Ischemic heart disease: symptoms

In accordance with the modern classification of IHD, there are two main variants of myocardial infarction: myocardial infarction with Q-wave (synonyms: large-focal, transmural) and myocardial infarction without Q wave (synonyms: fine-focal, nontransmural, subendocardial, intramural). Diagnosis of myocardial infarction with Q tooth is established on the basis of recording characteristic ECG changes in dynamics and, above all, the appearance of abnormal Q wave, and for the diagnosis of myocardial infarction without Q wave, registration of an increase in activity of cardiospecific isozymes and troponins is necessary, since ECG changes in infarction without a Q wave are not specific.

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Postinfarction cardiosclerosis

The diagnosis of postinfarction cardiosclerosis is established 2 months after the onset of myocardial infarction. Much more reliable is the diagnosis of postinfarction cardiosclerosis after myocardial infarction with a Q wave. Diagnosis of postinfarction cardiosclerosis after a heart attack without a Q wave is often questionable, since in practice, it is not always possible to verify the diagnosis of myocardial infarction without a Q wave.

Sudden coronary death

Sudden death is usually considered to be death within one hour after the onset of the first symptoms in a patient who is in a stable state before. Approximately 60% of all deaths in IHD are sudden. Moreover, about 20% of patients sudden death is the first manifestation of CHD. The immediate cause of sudden death in the vast majority of cases is ventricular fibrillation due to myocardial ischemia. Usually, at first, a ventricular tachycardia occurs, which quickly becomes fibrillation.

According to its external manifestations, death can be sudden in any cardiovascular and many extracardiac diseases (sudden death syndrome), but approximately 80% of sudden deaths are diagnosed with coronary artery disease, including 70% of them postinfarction cardiosclerosis. Approximately 20% are diagnosed with myocarditis, cardiomyopathies, heart defects, pulmonary artery pulmonary embolism, Wolff-Parkinson-White syndrome, QT interval prolongation on the ECG. In 4-10% of sudden death, it is not possible to detect any disease of the cardiovascular system (sudden death without a morphological substrate - "unexplained heart failure").

Heart rhythm disorders in IHD

Heart rhythm disturbances often complicate the course of other clinical forms of IHD. In many cases, it remains unclear whether the arrhythmia is due to coronary artery disease or simply a concomitant disorder. Causal relationship is evident only in cases of arrhythmias during episodes of ischemia or after myocardial infarction.

Although rhythm disturbances may be the only clinical manifestation of IHD (i.e., in patients without angina and myocardial infarction in the anamnesis), the diagnosis of CHD always remains only a presumptive, requiring clarification with the help of instrumental research methods.

You can imagine 2 variants of rhythm disturbances, as the only clinical manifestation of IHD:

1. Episodes of painless myocardial ischemia cause the occurrence of arrhythmias.
2. Myocardial damage due to painless ischemia leads to the formation of an arrhythmogenic substrate, electrical instability of the myocardium and 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 IHD, the cause is painless myocardial ischemia.

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

It should be noted, atrial fibrillation is very rarely a consequence of CHD. So, for example, only 2.2-5% of patients with a constant form of atrial fibrillation in coronary angiography revealed a lesion of the coronary arteries. Out of 18 thousand patients with coronary heart disease - only 0.6% of patients 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

Also, like arrhythmias, heart failure is usually a complication of various clinical forms of IHD, especially myocardial infarction and postinfarction cardiosclerosis, and not the only manifestation of IHD. Often such patients have an aneurysm of the left ventricle, a chronic or transient mitral insufficiency due to dysfunction of the papillary muscles.

There are cases of acute left ventricular failure during episodes of painless myocardial ischemia or chronic circulatory failure due to myocardial damage in painless ischemia.

The cause of acute heart failure is most often a myocardial infarction. Chronic heart failure is usually noted in patients with postinfarction cardiosclerosis, especially in the presence of an aneurysm of the left ventricle. The formation of an aneurysm in most cases occurs during myocardial infarction.

Most often (approximately 80%), an aneurysm is formed in the anterior-lateral wall and apex. Only 5-10% of the patients have aneurysms in the posterior-inferior wall area, and the posterior-inferior aneurysms in 50% of cases are false ("pseudoaneurysm" - localized "healed" myocardial rupture with hemorrhage into the subepicardial layers). True aneurysms are almost never ruptured (only in the first 1-2 weeks of a myocardial infarction, and that is very rare), and this should be told to the patient, since many are afraid of aneurysm rupture (but the threat of rupture of a false aneurysm is very high, therefore after the diagnosis of a false aneurysm, urgent surgery is necessary).

Signs of a true aneurysm of the left ventricle are a paradoxical ripple inside the apical impulse in the region of III-IV intercostal space and the frozen rise of the ST segment on the ECG in leads with a pathological Q-wave. The best method for detecting an aneurysm is echocardiography.

Complication of an aneurysm of the left ventricle:

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 in echocardiography in approximately 50% of patients with an aneurysm, but thromboembolism is relatively rare (in about 5% of patients), mainly in the first 4-6 months after myocardial infarction.

In addition to postinfarction cardiosclerosis, including the formation of an aneurysm of the left ventricle, the cause of heart failure in patients with IHD may be several more conditions:

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

Constant expressed 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 changes in the myocardium). It is possible that this is a protective mechanism - the preservation of the viability of the myocardium at the cost of a sharp decrease in contractility. In myocardial scintigraphy with Thallium-201, Thallium is admitted to the sites of reversible myocardial dysfunction (in contrast to scar tissue), the viability of the myocardium is also revealed with the help of positron emission tomography, and in the course of ventriculography there can be an improvement in regional contractility against dobutamine infusion. In such patients, there is an improvement after revascularization: aorto-coronary bypass or coronaroangioplasty. It is interesting that in patients with a "sleeping" myocardium there may be no changes on the ECG.

"Ischemic cardiomyopathy" ("the last stage of IHD"). A very common lesion of the coronary arteries, repeated episodes of myocardial ischemia, including postischemic "stunnedness", can cause necrosis of the myocardium with subsequent scarring. With diffuse lesions of the coronary arteries, slowly progressive diffuse damage to the myocardium 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 and aortocoronary shunting, is ineffective or ineffective, since there is almost no viable myocardium.

In some patients, repeated episodes of acute left ventricular failure (cardiac asthma, pulmonary edema) caused by transient ischemia of the papillary muscles, with the emergence of papillary muscle dysfunction and acute mitral insufficiency, or as a result of diastolic myocardial relaxation during episodes of ischemia.

There are interesting reports of the presence of some protective effect of repeated episodes of ischemia. This phenomenon was called ischemic "prikondishen" - after an episode of ischemia, the resistance of the myocardium to the subsequent occlusion of the coronary artery increases, i.е. There is a training or adaptation of the myocardium to repeated effects of ischemia. For example, when the balloon is repeatedly inflated during coronaroangioplasty, the height of the ST segment is decreased each time during coronary artery occlusion.