|
|
|
E. Initiate Medical Therapy
OBJECTIVE Initiate medical therapy that may improve cardiac symptoms and reduce cardiovascular mortality, while preparations are made for reperfusion therapy. ANNOTATIONMedical therapy should be initiated while preparations are made for reperfusion therapy. Medications that may be given at this time include the following:
Although the focus in initial management of AMI is on reperfusion of the occluded artery, studies have shown that initial medical management can also have an impact on patient outcomes. Aspirin
ISIS-2 (1988) demonstrated
that administration of 162 mg of aspirin during an AMI reduced mortality
by 23% at 35 days. The mortality rate improved to 42% when aspirin was given
in conjunction with streptokinase. This improvement was maintained for up
to 15 months, following initial presentation. Aspirin, as noted above, should
be given within 10 minutes of presentation. Aspirin should be non-coated
and chewed and should be given even if the patient reports taking aspirin
prior to arrival.Clopidogrel should be administered to hospitalized atients who are unable to take aspirin due to gastrointestinal intolerance or hypersensitivity CURE trial (2001) Beta-blockers
Since the original BHAT trials (1982), it has been known that beta-blockers improve mortality following a MI and the people who benefit the most have the worst LV systolic function. In the ISIS-1 trials (1986) and TIMI-IIB trials (Roberts et al., 1991), intravenous metoprolol (5 mg IV, which may be repeated to a total dose of 15 mg) and atenolol (5 mg to 10 mg IV) were both shown to have a beneficial effect on infarct size, recurrent ischemia or infarction, and death in those patients presenting with AMI. This benefit was seen whether patients received thrombolytics or not.
Accordingly, patients should be treated with beta-blockers, within 12 hours of presentation, unless there is a contraindication. Following administration of intravenous beta-blockers, patients should be started on oral beta-blockers. Relative contraindications to beta-blockers, include heart rate <60 bpm, systolic blood pressure <100 mm Hg, moderate or severe CHF, signs of peripheral hypoperfusion, PR interval >0.24 seconds on the ECG, second or third degree AV block, severe COPD, and history of asthma. Calcium Channel Blockers (CCB)
Per ACC/AHA AMI guidelines from 1996, short-acting nifedipine "is contraindicated in routine treatment of AMI," while verapamil and diltiazem "are contraindicated in patients with AMI and associated LV dysfunction or CHF." Verapamil or diltiazem may be given to patients for whom "beta-adrenoreceptor blockers are ineffective or contraindicated (i.e., bronchospastic disease) for relief of ongoing ischemia or control of a rapid ventricular response with atrial fibrillation (AF) after AMI in the absence of CHF, LV dysfunction, or AV block."Intravenous Heparin
Intravenous heparin should be considered in all patients referred for emergent percutaneous or surgical revascularization. It should also be used in patients who are to receive alteplase, reteplase, or tenecteplase, for an AMI. The optimal APTT goal should be 50 to 75 seconds (Granger et al., 1996). Intravenous heparin should be used in patients at risk for systemic emboli (i.e., large anterior wall MI, atrial fibrillation, previous embolic event, and LV thrombus). Patients who receive a nonselective thrombolytic agent (e.g., streptokinase) should not routinely receive intravenous heparin, unless they are at high risk for an embolic event (GUSTO, 1993a).Nitroglycerin
Nitroglycerin serves as a vasodilator, by its conversion to nitric oxide (NO) at the cellular level. The effect of NO includes both venous and arterial vasodilation. The net effect is a reduction in both cardiac preload and afterload, and a decrease in myocardial oxygen requirements. These beneficial hemodynamic effects improve myocardial ischemia (angina) and can also help patients with cardiac systolic dysfunction, by reducing infarction size (Jugdutt, 1993). Because nitrates can lower blood pressure, they should be avoided in patients with hypotension (i.e., systolic blood pressure <90 mm Hg) or significant bradycardia (i.e., heart rate <50 bpm) (Come & Pitt, 1976). Nitrates should be used with caution, if at all, in patients presenting with right ventricular infarction, as cardiac output is preload-dependent in patients with right ventricular infarction (Ferguson et al., 1989).Angiotensin-Converting Enzyme Inhibitors (ACE-inhibitor)
Four large-scale trials have demonstrated improved survival with oral ACE-inhibitor therapy started during the acute phase (0 to 36 hours) of MI (ISIS-4, 1995; GISSI-3, 1994; Ambrosioni, 1995; Chinese Cardiac Study Collaborative Group, 1995). These trials enrolled MI patients irrespective of the presence of clinical heart failure or known LV dysfunction, but patients with cardiogenic shock or low systolic blood pressure (i.e., less than 100 mm Hg) were generally excluded. A systematic overview of these trials, which included nearly 100,000 patients, was published in 1998 (ACE Inhibitor Myocardial Infarction Collaborative Group, 1998). The principal finding of this analysis was that ACE-inhibitor treatment improves 30-day mortality following MI (approximately 5 lives will be saved per 1000 patients treated). Most of the mortality benefit accrues during the first several days of treatment and in patients at highest risk (i.e., anterior wall MI, moderate-severe heart failure, heart rate >100). Adverse effects of ACE-inhibitor treatment were infrequent, although hypotension and renal dysfunction were more common in patients 75 years old or older. The only trial that did not show a benefit was the CONSENSUS-II trial (Swedberg et al., 1992), where intravenous enalapril was given to patients presenting with an AMI. Importantly, administration of intravenous enalapril was associated with excess hypotension. Accordingly, intravenous ACE-inhibitor should not be given within 48 hours of the infarction, and all ACE-inhibitor should be avoided in patients who are hypotensive or have other contraindications. ACE-inhibitor should be started at a low dose (e.g., captopril at 6.25 mg P.O. t.i.d.), then titrated upward over the following 24 to 48 hours.EVIDENCE
QE = Quality of Evidence; R = Recommendation (See
Introduction.)
*Note: This link will take you out of Module A.
|