Hungry Heart
The heart, like any other body, nourish the blood vessels, called coronary arteries. Narrowing of the coronary arteries leads to malnutrition of the heart muscle, to oxygen "starvation", which doctors termed "ischemia." Ischemia can occur when the heart needs more nutrients, such as during exercise. In this case, the patient experienced an attack of chest discomfort or angina. If blood flow in coronary artery thrombus suddenly blocked, then there is an acute lack of oxygen and is formed by immobilization of the heart muscle, called myocardial infarction.
Two Faces of threatening illnesses
Often in the literature used two different terms - "angina" and "myocardial infarction". Angina and myocardial infarction - two manifestations of one disease - coronary heart disease (CHD). However, many patients who suffered a heart attack, a well-known symptoms of angina and, conversely, patients suffering from angina, ever suffered a myocardial infarction. Risk of myocardial infarction is that often it deals a blow at once - about half of a myocardial infarction occurs without any obvious precursors was imminent disaster.
When the account goes on the clock ...
A fair question: whether it can effectively treat a myocardial infarction? Because it is a consequence of necrosis of cardiac muscle. If, in the developing myocardial eliminate its causes, that is to restore patency of occluded arteries of the heart, the negative consequences of a heart attack can be greatly reduced.
The most widely available method of treating a heart attack - is the introduction of drugs which dissolve the clot. Such treatment can begin immediately, as soon as the doctor prodiagnostiruet infarction. But it is most effective only in the early hours of the onset of the disease. Later, the clot becomes resistant to drugs. Moreover, after 6 hours of early myocardial most cells in the affected area die and use drugs, which by this time are not effective enough, it is meaningless. Another approach - the mechanical removal of obstacles in the coronary artery. For this, special thin catheter under X-ray control, rekanaliziruyut thrombus and a special balloon expanding the lumen of artery narrowing. Call this method of treatment of coronary angioplasty. Angioplasty is more effective than medication in the late periods after a heart attack, at a relatively "old" thrombosis.
Bypass pipe
If blood flow can not be restored in such a minimally traumatic technique as coronary angioplasty, then resort to open surgery - coronary artery bypass. At the same time from the aorta - the main blood line - to the arteries of the heart sum taken from other parts of the body vein or artery, so that the bypass (shunt) zone narrowing or blockage.
Similar methods can be used in the treatment of angina pectoris. Moreover, in developed countries, they are universally applied. The advantage of surgical techniques to the medication that they are rapidly and completely eliminate the symptoms of the disease.
Light at the end of the vessel
We can say that there are certain categories of persons whose presence of atherosclerosis is very likely. In most cases, narrowing of the coronary arteries is due to the development of deposits on the walls of the vessel - the atherosclerotic plaques - narrowing its lumen. Increased levels of cholesterol, family history of cardiovascular disease, obesity, smoking, hypertension, diabetes - that risk factors for atherosclerosis.
Bypass surgery, angioplasty or drugs
What is the best method - coronary bypass surgery, coronary angioplasty or medical treatment? Each of these methods has its own testimony. Sometimes at different stages should apply to different treatments. Certainly, drug prophylaxis and therapy are needed in almost all cases. Coronary angioplasty can also be used successfully in most patients. Brief treatments for coronary artery disease can be grouped as follows:
Medications. Some of them are needed to reduce blood cholesterol levels or high blood pressure. Other medications allow people suffering from angina, avoid attacks during exercise. Some drugs prevent cardiac arrhythmias, often associated with CHD. A number of drugs needed to prevent heart failure after myocardial infarction;
Thrombolytic therapy. This type of treatment used to remove a blood clot in acute myocardial infarction, where blood flow is difficult blood clots. Thrombolytic agents dissolve clots and restore patency of coronary artery disease. Thrombolytic therapy is often combined with angioplasty;
Angioplasty - a way to expand the internal lumen of blood vessels using a special container. At the same time through a small puncture, the doctor inserts a thin tube (catheter), and leads him to a narrowing section of the vessel, controlling the process using X-rays. Balloon expands under pressure, pushing, flatten atherosclerotic plaques, creating conditions for normal blood flow. In some cases, then install a metal frame - a stent, which is implanted in the artery wall, prevents her from re-narrowing.
Bypass surgery. During bypass surgery, a new way of blood supply to bypass the blocked section of artery. Shunts are typically created from his own veins or arteries, isolated, for example, from foot patient. Bypass surgery is usually performed surgically, although recently developed and more forgiving, non-surgical methods of grafting.
All of these techniques for many years been successfully used by doctors offices Cardiovascular Surgery Center. At the same time apply authoring, including a unique vascular stent, developed by the head office ZA Kavteladze with staff and is now produced by WILLIAM COOK (USA).
Provocative diagnosis
In the presence of a human multiple risk factors for CHD is necessary to conduct further investigation, which aims to find out whether there is ischemia of the person or not. To do this, carry out various so-called "provocative tests, such tests with physical exercise. Comparing the parameters of the heart at rest and under heavy loads, make a conclusion on the need for further examination. In the next step is usually carried out research vessels of the heart - coronaroangiography. And provocative tests and drug tests, and coronary angiography are a vast arsenal of diagnostic methods specialists of our clinic. According to the results of coronary angiography doctor chooses treatment strategy. After such a comprehensive survey may have enough to accurately predict the risk of heart attack and take the necessary measures to prevent it.
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Risk factors for coronary heart disease
≤ 75 years> 75 years
Heart failure 3,5% 14,4%
Renal failure 3,9% 11,5%
Diabetes 24,3% 37,3%
Stagnation in the lungs 19,7% 45,4%
Left bundle branch block 3,6% 12,7%
Accompanying a myocardial infarction disease aggravates the course of the underlying disease. The most frequent comorbidities are listed in the table below: [7]
Risk factors for coronary heart disease - it's the circumstances, the presence of which predisposes to CHD. These factors are largely similar to the risk factors for atherosclerosis, since the main link of pathogenesis of coronary heart disease is coronary atherosclerosis.
To classify the set of risk factors associated with cardiovascular disease in epidemiological studies suggested different models. Risk factors can be classified as follows.
Biological determinants or factors:
* Advanced age;
* Male gender;
Genetic factors that contribute to dyslipidemia, hypertension, glucose tolerance, diabetes and obesity.
Anatomical, physiological and metabolic (biochemical) features:
* Dyslipidemia;
* Hypertension;
* Obesity and the distribution of body fat;
* Diabetes.
Behavioural (behavioral) factors that may exacerbate coronary artery disease:
* Eating habits;
* Smoking;
* Lack of physical activity or physical exertion exceeding the adaptive capacity of an organism;
* Alcohol consumption;
* The behavior that contribute to coronary artery disease.
The likelihood of developing coronary heart disease and other cardiovascular diseases increases with the number and "power" of these risk factors.
For the doctor determines the nature and scope of preventive and therapeutic interventions are important as recognition of risk factors at the individual level as well as a comparative assessment of their significance. First and foremost, it is necessary to identify atherogenic dyslipoproteinemia at least at the level of detection of hypercholesterolemia (deviation of the concentration of cholesterol in the blood upwards compared to the norm). Proved that when the cholesterol content in blood serum from 5.0-5,2 mmol / l the risk of death from coronary heart disease is relatively small. The number of deaths from coronary heart disease within the next year increased from 5 cases per 1000 men at the level of blood cholesterol 5.2 mmol / l to 9 cases at the level of cholesterol in the blood 6,2-6,5 mmol / l and up to 17 cases per 1000 population at the level of blood cholesterol 7.8 mmol / L [8]. The specified pattern is typical for all people aged 20 years and older. Opinion on improving border permissible level of blood cholesterol in adults with increasing age as a normal phenomenon have failed [8].
Hypercholesterolemia refers to important elements of the pathogenesis of atherosclerosis of any arteries, the question of the causes of preferential formation of atherosclerotic plaques in the arteries of an organ (brain, heart, limbs) or in the aorta studied enough. One of the possible prerequisites for formation of stenotic atherosclerotic plaques in coronary arteries may be the presence of musculo-elastic hyperplasia of the intima (the thickness of the media can not exceed the thickness of 2-5). Intimal hyperplasia of coronary arteries, identified already in childhood, can be attributed to a number of factors, genetic susceptibility to coronary heart disease [8].
[Edit] Pathogenesis
Ultrasound diagnosis revealed a narrowing of the coronary artery. Area plaque marked in green.
According to modern concepts [9], coronary heart disease - it's pathology, which is based on myocardial damage caused by insufficient blood supply to it (coronary insufficiency). Imbalance between myocardial perfusion and real needs of its blood supply may occur in due the following circumstances:
1. Reasons inside the vessel:
* Atherosclerotic narrowing of coronary arteries;
* Thrombosis and thromboembolism of the coronary arteries;
* Spasm of the coronary arteries.
2. Causes outside the vessel:
* Tachycardia;
* Myocardial hypertrophy;
* Hypertension.
The concept of coronary heart disease is a group [9]. It combines both acute and chronic conditions, including regarded as an independent nosological forms, which are based on ischemia and resulting myocardial changes (necrosis, degeneration, multiple sclerosis), but only in cases where ischemia is caused by narrowing of coronary arteries associated with atherosclerosis, or cause mismatch of coronary blood flow with metabolic needs of the myocardium is not known.
Formation of atherosclerotic plaques occurs in several stages. First, the lumen of the vessel does not change significantly. With the accumulation of lipids in the plaque ruptures occur its fibrous sheet that accompanied the deposition of platelet aggregates, contributing to the local deposition of fibrin. Zone location parietal thrombus is covered by the newly formed endothelium and acts in the lumen of the vessel, narrowing it. Along with lipidofibroznymi plaques formed almost exclusively by fibrous stenosing plaques undergoing calcification [9].
As development and growth of each plaque, increasing the number of plaques increases and the degree of stenosis of the lumen of the coronary arteries, is largely (though not necessarily) determined by the severity of clinical manifestations and course of CHD. Narrowing of the arteries to 50% is often asymptomatic. Usually clear clinical manifestations of disease occur when luminal narrowing of up to 70% or more. What is located proximal stenosis, the greater the mass of myocardium subjected to ischemia, in accordance with the area's blood supply. The most severe manifestation of myocardial ischemia observed in stenosis of the main trunk or the mouth of the left coronary artery.
At the origin of myocardial ischemia can often play the role of a sharp increase in its oxygen demand, coronary thrombosis or angiospasm. Prerequisites to thrombosis due to damage of vascular endothelium may occur at early stages of atherosclerotic plaque, especially in the pathogenesis of CHD, and especially its exacerbation, the essential role played by the processes of hemostasis disorders, primarily the activation of platelets, which cause is not fully installed. Platelet mikrotrombozy and microemboli may exacerbate impaired blood flow in the stenotic vessel.
Significant atherosclerotic arteries is not always prevent their cramps. The study of serial transverse sections of diseased coronary arteries showed that only 20% of atherosclerotic plaque is concentric narrowing of the arteries, preventing the functional changes of the lumen. In 80% of the cases reveals the eccentric location of the plaque, which retained the ability of the vessel and to expand, and to spasm.
[Edit] Pathological anatomy
Atherosclerotic narrowing of coronary arteries (the scheme).
Nature of the changes detected in CHD, independent of clinical disease and the presence of complications - heart failure, thrombosis, thromboembolism, etc.
[Edit] With Myocardial Infarction
Histological preparation (increase in 100x, hematoxylin and eosin). Myocardial infarction, seven days ago.
The most pronounced morphological changes of the heart in myocardial infarction and postinfarction cardiosclerosis. Common to all clinical forms of CHD is a picture of the atherosclerotic lesion (or thrombosis) of arteries of the heart, usually detectable in the proximal parts of large coronary arteries. Most often affects the anterior interventricular branch of left coronary artery, at least right coronary artery and circumflex branch of left coronary artery. In some cases, revealed stenosis of left coronary artery. In the basin of the affected artery is often determined by changes in the myocardium, corresponding to ischemia or fibrosis, are characterized by a mosaic of changes (lesions coexist with areas of unaffected myocardium), with complete blockage of the lumen of coronary arteries in the myocardium, usually found postinfarction scar. In patients with myocardial infarction can be detected cardiac aneurysm, perforation of the interventricular septum, the gap between papillary muscles and chords, intracardiac thrombus [10].
[Edit] When angina
A clear correspondence between the signs of angina and anatomical changes in the coronary arteries is not, however, shown that for stable angina is more characteristic of the presence of atherosclerotic plaques in vessels with a smooth-coated surface of the endothelium, while in progressive angina often found plaques with ulceration, tears, forming parietal thrombus.
[Edit] Clinical forms
To substantiate the diagnosis of CHD should conclusively establish its clinical form (of those represented in the classification) according to generally accepted criteria for diagnosis of this disease. In most cases, the key to diagnosis is recognition of angina or myocardial infarction - the most frequent and most typical manifestations of CHD, other clinical forms of the disease found in everyday medical practice less and their diagnosis more difficult.
[Edit] Sudden coronary death
Sudden coronary death (primary cardiac arrest), presumably related to myocardial electrical instability. To form an independent CHD sudden death attributed to the event that there is no basis for the diagnosis of other forms of heart disease or other illness: for example, the death that occurs in the early phase of myocardial infarction is not included in this class and should be considered as death from myocardial infarction. If resuscitation is not performed or were unsuccessful, the primary cardiac arrest is classified as sudden coronary death. The latter is defined as a death that occurs in the presence of witnesses immediately or within 6 hours after onset of heart attack [11].
[Edit] Angina
Main article: Angina
Angina as a form of CHD combines angina, subdivided into:
* First mooted
* Stable
* Progressive
* Spontaneous angina (so-called. Angina of rest), which is a variant of Prinzmetal angina.
[Edit] angina
Angina is characterized by transient episodes of retrosternal pain due to physical or emotional stress or other factors leading to increased metabolic needs of the myocardium (increased blood pressure, tachycardia). In typical cases of angina appeared during physical or emotional stress retrosternal pain (heaviness, burning, discomfort) usually radiates into the left-hand shoulder. Rarely localization and irradiation of pain are atypical. Angina lasts from 1 to 10 minutes, sometimes up to 30 minutes, but no more. Pain is usually quickly stopped by after-load or 2-4 min after sublingual (under the tongue) nitroglycerin.
For the first time by having angina varied on the manifestations and prognosis therefore can not be confidently attributed to the category of angina pectoris with a particular course without the results of monitoring patients over time. The diagnosis is established in the period up to 3 months from the date of the patient first pain attack. During this time, determined by the course of angina pectoris: its convergence to zero, the transition to a stable or progressive [12].
The diagnosis of stable angina is established where sustainable downstream manifestations of the disease in the form of law-of pain attacks (or ECG changes preceding the attack) to load a certain level for a period of not less than 3 months. The severity of stable angina threshold characterizes patients tolerated exercise, which determine the functional class of its gravity, necessarily indicate a diagnosis is formulated.
Progressive angina is characterized by relatively rapid increase in frequency and severity of pain attacks with a decrease in exercise tolerance. Attacks occur at rest or with less than before, loading, harder cropped nitroglycerin (often required to improve its single-dose), sometimes cropped only the introduction of narcotic analgesics.
Spontaneous angina is different from angina that pain attacks occur for no apparent connection with the factors leading to increased metabolic needs of the myocardium. Seizures may develop in peace with no apparent provocation, often at night or in the early hours, are sometimes cyclical. Localization, and duration of irradiation, the effectiveness of nitroglycerin, a spontaneous attacks of angina differ little from the attacks of angina.
Variant angina or Prinzmetal angina, represent cases of spontaneous angina, accompanied by transient elevations in the ECG ST segment.
[Edit] Myocardial infarction
Main article: Myocardial infarction
Such a diagnosis is the presence of clinical and (or) laboratory (the change of enzyme activity), and electrocardiographic evidence of the occurrence of necrosis in the myocardium, large or small. If in the event of a heart attack patient will not be in the shortest possible time hospitalized in the ICU may develop severe complications and a high probability of death.
Macrofocal (transmural) myocardial infarction substantiated pathognomonic ECG changes or increased activity of specific enzymes in serum (certain factions of creatine kinase, lactate dehydrogenase, etc.), even with an atypical clinical picture.
The above enzymes - enzymes are redox reactions. Under normal conditions, they found only inside cells. If the cell is destroyed (eg, necrosis), these enzymes are released and are determined by laboratory tests. Increased concentrations of these enzymes in the blood during myocardial infarction has been called resorption of necrotic syndrome [13].
The diagnosis of small focal myocardial infarction put in developing the dynamics of changes in ST segment or T wave showed no pathological changes of the complex QRS, but in the presence of typical changes in enzyme activity.
[Edit] Postinfarction cardiosclerosis
Indication of myocardial infarction as a complication of coronary heart disease contribute to the diagnosis is not earlier than 2 months from the date of occurrence of myocardial infarction. Diagnosis of postinfarction cardiosclerosis as an independent clinical form of coronary heart disease set in the case of angina and other forms provided for the classification of coronary artery disease in a patient lacking, but there is clinical and electrocardiographic signs of focal sclerosis infarction (sustained arrhythmias, conduction, congestive heart failure, signs of scarring in the myocardium ECG). If in the late period patient survey electrocardiographic signs of myocardial infarction are not available, then the diagnosis can be justified by the data of medical records pertaining to the period of acute myocardial infarction. The diagnosis indicates the presence of chronic heart aneurysm, internal breaks myocardial dysfunction of papillary muscles of the heart, intracardiac thrombosis, determined by the nature of the violations of the conduction and cardiac rhythm, form and stage of heart failure.
[Edit] arrhythmic form
Cardiac arrhythmia or signs of left ventricular heart failure (in the form of attacks of breathlessness, cardiac asthma, pulmonary edema) appear as equivalents attacks angina or spontaneous angina. Diagnosis of these forms is difficult and is finally formed on the basis of aggregate results of electrocardiographic studies in samples with a load or when the monitor observation data and selective coronary angiography.
[Edit] Diagnosis
[Edit] Clinical symptoms
[Edit] Complaints
Irradiation of the pain of IBS. The color intensity indicates the frequency of occurrence of irradiation in this region.
The most typical complaint for coronary heart disease are:
* Retrosternal pain associated with exercise or stressful situations
* Shortness of breath
* Disruptions in the heart, a sense of rhythm disturbances, weakness,
* Signs of heart failure, such as swelling, starting with the lower extremities, involuntary sitting position.
[Edit] Medical history
From the data of history are of great importance the length and nature of pain, dyspnea, or arrhythmias, their connection with physical activity, the amount of physical exertion that the patient can sustain without the occurrence of an attack, the effectiveness of various medicines in case of attack (in particular, the effectiveness of nitroglycerin). It is important to ascertain the presence of risk factors.
[Edit] Physical Examination
At physical examination to identify possible signs of heart failure (moist rales and crackling in the lower parts of the lungs, "heart" edema, hepatomegaly - enlarged liver). Objective symptoms, typical for coronary heart disease, not requiring laboratory or instrumental examinations, no. Any suspicion of coronary heart disease requires electrocardiography.
[Edit] Electrocardiogram
ECG - an indirect method of investigation, that is, he does not say how many myocardial cells have died, but allows us to estimate some function of the myocardium (automaticity and with certain assumptions - for). For diagnosis of most pathological conditions infarction (cardiomyopathy, hypertrophy, and some other diseases), ECG is a secondary, supportive function.
[Edit] Some symptoms of acute myocardial infarction
Characteristic feature of myocardial macrofocal miokrada (transmural) is the presence of ECG pathological tooth Q.
1. in I leads:
* Is a pathological tooth Q (> 0.03 c, the amplitude exceeds 1 / 3 wave amplitude R)
* Is negative prong T.
2. in II abduction is abnormal tooth Q (> 0.03 c, the amplitude exceeds 1 / 4 R-wave)
3. III in abduction is abnormal tooth Q (> 0.03 c, the amplitude exceeds 1 / 2 R-wave)
4. in leads V1, V2, V3 is a tooth of QS or QR, and at the same tine T is negative.
5. in leads V4, V5, V6 is abnormal tooth Q (> 0.04 c) and the negative prong T.
Barb T can determine the dynamics of the process. For example, in II leads: in acute myocardial infarction - he strongly positive (curve Pardee, "cat back"), in the island - negative (usually with lower amplitude) in the subacute stage and the stage of scarring T-prong rises to the contours, but often does not reach it (if there macrofocal heart attack). Pathological Q wave and a weakly pronounced negative prong T, which do not change within a few days - electrocardiographic signs of scar tissue in the myocardium.
ST elevation acute myocardial infarction.
Depression, ST (arrow) - a characteristic feature of myocardial ischemia. Shows the ECG chest leads.
ECG data are objective instrumental criterion of myocardial infarction, limitation of damage and its localization.
[Edit] Echocardiography
Main article: Echocardiography
The essence of the method consists in irradiating the tissue ultrasound pulses of fixed frequency and receiving the reflected signal. Based on the value of the reflection pattern is formed by the density of tissue through which the impulse has passed. Modern devices to implement the findings of graphical information in real time, with possibility to assess blood flow through the Doppler effect.
In CHD echocardiography to evaluate the state of the myocardium, the preservation of valvular heart of its contractile activity.
[Edit] Laboratory indicators
CHD combines many diseases of the heart, and, accordingly, the biochemical changes occurring in the course of their development are different. May develop the following changes.
Troponin and creatine kinase in different periods of flow myocardial infarction.
[Edit] Changes typical for myocardial infarction
For myocardial infarction is characterized by increasing concentrations of specific proteins. Among them:
* CK (the first 4-8 hours);
* Troponin-I (7-10 days).;
* Troponin-T (10-14 days).;
* Lactate dehydrogenase;
* Aminotransferase;
* Myoglobin (first day).
All of these proteins are found only inside cells. When the mass destruction of cells, these proteins enter the bloodstream and are determined by laboratory tests. This phenomenon is known as resorption of the necrotic syndrome [13].
At the present time in Russia much of the medical institutions do not have the equipment and materials for determining the level of troponin. This analysis is often conducted in patients with private facilities on a commercial basis (with the consent of the patient to increase the volume of research).
Nonspecific response to myocardial injury include:
* Neutrophilic leukocytosis (lasts 3.7 days.) - As a manifestation of inflammation in response to necrotic changes;
* Increase ESR (1-2 weeks) - as a reflection of changes in the quantitative ratio between the fractions of proteins, which occurs also mainly due to the development of inflammation.
* Increased ALT AST. (Nonspecific markers of cytolysis)
[Edit] Changes specific to atherosclerosis
For the diagnosis of atherosclerosis requires information on the following indicators:
* The concentration of triglycerides;
* Total cholesterol;
* HDL cholesterol (antiatherogenic);
* LDL cholesterol (considered to be atherogenic);
* The concentration of apolipoprotein A1 (responsible for the removal of excess cholesterol from tissues);
* The concentration of apolipoprotein B (responsible for the delivery of cholesterol in the tissues);
* Atherogenic index.
