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#46
01.10.2007, 20:43
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Öèòàòà:
 Ìíå ïîêàçàëîñü êîëëåãà acha, ïîäòâåðäèë òåçèñ, ÷òî áîëüíûõ ñî ñòàáèëüíîé ñòåíîêàðäèåé, áåç ÈÌ íå òàê óæ ìíîãî...ÈÌÕÎ Âàì íàäî îáúåäèíèòüñÿ ñ Dr ìîæåò, ÷òî-íèáóäü ïîëó÷èòüñÿ.  Åñëè ó÷èòûâàòü ðàçíûå ïðåïàðàòû èç áåòà-áëîêàòîðîâ, òî ïî 500 ÷åë. â ãðóïïå áóäåò ìàëî...PS Î÷åíü ìíîãî "íî" è ðàçíûõ äîïóùåíèé. Ýòî ìîå ìíåíèå. 
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#47
12.10.2007, 19:18
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Á-ÀÁ ïîñëå ÈÌ
Îäèíîêîå ìíåíèå äîêòîðà èç Ñåðáèè î ðîëè Á-ÀÁ ïîñëå ïåðåíåñåííîãî ÈÌ.
Igor B. Mrdovic. Is the level of evidence for the use of beta-blockers in acute myocardial infarction satisfactory enough? European Heart Journal 2006 27(1):118-119 Institute for Cardiovascular Diseases Emergency Hospital Coronary Unit A Clinical Centre of Serbia Pasterova 2 Makenzijeva 85/8 11000 Belgrade Serbia and Montenegro 1. Á-ÀÁ â îñòðîé ôàçå ÈÌ. The cornerstone of each therapy's recommendation should be the impact on survival. In the August 2004 issue of the European Heart Journal, expert consensus opinion on beta-blockers stated that during the acute phase of myocardial infarction, oral beta-blockers are indicated in all patients without contraindications (Class I, level of evidence A).[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] The consensus group opinion was supported by the data from the pre-reperfusion ISIS-1[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] and MIAMI[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] trials and post-reperfusion TIMI-II trial[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] which compared two time protocols of metoprolol administration and, therefore, was not controlled with a non-beta-blocker or another beta-blocker. It is understandable that the results from pre-reperfusion studies cannot be simply incorporated into a modern concept of AMI treatment. 2. Á-ÀÁ ïîñëå ÒÁÊÀ. Retrospective analysis from PCI studies (PAMI-2, Stent PAMI, Air PAMI, PAMI noSOS, and CADILLAC) was used to support the premise of mortality reduction with pre-PCI intravenous and post-PCI peroral use of beta-blockers.[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ],[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] However, none of these studies were designed to randomly assess the effects of beta-blockers on mortality. 3. Á-ÀÁ ó ïîñòèíôàðêòíûõ ïàöèåíòîâ. Oral beta-blockers are further recommended for long-term use and for survival improvement in all patients who recover from AMI and do not present contraindications (Class I, level of evidence A); this recommendation is based on the data from a meta-analysis of 31 randomized trials, Hjalmarson's trial, Cooperative Cardiovascular Project, BHAT and Norwegian trial.[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ],[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] However, all these trials are from the pre-reperfusion era or use registry as a database. None of these trials included random assessment of beta-blockers in the post-reperfusion modern algorithm, including PCI, fibrinolysis, ACE-inhibitors, aspirin, and statines. Furthermore, the document states that the benefit of beta-blockers in low-risk patients is questionable. CAPRICORN, the only randomized post-reperfusion trial in AMI patients with ventricular dysfunction, showed all-cause mortality reduction with carvedilol when compared with placebo.[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] However, CAPRICORN did not reach the pre-specified higher level of statistical significance for the original primary endpoint of all-cause mortality (the primary endpoint was changed for co-primary during the study). Therefore, the statistical power of CAPRICORN is only borderline in favour of mortality reduction with carvedilol in high-risk AMI patients (P=0.031).
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#48
12.10.2007, 19:23
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4. Â/â Á-ÀÁ ïðè ÈÌ äëÿ ïðîôèëàêòèêè âíåçàïíîé ñìåðòè.
Intravenous beta-blocker administration for primary prevention of sudden death was marked as a Class I, level of evidence B. The document admitted that post hoc analysis of GUSTO-1 trial does not support intravenous use of beta-blockers in the reperfusion era.[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] In TIMI-IIB trial, early intravenous metoprolol administration had no advantage over the peroral treatment (4) 5. Âûâîäû: Evidence for the use of beta-blockers in the early stage of AMI thus results from studies in the pre-reperfusion era, registries, meta-analyses, and post hoc analysis, not designed for beta-blockers' random assessment in regard to mortality reduction after AMI. 6. Áóäóùåå: In the absence of powerful statistical evidence for mortality reduction in the reperfusion time, we believe the impact of beta-blockers on survival after AMI has not been proved sufficiently. For a better evaluation of the role of beta-blockers in patients with AMI, randomized large trials assessing the impact on survival are obviously missing. [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ]
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#49
12.10.2007, 19:33
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Íåëüçÿ èñêëþ÷èòü, ÷òî ïîëîæèòåëüíîå âëèÿíèå Á-ÀÁ/èÀÏÔ íà ïðîãíîç ïàöèåíòîâ ïîñëå ïåðåíåñåííîãî ÈÌ ñâÿçàíî ñ ïðîôèëàêòèêîé/ëå÷åíèåì ÕÑÍ.
1. Âîçìîæíî, ïðè ðàçäåëüíîì àíàëèçå ïåðåäíèé, îáøèðíûé ïî ïëîùàäè ÈÌ (âûñîêî ðèñêîâûõ ïî ÕÑÍ/âíåçàïíîé àðèòìîëîãè÷åñêîé ñìåðòè è ò.ä.) vs íèæíèé ÈÌ ïîêàæåò îòñóòñòâèå âëèÿíèÿ Á-ÀÁ íà ÑÑ ñìåðòíîñòü. Êîíå÷íî æå ýòè äîêàçàòåëüñòâà ñëåäóåò èñêàòü â ðåòðîñïåêòèâíîì èññëåäîâàíèè. 2. Äàëåå ïðè îòñóòñòâèè ïðåèìóùåñòâ Á-ÀÁ ïðè íèæíåì ÈÌ ìîæíî òåîðåòè÷åñêè çàäóìûâàòüñÿ íàä ïëàöåáî-êîíòðîëèðóåìîì èññëåäîâàíèè â ïîñò-ðåïåðôóçèîííóþ ýðó ó ýòîé êàòåãîðèè ïàöèåíòîâ. 3. Íå èñêëþ÷åíî, ÷òî èÀÏÔ òàêæå ðàáîòàþò ïðè áîëüøèõ ïåðåäíèõ ÈÌ è ìàëî ïîëåçíû ïðè íèæíèõ íåîñëîæí¸ííûõ ÈÌ.
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#50
01.11.2007, 20:43
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Ïóáëèêàöèÿ ñâåæåãî ìåäèöèíñêîãî àïòóäåéòà â òåìó
Beta blockers in the management of stable angina pectoris
Joseph P Kannam, MD Julian M Aroesty, MD Bernard J Gersh, MB, ChB, DPhil, FRCP UpToDate performs a continuous review of over 375 journals and other resources. Updates are added as important new information is published. The literature review for version 15.2 is current through April 2007; this topic was last changed on February*05,*2007. The next version of UpToDate (15.3) will be released in October 2007. INTRODUCTION*—*Beta blockers are first-line therapy in the treatment of chronic stable angina, particularly effort-induced angina. They were recommended for use in such patients by both the American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (show table 1A-1B) [1,2]. The major issues regarding the use of beta blockers in the medical management of the patient with stable angina and the evidence that these drugs are effective will be reviewed here. Their role, compared with other drugs, in the overall management of angina is discussed separately. (See "Overview of the management of stable angina pectoris"). MECHANISM OF ACTION*—*The physiologic effects of catecholamines (norepinephrine and epinephrine) are mediated by activation of specific alpha and beta adrenergic receptors. There are at least three distinct types of beta receptors [3-5]: Beta-1, which are found primarily in heart muscle. Activation of these receptors results in increases in heart rate, contractility, and atrioventricular (AV) conduction, and a decrease in AV node refractoriness. Beta-2, which are present in heart muscle but are more prominent in bronchial and peripheral vascular smooth muscle. Activation of these receptors result in vasodilatation and bronchodilatation. Beta-3, which are found in adipose tissue and the heart. Activation of these receptors may mediate catecholamine-induced thermogenesis and may reduce cardiac contractility [4,5]. Beta blockers act by competitively inhibiting catecholamines from binding to these receptors. Some are more selective for the beta-1 receptor. (See "Cardioselectivity" below). Upregulation of beta receptors*—*Beta receptor density is a dynamic process that can change under varying physiologic conditions. In particular, chronic beta blocker therapy leads to an increase in receptor density [6]. This can be clinically important, since sudden withdrawal of the beta blocker results in transient supersensitivity to catecholamines, possibly precipitating angina, myocardial infarction, or death [7,8]. These complications can occur even in patients without previously apparent coronary disease [8] (See "Major side effects of beta blockers", section on Beta blocker withdrawal). Cardiovascular effects of beta blockers*—*The beneficial therapeutic effects of beta blockade in patients with stable angina pectoris are mediated by a reduction in myocardial oxygen demand. Myocardial oxygen demand varies directly with heart rate, contractility, and left ventricular wall stress, each of which is diminished by beta blockade. The decrease in wall stress is mediated in part by the antihypertensive action of these drugs. The decline in heart rate is determined both by the degree to which the heart rate is sympathetically activated (as with exercise or stress) [9] and to the properties of the beta blocker. Those drugs with intrinsic sympathomimetic activity may actually increase the resting heart rate. They are, however, still effective in the treatment of angina because it is the reduction in the exercise heart rate that is of primary importance. (See "Intrinsic sympathomimetic activity" below). The negative inotropic effects of beta blockers may, at least theoretically, have a favorable impact on myocardial oxygen consumption in the patient with angina. In the past, beta blockers were avoided in patients with left ventricular dysfunction, from concern that negative inotropic effects could precipitate or worsen heart failure. However, extensive clinical experience and the results of major clinical trials have demonstrated that these agents actually prolong survival in patients with heart failure. In such patients, beta blocker therapy should be initiated at low dose, and volume overload should be corrected prior to the initiation of therapy. (See "Use of beta blockers in heart failure due to systolic dysfunction"). Beta blockers may also affect coronary blood flow, although there are competing effects. Beta blockers inhibit adrenergically mediated coronary vasodilation, thereby increasing coronary vascular resistance and decreasing coronary blood flow [10]. However, this potentially deleterious effect is overcome by the reductions in heart rate (which enhances coronary perfusion by prolonging diastole) and myocardial oxygen demand. Nonselective beta blockers may exacerbate coronary vasospasm in patients with variant angina and should be avoided. (See "Variant angina"). PHARMACOLOGIC CHARACTERISTICS*—*A number of different beta blockers are available for clinical use. Properties such as pharmacokinetics, cardioselectivity, intrinsic sympathomimetic activity, and alpha adrenergic blocking activity are important characteristics that should be considered when choosing a particular agent. Pharmacokinetics*—*Although the beta blockers have similar pharmacotherapeutic effects, their pharmacokinetic properties differ significantly in ways that may influence their clinical usefulness and side effects [11]. Among individual drugs, there are differences in completeness of gastrointestinal absorption, amount of first-pass hepatic metabolism, lipid solubility, protein binding, extent of distribution in the body, penetration into the brain, concentration in the heart, rate of hepatic biotransformation, pharmacologic activity of metabolites, and renal clearance of the drug and its metabolites [11-13]. On the basis of their pharmacokinetic properties, the beta blockers can be classified into two broad categories [12]: Those eliminated by hepatic metabolism Those excreted unchanged by the kidney Drugs in the first group (such as propranolol and metoprolol) are lipid-soluble, almost completely absorbed by the small intestine, and largely metabolized by the liver. They enter the central nervous system (CNS) in high concentrations, possibly resulting in an increased incidence of CNS side effects. They tend to have highly variable bioavailability and relatively short plasma half-lives. In contrast, drugs in the second category (such as atenolol and sotalol) are more water soluble, incompletely absorbed through the gut, eliminated unchanged by the kidney, and do not as readily enter the central nervous system [12,13]. They show less variance in bioavailability and have longer plasma half-lives. Cardioselectivity*—*Cardioselectivity refers to the ability of a drug to preferentially block the beta-1 receptors. Nonselective beta blockers have equal affinity for the beta-1 and beta-2 receptors, while cardioselective agents will primarily inhibit the beta 1-receptors. Cardioselectivity is a relative property and substantial beta-2 receptor blockade can also occur at the higher doses that are often required to treat angina [14]. Intrinsic sympathomimetic activity*—*Some beta blockers (such as pindolol and acebutolol) have intrinsic sympathomimetic activity (ISA), also called partial angonist activity, providing low-grade beta stimulation at rest but acting as typical beta blockers when sympathetic activity is high [15]. Alpha-adrenergic blocking activity*—*Labetalol and carvedilol block both beta and alpha receptors. As a result, they reduce peripheral and coronary vascular resistance. They are both non-selective beta blockers without ISA. ADVERSE EFFECTS OF BETA BLOCKERS*—*Beta blockers are generally well tolerated in patients with stable angina, but have a well recognized set of potential side effects that can limit their use. The major side effects of beta blockers are discussed fully elsewhere. (See "Major side effects of beta blockers").
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#51
01.11.2007, 20:44
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The most frequent adverse effects include: Decreases in heart rate, contractility, and AV node conduction. Bronchoconstriction, due to beta-2 receptor blockade, can be induced by nonselective agents and high doses of cardioselective agents. As a result, many clinicians have assumed that chronic obstructive pulmonary disease (COPD) or asthma is a contraindication to beta blocker therapy. However, beta blockers are safe and effective in patients with mild COPD/asthma who are not taking a beta-2 adrenergic agonist. Furthermore, some patients carry a diagnosis of COPD that has not been confirmed. The data supporting these observations primarily come from studies of patients with an acute coronary syndrome and are discussed elsewhere. (See "Beta blockers in acute myocardial infarction", section on COPD/asthma). Worsening of symptoms of peripheral arterial disease or Raynaud phenomenon. However, there appears to be no adverse effect on mild to moderate claudication symptoms when beta-1 selective blockers are used. (See "Medical management of claudication", section on Hypertension, and see "Clinical manifestations and diagnosis of the Raynaud phenomenon"). Fatigue may be due to the reduction in cardiac output or to direct effects on the central nervous system. Central side effects that can occur include nightmares, insomnia, and hallucinations. Although depression is often mentioned as a side effect of beta blockers, this association was not seen in randomized trials. Central side effects may be more common in the elderly. Erectile dysfunction is often a problem [16].
EFFICACY OF BETA BLOCKERS IN STABLE ANGINA — All of the beta blockers, regardless of pharmacologic properties, appear to be equally effective in the treatment of stable angina pectoris. They improve exercise capacity, reduce exercise-induced ST depression, decrease the frequency of anginal episodes, and diminish the requirement for sublingual nitroglycerin. No randomized trials have examined the effect of beta blockers on survival in patients with stable angina. (See "Improved survival in high-risk patients" below). Nonselective agents — Propranolol was the first beta blocker introduced clinically. It is a nonselective agent that has been used extensively for stable angina. Evidenced of long-term efficacy was provided in a study of 63 patients with severe stable angina who were treated with propranolol for five to eight years [17]. A 50 percent or greater reduction in anginal episodes occurred in 84 percent of patients (show figure 1). Those with a lesser or no response had a four-fold increase in mortality. There was no evidence of tachyphylaxis to beta blockade. Drug dose is an important determinant of response in patients with angina. Daily doses of 160 and 320 mg of propranolol, but not 80 mg, appear to be required [18]. Cardioselective drugs — As noted above, cardioselective beta blockers (the most commonly used being atenolol and metoprolol) offer the potential advantage of not interfering with bronchodilatation or peripheral vasodilatation. The clinical applicability of this effect is uncertain since cardioselectivity may be lost at the high doses needed to treat angina [14]. Nevertheless, cardioselective drugs are used in most patients with stable angina. Atenolol, metoprolol, and nadolol are as effective as propranolol (and more effective than placebo) and nitroglycerin in reducing anginal attacks and increasing exercise capacity [19-21]. In addition, once daily dosing of atenolol is as effective (and more convenient) as twice daily dosing [20]. Metoprolol is available in a short acting form (metoprolol tartrate) for twice daily dosing and in a long acting form (metoprolol succinate) for once daily dosing. The efficacy of metoprolol was demonstrated in the International Multicenter Angina Exercise (IMAGE) study in which 280 patients with chronic stable angina were randomly assigned to six weeks therapy with long-acting preparations of metoprolol (200 mg daily) or nifedipine (20 mg twice daily) [22]. Metoprolol reduced the frequency of angina and increased the mean exercise time to 1-mm ST segment depression. Furthermore, the increase in exercise time was significantly greater than that seen with nifedipine (70 versus 43 seconds). Use of an appropriate dose is important. One report compared 25, 50, 100, and 200 mg once daily dosing of atenolol with placebo in patients with angina [23]. All doses were more effective than placebo in reducing angina and the need for sublingual nitroglycerin; however, only the 100 and 200 mg doses increased exercise capacity (show figure 2). Agents with intrinsic sympathomimetic activity — Pindolol and acebutolol are as effective in treating angina as other beta blockers but have the potential advantage of causing less depression of cardiac function. One report, for example, compared the efficacy of propranolol and pindolol in 52 patients with stable angina [24]. Both agents were equally effective in relieving angina, but pindolol caused less pronounced resting bradycardia or impairment in left ventricular function. In another study, pindolol (when compared to propranolol) was associated with a higher resting heart rate and, at low levels of exercise, a higher heart rate, cardiac output, oxygen consumption was higher in the pindolol group [15]. These differences disappeared at higher rates of exercise. Despite some potential benefits, these drugs are rarely used in the treatment of stable angina except possibly in patients with underlying resting bradycardia. They may not decrease heart rate and blood pressure at rest and should not be given to patients with a prior myocardial infarction or heart failure in whom beta blockade improves survival. Agents with alpha blocking activity — Carvedilol is a nonselective beta blocker that has vasodilating properties as a result of selective alpha-1 antagonism. One study of 122 patients with chronic stable angina found that carvedilol, at doses of 25 or 50 mg twice daily, was superior to placebo, significantly increasing the time to angina and to one mm ST segment depression during exercise testing [25]. There was no difference in the frequency of side effects when compared to placebo. In another randomized trial, carvedilol was at least as effective as verapamil [26]. Data are more limited with labetalol but demonstrate significant reductions in heart rate and angina frequency and an increase in exercise time [27]. Improved survival in high-risk patients — In addition to control of angina symptoms, beta blockers improve survival in certain subgroups of patients with stable coronary disease: Patients who have had a myocardial infarction. (See "Beta blockers in acute myocardial infarction"). Patients with systolic heart failure. (See "Use of beta blockers in heart failure due to systolic dysfunction"). In contrast, beta blockers have never been shown to improve survival or reduce the incidence of myocardial infarction in patients with chronic stable angina in the absence of myocardial infarction or heart failure.
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#52
01.11.2007, 20:47
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THERAPEUTIC GOALS — The primary therapeutic goal of beta blockers in chronic stable angina is to reduce the frequency and severity of angina and to improve exercise capacity without significant side effects. As noted above, the efficacy of beta blockers in relieving angina is dose-dependent. It is therefore important to be certain that adequate beta blockade has been attained.
Reasonable goals when titrating the dose include: Resting heart rate between 50 and 60 beats/min. The 2002 ACC/AHA guidelines on stable angina recommend adjusting the beta blocker dose to achieve a resting heart rate of 55 to 60 beats/min [1]. Among patients with more severe angina, the goal may be less than 50 beats/min assuming the absence of symptoms due to bradycardia or heart block. In addition, the exercise heart rate should not exceed 75 percent of the heart rate associated with the onset of ischemia. Patients with resting bradycardia prior to therapy can be treated with a calcium channel blocker (such as diltiazem or nifedipine), nitrates, or, if a beta blocker is necessary, a drug with intrinsic sympathomimetic activity. Similar considerations apply to patients with atrioventricular conduction delay. Blunting of peak heart rate and blood pressure during exercise which can be measured by the patient or during exercise testing, if performed. Reduction in the frequency and severity of angina as well as the use of sublingual nitroglycerin. Absence of significant side effects. CHOOSING AN AGENT — Given the general efficacy of most beta blockers in the management of stable angina, ancillary properties, such as dosing interval and cost, become important considerations when determining which beta blocker to use (show figure 3). We generally use a cardioselective agent (atenolol or metoprolol). There are no major advantages of a nonselective agent, other than the low cost of propranolol, and there are potential disadvantages in patients with certain underlying diseases such as obstructive lung disease, asthma, peripheral arterial disease, diabetes, and depression. Beta blockers with intrinsic sympathomimetic activity are rarely used in the treatment of stable angina except possibly in patients with underlying resting bradycardia. They may not decrease heart rate and blood pressure at rest and should not be given to patients with a prior myocardial infarction or heart failure in whom beta blockade improves survival. We agree with the 2002 ACC/AHA guidelines on the management of chronic stable angina, which reached the following conclusions on the role of beta blockers: Beta blockers are recommended as initial therapy in the absence of a contraindication to its use in all patients. Although other drug classes have similar efficacy, long-acting nitrates are associated with the problem of nitrate tolerance and long-acting calcium channel blockers may be associated with worse outcomes in patients with left ventricular systolic function. (See "Nitrates in the management of stable angina pectoris", section on Nitrate tolerance and see "Calcium channel blockers in the management of stable angina pectoris", section on Are calcium channel blockers safe?). Long-acting calcium channel blockers and long-acting nitrates are recommended when beta blockers are contraindicated or poorly tolerated and in addition to beta blockers when angina persists with beta blocker monotherapy. SUMMARY AND RECOMMENDATIONS — Beta blockers are highly effective in the reduction of symptoms of angina and the development of myocardial ischemia in stable patients. However, they have never been shown to decrease mortality in these individuals in the absence of myocardial infarction or heart failure associated with a reduction in left ventricular systolic function. There are many different beta blockers approved for use for cardiovascular disorders. Since it is difficult to remember the ancillary properties, pharmacokinetics, and doses of all these agents, the physician should become familiar with one or two agents in each class (eg, atenolol or metoprolol, propranolol, and pindolol) for cardioselective, nonselective, and ISA, respectively (show figure 3). The choice of agent depends upon the clinical setting since all beta blockers are equally effective in treating angina. Unless contraindicated, we recommend that all patients with stable angina pectoris receive a beta blocker as first-line antianginal therapy (Grade 1A). We suggest using a cardioselective agent, such as atenolol or metoprolol (Grade 2C).
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#53
08.11.2007, 09:41
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POISE-study
Ìåòîïðîëîë ïðè íåñåðäå÷íîé õèðóðãèè ñíèæàåò ÷èñëî ÈÌ, ÑÑ ñìåðòíîñòü, íî óâåëè÷èâàåò 30-äíåâíóþ ñìåðòíîñòü îò ëþáûõ ïðè÷èí, ÎÍÌÊ.
[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] Title: Perioperative Ischemic Evaluation (POISE - Presented at AHA 2007) Trial Sponsor: AstraZeneca Year Presented: 2007 Topic(s): Prevention/Vascular Summary Posted: 11/7/2006 Writer: [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] Description The goal of the trial was to evaluate the effect of treatment with the beta-blocker metoprolol compared with placebo on major CV events in patients undergoing noncardiac surgery. Drugs/Procedures Used Patients were randomized in a double-blind manner to treatment with metoprolol (n = 4174) or placebo (n = 4177). A dose of study drug (metoprolol 100 mg controlled release or placebo) was given 2 to 4 hours prior to surgery and again 0 to 6 hours after surgery. Daily doses of study drug (metoprolol 200 mg or placebo) were then taken for the next 30 days. Principal Findings At study entry, 43% of patients had coronary artery disease, 41% had peripheral vascular disease, and 15% had a prior stroke. Type of surgery performed was vascular in 42% of patients, intraperitoneal in 22%, orthopedic in 21%, and other types in 15%. The primary endpoint of CV death, MI or cardiac arrest was reduced in the metoprolol group compared with placebo (5.8% vs. 6.9%, hazard ratio [HR] 0.83, 95% CI 0.70-0.99, p = 0.04), driven by a reduction in non-fatal MI (3.6% vs. 5.1%, HR 0.70, p = 0.0007). There were also reductions with metoprolol in revascularization (0.3% vs. 0.6%, p = 0.01), atrial fibrillation (2.2% vs. 2.9%, p = 0.04). However, total mortality was increased in the metoprolol group (3.1% vs. 2.3%, HR 1.33, p = 0.03) as was stroke (1.0% vs. 0.5%, HR 2.17, p = 0.005). The metoprolol group also had increased rates of significant hypotension (15.0% vs. 9.7%, p < 0.0001) and significant bradycardia (6.6% vs. 2.4%, p < 0.0001). Interpretation Among patients undergoing noncardiac surgery, treatment with the beta-blocker metoprolol was associated with a reduction in the primary endpoint of CV death, MI or stroke at 30 days compared with placebo, but total mortality was higher in the metoprolol group. Prior studies have evaluated prophylactic beta-blocker use for patients undergoing vascular surgery and have shown mixed results, with the MaVS and DIPOM trial finding no benefit on clinical events but an earlier trial using bisoprolol finding a reduction in cardiac death and MI. However, as with the present study, hypotension and bradycardia increased with metoprolol in MaVS and DIPOM. Additionally, in the present trial total deaths and strokes were more frequent in the metoprolol arm, with the reduction in the primary endpoint driven by non-fatal MIs. While the post-surgical CV event rate was high, even in this population of patients undergoing noncardiac surgery, given the increased risk of death, stroke, and severe hypotension with metoprolol, routine prophylactic therapy does not appear to be a safe approach to reducing CV events in this population.
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#54
13.12.2007, 09:56
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 íîâîì Update îò ACC/AHA ïî ñòàáèëüíîé ñòåíîêàðäèè Á-ÀÁ ïîêàçàíû òîëüêî ïîñëå ÈÌ, ÎÊÑ è ÕÑÍ (I A).
2007 Chronic Angina Focused Update of the ACC/AHA 2002 Guidelines for the Management of Patients With Chronic Stable [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] Angina 2002 Chronic Angina Recommendations: Start in all post-MI and acute patients (arrhythmia, LV dysfunction, inducible ischemia) at 5 to 28 days. Continue 6 months minimum. Observe usual contraindications. Use as needed to manage angina, rhythm, or blood pressure in all other patients. 2007 Chronic Angina Recommendations (2007 COR and LOE): It is beneficial to start and continue beta-blocker therapy indefinitely in all patients who have had MI, acute coronary syndrome, or left ventricular dysfunction with or without heart failure symptoms, unless contraindicated. I (A) Comments: Modified recommendation (changed text and COR LOE added)
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#55
13.12.2007, 13:15
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Öèòàòà:
Blood Pressure Control For hypertensive patients with well established coronary artery disease, it is useful to add blood pressure medication as tolerated, treating initially with beta blockers and/or ACE inhibitors, with addition of other drugs as needed to achieve target blood pressure. New recommendation (IC)
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#56
14.05.2008, 15:57
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Á-ÀÁ ïðè íåñåðäå÷íîé õèðóðãèè. POISE trial.
Äîñòóïíû ðåçóëüòàòû èññëåäîâàíèÿ POISE, îïóáëèêîâàííîãî â Lancet.
The Lancet Early Online Publication, 13 May 2008 Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ]
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#57
13.11.2008, 09:10
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Perioperative Use of Beta-Blockers in Noncardiac Surgery Questioned
Findings from a Lancet meta-analysis raise questions about the use of beta-blockers in intermediate- or high-risk patients undergoing noncardiac surgery, as current guidelines recommend. Researchers pooled data from 33 randomized trials comparing beta-blockers with control therapy among some 12,300 surgical patients. In analyses of 30-day outcomes, beta-blockers were associated with:
However, in Journal Watch Cardiology, Beat J. Meyer says the meta-analysis was "confounded by ... methodologic weaknesses." He concludes that the benefits of treatment still outweigh the risks when the "type and dose of beta-blocker are carefully selected according to individual patients' risk profiles" and "patients are properly monitored for perioperative hypotension and bradycardia." [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] (Free PDF) [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] (Free PDF) [Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] (Free)
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#58
04.10.2012, 08:18
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REACH Registry
β-Blocker Use and Clinical Outcomes in Stable Outpatients With and Without Coronary Artery Disease
[Ññûëêè äîñòóïíû òîëüêî çàðåãèñòðèðîâàííûì ïîëüçîâàòåëÿì ] Context β-Blockers remain the standard of care after a myocardial infarction (MI). However, the benefit of β-blocker use in patients with coronary artery disease (CAD) but no history of MI, those with a remote history of MI, and those with only risk factors for CAD is unclear. Objective To assess the association of β-blocker use with cardiovascular events in stable patients with a prior history of MI, in those with CAD but no history of MI, and in those with only risk factors for CAD. Design, Setting, and Patients Longitudinal, observational study of patients in the Reduction of Atherothrombosis for Continued Health (REACH) registry who were divided into 3 cohorts: known prior MI (n = 14 043), known CAD without MI (n = 12 012), or those with CAD risk factors only (n = 18 653). Propensity score matching was used for the primary analyses. The last follow-up data collection was April 2009. Main Outcome Measures The primary outcome was a composite of cardiovascular death, nonfatal MI, or nonfatal stroke. The secondary outcome was the primary outcome plus hospitalization for atherothrombotic events or a revascularization procedure. Results Among the 44 708 patients, 21 860 were included in the propensity score–matched analysis. With a median follow-up of 44 months (interquartile range, 35-45 months), event rates were not significantly different in patients with β-blocker use compared with those without β-blocker use for any of the outcomes tested, even in the prior MI cohort (489 [16.93%] vs 532 [18.60%], respectively; hazard ratio [HR], 0.90 [95% CI, 0.79-1.03]; P = .14). In the CAD without MI cohort, the associated event rates were not significantly different in those with β-blocker use for the primary outcome (391 [12.94%]) vs without β-blocker use (405 [13.55%]) (HR, 0.92 [95% CI, 0.79-1.08]; P = .31), with higher rates for the secondary outcome (1101 [30.59%] vs 1002 [27.84%]; odds ratio [OR], 1.14 [95% CI, 1.03-1.27]; P = .01) and for the tertiary outcome of hospitalization (870 [24.17%] vs 773 [21.48%]; OR, 1.17 [95% CI, 1.04-1.30]; P = .01). In the cohort with CAD risk factors only, the event rates were higher for the primary outcome with β-blocker use (467 [14.22%]) vs without β-blocker use (403 [12.11%]) (HR, 1.18 [95% CI, 1.02-1.36]; P = .02), for the secondary outcome (870 [22.01%] vs 797 [20.17%]; OR, 1.12 [95% CI, 1.00-1.24]; P = .04) but not for the tertiary outcomes of MI (89 [2.82%] vs 68 [2.00%]; HR, 1.36 [95% CI, 0.97-1.90]; P = .08) and stroke (210 [6.55%] vs 168 [5.12%]; HR, 1.22 [95% CI, 0.99-1.52]; P = .06). However, in those with recent MI (≤1 year), β-blocker use was associated with a lower incidence of the secondary outcome (OR, 0.77 [95% CI, 0.64-0.92]). Conclusion In this observational study of patients with either CAD risk factors only, known prior MI, or known CAD without MI, the use of β-blockers was not associated with a lower risk of composite cardiovascular events.
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