Treatment of angina pectoris (IHD) without surgery in Krasnoyarsk

home
Articles
For a healthy lifestyle!
Treatment of angina

If you have been diagnosed with coronary heart disease

,
angina pectoris
, your doctor will definitely prescribe you treatment - drug therapy, which he will recommend taking constantly, without interruptions. Why do you need to take medications regularly? And what drugs are used to treat angina pectoris, in what doses?

The first and most important thing in the presence of angina is to prevent complications of the disease ( myocardial infarction

, life-threatening heart rhythm disturbances, development of severe heart failure) and death, prolong your life.
Second and no less significant: improve the quality of your life, make it complete, eliminate pain. There are several main groups of drugs for the treatment of angina
. Let's figure out how they work and why doctors prescribe them for treatment.

Antiplatelet agents

Antiaggregates help prevent the formation of blood clots (thrombi), reduce the aggregation (sticking together) of platelets - blood cells that are responsible for the formation of a blood clot. The list of antiplatelet agents includes: aspirin, cardiomagnyl, thienopyridines.

Aspirin (acetylsalicylic acid)

Aspirin (acetylsalicylic acid)

– the main antiplatelet agent, it is prescribed to all patients suffering from angina pectoris (with the exception of those who cannot tolerate it, for example, allergy sufferers with the “aspirin triad”). The dose of aspirin is 75-150 mg daily. Taken once, every 20-30 minutes. after meal. Typically in the afternoon. Pay attention to the low dose! A typical aspirin tablet contains 500 mg, a dose that has been taken as an analgesic and antipyretic for over 100 years! For angina pectoris, no more than 1/4 tablet is recommended. This dose effectively prevents thrombosis and is quite safe for the stomach. When regularly taking higher doses of aspirin (acetylsalicylic acid), there is a risk of developing erosions and stomach ulcers. Since patients with angina pectoris require constant use of aspirin as treatment, special, safer forms for long-term use have been developed.

Cardiomagnyl (aspirin + magnesium hydroxide)
Cardiomagnyl (aspirin + magnesium hydroxide)
75 and 150 mg. Magnesium hydroxide, which is part of the tablet, stimulates the formation of special protective substances in the stomach wall of a patient with angina pectoris that prevent the formation of ulcers and erosions.

Enteric-coated aspirin (AspirinCardio 100 mg, ThromboAss 50 and 100 mg, CardiASK 50 mg, etc.)

. The special coating does not allow the tablet to dissolve in the stomach; absorption of aspirin occurs in the intestines. Important: these tablets must be taken whole, you cannot break them or chew them (otherwise you will damage the shell and the protective effect will disappear)!

Thienopyridines (clopidogrel, prasugrel, ticlopidine)

Thienopyridines (clopidogrel, prasugrel, ticlopidine)

– have a very pronounced antiplatelet effect, hundreds of times stronger than aspirin.
The prescription of these drugs (usually together with aspirin) is necessary in cases where the risk of thrombosis is very high: unstable angina
,
acute coronary syndrome
(“pre-infarction conditions”),
acute myocardial infarction
and cardiac surgery (
stenting
,
coronary artery bypass grafting
and etc.). Thienopyridines are also prescribed as a treatment for those patients who cannot take aspirin due to intolerance or contraindications.

Important:

Tell your doctor if you have previously had a stomach ulcer, duodenal ulcer (DU) or erosive gastritis, as well as unstable blood pressure with frequent crises, rises above 160-170/100 mm Hg. Art. This information will help your doctor make your antiplatelet treatment safe. It has been proven that regular use of antiplatelet drugs can reduce the incidence of myocardial infarction, strokes and death in patients with angina pectoris by up to 23% (in every 23 people out of 100)! After coronary angioplasty and stenting operations, doctors recommend taking aspirin and clopidogrel together for a certain period of time (from a month to several years).

Drug treatment of angina: hopes and disappointments

WITH

Modern cardiology is rightfully considered one of the most dynamically developing medical specialties. The rapid development of evidence-based medicine, along with numerous developments of new medications and methods of invasive interventions, leads to the fact that recommendations for the diagnosis and treatment of cardiovascular diseases are regularly updated with new data. At the same time, new methods for detecting and correcting cardiovascular diseases are subject to strict “selection” through rigorous clinical trials with a large number of participants and careful statistical analysis. And only diagnostic and therapeutic interventions that have convincingly proven their effectiveness are recommended for widespread use.

Angina pectoris, as a form of coronary heart disease (CHD), has long been considered one of the main cardiac problems. Of course, this is primarily due to the high prevalence of this disease and the high risk of developing myocardial infarction (MI) and other adverse consequences. In our country, as in many other countries, IHD and its consequences are the main cause of mortality

. Over the past 10–15 years, much has changed in the management of patients with angina. Beyond the scope of this review, the problems of treating unstable and vasospastic forms of angina remain. The main focus will be on new data regarding the drug treatment of stable angina, one of the most resource-intensive areas of modern cardiology.

Goal of treatment for angina pectoris

Treatment of stable angina has two goals. The first is the prevention of the development of MI and death and, accordingly, an increase in life expectancy. The second is a decrease in the frequency and intensity of angina attacks.

(ideally their complete elimination), which improves the quality of life.

From the patient's point of view, the latter goal often has a certain advantage, since it is subjectively perceived as more relevant.

However, the highest priority is given to therapy aimed at reducing the risk of MI and death. Therefore, if different therapeutic strategies are equally effective in alleviating disease symptoms, preference should be given to therapies with proven or very likely benefit in preventing death. The ideal drugs for treating a patient with coronary artery disease and angina are those that simultaneously provide a high quality of life and increase its duration. The choice of treatment often depends on the clinical response to initial drug therapy, although some patients immediately prefer myocardial revascularization procedures (angioplasty and stenting, coronary artery bypass grafting). Therefore, in the decision-making process regarding the choice of treatment, factors such as the cost-effectiveness ratio of the proposed therapy and the patient’s opinion should be taken into account. We should not forget that in many cases, using various methods of restoring coronary circulation, only one of the goals is achieved - eliminating or reducing pain, i.e. improving the quality of life, while regular drug therapy is necessary to prevent further development and progression of atherosclerosis .

Drug therapy to prevent myocardial infarction and death

Antiplatelet agents

In all modern cardiological guidelines, the use of antiplatelet drugs is a mandatory component of the treatment of coronary artery disease and angina pectoris.

, in particular. The main antiplatelet drugs in the arsenal of a modern doctor are aspirin, ticlopidine, clopidogrel.

of acetylsalicylic acid (aspirin) is based on

inhibits cyclooxygenase and platelet thromboxane A2 synthesis.
, the risk of adverse cardiovascular outcomes - MI, sudden death - is reduced
by an average of .

Ticlopidine inhibits platelet aggregation caused by ADP, thrombin, collagen, thromboxane A2 and platelet aggregation factor. In addition, in stable angina, ticlopidine reduces blood viscosity, reducing the concentration of plasma fibrinogen. Long-term use of the drug is limited due to side effects, the most dangerous of which are neutropenia and thrombocytopenic purpura.

Clopidogrel, like ticlopidine, is a thienopyridine derivative, but is superior to ticlopidine in its antithrombotic effect. In comparative studies, clopidogrel was superior to aspirin in reducing the combined risk of MI, vascular death, and stroke among patients with post-infarction cardiosclerosis, stroke, and peripheral atherosclerosis.

CURE Randomized Trial

, which included more than 12,500 patients, convincingly proved the effectiveness of clopidogrel (300 mg/day in the acute period, then 75 mg/day) in combination with aspirin (75–325 mg/day) in preventing (on average 20%) the likelihood of heart attack and stroke and death from cardiovascular complications in patients with unstable angina and other acute coronary syndromes.
Recently, this drug was recommended by the American Food and Drug Administration as a drug of choice in the intensive care of acute coronary syndromes. However, the advisability of prescribing clopidogrel for stable angina in randomized prospective studies has not yet been sufficiently studied. Despite the CAPRIE
a reduction in the combined risk of cardiovascular complications during long-term use of clopidogrel, the widespread use of this drug for coronary artery disease is still hampered by the unclear risk-benefit ratio with long-term use, as well as the relatively high cost. It should also be remembered that although clopidogrel is less likely than aspirin to cause dangerous gastrointestinal bleeding, taking clopidogrel is 30% more likely to cause diarrhea and skin rashes.

The results of a meta-analysis of the comparative effectiveness and safety of prescribing various doses of aspirin for the purpose of long-term secondary prevention of cardiovascular complications are interesting (Table 1).

Considering the widespread prescription of aspirin for long-term use for a variety of cardiovascular diseases (including the elderly), questions of the safety of therapy with this drug become very relevant. It should be noted that a special prospective study on the comparative assessment of different doses of aspirin is only being planned. However, data obtained earlier and summarized in a meta-analysis indicate that when taking small doses of aspirin (75–150 mg/day), all platelet cyclooxygenase is almost completely blocked after a few days, which ensures the antithrombotic effect of the drug. Taking medium (160–325 mg/day) and high (500–1500 mg/day) doses of aspirin does not enhance its antithrombotic activity and, accordingly, does not increase the preventive feasibility of taking it. Along with this, medium and high doses of aspirin cause significantly more frequent complications (usually gastrointestinal bleeding, including life-threatening ones).

It appears that low-dose aspirin (75–150 mg/day) should be prescribed to stable patients until solid evidence is available for secondary prevention of vascular complications.

, and in acute vascular complications (unstable angina, MI) and invasive interventions on the coronary arteries (angioplasty, stenting, atherectomy), when a rapid antiplatelet effect is required, it is necessary to use higher doses (>325 mg/day) - followed by a decrease to reduce risk of hemorrhagic complications.

Anticoagulants

Small placebo-controlled studies have examined the effect of daily subcutaneous administration of low molecular weight heparin in patients with stable angina. A decrease in plasma fibrinogen levels, an improvement in exercise tolerance, an increase in the time of exercise before the appearance of signs of ischemia on the ECG, and a decrease in the amplitude of ST segment depression on the ECG were demonstrated. But clinical experience with such therapy is still small, and its effect on prognosis has not been studied. More modern drugs, recombinant hirudin and platelet IIb/IIIa receptor antagonists, have also not demonstrated effectiveness in clinical studies in patients with stable angina. Therefore, these drugs should not yet be recommended for widespread use in stable angina.

Taking indirect anticoagulants in the absence of antiplatelet therapy

The effectiveness of indirect anticoagulants in ischemic heart disease was assessed in a meta-analysis of 20 randomized clinical trials. In 16 of these studies, patients received high-dose anticoagulants (INR>2.8) (total of 1056 patients), and in 4 studies medium-dose anticoagulants were prescribed (total of 1365 patients). No studies included concomitant regular antiplatelet therapy. It turned out that against the background of high doses of anticoagulants, the combined risk of developing myocardial infarction and stroke was significantly lower than in the control groups (reduced odds of development – 43% with a 95% confidence interval of 37–49%, reduction in absolute risk 9.8%) . The effect of average doses of anticoagulants was smaller and statistically insignificant. In a direct comparison of high- and medium-dose anticoagulants with aspirin, there was no difference in the effect on mortality and the combined risk of myocardial infarction and stroke (odds ratio 1.04, 95% confidence interval 0.80–1.34). However, compared with placebo, high-dose anticoagulants were associated with an almost sixfold increase in the incidence of major (usually intracranial) bleeding (odds ratio 6.0, 95% confidence interval 3.3–17.6). Compared with aspirin, prophylactic anticoagulants increased the risk of major bleeding by almost 2-fold (odds ratio 2.4, 95% confidence interval 1.6–3.6).

Thus, isolated use of high doses of anticoagulants is accompanied by a significant reduction in the risk of cardiovascular complications in coronary artery disease. Due to the fact that the risk of severe bleeding exceeds that while taking antiplatelet agents, constant monitoring of patients and monitoring of coagulograms is necessary. Taking low to medium doses of aspirin is as effective as taking anticoagulants

, however, the risk of complications of antiplatelet therapy is much lower, and it is easier to monitor patients taking aspirin.
The frequency of bleeding against the background of various doses of aspirin is presented in Table 2. Taking indirect anticoagulants in combination with antiplatelet agents
The same meta-analysis assessed the effectiveness of the combination of indirect anticoagulants and antiplatelet agents in the secondary prevention of coronary artery disease. A total of 6 randomized studies with a total number of 8915 participants were reviewed. In 3 studies (8435 patients), taking low doses of anticoagulants (INR <1.5) did not lead to a significant change in the combined risk of MI and stroke (odds ratio 0.91 with 95% confidence interval 0.79–1.06). At the same time, an unreliable increase in the risk of severe bleeding was shown when combining aspirin with low and high doses of indirect anticoagulants. In the remaining studies, where patients received more active anticoagulant therapy (INR 2–3), the sample size was insufficient (480 patients) to calculate the effectiveness and safety of treatment. Several randomized clinical trials are currently investigating this issue.

The same meta-analysis assessed the effectiveness of a combination of indirect anticoagulants and antiplatelet agents in the secondary prevention of coronary artery disease. A total of 6 randomized studies with a total number of 8915 participants were reviewed. In 3 studies (8435 patients), taking low doses of anticoagulants (INR <1.5) did not lead to a significant change in the combined risk of MI and stroke (odds ratio 0.91 with 95% confidence interval 0.79–1.06). At the same time, an unreliable increase in the risk of severe bleeding was shown when combining aspirin with low and high doses of indirect anticoagulants. In the remaining studies, where patients received more active anticoagulant therapy (INR 2–3), the sample size was insufficient (480 patients) to calculate the effectiveness and safety of treatment. Several randomized clinical trials are currently investigating this issue.

Lipid-lowering drugs

To date, there is no doubt that a decrease in plasma cholesterol levels with a high risk of complications of coronary artery disease is accompanied by a significant decrease in the risk of cardiovascular complications, including fatal ones, as well as a decrease in overall mortality. Among all methods of drug monotherapy, HMG-CoA reductase inhibitors (statins) most effectively reduce both cholesterol levels and the risk of cardiovascular complications

. The last decade has been marked by an avalanche-like accumulation of evidence of the beneficial effect of statins on morbidity and mortality rates in a variety of categories of patients - men, women, with concomitant diabetes, atherosclerosis of peripheral and cerebral arteries, etc. This has led medical practitioners to become more proactive in prescribing statins. However, there is evidence that many categories of patients are “undertreated” with statins, largely due to the lack of convincing evidence of the effectiveness of this class of drugs in women, in the elderly, and with initially normal and low plasma cholesterol levels. Questions also remain unclear about the doses at which statins should be prescribed, as well as the comparative effectiveness of various drugs.

To date, the most data has been obtained on the secondary prevention of coronary artery disease with pravastatin and simvastatin.

As part of the meta-study The Prospective Pravastatin Pooling project

A cumulative analysis of the results of 3 large prospective randomized trials of pravastatin in the primary and secondary prevention of coronary artery disease was conducted. The effectiveness of pravastatin in secondary prevention was assessed in a total of 13,173 patients treated with pravastatin 40 mg/day for 5 to 6 years. Among those taking pravastatin, there was a reduction in overall mortality to 7.9% versus 9.8% in the placebo group (a relative risk reduction of death of 20% with a 95% confidence interval of 12–27%). In addition, pravastatin reduced the risk of coronary death by 24% (95% confidence interval 14–33%).

A new stage in the prevention of cardiovascular diseases was the results of the use of simvastatin for primary and secondary prevention of cardiovascular diseases and complications in the Heart Protection Study (HPS)

, which will have a significant impact on the management strategy of patients suffering from angina pectoris.

Angiotensin-converting enzyme inhibitors

ACE inhibitors (ACE inhibitors) have not confirmed direct anti-ischemic effectiveness, although this group of drugs is used very widely in the treatment of angina attacks provoked by increased blood pressure.

A review of randomized clinical trials (with a total of 5966 participants) found convincing evidence that the use of ACE inhibitors for left ventricular dysfunction after myocardial infarction significantly reduces mortality, the rate of hospitalization for congestive heart failure, and the risk of recurrent nonfatal myocardial infarction compared with placebo. The effectiveness of the use of ACE inhibitors after MI in the absence of left ventricular dysfunction or in patients with stable coronary artery disease without clinical manifestations of circulatory failure has not yet been sufficiently studied. HOPE trial

(9297 patients with a high risk of developing cardiovascular complications, average follow-up period of 4.7 years) indicate a beneficial effect of ramipril at a dose of 10 mg/day on the main indicators of morbidity, overall and cardiovascular mortality and on the need for myocardial revascularization.

This issue is currently being investigated in two large multicenter studies. In the PEACE

During a 5-year follow-up, the addition of the ACE inhibitor trandolapril 4 mg or placebo to standard therapy in more than 8000 patients with stable coronary artery disease without left ventricular dysfunction (ejection fraction more than 40%) and its effect on such “hard” endpoints as death from heart disease –vascular causes and MI.

Another major study, results expected in 2003, is EUROPA.

.
In 10,500 patients with coronary artery disease without significant left ventricular dysfunction, the effect of long-term (more than 3 years) treatment with perindopril, an inhibitor with high specificity for tissue ACE, is being studied. The primary objective of the EUROPA trial is to evaluate the effect of perindopril at a daily dose of 8 mg on the composite endpoint of all-cause death, nonfatal myocardial infarction, unstable angina, and cardiac arrest followed by successful resuscitation. A wide range of cardiovascular complications (death from cardiovascular causes, heart failure, the need for myocardial revascularization procedures, stroke, etc.) was selected as secondary goals. As part of this study, to study the mechanisms of the beneficial effect of ACE inhibitors in this category of patients, 2 fragments are planned - PERSPECTIVE and PERFECT, which will clarify the mechanisms of the beneficial effect of ACE inhibitors on the development of atherosclerosis. PERSPECTIVE
trial will evaluate the effect of perindopril on coronary artery wall structure as measured by quantitative coronary angiography and intravascular ultrasound (IVUS). In this study, using the most accurate assessment method to date, IVUS, the effect of perindopril on the progression of coronary atherosclerosis over 3 years will be studied in 400 patients with stable coronary artery disease without signs of left ventricular dysfunction.

PERFECT Study

will study the effects of perindopril on brachial artery endothelial function in 300 patients. Flow-dependent dilatation of the brachial artery using high-resolution ultrasound will be determined before randomization and after 6, 12, 24 and 36 months of treatment with perindopril or placebo. The primary purpose of this excerpt will be to assess the percentage of change in flow-dependent dilatation of the brachial artery between baseline and 36 months of follow-up, as well as the percentage of change in the severity of brachial artery vasoconstriction due to neurohormonal activation during the cold test at the same time. These studies will help to definitively determine the place of ACE inhibitors in the treatment of patients with stable angina without impairment of the functional state of the left ventricle in order to improve the prognosis.

Hormone replacement therapy with estrogen

Many early observational studies showed that the administration of isolated or combined hormone therapy with estrogens and progestins to postmenopausal women with signs of coronary artery disease reduces the severity of risk factors for coronary artery disease (normalizes plasma lipids) and the risk of adverse complications of coronary heart disease by 35–80%. However, in the large prospective placebo-controlled HERS

(2763 postmenopausal women with coronary artery disease, follow-up period 4.1 years), the administration of combined hormone replacement therapy did not lead to a significant reduction in the risk of developing unstable angina, congestive heart failure, circulatory arrest, transient cerebrovascular accident, peripheral arterial thrombosis, non-fatal myocardial infarction, general mortality and mortality from ischemic heart disease. Hormone replacement therapy also did not reduce the need for myocardial revascularization. The isolated use of estrogens without progestins for the prevention of coronary artery disease has not been studied in randomized clinical trials.

At the same time, long-term use of estrogens was more often accompanied by the development of peripheral venous thrombosis and pulmonary embolism, endometrial and breast cancer, as well as gallbladder diseases.

Nitrates

Many doctors traditionally begin treatment of angina by prescribing nitrates, which are available in various dosage forms. These drugs improve exercise capacity, increase the time to onset of angina, and reduce ST segment depression on the exercise ECG. The disadvantage of nitrates is the development of tolerance to them and side effects that make their use difficult. It is also unknown whether nitrates improve the prognosis in patients with stable angina with long-term use, which makes the advisability of their use in the absence of angina pectoris (myocardial ischemia) questionable. In many cases, nitrates are used during periods of deterioration or when additional stress is expected (on demand).

b-blockers

β-blockers reduce heart rate and blood pressure during exercise, delay or prevent the development of pain and ischemic ECG changes. When selecting a dose, they are guided by the frequency of attacks; usually they try to slow down the heart rate to 55–60 beats/min. In the absence of contraindications

(and there are quite a lot of them)
we should strive for the mandatory prescription of b-blockers to all patients with stable angina
, since it is assumed (albeit less proven than after MI) that they have a beneficial effect on the prognosis. The previously described negative metabolic effects of b-blockers (deterioration of lipid parameters) are usually insignificant and are most often not taken into account. New members of the β-blocker class with additional vasodilator, antioxidant, and endothelial protectant properties are generally better tolerated and have a more favorable metabolic profile, but it is not yet known to what extent these benefits are realized with long-term use. The need to monitor the prescription of b-blockers and the side effects encountered lead to the fact that doctors do not always use this valuable class of drugs.

Calcium antagonists

Usually prescribed when the antianginal effect of nitrates or b-blockers is insufficient. Calcium antagonists are especially indicated for the treatment of vasospastic angina.

.
These are drugs with different hemodynamic effects (the group of dihydropyridines and drugs with rhythm-slowing effects verapamil and diltiazem) and, accordingly, a spectrum of side effects, which must be taken into account when choosing a drug. For long-term treatment of angina from dihydropyridine derivatives, it is recommended to use only long-acting dosage forms or long-acting new generations of calcium antagonists ( amlodipine
).
In addition, the use of amlodipine
is particularly effective for controlling increased blood pressure and treating arterial hypertension, which is a risk factor for the development of coronary artery disease.
Short-acting forms of nifedipine are not indicated for the treatment of patients with coronary artery disease. It is also necessary to take into account the negative inotropic effect of diltiazem and verapamil and avoid their use in patients with impaired left ventricular systolic function and especially in clinical manifestations of heart failure. Although a beneficial effect of calcium antagonists on the course of atherosclerosis (prevention of the development of new atheromas) is expected, evidence of an improvement in the prognosis of patients with angina pectoris with their regular use is not yet available. This issue is being studied in large studies - CAMELOT
(amlodipine),
ACTION
(nifedipine SL, GITS),
INVEST
(verapamil).

Other antianginal agents

Nicorandil is an activator of ATP-dependent potassium channels. Developed in 1984 in Japan, it is used for angina pectoris in European countries. Similar to nitrates in terms of the mechanism of venodilating action, it also has the properties of an arteriolodilator - through its effect on ATP-dependent potassium channels in the cell membrane. In experimental and clinical observations, nicorandil

has repeatedly demonstrated anti-ischemic properties, which were explained by its ability to “adapt” the myocardium to prolonged episodes of ischemia.

The IONA trial, a large, randomized, placebo-controlled trial, was conducted in the UK to test the effect of nicorandil on clinical outcomes in angina.

(Impact Of Nicorandil in Angina), which involved 5126 patients with stable angina (mean age 67 years, 24% women) and various associated cardiovascular risk factors (left ventricular hypertrophy, arterial hypertension - 46%, left ventricular systolic dysfunction , diabetes mellitus – 8%). 89% of patients included in the study had functional class I–II angina (according to the NYHA classification). In addition to antiplatelet agents, antianginal (b-blockers, calcium antagonists) and lipid-lowering therapy (statins) and ACE inhibitors, according to indications, study participants received nicorandil (40 mg/day in 2 doses) or placebo for 12–36 months (average 1 ,6 years). The summary primary endpoint was death from coronary artery disease, nonfatal myocardial infarction, and hospitalization for angina. Secondary endpoints were death from coronary artery disease and nonfatal myocardial infarction. Nicorandil significantly (by 17%) reduced the risk of the primary endpoint, mainly due to a reduction in the incidence of acute coronary syndromes without MI (by 21%) and the total number of cardiovascular complications (14%). Overall mortality did not change significantly during treatment with nicorandil, although a tendency towards its decrease was noted (by 15%). One of the side effects when taking nicorandil is headache.

Metabolic drugs

Recently, there has been significant interest in the metabolic approach in the treatment of stable angina. This approach allows you to avoid adverse consequences when prescribing or increasing doses of hemodynamic active agents (nitrates, b-blockers, calcium antagonists) in the form of a decrease in blood pressure, bradycardia, etc. A number of controlled studies have shown that trimetazidine

, so far the only approved drug of this group for the treatment of angina, both in monotherapy and in combination with any class of antianginal drugs, not only reduces the number of angina attacks and the need for nitroglycerin, but also significantly increases the duration of physical activity and the time until the onset of segment depression ST on ECG.
Recently, the mechanism of action of trimetazidine has been more precisely established - selective inhibition of “long-chain” 3-ketoacyl-CoA thiolase, an enzyme involved in the oxidation of free fatty acids, and this class is called 3-CAT inhibitors
.
A new dosage form of the drug, trimetazidine MB
, prescribed 35 mg twice a day, should significantly increase patient adherence to treatment.

Another representative of this group is ranolazine

, a partial inhibitor of fatty acid oxidation, was evaluated in 2 clinical placebo-controlled studies - as monotherapy at doses of 500 mg, 1000 mg and 1500 mg twice daily (
MARISA
) and as part of combination therapy when added to other antianginal agents in doses of 750 mg and 1000 mg 2 times a day (
CARISA
). By the 12th week of administration, ranolazine, according to the treadmill test, increased the time of pain-free walking, the total time of physical activity and the time until the appearance of ischemic changes on the ECG. A small but significant dose-dependent increase in the duration of the QT segment on the ECG was noted, although not accompanied by clinically significant rhythm disturbances. The study of the safety and tolerability of ranolazine, as well as its effect on the prognosis of stable angina, is currently ongoing (the drug has not yet been registered).

Thus, in the doctor’s arsenal for the successful treatment of a patient with stable angina, there are many drugs with proven clinical effects, including a beneficial effect on the prognosis.
Literature:
1. “Evidence-based medicine.” Annual directory. Issue 1. Moscow, MediaSphere Publishing House, 2002. P.140–184

2. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST–segment elevation. N Engl J Med, 2001 Aug 16; 347(7):494–502

3. CAPRIE Steering Committee. Clopidogrel vs Aspirin in Patients at Risk of Ischemic Events A randomized, blinded trial of clopidogrel versus aspirin in patients at risk of ischemic events (CAPRIE). Lancet 1996;348:1329–39

4. Collaborative meta-analysis of randomized trials of antiplatelet therapy for prevention of death, myocardial infarction and stroke in high risk patients. BMJ 2002 Jan 12;324(7329):71–86

5. Hankley GJ, Sudlow CLM, Dunbabin DW, et al “Thienopiridine derivatives (ticlopidine, clopidogrel vs aspirin) for preventing stroke and other serious vascular events in high vascular risk patients” In: The Cochrane Library, Issue 2, 2000. Oxford: Update Software

6. Anand SS, Yusuf S “Oral anticoagulant therapy in patients with coronary artery disease: a meta-analysis” JAMA, 1999;282:2058–2067

7. Flatber M, Kober L, Pfeffer MA, et al “Metaanalysis of individual patient data from trials of long-term ACE-inhibitor treatment after acute myocardial infarction (SAVE, AIRE and TRACE studies)” Circulation, 1997;96(suppl 1 ):I–706

8. The Heart Outcomes Prevention Evaluation (HOPE) Investigators. Effects of angiotensin–converting enzyme inhibitor, ramipril, on cardiovascular events in high–risk patients. N Engl J Med 2000;342:145–153

9. Hulley S, Grady D, Bush T. et al “Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women.” JAMA 1998;280:605–613

10. The LIPID Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med 1998;339:1349–1357

11. Simes J, Furberg CD, Braunwald E, et al “Effects of pravastatin on mortality in patients with and without coronary heart disease across a broad range of cholesterol levels. The Prospective Pravastatin Pooling project" Eur Heart J, 2002; 23(3):207–215

12. Shepherd J, Cobbe SM, Ford I, et al. “Prevention of coronary heart disease with pravastatin in men with hypercholesterolaemia.” N Engl J Med 1995;333:1301–1307

13. Sacks FM, Pfeffer MA, Moye LA, et al “The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels.” N Engl J Med 1996;335:1001–1009

14. Zhilyaev EV, Urzhumova TV, Glazunov AV, et al. “Clinical aspects of the use of trimetazidine (preductal) as an antianginal drug” Ter. Archive 2000;72(8):20–3

15. Zaslavskaya RM, Kelimberdieva ES, Komissarova IA, et al. “Comparative effectiveness of combination therapy with preductal and a combination of amino acids in elderly patients with coronary heart disease and angina pectoris of functional class II–III” Ter. Archive 1999;71(11):58–61

16. “The IONA Study Group. Effect of nicorandil on coronary events in patients with stable angina: the Impact Of Nicorandil in Angina (IONA) randomized trial" The Lancet 2002;359(9314):1269–1275

17. ACC/AHA/ACP–ASIM Guidelines for the management of patients with chronic stable angina. J Am Coll Cardiol 1999;33(7):2081–2118

18. Melandri G, Semprini F, Cervi V, et al “benefit of adding low-molecular weight heparin to the conventional treatment of stable angina pectoris. A double-blind randomized placebo-controlled trial.” Circulation 1993;88:2517–23

19. Van der Bos AA, Deckers JW, Heyndricks GR, et al. “Safety and efficacy of recombinant hirudin vs heparin in patients with stable angina undergoing coronary angioplasty.” Circulation 1993;88:2058–66

20. Simoons ML, Vos J, de Feyter PJ, et al. EUROPA substudies, confirmation of pathophysiological concepts. Eur Heart J 1998; 19 (Suppl J): 56–60.

21. The HOPE Study Investigators. Effects of an angiotensin–converting enzyme inhibitor, ramipril, on death from cardiovascular causes, myocardial infarction, and stroke in high–risk patients. N Engl J Med 2000; 342:145–53.

22. Pfeffer MA, Domanski M, Rosenberg Y, et al. Prevention of events with angiotensin–converting enzyme inhibition (the PEACE study design). Am J Cardiol 1998; 82(Suppl H): 25–30.

23. Fox KM, Henderson JR, Bertrand ME, et al. The European trial on reduction of cardiac events with perindopril in stable coronary artery disease (EUROPA). Eur Heart J 1998; 19 (Suppl J): 52–55

Statins

Statins – antiatherosclerotic drugs

, reduce the level of “bad” cholesterol in the blood (total cholesterol, LDL, triglycerides), increase the level of “good” cholesterol (HDL). With long-term use of the drug in a dose that allows you to control cholesterol at the target level, they can stop the growth of atherosclerotic plaques and even reduce their size. Target cholesterol levels depend on the prevalence of atherosclerosis in the body and associated diseases (for example, diabetes). Ask your doctor what your target levels should be and monitor the effectiveness of treatment (blood tests for cholesterol and lipids) at least 4 times a year. There is no habituation to statins or development of dependence; treatment with statins should be carried out continuously. If you stop taking it on your own, then within one month after stopping the drug, your blood lipid levels return to baseline.

Statins

can reduce the risk of
myocardial infarction
and stroke by up to 30-40% (in every 30-40 people out of 100), and this effect is more pronounced in diabetics!
The fact that statins save lives became known after several large studies, which involved thousands and tens of thousands of patients with angina pectoris
, diabetes mellitus, and peripheral atherosclerosis.
Today, statins are recommended for treatment not only for patients with angina
, but also for people without coronary artery disease, with several risk factors, for the prevention of atherosclerosis, heart attack and stroke.
Four drugs in this group are registered in Russia: simvastatin (Zocor), rosuvastatin (Crestor), atorvastatin (Liprimar) and fluvastatin (Leskol).

How to take statins

Take statins in the evening (before bedtime). There are medications that can be taken at any time of the day. Nausea and stool disturbances are possible. The use of statins is not recommended for persons with active liver disease or during pregnancy and breastfeeding. A very rare side effect is muscle pain. If you start taking the drug and notice soreness in all the muscles of your body, be sure to tell your doctor to avoid unwanted complications. If you do not tolerate statins well or taking the maximum therapeutic dose does not allow you to control lipid levels, then it is possible to reduce the dose and add a cholesterol absorption inhibitor, ezetimibe. Your doctor may also recommend the use of other lipid-lowering drugs for treatment: fibrates, delayed-release nicotinic acid.

Methods for diagnosing angina pectoris

Treatment of angina begins with diagnosing the condition of the coronary vessels. For this purpose, procedures such as:

ECG

Electrocardiography (ECG) is a basic diagnostic procedure in cardiology. Patients with angina pectoris are also recommended to undergo daily ECG monitoring.