12. Epidemiology, pathophysiological background, types and clinical syndromes of heart failure

Definition and epidemiology

Heart failure is a clinical syndrome where the patient has symptoms and/or signs of insufficient cardiac output and/or backwards congestion. This is due to an underlying decrease in systolic or diastolic function of the heart. Decreased systolic function refers to decreased ability of the heart to eject blood, reflected as a decreased left ventricular ejection fraction (LVEF, usually shortened to simply EF). Decreased diastolic function refers to decreased ability of the heart to fill with blood.

Not all people with heart failure have symptoms of volume overload, and as such, the term “congestive” heart failure is no longer preferred.

People may have decreased systolic function (decreased EF) or decreased diastolic function without having overt heart failure. However, these are precursors to heart failure and should be treated accordingly.

Some people with heart failure experience a stable course throughout their life, with no worsening of their symptoms. However, most people with HF experience at least one episode of worsening. This is called an acute decompensation or an exacerbation, and may occur over days or weeks or months. From there, the condition may continue to worsen or return to the condition before the worsening.

The mortality of heart failure has decreased significantly with modern treatment. According to one study, the 1-year mortality without medical therapy was approximately 52%, but with optimal modern medical therapy the 1-year mortality was approximately 7%.

Etiology

Heart failure is most common in persons with certain risk factors, especially coronary heart disease, cigarette smoking, hypertension, overweight, and diabetes. The most common causes of HF are myocardial infarction and hypertension.

This is a more comprehensive list of conditions which can cause heart failure:

  • Intrinsic myocardial disease
    • Myocardial infarction
    • Cardiomyopathy
    • Myocarditis
    • Toxic agents
      • Alcohol
      • Cocaine
      • Anthracyclines
      • Cyclophosphamide
  • Arrhythmias
    • Atrial fibrillation
    • Significant bradycardia
    • Bundle branch block
  • Excess cardiac workload
    • Pressure overload
      • Hypertension
      • Aortic or pulmonary stenosis
      • Hypertrophic cardiomyopathy
    • Volume overload
      • Aortic insufficiency
      • Mitral insufficiency
      • Tricuspid insufficiency
      • Congenital left-to-right shunts
  • Increased body demand of CO (“high output heart failure”)
    • Thyrotoxicosis
    • Anaemia
    • Pregnancy
    • AV fistula

In those who already have heart failure, many precipitators can trigger an episode of decompensation. This occurs most commonly due to excessive fluid intake or a myocardial infarction. However, any of the above mentioned causes can precipitate decompensation, in addition to:

  • Excessive salt intake
  • Physical or emotional stress
  • Infection

Pathophysiology

When the cardiac output becomes insufficient to supply the needs of the body, the body will try to increase the cardiac output by compensatory mechanisms. These compensatory mechanisms achieve the goal of increasing cardiac output initially and to some extent, but they’re deleterious in the long run. For this reason, many of the pharmacological targets in heart failure inhibit these compensatory mechanisms.

The most important compensatory mechanisms clinically are the neurohumoral systems, most importantly the sympathetic nervous system activation, the activation of RAAS, and the release of natriuretic peptides. Over time and as the result of these stimuli, myocardial remodelling occurs. This is also detrimental, as it causes the chambers to dilate, change their geometry, and accumulate fibrosis, causing systolic and/or diastolic dysfunction. Inhibition of the neurohumoral systems is shown to significantly decrease myocardial remodelling.

The body’s compensatory responses overshoot as well. The sympathetic nervous system gets so strongly activated that the vasoconstriction eventually decreases CO. The compensatory increase in heart rate increases the energy expenditure, increasing the demand for CO. Activation of RAAS causes fluid retention, which (after the Frank-Starling mechanism has been maxed out) worsens the myocardial contractility.

Types and classification

There are three types of heart failure, depending on the EF:

  • Heart failure with reduced ejection fraction (HFrEF) – EF < 40%
  • Heart failure with mid-range ejection fraction (HFmrEF) – EF 40 – 50%
  • Heart failure with preserved ejection fraction (HFpEF) – EF > 50%

HFrEF was historically called “systolic heart failure” while HFpEF was called “diastolic heart failure”, which reflects the underlying pathophysiology of each type. This distinction is important because each type have different underlying cause, pathophysiology, and most importantly, response to therapy. It is only in HFrEF that research has shown that medical therapy reduces both morbidity and mortality. For HFpEF, science is not yet at a place where we know the optimal medical therapy.

We can also classify HF according to the severity. This is accomplished with the New York Heart Association (NYHA) classification of heart failure:

  • NYHA class I
    • Symptoms of heart failure only in excessive exercise, or no symptoms of heart failure at all
  • NYHA class II
    • Symptoms of heart failure during normal daily activity like climbing stairs, making food, etc.
  • NYHA class III
    • Symptoms of heart failure during easy daily activity like dressing, walking on flat surface
  • NYHA class IV
    • Symptoms present during rest

We can also artificially divide heart failure into “right” and “left” heart failure, depending on which ventricle is the offender, but this distinction offers no advantage. Failure of one side of the heart quickly causes failure of the other, and so in most patients, symptoms of both “right” and “left” heart failure is seen.

Clinical features

The most characteristic symptoms of heart failure are dyspnoea, orthopnoea, and fatigue, although a wide variety of symptoms may occur. The most characteristic signs are elevated jugular venous pressure, lower extremity pitting oedema, and pulmonary crackles on auscultation.

Other clinical features include:

  • General features
    • Cardiac cachexia
    • Fatigue
    • Pulsus alternans
    • Tachycardia
  • Features of left-sided heart failure
    • Pulmonary symptoms dominate
    • Dyspnoea
    • Orthopnoea
    • Cardiac asthma
    • Paroxysmal nocturnal dyspnoea
  • Features of right-sided heart failure
    • Congestive symptoms dominate
    • Peripheral pitting oedema
    • Jugular vein distension
    • Hepatosplenomegaly
    • Jaundice
    • Ascites
    • Loss of appetite

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13. Diagnosis and therapy of heart failure

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