[prog4]

Я-провинциалка,живу в районном городке.
Подскажите,какой препарат предпочтителен в начальной
стадии гипертонии,т.к.в Альфа и Бета блокираторах не понимаю,а врачи назначают всем одно и тоже - Энап или ,если побочный кашель,то Тенорик. Прошу вас обьяснить,
почему у меня стабильно высокое диастолическое давление(110),а систолическое может быть разным (130-180).
Кардиограмма в норме,не полная,возраст -55 лет.Заболеваний почек не замечаю.Образ жизни-здоровый.

[Dr.Vad]

уважаемая провинциалка!
Ничего не сообщили о частоте пульса (сердечных сокращениях), но похоже, что лучше Вам может подойти препарат из так сказать группы энапа (ИАПФ), проверьте свои холестерин и триглицериды, лучше начать с дозы энапа 2,5 мг в 2 приема (утром и вечером), давление измерять за 0,5 - 1 час до ожидаемого следующего приема (или если получается каждые 2-3 часа). Цель лечения - подобрать инд. дозу, при которой давление не будет превышать 120/80-125/85 в течение суток. Дозу препарата повышать на 2,5 мг до получения целевых значений, не будет получаться на одном энаме, можно будет добавить легенькое мочегонное утречком (но это на будущее).
Когда давление нормализуете, то НЕОБХОДИМО принимать данный препарат неопределенно долго (до тех пор пока не перестанет удерживать давление, тогда повышение дозы, или добавление др. препарата, или переход на другой).
Успехов в лечении!

[Доктор Лектор]

Опубликовано: prog4
Я-провинциалка,живу в районном городке.
Подскажите,какой препарат предпочтителен в начальной
стадии гипертонии,т.к.в Альфа и Бета блокираторах не понимаю,а врачи назначают всем одно и тоже - Энап или ,если побочный кашель,то Тенорик. Прошу вас обьяснить,
почему у меня стабильно высокое диастолическое давление(110),а систолическое может быть разным (130-180).
Кардиограмма в норме,не полная,возраст -55 лет.Заболеваний почек не замечаю.Образ жизни-здоровый.

Уважаемая провинциалка!

Возьму на себя смелость подсказать Вам, что не мешало бы проверить ваши почки. Хоть нет жалоб, но высокое диастолическое давление чаще всего встречается при почечной патологии. Исходя из этого, группа энапа, как сказал, ошибившись (видимо опечатался), наш колега, Вам не желательна. Ингибиторы АПФ (куда входити энап), противопоказана при заболеваниях почек, и, как показывает практика, при назначении оказываются практически не эффективны. А в качестве скоропомощного препарата (при кризе), рекомендую группу нифидепина. 10-20 мг под язык. Но это только в качестве скорой помощи.

Посему, идите на УЗИ, на ОАМ (общий анализ мочи), и проч... и проч... Большая вероятность, что вам надо лечить не давление, а почки. Тогда и давление нормализуется.

Удачи. Прошу сообщить о результатах Ваших действий (если не затруднит)

[Gilarov]

Действительно, прежде, чем начинать лечение "препаратами из группы энапа", они же ингибиторы АПФ, не лишним было бы определить уровень мочевины и креатинина крови и сдать анализ мочи. Попутно, уважаемые коллеги, а как Вам результаты исследования ALLHAT, где хлорталидон - лучший?

[Dr.Vad]

Уважаемый Михаил Юрьевич!
Тк не спец по АГ, то приведу отрывок из недавнего комментария о ALLHAT.
Curr Atheroscl Rep (April 16, 2003) Volume 5, Number 3: May 2003 • Vascular Biology • pp. 199-200
The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT): It's not "either/or" in Hypertension Therapy
by Peter Libby, MD
...ALLHAT provides some important guidance for the care of "real world" patients with multiple risk factors, including hypertension. The study also offers solid affirmation that pharmacologic control of blood pressure benefits outcomes regardless of which agent was used. Over the 5-year horizon of ALLHAT, the thiazide diuretic proved overall the most effective and cost-efficient approach to initial therapy for hypertensive individuals. These results are reminiscent of those determined by the smaller Swedish Trial in Old Patients with Hypertension (STOP-2) trial [1], which showed that diuretics and/or b-blockers, ACE inhibitors, or calcium channel blockers achieved equivalent levels of prevention of cardiovascular mortality. To attain the blood pressure goals mandated by current guidelines, a large number of our patients with multiple risk factors will require more than one antihypertensive agent [2]. Accordingly, 63% of ALLHAT patients required two or more antihypertensive agents to achieve target blood pressure [3]. Certainly, diabetic subjects or patients who have survived acute myocardial infarction may have indications for interference with the action of angiotensin II, based on other indications from clinical trials. The ALLHAT results reinforce the view that treatment of hypertension in most patients is not usually a simple "either/or" choice of a single agent, but most often will require combination therapy, including a thiazide, guided by the individual comorbidities and other patient-specific criteria, including ethnicity and age. In this regard, a recently reported Australian study showed a benefit of the ACE inhibitor enalopril versus the thiazide hydrochlorothiazide in men between 65 and 84 years of age [4].
Interestingly, ALLHAT did not study b-adrenergic blocking agents. The Joint National Committee on Hypertension VI guidelines for antihypertensive therapy recommend b-blockers or diuretics as first-line choices for initial treatment of uncomplicated hypertension. A meta-analysis by Messerli et al. [5] showed that b-blockers are less effective than diuretics in preventing coronary heart disease events or coronary heart disease or overall mortality in individuals older than 60 years of age. Moreover, the recent Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial [6] showed that an angiotensin receptor blocker was more effective in stemming further cardiovascular events in a high-risk population of hypertensive subjects with left ventricular hypertrophy than treatment with doses of b-blockers alone that attained the same level of blood pressure control. Thus, excellent clinical trial evidence suggests differences between antihypertensive strategies depending on the pharmacologic class of the agent studied. b-blockers do exert cardioprotective effects in repeated studies of survivors of acute myocardial infarction, however. Thiazide diuretics may cause worsening of glucose tolerance, hyperuricemia, and abnormalities of the lipoprotein profile. Whether these potentially adverse actions might have untoward effects on patient outcomes over a horizon longer than 5 years remains a matter for conjecture and further study.
Pravastatin's apparent lack of efficacy in ALLHAT bears comment. Well-known, randomized clinical trials have studied more than 100,000 patient-years of pravastatin treatment, and all of these large trials showed an unequivocal benefit. A likely explanation for the apparent lack of efficacy of pravastatin in ALLHAT is the secular trend towards adoption of lipid-lowering strategies that followed in the wake of the Scandinavian Simvastatin Survival Study [7], which was published in 1994, the same year that ALLHAT began. The 36% "drop-in" of hypolipidemic therapy probably provided protection to the usual care group in this study, which was analyzed according to the "intention to treat" principle. The modest difference in LDL cholesterol levels between the pravastatin and control groups in this arm of ALLHAT agrees with the interpretation that LDL cholesterol decreased by 28% in the pravastatin group versus 11% in the usual care group, yielding a net LDL cholesterol difference of only 17% between groups. The benefit of this decline may be too small to have been detected by ALLHAT. Certainly, given the consistency and weight of the evidence for benefits of statins in survivors of myocardial infarction, we should not withhold therapy from this group based on the results of ALLHAT. In my judgement, the results of the lipid arm of ALLHAT should not deter us from conscientious application of the Adult Treatment Panel III guidelines of the National Cholesterol Education Project.

[Dr.Vad]

The ALLHAT study: if you believe in evidence-based medicine, stick to it!
Stevo Julius
University of Michigan Health System, Department of Internal Medicine, Division of Hypertension, Ann Arbor, Michigan, USA
Journal of Hypertension 2003; 21(3):453-454 .
The recent results of the ALLHAT study [ 1] are an important contribution to the therapeutics of hypertension. However, the early conclusions in the press, and comments by some opinion leaders that ALLHAT proved that diuretics ought to be the firstline treatment in all patients with hypertension, are surprising. There is nothing in ALLHAT to support such a wide generalization.
Let us start with the obvious: ALLHAT did not investigate initiation of treatment. In 90% of patients, ALLHAT evaluated the effect of 'roll over' from previous treatment to a well defined and, by design, restrictive treatment scheme; a scheme that excluded what is usually carried out in clinical medicine. Diuretics could not be combined with angiotensin-converting enzyme (ACE) inhibitors and a calcium antagonist could not be added to the other two treatment regimens. How this relates to starting treatment, and what should be the next step when the first step fails, is beyond me. Nevertheless, it is predictable that the ALLHAT results will be neatly ensconced as the first mandatory step in future guidelines. I understand the economics of this, but not the science.
However, the above is a minor concern compared to the fact that proponents of generalization chose to ignore what kind of population has been studied in ALLHAT. Is it really possible to project findings from high risk-advanced hypertension to the population of mild hypertension (stage 1, to be guideline-wise correct), the population in which we are presumed to start treating hypertension? In my opinion, such a generalization is not tenable on epidemiological, physiological and clinical grounds.
Epidemiologically, the largest proportion of all patients with hypertension have stage 1 hypertension and, in a decade of follow-up, 70% of hypertension-related mortality occurred among patients who at baseline had stage 1 hypertension [ 2]. From the population-risk standpoint, these are the most important patients.
How is it then that ALLHAT, and most current outcome trials comparing different drugs, opted to study high-risk populations? It is not because the investigators are unaware of the importance of mild hypertension; the choice is rooted in calculations of sample sizes needed to prove the point. In their infancy, outcome studies in hypertension could compare the effect of blood pressure-lowering-drugs with placebo. The differences from placebo were so large that, even in mild hypertension [ 3], it was possible to demonstrate the superiority of treatment in relatively small sample sizes. Present studies seek to show outcome differences when the blood pressure is lowered to a similar degree with different antihypertensive agents. Obviously in such a setting, only small difference can be expected and a large number of events are needed to show the difference. Thus, high-risk patients in whom many events are expected are chosen for study. The euphemism of 'high risk' stands for hypertensive patients with advanced vascular disease, target organ damage and metabolic abnormalities.
Many epidemiological studies have shown that each added risk factor greatly enhances the effect of blood pressure on mortality and morbidity. Blood pressure lowering in such patients has an overwhelming effect. In the UKPD study [ 4], control of blood pressure had a larger impact on outcomes than glucose control. Recent studies [ 5, 6] have demonstrated that patients with diabetes benefit more from blood pressure lowering than non-diabetic patients. In the LIFE study [ 7], the advantage of losartan over atenolol was particularly well demonstrated in atherosclerotic patients with isolated systolic hypertension.
Current drug comparison studies are caught in a conundrum. High-risk patients are needed to complete the study, but the higher the risk, the more impressive is the blood pressure lowering effect, and the harder it is to show subtle differences between various drugs. It is not surprising that, akin to other trials which preceded it [ 8-10], ALLHAT failed to find between-drugs differences in major outcomes. The results of the LIFE study are a refreshing exception and, hopefully, other forthcoming trials of angiotensin receptor blocking agents will confirm that it is possible to show differences even in patients in whom blood pressure lowering has such an overwhelming positive effect.
Physiologically, there is a huge difference between mild and high-risk hypertension. Most patients with borderline hypertension have no target organ damage but, as we have shown in the Tecumseh study [ 11], in addition to a slight pressure elevation, they are also overweight, have higher cholesterol, triglycerides, insulin, blood sugar and haematocrit levels. Their high-density lipoprotein levels are decreased. At the very outset, hypertension is a syndrome of multiple cardiovascular risk factors and a patient's long-term outcome will depend on how these risk factors, including blood pressure, are managed and how they evolve with time.
Clinically, an individual with stage 1 hypertension is middle-aged and has no visible cardiovascular complications. A patient with high-risk hypertension is old and has multiple abnormalities. In stage 1 hypertension, the goal is to prevent the development of the high-risk state; in a high-risk individual, the goal is to postpone life-threatening manifestations of an existing underlying disease. Obviously, a younger patient will be longer under the care of a physician than his high-risk counterpart.
It is now clear that diuretics and β-blockers have a negative effect on insulin sensitivity [ 12] and it is a well proven that, compared to traditional drugs, ACE inhibitors and angiotensin blocking agents decrease the incidence of new-onset diabetes [ 6, 13]. In the ALLHAT study, among those patients treated with chlorthalidone, the blood glucose increased from baseline to 2 years and remained increased at 4 years. At 2 and 4 years, the fasting glucose and the percentage of individuals with glucose ≥ 126 mg/dcl were significantly higher in the chlorthalidone compared to lisinopril group. A similar difference was seen between chlorthalidone and amlodipine groups at 2 years but, at 4 years, the difference was only marginally significant.
A practicing physician must be aware that the ALLHAT study does not provide any clues about the management of stage 1 hypertension (i.e. the type of hypertension he is most likely to see in his practice). The question is whether he is willing to expose a younger patient to 30 years of treatment with an antihypertensive drug, which favours acceleration of cardiovascular risk. I certainly am not prepared to do so.
Finally, opinion leaders should not endorse the illogical conclusion that the ALLHAT results justify a primary use of diuretics in all patients with hypertension. An outcome trial comparing various drugs in stage 1 hypertension might require huge numbers of patients, be expensive and necessitate a superb multinational organization, but it is not impossible. In this age of evidence-based medicine, we should state the obvious: that there is no evidence of how to treat mild hypertension. We need an ALLHAT-like trial in stage 1 hypertension and, accordingly, should relentlessly push for the realization of such a trial.

[Gilarov]

Так и я не спец. Поэтому на мой неокрепший ум так и подействовали результаты. В общем, новое - этохорошо забытое старое. Жаль хлорталидона в России нет...

[prog4]

Спасибо всем за советы,УЗИ делала 2-года назад, есть песок в одной почке,но не беспокоит.
Не знаю,как лечить, врач ничего не назначил,пью курсами живые соки,иногда спорыш, а что это за совет и проч...проч., я ведь не медик ,а программист.Вот и не знаю,начинать пить табл.от давления или как-то проверить почки.Дайте дельный совет.С ув.провинциалка.

[Gilarov]

Уважаемая Провинциалка!
Давать дельные советы заочно - трудно. Попробуйте все же сходить к врачу, ну, невеликая проблема гипертонию лечить. И еще, помимо соков, нужны физические нагрузки...