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At what ejection fraction we say heart failure with reduced ejection fraction and heart failure with preserved ejection fraction

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"heart failure"[MeSH Terms] AND "ejection fraction"

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2022 AHA ACC HFSA guideline HFrEF LVEF 40% HFpEF 50% definitions

  • HFrEF, heart failure with reduced ejection fraction: LVEF 40% or less
  • HFpEF, heart failure with preserved ejection fraction: LVEF 50% or greater
The intermediate group is:
  • HFmrEF, heart failure with mildly reduced ejection fraction: LVEF 41% to 49%
These labels require clinical heart failure, not just an echocardiographic EF value. For HFpEF especially, there should also be evidence of raised filling pressures or structural/diastolic cardiac abnormality. The ACC classification summary uses these cutoffs.

Pathophysiology of dilated cardiomyopathy

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"dilated cardiomyopathy" AND pathophysiology

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dilated cardiomyopathy pathophysiology review cardiac remodeling neurohormonal activation

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dilated cardiomyopathy gross pathology dilated left ventricular chamber mural thrombus

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https://www.ncbi.nlm.nih.gov/books/NBK553848

Pathophysiology of dilated cardiomyopathy (DCM)

DCM is a disorder of ventricular dilatation and impaired systolic contraction, usually affecting the left ventricle and often both ventricles. The primary functional defect is reduced myocardial contractility, producing a reduced ejection fraction, often <40%.

Pathophysiologic sequence

1. Initial myocardial injury or intrinsic defect
The trigger may be:
  • Genetic defects, especially in sarcomeric, cytoskeletal, nuclear-envelope, or cell-adhesion proteins. Titin mutations are common.
  • Myocarditis, often viral, with persistent injury or post-inflammatory remodeling.
  • Toxins, especially alcohol, anthracyclines, cocaine, and other cardiotoxic exposures.
  • Peripartum, metabolic, endocrine, nutritional, infiltrative, or idiopathic causes.
These insults impair force generation, myocyte integrity, energy handling, or calcium cycling. - Robbins & Kumar Basic Pathology, p. 370-371
2. Reduced contractility causes a fall in stroke volume and cardiac output
A weak ventricle cannot eject blood effectively:
[ \downarrow \text{Contractility} \rightarrow \downarrow \text{Stroke volume} \rightarrow \downarrow \text{Cardiac output} ]
More blood remains in the ventricle after systole, so end-systolic volume rises.
3. Ventricular dilatation and increased wall stress
Retained volume increases LV end-diastolic volume and stretches the chamber. As ventricular radius increases, wall stress rises according to Laplace's law:
[ \text{Wall stress} \propto \frac{\text{Pressure} \times \text{Radius}}{\text{Wall thickness}} ]
Thus, a dilated ventricle must generate more force to produce the same pressure. This further worsens systolic function. Initially, eccentric hypertrophy develops as an attempt to reduce wall stress, but it eventually becomes maladaptive.
4. Neurohormonal compensation becomes harmful
Reduced forward output and reduced effective arterial filling activate:
  • Sympathetic nervous system: tachycardia, vasoconstriction, increased contractility initially
  • RAAS: angiotensin II causes vasoconstriction and remodeling; aldosterone causes sodium and water retention and fibrosis
  • ADH: water retention
  • Endothelin, inflammatory cytokines, and oxidative-stress pathways
Initially these preserve perfusion. Chronically, they increase preload and afterload, promote hypertrophy, fibrosis, arrhythmias, myocyte apoptosis, and progressive remodeling.
5. Adverse remodeling
Chronic stretch and neurohormonal activation cause:
  • Myocyte hypertrophy but progressive myocyte loss through apoptosis/necrosis
  • Interstitial and replacement fibrosis
  • Abnormal extracellular-matrix turnover
  • Impaired calcium handling
  • A more spherical ventricle with worsening mechanical inefficiency
The result is a self-perpetuating cycle:
[ \text{Myocardial dysfunction} \rightarrow \text{dilatation} \rightarrow \text{increased wall stress} \rightarrow \text{remodeling/fibrosis} \rightarrow \text{further dysfunction} ]
6. Consequences of chamber dilatation
  • Functional mitral and tricuspid regurgitation: annular dilatation and papillary-muscle displacement prevent normal leaflet coaptation.
  • Raised ventricular filling pressures: causes pulmonary venous congestion, dyspnea, orthopnea, and eventually right-sided failure.
  • Arrhythmias: fibrosis and chamber enlargement predispose to atrial fibrillation and ventricular tachyarrhythmias.
  • Mural thrombus and embolism: low-flow, poorly contracting dilated chambers can form thrombi, which may embolize systemically.
  • Sudden cardiac death: may occur from malignant ventricular arrhythmias.

One-line exam summary

DCM results from genetic or acquired myocardial injury causing systolic pump failure; compensatory ventricular dilatation and neurohormonal activation initially support output but ultimately cause increased wall stress, eccentric remodeling, fibrosis, valve regurgitation, arrhythmias, and progressive HFrEF.
Recent mechanistic reviews also emphasize the roles of maladaptive RAAS and sympathetic activation, oxidative stress, inflammation, calcium-handling abnormalities, apoptosis, and extracellular-matrix remodeling in this vicious cycle, as summarized in this NCBI pathophysiology review.
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