Tension angina: treatment

Modifiable risk factors should be eliminated as much as possible. People with nicotine addiction should quit smoking: after 2 years of quitting smoking, the risk of myocardial infarction decreases to the level of patients who have never smoked. Appropriate treatment of arterial hypertension is necessary, since even moderate arterial hypertension leads to an increase in the workload of the heart. Weight loss (even as the only modifiable factor) often reduces the severity of angina.

Sometimes, treatment of even mild left ventricular failure results in marked improvement of angina. Paradoxically, digitalis preparations sometimes worsen angina, possibly by increasing myocardial contractility and thus increasing oxygen demand, or by increasing arterial tone (or both). Significant reduction of total and LDL cholesterol (by diet and medication as needed) slows the progression of coronary heart disease, may reverse some of the pathological changes, and improves endothelial function and thus arterial resistance to stress. An exercise program, especially walking, often improves quality of life, reduces the risk of coronary heart disease, and increases resistance to physical exertion.

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Medicines for angina pectoris

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

In case of an acute attack, the most effective method is to take nitroglycerin sublingually.

To prevent ischemia, all patients with diagnosed coronary artery disease or at high risk for its development should take antiplatelet drugs daily. β-Adrenergic blockers, unless contraindicated and tolerated, are prescribed to most patients. Some patients require calcium channel blockers or prolonged-release nitrates to prevent attacks.

Antiplatelet drugs prevent platelet aggregation. Acetylsalicylic acid binds irreversibly to platelets and inhibits cyclooxygenase and platelet aggregation. Clopidogrel blocks adenosine diphosphate-induced platelet aggregation. Each drug can reduce the risk of ischemic complications (myocardial infarction, sudden death), but the greatest effectiveness is achieved when they are prescribed simultaneously. Patients with contraindications to one drug should receive the other, at least one. Beta-blockers reduce the manifestations of angina and prevent myocardial infarction and sudden death better than other drugs. These drugs block sympathetic stimulation of the heart, reduce systolic blood pressure, heart rate, myocardial contractility and cardiac output, thus reducing the 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-blockers are available and effective. The dose is selected by gradually increasing it until bradycardia or side effects occur. Patients who cannot receive b-blockers, such as those with bronchial asthma, are prescribed calcium channel blockers with a negative chronotropic effect (such as diltiazem, verapamil).

Medicines used for ischemic heart disease

Medicine

Doses

Application

Antiplatelet drugs

Acetylsalicylic acid (aspirin)	For stable angina: 81 mg 1 time per day (soluble form). For ACS: 160-325 mg chewed (tablet form) upon delivery to the emergency room, then 81 mg* 1 time/day throughout hospitalization and after discharge	All patients with coronary heart disease or high risk of its development, except for intolerance to acetylsalicylic acid or contraindications to its administration; used for a long time
Clopidogrel (primarily) or Ticlopidine	75 mg 1 time/day 250 mg 2 times/day	Used with acetylsalicylic acid or (in case of intolerance to acetylsalicylic acid) as monotherapy
Glycoprotein receptor IIb/IIIa inhibitors	Intravenously for 24-36 hours	Some patients with ACS, mainly those undergoing PCI with stenting, and patients with
Abciximab	0.25 mg/kg bolus, then 10 mcg/min	High-risk unstable angina or non-ST-segment elevation MI
Eptifibatide	180 mcg/kg bolus, then 2 mcg/kg per minute
Tirofiban	0.4 mcg/kg per minute for 30 min, then 0.1 mcg/kg per minute

Beta-blockers

Atenolol	50 mg every 12 hours in the acute phase. 50-100 mg 2 times a day for a long time.	All patients with ACS, except for intolerance to beta-blockers or contraindications to their use, especially high-risk patients; used long-term
Metoprolol	1-3 boluses of 5 mg are administered at intervals of 2-5 minutes, as tolerated (up to a dose of 15 mg); then 25-50 mg every 6 hours, starting 15 minutes after the last intravenous administration, for 48 hours; then 100 mg 2 times a day or 200 mg 1 time per day (at the discretion of the physician)

Opiates

Morphine

2-4 mg intravenously as needed

All patients with chest pain due to ACS

Short-acting nitrates

Nitroglycerin sublingual (tablets or spray)	0.3-0.6 mg every 4-5 minutes until 3 times a day	All patients - for rapid relief of chest pain; taken as needed
Nitroglycerin as continuous intravenous administration	The initial rate of administration is 5 mcg/min with an increase of 2.5-5.0 mcg every few minutes until a tolerable rate is achieved.	Some patients with ACS: during the first 24-48 hours. Also patients with heart failure (except patients with hypertension), extensive anterior MI, ongoing attack of angina, hypertension (BP decreases by 10-20 mm Hg, but not more than 80-90 mm Hg for systolic pressure). For long-term use - in patients with recurrent angina and persistent pulmonary insufficiency

Long acting nitrates

Isosorbide dinitrate	10-20 mg 2 times a day; up to 40 mg 2 times a day is possible	Patients with unstable angina who continue to experience attacks after reaching the maximum dose of beta-blockers
Isosorbide mononitrate	20 mg 2 times a day with a 7-hour interval between the first and second doses
Isosorbide mononitrate sustained release	30-60 mg once a day, possibly increasing to 120 mg, sometimes up to 240 mg
Nitroglycerin patches	0.2-0.8 mg/h, apply between 6 and 9 am, remove after 12-14 hours to prevent tolerance
Ointment with nitroglycerin 2% (15 mg / 2.5 cm ointment)	1.25 cm distributed over upper chest or arm every 6-8 hours, increasing to 7.5 cm if ineffective, cover with cellophane, remove after 8-12 hours; daily to prevent tolerance

Antithrombotic drugs

Enoxaparin sodium	30 mg IV (bolus), then 1 mg/kg q sec for 12 h, maximum 100 mg	Patients with unstable angina or non-segment elevation MI Patients younger than 75 years receiving tenecteplase Almost all patients with STEMI, except those undergoing PCI within 90 min; treatment continued until PCI, CABG, or patient discharge
Unfractionated form of sodium heparin	60-70 U/kg intravenously (maximum 5000 U bolus), then 12-15 U/kg per hour (maximum 1000 U/hour for 3-4 days	Patients with unstable angina or NSTEMI may use enoxaparin sodium as an alternative.
	60 U/kg intravenously (maximum 4000 U bolus) is administered at the start of alteplase, reteplase, or tenecteplase administration, then continued at 12 U/kg per hour (maximum 1000 U/hour) for 48-72 hours	Patients with STEMI may use enoxaparin sodium as an alternative, especially in those over 75 years of age (since enoxaparin sodium combined with tenecteplase may increase the risk of hemorrhagic strokes)
Warfarin	The dose is selected until the INR is within 2.5-3.5.	Long-term use is possible

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

Nitroglycerin is a powerful smooth muscle relaxant and vasodilator. Its main points of action are in the peripheral vascular bed, especially in the venous depot, as well as in the coronary vessels. Even vessels affected by the atherosclerotic process are capable of expanding in places where there are no atheromatous plaques. Nitroglycerin lowers systolic blood pressure and expands systemic veins, thereby reducing myocardial wall tension - the main cause of increased myocardial oxygen demand. Sublingual nitroglycerin is prescribed to relieve an acute attack of angina or to prevent it before physical exertion. Significant relief usually occurs within 1.5-3 minutes, complete relief of the attack - after 5 minutes, the effect lasts up to 30 minutes. The intake can be repeated after 4-5 minutes up to 3 times if the full effect does not develop. Patients should always carry nitroglycerin tablets or aerosols in an accessible place to use quickly at the onset of an angina attack. Tablets are stored in a tightly closed glass container that does not allow light to pass through to preserve the properties of the drug. Since the drug quickly loses its effectiveness, it is advisable to keep it in small quantities, but often replace it with a new one.

Long-acting nitrates (oral or transdermal) are used if angina persists after the maximum dose of beta-blockers has been administered. If the onset of angina attacks can be anticipated, nitrates are prescribed to cover this time. Oral nitrates include isosorbide dinitrate and isosorbide mononitrate (the active metabolite of dinitrate). Their effect occurs within 1 to 2 hours and lasts from 4 to 6 hours. Slow-release forms of isosorbide mononitrate are effective throughout the day. Transdermal nitroglycerin patches have largely replaced nitroglycerin ointments, primarily because ointments are inconvenient and can stain clothing. Patches release the drug slowly, which provides a prolonged effect; Exercise tolerance increases 4 hours after patch application and continues for 18-24 hours. Tolerance to nitrates may develop primarily in cases where plasma drug concentrations are constant. Since the risk of MI is highest in the early morning hours, breaks in nitrate administration at lunchtime and early evening are reasonable unless the patient develops angina attacks during this time. For nitroglycerin, 8-10 hour intervals are probably sufficient. For isosorbide dinitrate and isosorbide mononitrate, a 12-hour interval may be required. Extended-release forms of isosorbide mononitrate do not appear to induce tolerance.

Calcium channel blockers may be used if angina symptoms persist despite nitrates or if nitrates cannot be administered. Calcium channel blockers are particularly indicated in hypertension or coronary artery spasm. Different types of these drugs have different effects. Dihydropyridines (such as nifedipine, amlodipine, felodipine) have no chronotropic effect and differ only in their negative inotropic effect. Short-acting dihydropyridines may cause reflex tachycardia and increased mortality in patients with coronary artery disease; they should not be used to treat stable angina. Long-acting dihydropyridines are less likely to cause tachycardia; they are most often used with beta-blockers. In this group, amlodipine has the weakest negative inotropic effect, which can be used in left ventricular systolic dysfunction. Diltiazem and verapamil, other types of calcium channel blockers, have negative chronotropic and inotropic effects. They can be given as a single agent to patients with beta-blocker intolerance and normal left ventricular systolic function, but they may increase cardiovascular mortality in patients with left ventricular systolic dysfunction.

Percutaneous coronary artery bypass grafting

NOVA (eg, angioplasty, stenting) is considered when angina symptoms persist despite drug treatment and are detrimental to the patient's quality of life, or when coronary artery anatomical defects (detected by angiography) suggest a high risk of mortality. The choice between NOVA and CABG depends on the extent and location of the anatomical defects, the experience of the surgeon and the medical center, and (to some extent) the patient's choice. NOVA is usually preferred when one or two vessels with suitable anatomical features are involved. Defects that are longer or located at branching sites often preclude NOVA. Most NOVA is performed with stenting rather than balloon dilation, and as stenting technology improves, NOVA is being used in increasingly complex cases. The risks of the procedure are comparable to those of CABG. The mortality rate is 1 to 3%; The incidence of left ventricular stenting is 3 to 5%. In less than 3% of cases, the vessel wall dissection occurs, creating a critical obstruction to blood flow, requiring emergency CABG. After stenting, clopidogrel is added to aspirin for at least 1 month, but preferably for 6 to 17 months, and statins, if the patient has not received them before. About 5 to 15% of stents become restenotic within a few days or weeks, requiring placement of a new stent within the previous one or CABG. Sometimes, closed stents do not cause symptoms. Angiography performed after 1 year reveals a virtually normal lumen in about 30% of the vessels in which the manipulation was performed. Patients can quickly return to work and normal physical activity, but strenuous work should be avoided for 6 weeks.

Coronary artery bypass grafting

Coronary artery bypass grafting uses sections of autologous veins (such as the saphenous vein) or (preferably) arteries to bypass diseased sections of the coronary arteries. Approximately 85% of vein grafts are functional at 1 year, while up to 97% of internal mammary artery grafts are functional at 10 years. Arteries can also hypertrophy to accommodate increased blood flow. Coronary artery bypass grafting is preferred for patients with left main disease, three-vessel disease, or diabetes.

Aortocoronary bypass grafting is usually performed using a cardiopulmonary bypass machine (CPB) on a stopped heart. The CPB pumps and oxygenates the blood. Risks of the procedure include stroke and myocardial infarction. In patients with normal-sized hearts, no history of myocardial infarction, good ventricular function, and no other contributing factors, the risk of perioperative myocardial infarction is <5%, stroke is 2% to 3%, and death is <1%; the risk increases with age and the presence of another disease. The operative mortality rate for a second aortocoronary bypass graft is 3-5 times higher than for the first; thus, the timing of the first aortocoronary bypass graft should be optimal.

After CPB, approximately 25% to 30% of patients develop cognitive impairment, possibly caused by microemboli that form during CPB. The impairment ranges from moderate to severe and may persist for weeks or even years. To minimize this risk, some centers use off-pump (i.e., off-pump) techniques, in which special devices mechanically stabilize the part of the heart that is being operated on.

Aortocoronary bypass grafting is very effective when patients with angina are selected correctly. The ideal candidate has severe angina and localized arterial lesions, without other organic myo(endo)cardial changes. Approximately 85% of patients experience complete resolution of symptoms or a marked reduction in symptoms. Exercise stress testing shows a positive correlation between bypass patency and increased exercise tolerance, but in some cases the increase in exercise tolerance persists even with bypass occlusion.

IHD may progress despite aortocoronary bypass grafting. Obstruction of the proximal bypass site vessels often increases in the postoperative period. Venous grafts are closed earlier in case of thrombosis and later (after several years) if atherosclerosis leads to slow degeneration of the intima and media of the vessel. Acetylsalicylic acid prolongs the functioning of the venous bypass; smoking has a pronounced adverse effect on the functioning of the bypass.

Aortocoronary bypass grafting improves survival in patients with left main disease, three-vessel disease, and poor left ventricular function, and in some patients with two-vessel disease. However, in patients with mild to moderate angina (class I or II) or three-vessel disease and good ventricular function, Aortocoronary bypass grafting only marginally improves survival. In patients with single-vessel disease, the results of medical therapy, NOVA, and Aortocoronary bypass grafting are comparable. The exceptions are left main and proximal left anterior descending artery disease, for which revascularization is superior. Patients with type 2 diabetes also have better outcomes after Aortocoronary bypass grafting than after PCI.

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