Chronic heart failure: types, treatment. Heart failure due to disease. Signs and treatment of restrictive cardiomyopathy

Research Institute of Cardiology named after A.L. Myasnikov of the Republic of Kazakhstan NPK of the Ministry of Health of the Russian Federation, Moscow

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In recent years, the dialectics of our ideas about the priority pathogenetic mechanisms responsible for the development of chronic heart failure (CHF) has completed the classical evolutionary spiral (Fig. 1): today, again, like 50 years ago, the attention of physiologists and clinicians is focused on central hemodynamic disorders.
However, if "at the dawn" of pathogenetic studies, the main cause of the onset and development of CHF was considered to be a decrease in the contractile (systolic) ability of the myocardium, then in recent years it has been customary to talk about the different "contribution" of systolic and diastolic dysfunction in the pathogenesis of the disease, as well as systolic-diastolic relationships in heart failure. At the same time, a violation of the diastolic filling of the heart is assigned no less, and perhaps even a greater role than systolic disorders.

What caused the increased attention to diastolic dysfunction? The role of assessing systolic and diastolic function for patients with CHF
Back in the middle of the century, in the experimental works of E. Sonnenblick, E. Braunwald, FZ Meyerson, the postulate of the unity of systolic and diastolic disorders underlying the development of heart failure was substantiated (1,2). By the beginning of the 80s, a lot of clinical evidence had accumulated, casting doubt on the "monopolistic" role of systolic dysfunction as the main and only hemodynamic cause responsible for the occurrence, clinical manifestations and prognosis of patients with heart failure. The essence of these facts is that poor contractility and low fraction left ventricular ejection (LVEF) does not always unequivocally predetermine the severity of decompensation, exercise tolerance, and even the prognosis of patients with CHF (Table 1.)
Table 1. Studies indicating a weak relationship between systolic dysfunction and clinical manifestations and prognosis of patients with CHF

At the same time, strong evidence was obtained that indicators of diastolic dysfunction, to a greater extent than myocardial contractility, correlate with clinical and instrumental markers of decompensation and even with the quality of life of patients with CHF. So, in a study conducted in the Department of Myocardial Diseases and Heart Failure, Research Institute of Cardiology named after A.I. A.L. Myasnikov, it was shown that the level of quality of life measured in 92 patients with CHF is practically not associated with cardiac contractility and LVEF (r=0.03; p>0.1), but has a significant (albeit weak) relationship with diastolic index Ve/Va (r=0.26; p=0.05).
Table 2. What are CHF patients with diastolic dysfunction? (MISCHF study data)

Rice. 1. Change of pathogenetic models of CHF development.
50s: cardiac model. main reason CHF - hemodynamic disorders associated with a decrease in cardiac contractility (treatment - cardiac glycosides)
60s: cardiorenal model. The cause of CHF is a violation of the function of the heart and kidneys (glycosides + diuretics)
70s: circulatory model. The cause of CHF is a violation of the function of the heart and peripheral vessels (glycosides + peripheral vasodilators)
80s: neurohumoral model. The cause of CHF is hyperactivation of neurohormones ( ACE inhibitors, b-blockers)
90s: myocardial model. The cause of CHF is hemodynamic disorders associated with myocardial changes occurring under the influence of neurohormones, and manifested by a deterioration in diastolic and systolic properties (treatment - ACE inhibitors, Ca antagonists 2+ (?), b -blockers)

In the same years, there was evidence of a direct connection between diastolic disorders and the prognosis of patients with CHF.
All this made us re-evaluate the importance of LV systolic dysfunction as the only and indispensable hemodynamic constant, and take a fresh look at the role of diastolic disorders in the pathogenesis of CHF.
Currently, systolic function, which is assessed mainly by the LV ejection fraction, is still assigned the role of an independent predictor of the prognosis of patients with CHF (Fig. 2). In addition, low LVEF remains a reliable marker of myocardial injury; contractility assessment is mandatory to determine the risk of cardiac surgery and can be used to determine the effectiveness of treatment.

Assessment of diastolic function has not yet become mandatory procedure, which is largely due to the lack of proven and accurate methods for its assessment.Nevertheless, even now there is no doubt that it is diastolic disorders that are responsible for the severity of cardiac decompensation and the severity of clinical manifestations of CHF. Diastolic markers more accurately than systolic ones reflect the functional state of the myocardium and its reserve (ability to perform a load), and more reliably than other hemodynamic parameters can be used to assess the quality of life and efficiency medical measures. In addition, there are all the prerequisites for the use of diastolic indices as predictors of prognosis in heart failure.

What do we mean by the terms "diastolic dysfunction" and "diastolic heart failure"?

The classical definition of diastolic dysfunction implies a purely pathophysiological aspect - the inability of the LV to take in (fill) a volume of blood sufficient to maintain adequate cardiac output at normal mean pulmonary venous pressure (< 12 мм рт.ст.) . Согласно этому простому определению, диастолическая дисфункция является следствием такого повреждения сердца, при котором для адекватного заполнения полости ЛЖ требуется high blood pressure in the pulmonary veins and left atrium. What can prevent LV filling? There are only two main reasons for worsening LV filling in diastolic dysfunction: 1) impaired active relaxation of the LV myocardium and 2) deterioration in LV wall compliance (Fig. 3). It should be remembered that the definition of diastolic dysfunction does not include patients with mitral stenosis, who also have an increase in pressure in the left atrium and impaired filling of the LV chamber, but not due to myocardial damage, but due to a mechanical obstruction to blood flow at the level of the A-V holes.
diastolic dysfunction may be combined with preserved or slightly reduced systolic function. In such cases, it is customary to speak of "primary" diastolic dysfunction, which is very often associated in our country exclusively with hypertrophic cardiomyopathy, constrictive pericarditis, or exotic restrictive myocardial diseases. Although in the vast majority of cases, diastolic dysfunction with preserved systolic function is characteristic of the most common diseases - arterial hypertension and coronary artery disease. As already mentioned, in about 1/3 of patients with clinically severe CHF, the development of decompensation is not associated with a clear violation of myocardial contractility and occurs, probably, due to diastolic disorders. To refer to such patients in the English literature, the terms are used: "heart failure with preserved systolic function" or "stiff heart syndrome".
However, the most common group of patients is that in which diastolic dysfunction is combined with systolic disorders. In fact, a decrease in systolic function in itself is the most common marker of diastolic disorders, and reduced contractility is always accompanied by impaired diastolic filling of the heart. In other words, if diastolic dysfunction can exist without visible systolic disorders, then systolic dysfunction always occurs against the background of impaired diastolic function. The pathophysiology of this phenomenon is described in more detail later in the article, as well as in the lecture and review presented in this issue of the journal. From a clinical point of view, in the treatment of heart failure, such a pattern dictates in our time the need to assess not only and not so much the known systolic, but the diastolic effects of the drugs used, which is extremely rare and, as a rule, only in patients with the so-called diastolic cardiac insufficiency.
As recommended working group European Society of Cardiology, the diagnosis of primary (isolated) diastolic heart failure is eligible with the mandatory presence of all three the following criteria:
1. Clinical signs actually CHF;
2. normal or slightly reduced myocardial contractility (LVEF > 45% and LVCD index< 3,2 см.м -2 );
3. data on disturbed relaxation or filling of the LV, signs of increased rigidity of the LV chamber.
The difference between the terms "diastolic dysfunction" and "diastolic heart failure" should be taken into account: diastolic heart failure always includes diastolic dysfunction, but the presence of diastolic dysfunction does not yet indicate the presence of heart failure.

Features of the epidemiology of diastolic dysfunction and diastolic heart failure

Diastolic dysfunction is probably extremely common. According to the Framingham study, such an indirect marker of diastolic dysfunction as LV hypertrophy occurs in 16-19% of the population and in at least 60% of patients with arterial hypertension. Diastolic dysfunction is more common in elderly patients, which are more sensitive to factors causing diastolic disorders, such as tachycardia, hypertension, ischemia. In addition, with age, the mass of the myocardium increases and its elastic properties deteriorate. Thus, in the future, due to the general "aging" of the population, one should expect an increase in the role of diastolic dysfunction among pathogenetic diseases. causes of CHF. So, according to McDermott, in the period from 1987 to 1993, the number of patients with CHF that developed against the background of diastolic dysfunction increased from 36 to 44%, i.e. the increase is 1.0-1.5% annually.
diastolic cardiac insufficiency is much less common than diastolic dysfunction, and is observed on average in 30% of patients with CHF, although some specialized echocardiographic studies show an even lower figure - 12%. This gives reason to believe that isolated diastolic heart failure is still not as common as it is believed.
Another feature of diastolic heart failure is a relatively better prognosis than in patients with "classic" systolic CHF: the annual mortality rate is 5-12% versus 15-30%, respectively. However, such "well-being" is deceptive, since the mortality of patients with "classic" systolic CHF is constantly decreasing, and in patients with diastolic heart failure, it remains at the same level from year to year. The reason for this phenomenon is clear - the lack of effective treatments for diastolic CHF; the consequences for such patients are sad: if this trend continues in the new century, we will mainly treat only diastolic CHF.

What is a "standard" patient with diastolic heart failure?

What is and what does a "standard" patient with diastolic heart failure look like? As can be seen from Table. 2, this is usually an elderly woman with arterial hypertension, often suffering from diabetes and atrial fibrillation. According to the severity of decompensation, she differs little from the "classic" patients with systolic dysfunction, but her heart size is noticeably smaller.,and the ejection fraction is greater.
But most importantly, neither she nor her doctors (!) really know how to behave and how to be treated.
To understand this issue, one should turn to the pathophysiology of the process.

From diastolic disorders to heart failure: three steps down

The issues of the pathophysiology of the development of diastolic heart failure are covered in detail in the review published in this issue of the journal. Schematically, the pathophysiology of the process is shown in fig. 3. At the 1st stage, under the influence of various damaging agents (overload, ischemia, infarction, LV hypertrophy, etc.), the process of active relaxation of the myocardium and early filling of the LV is disrupted, which at this stage is completely compensated by the activity of the left atrium and therefore does not manifest itself in any way even under load. The progression of the disease and an increase in the rigidity of the LV chamber is accompanied by a forced increase in LV filling pressure (the atrium can no longer cope!), which is especially noticeable during exercise. There is an even greater difficulty in blood flow to the left ventricle and a pathological increase in pressure in the pulmonary artery, which reduces exercise tolerance (stage 2). A further increase in LV filling pressure (3rd stage) completely "disables" the atrium; blood flow to the ventricle (blood outflow from the lungs) is critically reduced, which is accompanied by a drop in cardiac output, sharp decline tolerance and congestion in the lungs (detailed picture of CHF).
Thus, the mechanism of the process is a classic version of the development of stagnation caused by a deterioration in the outflow of blood from the lungs (backward failure), due to a deterioration in active relaxation of the myocardium and an increase in the rigidity of the LV chamber.
The key to solving the problem is to improve active relaxation and increase LV chamber compliance.

Treatment of diastolic heart failure: challenges and prospects

Obviously, the diagnosis and treatment of diastolic disorders should be started as early as possible, before the appearance of irreversible structural changes in the myocardium and systolic dysfunction. However, none of the existing medicines does not have a "pure" diastolic effect: selectively improving myocardial relaxation, drugs, as a rule, inhibit contractility and pumping function of the heart. Therefore "ideal" there is no treatment strategy for such patients, drugs are selected empirically, without a clear pathophysiological concept.
Using positive properties existing classes of drugs, one can try to substantiate 4 main directions of therapy for such patients:
1. Reducing congestion in the lungs by reducing the BCC (diuretics);
2. Improvement of LV active relaxation (Ca antagonists 2+ or ACE inhibitors)
3. Regression of LV hypertrophy and improvement of wall compliance (decrease in myocardial thickness and excess collagen in it - ACE inhibitors, AII receptor blockers or spironolactone);
4. Support for compensatory (contractile) atrial function and heart rate control ( b blockers, antiarrhythmics).
Some usage details various drugs presented in the review published in this issue of the journal. To this it must be added that to date, not a single prospective, multicenter study has been completed to evaluate the effect of any therapy on the survival of patients with diastolic CHF, and the number of such studies is disproportionately smaller than in systolic CHF.
In the works, in which patients with diastolic dysfunction nevertheless participated, the drugs from the group of Ca antagonists turned out to be the most studied. 2+ (verapamil and diltiazem), ACE inhibitors (captopril, enalapril, periodopril) and b blockers (metoprolol). Unfortunately, the data obtained do not inspire much optimism and rather indicate the absence of an "ideal" drug in the treatment of diastolic heart failure.
For example, antagonists of Ca 2+ , improving the active relaxation of the myocardium and increasing the compliance of the LV walls, are the means of choice in the treatment of diseases accompanied by severe LV hypertrophy. However, the addition of severe systolic disorders and congestive heart failure to LV hypertrophy makes the use of Ca antagonists 2+ dangerous due to the increased risk of death, especially sudden death.
Even ACE inhibitors - the most effective means of treating CHF - when used in patients with primary diastolic disorders partially "lose" their effectiveness in comparison with patients with "classic" systolic dysfunction. Thus, according to the large-scale MISCHF study, the reduction in mortality with the use of ACE inhibitors in patients with "classic" systolic CHF was expected and averaged 11% (p=0.04); at the same time, in patients with preserved systolic function, the decrease in mortality was no longer significant (p=0.08) and did not exceed 7%.
maybe, selective blockers receptors for AII (losartan, irbesartan, candesartan, etc.), due to a more powerful inhibitory effect on the proliferation of smooth muscle cells and fibroblasts, will be more effective in the treatment of such patients than ACE inhibitors. We hope to get an answer to this question after the completion in 2001 of the multicenter CHARM study, which evaluates the effectiveness of candesartan therapy in patients with CHF and high LV EF.
It is also interesting to use aldosterone antagonists (aldactone) in such patients, which can be useful due to the ability to slow down the expansion of collagen and reduce LV hypertrophy, as well as have a normalizing effect on fibrinogen and electrolytes.
Among the new classes of drugs, the most promising are "double" neurohumoral modulators - inhibitors of neutral endopeptidase (omopatrilat). Providing the same effects as ACE inhibitors, homopatrilat additionally prevents the destruction of natriuretic peptides - vasodilating hormones that have a diuretic and antiproliferative effect, which is extremely useful in diastolic disorders.

Conclusion

Diastolic heart failure is not a new disease or new form CHF: at the beginning of the century, E. Starling (1918) pointed out the fundamental importance of diastolic filling for the work of the whole heart, and in the 50-70s, the Sarnoff and Braunwald school proved the fundamental role of the diastolic properties of the ventricles for normal operation hearts. However, the key role of diastolic dysfunction in the pathogenesis and treatment of CHF has become recognized only in recent years, mainly due to the widespread prevalence of arterial hypertension and coronary artery disease - the main substrates of diastolic disorders.
What are the main difficulties associated with resolving the issue of diastolic CHF today?
First, the "Achilles' heel" of diastology is still the lack of accurate and safe technique to assess diastolic function of the heart. This issue is partly covered in a lecture published in this issue of the journal.
Another problem is the treatment of diastolic CHF: despite the wide range of drugs that are potentially effective for the treatment of such patients, none of them can be considered ideal, even ACE inhibitors.
Finally, the last and probably the most important problem is the lack of attention of researchers and doctors to this issue. Simple logic suggests that, according to the prevalence of the phenomenon, patients with diastolic CHF should be devoted to at least 1/3 of all large multicenter studies to assess the survival of patients with heart failure. In fact, such studies are rare and can be listed on the fingers: PEP-CHF (with perindopril) and CHARM (with candesartan).
We are on the threshold of the 21st century, and it depends only on the combination of our efforts and attention whether this century will become the century of "diastolic heart failure".

Literature:
1. Meyerson F.Z. Hyperfunction. Hypertrophy. Heart failure. M.: Medicine, 1968; 388 p.
2. Sonnenblick E.H, Downing S.E. Afterload as a primary determinant of ventricular performance. Am J Physiol 1963; 204:604-10.
3. Ageev F.T. The influence of modern drugs on the course of the disease, quality of life and prognosis of patients with various stages of chronic heart failure. Diss. … Dr. med. 1997; 241.
4. Shen W., Tribouilloy C., Rey J-L. et al. Prognostic significance of doppler-derived left ventricular diastolic filling variables in dilated c ardiomyopathy. Am Heart J 1992; 124:1524-32.
5. Little W.C., Downes T.R. Clinical evaluation of left ventricular diastolic performance. Prog in Cardiovas Diseases 1990; 32:273-90.
6. How to diagnose diastolic heart failure. European Study Group on Diastolic Heart Failure. Eur Heart J 1998; 19:990-1003.
7. Levy D., Anderson K., Savage D. Echocardiographically detected left ventricular hypertrophy: prevalence and risk factor. The Framingham Heart Study. Ann Intern Med 1988; 108:7-13.
8. McDermott M.M. et al. Heart failure between 1986 and 1994: temporal trend in drug-prescribing practices, hospital readmissions, and survival at an academic medical center. Am Heart J 1997; 134:901-9.
9. Cowie M.R., Wood D.A., Coats A.J.S. et al. Incidence and aetiology of heart failure. A population-based study. Eur Heart J 1999; 20:421-28.
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Diastolic heart failure is a violation of relaxation and filling of the left ventricle, due to its hypertrophy, fibrosis or infiltration and leading to an increase in end-diastolic pressure in it and the development of heart failure.

Prevalence of symptoms of diastolic heart failure

Symptoms of diastolic heart failure account for 20-30% of all cases of heart failure. It can be combined with systolic heart failure.

Causes of diastolic heart failure

Causes of diastolic heart failure include the following diseases:

• IHD (with or without myocardial infarction);
• Hypertrophic cardiomyopathy;
• Amyloidosis of the heart;
• Arterial hypertension;
• Valvular heart disease;
• Diabetes;
• Constrictive pericarditis.

Symptoms of diastolic heart failure

As a result of reduced compliance and impaired filling of the left ventricle, end-diastolic pressure in the left ventricle increases, which leads to symptoms of reduced cardiac output. There is an increase in pressure in the left atrium, a small circle of blood circulation. Subsequently, a symptom of right ventricular heart failure may occur.

Mandatory symptoms diastolic heart failure is considered the following:

• The main symptom is the presence of normal or slightly reduced contractile function of the left ventricle.
• Symptoms of pathological filling and relaxation of the left ventricle, impaired diastolic stretching of the left ventricle.
• Symptoms of chronic heart failure include symptoms of increased pressure in the left atrium: shortness of breath when physical activity, orthopnea, "gallop rhythm", wheezing in the lungs, pulmonary edema.
• Symptoms of normal or slightly reduced contractile function of the left ventricle are determined by echocardiography in heart failure.
• One of the many symptoms is a left ventricular ejection fraction of at least 45%.
• The index of the internal final diastolic size of the left ventricle is less than 3.2 cm per 1 m2 of the body surface.
• The index of the end diastolic volume of the left ventricle is less than 102 ml per 1 m2 of body surface.
• Symptoms of pathological filling and relaxation of the left ventricle, abnormal diastolic stretching of the left ventricle are determined by echocardiography (sometimes catheterization of the heart cavities).
• Auxiliary symptoms of heart failure of this type are the time of isovolumic relaxation of the left ventricle more than 92 ms (for the age of less than 30 years), more than 100 ms (for the age of 30-50 years), more than 105 ms (for the age of over 50 years).
• The ratio of the E peak amplitude to the A peak amplitude is less than 1 (for an age younger than 50 years), less than 0.5 (for an age older than 50 years).
• End diastolic pressure of the left ventricle more than 16 mm Hg. Art. or mean pulmonary capillary wedge pressure greater than 12 mm Hg. Art. (according to the catheterization of the cavities of the heart).

Forms of heart failure

The following forms of heart failure are distinguished: according to the speed of development of symptoms of heart failure - acute and chronic.

• acute form heart failure occurs with myocardial infarction, acute insufficiency mitral and aortic valves rupture of the walls of the left ventricle.
• Symptoms of chronic heart failure develop gradually. Acute heart failure can complicate the course of chronic heart failure.

UDC 616.122

TREATMENT OF DIASTOLIC DYSFUNCTION IN CHRONIC HEART FAILURE

LAKamyshnikova1 OA Efremova2

1 Municipal health care institution "Gorodskaya clinical Hospital№1, Belgorod

A review of current data on the treatment of diastolic chronic heart failure is presented.

Key words: diastolic dysfunction, chronic heart failure, treatment.

2 Belgorod

state

university

e-mail: [email protected]

To date, the prevalence in the population of the European part of Russia of chronic heart failure (CHF) III-IV functional class (FC) is 2.3%, the number of people suffering from CHF I-II functional class reaches 9.4%, which significantly exceeds similar foreign indicators .

Deterioration of systolic function has ceased to be a mandatory criterion for CHF. Moreover, low contractility of the left ventricle (LV) in outpatients with CHF is rather an exception to the rule: a left ventricular ejection fraction (EF) of less than 40% is detected in only 8.4% of patients. The most common finding is a normal or almost normal EF in the range of 40-60% (in 52.4% of patients). And, finally, 38.8% of outpatients with CHF have a hyperkinetic type of circulation with LV EF> 60%, which is associated with the presence of hypertension, an increase in the left ventricle (mainly due to myocardial hypertrophy), normal sizes cavities.

In recent years, the issue of treating CHF with preserved LV systolic dysfunction (HF-SSF) has become increasingly relevant, while there is no convincing evidence base for improving survival when using any specific drug treatment in CHF patients with diastolic dysfunction (DD). However, the effectiveness of some drugs has been shown in separate studies and is currently being studied.

Theoretically, drugs that reduce LV hypertrophy (LVH), improve active relaxation, and increase LV compliance should improve diastolic function.

For the treatment of CHF caused by LV diastolic dysfunction, it is usually recommended to use β-blockers, cardioselective calcium antagonists (verapamil and diltiazem), ACE inhibitors (ramipril, in particular), as well as AT1-angiotensin receptor blockers (losartan, valsartan, irbesartan and etc.).

There are certain features in the treatment of various CHF syndromes with preserved LV systolic function. So, for example, to improve heart function in patients with hypertrophic cardiomyopathy, β-blockers, verapamil and (or) disopyramide should be used; in patients with chronic cor pulmonale- calcium antagonists of the dihydropyridine series. Dihydropyridine calcium antagonists, as well as hydralazine and ACE inhibitors, may be useful in the treatment of patients with aortic or mitral regurgitation because as arterial vasodilators they reduce left ventricular afterload and thus reduce valvular regurgitation.

ACE inhibitors

The beneficial effect of ACE inhibitors (ACE inhibitors) in these patients may be associated with an effect on myocardial remodeling and a decrease in myocardial mass, the regression of fibrosis and an increase in the elasticity of the left ventricular wall.

Data on the beneficial effect of ACE inhibitors on the diastolic function of the heart in patients with hypertension were obtained in most of the studies. Improvement in LV diastolic function is observed in a fairly short time - as a rule, after 8-16 weeks of therapy, i.e. even before a statistically significant regression of LV hypertrophy. Significant improvement in surrogates endpoints(functional status, exercise tolerance, quality of life) in patients with CHF and relatively preserved contractility (EF > 45%) was shown in a prospective Russian study of FASON with ACE inhibitor fosinopril. A placebo-controlled study to evaluate the effect of ACE inhibitors on the survival of elderly patients with diastolic heart failure (DSF) (PEP-CHF), performed with perindopril, did not show a significant reduction in overall or cardiovascular mortality during treatment with ACE inhibitors. However, 1 year after the start of the study, ACE inhibitor therapy was associated with a significant reduction in the risk of unscheduled hospitalization due to decompensation. Thus, ACE inhibitors have not yet proven their ability to improve the prognosis of patients with HF-SSF and DHF, however, their use in such patients is absolutely justified, according to at least, in connection with the improvement of the functional status of patients and a decrease in the risk of involuntary hospitalizations.

Kuimov A.D. et al. a study was made of the effect of ACE inhibitor lisinopril on disorders of LV diastolic function and on the endothelial response in patients arterial hypertension with chronic heart failure and without CHF. As a result, a significant improvement in diastolic function was found in both groups, the endothelial response significantly improved only in patients without signs of CHF. The quality of life of patients, according to the analysis of questionnaires, significantly improved in both groups.

Angiotensin II receptor antagonists (ARA)

In terms of the degree of positive effect on LVH and the severity of fibrosis, ARA is not inferior to ACE inhibitors, and in terms of the ability to eliminate diastolic disorders, they can even surpass ACE inhibitors. Thus, in the Russian comparative study PIRANHA, the use of ARA irbesartan in patients with HF-CSF and severe diastolic disorders was associated with a more pronounced improvement in both hemodynamics and the functional status of patients than ACE inhibitor therapy with perindopril. However, as with ACE inhibitors, only one multicenter placebo-controlled study has been completed to assess the effect of ARA on the survival of patients with CHF with preserved systolic function - this is CHARM-preserved, performed with candesartan. This study also did not reveal a significant reduction in the risk of cardiovascular mortality in patients with HF-CVF with the use of ARA. But the frequency of hospitalizations associated with exacerbation of decompensation, and the number of new cases diabetes in the candesartan group was significantly less than in the placebo group. Currently, several more multicenter controlled studies with ARA are ongoing (I-PRESERVE, HK-DHFONTARGET/TRANSCEND), including those involving Russian patients. Thus, ARAs have not yet proven their ability to improve the prognosis of patients with HF-SSF. Nevertheless, the results of the CHARM-preserved study showed that the use of candesartan ARA in diastolic disorders at least reduces the frequency of hospitalizations, and its use in such situations is justified, especially in cases of intolerance to ACE inhibitors.

P-adrenergic receptor blockers (BABs)

Potentially, β-blockers can improve the course of CHF with preserved systolic function due to several mechanisms: slowing the heart rate (HR) and, as a result, improving LV diastolic filling, reducing LV hypertrophy, and inhibiting renin release. However, on the other hand, the activation of P-adrenergic receptors is compensatory in nature, helping to reduce diastolic dysfunction, therefore, it is effective

The possibility of long-term use of β-blockers in patients with EF above 45% requires further study.

BAB can be prescribed to reduce heart rate (increase the period of LV diastolic filling) and the severity of LVH (decrease the rigidity of the LV chamber). The SWEDIC study showed that the α-β-blocker carvedilol, in addition to lowering heart rate, has a positive effect on Doppler echocardiography of LV relaxation parameters in patients with DHF. Special works on the study of the effect of BAB on the survival of patients with DHF have not been carried out. However, in the SENIORS study with non-bivolol, which included more than 700 elderly patients with slightly reduced contractility (LV EF > 35%), therapy with this β-blocker was associated with a decrease in the combined rate of total mortality or hospitalization for cardiovascular reasons.

Given the lack of adherence to the prescription of recommended β-blockers for patients with CHF, the first multicenter open study in Russia in real outpatient practice, called "Optimization of the use of Betaloc ZOK in patients with CHF in everyday medical practice (BEZE)", was conducted in order to study the efficacy and safety of using Betaloc ZOK in complex treatment CHF and train physicians to use in real practice tools for monitoring the condition of patients with CHF. A total of 1427 patients with CHF were examined. It was shown that the treatment of patients with CHF with Betaloc ZOK, even at low doses under outpatient supervision, was not accompanied by clinical deterioration in the first weeks, that is, effectively and safely. Betaloc ZOK was optimally suited for the treatment of patients with systolic CHF, as well as those with hypertension and diastolic dysfunction, complicated by symptoms of cardiac decompensation. After the BEZE study, there can be no real grounds for refusing to prescribe BAB (Betaloc ZOK) to patients with CHF who are at the outpatient stage of treatment.

calcium antagonists

Calcium antagonists (ACs) also have a beneficial effect on LV diastolic dysfunction by controlling blood pressure levels, reducing myocardial oxygen demand, causing dilatation coronary arteries and regression of LV hypertrophy. The pathophysiological justification for the use of AAs is their ability to improve myocardial relaxation and thereby increase diastolic ventricular filling. However, if their positive effect in patients with hypertension is indisputable, then the effect on the survival of patients with CHF and the progression of this disease has not been studied enough. For example, AAs are the drugs of choice in the treatment of diseases accompanied by severe LV hypertrophy, but the addition of severe systolic disorders and congestive heart failure to LV hypertrophy makes their use impractical and even dangerous due to a decrease in the pumping function of the heart and an increased risk of death. In patients with preserved systolic function of the heart and existing diastolic dysfunction, only AKs of the dihydropyridine structure can be used. III generation, amlodipine. This drug, along with ACE inhibitors, has the most pronounced ability to cause regression of left ventricular hypertrophy and improve the state of diastolic function of the heart. Research conducted by M.R. Bokhua et al. have shown that normodipine has favorable influence on remodeling processes: causes regression of LV myocardial hypertrophy, improves diastolic function of the heart.

Diuretics

The use of diuretics should be strictly justified, be sure to be combined with the use of neurohormonal modulators, such as ACE inhibitors and aldosterone antagonists, as well as drugs that retain fluid in the vascular bed and improve renal blood flow and filtration.

Oddly enough, but there have been practically no serious placebo-controlled studies on the use of diuretics (with the exception of aldosterone antagonists), so all statements are based on expert opinion.

Diuretics may be needed in case of fluid retention but should be used with caution in patients with DHF to avoid excessive reduction in LV preload and fall in cardiac output.

Hypothiazide - the main representative of the class of thiazide diuretics, is used, as a rule, in patients with moderate CHF (FC II) and should be considered as a starting drug for the treatment of edematous syndrome. The starting dose of the drug is 25 mg, the maximum is 100 mg, because. when it is exceeded, the diuretic effect increases minimally, and the risk of typical side effects increases significantly. As with all active diuretic saluretics, including loop ones (the action is based on a decrease in the reabsorption of sodium and osmotically bound fluid), the main disadvantages are hyperactivation of the renin-angiotensin-aldosterone system (RA-AS), leading to rebound fluid retention, as well as electrolyte disorders (hypokalemia and hypomagnesemia). Therefore, the use of both thiazide and loop diuretics should always be combined with RAAS blockers (ACE inhibitors, ARA, aldosterone antagonists) and potassium-sparing drugs (aldosterone antagonists, rarely triamterene). It should be remembered that hypothiazide, for all its positive effects- a drug that requires careful and correct application to avoid serious adverse events.

Indapamide is significantly superior to hypothiazide in terms of safety profile, however, data on its use in the treatment of CHF are currently insufficient.

Loop diuretics (furosemide, ethacrynic acid, bumetanide, torasemide) are the most effective diuretics that block sodium reabsorption throughout the ascending part of the loop of Henle and remain active even with chronic renal failure and filtration up to 5 ml / min. Today, it is loop diuretics that are the basis for the treatment of edematous syndrome in CHF.

In 2006, the most effective and safest loop diuretic, torasemide, was registered in Russia. The starting dose of the drug is 5-10 mg, which, if necessary, can be increased to 100-200 mg per day. The main positive difference between torasemide and other loop diuretics is its additional effects, in particular, associated with the simultaneous blockade of the RAAS.

A dose-dependent blocking effect of torasemide on angiotensin II-stimulated calcium entry into cells has been proven. Numerous studies have shown the anti-aldosterone effects of torasemide, accompanied by an improvement in the diastolic properties of the myocardium.

Thus, the use of torasemide makes it possible to overcome the main disadvantages of active diuretic therapy. Not only the diuretic effect itself is enhanced, but also blocked side effects(electrolyte disturbances and activation of the RAAS).

In comparative controlled studies with furosemide, torasemide demonstrated higher clinical efficacy and tolerability, as well as the ability to reduce the number of readmissions due to exacerbation of CHF. In the TORIC study, torasemide demonstrated the ability to better influence the prognosis of patients with CHF, which makes this modern diuretic the drug of choice.

This drug has a lower kaliuretic effect than furosemide, has its own antifibrotic effect on the myocardium, which may be especially important for patients with DHF. However, studies on survival with the use of torasemide in patients with diastolic disorders have not yet been conducted.

Aldosterone antagonists

Modern look for the treatment of CHF - a combination of three neurohormonal modulators ACE inhibitor + BAB + aldosterone antagonist, is the most rational treatment regimen for patients with severe CHF.

Aldosterone receptor blockers have been used to treat CHF for many years. Spironolactone is the only drug of this class that has been studied in randomized trials. A large long-term study showed that

the addition of low doses of spironolactone (25 mg/day) to standard therapy, including an ACE inhibitor, reduces the risk of death and hospitalization in patients with functional class IV CHF. Based on the data obtained, low-dose spironolactone (25 mg/day) is recommended for the treatment of patients with functional class III-IV CHF, in whom the combination of digoxin, a diuretic, an ACE inhibitor, and usually a β-blocker is not effective enough.

In Russia, due to relatively high cost ACE inhibitors, these drugs are often not prescribed to patients with CHF at the “target” doses that are recommended in current guidelines. At best, ACE inhibitors are prescribed at doses that are about half of the "target". The cost of 25-5o mg of spironolactone per day is much less than the cost of therapy with "targeted" doses of most inhibitors. Therefore, according to Napalkov D.A. et al. (2008), spironolactone should be used in the treatment of not only severe cases CHF. Small doses of spironolactone may also be useful in the treatment of patients with less severe CHF who, for economic or other reasons, are not receiving “targeted” doses of ACE inhibitors and/or β-blockers. It can be assumed that in everyday clinical practice wide application spironolactone (2B-50 mg/day) to some extent can help compensate for the underuse of ACE inhibitors and β-blockers in patients with CHF due to LV systolic dysfunction. In addition, the addition of spironolactone may be useful in those cases of CHF, when the “target” doses of ACE inhibitors cannot be used due to the development of hypotension. After all, small doses of spironolactone cause a smaller decrease in blood pressure than the relatively high doses of ACE inhibitors currently recommended.

Thus, spironolactone seems to be used in all cases of functional class II-IV CHF when ACE inhibitors and β-blockers are prescribed at low doses or not prescribed at all (for example, due to low availability, hypotension, or other side effects ).

Before the appointment of spironolactone serum levels potassium should not exceed 5.0 mmol/l and serum creatinine levels should not exceed 2.5 mg/dl. Per biochemical indicators should be carefully observed during treatment with spironolactone. Hyperkalemia at any time can complicate therapy and lead to life-threatening bradyarrhythmias. Therefore, at the beginning of treatment with spironolactone, potassium supplements should be discontinued or their doses reduced. If serum potassium levels rise above 5.4 mmol/l, the dose of spironolactone should be reduced. The drug is canceled in case of development of significant hyperkalemia or gynecomastia.

The question of the use of low doses of aldosterone antagonists in combination with other neurohormonal modulators for the treatment of patients with initial stages CHF (I-II respiratory function remains open. Although there is already evidence that in patients who underwent MI, complicated by the development of CHF II F^, the use of a new aldosterone antagonist eplerenone made it possible to reduce the risk of death, including sudden death.

Despite the need to control the use, aldosterone antagonists rightfully occupy a place in the list of the main groups of drugs used to treat CHF. According to the results of the EPHESUS and RALES studies, there were no differences in the severity of the effects of aldosterone antagonists in CHF patients of different sexes.

Aldosterone antagonists in patients with diastolic disorders should be considered not so much as potassium-sparing diuretics, but as antifibrotic drugs. To date, no placebo-controlled studies have been conducted to evaluate the effect of aldosterone antagonists on the survival of patients with diastolic HF. The first multicenter controlled trial (TOPCAT) is currently underway, the purpose of which is to study the effect of spironolactone on the survival of patients with initial and moderate stages of CHF and

LV EF>45%. Since the end of 2006, the 3rd phase of the study has been going on, the planned duration clinical trial- 53 months, number of clinical bases - 35, number of patients - 2000.

cardiac glycosides

The rhythm-reducing effect of cardiac glycosides (digoxin) may be useful for patients with atrial fibrillation, which occurs in approximately 30% of patients with diastolic HF. However, the results of the DIG study showed that even regardless of the nature of the underlying rhythm, the use of digoxin is associated with more than 30% reduction in hospitalizations due to decompensated CHF in patients with both reduced (<45%), так и с относительно сохраненной (>45%) LV EF. Moreover, a subanalysis of this study showed that low concentrations drug in plasma<0,9 ng/ml) отмечается достоверное снижение риска смерти и госпитализаций по любым причинам, в т.ч. и у больных с сохраненной систолической функцией . Тем не менее, следует воздержаться от рутинного использования дигоксина у этой категории больных, при необходимости снижения ЧСС отдать предпочтение БАБ. При невозможности применения БАБ и выборе терапии в пользу дигоксина доза препарата не должна превышать 0,25 мг/сут.

Currently, there is evidence of a certain benefit from the use of drugs such as direct vasodilators (hydralazine, isosorbide dinitrate, isosorbide mononitrate (IMN)) in the complex therapy of CHF.

To develop rational tactics for their use, it is necessary to take into account not only the impact on clinical symptoms and hemodynamics, but also on the nature and severity of diastolic disorders present in most patients. The study showed that the combination of IMN with bisoprolol in patients with CHF-CVF has a beneficial effect on the clinical and functional status, structural, functional and hemodynamic parameters of the left ventricle, improves LV diastolic filling in violation of its relaxation, and also reduces clinical symptoms and slows down the progression of remodeling and diastolic disorders in patients with initial pseudo-normalization and restriction of TMDP. The data obtained may be a prerequisite for the appointment of nitrates in combination with BB for the correction of ischemic CHF with predominantly diastolic disorders, which is most indicated in the early stages of the disease in order to prevent its progression. However, indisputable evidence of the benefits and risks of such a combination in CHF can only be obtained in specially designed large-scale clinical trials.

Thus, CHF is a heterogeneous pathophysiological condition, the treatment of which should be carried out taking into account its etiology, pathogenesis, and, most importantly, the state of LV contractile function.

Literature

1. Belenkov Yu.N. Patients with chronic heart failure in Russian outpatient practice: features of the contingent, diagnosis and treatment (based on the materials of the EPOKHA-O-CHF study) / / Heart failure. 2004. - V. 5, No. 1. - S. 4-7.

2. Napalkov D.A., Sulimov V.A., Seidov N.M. Chronic heart failure: a shift in focus to the initial stages of the disease / / Attending physician. - 2008. - No. 4. - P.122-128.

3. Pristrom M.S., Sushinsky V.E. Diastolic myocardial dysfunction: diagnosis and treatment approaches //Medical news. - 2008. - No. 12. - S. 17-19.

4. Shevchenko O.P., Shevchenko A.O. ACE inhibitors in patients with heart failure // Russian Journal of Cardiology. - 2008. - No. 5. - S. 76-84.

5. Cleland J. The perindopril in elderly people with chronic heart failure (PEP-CHF) study. Hot Line .I Session on XVth World Congress of Cardiology, Barcelona, ​​03 .September .2006.

7. Kuimov A.D., Belyaeva O.N., Volkova I.I. Influence of ACE inhibitor lisinopril on disorders of left ventricular diastolic function and endothelial response in patients with arterial hypertension with and without chronic heart failure // Russian Journal of Cardiology. - 2004.- N 3. - S. 58-63.

8. Mareev V.Yu., Ovchinnikov A.G., Ageev F.T., Belenkov Yu.N. The effect of ACE inhibitors and angiotensin-II receptor antagonists on left ventricular diastolic function in patients with relatively intact left ventricular systolic function: results of the study "Perindopril, IRbesartan and Amlodipine in patients with CHF and preserved left ventricular systolic function (PIRANHA) // Seredechnaya Journal Failure. -2005. - No. 6 (1). - P.4-14.

9. Bergstrom A, Anersson B, Ender M et al. Effect of carvedilol on diastolic function in patients with diastolic heart failure and preserved systolic function. Results of the Swedish Doppler-echocardiographic study (SWEDIC) // Eur J Heart Fail. - 2004. - No. 6 (4). - R. 453-461.

10. Flather M., Shibata M., Coats A. et al. Randomized trial to determine the effect of nebivolol on mortality and cardiovascular hospital admission in elderly patients with heart failure (SENIORS) // Eur Heart J - 2005. - 26 (3). - R. 215-225.

11. Mareev V.Yu., Danielyan M.O. Optimization of the use of Betaloc ZOK in patients with CHF in everyday medical practice. BEZE study design and results // Heart Failure. - 2005. - V. 6, No. 6. - S. 251-257.

12. Lopez B., Querejrta R., Gonzalez A et al. Effects of loop diuretics on myocardial fibrosis and collagen type I turnover in chronic heart failure.// J Am Coll Cardiol - 2004 -43 (11) - R. 2028-2035.

13. Blockade of aldosterone receptors - a step forward in improving the survival of cardiac patients. Prepared by Ovsienko N. // Medical newspaper "Health of Ukraine". - 2008. - No. 21/1. - S. 14-15.

14. Drexler G, Komazda M, Struthers A, et al. Aldosterone blockade: life-saving benefits. Expansion of standards for the treatment of postinfarction congestive heart failure. As a result of the congress European Society cardiologists 2008. Prepared by Tatarenko O. // Medical newspaper "Health of Ukraine" - 2008 - No. 19 - P. 22-25.

15. Study Title: TOPCAT Aldosterone Antagonist Treatment of Heart Failure with Preserved Systolic Function. Clinical Research Portal / http://craclub.ru/component/option,com_tobi2/tobi2Task,tobi2Details/catid,7/tobi2Id,15616/Itemid,123/

16. Tareev V.Yu., Danielyan M.O., Belenkov Yu.N. On behalf of the EPOCHA-O-CHF research working group. Comparative characteristics of patients with CHF depending on the value of EF according to the results of the Russian multicenter study EPOCHA-O-CHF // Heart failure. - 2006. - 7 (4). - P.164-171.

17. Ali Ahmed, Rich M., Love T. et al. Digoxin and reduction in mortality and hospitalization in heart failure: a comprehensive post hoc analysis of the DIG trial // Eur Heart J - 2006 - 27 (2) -P. 178-186.

18. Otrokhova E.V., Ivanova N.V. Nitrates in chronic heart failure: paradoxes of application in medical practice // Farmateka. - 2008. - No. 7 (161). - S. 34-38.

TREATMENT OF DIASTOLIC DYSFUNCTION OF CHRONIC CARDIAC INSUFFICIENCY

L.A. Kamyshnikova1 O.A. Efremova2

1 Municipal health establishment

"Clinical hospital №1", Belgorod

2 Belgorod State

It is shown in the review of up-to-date facts by treatment of diastolic dysfunction of chronic cardiac insufficiency

Key words: diastolic dysfunction in the left ventricle, chronic cardiac insufficiency, treatment.

diastolic heart failure. This variant of heart failure reflects a situation in which the heart is unable to accept the necessary venous return of blood. This may be due to obstruction of filling (stenosis of the pulmonary vein collectors or atrioventricular valves, triatrial heart) or poor relaxation of the ventricles (pulmonary stenosis, aortic stenosis, cardiomyopathy). The latter option generally requires increased venous pressure to maintain adequate cardiac output. In newborns, temporary physiological "stiffness" of the right ventricle is often observed. The combination of the latter factor with increased afterload (due to semilunar valve stenosis or high RLV) leads to the rapid development of low cardiac output syndrome shortly after birth (a "critical" heart disease).

Diastolic function of the heart assessed by transmitral and transtricuspid diastolic blood flow, in which the early filling flow (peak E on echocardiography) and atrial systole flow (peak A) are distinguished.

In the fetus the E/A ratio is less than one; ventricular filling depends mainly on atrial systole. After birth, as the myocardium matures and its resistance decreases, the role of passive filling increases; in the period from one to 3-6 months, the E / A ratio becomes greater than one.

In most cases, violations of systolic and diastolic heart functions are combined.

Hypoxia and ischemia.

end result insufficient oxygen delivery to cells is their hypoxia and death. However, this process may be based on various mechanisms - hypoxia itself or ischemia. Both of these terms reflect the malnutrition of organs and tissues, however, they have a different physiological meaning. With hypoxia, the oxygen content in the blood flowing to the tissues is reduced, with ischemia, the volume of blood flowing is reduced. Congenital malformations can be accompanied by both of these mechanisms of circulatory disorders, and they concern both the heart itself and other organs. Typical examples are aortic stenosis and transposition of the main arteries.

With aortic stenosis with significant hypertrophy of the myocardium of the left ventricle, the growth of small coronary vessels lags behind the needs, the blood flow is disturbed mainly in the subendocardial layers of the myocardium, and ischemia of this zone occurs. During the transposition of the main arteries, the volumetric blood flow to the coronary vessels is not reduced, however, blood with a sharply reduced oxygen content comes from the aorta, which leads to myocardial hypoxia.

Type of circulatory disorder determines therapeutic and surgical measures: in case of ischemia, it is necessary to strive to restore the volume of blood flow, in case of hypoxia, to increase the oxygen content in the blood.

oxygenation index.

This index is used to evaluate the effectiveness artificial lung ventilation. It reflects the intensity of effort required to achieve a given oxygenation of arterial blood and is calculated by the formula: AI \u003d (avg Fp2 100) / рО2, where AI is the oxygenation index, Avg is the average airway pressure (cm wg), F02 — fractional oxygen content in the inhaled mixture (decimal fraction), pa02 - partial pressure of oxygen in arterial blood (mm Hg). The higher the index, the more severe the patient's condition.

Chronic diastolic heart failure

Diastolic CHF is heart failure with normal or slightly reduced contractile function of the left ventricle, but with a pronounced violation of its diastolic relaxation and filling, which is accompanied by an increase in end-diastolic pressure in the ventricle, blood stasis in the pulmonary circulation and other signs of heart failure. Thus, there are 3 main criteria for distinguishing diastolic CHF as one of the special forms of cardiac decompensation (recommendations of the working group of the European Society of Cardiology, 1998).

1. The presence of clinical signs of CHF (shortness of breath, fatigue, wet rales in the lungs, edema, etc.).

2. Normal or slightly reduced myocardial contractility (LV EF more than 45-50%).

3. The presence of objective signs indicating impaired relaxation and filling of the left ventricle and / or signs of increased LV stiffness.

The isolation of diastolic CHF is of great practical importance, since this form of heart failure occurs in 20–30% of patients with clinical signs of cardiac decompensation, and there are fundamental differences in the tactics of treating such patients. However, two important practical circumstances should be borne in mind:

1. The progression of diastolic CHF over time leads to such a sharp decrease in LV filling that the value of SI and EF begins to decrease, i.e. there are signs of LV systolic dysfunction.

2. In almost all patients with CHF, in whom the process of decompensation from the very beginning has the character of systolic CHF and is accompanied by a clear decrease in EF and CI, more or less pronounced signs of LV diastolic dysfunction can also be detected, which significantly aggravates hemodynamic disorders.

Thus, a clear division of CHF into two pathophysiological variants - systolic and diastolic - is true mainly in the early stages of CHF formation (S.N. Tereshchenko et al. 2000). Far advanced process of cardiac decompensation is, as a rule, a combination of disorders of the diastolic and systolic functions of the left ventricle

Chronic diastolic heart failure

DEFINITION

Diastolic CHF is heart failure with normal or slightly reduced contractile function of the left ventricle, but with a pronounced violation of its diastolic relaxation and filling, which is accompanied by an increase in end-diastolic pressure in the ventricle, blood stasis in the pulmonary circulation and other signs of heart failure. This form of heart failure occurs in 20-30% of patients with clinical signs of cardiac decompensation.

There are 3 main criteria for the selection of diastolic CHF (European Association of Cardiology, 2004): the presence of clinical signs of CHF (shortness of breath, fatigue, moist rales in the lungs, edema); normal or slightly reduced myocardial contractility (LV EF more than 45-50%); objective signs indicating impaired relaxation and filling of the left ventricle and / or signs of increased LV stiffness. The division of CHF into two pathophysiological mechanisms is possible in the early stages. The advanced process of cardiac decompensation is a combination of disorders of the diastolic and systolic functions of the left ventricle.

ETIOLOGY

2 causes underlie the occurrence of LV diastolic dysfunction: violation of active relaxation of the ventricular myocardium, which is associated with damage to the energy-intensive process of diastolic Ca2+ transport; deterioration of LV wall compliance, which is due to a change in the mechanical properties of cardiomyocytes, the state of the connective tissue stroma (fibrosis), pericardium, as well as a change in the geometry of the ventricle. The diastolic form of CHF most often develops with severe ventricular myocardial hypertrophy, severe cardiofibrosis, prolonged chronic myocardial ischemia, a significant increase in afterload, and pericarditis.

PATHOGENESIS

As a result of a slowdown in active relaxation of the LV and a decrease in its compliance in diastole, the normal filling pressure of the ventricle (less than 12 mm Hg) can no longer ensure its sufficient filling with blood. The first consequence of LV diastolic dysfunction is an increase in EDV in the ventricle, which contributes to the maintenance of normal EDV and cardiac output. The second consequence of LV diastolic dysfunction is the various redistribution of diastolic blood flow from the atrium to the ventricle during diastole.

The flow of blood from the atrium into the ventricles is carried out in two phases: in the phase of rapid filling, when, under the action of a pressure gradient between the atrium and the ventricle, about 60-75% of the total diastolic blood volume enters the latter; during atrial systole as a result of its active contraction (25% of the total blood volume). The early stages of impaired LV diastolic function are characterized by a moderate decrease in the rate of isovolumic relaxation and the volume of early filling. As a result of such a structural restructuring of the diastole, there is a pronounced overload of the LA, an increase in its volume and pressure in it. In later stages, a "restrictive" type of diastolic dysfunction develops. LA overload contributes to the early onset of supraventricular arrhythmias, atrial fibrillation and flutter. The third consequence of diastolic dysfunction is an increase in pressure in the venous bed of the pulmonary circulation and stagnation of blood in the lungs.

For diastolic CHF, LV dilatation is not characteristic until a violation of the pumping function of the heart joins the diastolic dysfunction. Left ventricular diastolic dysfunction, an increase in blood pressure in the ventricle and pressure in the pulmonary circulation contribute to the activation of the body's neurohormonal systems. This contributes to the retention of Na + and water in the body, the development of edematous syndrome and a tendency to vasoconstrictor effects. The late stages of diastolic CHF are characterized by a significant increase in LV end pressure, inefficiency of LA systole, and a critical decrease in LV filling. Due to high pressure in the pulmonary artery, hypertrophy and dilatation of the pancreas develops, followed by signs of right ventricular heart failure. Diastolic CHF is characterized by the predominance of left ventricular failure.

CLINICAL PICTURE

It is characterized by symptoms of congestive left ventricular heart failure against the background of normal systolic function of the left ventricle, signs of violation of its relaxation, detected by Doppler echocardiography. Diastolic CHF is more common in elderly patients. Patients with hypertension, coronary artery disease, aortic stenosis, GC.

MP. diabetes mellitus, have a high risk of developing diastolic CHF. Patients complain of shortness of breath during exertion, orthopnea and dry cough, appearing in the horizontal position of the patient with a low headboard; fatigue and reduced performance. Physical examination may reveal orthopnea; congestive moist rales in the lower parts of the lungs; enhanced apical impulse; "double" apex beat; presystolic gallop rhythm (pathological IV tone); atrial fibrillation is often detected.

INSTRUMENTAL DIAGNOSIS

The use of modern instrumental studies makes it possible to determine the signs of LV diastolic dysfunction, make sure that there are no significant violations of the LV systolic function, and determine the cause of diastolic CHF (IHD, MI, angina pectoris).

echocardiography

Echocardiographic criteria for the absence of LV systolic dysfunction are: 1. LV ejection fraction (EF) more than 45-50%. 2. The LV EDV index is less than 102 ml / m. 3. CI is greater than 2.2 l / min / m. Often, with diastolic dysfunction, EF remains normal, may be increased (more than 60%). This indicates the presence of a hyperkinetic type of blood circulation in patients with diastolic CHF. In 70% of patients with diastolic CHF, echocardiographic signs of severe LV hypertrophy are found.

To assess diastolic and LV function, the following are determined: the maximum rate of the early peak of diastolic filling (Vmax Peak E), the maximum rate of transmitral blood flow during left atrial systole (Vmax Peak A), the ratio of the maximum rates of early and late filling (E / A) , LV isovolumic relaxation time (IVRT), early diastolic filling deceleration time (DT).

LV isovolumic relaxation time (IVRT), which is the interval between the end of flow in the LV outflow tract and the start of flow through the mitral valve, is a good indicator of the rate of initial ventricular relaxation. Normally, LV IVRT is no more than 70-75 ms, and the deceleration time of early diastolic filling (DT) is 200 ms. At the end of diastole, during LA contraction, the blood flow rate increases again, forming a second peak (Peak A), and when the mitral valve closes, it returns to the zero line.

With normal diastolic function, the dopplerogram is dominated by the peak of early diastolic filling, which is 1.5-1.7 times higher than the peak of late ventricular filling (Table 63).

Table 63

Normal values ​​of LV diastolic function

Dopplerograms of the transmitral blood flow reveal a decrease in the amplitude of the E peak and an increase in the height of the A peak. The E/A ratio decreases to 1 and below. At the same time, an increase in the time of LV isovolumic relaxation (1VRT) is more than 90-100 ms and the time of deceleration of early diastolic filling (DT) is more than 220 ms. This type of LV diastolic dysfunction has been termed the “delayed relaxation” type. The most common factors leading to the formation of this type of LV diastolic dysfunction are chronic or transient myocardial ischemia in patients with coronary artery disease, cardiosclerosis of any origin, myocardial hypertrophy, pericardial lesions, bundle branch block.

Further progression of intracardiac hemodynamic disorders leads to an increase in LA pressure and an increase in the atrioventricular pressure gradient during the rapid filling phase. There is a significant acceleration of early diastolic ventricular filling (Peak E) with a simultaneous decrease in blood flow velocity during atrial systole (Peak A). The increase in end-diastolic pressure in the LV contributes to the restriction of blood flow during atrial systole. There is a pathological "pseudo-normalization" of LV diastolic filling with an increase in the values ​​of the maximum early diastolic filling rate (Peak E) and a decrease in atrial filling rate (Peak A). As a result, the E/A ratio increases to 1.6-1.8 or more. These changes are accompanied by a shortening of the isovolumic relaxation phase (IVRT) of less than 80 ms and an early diastolic filling deceleration time (DT) of less than 150 ms.

A restrictive type of diastolic dysfunction is observed in congestive heart failure, indicating a significant increase in LV filling pressure.

Often, the described signs of LV diastolic dysfunction precede violations of its systolic function. An adequate assessment of LV diastolic function by the described method is possible in patients with a heart rate of less than 90 per minute, in the absence of mitral stenosis, aortic, mitral insufficiency.

Radiography

X-ray of the chest organs makes it possible to detect the absence of severe cardiomegaly and assess the state of the pulmonary circulation. In most cases, signs of venous plethora of the lungs are revealed, sometimes in combination with signs of pulmonary arterial hypertension. Instrumental studies reveal the following signs of diastolic CHF: absence of LV systolic dysfunction (according to echocardiography); the presence of ECG and EchoCG signs of severe LV hypertrophy (symmetric or asymmetric); the presence of echocardiographic signs of LV diastolic dysfunction (the type of "delayed relaxation" - a decrease in the amplitude of the E peak; an increase in the height of the A peak; a decrease in the E / A ratio to 1 and below; "restrictive" type of diastolic dysfunction - an increase in the height of the E peak; a decrease in the amplitude of the A peak , an increase in the E / A ratio to 1.8 and above); absence of pronounced cardiomegaly on radiographic examination; increased LA wedge pressure, detected during catheterization of the right heart and LA.

There are no generally accepted algorithms for the treatment of diastolic CHF. According to the recommendations of the European Association of Cardiology (2004), several principles of drug therapy can be distinguished:

1. Restoration of sinus rhythm in patients with supraventricular tachyarrhythmia (atrial fibrillation or flutter) leads to a significant improvement in diastolic filling of the ventricles by restoring the normal physiological sequence of atrial and ventricular contraction.

A decrease in heart rate helps to reduce afterload, intramyocardial tension and myocardial oxygen demand. To correct heart rate, b-blockers (atenolol, metoprolol, carvedilol), calcium antagonists - verapamil and diltiazem are used.

3. To reduce stagnation in the pulmonary circulation, it is advisable to use diuretics that reduce BCC and pressure in the pulmonary artery.

To influence the factors that determine the diastolic filling of the ventricles and the degree of diastolic dysfunction, ACE inhibitors can be used, which are more effective in the treatment of patients with diastolic CHF. Calcium antagonists (verapamil and diltiazem) can improve active myocardial relaxation and diastolic filling of the ventricles, reduce myocardial mass, and improve the passive elastic properties of the heart muscle. B-blockers may be the drug of choice. The positive effect of long-term use of b-blockers is associated with a decrease in the degree of LV myocardial hypertrophy and a decrease in the stiffness of the heart muscle. The presence of a negative inotropic effect limits the use of these drugs in patients with severe cardiac decompensation (NYHA FC III-1V). B-blockers are advisable to use in patients with hypertension or coronary artery disease, when there is tachycardia or tachyarrhythmia.

Angiotensin II receptor blockers (losartan, valsartan, candesartai) have a more pronounced effect on local tissue RAS, myocardial hypertrophy and its elastic properties than traditional ACE inhibitors. Nitrates do not have a direct effect on diastolic relaxation, the formation of hypertrophy and cardiofibrosis, but they reduce myocardial oxygen demand, reduce ischemia of the heart muscle, and thus indirectly affect the elasticity of the ventricular myocardium. Cardiac glycosides are contraindicated in the treatment of patients with diastolic CHF.

The main principles of long-term treatment of patients with diastolic CHF are: restoration of sinus rhythm and full atrial systole in patients with supraventricular tachyarrhythmias. a decrease in tachycardia (verapamil and b-blockers), a decrease in signs of blood stagnation in the pulmonary circulation, long-term use of drugs that have the properties of reverse development of ventricular myocardial hypertrophy: ACE inhibitors; b-blockers; calcium antagonists; angiotensin II receptor antagonists, the use of nitrates.

Restrictive cardiomyopathy is a rare heart disease in which the myocardium is involved in the pathological process, and also in most cases the endocardium.

• Etiology and pathogenesis
• Symptoms
• Diagnostics
• Radiography of the heart and lungs
• Electrocardiogram
• CT and MRI
• echocardiography
• Endomyocardial biopsy
• Treatment
• Forecast

The main symptom of this disease is a violation of the filling of one or both ventricles of the heart, while their volume is significantly reduced without changing the wall thickness.

Etiology and pathogenesis

This disease is extremely rare. Most of all, this disease affects residents of tropical and subtropical countries. Where death from the disease is 15% of all cases of congestive heart failure. The disease occurs in all age categories, but children, adolescents and young men are most often affected.

The exact cause of this disease has not yet been established. But most physicians associate the development of this pathology with hypereosinophilic syndrome, which persists in the body for several months (bronchial asthma, helminthic invasion, eosinophilic leukemia, oncological neoplasms).

There is also reliable data on the relationship between endomyocardial fibrosis and the content of monocytes in the soil, which accumulate in the cardiac myocardium and endocardium of patients, certain types of this family of chemical elements (thorium, cerium), which contribute to the synthesis of collagen by heart fibroblasts.

The main factor in the pathogenesis of the disease is an increase in the stiffness of the walls of the ventricle of the heart, which develops as a result of fibrosis of the endocardium and myocardium, or as a result of infiltrative diseases.

As a result of these pathological processes, the filling of the left ventricle is disturbed, the rigidity of the myocardium and endocardium increases.

Significantly increased diastolic pressure in both ventricles, pulmonary hypertension develops. With fibrosis, not only the walls of the ventricles are affected, but also the valvular apparatus, resulting in the development of a defect (insufficiency or stenosis). In the absence of adequate treatment, diastolic heart failure may occur.

There are several types of such a disease as restrictive cardiomyopathy:

1. idiopathic
   • endomyocardial fibrosis;
   • Loeffler's disease (eosinophilic endomyocardial disease).

1. Secondary
   • hemochromatosis;
   • amyloidosis;
   • scleroderma;
   • sarcoidosis;
   • carcinoid heart disease;
   • radiation damage to the heart.

Depending on the damaged tissues, there are two forms of restrictive cardiomyopathy:

• primary myocardial - the pathological process affects the myocardium in isolation;
• endomyocardial - involved in the pathological process of the endocardium, resulting in thickening of the walls, infiltration, necrosis, fibrosis of the heart tissue.

Symptoms

At an early stage, the disease proceeds without pronounced clinical manifestations. Later, when the symptoms of heart failure increase, patients are concerned about:

• weakness and increased fatigue, unrelated to physical exertion;
• shortness of breath and pain in the heart after small physical exertion;
• coughing fits;
• pain in the right hypochondrium and an increase in the abdomen;
• sudden weight loss;
• lack of appetite;
• increase in body temperature;
• peripheral edema.

The clinical picture of the disease depends on the severity of chronic heart failure.

Diagnostics

Only a highly qualified doctor can make a diagnosis of "Restrictive cardiomyopathy" by conducting an examination and additional diagnostics in a hospital setting. Before prescribing the necessary amount of diagnostic studies, the doctor will conduct a thorough examination of the patient:

• collect an anamnesis of the disease;
• pay attention to family history;
• examine the skin and mucous membranes, where it can reveal a cyanotic blush, swollen neck veins, swelling of the upper and lower extremities, an enlarged abdomen disproportionately to the body;
• on palpation - pain in the right hypochondrium, the lower edge of the liver protrudes significantly from under the costal arch, ascites;
• during auscultation, a “gallop rhythm” is heard, a systolic murmur resulting from mitral and tricuspid valve insufficiency, the upper border of the heart is significantly shifted upwards, fine bubbling rales are heard in the lungs;
• when measuring blood pressure, the systolic pressure will be lowered, the pulse is weak filling.

Laboratory research methods include:

• radiography of the chest cavity;
• CT and MRI;
• echocardiography;
• endomyocardial biopsy.

Radiography of the heart and lungs

The x-ray shows a slightly enlarged heart, enlarged atria, venous congestion in the lungs.

Electrocardiogram

After deciphering the cardiogram, the attending physician should be alerted by signs of blockade of one or both legs of the His bundle, changes in the 5T segment, G wave, cardiac arrhythmias, signs of left atrial overload, ventricular and atrial hypertrophy.

CT and MRI

These methods of non-invasive laboratory studies are carried out for the purpose of differential diagnosis with constrictive pericarditis, the main feature of which is a significant thickening of the pericardium, uncharacteristic of restrictive cardiomyopathy.

echocardiography

Signs of this disease during echocardiography will be:

• severe atrial dilatation;
• reduction of the cavity of the damaged ventricle of the heart;
• unchanged systolic function;
• mitral functional regurgitation;
• violation of diastolic function of the left ventricle of the heart;
• thickening of the endocardium.

Endomyocardial biopsy

Myocardial biopsy is not always negative, and the diagnosis of restrictive cardiomyopathy is not ruled out. Most often, eosinophilic infiltrates are detected at an early stage of the disease, and fibrosis and dystrophy of myocardial cells are found at a late stage.

When conducting laboratory blood tests, anemia, non-specific inflammatory changes caused by a significant increase in eosinophils in the patient's peripheral blood are detected in the tests.

Treatment

Restrictive cardiomyopathy is a serious heart disease that is difficult to treat. More precisely, there is no effective treatment. Basically, the therapeutic course has a symptomatic direction. To alleviate the patient's condition, prescribe drugs for the treatment of heart failure:

• to reduce pressure in the left ventricle;
• to eliminate stagnation in the circles of blood circulation;
• for the prevention of thromboembolism.

• diuretic drugs;
• vasodilators;
• antiarrhythmic drugs;
• cardiac glycosides.

It should be noted that only a highly qualified doctor should prescribe treatment, taking into account the severity of the disease and the individual characteristics of the patient. So, with restrictive lesions of the heart, it is not always possible to use drugs used to treat heart failure. Diuretics (diuretics) reduce the amount of blood flowing to the heart, lower blood pressure, which can adversely affect the patient's overall health.

Cardiac glycosides are also prescribed as needed, because often the systolic function of the heart is not impaired. And in patients with amyloidosis, there is an increased sensitivity to cardiac glycosides.

The surgical method of treatment is used for fibroplastic endocarditis. The function of the damaged ventricle is restored by excision of the thickened endocardium. In case of insufficiency of heart valves, their prosthetics are performed. These operations improve not only the well-being, but also the prognosis for the patient's future life. A heart transplant is not a panacea, because fibrosis will soon damage the new heart as well.

Secondary restrictive cardiomyopathy is treated, but only if the underlying disease is treated. In some cases, effective treatment can prevent further damage to the heart and restore some of its function. In the acute phase of the disease, glucocorticosteroids and immunosuppressants are prescribed.

Forecast

It is difficult to make predictions for this heart disease. In most cases, the prognosis is poor. More than 50% of all patients die within 2 years after the onset of the first symptoms of the disease from such complications:

• thromboembolism;
• progressive heart failure;
• arrhythmias.

To date, the prevention of this disease has not been developed.

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If you have read the article “What is chronic heart failure”, then you already know that the diagnosis always indicates the stage of the disease and the functional class. In addition, if an ultrasound of the heart was performed, then the type of insufficiency is also established - systolic or diastolic.

What is systolic heart failure or systolic function?

To answer this question, we need to talk a little about the cardiac cycle.

The cardiac cycle consists of diastole (relaxation) and systole (contraction) of the ventricles. In diastole, the ventricles draw blood from the atria, and in systole they expel it throughout the body. Depending on how well the heart contracts, its systolic function is determined. At the same time, they are guided by such an indicator obtained by ultrasound of the heart as an ejection fraction. If the fraction is below 40%, then this means that the systolic function is impaired, and only no more than 40% of the blood enters the general channel at a rate of 55-70% - this is systolic heart failure or heart failure with systolic dysfunction of the left ventricle.

If the ejection fraction is normal, but the symptoms of heart failure are obvious, then this will be diastolic heart failure or heart failure with preserved systolic function, the latter statement is more true if diastolic dysfunction is not confirmed by a special Doppler study.

With diastolic dysfunction, the heart contracts well, but fills with blood poorly. In diastole, the ventricle must stretch almost twice in order to draw more blood and provide a good ejection, and if it loses this ability, then even with good contractility, the efficiency of such work will be low. Figuratively speaking, in order for such a heart to provide an adequate pumping function, it needs to contract twice as often as a healthy one. But this does not mean that with diastolic heart failure it is necessary to have a high pulse.

All about the causes and prevention of acute heart failure

What are the sources of the disease

In acute deficiency, it is associated with damage to the heart or a failure in the process of pumping blood through the vessels. Therefore, the main causes of acute heart failure are:

• hypertension;
• ischemia;
• heart defects.

In women, the primary cause is considered to be blood pressure, in men, ischemic disease is the culprit.

In reality, there are many reasons for the development of acute heart failure.

This list includes:

• type 1 and type 2 diabetes;
• violation of the heart rhythm;
• cardiomyopathy;
• drinking alcohol, smoking;
• myocarditis.

Influence of age and risk factors

The prognosis for acute failure worsens if the heart rhythm is significantly disturbed. The gender and age of the patient also affects. Women recover faster than men. In addition, there is a favorable prognosis in people younger than 65 years of age, when compared with patients older than this age.

Before the age of 50, a man is more prone to heart disease than a woman. After this milestone, the probability levels off. Heart attacks are rare in people younger than 40 years of age.

From the age of 45, the leading cause of death in men is acute heart failure. In women - after 65.

Important! Coronary disease in parents, grandparents - a high probability of developing pathology in descendants.

It is noted that more than half of deaths due to heart failure are caused by such provocateurs as:

• Smoking. Such an activity doubles the risk of developing a heart attack. Smokers with many years of experience who quit smoking can significantly improve their health;
• Passive lifestyle. Physical activity is needed at any age. Exercises are selected individually, but according to the standard, a 30-minute walk a day is enough for a person to maintain health;
• Elevated cholesterol. With a slight increase in the level, the risk of developing pathology increases several times. In this case, it is recommended to balance the diet;
• Hypertension. 50 million people have high blood pressure. The disease proceeds without pronounced signs, which is dangerous;
• Diabetes. People with this disease are at risk of leaving this world more often than those who are sick without such a diagnosis. It is recommended to maintain the sugar level on the optimal scale, change lifestyle, take medications;
• Alcohol. Moderate consumption of strong drinks reduces the development of acute heart failure by 40%;
• Obesity. If you are over 20% overweight, your risk of heart disease doubles. The most dangerous place for the accumulation of fat is the stomach.

Watch a video about the symptoms and causes of chronic insufficiency:

When to seek help: the main symptoms of the disease

Acute deficiency occurs suddenly. In most cases, the condition leads to the death of a person. A dangerous pathology occurs due to stagnation in a certain circle of blood flow, thereby disrupting gas exchange in the lungs. The death process is manifested by the following symptoms:

• sudden shortness of breath;
• frequent heartbeat;
• dry cough;
• sudden weakness;
• blanching of the skin;
• low blood pressure.

The patient should sit down and dangle his legs. Symptoms may increase.

First aid for a person with an attack

In an acute attack, 3 minutes is enough for ventricular work to be disrupted. In the event of such a situation, immediate assistance should be provided. Hospitalization is mandatory, so help should be called immediately after the first signs appear.

First of all, immediately call an ambulance, reassure the patient. You yourself should not panic either, since anxiety will only aggravate a person’s condition. If the attack happened indoors, it is recommended to provide fresh air. On the clothes, unbutton the top buttons, thereby facilitating the patient's breathing.

Before the arrival of specialists, it is recommended to put the victim in a semi-sitting position, this will help the blood to go to the legs. After a couple of minutes, apply a tourniquet to the thigh area. Put nitroglycerin under the tongue, repeat the medication every 10 minutes. If possible, control the pressure.

We offer you to learn about first aid for a heart attack:

Preventive measures

Prevention and lifestyle changes can help reduce your chances of developing acute heart failure.

A prerequisite is a visit to a cardiologist twice a year. This way you can identify the problem at an early stage.

You can not expose the body to intense physical exertion.

This is especially true for unprepared people. You should avoid a set of body fat, monitor nutrition and salt intake.

It is advisable to walk daily in the fresh air, start swimming. With a constant stay in the room, hypodynamia may develop.