Ischemic heart disease symptoms

Ischemic heart disease is one of the leading causes of death in the population of industrialized countries, is the narrowing of the coronary arteries that supply blood to the heart muscle. Physical activity increases the body's need for oxygen, and the heart responds by pumping blood more vigorously, which in turn increases the heart muscle's oxygen needs.

In coronary artery disease, narrowed arteries restrict the supply of blood to the heart muscle. If the constriction is not very large, difficulties can occur only with physical exertion, when the narrowed arteries are unable to meet the increased needs of the heart in oxygen. However, when the disease worsens, the narrowed arteries can limit the supply of oxygen to the heart muscle during normal activities or even at rest.

Coronary heart disease mainly occurs as a result of the accumulation of cholesterol plaques in the walls of the arteries;this process is called atherosclerosis. Cholesterol plaques consist of cholesterol-rich fatty deposits, collagens, other proteins and excess smooth muscle cells. Atherosclerosis, which usually develops very slowly throughout life, leads to thickening and narrowing of the walls of the arteries, preventing the flow of blood. Blood clots are formed more easily in the walls of arteries, which coarsen as a result of the deposition of cholesterol plaques. Clots can block the narrowed coronary artery completely and cause a heart attack. Arteries can also contract suddenly as a result of an arterial spasm.(Spasm most often occurs with smoking.)

Symptoms of coronary heart disease usually appear unexpectedly. In the early stages of the disease, there are no symptoms. As the disease develops during periods of physical activity or emotional stress, chest pain( angina pectoris) may occur, since narrowed arteries can not supply the heart with the increased amount of blood and oxygen needed during this period. Angina usually passes quickly during rest, but after a while the symptoms occur with less stress and, ultimately, the disease can lead to a heart attack. However, in one third of cases of coronary heart disease, angina never develops, and a heart attack can occur suddenly.

Clinical classification of IHD( VKNCs AMN USSR, 1984)

1. Sudden cardiac death( primary cardiac arrest).

2. Angina pectoris.

2.1.Stenocardia of the tension:

2.1.1.For the first time arisen angina.

2.1.2.Stable angina( indicating the functional class from I to IV).

2.1.3.Progressing angina( unstable).

2.2.Spontaneous( special, variant, vasospastic) angina.

3. Myocardial infarction.

3.1.Large-focal( transmural).

3.2.Small-focal.

4. Postinfarction cardiosclerosis.

5. Heart failure( indicating the form and stage).

6. Heart rhythm disturbances( indicating the form).

Working Classification of IHD

1. Sudden cardiac death( primary cardiac arrest).

2. Angina pectoris.

2.1.Stable exertional angina( indicating the functional class from I to IV).

2.2.Unstable angina:

2.2.1.For the first time arisen angina( air force). *

2.2.2.Progressing angina( PS).

2.2.3.Early postinfarction or postoperative angina.

2.3.Spontaneous( vasospastic, variant, Prinzmetal) angina pectoris.

3. Pain-free ischemia of the myocardium.

4. Mikrovascular angina pectoris( "syndrome X")

5. Myocardial infarction

5.1 Myocardial infarction with Q-wave( large focal, transmural)

5.2 Myocardial infarction without Q-wave( fine-focal)

6. Postinfarction cardiosclerosis.

7. Heart failure( indicating the form and stage)

8. Cardiac rhythm and conduction abnormalities( indicating the form)

Symptoms of

• No symptoms in the early stages of coronary heart disease

• Pain in the chest( angina) or a slight feeling of pressure, burning or heaviness can last for 30 seconds to five minutes. Pain( or discomfort) is usually felt in the center of the chest, directly under the breastbone, and can give in the arm( usually in the left), in the neck or in the jaw. Pain mainly occurs during physical exertion or stress and weakens when resting. The magnitude of the load that can cause angina may be determined in advance.

• Shortness of breath, dizziness or a feeling of suffocation, accompanied by pain in the chest.

• Sudden intensification of angina or its appearance at rest is a symptom of unstable angina that requires immediate treatment, as a heart attack can occur very quickly.

Although coronary heart disease can be life threatening, the outcome of the disease largely depends on the patient himself. Damage to the arteries can be slowed down or stopped as a result of lifestyle changes, including stopping smoking, changing eating habits and regular exercise, or by using medications to lower blood pressure and cholesterol levels in the blood. The goal of treatment, which may include the use of drugs and sometimes an operation, is to remove symptoms, improve blood circulation and prolong the life of the patient.

Causes of

• Cholesterol is promoted by the growth of cholesterol plaques in the arteries. By increasing the level of carbon monoxide in the blood and reducing the amount of oxygen available to the heart, smoking increases the risk of angina pectoris.

• High cholesterol levels in the blood cause ischemic heart disease. Lipoprotein penetrates the walls of the artery, where, as a result of a chemical reaction, it is part of cholesterol and can be part of cholesterol plaques.

• High blood pressure contributes to a person's predisposition to coronary heart disease.

• People with diabetes are at greater risk of developing atherosclerosis.

• Obesity can contribute to the development of atherosclerosis.

• Lack of physical activity( sedentary lifestyle) can contribute to the development of atherosclerosis.

• Men are at greater risk of developing coronary heart disease than women, with the exception of women in the postmenopausal period, when estrogen production is declining.

• Women aged 35 years who take oral contraceptives and smoke, are at a higher risk of developing atherosclerosis.

• The presence of heart attacks at an early age in family members is associated with an increased risk of coronary heart disease.

• Spasm of muscles in the walls of the artery can lead to its contraction and the appearance of angina pectoris. Spasms can be caused by smoking, severe emotional stress, or being in the cold.

Until recently, it was believed that the basis of IHD is solely environmental factors, but over the past 25 years, data have been obtained that such risk factors for IHD, as a high concentration of cholesterol in the blood serum and hypertension, are largely genetically determined. Risk factors for IHD also include high concentrations of fibrinogen, homocysteine, LP( a), apo-E, increased activity of ACE I, which usually reflect mutations in genes responsible for their synthesis or regulation of metabolism in the body.

The multifactorial nature of ischemic heart disease is not in doubt at this time. The study of the structure of the hereditary predisposition to ischemic heart disease is aimed at finding specific genetic factors that potentially predetermine the risk and onset of the disease. Important for understanding the genetics of IHD as a multifactorial disease the following provisions: a physiological sign in its qualitative or quantitative expression is genetically determined;the effect of

of polygenia is significant( hereditary predisposition to CHD is caused by the effects of many genes), and on the general polygenic background only a few potentially identifiable "main genes" can play a major role, as well as a fundamental property of the genome, like the polymorphism of its loci.

Among the many genetically determined risk factors for coronary artery disease, the following are of primary importance.

• Concentrations in the serum of total cholesterol, LDL, apo-B.
• Serum concentrations of HDL-C, apo-A.
• Concentration in the blood serum of LP( a)).
• Concentrations in serum of TG and VLDL.
• Receptor activity of LDL.
• Concentration in plasma of fibrinogen.
• Concentrations in the serum of estradiol.
• Heterozygosity for homocystinuria.
• ACE activity.

Numerous studies on the problem of atherosclerosis and coronary artery disease confirm the fact that an increase in the concentration of cholesterol in the blood is one of the main risk factors for the development of these diseases. The development of HLP can be caused by genetic defects and environmental factors( primary GLP), as well as by diseases such as diabetes mellitus, liver pathology, kidneys, hormonal disorders( secondary GLP).In the emergence of primary GLP, the main role is played by hereditary predisposition. Many hereditary anomalies of lipoprotein exchange have been studied, for which the development of IHD is characteristic, but only for certain precise genetic defects are known, which allow diagnosing the disease.

More than a dozen different polymorphic sites have been described in the apo-B gene( * 107730, 2p24-p23, APOB gene, ED) or in adjacent regions of the gene. The functional significance of most of them is not clear, nevertheless in a number of works some associative relationship between lipid levels and apo-B in serum and DNA variants in the apo-B gene was found. The study of the polymorphism of the apo-B gene for the EcoRI, MspI, PvuII and XbaI restrictionases showed that the EcoRI and MspI polymorphism of restriction fragment lengths exhibits a pronounced association with premature coronary atherosclerosis. The allele RI is due to the replacement of G-A at position 4154 in exon 29, leading to the replacement of Glu-Lys in the apo-B T2 peptide. The MspI polymorphism of the length of the restriction fragments of the apo-B gene is determined by insertions or deletions in the hypervariable 3-terminal region, and in exon 26 of the apo-B gene.

The hypothesis of the existence of a pathogenetic link between hyperhomocysteinemia and atherosclerosis was first proposed by K. McGully in 1969. In recent years, it has been established that hyperhomocysteinemia is often caused by genetic defects in enzymes involved in homocysteine ​​metabolism. The most common cause of hyperhomocysteinemia is point mutations in genes encoding the synthesis of cystation p-synthetase( * 236200, 21q22.3, CBS gene, p) and N( 5,10) -methylenetetrahydrofolate reductase( * 236250, MTHFR gene).

In homozygous for the defective gene, cystathione p-synthetase develops homocysteinuria, myopia, osteoporosis, mental retardation, propensity to thrombosis and early development of atherosclerosis. In heterozygotes, the main manifestation is hyperhomocysteinemia.

More than 9 mutations of the MTHFR gene have been identified, the most frequent of which is the replacement of the alanine residue with valine in the enzyme molecule, which makes the mutant protein thermolabile. In patients with the thermolabile form of N( 5,10) -methylenetetrahydrofolate reductase( 10-13% of the representatives of the Caucasoid race), arterial and venous thromboses develop significantly. The concentration of homocysteine ​​in them is increased by 50% of the norm, especially when folic acid is not consumed with food.

Currently, the participation of ACE in the pathogenesis of IHD is actively studied. ACE is a key component of the renin-angiotensin system( forms angiotensin II, which has a potent vasoconstrictor effect), as well as the kallikrein-kinin system( inactivates the bradykinin vasodilator).

Genetic polymorphism of the ACE gene is widespread, due to the presence / absence of Alu-repeat( insert in 287 pairs of nucleotides) in its 16th intron. The presence of this repetition is denoted as an I-allele, absence - as a D-allele. In homozygous carriers of the D-allele( DD-genotype), ACE activity is increased, in homozygous carriers of the I-allele( II-genotype) it is decreased, and in heterozygotes( ID-genotype) it has an intermediate value.

It is established that the genetic polymorphism of ACE is associated with a predisposition to the development of MI, especially in patients without such risk factors for atherosclerosis and ischemic heart disease as hyperlipidemia and overweight. DD-genotype is accompanied by high activity of ACE and promotes increased formation of angiotensin II.Angiotensin II can accelerate the development of atherosclerosis, directly damaging the intima of the vessels, inhibit the release of nitric oxide( a powerful endogenous relaxing factor), and enhance the action of endothelin-1.

Diagnostics

• Case history and physical examination. If you had a heart attack, the diagnosis can often be made by the doctor at the examination.

• An electrocardiogram can be performed to measure changes in the electrical activity of the heart as a result of circulatory disorders or a previous heart attack.

• Chest X-ray.

• Blood tests.

• Check for stress. While walking on the simulator, you measure blood pressure, change in heart rate and speed of breathing. If you do not endure physical exertion, you can enter the necessary medicine.

• To trace the flow of blood to the heart, after a physical load, a radioisotope, for example thallium, can be administered to the patient.

• An echocardiogram can be performed, in which ultrasonic waves are used to create an image of the movements of the heart.

• Heart angiography is performed to determine the presence of narrowing in the coronary artery. For this, a tiny catheter is inserted into the artery of the leg or arm and stretches into the coronary artery. Then a contrast material is injected through the catheter into the coronary artery and an X-ray is taken.

Treatment of

• In case of a heart attack, which is indicated by a sharp permanent chest pain, urgent medical care and hospitalization are necessary.

• Maintain a healthy lifestyle, eat low-fat foods, exercise. Avoid excessive consumption of alcohol, funds used with a blocked nose and other drugs that can cause high blood pressure.

• Rapidly acting nitrates, such as nitroglycerin, or long-acting nitrates, can be prescribed to dilate blood vessels and reduce or prevent symptoms of angina pectoris. A tablet of nitroglycerin placed under the tongue( sublingual) at the onset of an attack of angina usually reduces pain within a few minutes. Nitroglycerin can be put under the tongue also before the exercises that usually cause angina pectoris. However, in any attack of angina pectoris, you should not take more than three nitroglycerin tablets with breaks of five minutes, as a longer pain can mean a heart attack. Intravenous nitrate administration can be done to a patient with unstable angina. Nitrates can also be prescribed in the form of plates, aerosols or ointments to provide permanent protection.

• Beta-blockers such as propranolol or metoprolol are prescribed to reduce the need for the heart in oxygen by slowing down cardiac contractions and lowering blood pressure.

• Enalapril type inhibitors can be prescribed to reduce blood pressure and dilate blood vessels.

• Type verapamil, diltiazem or nifedipine blockers can be prescribed to reduce the need for oxygen in the heart and increase the flow of blood to the heart.

• Anticoagulants such as heparin or warfarin are used to reduce the risk of blood clots in patients with unstable angina.

• Vasodilators such as captopril, enalapril or hydralazine can be prescribed to dilate blood vessels and thereby reduce blood pressure and facilitate blood flow.

• The blocked coronary artery can be opened by percutaneous plastic surgery on vessels. In this procedure, a small balloon is introduced into the circulatory system through a catheter and directed to the blocked area of ​​the artery. Then the balloon is inflated, and it compresses the cholesterol plaque and widens the passage, improving the flow of blood. Then a stent is often placed in the artery to keep the artery open. With a plastic surgery on the vessels, the patient is in the hospital for only a few days.

• An operation to bypass the damaged area of ​​the artery can be performed to improve the flow of blood to the heart. The thoracic artery or vein taken from the leg is transplanted to the damaged coronary artery to bypass its narrowed or blocked part.

• In serious cases, when the heart muscle is severely damaged, there may be a question about heart transplant. The proportion of survivors after heart transplant is 80 percent in a year and 63 percent in four years.

Prevention

• Do not smoke.

• Eat low fat, cholesterol and salt foods.

• Exercise moderately intense exercises for at least 30 minutes at least three times a week. People aged 50 years who led a sedentary life, should first consult a doctor.

• If you are overweight, you need to lose weight.

• Visit your doctor regularly to measure blood pressure and cholesterol levels, and, if necessary, take action to treat.

• Your doctor may advise you to take a small dose of aspirin daily if you are at high risk for coronary artery disease. Aspirin reduces the tendency to form blood clots and, therefore, the risk of a heart attack. However, this medicine can be taken only by the doctor's advice.

• Attention! Call an ambulance if you experience severe chest pain, combined with nausea, vomiting, severe sweating, shortness of breath, weakness or fear, or without these symptoms.

• Attention! Call an "ambulance" if the pain in the chest with angina does not subside after 10-15 minutes.

• Attention! Call an "ambulance" if you experience severe chest pain.

• Visit the doctor if angina attacks become more frequent or more severe or occur when you are at rest.