Pharmacological properties of the drug Teveten
Eprosartan is a potent, non-peptide, orally active, non-biphenyl, non-tetrazole angiotensin II receptor antagonist that selectively binds to AT1 receptors. Angiotensin II plays an important role in the pathogenesis of hypertension (arterial hypertension) and is the main active hormone of the renin-angiotensin-aldosterone system. It selectively binds to AT1 receptors in various organs and tissues (vascular smooth muscle, adrenal glands, kidneys, heart) and causes important biological effects such as vasoconstriction, sodium retention and aldosterone release. It also takes part in the formation of hypertrophy of the heart and blood vessels through its effect on the hypertrophy of vascular smooth muscle and cardiac muscle. Eprosartan interferes with the effects of angiotensin II on blood pressure, renal blood flow and aldosterone release in healthy individuals. In patients with hypertension (arterial hypertension), a decrease in blood pressure occurs after a single dose of the drug and is subsequently maintained without fluctuations in blood pressure for 24 hours. Discontinuation of treatment with eprosartan does not cause a sharp increase in blood pressure (withdrawal syndrome). In patients with hypertension (arterial hypertension), a decrease in blood pressure after taking eprosartan is not accompanied by a change in heart rate. Eprosartan does not affect plasma levels of glucose, TG, cholesterol and LDL. Eprosartan does not interfere with the mechanisms of self-regulation of renal function. In healthy individuals, eprosartan improves effective renal blood flow. Eprosartan does not affect renal function in patients with essential hypertension and in persons with renal failure. It does not reduce the level of glomerular filtration in healthy individuals, in patients with essential hypertension and in patients with varying degrees of renal failure. Eprosartan increases natriuresis in healthy individuals on a low-salt diet. In patients with essential hypertension and in patients with varying degrees of renal failure, it does not cause sodium retention or deterioration of renal function. Eprosartan does not affect the secretion of uric acid. Unlike ACE inhibitors, eprosartan does not cause effects associated with increased bradykinin concentrations, such as cough. According to clinical data, the antihypertensive effect of eprosartan does not differ from the effect of the ACE inhibitor enalapril. The absolute bioavailability of eprosartan after a single oral dose of 300 mg is 13% due to its limited absorption. The maximum concentration of the drug in the blood plasma after oral administration on an empty stomach is observed after 1–2 hours. The half-life of eprosartan is usually 5–9 hours. With long-term use of eprosartan, its accumulation does not occur. Taking eprosartan with food delays absorption by less than 25%, which has no important clinical consequences. Plasma protein binding is high (approximately 98%) and constant over the therapeutic concentration range. Protein binding is independent of gender, age, liver dysfunction and the presence of mild/moderate renal failure, but is reduced in some patients with severe renal failure. In humans, following oral administration of 14C-eprosartan, eprosartan was the only compound detected in plasma and feces. 20% of radioactive eprosartan is excreted in the urine as acyl glucuronide and 80% as unchanged eprosartan. The volume of distribution of eprosartan is 13 l. Total plasma clearance is 130 ml/min. Eprosartan is excreted in urine and bile. After oral administration, 90% of 14C-eprosartan is excreted in feces and 7% in urine. The AUC value and maximum plasma concentration of eprosartan increase in elderly people (on average 2 times), but this does not require dosage changes. The AUC value of eprosartan increases in patients with liver failure (by an average of 40%), which also does not require dosage changes. The AUC value and maximum plasma concentration of eprosartan were 30% higher in patients with moderate renal failure (creatinine clearance - 30-59 ml/min) and 50% higher in patients with severe renal failure (creatinine clearance - 5-29 ml /min) compared to individuals with normal renal function. Dosage changes are not recommended. The pharmacokinetics of eprosartan are no different in women and men.
Teveten®
Angiotensin II receptor antagonist (ARA II) selectively acts on angiotensin receptors located in the blood vessels, heart, kidneys and adrenal cortex, forms a strong bond with them followed by slow dissociation.
Angiotensin II binds to AT1 receptors in many tissues (for example, vascular smooth muscle, adrenal glands, kidneys, heart) and causes vasoconstriction, sodium ion retention and aldosterone release, target organ damage - myocardial and vascular hypertrophy.
Eprosartan prevents the development or weakens the effects of angiotensin II, inhibits the activity of the renin-angiotensin-aldosterone system (RAAS). It has a vasodilating, antihypertensive and indirect diuretic effect. Reduces arterial vasoconstriction, total peripheral vascular resistance (TPVR), pressure in the pulmonary circulation, reabsorption of fluid and sodium ions in the proximal segment of the renal tubules, and aldosterone secretion. With long-term use, it suppresses the proliferative effect of angiotensin II on vascular and myocardial smooth muscle cells.
The antihypertensive effect after taking a single dose lasts for 24 hours, a persistent therapeutic effect appears with regular use - after 2-3 weeks without changing heart rate (HR).
Does not cause the development of orthostatic hypotension in response to the first dose of the drug.
In patients with arterial hypertension, eprosartan does not affect fasting blood concentrations of triglycerides, total cholesterol or low-density lipoprotein (LDL) cholesterol. In addition, eprosartan does not affect fasting blood glucose concentrations.
Increases renal blood flow and glomerular filtration rate (GFR), reduces the excretion of albumin (nephroprotective effect) while maintaining renal self-regulation, regardless of the severity of renal failure.
Does not affect purine metabolism, does not have a significant effect on the excretion of uric acid by the kidneys.
Less common than angiotensin-converting enzyme (ACE) inhibitors, it causes bradykinin-related effects (including dry persistent cough). The incidence of dry, persistent cough in patients receiving eprosartan is 1.5%. When replacing the ACE inhibitor with eprosartan in patients with cough, the incidence of dry persistent cough corresponds to placebo.
Discontinuation of treatment with eprosartan is not accompanied by withdrawal syndrome.
During clinical studies, the use of the drug in a daily dose of up to 1200 mg for 8 weeks was effective, with no apparent relationship between the dose and the frequency of reported side effects.
Eprosartan does not inhibit the isoenzymes CYP1A, 2A6, 2C9/8, 2C19, 2D6, 2E and 3A of the cytochrome P450 system in vitro.
The ONTARGET and VA NEPHRON-D studies, which examined the combined use of an ACE inhibitor with an ARB II, did not reveal significant beneficial effects on renal and/or cardiovascular function and mortality, while at the same time there was an increased risk of hyperkalemia, acute kidney injury and/or arterial hypotension compared with monotherapy. Given the similar pharmacodynamic characteristics, these results are also relevant for other ACE inhibitors and ARB II.
ACE inhibitors and ARB II should not be used simultaneously in patients with diabetic nephropathy.
The ALTITUDE trial (adding aliskiren to standard ACE inhibitor or AR II therapy) was terminated prematurely due to an increased risk of adverse outcomes. Cardiovascular death and stroke were significantly more common in the aliskiren-added group than in the placebo group, and adverse events and serious adverse events (hyperkalemia, hypotension, and renal dysfunction) were more common in the aliskiren group than in the placebo group. placebo group.
In the MOSES (Morbidity and Mortality after Stroke Comparison of Eprosartan and Nitrendipine for Secondary Prevention) study of 1,405 patients with hypertension and a history of cerebrovascular disease, 78% of patients in the eprosartan group received 600 mg once daily; 12% - up to 800 mg per day; in the nitrendipine group, 47% received 10 mg and 42% received 20 mg per day (in 11% of patients, doses reached 40 mg per day). Target blood pressure values were achieved in both groups and were maintained throughout the study. The eprosartan group had significantly better results (21% risk reduction) for the primary endpoint of all-cause mortality, cerebrovascular events (transient cerebrovascular accident, long-term reversible ischemic neurological deficit, stroke) and cardiovascular events ( unstable angina, myocardial infarction, heart failure, pulmonary embolism and fatal arrhythmia), including recurrent diseases. In the primary data analysis, the numerical risk index decreased by 12% for cerebrovascular and 30% for cardiovascular disorders. The overall mortality rate was better in the nitrendipine group; 8.4% in the eprosartan group (57 of 681 patients) versus 7.7% in the nitrendipine group (52 of 671 patients) (hazard ratio 1.07, 95% CI 0.73 to 1.56, p=0.725 ). Fatal and non-fatal myocardial infarction developed in 18 of 20, and stroke in 36 of 42 patients, which numerically supported eprosartan. According to the primary endpoint, the effect of eprosartan was more pronounced in patients who did not receive beta-blockers.
Use of the drug Teveten
The recommended dose for adults is 600 mg of eprosartan once a day in the morning. In most patients, the maximum reduction in blood pressure is achieved after 2–3 weeks of treatment. During clinical trials, the use of Teveten at a dose of 1200 mg/day for 8 weeks did not affect the incidence of side effects. Teveten can be used in monotherapy or in combination with other antihypertensive agents, such as thiazide diuretics or calcium channel blockers, if there is a need for a greater reduction in blood pressure. The drug can be taken regardless of meals. The duration of treatment is not limited. For elderly people, no dose change is required. Since the safety and effectiveness of Teveten in children have not been established, prescribing the drug to children is not recommended. No dosage changes are required for patients with liver failure. In patients with moderate or severe renal failure (creatinine clearance ≤60 ml/min), the daily dose should not exceed 600 mg.
Teveten plus overdose, symptoms and treatment
The most likely manifestation is arterial hypotension. Other symptoms may be associated with dehydration or decreased electrolyte levels (hypokalemia, hypochloremia, hyponatremia) and most likely include nausea and drowsiness. Treatment should be supportive and symptomatic. Depending on the time that has passed since the overdose, you can induce vomiting, lavage the stomach and/or apply activated charcoal. If arterial hypotension occurs, the patient must be placed in a horizontal position and the blood volume must be restored and the electrolyte balance corrected. Eprosartan is not removed by hemodialysis.
Side effects of the drug Teveten
In placebo-controlled clinical studies, the overall incidence of adverse events that occurred with eprosartan was comparable to placebo. Side effects were usually minor and disappeared on their own. Only in 4.1% of patients taking eprosartan did it become necessary to stop taking the drug. According to clinical studies, side effects occurred when using eprosartan with the following frequency: From the central nervous system - frequent (1/100, ≤1/10): headache, dizziness. From the cardiovascular system - frequency unknown: hypotension, including postural hypotension. From the skin and subcutaneous tissues - frequency unknown: allergic skin reactions (rash, itching, urticaria), angioedema, facial swelling. From the gastrointestinal tract - often (1/100, ≤1/10): nausea, vomiting, diarrhea, nonspecific gastrointestinal disorders. General disorders and reactions at the injection site - common (1/100, ≤1/10): asthenia. In addition to the side effects identified during clinical trials, the development of the following side effects was recorded during post-marketing use of eprosartan. Frequency unknown. From the urinary system - impaired renal function, including renal failure, in patients at risk (for example, with renal artery stenosis).
Special instructions for the use of the drug Teveten
In patients with significant fluid and/or salt deficiency (for example, due to the use of diuretics in high doses), arterial hypotension may occur. It is recommended to restore this deficiency before starting treatment with Teveten. During therapy with ACE inhibitors in patients whose renal function depends on the activity of the renin-angiotensin-aldosterone system (for example, patients with severe heart failure, bilateral renal artery stenosis or renal artery stenosis of a single kidney), oliguria and/or progressive azotemia develops and, less commonly, — OPN. Since there is no sufficient therapeutic experience with the use of Teveten in patients with severe heart failure and renal artery stenosis, it cannot be ruled out that it may also cause renal dysfunction in them due to blocking the renin-angiotensin-aldosterone system. If Teveten is used in patients with renal failure, it is necessary to check renal function before starting treatment and periodically during use of the drug. If deterioration in renal function is noted during therapy, the advisability of treatment with Teveten should be reconsidered. Patients with hereditary diseases such as galactose intolerance, lactase deficiency, Lapp syndrome or glucose-galactose malabsorption are not recommended to take the drug. There is insufficient experience with the use of Teveten during pregnancy. Drugs acting on the renin-angiotensin-aldosterone system can cause fetal death and disease and death in newborns when used for treatment in pregnant women in the second and third trimester of pregnancy. Like other drugs that affect the renin-angiotensin-aldosterone system, Teveten should not be prescribed during pregnancy, and if pregnancy is detected during therapy, treatment should be stopped as quickly as possible. Women who are breastfeeding are contraindicated to take Teveten. Based on the pharmacodynamic properties of the drug, it is unlikely that it will adversely affect the ability to drive a vehicle or operate machinery. However, caution should be exercised as sometimes during treatment of hypertension (arterial hypertension) a feeling of fatigue and dizziness may occur.
TEVETEN
Antihypertensive therapy: a new strategy to protect the brain
Specialization in medicine has become increasingly distinct in recent years. A striking example of this is cardiology. However, experience shows that it is rare that a cardiology scientific forum today goes without mentioning related problems. This is understandable: the pathogenesis of many diseases contains identical or similar aspects. To confirm this, I would like to cite the example of the recently completed Russian National Congress of Cardiologists, within the framework of which an extremely interesting and extremely relevant symposium “Antihypertensive therapy: a new strategy for protecting the brain” was held. The symposium took place on October 12, 2006 and was organized by the pharmaceutical company Solvay Pharma, .
It was also very significant that the first report was presented by Academician of the Russian Academy of Medical Sciences, Chairman of the All-Russian Scientific and Scientific Committee, R.G. Oganov. At the very beginning of his report “Secondary prevention of stroke - new data,” the academician noted that primary and secondary prevention of strokes are similar, which only increases interest in the problem. The risk factors for strokes, as well as cerebrovascular complications, are similar:
- Age, gender
- Arterial hypertension
- Diabetes
- Previous stroke
- IHD, atrial fibrillation, heart failure
- Obesity, alcohol abuse, smoking
Atrial fibrillation has the greatest strength, but the main quantitative contribution to the development of cerebral stroke in Russia is made by hypertension. Recently, against the backdrop of an increase in the number of people with hypertension, the number of not only strokes, but also vascular dementia is increasing. “The problem of controlling hypertension in our country is purely organizational, and if we do not take measures, then our incidence will be the highest in the world,” noted academician R.G. Oganov.
The relationship of hypertension with stroke and cardiovascular diseases is straightforward: the higher the level of hypertension, the higher the risk of primary and recurrent stroke. Risk stratification tables are built on this principle. The higher the blood pressure, the higher the individual risk. At SBP 120 the risk is 7%, at 180 – 23%.
The pattern of development of cognitive impairment in most cases is simple and develops according to the following pattern: hypertension-stroke-dementia. The PROGRESS study once showed that it is possible to reduce the risk of stroke, as well as influence the cognitive function and capacity of patients with the help of drugs that lower blood pressure. Then there was the MOSES study, which showed that the highly effective nitrendipine was significantly inferior to the drug eprosartan in the primary and endpoint: a reduction in overall mortality and cerebrovascular disorders. Eprosartan ( Teveten ) was 21% more effective in reducing the primary outcome (mortality and the number of cases of cerebrovascular and cardiovascular complications). Effect on all vascular events 25% (significantly reduced the incidence of fatal and non-fatal cerebrovascular events). The best result was achieved at a pressure of 120 to 140 mm Hg. The risk of recurrent strokes was significantly reduced and, of course, a cardioprotective effect was observed.
Academician R.G. Oganov drew the audience's attention to a simple fact: reducing risk in a population is more effective than treating individual patients, and lifelong prevention of risk in a population is even more effective. In other words, a drug reduction of a patient’s blood pressure to normal does not mean a reduction in risks to the level of healthy people; therefore, preventive measures and timely identification of risks are necessary. The task of doctors is to increase public awareness and adherence to treatment. Only in this case can we expect a significant reduction in cerebrovascular and cardiovascular risks, emphasized Academician R.G. at the end of his speech. Oganov.
The next report, “Features of blood supply to the brain in arterial hypertension,” was presented by senior researcher. Laboratory of Cardioneurology, Department of Cerebrovascular Disorders Lyudmila Aleksandrovna Geraskina. At the beginning of the report, it was noted that neurological complications in hypertension are not uncommon. With hypertension, the following changes occur:
- Adaptive: media hypertrophy, hyperelastosis, myoelastofibrosis, sclerosis;
- Destructive: primary necrosis of medial myocytes, plasmorrhagia, fibrinoid necrosis of the vessel wall
- Reparative: hyalinosis.
And if adaptive changes can undergo reverse development during the treatment process, then destructive changes are irreversible. Reparative changes are aimed at stabilizing the process at a new level. They occur in both large and small arteries, but the most serious changes occur in the microvasculature, which is not available in routine patient examination. A damaged vessel wall, increased blood pressure, and changes in trophism lead to plasmorrhagia. The patency of these arteries changes. As a result, there is an accumulation of organic changes in the blood vessels of the brain - hypertensive angioencephalopathy. On neuroimaging they look like small infarcts and diffuse changes - leukoaraiosis. And only then follows the clinical picture of atherosclerosis: decreased attention, memory, headaches. In the absence of adequate treatment, more severe chronic damage occurs and discirculatory encephalopathy occurs.
Every second patient with hypertension has the mildest initial manifestation of insufficient blood supply to the brain. No signs. A neurologist can detect only a set of small manifestations. Deformation of the carotid arteries and minor stenoses can be detected, but brain damage will be more pronounced, despite the silent course. In patients with minimal symptoms, there is a failure of perfusion and additional brain stealing.
As it progresses, changes in the vascular wall and rheological properties of the blood worsen. Focal and diffuse changes worsen. Cerebral symptoms increase - sensitive, coordination, and cognitive impairments appear (attention, memory, social, professional adaptation). There is a clear decrease in blood flow and an increase in the rigidity of the walls of large vessels. Multiple heart attacks and leukoaraiosis appear. If small focal changes are described, blood flow is already reduced.
Only a third of patients respond adequately to vasodilator stimuli. In most patients, blood flow is reduced, a perverted or exactly the opposite response. Factors that influence changes in the reactivity of the vascular wall: age, characteristics of the circadian rhythm. We find the greatest changes in patients with an additional increase in blood pressure at night, or with its excessive decrease. Reactivity is worse in patients with hemodynamically significant changes in the vessels of the neck or intracranial vessels and the presence of previous antihypertensive therapy.
The sooner we begin to treat hypertension, the more intact the vessels and their reactivity will remain with adequate treatment with modern drugs. Poor treatment (course, short-lived drugs) only aggravates the deterioration of vascular reactivity. How to recognize patients who have the least adaptation to changes in blood pressure during antihypertensive therapy? Usually this:
- persons over 60 years old,
- patients with diffuse damage to brain tissue: pyramidal syndrome, pseudobulbar syndrome, subcortical syndrome;
- patients who have markers of changes in brain matter: leukoaraiosis, cerebral infarction;
- patients with occlusive lesions of the vessels supplying the brain.
- persons with cardiac markers: left ventricular hypertrophy, coronary pathology.
Patients who already have neurological complications of hypertension and the lower limit of autoregulation of cerebral blood flow can be shifted to a mean pressure level of 120 mm Hg, then a disaster can occur. Moreover, this catastrophe may not necessarily be clinically obvious. He does not faint, does not pass out, nothing happens, but the trouble is that the patient may develop focal symptoms with a relatively moderate decrease in blood pressure, but loss of consciousness and global cerebral ischemia will not occur. It will occur if the level of cerebral blood flow drops to critical levels - 20 ml per 100 g of brain matter per minute. Here is a clinical example of the treatment of hypertensive crisis. It is recommended to reduce blood pressure by 25% of the initial value during the first 2 hours and to a level of 160/100 mmHg over the next 6 hours. But in case of chronic cerebral pathology, only a decrease in blood pressure to 20% of the initial value is tolerated normally. Those. preferably no more than 20% within 2 hours.
In terms of cerebroprotection, the MOSES study is indicative. Ca antagonists are considered the drugs of choice in the prevention of cerebral stroke. Eprosartan ( Teveten ) belongs to a new class of antihypertensive drugs. 2 advanced drugs collided. The result is a 25% reduction in the risk of recurrent stroke on eprosartan. Mechanism of cerebroprotection: improvement of endothelial properties, reverse remodeling, reduction of vascular stiffness, antiplatelet effect. Blockade of type 1 angiotensin receptors leaves no room for angiotensin to circulate in the vessels. But there remains room for receptors of the second type, which leads to a revival of blood flow: cerebroprotection due to activation of collateral blood flow. This is an additional positive non-antihypertensive effect that must be taken into account when treating patients with cerebrovascular pathologies. The conclusion is simple: in the presence of hypertension and cerebrovascular pathology, it is necessary to include Teveten with its strong cerebroprotective effect.
Professor Evgeniy Vladimirovich Shlyakhto continued the symposium. The topic of his report: “Cognitive impairment in patients with arterial hypertension: results of the OSCAR study” also turned out to be relevant and interesting. The professor noted that the fate of a patient with cardiovascular pathology is determined, among other things, by the development of cognitive impairment. The patient management strategy is based on risk factors:
- Preventing progression of the cardiovascular continuum
- Impact on risk factors (insulin resistance, cardiovascular remodeling, atherogenesis, prevention of MI, stroke, heart and kidney failure)
- Prevention of cognitive impairment
In Europe, older age groups have seen an increase in the number of people with cognitive impairment. More and more attention is being paid to mild cognitive impairment, when memory suffers, but self-care is at the proper level. 2% of mild to moderate dementia occurs before age 65, about 9% over age 65, and 20% over age 80. “We underestimate the importance of mild cognitive impairment,” said Professor E.V. Nobles. Prevention of cognitive impairment is the treatment of the underlying disease (atherosclerosis, hypertension, heart failure), elimination of neurological syndromes, improvement of cerebral circulation and metabolism in the brain.
Studies on primary and secondary prevention of strokes, as well as effects on cognitive function, showed that a decrease in blood pressure by 11% did not significantly improve cognitive function. However, in relation to angiotensin receptor blockers, improvement in the prevention of dementia has been shown, which is associated with a decrease in the amount of ischemia in brain tissue. A drug that increases the level of angiotensin II improves the prognosis of cognitive impairment. In this regard, the MOSES study is indicative, which for the first time highlighted the significant benefits of eprosartan ( Teveten ):
- the number of brain events decreased by 25%
- cardiac events - by 30%, even compared with calcium antagonists, the effectiveness of which on cerebral blood flow is considered proven.
- There were no differences in stroke prevention for these drugs.
Experimental data also fully confirm clinical studies of eprosartan. At the next stage of research, the multicenter OSCAR study showed extremely interesting results on the use of the drug Teveten . The first global analysis showed that the dynamics of blood pressure normalization for the majority of patients was positive and in more than 60% of cases it decreased to normal. At the same time, the decrease in SBP averaged 26 mm Hg, and DBP – 12.6 mm Hg. The dynamics of changes in cognitive functions were also positive. The most radical changes were typical for people over 60 years of age. Obese patients showed less improvement in cognitive function compared to those with normal BMI. However, with concomitant atherosclerosis, the increase in the MMSE (Mini - Mental State Examination) index was greater.
Side effects were observed in only 0.1% of cases, and good tolerability was noted on average in 94% of cases. High effectiveness of treatment with Teveten is observed in approximately 95% of cases.
Conclusions:
- Hypertension is the most important risk factor for the development of stroke and loss of cognitive function
- The results of multicenter randomized trials on the treatment and prevention of strokes showed the possibility of preventing strokes and dementia with antihypertensive drugs
- Teveten appears to be the most effective drug for preventing cerebral strokes (MOSES) in patients with hypertension and improving cognitive impairment (OSCAR).
The final message of the symposium was presented by Professor S.A. Boytsov: “Combination therapy of arterial hypertension.” He noted that in a real clinic there is a well-known rule: it is necessary not only to correct blood pressure levels, but also to influence risk factors. The reason is simple - today organ protection is needed - a relatively new and not always clear goal of therapy. The basis of vascular protection is the influence on their remodeling. Cerebrovascular pathology is 5.8 cases per 1000 people and in 92% of cases cerebral stroke is associated with hypertension. Therefore, neurologists, cardiologists and therapists should remember about the prevention of stroke and chronic stroke, including dementia. An indicative risk factor is an increase in pulse pressure and a decrease in the elasticity of large arteries.
It should be taken into account that 77% of patients with hypertension are over 55 years of age. According to a 10-year observation, in people over 60 years of age, isolated hypertension with high pulse pressure is observed in 8% of cases. Therefore, a separate consideration of this problem is necessary.
In young and middle-aged people, a proportional reduction in SBP and DBP is required, but in people over 60 years of age, it is more necessary to reduce SBP in order to reduce pulse pressure. Ensuring adequate cerebral perfusion also requires reducing systemic SBP and pulse pressure while maintaining DBP. The evolution of ideas and blood pressure control is interesting:
- Before 1990, DBP control prevailed
- Until the end of the 90s - SBP control
- Before 2004 – PD in the brachial artery
- Today – PD in the aorta
What are the current recommendations? The results of numerous studies provide a clear answer: Angiotensin II receptor blockade is the method of choice for organ protection in antihypertensive therapy. Returning to the MOSES study, I would like to note that the effect on SBP and DBP of nitrendipine and eprosartan was similar, however, the protective effect of eprosartan was significantly higher. Consequently, eprosartan ( Teveten ), other things being equal, has a special effect on hemodynamic characteristics. Why should hypertension therapy, according to the recommendations, be combined? There are several reasons:
- Possibility of simultaneous influence on several links of pathogenesis
- Possibility of enhancing the effect by acting on one mechanism using different means
- Inhibition of counter-regulatory mechanisms
- Reduced incidence of side effects
Rational combinations of antihypertensive therapy today include:
- Diuretic + ACE inhibitor (ARA)
- Ca antagonist + ACE inhibitor (ARA)
- Beta blocker + calcium antagonist
- Diuretic + beta blocker
- Alpha blocker + beta blocker
If we consider the main blocks of the pathogenesis of arterial hypertension, then the combination of an ACE inhibitor (ARB) + diuretic will have an optimal and universal effect on these blocks. Is there a ready-made drug? Yes, this is Teveten plus . It is extremely easy to use, and therefore is doomed to success. Teveten Plus is a combination of eprosartan and hydrochlorothiazide. Teveten Plus was registered in Russia only this year. The drug is not only highly effective, but also safe. At the end of the report, Professor S.A. Boytsov I once again reminded that organ protection and cerebroprotection are the most important goals of hypertension therapy, which are achieved mainly by controlling pulse blood pressure and carried out through combination therapy, and the most effective is the combination of ACE inhibitors or ARBs with diuretics. We can only hope that the advanced scientific achievements in the field of cardiology and neurology, presented at the symposium, will be picked up by doctors and transferred into practice.
Internet project "RMS-Expo" E-mail Web: Expo.rusmedserv.com
Drug interactions Teveten
No clinically significant interactions of the drug with other drugs have been established. Eprosartan does not affect the pharmacokinetics of digoxin or the pharmacodynamics of warfarin or glibenclamide. In turn, ranitidine, ketoconazole and fluconazole do not affect the pharmacokinetics of eprosartan. Concomitant use of Teveten with thiazide diuretics (eg, hydrochlorothiazide), calcium channel blockers (eg, long-acting nifedipine) and lipid-lowering agents (eg, lovastatin, simvastatin, pravastatin, fenofibrate, gemfibrozil and nicotinamide) is safe without any evidence of adverse interactions. There are reports of a reversible increase in serum lithium levels and toxic effects in the case of simultaneous use of lithium preparations with ACE inhibitors. The possibility of a similar effect when using Teveten cannot be excluded, therefore it is recommended to monitor the level of lithium in the blood during simultaneous use with lithium preparations. Eprosartan did not cause a blocking effect on human cytochrome P450 enzymes CYP 1A, 2A6, 2C9/8, 2C19, 2D6, 2E and 3A in vitro.
