Why ischemic heart disease occurs and how to treat it

What leads to the onset of ischemic heart disease

Ischemic heart disease (CHD) develops as a result of the action of mechanisms that lead to impaired blood circulation in the coronary vessels and oxygen starvation of the myocardium.

1. With atherosclerosis, blood cannot flow to the heart in sufficient quantities due to the fact that a fatty plaque narrows the lumen. For this reason, it becomes impossible to satisfy the oxygen demand of cardiomyocytes. As a result, a painful attack (angina pectoris) develops against a background of stress or physical exertion.
2. Thromboembolism. The formation of a blood clot is triggered by the breakdown of the cholesterol plaque. Sometimes a blood clot forms in the heart cavity, then breaks off and clogs the lumen of the artery. With endocarditis, a piece of valve tissue may act as a "plug".
3. Vascular spasm. A sharp contraction of smooth muscle fibers in the coronary artery system is provoked by a rapid transition from a horizontal to a vertical position. This phenomenon is observed when inhaling cold air, severe hypothermia of the whole body, stress, the use of certain drugs.

In addition to the main reasons, provoking factors also play a role in the appearance of acute or chronic myocardial ischemia:

• improper diet with an excess of fatty foods rich in cholesterol;
• obesity and metabolic disorders (including lipid);
• Sedentary lifestyle;
• endocarditis and heart defects;
• age after 45 in men and in women over 55;
• the presence of vascular diseases;
• diabetes;
• hypertension;
• constant stress, which is accompanied by increased blood pressure and increased heart rate;
• alcohol and smoking.

High cholesterol levels in violation of metabolic processes and a tendency to form blood clots are inherited. Therefore, the likelihood of coronary artery disease is higher in those people whose relatives had a history of heart attack at the age of 45-65 years, or died as a result of coronary insufficiency.

Classification

When establishing a diagnosis of coronary heart disease, my colleagues still use the classification that was adopted back in the 80s of the last century.

• Sudden cardiac death. Refers to all deaths within the first 60 minutes after the onset of an attack, preceded by loss of consciousness, acute symptoms of ischemia, and cardiac arrest.
• Angina pectoris.
  • Voltage. It occurs as a result of physical or psycho-emotional stress.
    • First appeared.
    • Stable.

1. The first class appears only during pronounced overloads and never occurs during normal work;
2. The second is placed for those who cannot walk quickly 500 or more meters without pain, as well as climb to the 6th floor and higher;
3. The third class characterizes the development of an attack with insignificant stress (it is conventionally assumed that when walking up to 100 meters and climbing the first flight);
4. The fourth class corresponds to the appearance of chest pain under the condition of complete rest, while a person cannot make any movement without developing acute cardiac ischemia with its characteristic signs.

• • Progressive (unstable). With this form, the condition worsens and the effectiveness of treatment decreases while maintaining a normal lifestyle.
• Spontaneous (Prinzmetal). A special form of ischemia, in which vasospasm occurs, causing pain. External reasons do not play a role in this. The course is difficult, poorly stopped by nitroglycerin.
• Painless ischemia. It was added to the general list much later. Revealed by chance after ECG and stress tests.
• Myocardial infarction.
  • Large focal (transmural) with a Q wave. It leaks with a large area and (or) all layers of the myocardium. Well defined by ECG.
  • Small focal, without Q wave. Myocardial ischemia and necrosis affect small areas and do not always appear on the cardiogram.

• Postinfarction cardiosclerosis.
• Heart failure.
• Heart rhythm disorders.

How and why pain syndrome occurs in coronary artery disease

The pathogenesis of the onset of pain during an attack is well understood. A decrease in blood flow or an increase in oxygen demand leads to the development of ischemia. An enhanced release of active substances (mediators) that irritate pain receptors (histamine, bradykinin) begins in the focus. From the affected area, signals begin to flow along the nerve fibers. First, they pass into the cervical and thoracic plexuses, localized in the spine. From there, impulses go through the thalamus to the cerebral cortex, and a sensation of pain is already formed there.

The severity of the pain symptom in IHD depends not only on the degree of damage. That is why there are "mute" and atypical forms of angina pectoris and even heart attack.

Symptoms

In my practice, I constantly come across the fact that patients with coronary artery disease do not seek help immediately. This is because the first symptoms of coronary artery disease build up gradually.

Pain

The most common complaint of a patient with angina pectoris or heart attack is pain in the chest region - in most cases it is accompanied by a feeling of fear and panic. Irradiation is usually observed under the scapula, in the arm, and part of the lower jaw on the virgin side. Some complain of numbness of the upper limb, aches in the wrist joint. With a lack of oxygen in the posterior basal region of the heart, soreness spreads to the stomach area. And very rarely it is noted in the right hand.

When I ask to describe the type of pain, the person indicates that it is:

• baking;
• oppressive;
• compressive.

The appearance of pain syndrome is associated with physical exertion - when a person ran, walked quickly, or climbed stairs. Sometimes an attack was observed after stress, strong emotional stress, going outside in cold weather. A sharp flow of blood to the heart is also noted when standing up from a prone position. All these factors lead to an increase in pressure, an increase in heart rate and an increase in myocardial oxygen demand.

Pain with angina pectoris is short-term and does not last more than 5-15 minutes. As soon as a person stops, sits down, calms down, it subsides, as the causes of acute ischemia are eliminated. Experienced patients always carry nitroglycerin with them, which quickly relieves symptoms. If the intensity of the discomfort does not subside after taking the drug, then this most often indicates non-cardiac pathology, or indicates the development of a heart attack.

With vasospastic or spontaneous angina pectoris, pain and other signs of myocardial ischemia develop without connection with physical activity, it is noted in the morning, often provoked by exposure to cold. Well removed only by calcium antagonists.

Other common manifestations

Other signs of coronary heart disease do not always appear; in some patients during an attack, I observed the following symptoms:

• nausea, vomiting;
• severe fatigue;
• severe shortness of breath with difficulty breathing;
• sweating;
• pallor of the skin;
• increase or decrease in blood pressure;
• increased heart rate (less often decrease), arrhythmia.

In some cases, instead of a classic attack indicating the presence of coronary heart disease, one can see its equivalents: shortness of breath, fatigue after minimal exertion.

Diagnostics

Diagnosis of coronary heart disease includes laboratory and instrumental techniques.

Analyzes

Biochemical methods for detecting a number of enzymes in the blood help in determining the acute phase of a heart attack, since they are released as a result of the destruction of cardiomyocytes. The first day after the attack, when there is acute myocardial ischemia and necrosis, an increase in LDH and myoglobin occurs. An increase in CPK occurs in the first 8 hours from the beginning, troponins are detected after 1-2 weeks

Cardiogram

Without fail, an admitted patient with complaints and signs of a heart attack, I send for an urgent cardiogram. It allows you to detect the presence of an increase in the left ventricle, rhythm disturbances and the severity of the lesion in a specific area of ​​the heart.

Signs of acute ischemia in the myocardium on the ECG are as follows:

1. The appearance of a high and sharp T wave. Although I observed an ECG in tall asthenic people, in whom such signs are a variant of the norm. Subendocardial ischemia of the anterior wall of the heart can be characterized by negative T, and a biphasic wave appears at the border of the affected area and the normal part of the myocardium.
2. Another typical sign of acute ischemia is ST segment displacement more than 0.5 mm from the isoline. Its rise in the chest leads indicates damage to the left ventricle, and depression in the same areas indicates a violation of the blood flow of the posterior wall.
3. Necrosis during the development of a heart attack manifests itself in the form of the appearance of a pathological Q wave or a whole QRS complex in the corresponding leads.

For more details and about changes in the film in patients with ischemia, we talked in the article at the link here.

Other methods

In order to determine IHD, the following methods are also widely used:

1. Load tests. They are recommended at the initial stage of ischemia, help to determine the disease in case of atypical manifestation and implicit abnormalities on the electrocardiogram. The principle is to artificially create an increased myocardial oxygen demand and fix the changes. For this, veloergometry, transesophageal pacing and pharmacological tests with the drugs "Isoprotenol", "Dipyridamol" are most often used. In the presence of a violation of the passage of blood through the arteries of the heart, myocardial ischemia is recorded on the ECG.
2. Coronary angiography. Refers to the most informative methods for detecting coronary pathology. It allows you to conduct research without provoking or waiting for an attack. A contrast agent is injected into the right and left arteries of the heart, and a full picture of the state of the vascular bed is obtained on the angiograph.
3. EchoCG. In this case, it is an auxiliary diagnostic method. Allows to assess the local and global contractility of the myocardium, shows the usefulness of the heart in systole and diastole, to determine the presence of complications in coronary artery disease.

Treatment

Coronary heart disease treatment begins with lifestyle adjustments and dietary prescriptions. I have repeatedly encountered the fact that patients did not take this important part of therapy seriously enough, and then wondered why it took so long to improve their condition.

Lifestyle correction

So, before you go to the pharmacy for medicines, you need to remember two important things:

• Sparing regime. Elimination of physical activity leading to increased oxygen consumption by the myocardium.
• A diet that excludes animal fats, foods high in salt and easily digestible carbohydrates. If you are overweight, you should reduce the total calorie content of food.

Medicines

Of course, one correction of nutrition and lifestyle will not be enough, therefore, it is necessary to support the body with medication.

1. Disaggregants to prevent blood clots. I usually recommend Aspirin or Clopidogrel (Plavix).
2. Beta-blockers ("Nebivalol", "Bisoprolol"). Numerous and long-term studies prove an increase in the life expectancy of patients with coronary artery disease who constantly use this group of drugs.
3. Statins, they help to equalize the level of "bad" cholesterol. If you treat coronary heart disease with their help, then the patient's life is significantly extended. For a quick and strong reduction, Rosuvastatin is used, and in patients with diabetes mellitus and high triglycerides, it is better to take Atorvastatin.
4. For the relief of an acute attack, "Nitroglycerin" is used sublingually, or "Isosorbide mononitrate" for internal use. Expanding the venous bed, drugs of this series reduce the preload on the heart and quickly relieve an attack of angina pectoris.
5. Diuretics reduce the volume of the vascular bed and thereby facilitate the work of the heart. For quick removal of edema, "Furosemide" is used. For the purpose of continuous use, I recommend Indapamide or Torasemide.