The impact of boreal forest fire on climate warming.

We report measurements and analysis of a boreal forest fire, integrating the effects of greenhouse gases, aerosols, black carbon deposition on snow and sea ice, and postfire changes in surface albedo. The net effect of all agents was to increase radiative forcing during the first year (34 +/- 31 Watts per square meter of burned area), but to decrease radiative forcing when averaged over an 80-year fire cycle (-2.3 +/- 2.2 Watts per square meter) because multidecadal increases in surface albedo had a larger impact than fire-emitted greenhouse gases. This result implies that future increases in boreal fire may not accelerate climate warming.

Demonstration of an area of slow conduction in human atrial flutter.

Ten patients with chronic atrial flutter were studied prospectively using electrophysiologic mapping and pacing techniques to assess the mechanism of atrial flutter and the presence of an area of slow conduction in the atria. Electrograms recorded from greater than or equal to 30 right atrial sites for each patient during atrial flutter demonstrated that right atrial free wall activation was craniocaudal and that the interatrial septum activation was caudocranial, consistent with a reentrant circuit involving the right atrium. In six patients, slow conduction occurred during atrial flutter in the inferior right atrium and was spatially associated with fractionated electrographic recordings. In the other four patients, a "missing" interval of electrical activity occurred in the inferior right atrium for an average of 40% of the atrial flutter cycle. Transient entrainment criteria were demonstrated in each patient during rapid high right atrial pacing. The mean activation time from the high right atrial pacing site to the coronary sinus (inferior left atrial) recording site was long (228 ms) and consistent with activation through an area of slow conduction. During rapid pacing of atrial flutter from the coronary sinus site, no transient entrainment criteria could be demonstrated. The mean activation time from the coronary sinus pacing site to the high right atrial recording site was relatively short (134 ms) and consistent with orthodromic activation of the high right atrium not through an area of slow conduction. High right atrial pacing during sinus rhythm at rates similar to atrial flutter demonstrated a short activation time to the coronary sinus and low right atrial sites (mean 169 and 88 ms, respectively), indicating activation that did not traverse an area of slow conduction. Coronary sinus pacing during sinus rhythm demonstrated the same phenomena. Low right atrial electrograms recorded during sinus rhythm and during rapid pacing of sinus rhythm were not fractionated, although they were during atrial flutter. Thus, atrial mapping and pacing data were complementary, indicating that human atrial flutter in the patients studied was generated by a reentrant circuit in the right atrium, with an area of slow conduction in the low right atrium present only during atrial flutter.

A fourth criterion for transient entrainment: the electrogram equivalent of progressive fusion.

Prior data pertaining to transient entrainment and associated phenomena have been best explained by pacing capture of a reentrant circuit. On this basis, we hypothesized that rapid pacing from a single site of two different constant pacing rates could constantly capture an appropriately selected bipolar electrogram recording site from one direction with a constant stimulus-to-electrogram interval during pacing at one rate, yet be constantly captured from another direction with a different constant stimulus-to-electrogram interval when pacing at a different constant pacing rate. To test this hypothesis, we studied a group of patients, each with a representative tachycardia (ventricular tachycardia, circus-movement tachycardia involving an atrioventricular bypass pathway, atrial tachycardia, and atrial flutter). For each tachycardia, pacing was performed from a single site for at least two different constant rates faster than the spontaneous rate of the tachycardia. We observed in these patients that a local bipolar recording site was constantly captured from different directions at two different pacing rates without interrupting the tachycardia at pacing termination. The evidence that the same site was captured from a different direction at two different pacing rates was supported by demonstrating a change in conduction time to that site associated with a change in the bipolar electrogram morphology at that site when comparing pacing at each rate. The mean conduction time (stimulus-to-recording site electrogram interval) was 319 +/- 69 msec while pacing at a mean cycle length of 265 +/- 50 msec, yet only 81 +/- 38 msec while pacing at a second mean cycle length of 233 +/- 51 msec, a mean change in conduction time of 238 +/- 56 msec. Remarkably, the faster pacing rate resulted in a shorter conduction time. The fact that the same electrode recording site was activated from different directions without interruption of the spontaneous tachycardia at pacing termination is difficult to explain on any mechanistic basis other than reentry. Also, these changes in conduction time and electrogram morphology occurred in parallel with the demonstration of progressive fusion beats on the electrocardiogram, the latter being an established criterion for transient entrainment.(ABSTRACT TRUNCATED AT 400 WORDS)

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm.

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.

Echocardiographic features of combined membranous subaortic stenosis and acquired calcific aortic valvulopathy.

The M-mode echocardiographic features of aortic valve structure and motion in a 45-year-old male with combined congenital subaortic diaphragm and acquired deformity of the aortic valve are described. Clinical, hemodynamic, and angiographic studies suggested calcific aortic valve disease with stenosis and insufficiency, but the additional presence of a subaortic diaphragm was not appreciated. Cardiac ultrasonography demonstrated multiple, central diastolic aortic valve cusp echoes consistent with a thickened, calcified, tricuspid aortic valve. Despite calcification of the cusps, however, enough systolic cusp excursion remained to demonstrate an early systolic, rapid movement toward closure of the right coronary cusp-a finding suggestive of fixed subvalvular obstruction. Surgery confirmed a discrete subaortic diaphragm and a tricuspid, thichened, mildly calcified aortic valve with fusion of the cusp commissures at their origins and rolling back of the cusp edges. The value of echocardiography in the evaluation of the left ventricular outflow tract and aortic valve is emphasized.