Sudden cardiac death

Sudden cardiac death is a cardiac arrest, an acute hemodynamic syndrome caused by a complete cessation of the pump function of the myocardium, or a state where the remaining electrical and mechanical activity of the heart does not provide effective blood circulation.

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

Our attention should be paid to ensure that the effects of sudden cardiac arrest have a better prognosis due to early recognition of this pathology (in a matter of seconds) and immediately started competent resuscitation measures.

To a sudden cardiac death is attributed only to cases characterized by the following symptoms.

1. The 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 before the onset of death, the patient's condition was assessed as stable and did not cause serious concern.
3. Other causes (forcible death and death resulting from poisoning, asphyxia, trauma or other accident) are completely excluded.

According to ICD-10, there are:

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

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

• sudden cardiac death of a coronary nature - the stop of blood circulation is caused by exacerbation or acute progression of ischemic heart disease;
• sudden cardiac arrhythmic death - sudden cardiac arrest caused by impaired cardiac rhythm or conduction. The onset of such death occurs in a matter of minutes.

The main criterion for the diagnosis is the lethal outcome, which occurred within a few minutes in cases when autologous morphological changes were not found at the autopsy.

[1], [2], [3], [4], [5], [6], [7]

What causes sudden cardiac death?

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

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

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

• cardiomyopathies (primary and secondary);
• myocarditis;
• heart and vascular malformations;
• diseases that cause myocardial hypertrophy;
• alcoholic heart disease;
• prolapse of the mitral valve.

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

• syndromes of ventricular pre-excitation and an extended QT interval;
• arrhythmogenic dysplasia of the myocardium;
• Brugada syndrome, etc.

Other causes of sudden cardiac death include:

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

Risk factors for sudden cardiac arrest

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

The electrical instability of the myocardium is manifested by the development of "threatening arrhythmias": cardiac arrhythmias immediately preceding and transforming into ventricular fibrillation and asystole. Long-term electrocardiographic monitoring showed that ventricular fibrillation is most often preceded by paroxysms of ventricular tachycardia with a gradual increase in the rhythm, which translates into a flutter of the ventricles.

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

The highest probability of circulatory arrest in the first hours of acute myocardial infarction. Almost 50% of all deaths die in the first hour of the disease from sudden cardiac death. It should always be remembered: the less time has passed since the onset of myocardial infarction, the more likely the development of 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 significant reduction in the ejection fraction is up to 40% or less. The likelihood of developing an unfavorable outcome increases in patients with aneurysm of the heart, post-infarction scars and clinical manifestations of heart failure.

Violation of 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 a decrease in the variability of the sinus rhythm, an increase in the duration and dispersion of the QT interval.

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

Restoration of cardiac activity after ventricular fibrillation. In the high-risk group, the possibility of 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 ischemic heart disease

The most prognostically dangerous is fibrillation, occurring outside the acute period of myocardial infarction. With respect to the prognostic significance of ventricular fibrillation, which has arisen in acute myocardial infarction, opinions are contradictory.

Common Risk Factors

Sudden cardiac death is more common in people aged 45-75 years, and men experience sudden cardiac death 3 times more often than women. But the nosocomial lethality with myocardial infarction is higher in women than in men (4.89 vs. 2.54%).

The risk factors for sudden death are smoking, hypertension with myocardial hypertrophy, hypercholesterolemia and obesity. The long-term use of soft drinking water with insufficient magnesium content (predisposes to coronary artery spasms) and selenium (there is a disruption in the stability of cell membranes, mitochondrial membranes, disturbance of oxidative metabolism, and impairment of the functions of target cells).

Risk factors for sudden coronary death include meteorological and seasonal factors. The research data show that an increase in the rate of sudden coronary death occurs in the autumn and spring periods, different days of the week, with changes in atmospheric pressure and geomagnetic activity. The combination of several factors leads to an increase in the risk of sudden death by several times.

Sudden cardiac death in some cases can be triggered by inadequate physical or emotional stress, sexual intercourse, alcohol consumption, abundant food intake and Cold stimulus.

[8], [9], [10], [11], [12], [13], [14]

Genetically determined risk factors

Some risk factors are genetically determined, which is of special importance both for the patient himself, and for his children and close relatives. A high risk of sudden death at a young age is closely related to the syndrome of the extended QT interval, Brugada syndrome, sudden unexplained death syndrome, arrhythmogenic right ventricular dysplasia, idiopathic ventricular fibrillation, sudden infant death syndrome, and others pathological conditions.

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

• blockade of the right leg of the bundle;
• specific ST segment elevation in leads V1 -3;
• periodic elongation 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. When carrying out a sample with physical activity and a drug trial with sympathomimetics (isadrin), the electrocardiographic manifestations described above decrease. During the sample with slow intravenous antiarrhythmic drugs blocking the sodium current (aymalin at a dose of 1 mg / kg, novocaineamide 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:

• stenosing atherosclerosis of the coronary arteries;
• thrombosis of coronary arteries;
• hypertrophy of the heart with dilatation of the cavity of the left ventricle;
• myocardial infarction;
• contractural damage to cardiomyocytes (a combination of contractural lesions with fragmentation of muscle fibers serves as the histological criterion of ventricular fibrillation).

Morphological changes serve as substrata, 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), autopsy shows significant atherosclerotic changes in the coronary arteries (narrowing the lumen by more than 75%) and multiple lesions of the coronary bed ( at least two branches of the coronary arteries).

Atherosclerotic plaques located mainly in the proximal areas of the coronary arteries are often complicated, with signs of endothelial damage and the formation of near-wall or (comparatively rarely) completely occluding the lumen of the blood clot.

Thrombosis is relatively rare (in 5-24% of cases). It's natural that the longer the interval from the onset of a heart attack to the time of death, the more frequent thrombi occur.

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

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

Electron microscopy shows the onset of irreversible changes in myocardial cellular structures 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, electrical instability and fatal arrhythmias.

Trigger factors (trigger factors) are myocardial ischemia, cardiac innervation disorders, myocardial metabolism disorders, and the like. 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 in most cases of sudden death are absent.

Heart rate disorders are most likely due to the appearance of relatively small ischemic foci 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), ventricular tachycardia without pulse, electrical activity of the heart without pulse and myocardial asystole.

The trigger mechanism of ventricular fibrillation with sudden coronary death is the resumption of blood circulation in the ischemic area of the myocardium after a prolonged (not less than 30-60 minutes) ischemic period. This phenomenon was called the phenomenon of reperfusion of the ischemic myocardium.

The regularity is certain: the longer is myocardial ischemia, the more often ventricular fibrillation is recorded.

The arrhythmogenic effect of the resumption of blood circulation is caused by the washing out of the ischemic areas into the total bloodstream of biologically active substances (arrhythmogenic substances), leading to electrical instability of the myocardium. Such substances are lysophosphoglycerides, free fatty acids, cyclic adenosine monophosphate, catecholamines, free radical peroxide compounds of lipids and the like.

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

Harbinger of sudden cardiac arrest

Approximately 25% of cases of sudden cardiac death occur immediately and without visible precursors. In the remaining 75% of cases, a thorough questioning of relatives reveals the presence of prodromal symptoms 1-2 weeks before the onset of sudden death, which indicates an exacerbation of the disease. Most often it is shortness of breath, general weakness, a significant decrease in working capacity and tolerance of exercise, palpitations and irregularities in the work of the heart, increased pain in the heart or pain syndrome of atypical localization, etc. Immediately before the onset of sudden cardiac death, about half of the patients have a painful anginal attack accompanied by fear of a near death. If sudden cardiac death occurred outside the constant monitoring zone without witnesses, it is extremely difficult for the doctor to establish the exact time of cardiac arrest and the duration of clinical death.

How is sudden cardiac death recognized?

Great importance in identifying people threatened with sudden cardiac death, has a detailed history and clinical examination.

Anamnesis. With a high degree of probability sudden cardiac death threatens patients with coronary heart disease, especially those who underwent myocardial infarction, had postinfarction angina or episodes of painless myocardial ischemia, clinical signs of left ventricular failure and ventricular arrhythmias.

Instrumental methods of research. Holter monitoring and long-term recording of the electrocardiogram can reveal threatening arrhythmias, episodes of myocardial ischemia, assess sinus rhythm variability and QT interval variance. The detection of myocardial ischemia, threatening arrhythmias and exercise tolerance can be done by stress tests: veloergometry, treadmill, etc. Successfully used electrostimulation of the atria with the help of esophageal or endocardial electrodes and programmed stimulation of the right ventricle.

Echocardiography makes it possible 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. To detect coronary circulation disorders, radioisotope scintigraphy of the myocardium and coronary angiography are used.

Signs of a very high risk of developing ventricular fibrillation:

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

How is sudden cardiac death prevented?

Prevention of sudden cardiac arrest in people of threatening categories is based on the impact on major risk factors:

• threatening arrhythmia;
• myocardial ischemia;
• decreased left ventricular contractility.

Medication methods of prevention

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

Beta-blockers

The high prophylactic efficacy of these drugs is associated with their antianginal, antiarrhythmic and bradycardic effects. The constant therapy with beta-blockers of all postinfarction patients without contraindications to these drugs is common. 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 coronary heart disease, but also with hypertension.

[15], [16], [17], [18]

Calcium antagonists

Preventive treatment with calcium antagonist verapamil postinfarction patients without signs of heart failure may also contribute to a reduction in mortality, including sudden arrhythmic death. This is due to antianginal, antiarrhythmic and bradycardic effect of the drug, similar to the effect of beta-blockers.

Angiotensin converting enzyme inhibitors can correct left ventricular dysfunction, which leads to a reduction in the risk of sudden death.

[19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29]

Surgical methods of treatment

If there are life-threatening arrhythmias that are not amenable to preventive drug therapy, surgical methods of treatment are indicated (implantation of pacemakers with bradyarrhythmias, defibrillators for tachyarrhythmias and recurrent fibrillation of the ventricles, intersection or catheter ablation of abnormal pathways in premature ventricular syndrome, destruction or removal of arrhythmogenic foci in the myocardium , stenting and coronary artery bypass grafting in 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 the arrest of blood circulation in patients with a known high risk of sudden cardiac arrest. In these cases, the most important method to combat fatal arrhythmias to save the patient's life is the timely and competent resuscitation, when sudden cardiac death occurred.