Effectiveness of cardiac rehabilitation after percutaneous transluminal coronary angioplasty (PTCA)

In several large studies, the effectiveness of cardiac rehabilitation based on physical training (PT) has been studied in patients after percutaneous transluminal coronary angioplasty (PTCA). In the ETICA study (Execise Training Intervention after Coronary Angioplasty), the effect of PT on clinical outcomes was studied in 118 patients who underwent PTCA with one CA (n = 81) or two CA (n = 37).

Patients were randomized to the group in which they performed FT, and the group of routine practice. Physical training (FT) (3 times a week for 6 months) consisted of physical exertion (FN) on an exercise bike (30 min) and gymnastics (15 min). At the beginning and at the end of the study, a stress test was carried out, the stopping criteria for which were patient fatigue, the achievement of the target heart rate or ST-segment depression> 1 mm.

Indicators of VO2max and quality of life increased by 26% (p <0.001) only in the FT group. The frequency of angiographically confirmed CA restenoses (narrowing> 50%) for 6 months of observation did not differ in the two groups (29% vs 33%), but the intracavitary diameter of the CA at the intervention site in the TF group was 30% higher (p <0.05) .

Progression of the disease and new lesions in large CA (narrowing> 20%) in the TF group were observed much less frequently. Cardiac ischemia, which was assessed by the presence of defects during waist perfusion during myocardial scintigraphy, was also observed less frequently in trained patients. The observation period after the completion of the intervention was 33 ± 7 months. During this time, no deaths occurred in any of the groups, however, in the TF group, AMI (1 vs 3) was less frequently noted (p <0.008) and percutaneous transluminal coronary angioplasty (PTCA) was performed (4 vs 11) or CS ( 2 vs 5).

This study was conducted prior to the widespread use of stents during PTCA and the use of drug-eluting stents. Thus, only 19 patients from the FT group and 18 patients from the control group had stents installed.

In addition, they did not use lipid-lowering therapy because they evaluated the effect of TF on lipid levels. Consequently, it is not clear that PT would have given a similar slowdown in the development of atherosclerosis and a reduction in the frequency of cardiac events if they performed comprehensive modern therapy. In addition, it is not clear to what extent the improvement of the condition of the coronary artery (CA) occurred due to structural changes in atherosclerotic plaques, and to which due to the improvement of endothelial function.

Effectiveness of cardiac rehabilitation in myocardial infarction

In 4 meta-analyzes, the effect of cardiac rehabilitation based on physical training (PT) on clinical outcomes was studied. All of them showed similar results, since based largely on the same research.

The most recent analysis summarized 48 studies with a total of 8940 included patients, randomized or in cardiac rehabilitation groups, or in routine practice groups. Total mortality and mortality from cardiac causes were lower in the cardiac rehabilitation groups by 20 and 26%, respectively (p <0.05 for both indicators). Repetitive MIs were noted 20% less frequently, but this difference was not statistically significant.

Most of the studies included in this meta-analysis were conducted prior to the development of modern strategies for revascularization, so it is possible that many patients in these early studies showed residual coronary stenosis and inducible ischemia. At present, such patients are usually given PTCA or CSH.

Even with the established positive effect of cardiac rehabilitation on myocardial ischemia, due to the widespread use of myocardial revascularization interventions, there is no certainty that cardiac rehabilitation will show a similar decrease in cardiac mortality. The most recent meta-analysis revealed no differences in studies conducted before and after 1995, therefore, the positive effects of cardiac rehabilitation can be considered legitimate for modern cardiological practice.

There were also no differences between the effect of physical training (PT) and more comprehensive rehabilitation programs, which confirms the role of PT in reducing heart mortality.

The results of meta-analyzes confirm the positive effect of physical training (PT), however, none of the studies had sufficient statistical power to confirm the reduction in cardiovascular mortality after cardiac rehabilitation.

Meta-analyzes are often criticized because of their tendency to focus on positive research results. On the other hand, the inclusion of studies based only on TF in meta-analyzes can lead to an underestimation of the effectiveness of complex cardio-rehabilitation. To address these concerns, two large-scale comprehensive cardiac rehabilitation studies are currently underway.

The study GOSPEL (Global Secondary Prevention Strategies for Limit Events after Myocardial Infarction) included 3241 patients from 78 centers in Italy. All patients after 3 months of the standard rehabilitation program will be randomly assigned to a group of 3-year intensive rehabilitation program and a standard observation group in the district clinic.

In the intensive rehabilitation group, they will conduct physical training (TF), lifestyle counseling and RF, and regular clinical examinations once a month for 6 months and then 2 times a year until the end of the study.

In a study of DANREHAB (Danish Cardiac Rehabilitation) with 770 patients with IHD, HF, or those at high risk of developing IHD, an intensive hospital cardiorehabilitation program is carried out for 6 weeks, followed by outpatient observation for 12 months. The program includes TF, nutritional recommendations, counseling on RF, smoking cessation and clinical examinations. Supposed to recruit 1800 patients. When the results of the study will be presented and whether it will be possible to include such a number of patients in the study is unknown.

Effectiveness of cardiac rehabilitation in angina pectoris

Currently, most patients with angina pectoris can cope with the symptoms of the disease using drug therapy or myocardial revascularization with PTCA or CS. Most of the evidence (with rare exceptions) that physical exercise (PT) increases exercise tolerance (TFN) in patients with angina pectoris, was obtained before 1990. FT increases the duration of FN before the onset of angina pectoris or completely eliminates angina pectoris by at least least two mechanisms.

First, physical training (PT) reduces the oxygen demand of the myocardium during submaximal FN. FT endurance increase VO2max. Since the change in HR and SAD during an FN is associated more with the degree of increase in VO2max (depending on the nature of the FN, and not from its absolute value), an increase in VO2max with FT leads to a decrease in the increase in HR and SAD per submaximal load. This reduction in double work reduces myocardial oxygen demand and retards the onset of an attack of angina.

Secondly, physical exercise (TF) reduces ED. Normal CAs in response to FNs expand, and for atherosclerotic-affected CAs, ED is manifested, which is manifested in FN by vasoconstriction. According to continuous coronary angiography performed on the background of the introduction of endothelial acetylcholine agonist to patients, FN reduce ED. The fact that in some patients at the very beginning of the FN an increase in blood pressure is observed also confirms the concept of the significance of endothelial function.

Physical training (FT) is considered to be shown (at least in the USA) to patients with angina in cases where it is impractical or impossible to perform surgical interventions on spacecraft. However, a recent clinical study led to a reconsideration of this approach. Hambrecht S. et al. studied the dynamics of physical performance, anatomical features of spacecraft and clinical outcomes in 101 men <70 years old with stable angina, who were randomized into 2 groups: in the first group, PT was performed during the year, and the second group of patients underwent PTCA.

Physical training (FT) was performed for 2 weeks, 6 days a week. TF included a 10-minute FN with training heart rate = 70% of the maximum in combination with daily 20-minute home TF iodine weekly 60-minute controlled TF.

In each group, 47 patients completed the study. The level of physical performance increased by 30% in trained patients and by 20% in those who underwent PTCA. Moreover, the differences were not significant, however, the increase in the maximum physical performance (20% vs 0%) and VO2max (16% vs 2%) were significantly higher in the trained patients. In the latter, the degree of spacecraft lesion did not change, and among patients who underwent PTCA, only 15% had restenosis, defined as a narrowing (> 50%) of the vessel at the site of angioplasty.

The progression of coronary heart disease (CHD), as measured by angiography, was lower in the FT group. 88% of patients from the PTCA group and only 70% of the patients from the TF group suffered acute Ssob, including myocardial infarction, stroke, revascularization procedure, or hospitalization for angina pectoris. Moreover, the difference was statistically significant. These results require confirmation. Due to the specificity of the selection criteria, they cannot be applied to all patients with stable angina. However, these results clearly demonstrated that PT can make a definite contribution to the treatment of patients with angina.

Physiology of physical activity and training for heart disease

a) Maximum oxygen consumption. Aerobic and static loads increase the body’s need for oxygen to provide energy to working muscle groups. The amount of energy used during FN is determined through oxygen consumption (VO2). The modified Fick formula: CB = VO2 / L (A – B) 02, where CB is a cardiac output, VO2 is oxygen consumption, Δ (A – B) O2 is the difference in 02 between arteries (A) and veins (B). In other words, the oxygen consumption depends on the CB and Δ (A – B) O2.

Thus, the metabolic needs when performing FN require an increase in oxygen delivery, which is provided by an increase in Δ (A – B) O2 and an increase in CB, which, in turn, depends on the heart rate and stroke volume (EI) of the heart. Δ (A – B) O2 during the execution of FN increases due to the redistribution of blood and, accordingly, oxygen from non-working tissues (for example, the kidneys and organs of the abdominal cavity) to working muscles. In addition, in working muscles, blood viscosity increases due to the transition of a certain part of blood plasma into the interstitial space. An increase in CB during FN is closely related to VO2. Thus, an increase in VO2 per liter leads to an increase in the total nitrogen concentration by = 6 l.

The maximum power of FN is defined as the maximum oxygen consumption (VO2max) that is transported in a person when performing FN until the moment when it is stopped due to fatigue or shortness of breath. Individual VO2max is a stable and reproducible indicator of physical performance. It is expressed either in absolute terms (l / min) or relative to MT (ml / kg / min). The maximum increase in Δ (A – B) O2 is a fixed value and is = 15-17 vol%. Since the intensity of the FN determines the oxygen consumption, which depends on the CB and Δ (A – B) O2, and the maximum Δ (A – B) O2 is a relatively constant value, the maximum power of the FN and VO2max indirectly indicate the maximum myocardial contractility (or maximum CB) and PP).

b) Myocardial oxygen consumption. Oxygen consumption by the myocardium (MVO2) is determined by the levels of HR and SBP through the so-called dual product: HR (beats / min) x CAD (mm Hg). Human physical performance depends on the consumption of oxygen and CB, and the degree of increase in heart rate and SBP during the FN is determined by the increase in oxygen demand (as a percentage of VO2max). Consequently, for any absolute value of the FN, a person with a large VO2max uses less of his reserve and, at a high FN, has a lower heart rate and an AAD. The key point: the myocardial oxygen demand is determined not only by the severity of the FN, but by the ratio of the severity of the load to the maximum physical performance.

c) Respiratory threshold. Carbon dioxide emissions (VCO2) with FN also increase. The increase in VO2 and VCO2 occurs in parallel, but the intensity of the release of CO2 increases faster. The amount at which an increase in oxygen demand is not accompanied by a further increase in carbon dioxide emissions is called a respiratory threshold (VT). This discrepancy is due to the formation of lactate, the buffering of H + lactate ions with bicarbonate and the subsequent formation of additional CO 2. The respiratory threshold is also called the anaerobic threshold and the onset of lactate accumulation in the blood. Since CO2 stimulates the respiratory center, a nonlinear increase in the respiratory rate occurs at the respiratory threshold and moderate shortness of breath appears. The respiratory threshold during FN is usually marked at 50% of VO2max in untrained people and makes up a higher percentage of VO2max in trained individuals. Respiratory threshold is an important indicator of TFN, because it reflects the maximum sustainable level of performance that can be achieved during submaximal loads.

d) The effect of heart disease on physical performance. Physical performance in some cardiac patients may be normal and age and sex, while others may be limited if the heart’s CR decreases, the heart rate response to the FN is disturbed, there is myocardial ischemia, which, in turn, limits the FA of patients or increase in PP at peak FN. Drugs such as β-AB, which limit the changes in heart rate during FN, as well as the limitations of FA in patients with heart disease, which cause the effect of detraining, make a definite contribution to the reduction of TFN.

e) The effect of physical training on physical performance. The main purpose of FT (aerobic or static) is to increase the physical performance of patients with heart disease. With static loads, an increase in muscle strength and endurance occurs in a trained muscle. The main effect of aerobic exercise is to increase VO2max. This provides a lower percentage of VO2max at submaximal FN, which reduces the increase in heart rate and SBP during FN and myocardial oxygen demand. Increased endurance also increases both the absolute respiratory threshold and the respiratory threshold as a percentage of VO2max.

Many mechanisms contribute to the increase in TFN after FT, including PP and Δ (A – B) O2, although the magnitude of the latter has clear physiological limitations.

The degree of increase in VO2max during static loads depends on a number of factors, including the patient’s age, the intensity and duration of PT, the genetic characteristics of the patient and the clinical condition, as well as whether similar exercises are used in FT and testing. Usually the degree of increase in TFN is greatest in young people who have been intensively trained. The degree of increase in VO2max in patients after cardiac rehabilitation averages 11–36%, but depends on the severity of the underlying disease. For example, in patients with significantly reduced cardiac contractility, an increase in physical performance can be achieved by increasing Δ (A – B) O2, although in some patients after 12 months of TF an increase in CV is also observed.

In addition to increasing the maximum physical performance, endurance exercises increase stamina due to the effect on the respiratory threshold. This influence is extremely important because increased submaximal physical performance reduces shortness of breath with submaximal fn and provides for the implementation of most daily tasks, none of which require maximum effort.

The history of the rehabilitation of patients in cardiology

Prolonged (several weeks) hospitalization and restriction of physical activity over the subsequent months were the standard treatment for myocardial infarction until the early 1950s. But in the early 1970s. patients after myocardial infarction were usually hospitalized for 3 weeks.

Exercise-based cardiac rehabilitation programs have been put into practice since the 1950s. and had the goal to overcome the state of detraining and reduced physical performance in patients caused by prolonged hospitalization and deliberate restriction of FA.

Physical training (FT) is considered as key elements in overcoming the state of de-training and cardiac rehabilitation, since physical training (FT) was among the few interventions that had proven effectiveness in preventing attacks of angina pectoris, and long before the use of β-AB, calcium antagonists, coronary artery bypass surgery and percutaneous transluminal coronary angioplasty (PTCA).

The reduction in the length of stay of patients in the hospital, as well as effective medications and interventions for the correction of myocardial ischemia influenced the structure and design of cardiac rehabilitation programs. FT continues to be one of the key elements of cardioreabilitation, however, according to the requirements of today, rehabilitation must be comprehensive.

Other key elements of a comprehensive cardiac rehabilitation are training and counseling patients in order to improve their psychological state, quit smoking, increase adherence of patients to therapy and diet. These educational components are so important that their knowledge is necessary when obtaining accreditation from the American Association of Cardiovascular and Pulmonary Rehabilitation.

Physical training (FT) continues to be considered the most important component of cardiac rehabilitation programs due to the fact that FT increases TFN; reduce pain syndrome (stenocardia) and reduce myocardial ischemia caused by FN, and also correct such FR as serum lipid levels, arterial hypertension and endothelial dysfunction. This chapter is about cardiac rehabilitation in general, but with an emphasis on physical training.

Primary and secondary prevention

Primary and secondary prevention

Primary and secondary prevention has contributed a lot to reducing mortality from KBS, but problems remain. The first problem is the general aging of the population. In this regard, the number of persons with factors that attribute them to the risk group of CVDs will increase, because The prevalence of many factors increases with age. Similarly, the number of people with CVD will increase, which will require strengthening of secondary prevention measures.

This article provides a general approach to the patient, which can be presented in a few simple steps.

a) Step 1. First, assess the overall risk of the first or repeated cardiovascular event (SSSob) for each patient. Using a special algorithm, patients are classified into 4 groups: (1) with obvious CVD, including those with myocardial infarction, MI, PAD, angina pectoris or preliminary vascularization; (2) with no apparent CVD, but with diabetes or with a high risk, as assessed using a cumulative scale; (3) with moderate risk; (4) low risk. Patients with CVD and DM usually allocate immediately. For the remaining stratification, you need to use other prognostic information in the form of a scale developed, for example, by the Framingham Heart Study, ESC, New Zealand Guidelines Group.

b) Step 2. After assigning the patient to the appropriate risk group, 8 objectives of classes 1 and 2 should be used.

c) Step 3. The table below summarizes the approaches to the interventions of all 3 classes. For several RFs (smoking, DLP and AH), the strength and consistency of association with atherosclerotic diseases indicate a causal relationship; The benefits of intervention are well documented for both primary and secondary prophylaxis. Smoking cessation is mandatory for all.

DLP Drug Therapy should be administered to individuals who have 10-year risk of KBS> 10%; its goal should be a significant reduction in LDL cholesterol. Similarly, pharmacological treatment to reduce blood pressure should be prescribed to persons with moderate risk. There is little doubt that diabetes, NFA, obesity, and certain dietary habits increase the risk of CHD and that moderate alcohol consumption reduces the risk, but it was difficult to accurately determine the magnitude of the effect on these RFs associated with the intervention.

Low cost interventions are shown for everyone. Structured programs with a favorable cost-effectiveness indicator are indicated for persons with established illness.

e) Step 4. Periodic assessments of the dynamics of RF and general risk can be useful for assessing the adequacy of the intervention and motivating the patient to implement preventive recommendations. These recommendations need to be adjusted depending on the success of the modification of individual FRs.

Many of these activities can be performed by related medical personnel as part of preventive programs. The benefits of these prophylactic models in specific cases have been demonstrated in high-risk groups after MI or surgical bypass surgery.

e) Special populations. CVDs are the leading cause of death for women in most developed countries of the world. In the US,> 240 thousand women die each year from coronary heart disease (CHD), but a study with primary care physicians, obstetrician-gynecologists and cardiologists showed that less than 1 in 5 doctors knew that more women die from CVD every year. men. The American Heart Association has published a new guideline on CVD prevention for women that contains clinical guidelines adapted to the individual risk level of women.

The elderly also represent a special population group. The previously described interventions are usually applicable for healthy elderly people, but with pharmacological interventions, the initial doses of drugs may be even lower than in young people. It is necessary to take into account comorbidity and drug interactions. However, you should not abandon beneficial interventions based only on the age of the patient. Particular attention should be paid to improving patient education in order to increase adherence to the prevention advice of people with low socioeconomic status.

Recommendations for the prevention of coronary heart disease

Recommendations for the prevention of coronary heart disease

Most preventive interventions target one risk factor (RF), but several have attempted to simultaneously change several RFs. Theoretically, the possibility of synergism among RFs can lead to a significant reduction in the risk of cardiovascular diseases (CVD).

Multifactorial interventions have greatly contributed to the understanding of cardiovascular risk (CCP), as well as increased knowledge of the effectiveness or ineffectiveness of intervention strategies, but their results were different. It is obvious that multifactorial intervention can reduce the level of FR, and this reduction can be long-lasting. In the Belgian study, which was part of the World Health Organization European Collaborative Trial in the Multifactorial Prevention of Coronary Heart Disease, the intervention program consisted of staff counseling on nutrition, smoking and FA and led to a significant reduction in predictors of coronary risk compared to the control group . This effect has been persistent for 5 years.

The overall result of multifactorial interventions is a change in the levels of DF or indicators of total risk scales in the intervention group. However, these changes did not always translate into a reduction in the frequency of events. These discrepancies can be explained by the fact that the intervention was too small or the patients in the control group also changed their lifestyle for the better over time. However, it is clear from these studies that by using simultaneous multifactorial interventions, CCP can be reduced if the planned interventions are large enough and adequately implemented.

In the analysis of 7 multifactorial interventions, changes in the multiple logistical risk function were compared with a reduction in the risk of CHD. A strong linear relationship suggests that if the risk factor (DF) does change, the frequency of events will also decrease.

New markers of coronary heart disease

New markers of coronary heart disease

A detailed discussion of new biochemical and genetic markers of cardiovascular diseases (CVD) is presented in a separate article on the site. In general, several hemostatic and inflammatory markers, new lipid parameters, cell adhesion molecules, markers of infection and oxidative stress are associated with the stages of atherogenesis, thrombosis or cardiovascular events (SSSob).

Of these new risk factors (RF), only the level of CRP added prognostic information to general risk prediction models, such as the Framingham Risk Scale. High levels of CRP serve as a prognostic factor for cerebral stroke (MI), recurrent coronary events and cardiovascular death. The Centers for Disease Control and Prevention and American Heart Association guidelines endorse the definition of CRP as an adjunct to risk assessment, especially for those in the intermediate risk zone.

In the United States, recently obtained results for women show that 20–30% of people at risk of 5–20%, according to APT III, can be reclassified into a higher or lower group after measuring the level of CRV. Approval of the definition of SRV partially reflects the low cost of assessment, especially in comparison with other approaches to screening based on complex visualization technologies, such as CT, or the definition of calcification of spacecraft. In general, when the level of SRV is used in the general risk prediction algorithm, its values ​​<1.1–3 and> 3 mg / l correspond to the low, intermediate, and high risk of future vascular diseases. Adding a high level of CRP to the formal definition of MS also improves predictive accuracy with respect to vascular events or diabetes. To date, other inflammatory markers, such as lipoprotein-associated phospholipase A2, fibrinogen, and ligand CD40, are of limited value if CRP levels are known.

Other new risk factors (RF) – lipoprotein (a) and homocysteine ​​- are of limited value in general screening, but may be useful in the presence of a premature disease in families prone to atherosclerosis, when there are no clusters of traditional RF. In relation to lipoprotein (a), the availability of an assessment, regardless of apo re-screening, is a significant achievement that helps resolve the inconsistencies of previous reports.

A general restriction on the use of these new markers is the lack of data showing that reducing their level will lead to a decrease in vascular risk, therefore their use is limited to a risk assessment and a motivation for lifestyle changes. For example, although statin therapy reduces CRP, a post-hoc analysis suggests improved outcomes in individuals with elevated CRP, prospective studies testing the use of CRP to control statin treatment are only starting. Similarly, although folate decreases homocysteine, there is no evidence that this approach reduces vascular risk. The potential clinical benefits of these markers and today’s results regarding their modification are presented in a separate article on the site.

A number of common genetic polymorphisms are associated with coronary risk factors (RF). For example, carriers of a common mutation in the MTNFR gene have elevated levels of homocysteine ​​and multiple inherited lipid metabolism abnormalities associated with HLP and an increased vascular risk. Similarly, almost 50% of variations in the level of CRP are inherited. However, there is no evidence that screening for this polymorphism adds essential information to more easily detectable levels of homocysteine, lipids or CRP. Data concerning arterial thrombosis contrasts with data from venous thrombosis, when an assessment of factor V Leiden and prothrombin mutation is clinically useful. Thus, although genetic screening is a promising way to identify individuals at risk for future events, its role in primary and secondary prevention of atherothrombotic diseases remains unproved today. However, the time will come when genetic screening will play a role in identifying individuals at increased risk for appropriate therapy to reduce the risk of subsequent events.

The effectiveness of the treatment of stress and depression in coronary heart disease

The effectiveness of the treatment of stress and depression in coronary heart disease

The study of psychosocial factors as possible risk factors for coronary heart disease (RF KBS) is difficult due to the inaccuracy of definitions and units of measurement. Psychosocial factors such as depression, chronic hostility, social exclusion, and a feeling of lack of social support have always been associated with the risk of coronary heart disease.

However, it is necessary in further work to confirm this relationship and establish the effectiveness of interventions. With regard to the existence of a link between vascular risk and such psychosocial factors as work-related stress, type A behavior and anxiety, the data are heterogeneous.

Studies of therapeutic interventions, although not blind, noted the importance of improving psychosocial factors as part of preventive programs, especially with secondary prophylaxis.

The strongest evidence was obtained for patients after myocardial infarction (MI). Although many data show that stress and depression after MI are common and predictors of subsequent events, the results of interventions are limited. A meta-analysis of 37 small studies on the training of patients with coronary heart disease (CHD) in stress management showed that these efforts can reduce heart mortality by 34% and repeated myocardial infarction by 29%, possibly due to the favorable effect on blood pressure, cholesterol and MT. smoking, FA and eating habits.

In the randomized ENRICHD study, 2481 patients were included (26% – with a feeling of low social support, 39% – in clinical depression, and 34% – in both conditions) 4 weeks after MI. 50% of patients were randomized for cognitive behavioral therapy and drug therapy, if necessary, and the other 50% were in the conventional treatment group.

Intervention did not increase survival without events. It did have a positive effect on depression and a sense of social exclusion, however, the relative improvement in the intervention group compared with the conventional treatment group was less than expected, possibly due to the significant improvement in the condition of patients in the control group.

Preliminary evidence suggests that pharmacotherapy for depression after MI, revascularization, or diagnosis of CHD can improve morbidity and mortality. A randomized SADHART study (Sertraline Antidepressant Heart Attack Randomized Trial) showed the safety of sertraline (a selective serotonin reuptake inhibitor) in the treatment of recurrent depression in patients with cardiovascular diseases (CVD).

Sertralin did not affect LV EF, ventricular premature beats, or other cardiac indicators when compared with the placebo group. Depression and mood scales were better in the sertraline group, especially in depressed patients before heart attack, i.e. in a group in which the onset of depression after an attack is particularly likely. The frequency of repeated heart attacks, HF, episodes of chest pain and cardiac death was lower in the sertraline group than in the placebo group.

In the ENRICHD study, the use of antidepressants was also associated with significantly lower levels of nonfatal MI and deaths.

Efficacy of vitamins for coronary heart disease

Efficacy of vitamins for coronary heart disease

Micronutrients and specific foods are studied as substances for reducing the risk of cardiovascular diseases (CVD). Common supplements that many use to reduce the risk of heart disease include multivitamins, vitamins B and folic acid, antioxidants such as vitamins E and C, various carotenoids and ubiquinone (coenzyme Q10).

Foods that can reduce cardiovascular risk (SSR) are whole grains, fiber, fish and fish oil, and soy protein. Observational studies have shown a lower incidence of CHD among those who use antioxidant vitamins and folic acid, but the results of the research are contradictory and their effect is modest.

The significance of randomized clinical trials for heart-healthy foods and nutrients is best illustrated by a description of the advantages and disadvantages of vitamin E. In fundamental research, there is strong evidence that oxidative stress plays an important role in the development of diseases caused by atherosclerosis, and vitamin E can slow down or prevent various stages of atherosclerosis.

By the mid-1990s. observational studies have convincingly shown that high doses of vitamin E reduce the risk of CHD, especially with secondary prophylaxis. However, completed secondary prevention studies have revealed that the addition of vitamin E has little effect on the risk of coronary heart disease (CHD). Similar results were obtained in two long-term primary prevention studies – the Women’s Health Study and the SU.VI.MAX (Supplementation en Vltamines et Mineraux AntioXydants), which evaluated a combination of antioxidants, including vitamin E in a dose of 30 mg.

No significant reduction in the risk of cardiovascular disease (CVD) was found in these studies.

In the study of the cardiovascular effects of antioxidants in women in the framework of secondary prophylaxis, no positive cardiovascular effects were found among those taking any antioxidant: vitamin E, vitamin C or β-carotene for> 9 years. In the GISSI study, 11,324 patients who recently had myocardial infarction were divided into groups:

(1) taking daily supplements containing 1 g of omega-3 PUFA;
(2) taking vitamin E at a dose of 300 mg;
(3) receiving both supplements;
(4) not taking anything.

Observation was conducted 3.5 years. Treatment of omega-3 PUFA, but not vitamin E, reduced the relative risk of the primary endpoint (death, non-fatal MI and MI) by 10% (95% CI 1-18). This beneficial effect was primarily due to the reduced risk of death, and not due to nonfatal MI or cerebral stroke (MI).

Finally, in numerous prospective cohort studies, plasma homocysteine ​​levels have been consistently associated with increased vascular risk. On this basis, it was hypothesized that a decrease in homocysteine ​​with folic acid would lead to a decrease in the frequency of vascular events. However, numerous studies with the addition of folic acid to patients with vascular disease did not reveal a favorable clinical effect.

Recommendations. There are no results of studies supporting the use of food supplements for the prevention of KBS or other cardiovascular events (SSSob). Antioxidants did not show a clear benefit in preventing CHD, but observational studies revealed the possibility of various micronutrients and specific foods to reduce the risk of coronary heart disease (CHD). However, soy protein and isoflavone supplements lost their popularity in 2006, when the ANA, which had previously recommended soy, changed its position after analyzing the results of 22 studies, saying that it could not recommend supplements of isoflavones in pills or in food to prevent heart disease.

More research is needed on fish oil supplements before offering general recommendations. Several recent studies have failed to reveal the benefits of folach supplementation, thus showing that a decrease in homocysteine ​​is not associated with a reduction in vascular risk.