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FORENSIC MEDICAL ASPECTS OF PATHOLOGICAL CONDITIONS IN THE
THANATOGENESIS OF SUDDEN DEATH IN ISCHEMIC HEART DISEASE
S.A.Khakimov, B.M.Xotamov
Tashkent state medical university, Republican scientific and practical center for forensic
medicine
ABSTRACT:
A review of literature data on the role of cardiac conduction system pathology in the
thanatogenesis of sudden death in alcoholic cardiomyopathy and coronary heart disease from a
forensic medical perspective is provided. Modern data on the main pathological changes in the
heart's conduction system in alcoholic cardiomyopathy and coronary heart disease are presented.
Modern and historical aspects of pathology in the conducting system of the heart are highlighted.
Further ways to develop a more detailed study of the thanatogenesis of sudden death in ACMP
and coronary artery disease have been identified.
Keywords:
cardiac conduction system, sudden death, alcoholic cardiomyopathy,
ischemic heart disease.
Alcohol consumption is an integral element of the lifestyle, culture, and everyday life of
the majority of the population in many countries worldwide, and is perceived by the
public as a socially acceptable phenomenon. However, unreasonable and chronic
alcohol consumption causes numerous negative social and medical consequences,
leading to physical and moral degradation of a person, which "leaks out" as a chronic
alcohol disease or chronic alcohol intoxication. Prolonged alcohol abuse in more than
50% of cases leads to heart damage. However, alcohol affects not only the heart muscle;
in chronic alcohol intoxication, pathology also occurs in other internal target organs: the
liver, brain, pancreas, etc.
Alcoholic cardiomyopathy (ACMP) is one of the manifestations of chronic alcohol
intoxication, which is known to be characterized by multiple organ pathologies. It is one
of the relatively common forms of sudden cardiac death and ranks second in frequency
after sudden coronary death. Occurs the next day after alcohol exacerbation, and more
often after several days of alcohol abuse, at the patient's "emergence" from intoxication.
The appearance of pain is not related to physical exertion. The pain lacks the
characteristic seizure-like nature typical of angina, i.e., the clarity of its appearance and
disappearance, almost never occurs behind the sternum, and is not compressive or
pressing in nature. Unlike angina, nitroglycerin in ACMP does not relieve pain, which
can last for hours or days. ACMP can manifest as acute rhythm disturbances, atrial
flutter paroxysms, or tachycardia. Arrhythmia paroxysms always develop after alcoholic
exacerbations, while attacks of rhythm disturbances are often repeated multiple times.
The connection between arrhythmia and alcohol abuse is usually clearly observed by the
patients themselves. In the genesis of paroxysmal rhythm disturbances in ACMP, in
addition to the toxic effect of ethanol on the myocardium, it is necessary to consider the
sympathetic-tonic effect of alcohol. Myocardial dystrophy and cardiosclerosis, which
develop in ACMP and form its morphological basis, can be accompanied by a
disruption of the myocardial contractility and the appearance of heart failure symptoms.
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The mechanism of ethanol's damaging effect on tissues and organs is related to the
cytotoxic effect of its metabolite - acetaldehyde. These include both direct toxic effects on
cell membranes and indirect effects through other metabolic pathways. In particular, it has
been established that ethanol suppresses oxidation-reduction processes by separating the
respiration and oxidative phosphorylation processes in mitochondria, activates the
lysosomal system, stimulates the lipid peroxidation process, and activates phospholipase A.
This can result in damage to cell membranes, increasing their permeability. Death in
ACMP, like sudden coronary death, occurs due to fatal heart rhythm disorders resulting in
ventricular myocardial fibrillation.
Much remains unclear regarding the triggering mechanisms of ventricular fibrillation in
sudden cardiac death. In our time, a significant place in the genesis of this process has
begun to be given to arrhythmogenic substations (lysofosphoglycerides, cyclic
adenosine monophosphates, free fatty acids, lipid peroxidation products, some forms of
prostaglandins) formed in areas of myocardial hypoxia. Under conditions of complete
cessation of blood supply to the ischemic section of the myocardium, the
arrhythmogenic substances remain inactive in the zone of coagulation necrosis. When
residual blood flow or reperfusion persists, these substances spread through the
myocardium with blood flow, causing its fibrillation and often subsequent sudden death.
This phenomenon has been termed ventricular reperfusion fibrillation, possibly
primarily due to reperfusion secondary calcium-induced damage to cardiomyocytes.
Purposeful studies of arrhythmogenic substances have shown that in sudden death from
coronary heart disease, the content of phospholipids decreases in the myocardium of the
ventricles, interventricular septum, and atrium, while the concentration of free fatty
acids increases sharply. Such shifts in the biochemical composition of the myocardium
during sudden death, according to researchers, indicate the destruction of
myocardiocyte membrane phospholipids with the formation and accumulation of free
fatty
acid
lizoforms
of
phospholipids
(lysofosphhatidylcholine
and
lysofosphhatidylethanolamine), which have a cardiotoxic effect while simultaneously
reducing calcium content in the mitochondria of myocardiocytes. The accumulation of
lizoforms of phospholipids in mitochondria in coronary artery disease has a
thanatogenetic significance, as it causes electro-physiological changes in the
myocardium with a decrease in the maximum diastolic potential, amplitude and
duration of action potentials, its fractionation, which in combination gives an
arrhythmogenic effect. According to epidemiological studies conducted in recent years,
sudden death outside of medical institutions is the most frequent variant of death from
coronary artery disease, with about 70% of people dying suddenly, and in 2/3 of cases,
the duration of a fatal attack does not exceed 1 hour.
Among the many factors contributing to cardiac electrical instability, myocardial
hypertrophy, autonomic disorders, hyperthyroidism, intoxication with ethanol,
sympathomimetics, and monoamine oxidase inhibitors, etc., are indicated. According to
some data, the morphological manifestations of cardiac electrical instability are
characterized by: myocardial ischemia foci; hemorrhages and damaged areas along the
nodular tracts of the sinus node; hemorrhages or damaged areas involving most of the
specific muscle fibers of one of the central nodes of the PSS or a narrow part of the
bundle branch. These changes, as a rule, are combined with signs of focal exhaustion of
the adrenergic innervation of the heart with the loss of significant areas of
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catecholamines in the nerve plexuses of the myocardium, with relative preservation in
these zones of the cholinergic nerve plexuses. According to other authors who hold
somewhat different opinions, acute changes in the cardiac conduction system of sudden
death in the form of necrosis and hemorrhages are rare. Among this group, necrotic foci
in the myocardium were found in only 13-40% of cases in those who died within the
first 1-6 hours. Such phenomena are explained by L.V. Kaktursky by the fact that the
structure of the PSS is extremely resistant to ischemia, and even in the infarct zone, the
PSS fibers die later than the contractile fibers. This is evidenced by the fact that in the
early stages of ischemia, in cases of sudden cardiac death, structural damage to the PSS
cannot be detected. In a significant number of cases of sudden death in patients with
coronary heart disease at the preclinical and early clinical stages, acute changes in the
heart muscle are detected in the form of focal damage to cardiomyocytes, leading to
electrical instability and cardiac arrest. According to published data, in sudden coronary
death, focal myocardial damage of the contracture type occurs among acute changes in
the heart muscle in all observations, while foreign authors find contracture injuries in
sudden death only in 72-88% of observations. Some authors believe that focal
myocardial damage of the contracture type is characteristic of stress reactions and is
caused by the effects of catecholamines, therefore it is also found in the control group
of persons who died from violent death. The only difference is that the density of these
injuries in sudden death is 14 times greater.
If we delve deeper into history, we can note that cardiomorphologists hypothesized the
existence of the sinoatrial node of the heart even before describing its morphological
substrate. Later, as a result of a thorough histological examination, a sinus node, which
plays the role of a heart rhythm controller, was discovered, which was confirmed by
elegant comparison of anatomical and electrophysiological data. The PSS consists of
specialized cells that initiate heartbeat and coordinate the contraction of heart chambers.
The sinoatrial node is a small group of specialized heart muscle fibers located in the
wall of the right atrium. It is located to the right of the point where the superior vena
cava enters and normally produces an electrical impulse for contraction. The
atrioventricular node is located under the endocardium in the lower posterior part of the
interatrial septum. A Giss bundle branches from the atrioventricular node, passing
through the interventricular septum anteriorly and posteriorly. Inside the partition, the
Giss bundle is divided into a wide network of fibers that pass through the left part of the
partition - the left leg of the Giss bundle, and into a compact part in the form of a wire
running along the right side - the right leg of the Giss bundle. The rhythmic contraction
of the heart is ensured by the sequential passage of an electrical impulse through the
PSS. The sign of electrical stimulation is the excitation potential, which is formed due
to ion currents through the special channels of the sarcolemma. Heart cells responsible
for electrical excitation are divided into three types according to their
electrophysiological properties, studied through intracellular introduction of
microelectrodes:
- Pacemaker cells - rhythm drivers (for example, in the sinoatrial and atrioventricular
nodes);
- specialized, fast-conducting fabric (e.g., Purkinje fibers);
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- muscle cells of the ventricles and atria.
As noted above, in normal conditions, the heart rhythm is maintained by the function of
the sinoatrial node, in the cells of which the generation of sinus impulses occurs. If we
proceed from the generally accepted notions that the occurrence of fibrillation is
associated with impairments in the excitability, conductivity, and automaticity of the
heart, then the study of the PSS, which carries out the formation and propagation of
impulses of cardiac excitation, becomes particularly relevant. This issue is practically
not covered in the literature, and small morphological studies of PSS pathology in cases
of sudden death were usually limited to the study of its lower sections. The sinus-atrial
node is located constantly above the right ear at the point where the superior vena cava
enters the right atrium, on the lateral side under the epicardium, and is separated from
the endocardium only by a thin layer of connective and muscular tissue. The nodule is
not recognized by the naked eye, as it merges with the surrounding tissue in color. The
node has the shape of a flat ellipse or crescent located horizontally, its length is
approximately 10-15 mm, its height is 5 mm, and its thickness is 1.5 mm. A
characteristic feature of the sinus-atrial node is the presence of a disproportionately
large artery running in the center of the node along its longitudinal axis. This artery in
55% of cases is one of the first branches of the right coronary artery that branches
directly from the aorta; in the remaining 45% of cases, it branches from the initial part
of the left coronary artery's circumferential branch. This makes the node's position
superior in terms of its function as a control apparatus for central aortic pressure and
pulsation. The structural basis of the node is the connective tissue framework, consisting
of collagen, elastic, and reticular fibers, in which bundles of fine specialized muscle
fibers are located. The characteristic features of these fibers are their random
arrangement, lack of transverse stripes, and significantly smaller diameter compared to
the fibers of the atrial contractile myocardium. At the periphery of the node are located
nerve ganglia, single ganglion cells, and nerve fibers, which are also abundant in the
node's tissue.
Detailed analysis of electrocardiograms recorded immediately before death shows that
in most cases, the basis of any heart disease that led to sudden death lies in acute
disruptions in the rhythm of cardiac activity, which transition into ventricular fibrillation
or asystole.
Studies have shown that it is not always possible to identify specific morphological
signs explaining the genesis of the fatal outcome of an arrhythmia attack, and in a
number of cases, both chronic and acute pathological changes in the node tissue are
detected, indicating a possible weakening of its function. These include: a significant
increase in the proportion of the connective tissue trunk (fibrosis or fibroelastosis of the
node) with a simultaneous decrease in the number of specialized fibers; lymphoid
infiltrates in the node tissue; stenosis, and in some cases, fresh thrombosis of the sinus
artery; eosinophilia, homogenization, and swelling of the myocyte sarcoplasm,
myocytosis of individual specialized fibers; micro-hemorrhages around the node,
partially penetrating the node tissue and surrounding the nerve trunks and ganglia;
changes in the nerve ganglia located near the node - hyperchromatosis, vacuolization,
eccentric displacement of the nuclei, their pycnosis, and caryolysis.
Thus, to develop a more detailed study of the thanatogenesis of sudden death in ACMP
and coronary artery disease, the following tasks can be addressed in the future:
- screening of morphological changes in the PSS in death from ACMP;
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-study of the degree of fibrosis and lipomatosis of the PSS in patients with coronary
artery disease and ACMP in a comparative aspect;
- study of tissue levels of acetaldehyde in death from ACMP;
- Immunohistochemical analysis of plasma protein transudation products and PSS cell
cytoskeleton elements during death from coronary artery disease and ACMP in a
comparative aspect.
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