Supraventricular arrhythmias complicating AMI are commonly associated with increased sympathetic tone. Many factors in the AMI setting can cause a hyperadrenergic state, including fear, anxiety, fever, pain, ongoing ischemia, hypoxia, dyspnea, and pericarditis (93). Management of these arrhythmias requires careful attention to such provocative influences.
Persistent sinus tachycardia (see Fig. 12) is deleterious during AMI because of the increased oxygen demands imposed by the rapid heart rate. Refractory sinus tachycardia portends a poor prognosis, since it is usually associated with a large area of infarction (94).
Treatment of sinus tachycardia includes a search for and correction of precipitating factors. Fever should be suppressed with aspirin or acetominophen. Anxiety and chest discomfort may be relieved with sedation and iv morphine. If present, CHF should be
treated with diuretics, oxygen, nitrates, and morphine. If no specific cause of sinus tachycardia is found, careful administration of beta-blockers may be helpful unless significant heart failure or hypotension is present.
Atrial fibrillation (AF, see Fig. 13) and flutter (see Fig. 14) occur in 10-20% of AMI (95-96). The prevalence of AF with AMI probably increases with age. In a Medicare dataset, 22% of patients greater than 65 yr of age with AMI either had AF at presentation (11%) or developed AF during hospitalization (11%) (97). In the SPRINT study, the mortality in AMI patients with AF was 25.5% (95). Patients with chronic AF who experience AMI do not seem to have a higher mortality than their counterparts without chronic AF. Conversely, patients who develop AF in the setting of AMI have high rates of complications and in-hospital mortality (97). AF occurs more commonly in the setting of pump failure, perhaps because of left atrial distension related to high filling pressures. In multivariate analysis, this excess mortality in patients with AF was attributable entirely to CHF (95). The association between AF, CHF, and high mortality is even more pronounced in patients in whom AF occurs relatively late (>12 h) after the onset of MI (98). Thus, AF developing during AMI seems to be a marker for rather than a direct cause of poor outcome. Notably, AF tends to occur earlier in the course of IMI (within 12 h), than anterior MI (12 h-4 d) (98). In addition to heart failure and high sympathetic tone, atrial infarction, elevated right atrial pressure, pericarditis, right ventricular infarction (13,99) and pulmonary embolus have been specifically linked with paroxysms of AF during AMI. Both electrocardiographic (100) and angiographic (101) stigmata of atrial infarction may occur in patients who develop AF. Early betablockade reduces the incidence of AF complicating AMI (39). In GUSTO-1, AF was associated with a higher rate of stroke and in-hospital mortality, suggesting AF remains a significant risk factor even in the setting of thrombolytic therapy. Thrombolytic therapy may, however, reduce the incidence of AF during AMI (102).
Acceleration of the ventricular rate with the onset of AF or atrial flutter increases myocardial oxygen demand and reduces the time available for diastolic perfusion of the coronary arteries. With loss of the contribution of atrial contraction to left ventricular filling, cardiac output may decrease. As with sinus tachycardia, these rhythm disturbances may have an identifiable underlying cause, may persist if not treated correctly, and may cause infarct extension and clinical deterioration.
Specific measures used to treat AF or atrial flutter depend upon the degree of hemodynamic compromise present in association with the arrhythmia. The potential risk of thromboembolic complications with cardioversion should also be considered in patients with AF or atrial flutter of unknown duration who are not chronically anticoagu-lated. If significant hypotension, heart failure, or angina ensues, urgent electrical cardioversion may be required. The patient should be sedated with a short-acting agent if possible, and a synchronized electrical discharge should be delivered. An initial discharge of 200 J for AF and 50-100 J for atrial flutter is reasonable; subsequent shocks titrated to higher energy levels may be delivered if necessary. Lower energies are typically required for atrial flutter than for AF. Biphasic waveforms may increase the success of external cardioversion compared with traditional monophasic waveforms. After cardioversion, the potential benefits and risks of antiarrhythmic therapy to suppress further episodes of AF must be carefully considered.
Patients who develop AF but maintain hemodynamic stability should be treated medically. Therapy should focus initially on control of the ventricular response to AF. Because of the probable contributions of ischemia and adrenergic tone to the initiation of AF, beta-blockade is the preferred first-line therapy for AF in the setting of AMI. If it is unclear whether a beta-blocker will be tolerated, a trial of esmolol, an ultra-short-acting beta-blocker, may be employed. Other pharmacologic alternatives include diltiazem and verapamil. Digoxin may be employed, but generally takes several hours before slowing AV nodal conduction by increasing vagal tone; in contrast, beta-blockers and calcium-channel blockers act directly at the AV node.
The role of antiarrhythmic therapy for suppression of recurrences of AF has not been critically evaluated in AMI patients. Sotalol and amiodarone are frequently used in patients with coronary disease and AF, although there is little data in the AMI setting. In one small study, iv amiodarone appeared to be relatively effective in converting AF to SR in patients with AMI (103). Data are similarly scant with the IA agents, although proarrhythmic risks may be higher in the setting of acute ischemia and/or infarction. Although dofetilide appears to be relatively safe in post-infarct patients (104), no data exists for AF in the AMI setting. Nevertheless, in patients who experience recurrent symptomatic AF despite beta-blocker or other AV-nodal-blocking therapy, a course of an antiarrhythmic agent may be reasonable.
Atrial flutter, in which atrial activity is organized into a single macro-reentrant right atrial circuit, is much less common than AF during AMI (98). Pharmacologic options are the same as for AF, although ventricular rate control is typically more difficult to achieve in atrial flutter. In addition, atrial flutter may be terminated by overdrive atrial pacing. Catheter ablation for atrial flutter, although extremely effective in the non-AMI setting, has not been reported in AMI patients.
Initiating anticoagulation should also be considered in patients with AF and atrial flutter. Intravenous heparin is frequently used adjunctively in patients managed with thrombolytic therapy and primary angioplasty/stent, as well as in patients managed conservatively. No data exist with respect to the efficacy of low molecular weight heparins and the newer antiplatelet agents in preventing thromboembolic complications related to AF.
Finally, consideration should be given to the need for long-term oral antiarrhythmic therapy and anticoagulation if AF or atrial flutter recur or if conditions likely to precipitate these arrhythmias persist. Although such a decision must be individualized, a conservative approach with anticoagulation for at least 6 wk following restoration of sinus rhythm is reasonable. The long-term need for suppressive antiarrhythmic therapy should frequently be reassessed.
Paroxysmal supraventricular tachycardia (105) (PSVT, see Fig. 15) is a rare rhythm disturbance that occurs during acute MI (98). When PSVT does occur, it is often both transient and recurrent (93). Left ventricular failure and increased sympathetic tone may be precipitating factors, but this has not been firmly established.
The most common forms of PSVT, AV-nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia (AVRT) using an accessory pathway, are reentrant rhythms that utilize the AV node as one limb of the circuit. Vagal maneuvers will often terminate these tachycardias (106). If vagal maneuvers are ineffective, iv adenosine is the drug of choice in non-AMI patients (105); iv verapamil is also extremely effective. Unfortunately, few data exist in the AMI setting. Adenosine frequently causes transient anginal chest discomfort, dyspnea, and flushing. Clinically significant hypotension is more commonly a side-effect of iv verapamil than adenosine. Verapamil may be containdi-cated if there is significant left ventricular dysfunction. Intravenous metoprolol may be effective in terminating PSVT (107), and oral beta-blockers may prevent recurrences.
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