ISCHEMIC HEART DISEASE
Coronary heart disease occurs as a result of insufficient blood supply to the heart, the cause of which is narrowing of the coronary vessels.
The disease is more common after the age of 50, but may also be at a younger age.
Coronary disease occurs due to damage to the inner wall (endothelium) of the vessels. The cause of damage can be as viral (viral infections), bacterial (bacterial infections), toxic exposure (smoking, alcoholism, drug addiction, other harmful intoxications), hypertension (a sharp increase in pressure leads to a hydrodynamic impact on the vascular wall and it injures), as well as genetic predisposition of the walls to damage.
An inflammatory process is formed at the site of damage to the endothelium, and subsequently an atherosclerotic plaque is formed, leading to a narrowing of the vessel and a decrease in blood flow in the heart muscle.
Factors contributing to the development of coronary disease.
Fatal factors.
1. Gender: Men get sick more often than women
2. Age: The older age, the higher the risk of disease
3. Heredity: if one of the relatives had vascular atherosclerosis, then the risk of developing the disease is higher
Manageable risk factors.
1. Smoking - increases the risk of heart disease by 1.5 times
2. Hypercholesterolemia (total cholesterol > 5.2 mmol/L).
3. Dyslipidemia (change in the ratio of levels of different cholesterol fractions)
Increased LDL cholesterol (beta-lipoproteins or BAD cholesterol).
A decrease in HDL cholesterol (an increase of 0.03 mmol/L is associated with a 3% reduction in CVD risk, this is GOOD cholesterol).
Hypertriglyceridemia (many triglycerides in the blood).
4. Increase in systolic (upper) blood pressure > 140 mm Hg.
5. Increase in diastolic (lower, "cardiac") blood pressure > 90 mm Hg.
6. increased salt intake.
7. Obesity.
8. Alcohol abuse.
9. Hypodynamics (daily aerobic [i.e. airborne] exercises of mild or moderate intensity for 20 min reduce the risk of death from CHD by 30%).
10. Stresses.
Clinical manifestations:
Sudden coronary death.
- a naturally fatal outcome of cardiovascular disease within one hour from the beginning of its development in persons who were previously in a stable state (in the absence of signs that allow to make another diagnosis).
death occurred in the presence of witnesses within one hour of the first threatening symptoms
before the onset of death, the condition of patients was assessed by others as stable and not causing serious concern
death occurred under circumstances excluding its other causes (violent death, injuries, other fatal diseases)
Possible causes of sudden cardiac death are:
in the vast majority of cases (about 85-90%), the cause of sudden cardiac death is CHD, with any clinical variants of it, including asymptomatic course, when sudden death is the first and last
clinical manifestation of the disease
any heart disease accompanied by severe myocardial hypertrophy (for example, hypertrophic cardiomyopathy, aortic mouth stenosis, etc.)
congestive heart failure of any genesis
cardiogenic shock of any genesis
heart tamponade of any genesis
pulmonary embolism
primary electrophysiological disorders such as: Q-T prolonged syndrome, QT prolongation (congenital and acquired forms); sinus node weakness syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia
nonatherosclerotic diseases of the coronary arteries
inflammatory, infiltrative, neoplastic and degenerative processes
congenital diseases
rhythm disturbances as a consequence of neurohumoral influences or disorders of the central nervous system (disturbance of autonomic regulation of the heart with a predominance of sympathetic activity;
the most important marker of this condition is a decrease in sinus rhythm variability, as well as an increase in the duration and variance of the Q-T interval)
sudden infant death syndrome and sudden death in children
heart concussion (heart contusion)
aortic dissection
intoxication or metabolic disorders
CLINICAL PATTERN OF SUDDEN DEATH.
Most cases of sudden cardiac death occur in community-acquired settings, which determines the most frequent fatal outcome of this form of coronary heart disease.
Sudden cardiac death can be triggered by excessive physical or neuropsychiatric stress, but can occur at rest, such as in sleep.
Immediately before the onset of sudden cardiac death, about half of the patients have a painful anginous attack, often accompanied by fear of near death. About 1/4 of sudden cardiac death occurs with lightning speed and no visible harbingers; in the rest of the patients, 1-2 weeks before sudden death, various, not always specific, prodromal symptoms are noted, indicating an exacerbation of the disease: an increase in heart pain (sometimes atypical localization), shortness of breath, general weakness and a significant decrease in the performance and tolerance of physical activity, palpitations and interruptions in the work of the heart, etc.
Immediately during the sudden development of ventricular fibrillation or asystole of the heart, the patient develops sharp weakness, dizziness.
After a few seconds, as a result of a complete cessation of cerebral blood flow, the patient loses consciousness, tonic contraction of skeletal muscles, noisy breathing appear.
When examined, the skin is pale with a grayish tint, cold to the touch. Pupils begin to expand quickly. The pulse on the carotid arteries is not determined, the tones of the heart are not listened to. After about 1.5 minutes, the pupils are maximally dilated. There are no pupillary and corneal reflexes. Breathing quickly cuts down, becomes agonal, very rare individual "convulsive respiratory movements" appear. After 2.5-3 minutes, breathing stops altogether. It should be remembered that about 3 minutes after the onset of ventricular fibrillation or asisstolia, irreversible changes occur in the cells of the cerebral cortex.
Angina pectoris.
Angina pectoris is subdivided into:
Tension angina.
Tension angina is characterized by transient attacks of vaginal pain caused by physical or emotional exertion or other factors leading to increased metabolic needs of the myocardium (increased BP, tachycardia). In typical cases of tension angina, the pain that appeared during physical or emotional exertion (heaviness, burning, discomfort) usually irradiates into the left arm, shoulder blade. Quite rarely, localization and irradiation of pain are atypical. An attack of angina lasts from 1 to 10 minutes, sometimes up to 30 minutes, but no more. Pain, as a rule, is quickly relieved after the termination of the load or 2-4 minutes after sublingual intake (under the tongue) of nitroglycerin.
For the first time, tension angina is diverse in manifestations and prognosis, therefore, it cannot be confidently attributed to the category of angina with a certain course without the results of observing the patient in dynamics. The diagnosis is established up to 3 months from the date of the patient's first pain attack. During this time, the course of angina pectoris is determined: its convergence to no, transition to stable or progressive
Stable angina.
Stable angina is established in cases of a stable manifestation of the disease in the form of a regular occurrence of pain attacks (or ECG changes preceding the attack) on the load of a certain level for a period of at least 3 months. The severity of stable angina tension characterizes the threshold level of physical activity tolerated by the patient, by which the functional class of its severity, necessarily indicated in the formulated diagnosis, is determined.
Progressive angina.
Progressive tension angina is characterized by a relatively rapid increase in the frequency and severity of pain attacks with a decrease in exercise tolerance. Attacks occur at rest or with a lower load than before, it is more difficult to stop with nitroglycerin (often an increase in its single dose is required), sometimes they are copied only by the introduction of narcotic drugs..
Spontaneous angina pectoris.
Spontaneous angina pectoris
differs from tension angina in that pain attacks occur with no apparent association with factors leading to increased myocardial metabolic needs. Seizures can develop at rest without obvious provocation, often at night or in the early hours, sometimes of a cyclical nature.
In terms of localization, irradiation and duration, effectiveness of nitroglycerin, attacks of spontaneous angina do not differ much from attacks of tension angina.
Variant angina, or Prinzmetal angina, refers to cases of spontaneous angina, accompanied by transient ascents on the ST segment ECG.
Myocardial infarction.
Such a diagnosis is established in the presence of clinical and/or laboratory (change in enzyme activity) and electrocardiographic data indicating the occurrence of a focus of necrosis in the myocardium, large or small. If, in the event of a heart attack, the patient is not hospitalized as soon as possible, the development of severe complications is possible and the likelihood of death is high.
Large-lobed (transmural)
myocardial infarction is justified by ECG changes or a specific increase in the activity of enzymes in blood serum (certain fractions of creatine phosphokinase, lactate dehydrogenase, etc.) even with an atypical clinical picture.
The listed enzymes are enzymes of redox reactions. Under normal conditions, they are only found inside the cell. If a cell breaks down (for example, in necrosis), then these enzymes are released and determined at the laboratory. The increase in blood concentrations of these enzymes in myocardial infarction is called resorption-necrotic syndrome.
The diagnosis of small-focal myocardial infarction is made in dynamics-developing changes in the ST segment or T wave without pathological changes in the QRS complex, but in the presence of typical changes in enzyme activity.
Complaints in coronary heart disease are:
Stomach pain associated with physical activity or stressful situations, shortness of breath interruptions in the heart, sensation of rhythm disturbance, weak.Signs of heart failure, for example, swelling starting from the lower extremities, forced position of the site.Treatment of coronary disease. Drug therapy.
Aspirin - If you take it every day or every other day, the risk of angina or heart attack will decrease, as the likelihood of blood clots will decrease. Aspirin consumption reduces the possibility that a blood clot will form at the site of a platelet rupture in the coronary artery - this is usually the main cause of a heart attack (myocardial infarction). Side effects of aspirin: ulcer and bleeding. Check with your doctor before taking aspirin.
• Beta blockers - Reduce heart rate and lower blood pressure, that is, reduce the need for oxygen in the heart. Clinical studies have proven that it is possible to prevent a heart attack and sudden death.
Nitroglycerin - This drug reduces chest pain by reducing the heart's oxygen demand and dilating the coronary arteries, thereby increasing the amount of oxygen supplied. A spray solution or tablet placed under your tongue acts instantly when you need immediate help with an angina attack. Long-acting nitroglycerin tablets or skin patches act slowly for several hours.
Calcium channel blockers - These drugs dilate the coronary arteries and improve blood flow. They also lower blood pressure and heart rate.
ACE - inhibitors - Angiotensin-converting enzyme (ACE) dilates blood vessels, increasing blood flow. Recent studies have shown that ACE inhibitors reduce the number of heart disease, seizures, and deaths among people who have coronary artery disease; this effect is not related to their property of lowering blood pressure. Therefore, they may have additional beneficial effects on blood vessel and heart muscle tissues. They will help primarily people with diabetes and those with a weakened heart muscle
Statin - Medications on statin reduce the amount of lipids (cholesterol and other fats) in your blood. As a result, the internal walls of blood vessels change, and platelet formation or enlargement becomes less likely. They slow or stop the development of coronary heart disease and also prevent repeated heart attacks.
Not so long ago, clinical studies have shown that a statin has an even more beneficial effect if used immediately after a heart attack or the threat of its occurrence, even before reducing the level of fats, it stabilizes platelets. Medications on statin: atorvastatin (Lipitor), pravastatin (Pravahol), simvastatin (Zokor), lovastatin (Mevakor) and rosuvastatin (Crestor).
Surgical treatment of coronary heart disease - types of surgical interventions
In the case where angina symptoms worsen despite taking medication, you may need surgery in the cardio-catheterization laboratory that clears the blocked artery.
Coronary angioplasty (PTCA)
This procedure (catheterization of the heart or fluid examination, from which coronary arteries can be examined from the inside), but it is both therapeutic and diagnostic. A similar but stronger tube (guide catheter) is inserted into the artery in the groin or arm, after which a wire thick from the hair is inserted through it into your coronary artery. An even thinner catheter is inserted through the guide wire into the blocked artery. The thin catheter at the end has a tiny ball. Once the ball reaches the blockage, it inflates to widen the artery and improve blood flow. The platelet does not disappear anywhere, it simply flattens and remains on the wall of the artery. The ball is then removed with the catheter. This procedure is sometimes called PTCA, that is, an abbreviation for its full name is used: percutaneous (conducted through the skin) transluminal (through the axial opening of a blood vessel) coronary angioplasty.
A stent is a small, lattice helical metal tube or frame above the ball. The ball inflates in a blockage, thus freeing the stent. After that, the ball is removed, but the stent remains in place, preventing the artery from narrowing. Just like arteries treated with angioplasty alone, arteries treated with stenting can become clogged again over time. A stent for many people is a better decision, it lasts longer.
• Atherectomy
Sometimes platelets become too hard, large, turn into lime, because of this it is impossible to treat with angioplasty or stent. In such cases, platelets have to be removed using a drill-like device.
The procedure will only work if the blockage or constriction is localized in a relatively small separate section of the artery. Instruments commonly used in atherectomy: directed catheter for atherectomy, transluminal retrievable catheter (AngioJet), rotational atherectomy is also used. Platelets can also be burned using an excimer laser.
Brachytherapy
The blockage is exposed to radiation to get rid of it. The source of radiation is very small, it fits inside or near the artery. The procedure is used in cases where the patient has already passed through Anglioplasty or stent treatment, but blockages have appeared again (restenosis procedure occurs). In coronary heart disease, surgery threatens those people whose disease is in severe stages or who have not been helped by medication or less drastic measures than surgery.
Aorto-coronary bypass grafting (CABG)
This is standard surgery for blockages in the coronary arteries. If multiple coronary arteries are blocked or if there is significant blockage in the left main artery, bypass grafting is the best solution to the problem. Blocked parts of the artery are bypassed, or shunted, by blood vessels "borrowed" from your chest (internal thoracic artery), arm (radial artery), or leg (subcutaneous vein of the leg). During surgery, the heart is stopped for a while, and your body is connected to a machine called an artificial circulation machine, which takes over the functions of the heart.
Operations are usually very successful, the percentage of complications is very low. Surgery without an artificial circulation machine: sometimes surgeons can perform open heart surgery without using an artificial circulation machine, right during the beating of the heart. The procedure usually causes fewer side effects than the standard procedure, but it cannot be done in all cases.
Minimally invasive coronary bypass surgery
If bypass grafting needs to be done only for the anterior or right coronary artery, the surgeon can replace the blocked artery with an artery from the chest by making a small incision rather than opening the full thoracic cavity, and thus bypass the blockage.
Transmiocardial laser revascularization (TMR) of TMR is an alternative for people who do not want to resort to angioplasty or bypass surgery. The surgeon, using a laser catheter, makes several punctures in the heart muscle. These small openings allow new blood vessels to form. This procedure can be performed either separately or together with coronary bypass grafting.