Long-term prognosis of patients with incomplete bilateral bundle branch block complicating acute myocardial infarction. Role of cardiac pacing.
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Biomedical subjects
Publications and source records attributed to D D Waters.
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BACKGROUND: Dipyridamole imaging is widely used as an alternative to exercise testing to identify and risk stratify patients with coronary artery disease. Safety data on intravenous dipyridamole stress testing has been derived largely from individual institutional data. METHODS AND RESULTS: Data were collected retrospectively by 85 coinvestigators from 73,806 patients who underwent intravenous dipyridamole stress imaging in 59 hospitals and 19 countries to determine the incidence of major adverse reactions during testing. The dose of dipyridamole infused was 0.56 mg/kg in 64,740 patients, 0.74 mg/kg in 6551 patients, and 0.84 mg/kg in 2515 patients. Combined major adverse events among the entire 73,806 patients included seven cardiac deaths (0.95 per 10,000), 13 nonfatal myocardial infarctions (1.76 per 10,000), six nonfatal sustained ventricular arrhythmias (0.81 per 10,000) (ventricular tachycardia in two and ventricular fibrillation in four), nine transient cerebral ischemic attacks (1.22 per 10,000), (with speech or motor deficit), one stroke, and nine severe bronchospasms (1.22 per 10,000) (one intubation and eight near intubations). In addition to the safety data, detailed demographic, peripheral hemodynamic, side effect, and concomitant drug data were examined in a subgroup of 3751 patients. End points from subsets of patients were compared with those of the group as a whole. Multivariate analysis revealed that dipyridamole-induced chest pain was more common in patients less than 70 years old (p = 0.0017), those with a history of coronary revascularization (p = 0.002), or patients taking aspirin (p = 0.0001). Minor noncardiac side effects were less frequent among the elderly (p = 0.0053) and more frequent in women (p = 0.0001) and patients taking maintenance aspirin (p = 0.0034). When a patient was judged on the basis of the adequacy of hemodynamic response to be a dipyridamole "nonresponder" (< 10 mm Hg drop in systolic blood pressure and 10 beats/min increase in heart rate), the only significant predictor was angiotensin-converting enzyme inhibitor intake (p = 0.0025). Inferoposterior hypoperfusion was significantly more frequent in patients with dipyridamole-induced hypotension: 57% (44/77) (p < 0.0001) of those who had hypotension and 89% (8/9) (p = 0.0076) who had severe symptomatic bradyarrhythmias displayed inferoposterior defects on thallium scanning. Caffeine levels were determined in 391 consecutive patients: levels greater than 5 mg/L were observed in only eight patients (2%), suggesting that methylxanthine levels sufficient to alter the hemodynamic response to dipyridamole resulting in suboptimal hyperemic stress are unlikely when patients take nothing by mouth after midnight. CONCLUSION: The risk of serious dipyridamole-induced side effects is very low and is comparable to that reported for exercise testing in a similar patient population.
BACKGROUND: Newer diagnostic modalities such as serum markers and acute rest myocardial perfusion imaging (MPI) have been evaluated diagnostically in patients with chest pain in the emergency department (ED), but never concurrently. We compared these two modalities in distinguishing patients in the ED with symptomatic myocardial ischemia from those with non-cardiac causes. METHODS: Serum markers and acute technetium-99m sestamibi/tetrofosmin rest MPI were obtained in 75 patients admitted to the ED with chest pain and nondiagnostic electrocardiograms. Venous samples were drawn at admission and 8 to 24 hours later for total creatine kinase, CK-MB fraction, troponin T, troponin I, and myoglobin. Three nuclear cardiologists performed blinded image interpretation. Coronary artery disease (CAD) was confirmed either by diagnostic testing or by the occurrence of myocardial infarction (MI). RESULTS: Acute rest MPI results were abnormal in all 9 patients with MI. An additional 26 patients had objective evidence of CAD confirmed by diagnostic testing. The sensitivity of acute rest MPI for objective evidence of CAD was 73%. Serum troponin T and troponin I were highly specific for acute MI but had low sensitivity at presentation. Individual serum markers had very low sensitivity for symptomatic myocardial ischemia alone. In the multivariate regression model, only acute rest MPI and diabetes were independently predictive of CAD. CONCLUSION: At the time of presentation and 8 to 24 hours later, acute rest MPI has a better sensitivity and similar specificity for patients with objective evidence of CAD when compared with serum markers.
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Six patients hospitalized with active variant angina were treated for 3 days with the serotonin antagonist ketanserin after a 3 day control period on no medication. The number of variant angina episodes per patient per day was 1.52 +/- 1.42 during the control period and 2.05 +/- 2.30 during ketanserin therapy (p = NS). Ergonovine was administered in incremental doses of 0.0125 mg to 0.4 mg in the control period, during intravenous ketanserin administration and after 3 days of oral treatment. All 6 patients developed ST elevation during all 3 ergonovine tests. The ergonovine dose at which ST elevation developed was similar in each of the 3 periods. It is concluded that ketanserin is of no value in the treatment of variant angina and that both spontaneous and ergonovine-induced coronary spasm in man are unlikely to be mediated by a serotonergic mechanism.
A circadian pattern is present for all of the manifestations of coronary artery disease discussed in this review; typical angina, variant angina, myocardial infarction and sudden cardiac death. The peak incidence for typical angina is from 06:00 to noon, and earlier, from midnight to 09:00 in variant angina. The peak incidence of myocardial infarction and sudden cardiac death are the same as for typical angina, even though different mechanisms are involved.
The electrophysiologic effects of intravenous diltiazem were evaluated in 10 patients with recurrent supraventricular tachycardias. The tachycardia incorporated an accessory pathway in 7 patients and was due to AV nodal reentry in 3 patients. Diltiazem 0.25 mg/kg was administered intravenously over 5 minutes during sustained supraventricular tachycardia. Programmed electrical stimulation was used to restore sinus rhythm if diltiazem failed to terminate the arrhythmia within 10 minutes. Conduction intervals, refractory periods and tachycardia characteristics were evaluated before and immediately after drug administration. Diltiazem did not significantly modify sinus cycle length, AH and HV intervals. Atrial and ventricular effective refractory periods were similar before and after diltiazem. The effective refractory period of the AV node was prolonged by 42 msec after diltiazem (p less than 0.05). Diltiazem increased the tachycardia cycle length from 320 +/- 41 to 353 +/- 36 msec (p less than 0.01) but terminated the arrhythmia in only 2 patients. After diltiazem, supraventricular tachycardia could not be reinitiated in only 2 patients and the tachycardia initiating window was not significantly reduced (56 +/- 26 to 41 +/- 33 msec). The infusion of diltiazem was accomplished without side effects. Thus, 0.25 mg/kg of intravenous diltiazem produces a modest depression of AV nodal function and is not very effective in terminating supraventricular tachycardia or preventing its initiation in this study population. Further studies using higher doses of intravenous diltiazem would be useful to determine its maximal therapeutic benefit in patients with recurrent supraventricular tachycardias.
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