Morphological picture and molecular pathogenesis
The core of cardiac injury in toxic forms of diphtheria is profound intracellular disruption. Pathological anatomy records the onset of these changes at the turn of the first and second weeks of the disease. Morphologically, the process is characterized by marked cardiomyocyte dystrophy, which is predominantly fatty in nature. Along with dystrophic changes, cell necrosis (death) and lymphomacrophage infiltration of the interstitial tissue are observed.
The molecular mechanism of this damage represents a complex two-component cascade:
- Lysosomal damage. The destruction of lysosomes inside cardiomyocytes leads to a massive release of lysosomal enzymes, which literally digest the cell from within, exacerbating necrobiotic processes.
- Mitochondrial damage. Enzymatic blockade of carnitine occurs, which is a critically important cofactor for mitochondrial fatty acid oxidation. Unoxidized lipids accumulate, forming fatty transformation of the myocardium.
The outcome of these processes is total cellular energy deficiency. Energy starvation entails a disruption of normal depolarization and repolarization of cell membranes, which clinically manifests as decreased conductivity and a drop in the contractile capacity of the heart muscle.
Clinical and temporal classification
The timing of inflammatory and dystrophic changes directly determines the severity of the course and the final prognosis for the patient. Traditionally, two main types of cardiac involvement in diphtheria are distinguished:
| Type of injury | Time of onset | Clinical features |
|---|---|---|
| "Early" myocarditis | Develops as an early complication (from the 2nd–3rd or 4th day). Manifestation in the 1st week is an extremely unfavorable sign | Proceeds with maximum severity. Associated with the highest risk of fatal outcome |
| "Late" myocarditis | Typical onset is on the 2nd–3rd week (sometimes stretching to 3–4 weeks), against the background of subsiding local symptoms in the oropharynx | Proceeds more favorably. Upon resolution of the disease, it leaves behind residual myocardial dystrophy |
Stages and diagnostic methods
The detection of dystrophic and necrotic changes in the myocardium is possible even before the appearance of classical instrumental or physical symptoms. Diagnostics is divided into preclinical and clinical stages.
Early (preclinical) markers that precede changes on the electrocardiogram:
- Biochemical shifts: cardiospecific enzymes appear in the blood serum (creatine phosphokinase — CPK, lactate dehydrogenase — LDH, and aspartate aminotransferase — AST). It is important to note that the level of AST has a direct correlation with the severity of developing myonecrosis.
- Ultrasound signs (US): edema of the heart muscle is visualized, expansion (dilatation) of the ventricles and a clear impairment of their contractile function are noted.
Physical and instrumental signs:
- Objective examination reveals tachycardia, and percussion determines the expansion of the boundaries of relative cardiac dullness.
- ECG records various rhythm disturbances, conduction system blocks, prolongation of the PR interval, and specific changes in the ST–T complex.
- According to echocardiography (EchoCG), the picture of structural changes may correspond to dilated or hypertrophic cardiomyopathy.
Prognosis and possible outcomes
Diphtheritic heart damage can be extremely aggressive. The main threat to life is posed by severe arrhythmias, which are associated with a high risk of sudden death due to acute heart failure.
In the case of favorable resolution of the disease, the myocardial tissue does not fully recover. Residual myocardial dystrophy forms as an outcome of inflammation. In the long-term period after suffering toxic myocarditis, the development of myocarditic cardiosclerosis is possible (replacement of dead cardiomyocytes with connective tissue), which ultimately becomes the morphological basis for the formation of chronic heart failure.
To memorize the pathogenesis of fatty degeneration, use the logical chain "M-C-F-E": Mitochondria damaged → Carnitine blocked → Fats accumulate → Energy drops.
Class and exam questions
Why does fatty myocardial degeneration occur specifically in diphtheria?
Due to mitochondrial damage, a blockade of carnitine occurs. Without this cofactor, full mitochondrial oxidation of fatty acids is impossible, which is why unoxidized lipids accumulate in the cell cytoplasm.
Which laboratory markers indicate early heart damage?
At the preclinical stage, an increase in cardiospecific enzymes is recorded in the blood: CPK, LDH, and AST. At the same time, the level of AST directly correlates with the volume and severity of myocardial necrosis.
What is the key clinical difference between early and late diphtheritic myocarditis?
Early myocarditis manifests in the first week of the disease, proceeds extremely severely, and often leads to a fatal outcome. Late myocarditis develops in the 2nd–4th week against the background of subsiding local symptoms and more often ends in recovery with the formation of residual dystrophy.
What are the long-term consequences of suffered diphtheritic myocarditis?
Surviving patients develop residual myocardial dystrophy. In the long-term period, it can transform into myocarditic cardiosclerosis, leading to chronic heart failure.
What else to study on this topic
- Pathomorphology of local changes in pharyngeal diphtheria
- Mechanisms of cell membrane damage by lysosomal enzymes
- Pathogenesis and virulence factors of the diphtheria causative agent
- Morphological differences of myocarditic cardiosclerosis from other forms
- The role of carnitine in normal cellular energy metabolism
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