Coronary heart disease: symptoms

According to the modern classification of coronary heart disease, there are two main types of myocardial infarction: myocardial infarction with a Q wave (synonyms: large-focal, transmural) and myocardial infarction without a Q wave (synonyms: small-focal, non-transmural, subendocardial, intramural). The diagnosis of myocardial infarction with a Q wave is established based on the registration of characteristic ECG changes over time and, above all, the appearance of a pathological Q wave, and for the diagnosis of myocardial infarction without a Q wave, it is necessary to register an increase in the activity of cardiac-specific isoenzymes and troponins, since ECG changes in infarction without a Q wave are nonspecific.

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Post-infarction cardiosclerosis

The diagnosis of post-infarction cardiosclerosis is established 2 months after the onset of myocardial infarction. Much more reliable is the diagnosis of post-infarction cardiosclerosis after myocardial infarction with a Q wave. The diagnosis of post-infarction cardiosclerosis after a non-Q wave infarction is often questionable, since in practical healthcare it is not always possible to verify the diagnosis of non-Q wave myocardial infarction.

Sudden coronary death

Sudden death is considered to be cases of death within one hour after the onset of the first symptoms in a patient who was previously in a stable condition. Approximately 60% of all deaths in ischemic heart disease are sudden. Moreover, in approximately 20% of patients, sudden death is the first manifestation of ischemic heart disease. The immediate cause of sudden death in the vast majority of cases is ventricular fibrillation due to myocardial ischemia. Ventricular tachycardia usually occurs first, which quickly turns into fibrillation.

In its external manifestations, death can be sudden in any cardiovascular and many extracardiac diseases (the "sudden death" syndrome), but in about 80% of those who die suddenly, coronary heart disease is detected, including postinfarction cardiosclerosis in 70% of them. Myocarditis, cardiomyopathy, heart defects, pulmonary embolism, Wolff-Parkinson-White syndrome, and QT prolongation syndrome on ECG are diagnosed in about 20%. In 4-10% of those who die suddenly, no cardiovascular disease can be detected (sudden death without a morphological substrate - "unexplained cardiac arrest").

Heart rhythm disturbances in coronary heart disease

Heart rhythm disturbances often complicate the course of other clinical forms of coronary heart disease. In many cases, it remains unclear whether the arrhythmia is a consequence of coronary heart disease or simply an accompanying disorder. The cause-and-effect relationship is obvious only in cases of arrhythmia occurring during episodes of ischemia or after myocardial infarction.

Although rhythm disturbances may be the only clinical manifestation of coronary heart disease (i.e. in patients without a history of angina pectoris or myocardial infarction), the diagnosis of coronary heart disease always remains only presumptive, requiring clarification using instrumental research methods.

There are 2 possible types of rhythm disturbances as the only clinical manifestation of coronary heart disease:

1. Episodes of painless myocardial ischemia cause the occurrence of arrhythmias.
2. Myocardial damage due to silent ischemia leads to the formation of an arrhythmogenic substrate, electrical instability of the myocardium and the occurrence of arrhythmias even in the intervals between episodes of painless ischemia.

A combination of these two options is possible. In any case, if arrhythmia is the only clinical manifestation of coronary heart disease, the cause is painless myocardial ischemia.

Arrhythmias are not a symptom of coronary heart disease in patients without other signs of myocardial ischemia and, as the only manifestation, are found in coronary heart disease no more often than in healthy individuals. Therefore, such a diagnosis formulation as "CHD: atherosclerotic cardiosclerosis" and then the name of any rhythm disorder is illiterate, since there are no clinical criteria for atherosclerotic cardiosclerosis, and signs of myocardial ischemia are not indicated. It is also unacceptable to indicate the name of the arrhythmia immediately after the abbreviation CHD. In the diagnosis of CHD, it is necessary to indicate signs of ischemia or ischemic damage to the myocardium: angina pectoris, infarction, post-infarction cardiosclerosis or painless ischemia. Examples of the formulation of the diagnosis of arrhythmia in patients with CHD: "CHD: post-infarction cardiosclerosis, paroxysmal ventricular tachycardia"; "IHD: angina pectoris, FC-II, frequent ventricular extrasystoles."

It should be noted that atrial fibrillation is very rarely a consequence of coronary heart disease. For example, only 2.2-5% of patients with a permanent form of atrial fibrillation had coronary artery disease detected during coronary angiography. Of 18 thousand patients with coronary heart disease, only 0.6% had atrial fibrillation. Most often, the occurrence of atrial fibrillation is associated with left ventricular dysfunction and heart failure or with concomitant arterial hypertension.

Heart failure

Like arrhythmia, heart failure is usually a complication of various clinical forms of coronary heart disease, especially myocardial infarction and postinfarction cardiosclerosis, and not the only manifestation of coronary heart disease. Often, such patients have left ventricular aneurysm, chronic or transient mitral insufficiency due to dysfunction of the papillary muscles.

Cases of acute left ventricular failure during episodes of silent myocardial ischemia or chronic circulatory failure due to myocardial damage during silent ischemia are possible.

The most common cause of acute heart failure is myocardial infarction. Chronic heart failure is usually observed in patients with post-infarction cardiosclerosis, especially in the presence of a left ventricular aneurysm. In most cases, aneurysm formation occurs during a myocardial infarction.

Most often (approximately 80%), aneurysms form in the area of the anterolateral wall and apex. Only 5-10% of patients have aneurysms in the area of the posteroinferior wall, and in 50% of cases, aneurysms of the posteroinferior wall are false ("pseudoaneurysm" - a localized "healed" rupture of the myocardium with hemorrhage into the subepicardial layers). True aneurysms almost never rupture (only in the first 1-2 weeks of myocardial infarction, and even then very rarely), and the patient should be told about this, since many are afraid of an aneurysm rupture (but the risk of rupture of a false aneurysm is very high, so after the diagnosis of a false aneurysm, urgent surgery is necessary).

Signs of a true left ventricular aneurysm are paradoxical pulsation inwards from the apical impulse in the region of the III-IV intercostal spaces and a frozen ST segment elevation on the ECG in leads with a pathological Q wave. The best method for detecting aneurysm is echocardiography.

Complications of left ventricular aneurysm:

1. heart failure,
2. angina pectoris,
3. ventricular tachyarrhythmias,
4. formation of a thrombus in the left ventricle and thromboembolism.

A thrombus in the left ventricle is detected by echocardiography in approximately 50% of patients with aneurysm, but thromboembolism is observed relatively rarely (in approximately 5% of patients), mainly in the first 4-6 months after myocardial infarction.

In addition to post-infarction cardiosclerosis, including the formation of a left ventricular aneurysm, several other conditions may be the cause of heart failure in patients with coronary heart disease:

"Stunned" myocardium is a transient, prolonged post-ischemic myocardial dysfunction that persists after restoration of coronary blood flow (from several hours to several weeks after an episode of acute ischemia).

Constant severe myocardial dysfunction due to frequent repeated episodes of ischemia or chronic reduction of coronary blood flow - the so-called "sleeping" or "inactive" myocardium ("hibernated" myocardium). In this case, coronary blood flow is reduced and only maintains tissue viability (reversible myocardial changes). It is possible that this is a protective mechanism - maintaining myocardial viability at the cost of a sharp decrease in contractility. Myocardial scintigraphy with Thallium-201 shows the entry of Thallium into areas of reversible myocardial dysfunction (in contrast to scar tissue), myocardial viability is also detected using positron emission tomography, and ventriculography may show an improvement in regional contractility against the background of dobutamine infusion. Such patients show improvement after revascularization: aortocoronary bypass or coronary angioplasty. Interestingly, patients with “sleeping” myocardium may not show any changes on the ECG.

"Ischemic cardiomyopathy" ("last stage of ischemic heart disease"). A very common lesion of the coronary arteries, repeated episodes of myocardial ischemia, including with post-ischemic "stunning", can cause myocardial necrosis with subsequent scarring. With diffuse coronary artery disease, slowly progressing diffuse myocardial damage occurs, up to the development of a condition almost indistinguishable from dilated cardiomyopathy. The prognosis is very poor, often even worse than with dilated cardiomyopathy. Treatment, including coronary artery bypass grafting, is ineffective or ineffective, since there is almost no viable myocardium.

Some patients experience repeated episodes of acute left ventricular failure (cardiac asthma, pulmonary edema) caused by transient papillary muscle ischemia, with the development of papillary muscle dysfunction and acute mitral regurgitation, or due to impaired diastolic relaxation of the myocardium during episodes of ischemia.

Of interest are reports of some protective effect of repeated episodes of ischemia. This phenomenon is called ischemic "preconditioning" - after an episode of ischemia, the resistance of the myocardium to subsequent occlusion of the coronary artery increases, i.e., the myocardium is trained or adapted to repeated exposure to ischemia. For example, with repeated inflation of the balloon during coronary angioplasty, the height of the ST segment elevation decreases each time during occlusion of the coronary artery.