In recent years, in the clinical practice, ACE inhibitors are increasingly prescribed. And this is quite natural, since the imbalance of the renin-angiotensin system plays an important role in the development of cardiovascular diseases. Throughout the last decade, numerous studies have been conducted in which the clinical efficacy of ACE inhibitors in various cardiovascular diseases has been studied. The results of these studies are reflected in domestic recommendations, according to which an ACE inhibitor should be prescribed to patients with arterial hypertension, heart failure, acute and myocardial infarction and diabetic nephropathy .

ACE inhibitors are one of the most studied classes of antihypertensive drugs, the effectiveness of which, following diuretics and BB, has been proven in large-scale randomized trials with endpoints. The first study of this kind was the CAPPP study, which compared the effectiveness of ACE inhibitors (captopril 50 mg per day) with atenolol and metoprolol (50–100 mg per day) or hydrochlorothiazide (25 mg per day) for 6 years in the treatment of 10985 patients with hypertension There were no differences in the frequency of the combined endpoint (fatal and non-fatal strokes and myocardial infarction, as well as mortality from other cardiovascular causes) between groups of patients who received ACE inhibitors and BB or diuretics.In this study, a more favorable metabolic profile of captopril was also demonstrated compared with BB and diuretic. The incidence of diabetes by the end of the study in the captopril group was 21%. lower than the other group .

A relatively new scope of ACE inhibitors is the prevention of complications and an increase in mortality in patients with high cardiovascular risk. This is explained by the fact that ACE inhibitors are one of the most effective classes of drugs in terms of improving endothelial function. At least two possible mechanisms of the effect of an ACE inhibitor on the endothelial function have been described. It is possible that ACE inhibitors increase the level of tissue bradykinin [37–38], a powerful stimulator of the release of endothelium-dependent relaxation factors: NO, endothelium-dependent hyperpolarization factor and prostacyclin (PGI2). Another mechanism of action of an ACE inhibitor is the blockade of the formation of angiotensin II, which is considered as an inducer of oxidative stress, leading to a decrease in the bioavailability of NO. AII has the opposite effect with respect to NO.Inhibition of ACE can restore the balance between two vasoactive systems . The dual mechanism of ACE inhibitors is to block the formation of angiotensin II and prevent the destruction of bradykinin, which stimulates the synthesis of endothelial NO, causes the antihypertensive, antiproliferative and angioprotective action of these drugs.

The ability of an ACE inhibitor to improve endothelial function and inhibit atherogenesis processes was first demonstrated in a study of TREND (Trial on Reversing Endothelial Dysfunction) [41]. In a randomized trial lasting half a year in the treatment of 129 IHD patients, the effectiveness of quinapril in relation to the restoration of impaired endothelial function of the coronary arteries was examined, which was assessed using a sample with intracoronary acetylcholine during coronaryography. A reduction of 10–20% in the severity of vasoconstrictor reactions after quinapril therapy was found.

In the BANFF Study, a comparative assessment of the correction of endothelial function was performed with 8 weeks of treatment with different classes of antihypertensive drugs (amlodipine, quinapril, enalapril, losartan) in 80 patients with CHD. The majority of the sample were men (80%), the average age was 58 ± 0.9 years. The risk factors were as follows: hypercholesterolemia was in 54% of patients, AH – in 26%, diabetes – in 10%. A history of myocardial infarction was recorded in 47% of patients, 95% of patients underwent coronary angioplasty. In the course of treatment, blood pressure and blood lipid spectrum did not differ significantly, and the endothelium-dependent vasodilation of the brachial artery in patients with risk factors improved only during treatment with quinapril, while amlodipine, enalapril and losartan did not affect endothelial function [42].

The powerful effect of ACE inhibitors on endothelial function is also confirmed by the results of our own research on the advantages of this class of drugs over others in the treatment of smoking patients with hypertension.

Analysis of large-scale studies indicates a decrease in the effectiveness of antihypertensive drugs in the treatment of smoking patients with hypertension. The use of b- blockers allowed to reduce the number of coronary episodes in non-smoking hypertensive patients, while smokers had no such effect . According to the results of the study using Smad in patients with arterial hypertension, it was found that in smoking patients the levels of systolic and diastolic blood pressure, as well as the heart rate, are statistically significantly higher than in non-smoking patients. The authors make the assumption that such results may indicate that patients with hypertension are not treated . . An analysis of the national sample of treated individuals with hypertension in Sweden, which included 4,424 patients, observed in 189 doctors, indicates a decrease in the effectiveness of antihypertensive therapy in smoking patients. The percentage of inadequately treated persons in relation to DBP (≥ 90 mm. Mercury) in the group of smokers is 32.7%, in the group of non-smokers – 25%, p <0.01. The corresponding figures of systolic blood pressure (≥ 140 mm Hg) are 72.8% and 68.9%, p <0.01 . In the Russian multicenter study Prologue in the group of the main treatment (starting therapy with an ACE inhibitor followed by the addition of hydrochlorothiazide and atenolol), the effectiveness of blood pressure reduction in the smoking group was significantly less than in the non-smoking group [46]. The most important reason for reducing the effectiveness of antihypertensive drugs for the treatment of smokers is endothelial dysfunction that develops in this category of patients [47, 48]. Endothelial dysfunction leads to pronounced peripheral vasospasm, which in turn reduces blood flow at the level of microcirculation followed by ischemia of organs and tissues, which leads to the maintenance of high blood pressure. Therefore, it can be assumed that antihypertensive drugs, corrective DE should have an advantage in smoking patients with hypertension. Such classes of drugs primarily include ACE inhibitors. Let us take an example of another study:23 smokers of patients with hypertension (mean age 38 ± 12 years, smoking experience – 21 years, the average number of cigarettes smoked – 19), who had no other risk factors for 8 weeks, received 20 mg of lisinopril and placebo alternately. The treatment with lisinopril showed a significant increase in the blood flow in the forearm in response to the intraarterial administration of acetylcholine. This fact indicates an improvement and endothelial function . There are few studies confirming the effectiveness of an ACE inhibitor in the treatment of smoking patients with hypertension. In the randomized crossover study, the antihypertensive efficacy of enalapril and atenolol was studied in the treatment of male smokers with AH. The ACE inhibitor enalapril in the smoking group was found to be more effective than the b- blocker atenolol .

In the randomized crossover study itself, 30 smoking patients, men aged 35–64 years with mild and moderate essential arterial hypertension, were included. Within 12 weeks, patients received the drug Iruzid, which is a fixed combination of 20 mg of lisinopril and 12.5 mg of hydrochlorothiazide, and a combination of 50 mg of atenolol with 12.5 mg of hydrochlorothiazide. The decrease in systolic blood pressure after Iruzid treatment amounted to an average of 16.6 mm Hg. Art., and diastolic blood pressure – 10.3 mm Hg. Art. The corresponding figures for a decrease in blood pressure during treatment with a combination of atenolol and hydrochlorothiazide are 11, 9, and 7.6 mm Hg. Art. Differences in decreases and systolic
 
 
 
 
 
 
 
 
 
 
 and diastolic blood pressure is significant (p <0.005). Thus, Iruzid provided a more pronounced decrease in blood pressure in smokers than the combination of 0.15 % atenolol and hydrochlorothiazide. These differences

Patients who reach the combined primary endpoint (myocardial infarction, stroke, cardiovascular death). H Ashley reflected in the effect of two strategies of treatment on endothelial hydrochloric function which is evaluated using a cuff test,
 
 
 
 
 
 those. assessment of endothelium- dependent vasodilation (EDVD) of the brachial artery using high-resolution ultrasound. Iruzid therapy led to a marked improvement in endothelial function. Against the background of therapy with Iruzid, a significant pronounced increase in EDVD was observed – 7.9% ± 3.0 before treatment and 15.5% ± 2.2 after treatment (p <0.05). During treatment with a combination of atenolol and hydrochlorothiazide, the change in EDVD was statistically insignificant – 8.2% ± 3.4 and 9.6% ± 3.6 (p> 0.05).

The hypothesis of the possibility of preventing complications and death in patients with high cardiovascular risk of ACE inhibitors has been tested in a number of large multi-site studies: HOPE (Heart Outcomes Prevention Evaluation Study), EUROPEA (EURopean trial coronary Arte-ry disease), PEACE (Prevention of events with Anti- ingin-converting Enzyme inhibition). This list stands out as the HOPE study [51], which involved 9297 men and women with confirmed atherosclerosis of various localization (coronary heart disease, peripheral arterial disease, stroke) or diabetes mellitus at least another risk factor (arterial hypertension, cigarette smoking, microalbuminuria, or dyslipidemia). 80% of patients had coronary heart disease,55% – angina, 52% – history of myocardial infarction, 43% – atherosclerosis of the peripheral arteries, 25% – unstable angina in history, and 26% – coronary artery bypass surgery in history, 18% – percutaneous regstrium, and 18% – acute coronary artery bypass graft bypass, in 18% – percutaneous regstrosis, in 18% – acute coronary artery bypass surgery. 11% have a stroke or transient ischemic attack. Almost half of the patients suffered from hypertension and about 40% – type 2 diabetes. Patients were given a placebo or an ACE inhibitor ramipril (with titration of doses from 1.25 to 10 mg) and continued monitoring for an average of 5 years. The primary endpoint (cardiovascular death, MI, or stroke) was recorded in 17.8% of patients in the placebo group and 14.0% of patients in the ramipril group, reflecting a 22% reduction in risk, p <0.001 (Fig. 3). Ramipril therapy led to a decrease in the frequency of the most important components of this end point – MI, MI (Fig. 4.5). Besides,a reduction in total mortality (from 12.2 to 10.4% within 5 years), the need for revascularization, diabetic complications, diabetes, heart failure, progression of angina pectoris, or cardiac insufficiency. An interesting fact is that the decrease in blood pressure in the ramipril group was relatively small (BP is 3/3 mm Hg), so the results of treatment cannot be explained only by antihypertensive drugs. the effect of the drug .

Thus, in this study, the protective role of ramipril was confirmed in terms of preventing the development of complications in patients with high risk. Moreover, the protective effect of ramipril is in no way associated with a decrease in blood pressure.

Additional evidence of the effectiveness of long-term treatment of ACE inhibitors for the purpose of secondary prophylaxis is the results of the EUROPA study [52]. It included 13,655 patients in the low-risk group, without heart failure, who suffered from stable coronary heart disease. For an average of 4.2 years, they were treated with perindopril or placebo. In patients with perindopril, a decrease in the incidence of cardiovascular outcomes (cardiovascular death, myocardial infarction, sudden death) from 10 to 8% was detected, which meant that for the prevention of a single cardiovascular outcome, treatment was necessary for 4 , 2 years in 50 patients. The benefits of ACE inhibitors were comparable in all subgroups of patients.

In recent years, ARA has made a huge leap forward in terms of conquering new niches for the treatment of hypertension in various clinical situations. If earlier this class of drugs was in the shadow of an ACE inhibitor (their prescription for hypertension was limited mainly by situations related to side effects due to the administration of ACE inhibitors), then at present the niche of their use, as follows from Table 1, extensive. To better understand the possibilities of ARA, it is necessary to recall their mechanism of action. It is known to inhibit the angiotensin II receptor AT1 – conductors of the main negative effects of this hormone – as a result of which, unlike the ACE inhibitor, the synthesis of AII is not disturbed. The negative effects of AII include vasoconstriction, increased secretion of endothelin, stimulation of the synthesis of peroxide radicals, hypertrophy of smooth muscle cells,increased activity of tissue activator inhibitor type 1 plasminogen. Many of these effects are atherogenic. On the other hand, angiotensin II stimulation of unblocked type 2 receptors (AT2) causes effects opposite to those listed above, namely, vasodilatation, increased production of nitric oxide, and stimulation of antiproliferative processes. Thus, ARA have a double positive mechanism of action, which has a powerful anti-thrombogenic potential.

An illustration of the possibilities of ARA is the LIFE study (a study of the effectiveness of losartan in reducing end points in people with arterial hypertension), the results of which were expected with great interest and are likely to be discussed for a long time [8, 59]. In this study, not only was antihypertensive efficacy of ARA proved for the first time in terms of its effect on end points, but other possibilities were also demonstrated.

In a double-blind, randomized, controlled international study, 9193 hypertensive patients aged 55–80 years participated, with left ventricular hypertrophy. The study participants were randomized into 2 groups for the purpose of treatment as initial with either losartan or atenolol. The initial dose of drugs was, respectively, 50 mg of lazan 1 time per day and 50 mg of atenolol 1 time per day. The drugs could be combined with hydrochlorothiazide – 12.5 mg per day and further increase their dose to 100 mg per day in order to achieve the target blood pressure reduction of less than 140/90 mm Hg. Art. Finally, if the maximum doses of the studied drugs in combination with a diuretic did not provide adequate control of blood pressure, then it was allowed to prescribe additional drugs (with the exception of ARA, ACE inhibitors and BB). The duration of the study averaged 4.8 years.

The objective of the study was to study the comparative efficacy of losartan and atenolol in order to reduce the main endpoint, which included a total of MI, MI and cardiovascular mortality. Other endpoints included the incidence of diabetes mellitus, all-cause mortality, regression of left ventricular hypertrophy, the frequency of hospitalizations for angina or heart failure.

In total, 508 cases of a combined endpoint were detected in the losartan group , and 588 in the atenolol group. Thus, compared to atenolol, losartan reduced the frequency of the main endpoint (cardiovascular mortality, MI and MI) by 13% (p <0.021). The frequency of fatal and nonfatal MI in the losartan group was 25% lower than in the atenolol group (p <0.001), despite the fact that the blood pressure in both groups decreased almost the same – by 30/17 mm Hg. in the group of losartan and at 29/17 mm Hg in the group atenolol. However, there were no differences in the incidence of myocardial infarction in both groups. Another important finding is the significantly lower incidence of diabetes in the Losar group – by 25% (p <0.001). In the subgroup of patients with initial diabetes, the frequency of the main endpoint was lower by 24% (p <0.031), and the rate of cardiovascular mortality was 37% (p <0.028) in the losartan group than in the atenolol group. This indicates a beneficial side effect of losartan. Thanks to this study, a new niche for ARA – AG and myocardial hypertrophy has appeared, since it was shown that a significantly more regressive hypertrophied left ventricle was observed in the subgroup of individuals with losartan compared with atenolol. It was also important thatthat the frequency of side effects when using losartan was significantly less than in the atenolol group. As a result, at the end of the study, significantly more patients continued to take losartan than atenolol.

New possibilities in the treatment of such a problematic group of patients as hypertension with concomitant CHF are associated with ARA. As is known, currently in the treatment of hypertension with CHF, an arsenal of drugs is successfully used that can effectively eliminate the symptoms of heart failure and prolong the life of such patients. These classes of drugs, as is known, include ACE inhibitors, BB, diuretics, and cardiac glycosides. For a long time, the ACE inhibitors, considered to be the gold standard for treating CHF, lacked an alternative to blocking the renin-angiotensin system, which is absolutely necessary in CHF. However, there are a number of situations where patients do not tolerate an ACE inhibitor. In addition, for unknown reasons, the effectiveness of ACE inhibitors in women is significantly lower than in men. In these situations, the doctor needs an alternative to an ACE inhibitor.And this alternative appeared due to the data obtained in the CHARM project, which combined three studies. In a placebo-controlled study CHARM-ALTERNATIVE with more than 2000 patients with CHF, the effectiveness of candesartan in the treatment of patients not taking ACE inhibitors due to their intolerance was studied [60]. The results showed that in case of an intolerance to an ACE inhibitor, the use of candesartan reduces the incidence of MTR and mortality from them, and also reduces the frequency of hospitalization due to the progression of CHF (Fig. 7).in the case of an intolerance to an ACE inhibitor, the use of candesartan reduces the incidence of mortality and mortality from them, and also reduces the frequency of hospitalization due to the progression of heart failure (Fig. 7).in the case of an intolerance to an ACE inhibitor, the use of candesartan reduces the incidence of mortality and mortality from them, and also reduces the frequency of hospitalization due to the progression of heart failure (Fig. 7).

In another study, CHARM-ADDED [61], it was found that the addition of candesartan to IAP F and BB in patients with CHF leads to a clinically significant decrease in the incidence of CCO and death from them, as well as hospitalization due to progression CHF .

In both of these studies , the use of candesartan was characterized by good tolerability. It is not unimportant to note that the effectiveness of desa-sartan was almost the same in both men and women. A comparative analysis of the results of the CHARM project and the SOLVD study showed that the effectiveness of candesartan in order to reduce the risk of death from SSO and the frequency of hospitalization due to the progression of CHF is comparable to the effectiveness of the standard ACE enalapril. It is very important for practical physicians to know the dose titration rules.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 candesartan, which was used in the CHARM project. The starting dose is 4 mg per day once, which
 
 
 
 
 with stable blood pressure and the absence of complications, it doubled every 3-5 days until reaching 16 mg per day. The maximum dosage per day is 32 mg. To date, the use of candesartan in the treatment of patients with CHF is the most reasonable, and it can be used on a par with an ACE inhibitor (evidence grade A). This fact is reflected in the latest European and Russian recommendations on the diagnosis and treatment of CHF. Moreover, in the latest European guidelines for the treatment of hypertension, a new niche for the use of ARA has appeared – a concomitant CHF. Of the other representatives of the ARA, it is also recommended to use losartan and valsartan. In the new recommendations for the diagnosis and treatment of hypertension, there is also a very interesting niche for the use of ARA – preventing the development of atrial fibrillation in patients with a history of arrhythmia paroxysms.All of these new APA niches indicate the most important pleiotropic effect of this class – organ protection, not associated with a decrease in blood pressure.

As clinical practice shows, in most cases it is possible to achieve target blood pressure against the background of combination therapy with drugs with different mechanisms of action, especially in groups of patients with high risk, which are observed among practitioners. This is quite natural, since a single class of drugs is not able to control all the pathogenetic mechanisms for increasing blood pressure: the activity of the CNS and the renin-angiotensin – aldosterone system, volume-dependent mechanisms. There are various combinations of antihypertensive drugs. Combinations of two anti-hypertensive drugs are divided into rational (effective), possible and irrational. All the benefits of combination therapy are found only in rational combinations of antihypertensive drugs. These include: ACE inhibitor + diuretic; ARA + diuretic; IAPF + AK; ARA + AK;dihydropyridine AK + β-AB; AK + Diu retic; β-ab + diuretic .

There are certain nuances of combination therapy. It can be of two types: starting monotherapy with a transition to a combination therapy in the absence of an effect (i.e. achieving the target level of blood pressure) or a combination therapy at the start of treatment . If you start from the strategy of starting monotherapy, then the doctor inevitably faces a situation of painstaking search for the most optimal antihypertensive agent for the patient with frequent changes drugs and their dosages, which often deprives the doctor and the patient of confidence in success and, ultimately, reduces adherence to treatment. This is especially true for patients with mild and moderate hypertension, most of whom do not experience discomfort from an increase in blood pressure and are not motivated to treat. Combined therapy at the start of treatment, provided effective doses of the drugs allow for faster adequate blood pressure control in most cases of hypertension.

The most popular in Russia is the combination of an ACE inhibitor and a diuretic. As the results of the Pythagoras study show, almost a third of physicians in Russia prefer the combination of these particular drugs [62]. It is possible that these two classes of drugs provide control of almost all mechanisms for increasing blood pressure. Fixed combinations of antihypertensive drugs, which are significant but increase patients’ commitment to the treatment of hypertension. Among the fixed combinations, noliprel and noliprel-forte (2–4 mg of perindopril and 0.625–1.5 mg of indapamide), korenitek (20 mg of enalapril and 12.5 mg of hypothiazide), tarka (180 mg of isoptin CP) are successfully used. and 2 mg of trandolapril). At the same time, fixed combinations of drugs limit titration of doses, if necessary, both upwards and downwards. Therefore, the emergence of the first non-fixed combination Enzix containing two drugs in one blister – enalapril and indapamide is important. The drug owes its appearance to the EPIGRAF project, which was carried out under the auspices of the All-Russian Scientific Society of Cardiology (coordinator Academician of the Russian Academy of Sciences Yu.N. Belenkov). The project consisted of two multicenter studies, EPIGRAF-1 and EPIGRAF-2.

A doctor and 38 polyclinics from 17 cities took part in the open study of EPIGRAPH-1 . A total of 550 patients with grade II – III hypertension (baseline systolic blood pressure> 160 mmHg) were included in the study, and among them were patients not only with essential, but also with symptomatic hypertension. A special feature of the study was that already at the beginning of treatment patients were prescribed a combination of enalapril and indapamide. Moreover, if the dose of indapamide was constant – 2.5 mg, then the dose of enalapril varied depending on the initial level of blood pressure. At the same time, doctors had the possibility of adjusting the doses of enalapril depending on the achievement of the target blood pressure within 4 weeks. As a result of the treatment of hypertensive patients with differentiated doses of enalapril and indapamide, a significant reduction in both systolic and diastolic blood pressure was achieved. At the same time, target BP was achieved in 70% of patients (<140/90 mmHg).The percentage of patients who responded to treatment in general (decrease in systolic and diastolic blood pressure –∆20 / 10 mm Hg) was 77.1. Adverse reactions were observed in only 8.2% of patients. Only 2.7% of patientsntov was a cough . The main conclusion of the study was that efficacy and safety The combination of enalapril with indapamide in the treatment of hypertension did not depend on gender, age, and the cause of the increase in blood pressure (primary hypertension or secondary hypertension of renal origin). It is especially necessary to pay attention to the latter circumstance, in connection with the ingrained opinion that the effectiveness of antihypertensive therapy in patients with symptomatic hypertension decreases. The combination of enalapril with indapamide was especially preferred in women, in whom the ACE inhibitor monotherapy may be less effective. The results of the EPIGRAPH-1 study allowed us to work out the most effective doses of enalapril and indapamide for hypertensive patients of varying degrees, which became the basis for the creation of 3 types of Enzix preparation: Enzixil – 10 mg of enalapril and 2.5 mg of indapamide (single dose in the morning) for hypertensive patients I degree; Enzix Duo – 10 mg enalapril and 2,5 mg of indapamide (in the morning) + 10 mg of enalapril (in the evening) for patients with hypertension of II degree; Enzaprim Enzapi Duo Forte – 20 mg of enalapril and 2.5 mg of indapamide (in the morning) + 20 mg of enalapril (in the evening).

The effectiveness and safety of the Enzix was evaluated in the study EPIGRAF-2, which by design was a comparative, randomized multicenter, which included 9 centers in Russia and 1 center in Serbia [64]. A total of 313 patients were included in the study, which were randomized into two groups. The Enzix group included 211 patients, the control group included 102 patients.

In the control group, treatment was carried out with antihypertensive drugs of any class, except for ACE inhibitors and diuretics.

This study also confirmed the high efficacy of the combination of enalapril and indapamide. In the group receiving Enzix – 72.5% of patients reached the target level of blood pressure. Thus, the early initiation of treatment of patients with hypertension of grades I – II with the unstable combination of enalapril and indapamide (Enzix), in comparison with routine antihypertensive therapy, makes it possible to achieve normalization of blood pressure more often. In addition, Ensix therapy is cost effective.

The presence of a diuretic of indapamide in the Enzix composition without undesirable side effects is of significant clinical importance. As already noted, diuretics and BB (especially non-selective) have a negative metabolic effect and increase the risk of diabetes.

This fully applies to combination therapy. In this regard, the components of the drug Enzix do not cause concern. Enalapril, as an ACE inhibitor, is by definition metabolically neutral, and indapamide occupies a special place among diuretics. At the recommended doses (1.5–2.5 mg per day), it not only provides an adequate antihypertensive effect, but is also metabolically neutral. It has been proven that indapamide does not cause hypokalemia, changes in the carbohydrate [65] and lipid profile [66]. Especially convincing evidenceThe metabolic neutrality of indapamide was obtained as a result of a meta-analysis of three studies involving a total of 1195 patients. According to the results of treatment with the retard form of indapamide for 9–12 months, no effect on the carbohydrate and lipid profile, as well as the level of uric acid was found .

Indapamide, in addition to the diuretic effect, has a vasodilating effect by reducing the sodium content in the artery wall, regulating calcium intake in vascular smooth muscle cells, as well as increasing the synthesis of prostaglandin E2 in the kidneys and prostacyclin in the endothelium . Thus, indapamide, having a more pronounced effect on the vessels than the other diuretics, affects endothelial function. It has an antioxidant effect, increasing the bioavailability of NO . Moreover, the LIVE study proved that indapamide therapy can cause regression of hypertrophy and left ventricular myocardium .

The presence of 2 antihypertensive drugs in a single double blister will certainly help to increase adherence to treatment. Three different dosages of Enzix will contribute to the adequate selection of non-fixed combination in various clinical situations related to the degree of increase in blood pressure.

In the concept of a multifactor approach, the most important is the correction of lipid metabolism disorders, which, as already mentioned, makes the most important contribution to the risk of complications. By impaired lipid metabolism, we mean an increase in the level of total cholesterol (cholesterol), cholesterol cholesterol of low-density lipoproteins (LDL), triglycerides (TG), and a decrease in cholesterol cholesterol of high-density lipoproteins (HDL). In large epidemiological studies, a direct relationship was found between cholesterol level and mortality from coronary heart disease [71,72], and also that a decrease in the level of LDL cholesterol leads, in turn, to a decrease in the risk of developing coronary heart disease [73,74]. Today, the most effective and safest drug-based lipid-lowering therapy is statins. They reduce LDL cholesterol by 20–60%, TG – by 10–40%, and HDL cholesterol increases by 5–15% . Prolonged use of statins leads to a significant reduction in the risk of cardio and cerebrovascular complications [76]. At the same time, the effectiveness of statins has been proven not only in patients with coronary artery disease, but also without coronary artery disease. The ASCOT-LLA (Anglo-Scandinavian Cardiac Outcomes Trial – Lipid Lowering Arm) study proved the effectiveness of statins for the prevention of cardiovascular complications in patients with hypertension and moderate hypercholesterolemia [77]. This fact is reflected in the recommendations of GFCF for the diagnosis and treatment of atherosclerosis, where statin administration is recommended not only for treating patients with various clinical manifestations of atherosclerosis, but also for treating patients without clinical manifestations of atherosclerosis and with a high risk of CVD death according to the SCORE scale. Thus, indications for lipid-lowering therapy are greatly expanded, as a means of not only secondary, but also primary prophylaxis.

At the same time, statins have a number of additional pleiotropic effects, which include the ability to improve endothelial function, reduce blood viscosity, and also have an anti-inflammatory, hypotensive effect. One of the most important effects of statins is an improvement in endothelial function [78,79]. It is with the improvement of endothelial function in the application of statins that their hypotension effect has been identified, which has been identified in a number of studies in recent years [80,81]. In this regard, the data of our own double-blind, randomized, placebo-controlled clinical study are of interest, the purpose of which was to study the hypotensive effect of pravastatin in patients with mild hypertension and HCS. The 12-week study included 52 male patients aged 35–60 years,who were randomly assigned to 3 groups. Group I received a placebo – 16 people, Group II – Pravastatin – 40 mg per day – 18 people and Group III – prolonged non-dihydropyridine calcium antagonist – diltiazem (altiazem PP ® ) – 180 mg per day – 18 people.

The treatment with pravastatin showed a significant decrease in the average daily GAD by 6.2 mm Hg. (p <0.001), the average daily dad – 5.4 mm Hg. Art. (p <0.001). At the same time, against the background of receiving a placebo, there was no change in the average daily GARDEN (total –0.1 mm Hg, p> 0.05), nor the average daily DBP (total –0.3 mm Hg. Art. , p> 0.05). At the same time, pravastatin provided a significant reduction in the average daily GARDEN and DBP compared with placebo. At the same time, it was slightly inferior in its hypotensive effect.

As for the hypolipidemic effect of pravastatin, the decrease in total cholesterol was 29.2 ± 3.3% of the initial level (p <0.001), LDL cholesterol – 37.7 ± 4.4% of the initial level (p <0.001) , increase in HDL cholesterol levels – 30.1 ± 5.7% from the initial level (p <0.001).

Interestingly, the degree of decline in cholesterol levels did not correlate with the degree of decline in either GARDEN or DBP. Thus, the hypotensive effect of pravastatin was not dependent on its hypolipidemic action.

Pravastatin’s hypotensive effect made an additional contribution to reducing the total coronary risk, calculated on the basis of the computerized model of the West German study PROCAM STUDY [82]. The main components of this formula are: age, CAD, level of total cholesterol or LDL cholesterol, HDL cholesterol, TG, smoking status, type 2 diabetes, history of coronary artery disease, myocardial infarction, history of coronary artery disease.

Taking into account only the hypolipidemic effect, the total risk was significantly reduced (–69%) and amounted to 7.2%, while taking into account the hypotensive effect, it reached 6.3%. Thus, the antihypertensive effect of pravastatin makes an additional contribution to the reduction in total coronary risk .

Perhaps the additional antihypertensive effect of pravastatin, which is a consequence of the improvement in endothelial function, can be attributed to the WOSCOPS (West of Scotland Coronary Prevention Study) study on primary ischemic heart disease prevention, where the efficacy of pravastatin in the treatment of 6550 people with lipid metabolism disorders was evaluated [83] . The reduction in coronary risk (combined endpoints – nephatal MI, coronary artery disease, coronary angioplasty, CABG) was significantly higher (by 12%) than expected, calculated on the basis of the Framingham model, which takes into account the level of total cholesterol.

With long-term statin therapy, it is necessary to take into account not only their hypopidemic effect, but also the hypotensive effect, which makes an additional contribution to the reduction in total coronary risk.

Since endothelial dysfunction is the cause of the disruption of the structure and normal functioning of the vessels of the microvasculature [84], it would be logical to assume that statins have a favorable effect on the microcirculation system, which is the basis for adequate organ and tissue perfusion. There are only a few data from foreign studies on the effect of statins on microcirculation. . No studies on this topic have been conducted in Russia. We have undertaken a study to study the effect of a new statin called Rosuvastatin (Crestor, AstraZeneca, UK) on the microcirculatory bed in patients with dyslipidemia and mild and moderate hypertension. The study involved 25 patients with cholesterol levels above 5.0 mmol / l and LDL cholesterol above 3.0 mmol / l and the level of the GARDEN 140–179 mm Hg. and dad 90–109 mm Hg For 12 weeks, patients took 10 mg of rosuvastatin without dose adjustment. The state of the microcirculatory bed was studied using laser Doppler flowmetry.

In general, the favorable effect of rosuvastatin on the microcirculatory bed has been established. At the same time, positive shifts were observed in various pathological types of microcirculation – in spastic and hyperemic. In the case of the spastic type of microcirculation, when the microcirculatory bed is depleted in blood, an increase in blood flow occurs during the treatment with Krestor, as evidenced by the increase in the microcirculation index. The same is evidenced by the decrease in the reserve of capillary blood flow (RSC), which is a consequence of the increase in the number of functioning capillaries. In the hyperemic type of microcirculation, when there is an overflow of the vascular bed, there is a decrease in blood flow, as evidenced by a decrease in the microcirculation index. In these patients, an increase in RCC is observed, which plays a positive role, since it facilitates unloading of the overfilled precapillary link.

At the same time, in both groups, a decrease in peripheral vascular resistance was observed, as evidenced by a significant increase in myospheric amplitudes. As a result, blood flow to the capillaries increases and organ and tissue perfusion improves.

Thus, in general, during the treatment with Crestor, patients with DLP and mild and moderate hypertension have seen favorable changes in the microcirculation system.

Another positive effect of rosuvastatin on the vessels was also revealed – a significant decrease in the SBP – by 8 mm Hg. Art., DBP – at 6 mm Hg. Art.

The study confirmed the pronounced hypolipidemic effect of Crestor.

Thus, the new hypolipidemic drug rosuvastatin has not only a pronounced hypolipidemic effect, but also a positive effect on the vessels, contributing to microcirculation and a decrease in blood pressure in patients with dyslipidemia and mild and moderate arterial hypertension . Of course, the indicated vascular effects of Crestor can positively affect the effectiveness of the prevention of CCO during long-term therapy with this statin.

As already noted, the problem of control of blood pressure and the correction of concomitant risk factors in the case of patients without clinical manifestations of atherosclerosis is that patients are not motivated for drug treatment (“risk factors do not hurt”), not to mention the motivation for non-pharmacological methods for the correction of concomitant risk factors. In this regard, one should note the successful experience of holding educational schools (in Ivanovo, Khabarovsk), which indicate that achieving better control not only of blood pressure, but also of correcting risk factors is quite possible .

Of particular note is the relevance of the development and implementation of motivational technologies in clinical practice. One of them can be the electronic version of SCORE (Systematic Coronary Risk Evaluation – Systematic (regular) coronary risk assessment) – a new system for assessing the risk of fatal outcomes of CVD for 10 years, developed by experts of the European Society of Cardiology together with specialists of the Federal Research Center The Ministry of Health and Social Development of Russia based on data from prospective studies conducted in European populations, including Russian (in total, more than 200,000 people). This The interactive system allows you to visually demonstrate to the patient the risk of a fatal outcome from CVD within 10 years and its positive dynamics in reducing the risk as a result of the intervention. Such a visual computer demonstration is designed to increase the motivation and commitment of patients to the drug and non-drug correction of risk factors and, ultimately, lead to a significant decrease in MDR. Currently, the Russian version of HeartScore has appeared on the Internet, which can be used by practical doctors.

The SCORE system includes the following risk factors: gender, age, smoking, systolic blood pressure (MAP), total cholesterol level. The high-risk criterion was defined as a risk of 5% and higher, in contrast to the previous figure of 20% and higher.

The status of smoking is determined when the patient is asked if he answers “yes” or “no”. A patient is considered to be a smoker if he smokes more than seven cigarettes a week.

The risk is considered very high if, when the patient data is projected onto the SCORE card, it is higher than 10%; high – if it is in the range from 5 to 10% medium – from 2 to 4% and low – less than or equal to 1%.

In case of high and very high risk, the patient needs to take active preventive and therapeutic measures aimed at eliminating and correcting risk factors.

Compared to the risk table, the advantages of using HeartScore for clinicians and patients are in their speed and ease of use, individual adaptation to the patient. The program offers:

.                                   –   graphic demonstration of absolute cardiovascular risk,

.                                   –   assessment of the relative role of corrected risk factors,

.                                   –   recommendations of intervention that contributes to a change in the behavior of treatment tolerance, i.e. patient adherence to treatment. HeartScore ® is a primary prevention tool for CVD, for assessing the risk of those who are not yet sick. But patients with existing symptoms of diseases associated with atherosclerosis require intensive treatment to prevent complications, so in such cases there is no need to resort to such a risk assessment, because these patients are already at high risk. HeartScore ®helps to assess the risk, and does not pretend to the absolute accuracy of the forecast. In HeartScore task ®
 
 
 
 
 It does not include an influence on the decision of the doctor regarding the tactics of treatment of patients and the starting point of treatment (from what level of risk to start treatment). These questions undoubtedly remain in the competence of the doctor.

In accordance with the European recommendations for the prevention of CVD, treatment should begin if the risk of death from CVD within 10 years exceeds 5%. For young patients, it is necessary to focus on the relative risk table. We have conducted a multicenter large-scale study on the effectiveness of integration into the clinical practice of the electronic version of SCORE.
 . The study involved 350 therapists from 47 cities of Russia. Each therapist included 3 high-risk patients with hypertension in the study (risk on the SCORE scale> 5%). A total of 1050 patients were included in the program. For the first time in the practice of research, not only in Europe, but also in Russia, the electronic version of SCORE was used to study the effect of its use in order to increase adherence to medical treatment of hypertension and effective control of associated risk factors. For this purpose, a subsample of 128 patients with AH was formed. In these patients, the risk was assessed using the electronic version of SCORE. Patients (n = 481 people) matched for age, sex, systolic blood pressure, frequency of smokers, body mass index were selected as the control group.In the control group, patients were shown a risk assessment according to the usual SCORE table. All patients were prescribed combination antihypertensive therapy as a starting therapy. The study lasted 1 year. By the end of the study, in the main group, a significantly larger number of patients reached the target level of blood pressure or responded to treatment (decrease in the GARDEN not less than 20 mm. Mercury. And / or decrease in DBP not less than 10 mm. Mercury. with a group of patients whose total risk was assessed according to the tables (without using the electronic version of SCORE), which corresponded to 90% to 82% of patients in the main and control group (p <0.005), Fig. 13. Thus, a more pronounced decrease in total cardiovascular risk was achieved in those patients whose risk was assessed using the electronic version of SCORE.All patients were prescribed combination antihypertensive therapy as a starting therapy. The study lasted 1 year. By the end of the study, in the main group, a significantly larger number of patients reached the target level of blood pressure or responded to treatment (decrease in the GARDEN not less than 20 mm. Mercury. with a group of patients whose total risk was assessed according to the tables (without using the electronic version of SCORE), which corresponded to 90% to 82% of patients in the main and control group (p <0.005), Fig. 13. Thus, a more pronounced decrease in total cardiovascular risk was achieved in those patients whose risk was assessed using the electronic version of SCORE.All patients were prescribed combination antihypertensive therapy as a starting therapy. The study lasted 1 year. By the end of the study, in the main group, a significantly larger number of patients reached the target level of blood pressure or responded to treatment (decrease in the GARDEN not less than 20 mm. Mercury. with a group of patients whose total risk was assessed according to the tables (without using the electronic version of SCORE), which corresponded to 90% to 82% of patients in the main and control group (p <0.005), Fig. 13. Thus, a more pronounced decrease in total cardiovascular risk was achieved in those patients whose risk was assessed using the electronic version of SCORE.By the end of the study, in the main group, a significantly larger number of patients reached the target level of blood pressure or responded to treatment (decrease in the GARDEN not less than 20 mm. Mercury. with a group of patients whose total risk was assessed according to the tables (without using the electronic version of SCORE), which corresponded to 90% to 82% of patients in the main and control group (p <0.005), Fig. 13. Thus, a more pronounced decrease in total cardiovascular risk was achieved in those patients whose risk was assessed using the electronic version of SCORE.By the end of the study, in the main group, a significantly larger number of patients reached the target level of blood pressure or responded to treatment (decrease in the GARDEN not less than 20 mm. Mercury. with a group of patients whose total risk was assessed according to the tables (without using the electronic version of SCORE), which corresponded to 90% to 82% of patients in the main and control group (p <0.005), Fig. 13. Thus, a more pronounced decrease in total cardiovascular risk was achieved in those patients whose risk was assessed using the electronic version of SCORE.compared with the group of patients in whom the total risk was assessed according to the tables (without using the electronic version of SCORE), which corresponded to 90% to 82% of patients in the main and control group (p <0.005), Fig. 13. Thus, a more pronounced decrease in total cardiovascular risk was achieved in those patients whose risk was assessed using the electronic version of SCORE.compared with the group of patients in whom the total risk was assessed according to the tables (without using the electronic version of SCORE), which corresponded to 90% to 82% of patients in the main and control group (p <0.005), Fig. 13. Thus, a more pronounced decrease in total cardiovascular risk was achieved in those patients whose risk was assessed using the electronic version of SCORE.

These data indicate the feasibility of introducing into clinical practice the management of patients without clinical manifestations of atherosclerosis of the electronic version of SCORE, not only as a tool for assessing the overall risk, but also as a motivational technology to improve adherence to drug and non-drug risk control methods. Ultimately, this should lead to a more effective reduction in total cardiovascular risk.

1. Hypotension is diagnosed if systolic blood pressure does not exceed 90 mm Hg. Art.
2. Shock is a clinical syndrome characterized by, in addition to hypotension, signs of reduced perfusion of peripheral tissues (cold skin, oligoanuria, lethargy and lethargy).
3. Breathing with 100% oxygen through a mask with a non-reversible valve and a bag-tank at an oxygen supply rate of 5–6 l / min).
4. To correct the pumping function of the left ventricle, blood pressure should be initially normalized. In case of arterial hypotension / cardiogenic shock, it is initially necessary to make sure that the ventricles of the heart are sufficiently filled with pressure (no absolute or relative hypovolemia). In an emergency in the absence of pulmonary edema, it is advisable to quickly inject 250 to 500 ml of fluid intravenously, possibly repeatedly (by controlling the degree of stagnation in the lungs and, if possible, at least central venous pressure). If a sufficient increase in blood pressure is not achieved, infusion of a pressor agent should be initiated, the choice of which depends on the level of blood pressure. In the presence of hypovolemia, it is important to identify and, if possible, eliminate its cause. In cases where pulmonary edema is combined with increased blood pressure, it is necessary to reduce it by infusion of nitroglycerin or sodium nitroprusside.To correct myocardial contractility, other existing disorders should also be eliminated (hypoxia, hypoglycemia, drug overdose). In addition, rapid restoration of normal myocardial blood supply (thrombolytic therapy or invasive methods of myocardial revascularization during occlusion of a large epicardial coronary artery), as well as surgical correction of existing intracardiac hemodynamics, may be required.as well as surgical correction of existing intracardiac hemodynamic disorders.as well as surgical correction of existing intracardiac hemodynamic disorders.
5. The norepinephrine infusion rate is 0.5–30 mcg / kg / min, the dopmin infusion rate is 2.5–20 mcg / kg / min.
6. Simultaneous (but not isolated infusion of dobutamine) is possible. Dobutamine is the drug of choice for myocardial infarction of the right ventricle (it is also important to administer intravenous fluids, not using vasodilators and diuretics).
7. Dobutamine infusion rate 2–20 mcg / kg / min.
8. Perhaps the use of intra-aortic balloon contraception (considered as a temporary measure before conducting invasive interventions – myocardial revascularization using angioplasty procedure, coronary artery bypass surgery, surgical correction of intracardiac hemodynamics, heart transplantation).
9. For the correction of high blood pressure in the acute phase of myocardial infarction, nitroglycerin is preferable, and in the absence of myocardial ischemia, sodium nitroprusside is preferable.
10. First-line interventions, in addition to intravenous administration of morphine and a diuretic (furosemide), also include giving the patient a half-sitting position with his legs down and ensuring breathing with 100% oxygen. With systolic blood pressure above 100 mm Hg. Art. you should start taking nitroglycerin (1 tablet every 5 to 10 minutes) or isosorbiddinitrate as an aerosol until it is possible to administer intravenous infusion of nitroglycerin. If there is no response to the first dose of furosemide, a double dose should be administered within 20 minutes. A ventilator should be started when the arterial blood oxygen saturation drops to 90%, the oxygen tension in the arterial blood reaches 60 mm Hg. Art. when breathing 100% oxygen, as well as clinical manifestations of brain hypoxia (drowsiness, lethargy), a progressive increase in the voltage of carbon dioxide in the blood or an increase in acidosis.In milder cases, it is possible to evaluate the effectiveness of creating a positive pressure at the end of exhalation or breathing under constant positive pressure.
11. Intravenous nitroglycerin is assigned to second-line drugs due to the time lag before the start of treatment. The administration of positive inotropic agents (dobutamine in the absence of arterial hypotension and dopmine in its presence) is assigned to the same group of interventions.
12. Amrinone as a positive inotropic agent and a vasodilator is administered at a loading dose of 0.75 mg / kg for 2–3 minutes followed by an infusion of 5–15 µg / kg / min. Euphyllinum is administered with severe bronchospasm at a loading dose of 5 mg / kg in 20-30 minutes, followed by an infusion of 0.5-0.7 mg / kg / h. Its use should be avoided with supraventricular tachyarrhythmias. Intra-aortic balloon contraception is considered as a temporary measure before invasive interventions (myocardial revascularization using an angioplasty procedure, coronary artery bypass surgery, surgical correction of intracardiac hemodynamics, heart transplant).

Clinical manifestations chronic heart not sufficiency can to arise on normal background or almost normal systolic LV function by according to Echocardiography . A common cause of chronic heart failure is LV diastolic dysfunction .

Diastolic dysfunction is detected at a whole range of cardio – vascular diseases . She is more sensitive at comparing with systolic cal function to natural aging processes . Violations of diastolic function can be iso Rowan , combined with systolic dysfunction or precede a clear violation of systole . Violations of diastole is dominated by about at thirdspatients with chronic heart failure . Required evaluate as systolic , so and diastolic function of the left ventricle , so as the causes of their violations and , that more importantly , their correction methods are different . Simplified times division on systolic and diastolic dysfunction is often unjustified . Systole and diastole – Inter – liyayuschie phase of the cardiac cycle . With minor systolic dysfunction some segments with on ruined local contractility can keep shrinking at diastole , resulting in to decrease in time for ventricular fillingand diastolic dysfunction . On the contrary , a stubborn LV , unable to adequately fill at diastole , provides low stroke volume at systole and leads to systolic dysfunction . High peak BUT It corresponds to the fourth auskultativ Nome tone of the heart , then as high peak E – the third auscultatory tone

Possible errors in identifying dysfunction of the right ventricle.

Echocardiographic assessment of the pancreas is difficult at svya communication with significant trabecular , complex geometry cal form and interaction with other chambers of the heart . More than that , the prostate is located directly behind the breastbone , which hinders its visualization . Evaluation The pancreas is especially difficult with increased airiness of the lung tissue ( emphysema ), pneumosclerosis and torus kotomii at history . For unfortunately , namely with of these states estimation function of the pancreas is the largest zna chenie . RV function depends not only from myocardial contractility , but and on the conditions of load , contractility of the left ventricle , excursions IVS and pressure atpericardium . With analysis of pancreas function should be considered everything these factors . Even an experienced researcher is able to conduct a full study of the pancreas less than in 50% of patients .

The clinical significance of right ventricular dysfunction

Identification of dysfunction of the pancreas is a principled nym with a number of congenital and acquired diseases of the heart for the choice of tactics of treatment , planning the timing of surgical intervention , determine the prognosis .

With congenital defects , such as defect MZhP , defect MPP or tetralogy of Fallot , evaluation function of the pancreas to and after surgery treatment allows define prognosis of the disease .

In a similar manner as possible surgical vmesha ments with defects of the heart , such as mitral ste ERA , stenosis of the mouth of the pulmonary artery or tricuspid regurgitation ( TR ) depends on the availability or lack of dysfunction of the pancreas . Patient long-term prognosis with chronic diseases of the lung ( chronic obstructive disease of the lungs , interstitial for bolevaniya light ) depends on the function of the pancreas . Dilatation of the pancreas , pulmonary hypertension and pulmonary heart are predictors of negative prognosis .

With myocardial infarction pancreas dysfunction observed at following situations :

.       lower myocardial infarction with involvement of the pancreas ;

.       anterior myocardial infarction with acute defect MZhP .

Tactics treatment pancreatic infarction is different from leche of LV infarction . Dysfunction of the pancreas due postin farktnogo defect IVS is an important cause of death ( see . Chapter ” Coronary disease of the heart ” ). Diastolic kollabirovanie pancreas is an important echocardiographic sign of tamponade of the heart ( see . Chapter ” Diseases of the pericardium ” ).

Indicators transmitral blood flow depends on many factors , and not only on tensile properties and LV relaxation . Therefore , when assessing diastolic function of the left ventricle to rely only on E / A ratio is incorrect .

On The transmitral bloodstream is affected by the following factors :

.       load capacity ( preload and afterload );

.       frequency of heart contractions ;

.       systolic function of the LP ;

.       respiratory phase .

Overload volume due to mitral or Aortic insufficiency reduces peak A , so as atrial contraction not at able to effectively push blood at already maximally stretched the desire of daughters . With tachycardia peak amplitude BUT increases at connections with shortening of diastole ( greater contribution of atrial systole ). On the contrary , if bradycardia peakBUT Decrease the creases due to the elongation phase of diastolic filling ( smaller contribution contraction of the atria ). So manner , high peak BUT It has a greater value onbackground bradycardia .

Ratio E / A incorrectly when atrial Arita mission , complete transverse blockade and lengthening the PR interval . Have elderly patients dominated by peak A. Ratios e E / A > 1 or E = A at combined with the shortening of time for slowing reflects the increase in course – diastolic pressure at LV . This type of diastolic dysfunction was the name pseudonormal .

For An adequate assessment of LV diastolic function is necessary to know the physiology of the diastolic phase of the cardiac cycle .

AT diastole there are four periods :

.       phase relaxation : on closing of the aortic valve stem Pan to the opening of the mitral valve ( phase 1);

.       early rapid filling phase : from the opening of the mitral valve to the end of filling ( fa for 2);

.       phase of diastasis — equilibrium ( phase 3);

.       phase systole predserdiy- active cut of auricles ( phase 4).

The first two phases correspond to the relaxation of the ventricular myocardium ( energy-intensive process ). Tre tya and The fourth phase reflects the passive extension of the myocardium , depending on its rigidity . So way , allocate two major type dia stolicheskoy dysfunction :

slow relaxation ;

restrictive type .

Diastolic dysfunction occurs at connections with by Vyshen stiff LV , which leads to disruption of diastolic blood flow of LP at LV .

Scanning in the M-mode at the level of the mitral valve

AT normal movement PSMK at diastole has character hydrochloric M – shaped form ( with waves E and A ) With diastema netocrystalline dysfunction LV tour PSMK reduced , wave BUT becomes higher , than the wave E , that leads to reducing the E / A ratio . These changes OCU by previously increased rigidity LV and subsequent increase in pressureat LP . Indicated signs not are highly sensitive or specific for identify diastolic dysfunction .

Practically everything diseases hearts early or late lead to systolic dysfunction of the left ventricle . The main reasons are given below at order decreasing frequency .

Ischemic disease of the heart : recurrent myocardial infarction , commonly infarction , multivessel lesion .

Hypertensive heart : LVH decompensation .

Valve pathology : mitral or aortic insufficiency ( volume overload ).

Primary myocardial damage : dilated ILC or acute myocarditis .

Congenital malformations of the heart : reset the left to right ( defect IVS ).

The clinical significance of left ventricular systolic dysfunction

Systolic dysfunction of the left ventricle at any zabole Vania heart is an independent negative prognostic factor .

Have Patients with ischemic disease of the heart with systolic cal dysfunction of the left ventricle is less than the survival rate after operations revascularization ( coronary artery shunt vanie ). The development of systolic dysfunction in a patient with LVH on background of arterial hypertension characterized by transition to phase decompensation hypertensive heart . Volumetric overload of the LV due to valve insufficiency or intracardiac discharge from left to right will inevitably lead to systolic dysfunction of the left ventricle . AT addition to prognostic information , devel term systolic dysfunction plays a key role at determining the tactics of managing patients with heart defects . LV systolic dysfunction is one of major diagnostic criteria for dilated CMP . Serial echocardiographic examinations allow not just trace the natural flow disease , but and define efficiency Spend my therapy . Minor violations of systolic function , imperceptible at alone , it can be identified at

research at load . On the background of adequate medical management of heart failure is also can observed only minor violations of systolic function .

One of The causes of LV systolic dysfunction are myocarditis — inflammation of the myocardium viral ( Coxsackie type B virus ), bacterial ( mycoplasma ) or parasitic ( Lyme disease ) nature .

Echocardiographic signs of myocarditis are similar. with picture dilated ILC , consisting By combining of systolic and diastolic dysfunction of the left ventricle , as well as insufficiency of the valvular apparatus . Occasionally can determined by the violation of local contractility due to focal nature of inflammation . By differential differential signs of myocarditis include the presence of febrile fever at recent past as well as sinus tachycardia at rest at combined with Inversion her teeth T on ECG . Rapid improvement in LV function and reduction of mitral insufficiency by according to serial echocardiographic studies allows you to lean at favor the diagnosis of myocarditis , and not dilated KMP .