Sudden cardiac death

Sudden cardiac death is cardiac arrest, an acute hemodynamic syndrome caused by complete cessation of the myocardial pumping function, or a condition in which the continuing electrical and mechanical activity of the heart does not provide effective blood circulation.

The incidence of sudden cardiac death ranges from 0.36 to 1.28 cases per 1000 population per year. About 90% of sudden cardiac death cases occur in out-of-hospital settings.

Our attention should be drawn to the fact that the consequences of sudden circulatory arrest have a better prognosis due to early recognition of this pathology (in a matter of seconds) and immediate initiation of competent resuscitation measures.

Only cases characterized by the following signs are classified as sudden cardiac death.

1. The onset of death occurred in the presence of witnesses within 1 hour after the appearance of the first threatening symptoms (previously this period was 6 hours).
2. Immediately prior to death, the patient's condition was assessed as stable and did not raise serious concerns.
3. Other causes (violent death and death resulting from poisoning, asphyxia, injury or any other accident) are completely excluded.

According to ICD-10, the following are distinguished:

• 146.1 - Sudden cardiac death.
• 144-145 - Sudden cardiac death due to conduction disturbance.
• 121-122 - Sudden cardiac death in myocardial infarction.
• 146.9 - Cardiac arrest, unspecified.

Some variants of the development of sudden cardiac death, caused by different types of myocardial pathology, are classified into separate forms:

• sudden cardiac death of a coronary nature - circulatory arrest caused by exacerbation or acute progression of ischemic heart disease;
• sudden cardiac death of arrhythmic nature - sudden cessation of blood circulation caused by disturbances in cardiac rhythm or conduction. The onset of such death occurs within minutes.

The main criterion for diagnosis is a fatal outcome occurring within a few minutes in cases where autopsy did not reveal morphological changes incompatible with life.

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What causes sudden cardiac death?

According to modern concepts, sudden cardiac death is a generalized group concept that unites various forms of cardiac pathology.

In 85-90% of cases, sudden cardiac death develops as a result of ischemic heart disease.

The remaining 10-15% of cases of sudden cardiac death are caused by:

• cardiomyopathies (primary and secondary);
• myocarditis;
• malformations of the heart and blood vessels;
• diseases causing myocardial hypertrophy;
• alcoholic heart disease;
• mitral valve prolapse.

Relatively rare causes that provoke a condition such as sudden cardiac death:

• ventricular pre-excitation and prolonged QT syndromes;
• arrhythmogenic myocardial dysplasia;
• Brugada syndrome, etc.

Other causes of sudden cardiac death include:

• pulmonary embolism;
• cardiac tamponade;
• idiopathic ventricular fibrillation;
• some other conditions.

Risk factors for sudden cardiac arrest

Myocardial ischemia, electrical instability and left ventricular dysfunction are the main triad of risk for sudden cardiac arrest in patients with coronary heart disease.

Electrical instability of the myocardium manifests itself in the development of "threatening arrhythmias": disturbances of the heart rhythm, immediately preceding and transforming into fibrillation and asystole of the ventricles. Long-term electrocardiographic monitoring has shown that ventricular fibrillation is most often preceded by paroxysms of ventricular tachycardia with a gradual increase in rhythm, turning into ventricular flutter.

Myocardial ischemia is a significant risk factor for sudden death. The degree of coronary artery damage is important. About 90% of those who died suddenly had atherosclerotic narrowing of the coronary arteries by more than 50% of the vessel lumen. In approximately 50% of patients, sudden cardiac death or myocardial infarction are the first clinical manifestations of ischemic heart disease.

The probability of circulatory arrest is highest in the first hours of acute myocardial infarction. Almost 50% of all deaths occur in the first hour of the disease due to sudden cardiac death. It should always be remembered: the less time has passed since the onset of myocardial infarction, the greater the probability of developing ventricular fibrillation.

Left ventricular dysfunction is one of the most important risk factors for sudden death. Heart failure is a significant arrhythmogenic factor. In this regard, it can be regarded as a significant marker of the risk of sudden arrhythmic death. The most indicative is a decrease in the ejection fraction to 40% or less. The likelihood of developing an unfavorable outcome increases in patients with cardiac aneurysm, post-infarction scars and clinical manifestations of heart failure.

Impaired autonomic regulation of the heart with a predominance of sympathetic activity leads to electrical instability of the myocardium and an increased risk of cardiac death. The most significant signs of this condition are decreased sinus rhythm variability and increased duration and dispersion of the QT interval.

Left ventricular hypertrophy. One of the risk factors for sudden death is severe left ventricular hypertrophy in patients with arterial hypertension and hypertrophic cardiomyopathy.

Restoration of cardiac activity after ventricular fibrillation. The high-risk group for sudden arrhythmic death (Table 1.1) includes patients resuscitated after ventricular fibrillation.

The main risk factors for arrhythmic death, their manifestations and methods of detection in patients with coronary heart disease

The most prognostically dangerous is fibrillation that occurs outside the acute period of myocardial infarction. Opinions are contradictory regarding the prognostic significance of ventricular fibrillation that occurs during acute myocardial infarction.

General risk factors

Sudden cardiac death is more often registered in people aged 45-75 years, and sudden cardiac death occurs 3 times more often in men than in women. However, in-hospital mortality in myocardial infarction is higher in women than in men (4.89 versus 2.54%).

Risk factors for sudden death include smoking, arterial hypertension with myocardial hypertrophy, hypercholesterolemia and obesity. Long-term consumption of soft drinking water with insufficient magnesium (predisposes to spasms of the coronary arteries) and selenium (impairs the stability of cell membranes, mitochondrial membranes, impairs oxidative metabolism and disrupts the functions of target cells) also has an effect.

Risk factors for sudden coronary death include meteorological and seasonal factors. Research data show that sudden coronary death increases in autumn and spring, on different days of the week, with changes in atmospheric pressure and geomagnetic activity. The combination of several factors leads to a several-fold increase in the risk of sudden death.

Sudden cardiac death in some cases can be provoked by inadequate physical or emotional stress, sexual intercourse, alcohol consumption, heavy meals and cold irritants.

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Genetically determined risk factors

Some risk factors are genetically determined, which is of particular importance both for the patient and for his children and close relatives. Long QT syndrome, Brugada syndrome, sudden unexplained death syndrome, arrhythmogenic right ventricular dysplasia, idiopathic ventricular fibrillation, sudden infant death syndrome and other pathological conditions are closely associated with a high risk of sudden death at a young age.

Recently, great interest has been shown in Brugada syndrome - a disease characterized by the young age of patients, frequent occurrence of syncope against the background of attacks of ventricular tachycardia, sudden death (mainly during sleep) and the absence of signs of organic myocardial damage at autopsy. Brugada syndrome has a specific electrocardiographic picture:

• right bundle branch block;
• specific ST segment elevation in leads V1-3;
• intermittent prolongation of the PR interval;
• attacks of polymorphic ventricular tachycardia during syncope.

A typical electrocardiographic pattern is usually recorded in patients before the development of ventricular fibrillation. During a test with physical exercise and a drug test with sympathomimetics (isadrine), the electrocardiographic manifestations described above are reduced. During a test with slow intravenous administration of antiarrhythmic drugs that block the sodium current (ajmaline at a dose of 1 mg / kg, novocainamide at a dose of 10 mg / kg or flecainide at a dose of 2 mg / kg), the severity of electrocardiographic changes increases. The introduction of these drugs in patients with Brugada syndrome can lead to the development of ventricular tachyarrhythmias (up to ventricular fibrillation).

Morphology and pathophysiology of sudden cardiac arrest

Morphological manifestations of sudden cardiac arrest in patients with ischemic heart disease:

• stenotic atherosclerosis of the coronary arteries of the heart;
• coronary artery thrombosis;
• cardiac hypertrophy with dilation of the left ventricular cavity;
• myocardial infarction;
• contracture damage to cardiomyocytes (the combination of contracture damage with fragmentation of muscle fibers serves as a histological criterion for ventricular fibrillation).

Morphological changes serve as a substrate on the basis of which sudden cardiac death develops. In the majority of patients with ischemic heart disease (90-96% of cases) who died suddenly (including patients with asymptomatic course), significant atherosclerotic changes in the coronary arteries (narrowing of the lumen by more than 75%) and multiple lesions of the coronary bed (at least two branches of the coronary arteries) are found at autopsy.

Atherosclerotic plaques, located predominantly in the proximal sections of the coronary arteries, are often complicated, with signs of endothelial damage and the formation of parietal or (relatively rare) completely occluding vessel lumen thrombi.

Thrombosis is relatively rare (5-24% of cases). It is natural that the longer the period of time from the onset of a heart attack to the moment of death, the more often thrombi occur.

In 34-82% of the deceased, cardiosclerosis is determined with the most frequent localization of scar tissue in the area of localization of the cardiac conduction pathways (posterior septal region).

Only 10-15% of patients with ischemic heart disease who died suddenly show macroscopic and/or histological signs of acute myocardial infarction, since the macroscopic formation of such signs requires at least 18-24 hours.

Electron microscopy shows the onset of irreversible changes in the cellular structures of the myocardium 20-30 minutes after the cessation of coronary blood flow. This process ends 2-3 hours after the onset of the disease, causing irreversible disturbances in myocardial metabolism, its electrical instability and fatal arrhythmias.

The triggering moments (trigger factors) are myocardial ischemia, disturbances in the innervation of the heart, disorders of myocardial metabolism, etc. Sudden cardiac death occurs as a result of electrical or metabolic disturbances in the myocardium,

As a rule, acute changes in the main branches of the coronary arteries are absent in most cases of sudden death.

Heart rhythm disturbances are most likely caused by the occurrence of relatively small foci of ischemia due to embolization of small vessels or the formation of small blood clots in them.

The onset of sudden cardiac death is most often accompanied by severe regional ischemia, left ventricular dysfunction and other transient pathogenetic conditions (acidosis, hypoxemia, metabolic disorders, etc.).

How does sudden cardiac death develop?

The immediate causes of sudden cardiac death are ventricular fibrillation (85% of all cases), pulseless ventricular tachycardia, pulseless electrical activity of the heart, and myocardial asystole.

The trigger mechanism of ventricular fibrillation in sudden coronary death is considered to be the resumption of blood circulation in the ischemic area of the myocardium after a long (at least 30-60 minutes) period of ischemia. This phenomenon is called the phenomenon of reperfusion of the ischemic myocardium.

There is a reliable pattern: the longer the myocardial ischemia, the more frequently ventricular fibrillation is recorded.

The arrhythmogenic effect of blood circulation restoration is caused by the washing out of biologically active substances (arrhythmogenic substances) from ischemic areas into the general bloodstream, leading to electrical instability of the myocardium. Such substances include lysophosphoglycerides, free fatty acids, cyclic adenosine monophosphate, catecholamines, free radical lipid peroxide compounds, etc.

Usually, in myocardial infarction, the reperfusion phenomenon is observed on the periphery in the peri-infarction zone. In sudden coronary death, the reperfusion zone affects larger areas of ischemic myocardium, and not only the border zone of ischemia.

Signs of sudden cardiac arrest

In approximately 25% of cases, sudden cardiac death occurs with lightning speed and without any visible precursors. In the remaining 75% of cases, a thorough questioning of relatives reveals the presence of prodromal symptoms 1-2 weeks before sudden death, indicating an exacerbation of the disease. Most often, these are shortness of breath, general weakness, a significant decrease in performance and tolerance of physical activity, palpitations and interruptions in the work of the heart, increased heart pain or pain syndrome of atypical localization, etc. Immediately before the onset of sudden cardiac death, approximately half of patients experience a painful angina attack, accompanied by fear of imminent death. If sudden cardiac death occurs outside the zone of constant observation without witnesses, then it is extremely difficult for the doctor to establish the exact time of circulatory arrest and the duration of clinical death.

How is sudden cardiac death recognized?

A detailed anamnesis and clinical examination are of great importance in identifying individuals at risk for sudden cardiac death.

History. Sudden cardiac death is highly likely to occur in patients with ischemic heart disease, especially those who have had a myocardial infarction, have post-infarction angina or episodes of painless myocardial ischemia, clinical signs of left ventricular failure and ventricular arrhythmias.

Instrumental methods of examination. Holter monitoring and long-term recording of electrocardiogram allow to detect threatening arrhythmias, episodes of myocardial ischemia, to evaluate variability of sinus rhythm and dispersion of QT interval. Detection of myocardial ischemia, threatening arrhythmias and tolerance to physical activity can be made by means of load tests: bicycle ergometry, treadmillmetry, etc. Electrical stimulation of atria by means of esophageal or endocardial electrodes and programmed stimulation of the right ventricle are successfully used.

Echocardiography allows to evaluate the contractile function of the left ventricle, the size of the heart cavities, the severity of left ventricular hypertrophy and to identify the presence of myocardial hypokinesis zones. Radioisotope myocardial scintigraphy and coronary angiography are used to identify coronary circulation disorders.

Signs of a very high risk of developing ventricular fibrillation:

• history of episodes of circulatory arrest or syncopal (associated with tachyarrhythmia) conditions;
• sudden cardiac death in family history;
• decreased left ventricular ejection fraction (less than 30-40%);
• tachycardia at rest;
• low sinus rhythm variability in individuals who have had a myocardial infarction;
• late ventricular potentials in patients who have had myocardial infarction.

How is sudden cardiac death prevented?

Prevention of sudden cardiac arrest in people at risk is based on the impact on the main risk factors:

• threatening arrhythmias;
• myocardial ischemia;
• decreased contractility of the left ventricle.

Medicinal methods of prevention

Cordarone is considered the drug of choice for the treatment and prevention of arrhythmias in patients with heart failure of various etiologies. Since there are a number of side effects with prolonged continuous use of this drug, it is preferable to prescribe it when there are clear indications, in particular, threatening arrhythmias.

Beta blockers

The high prophylactic effectiveness of these drugs is associated with their antianginal, antiarrhythmic and bradycardic action. Constant therapy with beta-blockers is generally accepted for all post-infarction patients who do not have contraindications to these drugs. Preference is given to cardioselective beta-blockers that do not have sympathomimetic activity. The use of beta-blockers can reduce the risk of sudden death not only in patients with ischemic heart disease, but also in hypertension.

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Calcium antagonists

Prophylactic treatment with the calcium antagonist verapamil in post-infarction patients without signs of heart failure may also help reduce mortality, including sudden arrhythmic death. This is explained by the antianginal, antiarrhythmic and bradycardic effects of the drug, similar to the effect of beta-blockers.

Angiotensin-converting enzyme inhibitors help correct left ventricular dysfunction, which reduces the risk of sudden death.

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Surgical treatment methods

If there are life-threatening arrhythmias that do not respond to prophylactic drug therapy, surgical treatment methods are indicated (implantation of pacemakers for bradyarrhythmias, defibrillators for tachyarrhythmias and recurrent ventricular fibrillation, intersection or catheter ablation of abnormal conduction pathways in premature ventricular excitation syndromes, destruction or removal of arrhythmogenic foci in the myocardium, stenting and aortocoronary bypass grafting for ischemic heart disease).

It is not possible to identify all potential victims of sudden death, despite the achievements of modern medicine. And it is not always possible to prevent circulatory arrest in patients with a known high risk of sudden cardiac arrest. In these cases, the most important method of combating fatal arrhythmias to save the patient's life is timely and competent resuscitation when sudden cardiac death has occurred.