Unstable angina non ST elevation myocardial infarction beta blockers
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Beta blockers in Unstable Angina(UA) / NSTEMI
In UA/NSTEMI, the primary benefits of beta blockers are due to inhibition of beta-1 adrenergic receptors, which results in a decrease in cardiac work and myocardial oxygen demand. Slowing of the heart rate also has a favorable effect, acting not only to reduce myocardial oxygen demand(MVO2) but also to increase the duration of diastole and diastolic pressure-time, a determinant of forward coronary flow and collateral flow[1]. In the absence of contraindication(especially hypotension, heart failure and hemodyanamic instability), beta blockers should be initiated either orally or intravenously within first 24 h. Patients with marked first-degree AV block (i.e., ECG PR interval greater than 0.24 s), any form of second- or third-degree AV block in the absence of a functioning implanted pacemaker, a history of asthma, severe left ventricular dysfunction or heart failure (e.g., rales or S3 gallop) or at high risk for shock (see above) should not receive beta blockers on an acute basis. Two recent studies(GUSTO-I and COMMIT) have revealed that early aggressive beta blockade poses a substantial net hazard in hemodynamically unstable patients and should be avoided. In the COMMIT study[2], the utility of early intravenous followed by oral beta blockade (metoprolol) was tested in 45,852 patients with MI (93% had STEMI, 7% had NSTEMI) which showed that neither the composite of death, reinfarction, or cardiac arrest nor death alone was reduced for up to 28 d in the hospital. Overall, a modest reduction in reinfarction and ventricular fibrillation (which was seen after day 1) was counterbalanced by an increase in cardiogenic shock, which occurred early (first day) and primarily in those who were hemodynamically compromised or in HF or who were stable but at high risk of development of shock. Risk factors for shock were older age, female sex, time delay, higher Killip class, lower blood pressure, higher heart rate, ECG abnormality, and previous hypertension. In GUSTO-I retrospective analyses[3] , the administration of intravenous atenolol combined with late oral administration was associated with higher mortality than late oral administration alone. The authors concluded that late oral administration of atenolol might be sufficient and may offer just as good of outcomes as that coupled with early IV administration. Overall, the rationale for beta-blocker use in all forms of CAD, including UA, is generally favorable, with the exception of initial heart failure.
ACC / AHA Guidelines (DO NOT EDIT) [1][4]
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References
- ↑ 1.0 1.1 Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE, Chavey WE, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS, Smith SC, Jacobs AK, Adams CD, Anderson JL, Antman EM, Halperin JL, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura R, Ornato JP, Page RL, Riegel B (2007). "ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". Journal of the American College of Cardiology. 50 (7): e1–e157. doi:10.1016/j.jacc.2007.02.013. PMID 17692738. Retrieved 2011-04-09. Unknown parameter
|month=ignored (help) - ↑ Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX, Xie JX, Liu LS; COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Lancet. 2005 Nov 5;366(9497):1622-32. PMID: 16271643
- ↑ Pfisterer M, Cox JL, Granger CB; et al. (1998). "Atenolol use and clinical outcomes after thrombolysis for acute myocardial infarction: the GUSTO-I experience. Global Utilization of Streptokinase and TPA (alteplase) for Occluded Coronary Arteries". J. Am. Coll. Cardiol. 32 (3): 634–40. PMID 9741504. Unknown parameter
|month=ignored (help) - ↑ Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE, Chavey WE, Fesmire FM, Hochman JS, Levin TN, Lincoff AM, Peterson ED, Theroux P, Wenger NK, Wright RS (2011). "2011 ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. doi:10.1161/CIR.0b013e318212bb8b. PMID 21444888. Retrieved 2011-04-08. Unknown parameter
|month=ignored (help)