with data on either side of the truth. Small studies suggested benefits. But large studies with Iron supplements and Erhytopoitn analogs failed to show benefits. IRON-OUT, RED -HF (Ref 2,3) . But in a popular study from the Lancet , showed ferric carboxymaltose improved the outcome. (Ponikowski P,l. Lancet. 2020 Dec 12;396(10266):1895-1904).

Final message

We, as modern-day cardiologists are always pre-occupied with measures to improve LV ejection fraction at any cost (Since we fell into a false knowledge trap of defining HF solely on the basis of  EF% ) To make HF patients walk 30 meters extra in a 6-minute walk test we have complex and costly procedures like CRT, Mitra clips, and IAS flow regulators,  etc.

However, experience tells us there are many parameters other than EF that can improve functional capacity and quality of life. Breathing exercise is the best example. Let’s add one more to this list. A simple correction of anemia with iron can make your cardiac failure patient walk many blocks more. Trials are not consistently confirming this though. Don’t bother them,  just have a try. If prescribing tablet iron without evidence bothers you with scientific guilt, ask your patient to take a diet with rich iron content and see the difference.

For advanced readers

Anemia and  Aortic afterload: The apparent advantage

There is one curious concept. Anemia makes the blood thin. Reason lowered viscosity. As a consequence afterload falls. , hypoxia-induced peripheral vasodilatation and enhanced nitric oxide activity also contribute to this.  Vasodilatation also involves the recruitment of microvessels and, in the case of chronic anemia, stimulation of angiogenesis. So, anemia apparently has a double edge, and one of them seems to be beneficial.

We must also beware, the risk of iron overload is genuine in some of these patients with HF. This makes us wonder, in ancient times venesection was used for so many undisclosed illnesses, which might include heart disease as well.

Reference

1. Melenovsky  V, Petrak  J, Mracek  T,  et al.  Myocardial iron content and mitochondrial function in human heart failure.  Eur J Heart Fail. 2017;19(4):522-530

2. Lewis GD, Malhotra R, Hernandez AF, et al. Effect of Oral Iron Repletion on Exercise Capacity in Patients With Heart Failure With Reduced Ejection Fraction and Iron Deficiency: The IRON OUT HF Randomized Clinical Trial. JAMA. 2017;317(19):1958–1966. doi:10.1001/jama.2017.5427

3. Swedberg K, Young JB, Anand IS, Cheng S, Desai AS, Diaz R, Maggioni AP, McMurray JJ, O’Connor C, Pfeffer MA, Solomon SD, Sun Y, Tendera M, van Veldhuisen DJ; RED-HF Committees; RED-HF Investigators. Treatment of anemia with darbepoetin alfa in systolic heart failure. N Engl J Med. 2013 Mar 28;368(13):1210-9. doi: 10.1056/NEJMoa1214865. Epub 2013 Mar 10. PMID: 23473338.

 

Posted in Uncategorized | Tagged |

Patient empowerment movement, definitely has a good intention , but …

November 11, 2022 by dr s venkatesan

 

 

The definition & intended purpose of patient empowerment

WHO defines empowerment as “a process through which people gain greater control over decisions and actions affecting their health” and should be seen as both an individual and a community process.1

Four components have been reported as being fundamental to the process of patient empowerment: 1) understanding by the patient of his/her role; 2) acquisition by patients of sufficient knowledge to be able to engage with their healthcare provider; 3) patient skills; and 4) the presence of a facilitating environment.2

Based on these four components, empowerment can be defined as A process in which patients understand their role* and are given the knowledge and skills by their healthcare provider to perform a task in an environment that recognizes community and cultural differences and encourages patient participation.

Reference 

Patient-empowerment—Toolkit

 

Posted in cardiology-ethics, Medical education | Tagged , |

« Newer Posts - Older Posts »