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Posts Tagged ‘HFrEF’

HFrEF vs HFpEF : Can we Bio-chemically differentiate the two ?

Posted in Uncategorized, tagged , , on September 15, 2025|

Some times I wished, I could have become a Nephrologist. This thought comes whenever we face a patient with unexplained dyspnea, normal EF, and heart size. Am I missing a HFpEF? The heart is not like the kidney, which injects the all too familiar BUN & creatinine into blood promptly (with a high degree of reliability). Even a medical neophyte can diagnose renal failure just like that.

Cardiologists don’t have that luxury. Of course, we do have NT-Pro BNP recently , which nowhere comes near to renal failure markers . Still, many of the youngsters are tuned to believe NT-Pro BNP is equivalent to creatinine for the heart. Remember, biochemical diagnosis is always an adjunct and never confirmatory This is because NT-Pro BNP is universal cardiac stretch molecule , that can elevate in big list of conditions. Similarly , to appear in the blood, there can be a time lag unlike creatinine. (Read the universal definition of heart failure below).

“The universal definition of HF , defines HF is a clinical syndrome with symptoms and/or signs caused by a structural and/or functional cardiac abnormality and corroborated by elevated natriuretic peptide levels and/or objective evidence of pulmonary or systemic congestion”

* Though , a key link word and /or is used widely, unfortunately , the definition fails to reiterate clinical signs will prevail over biochemistry at any given point of time. It has inadvertantly ? given some over wiegtage to biochemistry.

Also, the new definition has gotten rid of hemodynamic, metabolic, and chamber-wise RV, LV classification systems. I think the committee wanted to remove the clutter of terms. In a broad sense, it’s good. By using the word structural, it includes valve defects or pericardial pathology into the basket of HF.

Now getting deeper, can we differentiate differentiate HFpEF from HFrEF, based on biochemical markers ?

Differentiating HFpEF and HFrEF is vital but looks complex. One may say it is not really complex. Funnily , the purpose of the above chart becomes redundant if the EF of 50% has already differentiated the two conditions . what is the big deal about this table ? It is purely for prognostic and etiological purposes.

Summary

NT-proBNP is typically lower in HFpEF due to reduced ventricular wall stress, while MR-proANP which originates in the atria are expected to be more in HFpEF . Inflammatory and fibrotic markers and MicroRNA panels are high and more specific to HFpEF.

*Growth differentiation factor-15 . **ADM -Adrenomedulin a biomarker for arterial stiffness and arterial calcification . ***ucMGP refers Uncarboxylated Matrix Gla Protein. MGP to function as a calcification inhibitor,

Final message

Recognizing and confirming HFpEF, itself can be considered a partial clinical success. (Since more often it is missed) As mentioned earlier, biochemical differentiation is largely an academic exercise but gives us an idea of systemic pro-inflammatory and local fibrotic status.

There is a rough pathological rule of thumb (Note the word rough again). HFpEF is more often a systemic condition where the heart is affected. (In contrast to HFrEF where the pathology of the heart is central, and all systemic features are secondary to it.) Treatment options for heart failure have improved overall .However it is more limited in HFpEF as Inotropic agents are redundant here. Prognosis is highly variable and not necessarily better.

Reference

1.Ho JE, Lyass A, Lee DS, et al. Circulating biomarkers of incident heart failure with preserved ejection fraction: the ARIC study. JAMA Cardiol. 2018;3(5):415-423.

2.Zile MR, Desantis SM, Baldauff N, et al. Biomarker-guided risk assessment for the diagnosis and treatment of heart failure with reduced ejection fraction and preserved ejection fraction. JACC Heart Fail. 2021;9(12):893-903.

For Fellows . How do you diagnose HFpEF ?

  1. Clinical features of heart failure (Apply some criteria , ex-Framingham )
  2. Some evidence of elevated LV filling pressure at rest or exercise (Diastolic stress test)
  3. Normal LVEF > 50% (Must ensure this should not be a recovered and improved EF from HFrEF condition)
  4. NT-ProBNP -Supportive

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If EF% is a most flawed LV functional parameter,.. why we Insist HF to be classified based on it ?

Posted in Uncategorized, tagged , , , , , , , , , on September 25, 2020|

Heart failure has been classified in many ways, with prevailing levels of our knowledge and ignorance. It is based on a variety of factors like rapidity of onset, etiology, chambers involved, hemodynamics, etc. 

  • Forward vs backward failure
  • Acute vs chronic failure
  • RV/LV or Biventicular failure 
  • Systolic vs diastolic heart failure
  • High output vs low out failure
  • Ischemic vs non-ischemic failure 
  • Reversible vs Refractory HF 

None of them have really helped at the bedside though it helped us understand the condition. Now, in the last decade, we have crash-landed on our favorite obsession to classify HF ie based on Ejection fraction. We believe we have found an exciting new classification. (HFrEF/HFpEF/HFmrEF).We embraced it, even after recognizing EF as a battered LV functional parameter due to its high load-dependence with a dubious reproducibility.  

If we rely too much on echo, there can be a few more classifications for HF 

  1. HF failure with preserved diastolic function(25% of all DCMs with HFrEF )
  2. HF with preserved mitral valve function
  3. HF with preserved Global longitudinal strain(Still normal EF%)
  4. HF with preserved RV function
  5. HF with preserved Torsion and Twist.
  6. Finally, HF with normal Heart (Anemia/CKD etc)  In anemia heart never fails in true sense. In fact, it works at peak capacity.(More of a Success than failure). Similarly isn’t odd to put primary CKD/CRF in the CHF basket.

Probably the most important and practical classification  could be

  1. Primary vs secondary HF (Primary means all muscle diseases under MOGES system ) 
  2. Valvular vs non-valvular failure (Surgically correctable MVR/DVR/Mitral valve repair)
  3. Revascularisable  or Non-revascularisable HF (STICH study responders)
  4. ICD/CRT eligible HF vs Non-eligible HF ( Rule out DANISH study non-responders)
  5. Refractory failure -Novel drugs/ Assist device/TAH/ Transplant suited 

Final message

 Dr Thomas Lewis said over 100 years ago, the essence of the practice of cardiology is to recognize HF early. Looking back at the literature, there will be no dearth of classification for HF. It will come and go according to academic and Imaging whims. Of course, that may aid in ruling out primary cardiac conditions. But, we must always emphasize to the next-generation that HF is often due to systemic*(reversible too) conditions in substantial numbers. Here the heart is just a bystander watching helplessly, trying to adapt to a remote systemic comorbid problem. Such hearts don’t require cowboy aggression but gentle care by concerned physicians.(One study reveals weight reduction and systematic exercise program adds more life to HF than drugs and devices. Will link the reference/ or try google)

*Eg: Anemia is the commonest cause of HFpEF on a global scale. .CKD, undiagnosed autoimmune disorders, malignancy, are other classical examples. Let us be first a physician then a cardiologist, that will ensure our we don’t miss important treatable conditions with our short-sighted definition of heart failure based on EF%.

 Reference 

1.Y. Juilliere, J.N. Trochu, P. de Groote, et al.Heart failure with preserved systolic function: a diagnostic algorithm for a pragmatic definition  Arch Mal Coeur Vaiss, 99 (2006), pp. 279-286  View Record in ScopusGoogle Scholar
 

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