Aspirin: what is better to drink and when to take it

Not long ago, our gynecologists attended the XXVI European Congress of Perinatal Medicine (ECPM 2018). We, together with Svetlana Silenko, Deputy Head of the Center for Obstetrics and Gynecology GMS Clinic, decided to share with you the most interesting facts heard and seen at the congress.

Pharmacodynamics and pharmacokinetics

The main component of the medicine is acetylsalicylic acid (some mistakenly call it acetylic acid). The pharmaceutical drug belongs to anti-inflammatory medications.

It is useful to know that Aspirin and acetylsalicylic acid are the same thing.

C9H8O4 is the chemical formula of Aspirin.

Taking Aspirin in a dosage of 300 mg to 1 mg helps eliminate joint and muscle pain. In addition, a similar dose of the drug helps to improve well-being during colds and flu, and helps with fever.

Acetylsalicylic acid is suitable for the treatment of acute and chronic inflammatory diseases.

It is advisable to take aspirin for:

Bekhterov's diseases
Osteoarthritis
rheumatoid arthritis

For the above diseases, doctors prescribe higher doses of the drug than when fighting colds and high body temperature. Based on the specific course of the disease, patients are prescribed 4-8 g of medication per day.

Aspirin is also useful to take in the presence of many vascular diseases. In such cases, doctors recommend taking from 75 g to 300 mg of the substance daily (depending on the nature and danger of the disease).

Pharmacokinetics

After consuming the medicine, the active substance is rapidly and completely absorbed from the stomach. During and after absorption, it is converted to salicylic acid (the main active metabolite).

Decomposition products are primarily excreted through the kidneys.

Purpose of the drug

Doctors do not prescribe Aspirin for high blood pressure, but they do prescribe it to prevent possible complications. The drug helps prevent the development of heart attack and stroke. For hypertensive patients, Aspirin alone is not enough, but for patients with cerebral vascular pathologies, the medication is quite enough. The medicine can dilate blood vessels and stop headaches.

Doctors do not recommend medicine for high blood pressure. “Aspirin” is actively used by cardiologists and is included in standard treatment regimens for pathologies of the heart and blood vessels. Doctors also prescribe it in the postoperative stage after various interventions to prevent the formation of complications.

It is not advisable to take acetylsalicylic acid continuously. For patients with high blood pressure, the medicine helps well if cardiovascular pathologies are detected. In such situations, Aspirin reduces blood pressure. In other situations, therapy with this remedy does not make sense.

If the pressure has increased, in order to reduce it, doctors prescribe other medications: Cardiomagnyl, Aspecard. But their constant use is possible if there is a mortal danger:

in a post-infarction state;
there are blood flow disorders in the brain;
atherosclerosis was detected.

To reduce potential risks, the cardiologist determines which disorder in the body increases blood pressure. Then he prescribes the drug and determines an effective treatment regimen.

Chemical structure of aspirin

The medicine is a non-steroidal analgesic and is effective in eliminating inflammatory formations. It is a popular substance that can help with frequent headaches and migraines. The properties of the drug are aimed at reducing the activity of enzymes that are the cause of many ailments. Positively affects the cerebral hemispheres and areas responsible for thermoregulation.

Structure of aspirin:

Acetylsalicylic, citric acids.
Sodium bicarbonate.
Citrate, sodium carbonate.
Talc.

The effect of Aspirin on the body of a hypertensive patient has not been fully studied; doctors do not prescribe this medicine for treatment when diagnosing hypertension. But its ability to make blood less often is appreciated by cardiologists. Since the result of consuming acetylsalicylic acid is a reduction in the risk of acquiring serious heart pathologies (heart attack, stroke). Therefore, to the question of whether it is possible to take aspirin with high blood pressure, there is a clear answer - it is possible, but in the intervals between attacks, as a dosage form to prevent pathology or for complex therapy.

To treat hypertension, they resort to similar compositions with a similar name, confirming the inclusion of the same components in the structure, as an example - Aspirin Cardio.

Undoubtedly, the dosage form has an effective effect on symptoms. It is unlikely that it will be possible to cure hypertension or achieve effective effects on blood pressure. Taking the medicine daily can have a positive effect on the dynamics of the disease and slightly reduce the tonometer readings. Good results in the treatment of hypertension can be achieved with complex treatment in combination with more effective drugs aimed at reducing elevated values on the tonometer display.

A cardiologist or neurologist can prescribe a drug for the initial stage of hypertension (90 mmHg). Aspirin can reduce the tonometer readings by several positions, and the reason for this is its ability to thin the blood. The dose is prescribed by the attending physician.

The ability of the drug to reduce high intracranial pressure is invaluable; tablets can cope with this task on their own.

Indications for use of Aspirin

Acetylsalicylic acid is a symptomatic drug that should be taken for:

pain
inflammation
feverish

Indications for use:

toothache
headache
muscle and joint pain
algomenorrhea
sore throat due to a cold
back pain
cold
ARVI
Pain of moderate severity arising from inflammation of the joints

Contraindications for Aspirin

Prohibitions on taking Aspirin are divided into two types:

Relative
Absolute

Taking Aspirin is strictly prohibited if you are allergic to acetylsalicylic acid or other non-steroidal anti-inflammatory drugs. In addition to all this, the drug should not be used if there is an increased tendency to bleeding.

Relative contraindications:

Bronchial asthma
Combined use of anticoagulants
Breast-feeding
Pregnancy
Chronic stomach diseases
Kidney dysfunction
Diabetes
Age up to 12 years

If there are relative prohibitions, taking the medicine is possible only after approval by the doctor.

What do the doctor's say

Is it possible to take Aspirin for high blood pressure? Doctors say that it can be drunk in moderate dosages for hypertension. However, it is prohibited to use it constantly. If blood clotting is impaired, it is better to avoid Aspirin to reduce blood pressure. In addition, constant medical supervision is required while taking it. If hypertension is treated with Aspirin, this should be done in combination with other medications.

Doctors remind that with prolonged use, acetylsalicylic acid weakens the gastric mucosa, which can lead to internal bleeding. It is not recommended to use Aspirin for gastritis, ulcers and ulcerative colitis.

Side effects

Sometimes taking Aspirin can cause negative effects, these include:

Pain in the stomach
Decreased platelets in the blood
Bronchospasm
Various skin rashes

Taking Aspirin for a long time sometimes leads to the development of bleeding in the gastrointestinal tract. Signs characterizing this pathology:

Anemia
Tarry stool
Weakness, excruciating abdominal pain

If the above symptoms appear, you should stop taking Aspirin and seek medical help.

In 1997, the American Diabetes Association published recommendations on the use of aspirin for the primary and secondary prevention of cardiovascular complications in patients with diabetes mellitus (DM) [1, 2]. The recommendations were based on a meta-analysis of 145 prospective controlled trials of the effectiveness of anticoagulants and antiplatelet agents in 63,762 people with a history of cardiovascular disease [3, 4]. Taking aspirin significantly reduced the incidence of cardiovascular complications, and this effect was most noticeable among 4643 patients with diabetes [3, 4].

Among the antiplatelet drugs used for ischemic heart disease and atherosclerosis of cerebral and peripheral vessels, aspirin is the best studied and most frequently used [5].

Mechanisms of action and properties of aspirin

The antiplatelet effect of aspirin is based on its ability to inhibit cyclooxygenase-1 (COX-1) in platelets (Fig. 1). Aspirin irreversibly binds to active centers localized on the wall of the hydrophobic channel of the COX-1 molecule, leading from its surface to deep structures. By acetylating the active centers of COX-1, aspirin blocks the transport of arachidonic acid, a substrate for the synthesis of prostaglandins and thromboxanes [6, 7]. Thromboxane A2 activates platelet aggregation and thus promotes thrombus formation. Aspirin inhibits COX-1 irreversibly, and this effect persists throughout the life of the platelet (about 10 days). Therefore, the duration of action of aspirin significantly exceeds its relatively short half-life.

It is believed that 20% of intact platelets are sufficient to maintain normal hemostasis. Since approximately 10% of platelets are replaced daily, a single dose of aspirin produces an effect that lasts at least 48 hours.

Aspirin irreversibly suppresses COX-1 activity not only in platelets, but also in the endothelium. Unlike thromboxane A2, prostacyclin, secreted by the endothelium, inhibits platelet aggregation and has a vasodilatory effect. Impairment of prostacyclin secretion as a result of the action of aspirin is highly undesirable. However, unlike anucleated platelets, endothelial cells are capable of synthesizing active COX-1 and do this constantly even under the influence of aspirin. It takes 3–6 hours for complete restoration of COX-1 activity in the endothelium [8, 9].

Aspirin inhibits COX-1 in platelets as they pass through the liver. Here, aspirin is almost completely inactivated, so only trace amounts enter the systemic circulation. Aspirin is used as an antiplatelet agent in small doses, and its distribution throughout the body is very limited. T1/2 of aspirin is only 15–20 minutes, which shortens the duration of its contact with the body [10]. The risk of a decrease in prostacyclin production in the endothelium under the influence of aspirin is minimal, especially when using low doses of the drug.

One can debate for a long time which of the described effects of aspirin is the most physiologically significant (Fig. 2). However, it has been proven that in atherosclerosis it is the suppression of thromboxane A2 secretion that has a therapeutic effect [11]. From this point of view, aspirin appears to be a custom-made drug for antiplatelet therapy [12].

Modern experimental methods have made it possible to recreate a complex picture of the action of aspirin. The variety of effects distinguishes aspirin from other antiplatelet drugs and makes it a unique drug.

The antithrombotic effect of aspirin is believed to include effects on fibrinogen formation and the process of fibrinolysis. Aspirin acetylates lysine residues in the fibrinogen molecule and thus prevents their oxidation. Altered fibrinogen cannot be converted into fibrin and cause thrombus formation [13]. In addition, acetylation of lysine residues, which normally stabilize the network of fibrin elements, promotes thrombus dissolution [14, 15]. Moreover, aspirin causes the formation of thicker fibrin strands and networks with larger pores. This has a positive effect in patients with cardiovascular diseases, which are characterized by the presence of dense fibrin clots. In addition, an increase in pores facilitates access to fibrin threads of plasminogen activators, causing their dissolution [14, 15]. Aspirin inhibits the formation of thrombin, which catalyzes the conversion of fibrinogen to fibrin [16]. It has been shown that high doses of aspirin can have both an inhibitory and stimulating effect on fibrinolysis, with the fibrinolytic effect being dominant [17–19].

Of particular interest is the ability of aspirin to stabilize atherosclerotic plaques. There is evidence of its effect on the functional activity of the cellular components of the vascular wall. For example, in the endothelium, in addition to affecting COX-1 activity, aspirin feedback regulates the expression and activity of NO synthase and can both enhance and suppress NO production [21–24]. Long-term use of low-dose aspirin reduces elevated levels of tissue plasminogen activator [25, 26].

Aspirin suppresses the expression of genes involved in the activation of inflammatory processes [27, 28] and normalizes the level of C-reactive protein [29, 30]. This is of great importance, since inflammatory processes increase the risk of rupture of atherosclerotic plaques and thrombus formation [31–33]. The stability of atherosclerotic plaques also increases due to the antioxidant effect of aspirin [23, 34]. Aspirin and its metabolites help protect the endothelium from peroxidation products, in particular from OH radicals [34]. It turned out that aspirin stimulates the production of ferritin, which binds free iron ions in the blood and thereby protects the endothelium from free radicals arising under the influence of free iron ions. At therapeutic concentrations, aspirin increases ferritin production by 5 times. These observations allow us to understand why aspirin increases the resistance of the endothelium to free radical oxidation [35]. In addition, aspirin affects the synthesis of vitamin K in the liver, uncouples oxidative phosphorylation, depletes ATP reserves, and blocks the production of extracellular adenosine [36]. Many researchers believe that these properties of aspirin are no less significant than its effect on platelet aggregation [37].

Aspirin is rapidly absorbed from the stomach and upper small intestine. Its maximum plasma concentration is reached within 15–20 minutes [38]. At this point, aspirin at a dose of 80–160 mg completely suppresses platelet aggregation [39]. Aspirin is usually taken at night. This is due to the fact that the peak of the daily rhythm of platelet aggregation is observed at 22:00.

For long-term use, it is recommended to use enteric forms of aspirin. When prescribing these forms, the risk of damage to the gastric mucosa and gastrointestinal bleeding is the same as when prescribing placebo [40, 41]. Switching from regular aspirin to enteric forms reduces the number of days of disability by 78% and the number of hospitalizations during the year by 64%.

The enteric coating makes aspirin safer for the stomach, but delays the onset of action of the drug by an average of 2 hours. In emergency situations, instant aspirin is recommended, and regular or enteric aspirin tablets should be chewed or sucked [42–44]. If enteric aspirin tablets are chewed, the maximum antiplatelet effect occurs within 30 minutes [44]. With long-term use of the drug, the time of development of the effect does not matter [45].

Aspirin can be taken at longer intervals, but it is usually recommended that these intervals should not exceed 2 days. Frequent use of small doses of the drug is better tolerated, and the secretion of prostacyclin is less suppressed.

When taken in the evening, aspirin reduces blood pressure in people at high risk of cardiovascular disease, whereas this effect is absent when taken in the morning [46–49]. The antiplatelet effect also depends on the time of administration, since the number of platelets in the blood follows a circadian rhythm and is higher during the day than in the morning [50]. Aspirin taken in the morning is eliminated faster than when taken in the evening [47]. In addition, the proportion of aspirin entering the systemic circulation decreases with decreasing dose.

The dose of aspirin is selected depending on the indications and individual characteristics of the patient [51]. One of the amazing properties of aspirin is its ability to cause different effects at different doses. The antiplatelet effect decreases with increasing dose, possibly due to suppression of prostacyclin secretion. As the dose is reduced, the frequency of side effects decreases. It has been shown that a stable antiplatelet effect can be achieved in the dose range from 30 to 1500 mg. Typically, the desired level of platelet aggregation inhibition can be achieved with 100 mg aspirin [51].

The American Heart Association recommends a daily dose of 75–325 mg for preventive antiplatelet therapy [5]. The American Diabetes Association recommends the use of aspirin in a dose of 81–325 mg/day in patients with diabetes [40]. To achieve a rapid antiplatelet effect, aspirin treatment is always started with a dose of at least 2 mg/kg. This is especially important in emergency situations in patients with acute cardiovascular complications [51]. The use of low doses of aspirin sharply reduces the incidence of nosebleeds and massive post-traumatic hematomas.

The effect of aspirin is most pronounced when platelets are in a state of hyperactivity, that is, they have an increased tendency to aggregate. Myocardial infarction or atherosclerotic plaque rupture are typical conditions in which platelets are activated. Plasma thromboxane A2 levels may remain elevated for up to two years after these events [52, 53]. Smoking significantly increases platelet aggregation [54, 55].

Extremely high levels of thromboxane A2 are observed in patients with diabetes. This disease is accompanied by hyperactivation of platelets, a significant acceleration of their renewal, increased metabolism of arachidonic acid, decreased production of prostacyclin and NO, increased free radical oxidation, increased expression of adhesion molecules; acceleration of the development of atherosclerosis and an increase in the frequency of thromboembolism [56, 57]. This explains the effectiveness of prophylactic use of aspirin in patients with a combination of diabetes and coronary artery disease [1, 58], especially in the presence of type 2 diabetes [59].

Clinical trial data

The effectiveness of aspirin for the primary prevention of cardiovascular complications in patients with diabetes has been proven by the results of several studies.

The Early Treatment of Diabetic Retinopathy Study, a multicenter, randomized trial, enrolled 3,711 patients aged 18 to 70 years from 22 clinical sites in the United States [60]. The effectiveness of aspirin was assessed by total mortality and mortality from cardiovascular diseases. The dose of aspirin (Bayer) was 650 mg/day. After 5 years, overall mortality among patients receiving aspirin was 12.1 versus 14.9% in patients not receiving it. Mortality from cardiovascular diseases also differed significantly – 9.3 and 11.2%, respectively. The reduction in mortality in patients receiving aspirin was largely due to a reduction in the incidence of myocardial infarction.

No less important confirmation of the protective effect against cardiovascular diseases in patients with diabetes was obtained in the Hypertension Optimal Treatment study [61]. This double-blind, controlled study included 18,790 patients with hypertension, 1501 of whom had diabetes. Almost 10% of patients had symptoms of damage to the cardiovascular system at the beginning of the study. The addition of aspirin at a dose of 75 mg/day to antihypertensive therapy led to a significant reduction in the incidence of cardiovascular complications by 15% and a reduction in the incidence of myocardial infarction by 36%.

A double-blind, controlled study of the effect of aspirin on mortality from cardiovascular diseases, the Physicians' Health Study, continued for five years [62]. The study included 22,071 patients without cardiovascular disease, including 533 patients with diabetes. Aspirin was prescribed at 325 mg every other day. The cumulative five-year risk of myocardial infarction in patients with diabetes who received aspirin was 4%, and in patients receiving placebo it was 10.1%. Aspirin significantly reduced the risk of myocardial infarction in the age group over 50 years; this effect was strongest in men with low total cholesterol. In participants over 59 years of age, the risk of myocardial infarction was reduced by 39% when exposed to aspirin.

Recent studies, the Thrombosis Prevention Trial and the Primary Prevention Project, assessed the effectiveness of primary prevention of cardiovascular disease using low-dose aspirin (75–100 mg/day). In total, these studies involved about 6000 patients at high risk of cardiovascular diseases, including patients with diabetes [61, 63, 64]. Aspirin significantly reduced the incidence of myocardial infarction and mortality from cardiovascular diseases.

The American Diabetes Association, based on the results of a meta-analysis of studies, concluded that adult patients with type 1 and 2 diabetes mellitus at high risk of cardiovascular complications should take from 81 to 325 mg of enteric-coated aspirin daily for primary prevention of the latter [1, 2 , 40, 65]. Risk factors include: family history of coronary artery disease, smoking, arterial hypertension, excess weight (relative weight > 120%, BMI in men > 27.3 kg/m2, BMI in women > 27.8 kg/m2). In addition, the high-risk group for vascular complications of diabetes includes patients with micro- and macroalbuminuria and individuals with dyslipidemia (total cholesterol > 200 mg%, LDL cholesterol > 100 mg%, HDL cholesterol 200 mg%). Some authors also indicate such risk factors as increased levels of fibrinogen, glycosylated hemoglobin, tissue plasminogen activator inhibitor and severe insulin resistance [1]. Aspirin may reduce microalbuminuria in type 1 diabetes [66]. It is most effective in individuals with elevated levels of C-reactive protein [67]. These disorders may also serve as indications for the use of aspirin in patients with diabetes.

Since there is insufficient experience with the use of aspirin in young patients with diabetes, and in people under 21 years of age it can provoke Reye's syndrome, the recommendations of the American Diabetes Association apply only to people over 30 years of age [40].

To date, it has been convincingly proven that aspirin prevents repeated myocardial infarctions and acute cerebrovascular accidents, i.e., it is effective as a means of secondary prevention.

The American Diabetes Association suggests the use of aspirin for the secondary prevention of complications in patients with diabetes with cardiovascular diseases, primarily in patients with diabetes and coronary artery disease, angina pectoris, who have had myocardial infarction, or coronary artery bypass grafting.

According to the American Diabetes Association, coronary artery disease in patients with diabetes is an absolute indication for the use of aspirin [2]. In addition, the group of secondary prevention of cardiovascular complications includes patients who have suffered a cerebrovascular accident, transient ischemic attack, with damage to peripheral arteries, and intermittent claudication.

These recommendations are based on a meta-analysis of 145 prospective controlled trials of the effectiveness of antiplatelet therapy in people with a history of myocardial infarction, stroke, or transient cerebrovascular accidents with a history of cardiovascular disease. A meta-analysis was conducted by the Antithrombotic Therapy Research Group [3, 4, 68]. Among the 63,762 patients included in these studies, 4,643 had diabetes. Taking aspirin significantly reduced the incidence of recurrent cardiovascular events; this effect was more noticeable in patients with diabetes [3, 4]. The incidence of cardiovascular complications in patients with diabetes who took aspirin decreased to 19.3%, while in patients who did not take this drug it was 23.5% (p

A repeated meta-analysis conducted by the same group approximately 10 years later and including 212 thousand patients participating in 287 trials confirmed that in high-risk patients, including patients with diabetes, antiplatelet therapy reduces the frequency of heart disease. -vascular complications by 23% [69].

Aspirin and other antiplatelet drugs

Is there an alternative to aspirin prevention? Currently, in addition to aspirin, ticlopidine, clopidogrel, dipyridamole and glycoprotein IIb/IIIa receptor inhibitors are used to suppress platelet aggregation.

Ticlopidine and clopidogrel are antithrombotic drugs that irreversibly block the binding of ADP to type 2 purinergic receptors on platelets. By blocking this type of receptor, they prevent the activation of platelet glycoprotein IIb/IIIa receptors, their binding to fibrinogen and the formation of a platelet thrombus. Thus, the mechanism of action of ethiclopidine and clopidogrel differs from that of aspirin [68]. However, they do not have such a wide spectrum of action as aspirin.

Currently, clopidogrel is most often considered as an alternative to aspirin. The use of ticlopidine increases the risk of agranulocytosis and neutropenia and is therefore less acceptable. The CAPRIE (Clopidogrel vs. Aspirin in Patients at Risk of Ischemic Events) study compared the effectiveness of aspirin at a dose of 325 mg/day and clopidogrel at a dose of 75 mg/day for the prevention of cardiovascular complications in patients who had recently suffered a myocardial infarction, a brain disorder blood circulation or had severe damage to the peripheral arteries. In patients taking clopidogrel (1914 patients with diabetes), ischemic complications occurred significantly less often (Fig. 3) than in patients taking aspirin (1952 patients with diabetes) - in 15.6 and 17.7% of cases, respectively; p

The American College of Cardiology and the American Heart Association recommend the use of a combination of aspirin and clopidogrel for short-term antiplatelet therapy in acute coronary syndrome in patients with diabetes [71]. According to the CURE (Clopidogrel in Unstable Angina to Prevent Reccurent Events) study, combination therapy with aspirin and clopidogrel for 9 months was 20% more effective than treatment with aspirin alone (the incidence of myocardial infarction, cerebrovascular accidents and mortality from cardiovascular complications was assessed ) [72]. The incidence of major bleeding in patients receiving the combination of drugs was significantly higher than in patients receiving aspirin alone (3.7 and 2.7%, respectively), but the incidence of life-threatening bleeding did not significantly increase.

In acute coronary syndrome in patients with diabetes, a beneficial effect of inhibitors of glycoprotein IIb/IIIa receptors was noted. The use of these drugs significantly reduces mortality over 30 days. However, they can only be used short-term and therefore cannot be considered as an alternative to long-term aspirin use [73].

Combining aspirin with other antiplatelet agents is useful not only for acute coronary syndrome. Thus, its combination with dipyridamole in patients of different ages with stroke more effectively protects against recurrent stroke and death than aspirin monotherapy. The risk of stroke is reduced by 18% when taking aspirin, by 16% when taking dipyridamole, and by 37% when taking the combination [74, 75]. In patients with intracoronary stents, the combination of aspirin 325 mg/day and ticlopidine 250 mg/day is more effective than aspirin monotherapy at 325 mg/day or the combination of aspirin at the indicated dose with an individually adjusted dose of heparin or warfarin [76]. Unfortunately, all of these combinations prolong bleeding time and increase the risk of side effects.

It seems reasonable to conclude that currently aspirin is the drug of choice for long-term antiplatelet therapy in patients with diabetes [77, 78]. It is important to emphasize that the annual cost of treatment with aspirin is 230 and 600 times less than the cost of treatment with clopidogrel and ticlopidine, respectively [79].

In some patients, the antiplatelet effect of aspirin is not observed. Such aspirin resistance is due to genetic factors [80]. Platelets contain mainly COX-1, but they may also contain cyclooxygenase-2, the activity of which is much less affected by aspirin. This partly explains why platelets in some patients are less sensitive to the action of aspirin [81].

In such situations, attempts can be made to optimize therapy by monitoring urinary levels of thromboxane metabolites [51] and adjusting the dose of aspirin. If there is no effect, it is recommended to switch to clopidogrel.

Side effects of aspirin

Side effects of aspirin are observed in 5-8% of patients and most often affect the gastrointestinal tract. Tolerability improves with lower dosages of enteric aspirin. Patients who have a tendency to bleeding or concomitant gastrointestinal diseases require increased attention. Reducing the dose of aspirin does not always reduce the risk, but it always reduces the severity of bleeding [74]. The risk of side effects is higher in patients over 60 years of age, with a history of peptic ulcer disease, smokers, and patients taking other “high-risk” drugs (for example, glucocorticoids) [82]. Aspirin should not be prescribed to patients with an allergy to this drug, with active forms of liver disease, with a tendency to bleeding, with a recent history of gastrointestinal bleeding, or on anticoagulant therapy [40].

Regular use of nonsteroidal anti-inflammatory drugs, which include aspirin, increases the risk of chronic renal failure and worsens blood pressure control in people with arterial hypertension [40]. According to the Department of Medical Epidemiology at Stockholm University of Cardiology, in people with kidney failure, aspirin increases the risk of end-stage renal failure by 2.5 times, regardless of the cause. However, other data on the use of aspirin in patients with diabetes indicate that the risk of end-stage renal failure with aspirin is no different from the risk with placebo [60]. The 2002 American Diabetes Association guidelines do not include kidney disease as a contraindication for regular aspirin use in patients with diabetes [40]. It is believed that low doses of aspirin weakly suppress the synthesis of prostaglandins in the kidneys and therefore have virtually no effect on their function and blood pressure.

The real situation with aspirin use

Unfortunately, data on the reduction in the risk of cardiovascular complications in patients with diabetes under the influence of aspirin are not taken into account in everyday clinical practice. Even in specialized diabetes centers, few patients are prescribed antiplatelet therapy [83].

According to the NHANES III study, conducted in the United States from 1988 to 1994, 21% of patients with diabetes over 18 years of age had a history of coronary artery disease, and another 71% of patients had at least one risk factor for cardiovascular disease. Thus, based on the recommendations of the American Diabetes Association, 92% of adults with diabetes required treatment with aspirin. In fact, only 20% of patients received aspirin regularly. Among patients with diabetes and coronary artery disease, the proportion of those regularly taking aspirin reached 37%. At the same time, among patients without coronary artery disease and with one or more risk factors, the proportion of those who regularly took aspirin did not exceed 13%. It is obvious that the widespread and systematic introduction of an effective and cheap method of preventing cardiovascular complications in patients with diabetes is very promising. Between 80 and 90% of patients with type 2 diabetes are at high risk for cardiovascular complications and are primarily considered candidates for chronic aspirin treatment. However, aspirin treatment is not recommended for patients with diabetes under 30 years of age [40].

In conclusion, I would like to emphasize that in Russia, regular use of aspirin is indicated for almost 6 million patients with diabetes.