Heart hypertrophy

Cardiac hypertrophy is an increase in the myocardial mass of the heart as a result of continuous pressure or volume load on the heart (Krams 2010).

Cardiac hypertrophy is divided into 3 stages:

1. development of hypertrophy

Increased workload on the heart leads to the development of cardiac hypertrophy in this phase.

2nd phase of compensation

The growth of the heart can still compensate for the ratio of heart muscle mass to cardiac work. There are no serious limitations to the heart mechanics. Only the relaxation speed and shortening time of the heart muscle are reduced.

3rd phase of heart failure

In this phase, the heart is no longer able to deliver a normal cardiac output (Klinke 2010).

Pathologically and anatomically, cardiac hypertrophy is divided into:

- Concentric hypertrophy

In this case, a constant or reduced ventricular lumen is found as a result of chronic cardiac pressure load (Krause 2022). This is referred to as physiological cardiac hypertrophy (Nakamura 2018).

-Eccentric cardiac hypertrophy

In this case, cardiac dilatation occurs as a result of chronic cardiac volume load (Krause 2022). This form is also referred to as pathological cardiac hypertrophy (Nakamura 2018). Clinically, functional disorders occur at this stage (Oldfield 2020).

Depending on the localization, cardiac hypertrophy is pathophysiologically divided into:

- Left ventricular hypertrophy

- Right ventricular hypertrophy

- Biventricular cardiac hypertrophy (Krause 2022)

The causes of cardiac hypertrophy can be:

• Idiopathic, such as primary cardiomyopathy
• Athlete's heart without pathological value
• Chronic stress on the heart due to
  • Left ventricular pressure load due to e.g. arterial hypertension, hypertensive heart disease (Krause 2022), pulmonary embolism, post-myocardial infarction, congenital or acquired heart valve stenosis such as aortic valve stenosis (Krams 2010)
  • Left ventricular volume load due to e.g. congenital or acquired heart valve insufficiency (Krams 2010), e.g. aortic valve insufficiency
  • Right ventricular pressure load due to e.g. cor pulmonale, pulmonary hypertension
  • Right ventricular volume load due to congenital or acquired heart valve insufficiencies (Krams 2010) such as tricuspid insufficiency (Krause 2022)

The heart is able to increase cardiac output in stressful situations by stimulating the sympathetic nervous system or by pre-stretching. Only when the heart is exposed to an increased workload over a longer period of time do structural changes occur in the heart muscles in the form of cardiac hypertrophy (Klinke 2010).

In the case of a chronic pressure load, the heart muscle wall hypertrophies without the ventricular volume increasing, known as concentric cardiac hypertrophy. The systolic wall tension increases as a result (Krams 2010) and cardiac function improves (Oldfield 2020).

Chronic volume loading, on the other hand, leads to an enlargement of the ventricular wall with enlargement of the ventricle, also known as eccentric cardiac hypertrophy. The systolic wall tension remains unchanged (Krams 2010).

In the late stages of cardiac hypertrophy, relative hypoxia occurs, as the cardiac capillary volume remains constant, but the diffusion distance becomes steadily longer. There is a risk of deficiency supply from the critical heart weight, which is approx. 500 g or 7 g / kg bw (Krams 2010).

Cardiac hypertrophy can lead to:

- dyspnea

- heart failure

- Myocardial infarction (Krause 2022)

The diagnosis of cardiac hypertrophy consists of a physical examination, ECG, echocardiography and chest X-ray (Krause 2022).

Clinical examination

- Left ventricular hypertrophy: Lifting cardiac apex (Krause 2022)

- Right ventricular hypertrophy: Epigastric pulsations (Krause 2022)

ECG

• Left ventricular hypertrophy:
  • Rotation of the electrical axis of the heart to the left (position type: left or over-rotated left type)
  • P- sinistroatrial
  • Increase in amplitude of the R wave in I, aVL, V 4 - 6
  • Amplitude increase of the S-wave in III, aVF, V1 - 3
  • Sokolow index ≥ 3.5 mV
  • Lewis index ≥ 1.6 mV
  • Cornell index in men ≥ 2.8 mV, in women ≥ 2.2 mV
  • Delayed R progression with abrupt R / S transition (Krause 2022)

• Right ventricular hypertrophy
  • Rotation of the electrical axis of the heart to the right (position type: steep type, sagittal type or right type)
  • P- dextroatrial
  • Increase in amplitude of the R wave in III, aVF, V 1- 2
  • Amplitude increase of the S- prongs I, aVL, V 1 - 2
  • Sokolow index ≥ 1.05 mV
  • Whitebook index ≤ - 1.4 mV
  • Delayed R progression with S persistence and shift of the R / S transition to the left (Krause 2022)
  • In the case of pressure-induced hypertrophy of the right ventricle, a relatively high R wave in lead V1 (R ≥ S), usually associated with a right axis deviation. Alternatively, there may also be a qR pattern in V1 or V3R. ST depression and T wave inversion are often detectable in the right to mid precordial leads (Kasper 2017).

In higher-grade right or left ventricular hypertrophy, there are also:

• Changes in the ST segment and T wave in the form of excitation regression disorders with descending ST segment depression and preterminal negative T waves during pressure loading or ascension of the ST segment with excessive T waves during volume loading in both the right and left ventricular leads
• The QRS complex can show an intraventricular conduction delay in both the left and right ventricular leads (Krause 2022).

Echocardiography

Echocardiography allows the cardiac pressure and volume load to be assessed by:

• Measurement of the ventricular diameter
• Measurement of the end-diastolic volume index during cardiac dilatation
• Measurement of the myocardial wall thickness

In left ventricular hypertrophy, there is an increase in IVSDd (end-diastolic diameter of the interventricular septum) and PWDd (end-diastolic posterior wall diameter). (Krause 2022)

Chest X-ray

In the early stages, concentric hypertrophy caused by pressure loading cannot be detected on the X-ray. However, if there is eccentric hypertrophy due to volume loading, this can be detected radiologically at an early stage (Herold 2022).

- Left ventricular hypertrophy:

The apex of the heart is displaced further to the left and dips obliquely into the diaphragm at an obtuse angle. The lateral view shows a narrowing of the posterior space of the heart near the diaphragm (Herold 2022).

- Right ventricular hypertrophy

In this case, the heart is also shifted to the left by rotation. However, the apex of the heart is raised and the angle between the left edge of the heart and the diaphragm becomes acute. The lateral image shows a narrowing of the retrosternal anterior chamber of the heart (Herold 2022).

Histologically, cardiac hypertrophy is characterized by an enlargement of the myocytes without cell division (Zhu 2019).

The therapy depends on the underlying disease.

The prognosis also depends on the disease causing the cardiac hypertrophy.

Cardiac hypertrophy is normally a reversible process that can regress within a few weeks if the triggering factors are eliminated. Only in the case of long-term hypertrophy, in which structural changes in the form of fibrosis are detectable, is the hypertrophy only partially reversible and is then also referred to as "pathological hypertrophy" (Klinke 2010).

1. Herold G et al. (2022) Internal Medicine. Herold Publishers 214
2. Kasper D L, Fauci A S, Hauser S L, Longo D L, Jameson J L, Loscalzo J et al. (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1453
3. Klinke R, Pape H C, Kurtz A, Silbernagl S (2010) Pathophysiology. Georg Thieme Verlag Stuttgart / New York 155 - 156
4. Krams M, Frahm S O, Kellner U, Mawrin C (2010) Short textbook on pathology. Georg Thieme Publishers Stuttgart / New York 84
5. Krause U (2022) Cardiac hypertrophy. Pschyrembel online. Doi: https://www.pschyrembel.de/Herzhypertrophie/K09Q7
6. Nakamura M, Sadoshima J (2018) Mechanisms of physiological and pathological cardiac hypertrophy. Nat Rev Cardiol. 15 (7) 387 - 407
7. Oldfield C J, Dukamel T A, Dhalla N S (2020) Mechnisms for the transition from physiological to patholpgical cardiac hypertrophy. Can J Physiol Pharmacol. 98 (2) 74 - 84
8. Zhu L, Li C, Liu Q, Xu W, Zhou X (2019) Molecular biomarkers in cardiac hypertrophy. J Cell Mol Med. 23 (3) 1671 - 1677