Month: February 2019

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.

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.

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.