Stenocardia tension: treatment

Risk factors that are amenable to correction should be eliminated as much as possible. People with nicotine addiction should quit smoking: after 2 years of quitting, the risk of myocardial infarction decreases to a level in patients who never smoked. Proper treatment of hypertension is necessary, since even moderate arterial hypertension leads to an increase in the workload on the heart. Decreased body weight (even as the only correctable factor) often reduces the severity of angina pectoris.

Sometimes the treatment of even a small deficiency of the left ventricle leads to a marked decrease in the severity of angina pectoris. Paradoxically, foxglove preparations sometimes increase angina pectoris, possibly due to an increase in myocardial contractility and, accordingly, an increase in the need for oxygen, or due to an increase in the tone of the arteries (or with the participation of both mechanisms). A significant reduction in the total amount of cholesterol and LDL cholesterol (through diet and drugs as needed) slows the progression of IHD, can lead to the disappearance of some pathological changes, improves endothelial function and, thus, the stability of arteries to stress. The program of physical exercises, mainly walking, often improves the quality of life of patients, reduces the risk of coronary heart disease and increases resistance to physical exertion.

[1], [2], [3], [4], [5], [6]

Medicines for angina pectoris

The main goal is to reduce acute symptoms and prevent or reduce the extent of ischemia.

In case of an acute attack, nitroglycerin is most effective under the tongue.

To prevent ischemia, all patients with diagnosed IHD or a high risk of its development should take antiplatelet drugs daily. B-Adrenoblockers, if there are no contraindications and tolerance to them, are prescribed to the majority of patients. Some patients need calcium channel blockers or long-acting nitrates to prevent attacks.

Antiplatelet agents interfere with platelet aggregation. Acetylsalicylic acid binds irreversibly to platelets and inhibits cyclooxygenase and platelet aggregation. Clopidogrel blocks adenosine diphosphate-induced aggregation of platelets. Each drug can reduce the risk of ischemic complications (myocardial infarction, sudden death), but the greatest effectiveness is achieved with their simultaneous appointment. Patients with contraindications to any drug should receive another, at least one. Beta-adrenoblockers reduce manifestations of angina and prevent heart attack and sudden death better than other drugs. These medicines block sympathetic cardiac stimulation, reduce systolic blood pressure, heart rate, myocardial contractility and cardiac output, thus reducing myocardial oxygen demand and increasing resistance to physical exertion. They also increase the threshold for the development of ventricular fibrillation. Most patients tolerate these drugs well. Many b-adrenoblockers are available and effective. The dose is selected by gradually increasing it, until bradycardia or side effects occur. Patients who can not receive b-adrenoblockers, for example patients with bronchial asthma, are prescribed calcium channel blockers with a negative chronotropic effect (such as diltiazem, verapamil).

Medicines used in ischemic heart disease

Medicine

Doses

Application

Antiplatelet drugs

Acetylsalicylic acid (aspirin)	With stable angina: 81 mg once a day (soluble form). When ACS: 160-325 mg chew (tableted form) upon delivery to the receiving room, then 81 mg * 1 time / day throughout the hospitalization and after discharge	All patients with IHD or a high risk of its development, with the exception of intolerance to acetylsalicylic acid or contraindications to its use; apply for a long time
Clopidogrel (predominantly) or Ticlopidine	75 mg 1 time / day 250 mg 2 times / day	Applied with acetylsalicylic acid or (with intolerance of acetylsalicylic acid) in the form of monotherapy
IIb / IIIa inhibitors of glycoprotein receptors	Intravenously for 24-36 h	Some patients with ACS, mostly those who perform NDA with stenting, and patients with
Abciximab	0.25 mg / kg bolus, then 10 μg / min	Unstable high-risk angina, or IM without ST- segment elevation
Eptifibatid	180 μg / kg bolus, then 2 μg / kg per minute
Tirofiban	0.4 μg / kg per minute for 30 minutes, then 0.1 μg / kg per minute

B-adrenoblockers

Atenolol	50 mg after 12 hours in the acute phase. 50-100 mg twice a day for a long time	All patients with ACS, except for intolerance to b-blockers or contraindications to their use, especially those at high risk; apply for a long time
Metoprolol	1 -3 boluses of 5 mg are administered at intervals of 2-5 minutes, according to tolerability (up to a dose of 15 mg); then 25-50 mg every 6 hours, starting 15 minutes after the last intravenous injection, for 48 hours; further 100 mg 2 times a day or 200 mg once a day (at the doctor's discretion)

Opiates

Morphine

2-4 mg intravenously as needed

All patients with chest pain due to ACS

Nitrates of short action

Nitroglycerin sublingually (tablets or spray)	0,3-0,6 mg every 4-5 minutes to Sraz	All patients - for rapid relief of pain in the chest; take as necessary
Nitroglycerin in the form of continuous intravenous administration	The initial rate of administration is 5 μg / min with an increase of 2.5-5.0 μg every few minutes until the delivered rate	Some patients with ACS: during the first 24-48 hours. Also patients with heart failure (except for patients with AH), extensive anterior myocardial infarction, an ongoing attack of angina, hypertension (BP decreases by 10-20 mm Hg, but no more than than at 80-90 mm Hg for systolic pressure). For long-term use - in patients with recurrent angina and persistent pulmonary insufficiency

Nitrates of continuous action

Isosorbide dinitrate	10-20 mg 2 times a day; can be up to 40 mg 2 times a day	Patients with unstable angina continuing to detect seizures after reaching the maximum dose of b-adrenoblockers
Isosorbide mononitrate	20 mg 2 times a day with a 7-hour interval between the first and second doses
Isosorbide mononitrate with sustained release	30-60 mg once a day, possibly with an increase to 120 mg, sometimes up to 240 mg
Plasters with nitroglycerin	0,2-0,8 mg / h, paste between 6 and 9 o'clock in the morning, remove after 12-14 hours to prevent tolerance
Ointment with nitroglycerin 2% (15 mg / 2.5 shmmazi)	1.25 cm spread on the upper half of the chest or arm every 6-8 hours, increasing the dose to 7.5 cm with ineffectiveness, cover with cellophane, remove after 8-12 hours; daily to prevent tolerance

Antithrombotics

Sodium Enoxaparin	30 mg intravenously (bolus), then 1 mg / kg per second for 12 hours, a maximum of 100 mg	Patients with unstable angina or MI without segment elevation Patients younger than 75 years who receive tenecteplase. Almost all patients with MI and ST- segment elevation, except for those who will be given NDA within 90 minutes; treatment is continued until NDA, CABG or discharge
The unfractionated form of sodium heparin	60-70 units / kg intravenously (maximum 5000 units bolus), further 12-15 units / kg per hour (maximum 1000 U / h for 3-4 days	Patients with unstable angina or myocardial infarction without rising segments can use sodium enoxaparin as an alternative
	60 units / kg intravenously (maximum 4000 units bolus) is administered at the beginning of the introduction of alteplase, retiplaza or tenecteplase, then continue at 12 U / kg per hour (maximum 1000 U / h) for 48-72 hours	Patients with myocardial infarction with an elevation of segments may use sodium enoxaparin as an alternative, especially those over the age of 75 (since sodium enoxaparin together with tenecteplase can increase the risk of hemorrhagic strokes)
Warfarin	The dose is adjusted to achieve an MHO of 2.5-3.5	Possible long-term use

* Higher doses of acetylsalicylic acid do not lead to a more pronounced disaggregant effect, but increase the risk of side effects. Enoxaparin sodium is preferred over other low molecular weight forms of sodium heparin.

Nitroglycerin is a powerful relaxant of smooth muscles and a vasodilator. The main points of application of its action are in the peripheral vascular bed, especially in the venous depot, as well as in the coronary vessels. Even the vessels affected by the atherosclerotic process are able to expand in places where there are no atheromatous plaques. Nitroglycerin lowers systolic blood pressure and dilates the systemic veins, thus reducing the stress of the myocardial wall - the main reason for the increase in myocardial oxygen demand. Sublingually, nitroglycerin is prescribed for relief of an acute attack of angina or preventing it before physical exertion. The expressed relief usually comes within 1,5-3 minutes, complete arresting of an attack - in 5 minutes, the effect lasts up to 30 minutes. Admission can be repeated 4-5 minutes to 3 times, if the full effect does not develop. Patients should always wear nitroglycerin tablets or aerosol in an accessible place to use quickly at the beginning of an attack of angina. The tablets are stored in a tightly closed glass container that does not allow light to retain the properties of the preparation. As the drug quickly loses its effectiveness, it is advisable to keep it in a small amount, but often replaced with a new one.

Nitrates of long-acting (for ingestion or active transsexposure) are used if the manifestations of angina persist after the administration of the maximum dose of b-blockers. If the occurrence of attacks of angina can be foreseen, nitrates are prescribed with the expectation of "blocking" this time. Nitrates for oral administration include isosorbide dinitrate and isosorbide mononitrate (active metabolite dinitrate). Their effect occurs within 1-2 hours and lasts from 4 to 6 hours. The forms of isosorbide release of mononitrate with slow release are effective throughout the day. Plasters with nitroglycerin, acting percutaneously, largely replaced ointments with nitroglycerin, primarily because the ointments are uncomfortable and can stain clothing. Patches slowly release the drug, which provides a prolonged effect; the tolerance of physical loads increases after 4 hours after gluing of the patch and lasts for 18-24 hours. Nitrate tolerance can develop mainly in those cases when the concentration of the drug in the blood plasma is constant. Since the risk of myocardial infarction is highest in the early morning hours, reasonable interruptions in the intake of nitrates in the lunch and early evening hours, if the patient does not develop angina attacks on this background. For nitroglycerin, 8-10 hour intervals can probably be considered sufficient. For isosorbide dinitrate and isosorbide mononitrate, a 12-hour interval may be required. Prolonged forms of isosorbide mononitrate release, apparently, do not lead to the formation of tolerance.

Calcium channel blockers can be used if the symptoms of angina persist despite the use of nitrates, or if nitrates can not be prescribed. Calcium channel blockers are especially indicated for hypertension or spasm of coronary arteries. Different types of these drugs have different effects. Dihydropyridine (such as nifedipine, amlodipine, felodipine) do not have a chronotropic effect and differ only in their negative inotropic effect. Short-acting dihydropyridines can cause reflex tachycardia and increased mortality in patients with IHD; they should not be used to treat stable angina pectoris. Long-acting dihydropyridines less than expression "cause tachycardia; they are most often used with b-adrenoblockers. In this group, the weakest negative inotropic effect is amlodipine, which can be used for systolic dysfunction of the left ventricle. Diltiazem and verapamil, other types of calcium channel blockers, have negative chronotropic and inotropic effects. They can be prescribed as one drug for patients with intolerance to b-adrenoblockers and normal systolic function of the left ventricle, but they can increase cardiovascular mortality in patients with left ventricular systolic dysfunction.

Percutaneous surgery on coronary arteries

The possibility of NOVA (for example, angioplasty, stenting) is considered in those cases when the symptoms of angina persist despite treatment with medications and worsen the quality of life of the patient or if the anatomical defects of the coronary artery (revealed by angiography) indicate a high risk of death. The choice between NOVA and CABG depends on the degree and location of anatomical defects, the experience of the surgeon and the medical center, and (to some extent) on the choice of the patient. NOVA is usually preferred for the lesion of one or two vessels with suitable anatomical features. Defects of a large extent or located in the junction of the vessel often become an obstacle to the implementation of NOVA. In most cases, NOVA is performed with stenting, rather than with balloon dilatation, and, as stenting technologies improve, NOVA is used in increasingly complex cases. The risk created by the operation is comparable to that of CABG. Mortality ranges from 1 to 3%; the frequency of development of the left ventricle - from 3 to 5%. Less than 3% of cases, there is a stratification of the vessel wall, which creates a critical obstacle to the blood flow, which requires an emergency CABG. After stenting, clopidogrel is added to the acetylsalicylic acid for at least 1 month, but preferably for a period of 6-17 months, as well as statins if the patient has not received it before. Approximately 5 to 15% of the stents are restenosed after a few days or weeks, which requires placing a new stent inside the previous stent or holding a CABG. Sometimes closed stents do not cause symptoms. Angiography performed after 1 year, reveals an almost normal lumen of about 30% of the vessels in which the manipulation was performed. Patients can quickly return to work and normal physical activity, but hard work should be avoided for 6 weeks.

Aortocoronary bypass surgery

In aortocoronary bypass, the sites of autologous veins (for example, the saphenous vein of the leg) or (preferably) the arteries are used to bypass the affected areas of the coronary arteries. After 1 year, approximately 85% of venous shunts function, while in 10 years up to 97% of the shunts from the internal thoracic artery function. Arteries are also able to hypertrophy to adapt to increased blood flow. Aortocornary shunting is preferable for patients with left main artery disease, pathology of three vessels or the presence of diabetes mellitus.

Aortocornary shunting is usually performed using an artificial circulatory system (AIC) on a stopped heart. AIC pumps and oxygenates the blood. The risk of surgery includes stroke and myocardial infarction. In patients with normal heart size, no history of myocardial infarction, good functioning of the ventricles, and absence of other additional factors, the risk of perioperative myocardial infarction is <5%, stroke 2% to 3%, death <1%; the risk increases with age and in the presence of another disease. Operational mortality in the second aortocorn shunting is 3-5 times higher than in the first; Thus, the time of the first aortocornary shunting should be optimal.

After AIC, approximately 25-30% of patients develop cognitive disorders, possibly caused by microemboli produced in AIC. Disorders range from mild to severe and can persist for weeks or even years. To minimize this risk, some centers use the "beating heart" technique (i.e., without AIC), in which special devices mechanically stabilize the part of the heart involved in the operation.

Aortocornary shunting is very effective with proper selection of patients with angina pectoris. The ideal candidate has severe angina and limited localization of arterial lesions, without other organic changes to myo (endo) carda. Approximately 85% of patients experience complete disappearance of symptoms or a marked decrease in symptoms. A stress test with physical exertion demonstrates a positive correlation between shunt patency and increased resistance to exercise, but in some cases, an increase in exercise tolerance is maintained even with shunt occlusion.

IHD can progress despite aortocornar shunting. In the postoperative period, obstruction of proximal vessels bypass grafts is often increased. Venous implants are closed earlier in the case of thrombosis and later (after several years) if atherosclerosis leads to a slow degeneration of the intima and the middle shell of the vessel. Acetylsalicylic acid prolongs the functioning of the venous shunt; Smoking has a pronounced adverse effect on the functioning of the shunt.

Aortocornary shunting improves survival of patients with left main artery disease, pathology of three vessels and low left ventricular function, as well as some patients with involvement of two vessels. However, in patients with moderate or moderate angina (grade I or II) or a pathology of three vessels and good ventricular function, aortocornary bypass surgery only slightly improves survival. In patients with single vessel damage, the results of drug treatment, NOVA and aortocornary shunting are comparable. The exceptions are lesions of the left main and proximal part of the left anterior descending artery, for which revascularization has advantages. Patients with type 2 diabetes also have better results after aortocorn bypass surgery than after NDA.

[7], [8], [9], [10]