Stage B
Structural heart disease without signs
or symptoms of heart failure (HF)

Patients categorized in ACC/AHA Stage B HF have impaired heart function but no symptoms of HF, e.g., exercise intolerance, fluid retention, etc.
According to Young et al., (2021) Stage B is defined as no previous diagnosis of HF with evidence of a structural or functional abnormality including the following:

• LV EF <50%
• Diastolic dysfunction at least moderate in severity
  
• LV hypertrophy (LVMI>134 g/m2 for men and >110 g/m2 for women) Click here to open the MDApp calculator for Left Ventricular Mass Index (LVMI)
  
• Significant valve disease per echocardiogram (defined as greater than moderate in severity),
  
• Presence of regional wall motion abnormalities on echocardiogram
  
• Enlarged left ventricle
  
• Abnormal Left Atrial Volume Index (LAVI) is (>33 mL/m2 for men and >30 mL/m2 for women).

In addition, preclinical diastolic dysfunction, and preclinical systolic dysfunction, have been associated with an increased risk of clinical HF and increased risk of mortality.

Myocardial infarction

• Myocardial infarction (MI) is usually the result of myocardial ischemia and hypoxia due to thrombosis associated with coronary artery disease. Hypoxic cardiomyocytes must switch to anaerobic metabolism which initiates a cascade of acidosis, inflammation, mitochondrial damage, reduction of ATP production, disrupted ion transport, loss of membrane integrity and cardiomyocyte death. The longer the duration of coronary occlusion the larger the infarct size (McAlindon, 2015).

Post-MI ventricular remodeling with reduced EF:

• Thrombosis
• Ischemia
• Necrosis
• Scar formation
• Scar stretching and thinning
• Ventricular dilation with reduced ejection fraction (systolic dysfunction)

• Ventricular remodeling refers to the changes in size, shape, structure, and function of the heart.

Physiologic remodeling

• Physiologic ventricular remodeling is a benign result of adaptive gene transcription by cardiomyocytes in response to increased cardiac workload associated with endurance training and pregnancy. Endurance training increases oxygen consumption, cardiac output, stroke volume, and systolic blood pressure, as well as decreasing peripheral vascular resistance.
• Ventricular hypertrophy of pregnancy is the result of a natural chronic volume overload. Physiological remodeling is a reversible hypertrophy characterized by a proportional increase in chamber dimension and wall thickness. (Fernandes, 2015)

Pathological remodeling

• Pathological remodeling is progressive and minimally reversible. It is the product of chronic stress, hemodynamic overload and injury induced maladaptive gene transcription associated with ventricular fibrosis, cardiomyocyte hypertrophy, abnormal sarcomere architecture, arrhythmia, and heart failure (Burchfield, 2013).
• The sarcomere is the primary motile unit in striated myocytes and cardiomyocytes. The normal cardiomyocyte has length to width ratio of ≈ 7:1. Eccentric hypertrophy can result in a length to width ratio of ≈ 11:1. Elongation of ventricular cardiomyocytes by eccentric hypertrophy is characterized by ventricular dilation with high end-diastolic volume (EDV) and reduced ejection fraction (EF).

• Valve disease
  The heart has four valves: the tricuspid, pulmonary, mitral, and aortic. (“Heart Valve Diseases | Types, Causes, Risks, Symptoms, Treatment”) The tissue flaps of these valves make sure the blood flows in the correct direction through the heart chambers. Infections, birth defects, age-related changes, or other conditions can cause incomplete closure of one or more of the heart valves. An incompetent valve can allow blood to backflow into a heart chamber instead of being ejected forward. This is commonly referred to as regurgitation of which ever valve is involved. For example, if the Mitral valve leaflets fail to close, blood flowing back into the left atrium during systole would be referred to Mitral valve regurgitation or sometimes mitral insufficiency or mitral incompetence. Valve damage can also lead to the heart valve not opening fully (stenosis) requiring more for heart muscles to produce sufficient cardiac output. If the heart valve is closed completely, with no open passage for blood flow, that is referred to as atresia. https://my.clevelandclinic.org/health/articles/17067-heart-valves
• Left Ventricular Hypertrophy (LVH)
  In response to pathophysiological stimuli, such as ischemia/reperfusion injury or excessive mechanical load, multiple molecular and cellular changes contribute to ventricular remodeling. These changes may include cardiomyocyte loss through cell death pathways e.g., necrosis, apoptosis, and possible excessive autophagy. Accumulation of excess extracellular matrix leading to fibrosis. Metabolic derangements, insulin resistance, and lipo-toxicity can occur. Finally, structural changes and alterations in ion transporting processes may culminate in malignant arrhythmia.

Some of the early signs of LVH are

• Shortness of breath
• Fatigue
• Chest pain, often after exercising
• Sensation of rapid, fluttering or pounding heartbeats (palpitations)
• Dizziness or fainting (Mayo clinic staff, 2020)

• Causes and Tests

Besides hypertension LVH can be caused by aortic valve stenosis, hypertrophic cardiomyopathy, and athletic training. An electrocardiogram, an echocardiogram and/or an MRI may be ordered to confirm a diagnosis of LVH.

Stages C and D will be discussed in detail in course #2, Treatment of Heart Failure.

References

Burchfield, J. S. (2013). Pathological Ventricular Remodeling. Circulation. 128(4), 388-400.

Fernandes, T., Baraúna, V., Negrão, C., Phillips, M. & Oliveira, E. (2015). Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs. American Journal of Physiology - Heart and Circulatory Physiology. 309(4), H543-H552.

Mayo Clinic staff. (2020). Left Ventricle hypertrophy – symptoms. Nov. 25, 2020 retrieved from https://www.mayoclinic.org/diseases-conditions/left-ventricular-hypertrophy/symptoms-causes/syc-20374314.

McAlindon, E., Bucciarelli-Ducci, C., Suleiman, M., Baumbach, A. (2015) Infarct size reduction in acute myocardial infarction. Heart. 101, 155-160.

Young, K.A., Scott, C.G., Rodeheffer, R.J. & Chen, H.H. (2022). Incidence of Preclinical Heart Failure in a Community Population. J Am Heart Assoc.11(15), e025519.

Young, K.A., Scott, C.G., Rodeheffer, R.J. & Chen, H.H. (2021). Progression of Preclinical Heart Failure: A Description of Stage A and B Heart Failure in a Community Population. Circ Cardiovasc Qual Outcomes. 14(5), e007216.

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