Low blood pressure, iron deficiency in the body: consult a doctor


Cardiovascular disease and anemia

The number of deaths from cardiovascular diseases (CVD) continues to rise worldwide. The conclusion that coronary heart disease (CHD) “... is the leading cause of death worldwide, its level is constantly growing and has now reached the proportions of a pandemic that knows no borders,” appeared on the website of the World Health Organization (WHO) in 2009 ., is perceived as increasingly relevant. In 2011, IHD caused the death of 7.3 million people [1, 2].

According to WHO estimates, 1.62 billion people suffer from anemia in the world [3]. The incidence of anemia, as well as coronary artery disease, increases significantly with age. More than 10% of people over 65 years of age and up to 50% of elderly patients with chronic diseases living in nursing homes have signs of anemia [4].

In the practice of general practitioners and cardiologists, a combination of cardiovascular pathology and anemia is often encountered. Anemia is detected in 25–40% of patients with chronic heart failure (CHF) and 10–20% of patients with coronary artery disease [5–7].

European and American recommendations for the management of patients with stable angina, issued in the last two years, require mandatory determination of hemoglobin levels in all patients and consider anemia as a factor provoking coronary insufficiency [8, 9]. In the latest recommendations for the diagnosis and treatment of patients with CHF, American and European experts note that anemia not only increases the symptoms of CHF, worsens the quality of life of patients, reduces exercise tolerance, and can cause the development of acute decompensation of CHF and an increase in the frequency of hospitalizations, but also an independent negative predictor of prognosis [10, 11]. The risk of death in CHF in patients with anemia is twice as high as without it, even when taking into account additional variables (renal dysfunction, severity of CHF, and others) [13]. Already latent iron deficiency can have a negative impact on the prognosis of CHF [14], which makes it advisable to determine its markers in all patients with CHF.

In acute coronary syndrome, the presence of anemia can quadruple the likelihood of death in patients and is considered an independent predictor of the risk of adverse clinical outcomes [15, 16]. Even chest pain syndrome in women, when combined with anemia, turns out to have a more unfavorable prognosis (the risk of death doubles) [17].

Preoperative anemia during cardiac surgery determines a high risk of subsequent blood transfusion and worse treatment results, which makes the task of early detection of anemia and high-quality, timely treatment urgent [18].

The role of anemia as an independent risk factor for poor prognosis in atrial fibrillation in elderly and senile people has been proven [19].

As shown by the analysis of the effect of the combination of anemia and impaired renal function on coronary artery disease in the population-based ARIC study (The Atherosclerosis Risk in Communities Study), anemia occurs in individuals with a slight and moderate decrease in renal function much more often than expected. And the combination of anemia and renal dysfunction significantly increases the risk of developing coronary artery disease, even after taking into account known risk factors such as diabetes mellitus, blood lipid levels, blood pressure and the use of antihypertensive therapy. The findings highlight the need for timely identification and treatment of anemia to improve patient prognosis [20].

The unfavorable mutual influence of CHF, anemia and renal dysfunction gave rise to the identification of new syndromes: “cardiorenal anemia syndrome”, “cardiorenal iron deficiency syndrome” and even “cardiorenal anemia and iron deficiency syndrome”. The latter terms emphasize the importance of iron deficiency as an independent risk factor for poor prognosis in CHF. The possibility of a direct effect of iron deficiency on diastolic function, hypertrophy, fibrosis and dilatation of the myocardium, the level of circulating erythropoietin, molecular signaling pathways and activation of inflammation has been proven in animal experiments [21]. This wide range of negative effects of iron deficiency is likely related to the role of iron in the body. It is not only part of hemoglobin and myoglobin, but is also found in enzymes involved in the conversion of adenosine triphosphate into adenosine diphosphate, promotes electron transport in mitochondrial chains, determines tissue metabolism and the absorption of free radicals [19]. Iron is involved in immune reactions and is necessary for the myelination of nerve fibers and DNA synthesis [22, 23].

Anemia in people with cardiovascular disease may have the same etiological factors as in the general population. An additional role in the development of anemia in cardiovascular pathology may be played by the older age of patients, which is itself associated with a lower hemoglobin value, the increasing incidence of chronic kidney disease, and the high prevalence of diabetes mellitus. It is assumed that the development of anemia in pathology of the cardiovascular system is contributed by: a chronic inflammatory process (increased synthesis of pro-inflammatory cytokines - tumor necrosis factor alpha, interleukin-6), ischemic depression of bone marrow hematopoiesis, decreased synthesis of endogenous erythropoietin due to renal dysfunction. In CHF, hemodilution with sodium and water retention and impaired absorption of iron and vitamins in the intestine may play a role in the formation of anemia. An additional factor for the development of anemia may be ongoing drug therapy that causes blood loss (when taking Aspirin, anticoagulants), a decrease in the production of erythropoietin and the sensitivity of the bone marrow to it (when using blockers of the renin-angiotensin-aldosterone system), etc.

The relevance of the issue of early diagnosis of anemia in patients with cardiovascular pathology is determined by the fact that its late detection leads to a delay or absence of the necessary intervention in relation to a potentially correctable condition.

A significant proportion of patients with cardiovascular pathology have latent iron deficiency, or iron deficiency anemia (IDA) or a combination of these conditions with other types of anemia.

Clinical signs of IDA consist of anemic and sideropenic syndromes, the latter is also determined by iron deficiency. Anemic syndrome may include the following manifestations: weakness, dizziness, syncope and orthostatic conditions, memory loss, epileptic seizures, symptoms of coronary insufficiency (anginal pain, repolarization disturbances on the ECG, arrhythmias), symptoms of myocardial insufficiency, systolic murmur on auscultation of the heart. Sideropenic syndrome leads to multiple disorders of various organs and systems. Lesions due to iron deficiency in the skin, skin appendages and mucous membranes (dryness, damage to hair and nails, etc.) are well known. No less common manifestations are symptoms from the gastrointestinal tract (decreased and perverted appetite, dysphagia, constipation or diarrhea, glossitis, burning tongue, esophagitis, dystrophic changes in the cells of the gastric mucosa); nervous system (increased fatigue, tinnitus, dizziness, headaches, decreased intellectual capabilities); cardiovascular system (tachycardia, diastolic dysfunction); urinary system (dysuria and urinary incontinence when coughing, laughing, nocturnal enuresis).

In the laboratory diagnosis of chronic IDA, microscopy of a peripheral blood smear reveals microcytic hypochromic anemia with hypoproliferation of reticulocytes. To confirm iron deficiency, reduced serum iron and ferritin levels are required.

Treatment of IDA is aimed at treating the disease underlying iron deficiency and actually compensating for iron deficiency.

Although patients with IDA need dietary advice, it is important to clearly explain that diet is not the basis of therapy. The largest amount of iron is found in meat (heme iron). All other foods contain less iron, and, most importantly, much less of them is absorbed (1–5% from apples, 10–15% from eggs and fish, and 25–30% from meat).

In drug therapy for IDA, the main focus has been and remains the use of iron supplements. The choice of iron drug is determined by its effectiveness (the amount and bioavailability of the iron it contains) and tolerability. An intake of 100 to 300 mg of elemental iron per day is required. The use of higher doses does not make sense, since iron absorption does not increase. Iron preparations on the domestic market are represented by hydroxypolymaltose complex, iron sorbitol complex, protein iron succinylate, iron sucrose complex. For patients with cardiac pathology, it is extremely important when carrying out additional drug therapy for IDA, in addition to high efficiency, the absence of negative drug interactions and good tolerability of the drug. The drug Maltofer, a polymaltose complex of iron sulfate (III), meets these requirements. Maltofer is a non-ionic iron preparation. Its absorption is ensured by active transport, without preliminary dissociation in the intestine, which eliminates the irritating effect on the mucous membrane and avoids most of the undesirable reactions from the gastrointestinal tract typical of ionized iron preparations [25, 26]. Maltofer does not interact with food or other medications, and the release form in the form of chewable tablets allows it to be used at any time and in any setting [27–30]. At the same time, the absorption of iron from other iron supplements may be reduced under the influence of substances contained in some foods - phytins (rice, soy), phosphates (fish, seafood), tannin (tea, coffee), while taking a number of medications (tetracyclines, antacids, calcium and magnesium salts), which requires taking these medications taking into account the time of consumption of food and these medications. Iron salt preparations contain divalent iron, which, after entering the blood, is converted into trivalent iron for its subsequent inclusion in the hemoglobin molecule, which can be accompanied by the formation of free radicals and have a negative effect on physiological processes in various organs and tissues [31]. Maltofer contains ferric iron, which is directly used to build the hemoglobin molecule, and therefore does not have a pro-oxidant effect [32]. When using iron supplements in adequate doses, a subjective improvement in well-being may be noted within a few days. The first objective criterion - reticulocyte crisis (an increase in the number of reticulocytes by 2-10 times compared to the initial one) is observed by the end of the first week of therapy. The absence of reticulocyte crisis indicates either an inadequate dose of the drug or an erroneous prescription of the drug. An increase in hemoglobin levels and the number of red blood cells is observed in the third week of therapy. After normalization of hemoglobin levels, a half dose of iron supplement is recommended for another 4–8 weeks to saturate the iron depot.

In 2013, the first recommendations for the treatment of anemia in patients with cardiovascular pathology were issued by the American College of Physicians [20]. They generally determine the tactics of managing a patient with cardiac pathology and anemia, regardless of its etiology. Three treatment strategies are considered: the use of erythropoietin-stimulating agents, red blood cell transfusion, and replenishment of iron deficiency. It is emphasized that red blood cell transfusion does not provide benefit and can cause harm to patients, so it is only possible in hospitalized severe patients with coronary artery disease with severe anemia. The use of erythropoietin-stimulating drugs for mild and moderate anemia in patients with CHF and coronary artery disease is not recommended due to the potential risk of thromboembolic complications and the lack of effect of therapy on the prognosis and frequency of hospitalizations. Positive data are currently available for the strategy of replenishing iron deficiency with intravenous administration of iron carboxymaltose; this tactic improves exercise tolerance, quality of life, reduces mortality and the frequency of hospitalizations [33].

Thus, anemia is a common comorbidity in cardiovascular diseases. Today in cardiology it is assessed as an independent predictor of the risk of adverse clinical outcomes, therefore patients with cardiovascular pathology need timely diagnosis of anemia in order to carry out adequate therapy.

Literature

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E. S. Temnikova, Doctor of Medical Sciences, Professor

State Budgetary Educational Institution of Higher Professional Education Omsk State Medical Academy of the Ministry of Health of the Russian Federation, Omsk

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What is anemia? Nine out of ten people will answer: anemia. This concept has become so common in everyday life that no one even thinks about deciphering it. But “little” does not mean that there is not enough blood in your body. Her quantity is just fine. Problems with “quality”: with anemia, there are not enough full-fledged red blood cells in the blood - red blood cells. And they contain hemoglobin, which is responsible for the “delivery” of oxygen to every cell of the body’s tissues. And if its level is reduced, very unpleasant things happen: organs and tissues experience oxygen starvation, which means they are unable to work at full capacity.

Anemia may be an inherited blood disorder, or it may be a temporary “abnormal” condition. For example, when the body experiences a deficiency of vitamin B12, folic acid, after an injury with large blood loss, etc. But 90% of anemias are so-called iron deficiency: the name itself suggests that the body lacks iron. Why? Let's try to figure it out.

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