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0PROBLEMS OF DIAGNOSING PATIENTS WITH CHRONIC HEART FAILURE ASSOCIATED WITH CHRONIC
OBSTRUCTIVE PULMONARY DISEASE
1Ruzieva Kh.O., 2Atakhodjaeva G.A.
1Assistant, Tashkent Pediatric Medical Institute 2TashPMI, Doctor of Medical Sciences, Associate Professor of Internal Medicine Department,
Nephrology and Hemodialysis https://doi.org/10.5281/zenodo.13332241
Abstract. It is important to suggest that at present time as one of the most common complaints of patients while visiting a general practitioner is shortness of breath, the causes of which may be chronic heart failure (CHF) and chronic obstructive pulmonary disease (COPD). Definitely, the problem of chronic obstructive pulmonary disease (COPD) is of significant importance in a number of clinical conditions, one of which is chronic heart failure.
Keywords: shortness of breath, chronic heart failure, chronic obstructive pulmonary disease, pulmonary hypertension.
Chronic heart failure (CHF) is a clinical syndrome that is the final outcome of most cardiovascular diseases and occupies a leading place among the causes of disability and mortality in patients with cardiac pathology [1, 2, 3]. The incidence of CHF in the population is at least 1.82%, but this figure is being increased among people over 65 years of age and reaches 6-10%, while decompensation becomes the most common cause of hospitalization in elderly patients. According to various authors, chronic heart failure was detected in 30-62% of observations among patients with COPD in older age groups. [4,5,6] COPD is one of the most common comorbid diseases in patients with CHF, which is associated with problems with late diagnosis of CHF and its treatment, primarily with the lack of use of P-blockers [1, 2]. The detection rate of COPD in patients with CHF is 10-32% [5-7].
According to the study by Framing, it is known that from the moment of diagnosis of CHF, 37% of men and 38% of women died within the first 2 years and 82% of men and 62% of women within 6 years [7,8]. With the development of pronounced congestion, mortality from CHF turns out to be even more significant. A number of authors note that the one-year survival rate of these patients is less than 50%.
The problem of COPD associated with CHF (PH-CHF) has been studied for a long time and is relevant at the moment. In a 2018 study, a correlation was established between the progression of heart failure and an increase in pulmonary hemodynamic parameters.
It is important to note that readmission and mortality in patients with CHF in combination with COPD are much higher than in patients with CHF without bronchopulmonary pathology [57]. According to the ARIC (Atherosclerosis Risk in Communities) study, which involved more than 13,000 people, it was shown that the presence of COPD and a decrease in forced expiratory volume in the first second (FEV 1) are independent predictors of the development of CHF [10].
The combination of COPD and CHF presents certain difficulties for diagnosis and treatment. These diseases have common risk factors, similar clinical manifestations and the commonality of some links in pathogenesis. Currently, the problem of the relationship between
COPD and cardiovascular pathology can be discussed both from the point of view of a simple combination of different nosologically forms, and from the point of view of the occurrence of conditions in COPD that contribute to the formation of arterial hypertension, coronary artery disease, and heart failure. The development of conditions for the formation of cardiovascular pathology in COPD indicates not just a combination of different forms of pathology, but the existence of a cardiorespiratory continuum in which COPD is a direct participant in the formation of arterial hypertension, coronary artery disease and heart failure.
The development of these nosology types is based on a complex of pathogenetic mechanisms acting directly on target organs or indirectly - through the development of endothelial dysfunction on the vascular wall, increased arterial stiffness, and factors include hypoxemia at rest or during physical activity, smoking, oxidative stress, low grade systemic inflammation [7]. Telling about the development of CHF in patients with COPD, it is important to mention the decompensation of chronic pulmonary heart disease (CHP), which is one of the important problems of modern medicine. According to some authors, COPD is accompanied by the development of pulmonary hypertension in 30-50% of cases [11]. The occurrence and development of pulmonary hypertension worsens the prognosis, and is also one of the main factors that determines the survival of patients with COPD [12-14]. It is important to note that the life prognosis of patients with COPD becomes unfavorable when pulmonary hypertension stabilizes and circulatory failure develops [12, 15]. More than 60% of patients with COPD die between 15 months and 5 years after the onset of circulatory decompensation, which ranks third after arterial hypertension and chronic coronary insufficiency among the causes of death in the age group over 50 years [16]. Despite the fact that decompensated CHL in 30-37% of cases is the cause of death from circulatory failure and in 12.6% of all cases the cause of death from cardiovascular diseases, the issues of early diagnosis of CHL, its decompensation and the development of effective treatment remain relevant, solutions which are inseparable from understanding the pathogenesis of CLS.
Thus, COPD and CHF constitute a dangerous duo that requires special attention. Both diseases are well studied, but independently of each other. Thus, pulmonologists are primarily involved in the study and management of patients with COPD and cardiologists are involved in the management of patients with CHF. This is probably why there is a late diagnosis of COPD in patients with CHF and CHF in patients with COPD. The combination of COPD and CHF gives rise to a number of clinical, including diagnostic, problems that have not yet been completely resolved. This review summarizes data on the features of diagnosing CHF in patients with COPD and COPD in patients with CHF. Difficulties in diagnosis begin with the similarity of clinical symptoms of CHF and COPD. From a modern clinical point of view, CHF is a syndrome with a complex of characteristic symptoms (shortness of breath, fatigue, decreased physical activity, edema), which are associated with inadequate perfusion of organs and tissues at rest or during exercise and often with fluid retention in the body. The root cause is a deterioration in the ability of the heart to fill or empty, caused by myocardial damage, as well as an imbalance of vasoconstrictor and vasodilating neurohumoral systems.
Symptoms typical of CHF include shortness of breath and fatigue, orthopnea, nocturnal attacks of cardiac asthma, poor exercise tolerance, fatigue, increased recovery time after cessation of exercise, and edema [5]. Most of these complaints (for example, shortness of breath, lack of air during physical activity, fatigue) are characteristic of both COPD and CHF. Dyspnea is one of the
first and for a long time the only complaint of patients with COPD. About 95% of patients with COPD and 56-74% of patients with CHF complain about shortness of breath. The majority (62%) of patients with COPD characterize shortness of breath as moderate or severe. [17, 18] Increased fatigue is noted by up to 72% of patients with COPD and 68% of patients with CHF [17]. In this regard, diagnosing CHF, especially in the early stages, can cause certain difficulties. In one study of 405 patients aged 65 years and older, 20.5% of subjects had previously unrecognized heart failure [19] of them, 50.6% had systolic dysfunction of the left ventricle (LV), 49.4% had diastolic dysfunction of the LV, although they were initially sent to the hospital with a diagnosis of COPD, but without a confirmed diagnosis of CHF. According to expert opinion, the most likely cause of systolic dysfunction was CAD, whereas hypertension, LV hypertrophy, and arrhythmia were common causes of diastolic dysfunction. Thus, the prevalence of CHF in stable COPD is 4 times higher than in the general population in people over 65 years of age.
Specific clinical signs of CHF are swelling of the neck veins, hepatojugular reflux, III heart sound (gallop rhythm), displacement of the apex beat to the left, systolic murmur; fewer specific ones include peripheral edema (ankle, sacrum, scrotum), wheezing in the lungs (crepitus), dullness in the lower parts of the lungs (pleural effusion), tachycardia, irregular pulse, tachypnea (respiratory rate more than 16 per minute), liver enlargement, ascites, cachexia. At the same time, in patients with COPD, severe emphysema can make it difficult to identify and evaluate such objective clinical signs that are pathognomonic for CHF, such as bilateral moist rales over the lower parts of the lungs, expansion of the percussion borders of the heart and even the third tone [3]. It is also important to note that difficulties arise when establishing the functional class of CHF based on the intensity of shortness of breath that limits physical activity, since in patients with COPD shortness of breath is both a symptom of CHF and a manifestation of COPD. In people with lung diseases, it is difficult to identify and correctly interpret the clinical manifestations of CHF. Typically, patients with CHF seek medical help precisely because of the occurrence of symptoms, many of which have low specificity and do not allow one to confidently distinguish CHF from other diseases, for example, shortness of breath with slight physical exertion, which can also occur in a patient with COPD. More specific symptoms, such as orthopnea and nocturnal attacks of cardiac asthma, are much less common, especially in patients with early stages of CHF, and therefore have low sensitivity [5]. The similarity of symptoms can lead to both underdiagnosis and overdiagnosis of CHF in patients with COPD. Thus, in one study, the presence of previously undiagnosed CHF was noted in 21% of patients with COPD [16]. According to the pooled data of a meta-analysis, including 6 studies (682 patients in total) studying LV ejection fraction (EF) in patients with COPD, 10-46% of patients had LVEF less than 40-50% [3, 7]. A thorough history taking is of great importance in diagnosing CHF. Heart failure is unlikely in patients without significant cardiac damage, while in the presence of those (especially a previous myocardial infarction), the likelihood of CHF in a patient with corresponding symptoms and signs increases significantly. In patients with CHF and COPD, there are frequent cases of overdiagnosis of the severity of CHF.
Besides that, the modern classification of the severity of CHF is based on a description of the severity of symptoms - functional classes of New York Heart Association [4], which is based on the patient's tolerance to physical activity. In patients with COPD, especially with severe and extremely severe course, there is also a decrease in tolerance to physical activity, regardless of the presence or absence of CHF. Radiography remains the standard diagnostic method for examining
patients with both COPD and CHF. It must be remembered that in the diagnosis of CHF, chest radiography has high variability and low reproducibility [5]. If CHF is suspected, the main attention should be paid to cardiomegaly (cardiothoracic index more than 50%) and pulmonary venous congestion. Cardiomegaly is evidence of the involvement of the heart in the pathological process. It should be noted that expansion of the boundaries of the cardiac shadow may be absent even with severe LV systolic dysfunction. The presence of venous stasis and its dynamics can be used to characterize the severity of the disease and serve as an objective criterion for the effectiveness of therapy. At the same time, severe pulmonary emphysema in patients with COPD can make it difficult to assess the severity of radiological signs of pulmonary congestion and measure the cardiothoracic index. Emphysematous areas of the upper lobes of the lungs, which are depleted in blood vessels, can mask the signs of CHF, and changes in the pulmonary vessels and radiolucent zones of the lungs can mask the manifestations of congestion in the lungs [3]. In recent years, important principles for the diagnosis of CHF have been the use of instrumental (echocardiography - Echo CG, magnetic resonance imaging - MRI) and laboratory (concentration of natriuretic peptide - CNP and its N-terminal precursor - NT-pro BNP) markers, imaging methods play a central role in the diagnosis of CHF.
The method of choice for suspected CHF is echocardiography, which is characterized by high diagnostic accuracy, widespread use, non-invasiveness and relatively low cost. Echo CG allows to assess quickly the size of the heart, the size of the cavities, the condition of the valve apparatus, and the systolic and diastolic functions of the ventricles. At the same time, it is important to note that the presence of COPD reduces the chances of satisfactory cardiac imaging. Thus, according to various studies, a satisfactory ultrasound window is present in 90% of patients with COPD and only in 65% of patients with severe and extremely severe COPD [3, 7, 9, 19, 20]. It is especially difficult to establish the diagnosis of heart failure in patients with COPD with preserved LVEF. The diagnosis of heart failure with preserved LVEF can be discussed in patients with COPD, LVEF greater than 40% and abnormal LV mass or dilated left atrium on echocardiography, or impaired LV filling on radionuclide ventriculography. Standard echocardiographic indicators of LV diastolic dysfunction do not allow us to establish accurately the presence of CHF with preserved LVEF, however, the accuracy of diagnosis can be increased with the combined use of Doppler echocardiography and myocardial tissue imaging methods, which provide evidence of impaired myocardial relaxation, increased LV filling pressure, etc. [4, 5, 21]. In addition to examining the LV, echocardiography allows one to assess the presence and severity of pulmonary hypertension and assess the structure of the right ventricle.
MRI is the gold standard for the accuracy of measuring the volume and mass of the heart, assessing the structure and function of the atria, but the disadvantages of this research method are its high cost and less common use than echocardiography.
A successful laboratory research method is measuring the concentration of natriuretic hormones in the blood. This is a family of peptides, the secretion of which increases with organic lesions of the heart, as well as with an increase in the hemodynamic load on the heart and for a number of extracardiac reasons (for example, renal failure) [5]. The role of natriuretic hormones is especially high when echocardiography is informative insufficiently, when patients have changes in the lungs. Normal levels of natriuretic hormones virtually exclude significant cardiac damage in the absence of previous treatment. In such cases, it is important to look for non-cardiac causes of patient's symptoms. Numerous studies have determined so-called threshold values for
natriuretic hormones. Different threshold values are used in patients with different onset of the disease. In case of acute onset of symptoms or their sharp increase, to exclude CHF, the CNP level should be less than 100 pg/ml, and NT-pro CNP should be less than 300 pg/ml [4, 5]. At the same time, a CNP level of more than 500 pg/ml in a patient with known COPD presenting with progressive dyspnea indicates the presence of left ventricular failure, regardless of whether it was previously diagnosed. The indicated CNP level does not allow differentiation of the respiratory or cardiac origin of dyspnea as the cause of the clinical deterioration of patient's condition, but indicates that therapy for CHF should be started or changed in addition to the treatment of patients with COPD [10]. A BNP level of 100-500 pg/ml may indicate right ventricular failure (which is also typical for patients with COPD), moderate left ventricular failure, or a combination of both [2, 4]. Accordingly, an NT-pro CNP level of more than 450 pg/ml (for patients under 50 years of age) and 900 pg/ml (for patients 50 years of age and older) indicates the presence of decompensated CHF in patients with COPD and increasing dyspnea [2, 4]. Similar data on the diagnostic level of NT-pro CNP in patients with exacerbation of chronic bronchitis were obtained in the work of Q. Wang et al. [22].
It was shown that when the NT-pro CNP level is more than 935 pg/ml, the sensitivity of left ventricular failure is 94.4%, the specificity is 68.2%, and the accuracy is 74.3%. The authors showed that when NT-pro CNP levels are included in the diagnostic algorithm, the likelihood of diagnosing left ventricular failure in patients with exacerbation of chronic bronchitis increases than when doctors focus only on clinical symptoms, X-ray and ECG data. Since 20-25% of patients with CHF have a CNP level of less than 100 pg/ml, with the gradual onset of symptoms, to exclude CHF, the CNP level should be less than 35 pg/ml, and NT-pro CNP - less than 125 pg/ml. The sensitivity and specificity of tests to determine the level of CNP and NT-pro CNP with gradual onset of symptoms is lower than with acute onset of CHF [5]. It should be noted that an increase in the level of CNP and NT-pro CNP in patients with COPD may be associated not only with the development of left ventricular failure, but also with pulmonary hypertension and right ventricular failure in CHL [3, 4, 23].
According to studies, the level of CNP correlates with pulmonary artery pressure [3]. According to the recommendations of the CNP Consensus Panel (2004), CLS is characterized by a CNP level of 100-500 pg/ml. In a stable period, patients with COPD have higher CNP levels than healthy people, but on average do not exceed 50 pg/ml [22]. At the same time, there is evidence that during an exacerbation, especially during a severe exacerbation of COPD with the development of acute hypoxemia, patients experience an increase in CNP levels, although not reaching the level in decompensated left ventricular failure [6, 23, 24]. This increase is associated with pressure or volume overload of the right ventricle. It should also be taken into account that obese patients have lower CNP levels than patients whose body mass index is less than 30 kg/m2 [25]. This may be due to the fact that adipocytes have receptors that bind and catabolize CNP, thereby reducing its levels in peripheral blood.
By summarizing it can be concluded that COPD is one of the important factors in the development of not only CHF, but cardiovascular diseases in general. There are quite a few cases of overdiagnosis of COPD in patients who are observed for CHF, but it is important to take into account the fact that CHF often remains undiagnosed, despite its high prevalence in patients with COPD. To formulate the correct therapy and increase the effectiveness of treatment for patients with a combination of COPD and CHF, it is important to determine the proportion of each of them
in the existing symptoms. Determining the severity of broncho-obstructive syndrome and the CNP level limits overdiagnosis and overestimation of the functional class of CHF when the CNP level is less than 100 pg/ml. An elevated level of CNP in the blood plasma should raise doubts about the presence of CHF in patient. Regular spirography in smoking patients with CHF will make it possible to increase the level of diagnosis of COPD and reduce the incidence of its overdiagnosis at the stage of decompensated CHF. Therefore, close cooperation between primary care physicians, pulmonologists and cardiologists is important to improve the diagnosis of combined cardiorespiratory pathology.
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