"Overall, these results suggest that T3 is capable of providing a safe alternative for beta blocker intolerant patients following MI." The researchers will continue studying the effectiveness of thyroid hormone after MI and encourage clinical researchers to consider examining low dose T3 treatment of MI patients who cannot tolerate beta blockers.
Full Answer
Should we reconsider beta blockers after mi?
They also suggested that physicians and patients with an uncomplicated course after MI may want to reconsider the continued use of beta blockers beyond 1 year.
Should beta-blockers be used after acute myocardial injuries?
Beta-Blockers [BB] have been used extensively in the last 40 years after acute myocardial infarction [AMI] as part of therapy and in secondary prevention. The evidence for “routine” therapy with beta-blocker use post AMI rests largely on results of trials conducted over 25 years ago.
How long should beta-blockers be used after mi or ACS?
It is reasonable to continue beta-blockers beyond 3 years as chronic therapy in all patients with normal LV function who have had MI or ACS. This evolution of the impact of beta-blockers post-MI follows trends in reperfusion and advances in medical therapy.
Are seniors taking beta-blockers to their detriment?
Beta-blockers are recommended in the JNC 7 Report as first-line therapy in patients with “compelling indications” such as ischemic heart disease and heart failure. CLINICAL CONTEXT: Seniors taking beta-blockers to their detriment? Many elderly patients are on beta-blockers, perhaps to their detriment.
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Which medication is the drug of choice for a patient with an acute myocardial infarction because of its vasodilation property?
Nitroglycerin remains a first-line treatment for angina pectoris and acute myocardial infarction. Nitroglycerin achieves its benefit by giving rise to nitric oxide, which causes vasodilation and increases blood flow to the myocardium.
What medications are prescribed after MI?
These medications include clopidogrel (Plavix), prasugrel (Effient), and ticagrelor (Brilinta). Similar to aspirin, P2Y12 inhibitors may raise your bleeding risk. P2Y12 inhibitors may be used for several reasons. As described above, they're an antiplatelet alternative to aspirin.
What is the drug of choice for myocardial infarction?
The pain of myocardial infarction is usually severe and requires potent opiate analgesia. Intravenous diamorphine 2.5–5 mg (repeated as necessary) is the drug of choice and is not only a powerful analgesic but also has a useful anxiolytic effect.
Which of the following medications are commonly advised after a myocardial infarction?
Clopidogrel and ticagrelor are recommended for conservative medical management of MI in combination with aspirin (162 to 325 mg per day) for up to 12 months. Early administration of beta blockers is recommended during hospitalization after an MI.
What is the first line treatment for myocardial infarction?
The early treatment of acute myocardial infarction consists of ensuring the patient is in an environment in which defibrillation is possible and then reducing the size of the potential infarct by re-opening the occluded coronary artery.
What drugs reduce mortality after MI?
ACE inhibitors reduce mortality rates after myocardial infarction. Administer ACE inhibitors as soon as possible as long as the patient has no contraindications and remains in stable condition. ACE inhibitors have the greatest benefit in patients with ventricular dysfunction.
Why are ACE inhibitors used after MI?
A meta-analysis concluded that administration of an ACE inhibitor within 3 to 16 days of infarction can slow the progression of cardiovascular disease and improve the survival rate (figure 1) [1].
What treatment is indicated in the first 12 hours of myocardial infarction?
Reperfusion. Early mechanical intervention (primary PCI) or pharmacologic reperfusion should be performed as soon as possible for patients with clinical presentation of STEMI within 12 hours of symptom onset and who have persistent ST-segment elevation or new or presumed new left bundle branch block (LBBB).
Why are beta-blockers given after MI?
For patients with acute myocardial infarction (MI), beta blocker therapy reduces infarct size and early mortality when started early and lowers the risk of death when continued long term.
Which of the following are medications commonly used to treat myocardial infarction MI or acute coronary syndrome ACS )?
Anticoagulant Drugs. Either a low molecular weight heparin (LMWH), unfractionated heparin, or bivalirudin is given routinely to patients with acute coronary syndrome unless contraindicated (eg, by active bleeding or planned use of streptokinase or anistreplase).
What drug classes are recommended in the long term treatment after an AMI?
Secondary preventive drug therapy, e.g. platelet inhibitors, statins, beta-blockers and angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor II blockers (ARB), is recommended following AMI to reduce the risk of new cardiovascular events and death [3–7].
What are ACS medications?
MedicationsThrombolytics (clot busters) help dissolve a blood clot that's blocking an artery.Nitroglycerin improves blood flow by temporarily widening blood vessels.Antiplatelet drugs help prevent blood clots from forming and include aspirin, clopidogrel (Plavix), prasugrel (Effient) and others.More items...•
How long after AMI can beta blockers be used?
One of the earliest studies suggesting benefit of beta-blockers after AMI was the Norwegian Timolol Trial [2]. It was a double-blind randomized study of 1,884 patients which examined the effect of timolol administered 7-28 days after AMI, and followed patients for 12-33 months. The study was conducted primarily in low risk, “clinically stable” patients. The study employed an “intention-to-treat” analysis. The authors found that use of timolol resulted in a 39.4% reduction in mortality, a 44.6 % reduction in sudden-death, and a 28.4% reduction in re-infarction rates. The mortality curves continued to diverge up to 30 months, after which the curves became parallel. The authors report that after 24 months the number of at risk patients was too small to derive conclusions with respect to mortality, and report a negligible difference between the two curves for re-infarction after six months. These findings were similar to those in the American beta-blocker Heart Attack Trial (BHAT) [47], the Goteborg Metoprolol Trial [7] and the Stockholm Metoprolol Trial [4].
How do beta blockers help with AMI?
Beta blockers reduce myocardial workload, and thus oxygen demand , via a reduction in heart rate and blood pressure [17-18] . They reduce catecholamine levels [19], decrease myocardial ischemia and limit infarct size, and may prevent the development of definite infarction in acute coronary syndrome (ACS) patients [18-25]. Early use of BBs in AMI has been shown to reduce the incidence of supraventricular and malignant ventricular arrhythmias, reduce the use of other anti-arrhythmic medications [7,26-30], decrease chest pain symptoms [31], and decrease sudden cardiac death and early and late re-infarction [2,7,26,28,32-36].
When to use beta blocker?
Beta-Blockers [BB] have been used extensively in the last 40 years after acute myocardial infarction [AMI] as part of therapy and in secondary prevention. The evidence for “routine” therapy with beta-blocker use post AMI rests largely on results of trials conducted over 25 years ago. However, there remains no clear recommendation regarding the appropriate duration of treatment with BBs in post AMI patients with normal left ventricular ejection fraction [LVEF] who are not experiencing angina, or who require BB for hypertension or dysrhythmia. Based on the latest ACC/AHA guidelines, BBs are recommended for early use in the setting of AMI, except in patients who are at low risk and then indefinitely as secondary prevention after AMI. This recommendation was downgraded to class IIa in low risk patients and the updated 2007 ACC/AHA guidelines suggest that the rationale for BB for secondary prevention is from limited data derived from extrapolations of chronic angina and heart failure trials. In this review, we examine the key trials that have shaped the current guidelines and recommendations. In addition, we attempt to answer the question of the duration of BB use in patients with preserved LVEF after acute MI, as well as which subgroups of patients benefits most from post AMI use of beta blockers.
What is beta blocker used for?
Beta-Blockers have been used extensively in the last 40 years after (AMI) as part of primary therapy and in secondary prevention. They are employed for multiple indications such as hypertension [11], perioperative cardioprotection [12-13], angina [14] post cardiac surgery atrial fibrillation prevention [15-16] and arrhythmias. Early BB therapy has been recommended as part of the emergency treatment of suspected AMI, especially if the patient is tachycardic or hypertensive. Current recommendations for the use of BB’s in AMI are found in the 2004 Task force and 2004/2007 ACC/AHA STEMI guidelines. The evidence for “routine” therapy with beta-blockers post AMI rests largely on results of the trials conducted over 25 years ago.
Does propranolol reduce mortality?
Another analysis of BHAT by Hawkins et al, found propranolol to improve mortality in older patients [3]. The study examined patients aged 30-59 years vs. 60-69 years. The older group had a 33.3% reduction in mortality versus placebo, compared to an 18.9% reduction in the younger age group. In this latter group, benefit from propranolol was confined to the first 6 months, while in the older group there was a continuing separation of the curves up to 36 months.
Does propranolol help with BHAT?
A sub-analysis of the BHAT database by Viscoli et alassessed the mortality rates in the study population after division into low, medium and high risk groups, and by 12 months or more of treatment [50] . The authors found that while propranolol therapy conferred an improvement in mortality of 43% among high risk patients, there was no evidence of long term benefit in the low risk population, calculated to be approximately 88% of the cohort. In addition, it highlighted that the overall risk reduction of 27% seen at 2 years occurred primarily in the first year, during which the risk reduction was 39%. In fact the risk reduction declined to 18% after 1 year, once adjusted for the effects of differences in the risk for death [50]. Overall, the authors concluded that the benefits of propranolol treatment in BHAT were confined to the highest risk patients. They also suggested that physicians and patients with an uncomplicated course after MI may want to reconsider the continued use of beta blockers beyond 1 year.
Can a patient with AMI be treated with BB?
In conclusion, it can be recommended that acutely, all hemodynamically stable AMI patients receive BB to reduce chest pain, as well as to reduce the risk of re-infarction and Ventricular arrhythmias. There may be a slight reduction in mortality if the patient has not previously been treated with BB. However, it remains inconclusive whether BB use beyond one year truly reduces mortality in the current era of AMI and post-AMI care, particularly in patients with preserved Left Ventricular systolic function. In these and other low risk patients (young, no arrhythmias or residual ischemia), prolonged use with Beta-Blockers is unlikely to confer mortality benefit. These findings can inform a practitioner’s decision regarding the risks and benefits of discontinuation of BBs in low risk patients, in the not infrequent clinical circumstance where discontinuation needs to be considered. It is important to keep in mind that most of the trials reviewed above were conducted before the widespread use of revascularization either by thrombolysis or PCI. Further studies are warranted to examine the effect of the duration of treatment with beta-blockers in asymptomatic patients treated with current medical therapy and interventions.
Which patients should receive beta blockers during an index hospitalization for ACS?
Which patients, then, should receive beta-blockers during an index hospitalization for ACS? Patients at low risk for cardiogenic shock should be started on a beta-blocker in-hospital to reduce the risk of reinfarction and angina; this is applicable for most patients with an MI. Extrapolating from pre-reperfusion-era trials, patients presenting late with large infarct size and perhaps without revascularization may have the greatest benefit from continuation of oral beta-blockers, including potential reduction in mortality and sudden death. These are also patients who will have reduced LVEF, where beta-blockers remain the standard of care.
When to start beta blocker?
Initiate oral beta-blockers within the first 24 hours in patients with ST-segment elevation MI in the absence of HF, low-output state, risk for cardiogenic shock, or other contraindications to beta-blockade.
How long should beta blockers be used?
Beta-blocker therapy should be started and continued for 3 years in all patients with normal LV function who have had MI or ACS.
Why do beta blockers cause stroke?
This signal toward increased stroke with beta-blockers may be due to ineffective reduction of central aortic pressures. Additional adverse metabolic side effects including new onset diabetes, weight gain, and hypercholesterolemia often lead to drug discontinuation as well.
How long does it take to start beta blocker?
Initiate oral beta-blockers within the first 24 hours in the absence of HF, low-output state, risk for cardiogenic shock, or other contraindications to beta-blockade.
What happens to sympathetic activation over the long run?
Sympathetic activation over the long run results in ventricular remodeling and heart failure (HF).
Can beta blockers be used for ST elevation?
The current 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes suggests that it is reasonable to continue beta-blocker therapy in patients with normal left ventricular (LV) function with ACS without ST-segment elevation (Class IIa, Level of Evidence C) (Table 2). 13 The 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction lends a Class I, Level of Evidence B recommendation that beta-blockers should be continued during and after hospitalization for all patients with ST-segment elevation MI and no contraindications. 14 However, these guidelines also comment that long-term duration of routine beta-blocker therapy in patients without HF or hypertension has not been prospectively addressed and refer to the AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update, recommending 3 years of beta-blocker therapy in this subset (Class I, Level of Evidence B). 15 Continuation of beta-blockers beyond 3 years in these patients is considered reasonable (Class IIa, Level of Evidence B). These guidelines are largely based on evidence pre-dating contemporary medical and reperfusion strategies. The 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation recommend only long-term management with beta-blockers post-MI in those patients with LV ejection fraction (LVEF) ≤ 40%, stating that contemporary randomized trials of beta-blocker therapy have not been conducted in patients after ACS without ST-segment elevation with normal LV function. 16
Study Questions
What is the association of beta-blocker dose with survival after acute myocardial infarction (MI), hypothesizing that higher-dose beta-blocker therapy will be associated with increased survival?
Methods
A multicenter registry enrolled 7,057 consecutive patients with acute MI. Discharge beta-blocker dose was indexed to the target beta-blocker doses used in randomized clinical trials, grouped as >0% to 12.5%, >12.5% to 25%, >25% to 50%, and >50% of target dose.
Conclusions
The authors concluded that data do not demonstrate increased survival in patients treated with beta-blocker doses approximating those used in prior randomized clinical trials compared with lower doses.
Perspective
This registry study reports no improvement in outcomes with higher-dose beta-blocker therapy, more specifically the target beta-blocker doses used in prior randomized clinical trials.
When should beta blockers not be used?
Beta-blockers should not be used to treat hypertension in patients older than age 60 unless they have another compelling indication to use these agents, such as heart failure or ischemic heart disease.1,2. Strength of recommendation. A:Based on a well-done meta-analyses. Khan N, McAlister FA.
What are the indications for beta blockers?
Heart failure and angina are indications for beta-blockers
What is the JNC 7 report for beta blockers?
Compelling indications. Beta-blockers are recommended in the JNC 7 Report as first-line therapy in patients with “compelling indications” such as ischemic heart disease and heart failure.
Is atenolol a beta blocker?
Although atenolol is one of the most commonly prescribed beta-blockers due to its low cost and once-daily dosing, it may be the least effective.
Is beta blocker a first line drug?
Beta-blockers are not 1st-line, even if thiazides are contraindicated. What is new about the Kahn and McAlister evidence is that beta- blockers should not be the first-line drug of choice even when thiazide diuretics are contraindicated.
Do elderly people need beta blockers?
Many elderly patients are on beta-blockers, perhaps to their detriment. Treatment choices for hypertension can have an enormous impact on outcomes among older patients:
Does beta blocker help with stroke?
Conclusion. This meta-analysis showed a “relatively weak effect of beta-blockers to reduce stroke, and the absence of effect on coronary heart disease when compared with placebo or no treatment” and a “trend toward worse outcomes in comparison with calcium channel blockers, renin-angiotensin system inhibitors, and thiazide diuretics.”
Why is it important to have a complete list of beta blockers?
Because beta-blockers can interact negatively with other drugs, it’s important that you provide your doctor with a complete list of the medications you’re taking.
How does beta blocker work?
Beta-blockers work by preventing the stress hormone adrenaline (epinephrine) from binding to beta receptors. This slows down your heart rate and lowers your blood pressure. Side effects of these medications may include fatigue and dizziness, poor circulation, and sexual dysfunction.
What are some complementary therapies for migraines?
Some complementary therapies may be useful in treating migraine. These include biofeedback and acupuncture.
How to reduce migraines?
Decrease overall stress. Stress is a common migraine trigger. Beta-blockers may help reduce migraine frequency by reducing anxiety. Beta-blockers are one of the first lines of treatment in migraine prevention, as they’re generally effective and have relatively mild side effects.
Which beta blocker is the most effective for migraines?
Research has shown that some beta-blockers tend to be more effective than others at preventing migraine. Based on studies that have been done to date, propranolol appears to be the most effective beta-blocker for treating and preventing migraine attacks.
When were beta blockers first used?
Beta-blockers were first introduced in the late 1960s and proved safe, inexpensive, and effective at treating heart conditions. They were found to also help with migraine by accident. This happened when people who had been prescribed beta-blockers found that the drugs also alleviated their migraine symptoms.
Which is the most effective migraine medication?
metoprolol. timolol. Among these, propranolol has been the most widely studied and appears to be the most effective. Several studies included in the above-mentioned literature review reported that propranolol has the ability to reduce migraine headaches by 50 percent.
How to reduce erectile dysfunction with beta blocker?
Talk to your doctor. Be sure to take your blood pressure drugs exactly as prescribed. This will help minimize side effects. If erectile dysfunction seems to be a side effect of your beta-blocker, talk with your doctor. They may lower your dosage or switch you to another drug.
How do beta blockers help with blood pressure?
Beta-blockers help lower blood pressure by blocking certain receptors in your nervous system. These are the receptors that are usually affected by chemicals such as epinephrine. Epinephrine constricts your blood vessels and causes blood to pump more forcefully.
What medications can cause erectile dysfunction?
Diuretics. Other common blood pressure-lowering medications that can contribute to erectile dysfunction are diuretics. Diuretics cause you to urinate more often. This leaves less fluid in your circulation, which leads to lower blood pressure. Diuretics may also relax muscles in your circulatory system.
How many medications are there for ED?
This can help them know if the ED drugs could interact with drugs you already take. Currently, there are six drugs on the market to treat erectile dysfunction: Caverject. Edex. Viagra. Stendra. Cialis. Levitra. Of these, only Caverject and Edex are not oral pills.
Is Caverject an oral drug?
Of these, only Caverject and Edex are not oral pills. Instead , they’re injected into your penis. None of these drugs are currently available as generic products. The side effects of these drugs are similar, and none of them interacts with beta-blockers.
Can beta blockers cause erections?
It’s thought that by blocking these receptors, beta-blockers may interfere with the part of your nervous system responsible for causing an erection. However, according to the results reported in one study in the European Heart Journal, ED associated with beta-blocker use was not common. The reported cases of ED in men who took beta-blockers may ...
Can blood pressure medications cause erectile dysfunction?
Other blood pressure drugs may be less likely to cause erectile dysfunction. Calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors may be as effective as beta-blockers at reducing high blood pressure. However, there have been fewer reports of erectile dysfunction by men who have used these drugs.
What medications interact with metoprolol?
Common medications that may interact with metoprolol include: antidepressants, such as fluoxetine, paroxetine, St John’s Wort, and monoamine oxidase inhibitors. antifungals, such as terbinafine. antihistamines, such as diphenhydramine.
How long does metoprolol affect heart rate?
With oral metoprolol tartrate, significant effects on the heart rate are seen within an hour, and effects last for six to 12 hours depending on the dose. With injectable metoprolol tartrate, significant effects are seen within 20 minutes, and a single injection lasts for approximately 5 to 8 hours, depending on the dose.
How long does it take for metoprolol to reach peak concentration?
With oral metoprolol succinate extended-release (ER) tablets, peak concentrations are reached in about seven hours following a single dose. With regular dosing; however, concentrations of metoprolol remain steady and do not fluctuate much. ER tablets are usually dosed once daily. The blood pressure lowering effects of ER tablets persist for about 24 hours.
What class of drugs is metoprolol?
Metoprolol belongs to a class of drugs known as beta-blockers.
Does metoprolol cause angina?
Avoid abrupt discontinuation. Stopping metoprolol ( both tartrate and succinate) suddenly can exacerbate angina and may increase the risk of a heart attack.
Does metoprolol succinate cause dizziness?
Side effects are similar for both metoprolol tartrate and metoprolol succinate because they both contain the same active drug, metoprolol. Dry eyes, blurred vision, dizziness (particularly when rising from a sitting to a standing position), fatigue, nightmares,a slow heart beat, and sweating are common.
Does metoprolol succinate help with heart failure?
Lowers blood pressure and relieves symptoms of angina in people with heart disease. Slow-release forms may be beneficial in people with certain types of heart failure. Available as a slow-release tablet which is usually dosed once a day.
How many people received blockers after MI?
A review of ≥200 000 patient records in the Cooperative Cardiovascular Project found that only 34% of patients received β-blockers after MI. 12 The percentage was lower among African Americans, the elderly, and patients with HF, COPD, low heart rate or blood pressure, or type 1 diabetes mellitus. 12 When all risk factors were accounted for, however, there was notably less mortality in each of these subgroups when β-blockers were administered. 12 16
Why are blockers not used?
All too often, β-blockers are not used because of their perceived side effects, namely fatigue, decreased heart rate, hypotension, and reduced sexual activity. In the BHAT trial, reduced sexual activity was reported by 43.2% in the propranolol group and 42.0% in the placebo group; the difference was not statistically significant. 8 Similarly, fatigue was present in 66.8% in the propranolol group compared with 62.1% in the placebo group. 8 Propranolol had to be discontinued in only 0.7% because of bradycardia, in 1.2% because of hypotension, in 1.5% because of fatigue, in 0.4% because of depression, and in only 0.2% because of reduced sexual activity. 8 It is clear from this study that even high doses of β-blockers are well tolerated in post-MI patients.
What is the best treatment for HF?
Present ACC/AHA guidelines advise that in patients with systolic HF, most of whom have coronary artery disease, 14 an ACE inhibitor should be used first, and a β-blocker such as carvedilol or metoprolol CR/XL should be started at low doses (see Figure 1) and gradually increased over ≈12 weeks. 15 There is now conclusive evidence that long-term β-blocker use results in improved rates of mortality and morbidity in patients with HF. 16–18,19
Does propranolol reduce mortality?
Since it was first reported in 1965 that administration of propranolol after acute MI reduced mortality, 4 a number of studies have been conducted to confirm this observation. 5 The largest were the β-Blocker Heart Attack Trial (BHAT) 6 and the Norwegian Multicenter Study Group 7 trial studying nonselective β-blockers. In the BHAT trial (which monitored 3837 post-MI patients for 27 months), propranolol significantly reduced overall mortality by 26% compared with placebo. 8 The Norwegian Multicenter Study Group (which monitored 1884 post-MI patients for 12 to 33 months) demonstrated a 39% reduction in mortality and a 28% reduction in the reinfarction rate with timolol ( Table 1 ). 7
Is blocker contraindicated for HF?
Because of their initial transient negative inotropic effects, β-blockers traditionally were considered contraindicated in HF. However, in a subset analysis in BHAT of patients who had HF before randomization, propranolol reduced total mortality and sudden death. 13 In CAPRICORN, carvedilol reduced mortality and reinfarction in post-MI patients with left ventricular systolic dysfunction, with or without signs of HF ( Table 2 ).
Is metoprolol safe for reactive airway disease?
In patients with mild reactive airway disease, short-acting β 1 -selective agents such as metoprolol or atenolol at low dose may be safer because of limited interaction with the β 2 -receptor. 21 Their selectivity, however, may be lost at higher doses.
Can a blocker be used in MI?
On the basis of much of the evidence presented here, the American Medical Association and 5 other collaborating medical organizations recently issued a “Quality of Care Alert,” which recommends that the benefits of β-blockers in reducing mortality and reinfarction may actually outweigh their risks, even in patients with relative contraindications such as asthma, diabetes mellitus, COPD, severe peripheral vascular disease, PR interval >0.24 seconds, and moderate or severe left ventricular failure. 35 Taken as a whole, this evidence leads to the conclusion that β-blockers should be administered to all post-MI patients without a contraindication and should be continued indefinitely, as recommended in the recent 2001 AHA/ACC Scientific Statement. 1