Myocardial Injury

Factors directly damaging the heart

Pathogenic agents causing primary heart muscle damage are divided into physical, chemical, and biological.

Physical factors include:

• Extracardiac compression of the heart (accumulation of exudate in pericarditis, blood in hemopericardium and tamponade, pressure from a tumor or emphysematous lungs).
• Exposure to electric current (household electrical injury or medical defibrillation).
• Mechanical trauma (chest contusions, penetrating wounds, consequences of surgical manipulations).

Chemical factors include:

• Non-drug compounds: heavy metal and calcium salts, enzyme inhibitors, lipid hydroperoxides, and uncouplers of oxidative phosphorylation.
• Medications in inappropriate doses: cardiac glycosides, beta-blockers, calcium channel blockers.
• Deficiency states: lack of oxygen (hypoxia) or ions essential for metabolism.

Functional overload and heart failure

Excessive myocardial stress is a leading cause of heart failure (HF). Functional overload is divided into two categories:

• Increased preload — overload of the heart with an excessive blood volume.
• Increased afterload — overload with pressure (resistance to ejection).

Depending on the ratio of damage and load, three forms of failure are distinguished:

1. Myocardial — caused by primary damage to the cardiomyocytes themselves.
2. Overload — occurs under excessive functional load on an initially intact (healthy) myocardium.
3. Mixed — combines elements of direct damage and hemodynamic overload.

The role of potassium and acidosis in arrhythmogenesis

During cell damage, a massive efflux of $K^+$ ions into the interstitial fluid occurs. This is facilitated by three factors: energy deficit (lack of ATP and creatine phosphate), ion pump dysfunction (decreased activity of plasmalemmal $K^+, Na^+$-ATPase), and structural abnormalities (abnormal membrane permeability).

Excess extracellular potassium triggers a cascade of electrophysiological disruptions:

• Excitability threshold decreases due to a reduced resting potential (partial membrane depolarization).
• Impulse conduction slows down, forming an electric current of injury in micro-areas of the tissue.
• Arrhythmogenic vulnerability increases: the refractory period shortens, the myocardium recovers its ability to excite faster, creating conditions for ectopic foci and re-entry waves.

Excess hydrogen ions ($H^+$) during tissue acidosis exhibit a similar but less pronounced arrhythmogenic effect.

cAMP accumulation and arrhythmia mechanisms

Excess intracellular cyclic AMP (cAMP) is a crucial factor in the development of arrhythmias. It accumulates due to two reasons:

• Activation of the enzyme adenylate cyclase under the action of catecholamines (adrenaline, noradrenaline).
• Inhibition of phosphodiesterases (enzymes that degrade cAMP) in ischemia, myocarditis, or cardiomyopathies.

High cAMP levels stimulate the slow inward calcium current ($I_{Ca}$). This overloads cardiomyocytes with calcium and induces triggered activity.

Ultimately, two main mechanisms of arrhythmias are formed:

1. Abnormal automatism (early or delayed afterdepolarization).
2. Circulation of the excitation wave (Reentry), which can manifest as retrograde conduction, wave "reflection," or longitudinal dissociation.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of excitation wave circulation (Reentry)
• Types of abnormal automatism: early and delayed afterdepolarization
• The effect of oxidative phosphorylation uncouplers on cardiomyocytes
• Electrophysiology of injury currents in myocardial microregions

Other topics in "Chapter 22. Typical Forms of Pathology of the Circulatory System"

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