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Archive for November, 2022

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 mechanically compromised heart should not be burdened with one more compromise, ie with a defective cargo.

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 DeficiencyThe IRON OUT HF Randomized Clinical TrialJAMA. 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.

 

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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

 

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We have enough evidence to question the superiority of the presumably best practice in cardiac pacing namely dual chamber pacing. Apparently, the DDD failed to show gross benefits in both  AV block as well as sinus node dysfunction. (UKPACE, MODE-Selection Trial) in studies done nearly two decades ago.

It is 2022. Here is one more study in the Indian heart journal, coming up from JIPMER Pondycherry,on this concept. It is an intelligently designed cross-over study. The same patients were switched between DDD and VVI modes. This study reaffirmed the lack of appreciable hemodynamic and clinical benefits with DDD mode yet again. 

We have also contributed a little on this issue. It was found cardiac failure in VVI pacing was not a real big issue in the long-term follow-up. We presented and published in world congrees of cardiology Dubai 2012, and Circulation journal. 

How is that? A dual chamber pacer with AV synchrony fails to show a hemodynamic benefit?

The answer is simple..VV desynchrony is a common denominator for both VVI and DDD pacers. Providing AV synchrony without VV synchrony doesn’t make real sense in the long term to overcome the altered physiology, Still, DDD pacing continues to enjoy a popular mandate by hiding behind a vague outcome measure called quality of life.

What is the physiological pacing then?

Just because, DDD and  VVI pacers are equipoise,  can we presume the new pacing kid LBBB pacing would be physiological? We wish so, but unless and until we replicate the entire conducting system right from SA, and the AV node which includes many miles length of delicate Purkinje cables, every pacing system we use is currently pathological. (If that sounds too harsh, let’s make it non-physiological)

Having said that, VVI pacing is one of the most remarkable Inventions in medical science since the last century, that plays God’s own function and gives a new lease of life to all those patients with critical AV blocks and trouble some SNDs.

Final message

It may be difficult to digest for true scientists. Restoring the atrial booster pump is not bringing in the desired benefits. It is clear that VVI pacing will never become obsolete. This fact was established long before. We must argue and wonder, why we need to keep proving a scientific truth again and again?  There could be a good justification too. Real-time cardiologist behavioral patterns clearly tell us, as a genre, they often struggle to get detached from futile modalities even after good published evidence (PCI for CTO, Revascularisation for Ischemic DCM, are a few more examples)

 

 

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