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Background— Although the hemodynamic changes associated with atrial fibrillation (AF) have been extensively studied, the neural changes remain unclear. We hypothesized that AF is associated with an increase in sympathetic nerve activity (SNA) and that the irregular ventricular response contributes to this state of sympathoexcitation. Methods and Results— In 8 patients referred for an electrophysiological study, SNA, blood pressure (BP), central venous pressure (CVP), and heart rate were recorded during 3 minutes of normal sinus rhythm (NSR) and 3 minutes of induced AF. In 5 of 8 patients who converted to NSR, right atrial (RA) pacing was performed for 3 minutes in atrial pacing triggered by ventricular sensing mode triggered by playback of an FM tape previously recorded from the right ventricle during AF (RA-irregular) and atrial pacing inhibited by atrial sensing mode at a rate equal to the mean heart rate obtained during AF (RA-regular). SNA data were expressed as percentage of baseline during NSR. SNA increased in all 8 patients during induced AF compared with NSR (171±40% versus 100%, respectively; P P =0.02). Similarly, SNA was significantly higher during RA-irregular pacing compared with RA-regular pacing (124±24% versus 91±20%, respectively; P =0.03). BP and CVP were not significantly different between the 2 pacing modes. Conclusions— Induced AF results in a significant increase in SNA, which is in part attributable to the irregular ventricular response. Our findings suggest that restoring NSR or regularity might be beneficial, particularly in patients with heart failure.

Background— The purpose of this study was to assess the effect of the serotonin reuptake inhibitor paroxetine hydrochloride (Paxil, SmithKline Beecham) on cardiovascular reflexes. We hypothesized that Paxil prevents neurally mediated syncope (NMS) by attenuating the sympathoinhibition and vagotonia associated with a vasovagal reaction. Methods and Results— In a double-blind randomized study, 25 healthy subjects with a positive response to either carotid sinus massage (CSM) or lower body negative pressure (LBNP) received Paxil (20 mg/d) or placebo for 6 weeks. Arterial baroreflex sensitivity (BRS), muscle sympathetic nerve activity (SNA), baroreflex control of SNA, blood pressure, and heart rate responses to CSM and LBNP were measured at baseline and at 6 weeks. Nineteen subjects completed the study (Paxil, n=9; placebo, n=10). In the Paxil group, BRS decreased significantly compared with baseline (15.8±4.0 ms/mm Hg versus 11.0±2.6 ms/mm Hg, P =0.05); however, all 9 subjects continued to have a positive response to LBNP with presyncope. Paxil did not attenuate the sympathoinhibition or vagotonia associated with a positive LBNP response and had no significant effect on baroreflex control of SNA. In the control group, no significant change in BRS was noted compared with baseline. Seven out of 9 subjects who had a positive LBNP response at baseline had a repeat positive LBNP response, and the subject with a positive CSM at baseline had a negative response at 6 weeks. Conclusions— Paxil decreases arterial BRS but does not prevent the presyncope associated with LBNP. The effect of Paxil on the autonomic reflexes in patients with neurally mediated syncope remains unclear.

Background: Atrial fibrillation (AF) is highly prevalent and poses a significant public health burden on the aging population. We hypothesized that AF independently predicts myocardial infarction (MI) in the Cardiovascular Health Study (CHS). Methods: AF was evaluated longitudinally in participants free of cardiovascular disease at baseline in the CHS. Participants were followed for a mean (standard deviation, SD) 12.7 (5.8) years for development of fatal or nonfatal MI. Cox regression models were utilized to assess the associations of time-updated AF and MI in fully adjusted models and models with gender interaction. Results: Of the 5888 participants in the CHS, 4158 met the inclusion criteria. The mean (SD) age was 72.3 (5.4) years old (38.3% male, 14.3% African-American). Eighty-two had prevalent AF; 1005 developed incident AF during follow up (AF group, n=1087). To avoid bias, participants diagnosed with AF at the same time as their MI were not included in the AF group. Baseline total cholesterol (212.4 [38.6] mg/dL), systolic blood pressure (SBP, 136.1 [21.4] mmHg), and diabetes mellitus prevalence (13.6%) were similar between groups. AF updated as a time-varying exposure was associated with a higher risk of MI: hazard ratio (HR) 1.61, [95% CI 1.32-1.96], after adjusting for age, gender, race, SBP, total and high-density lipoprotein cholesterol, current smoking, fasting glucose, education, alcohol use, C-reactive protein, body-mass index, diabetes, anti-arrhythmic use, and time-updated use of aspirin, anti-hypertensive and lipid medications. Women were at higher risk (HR 2.00 [95% CI 1.53-2.62]) than men (HR 1.33 [95% CI 0.99-1.77]) (p for interaction=0.02). Conclusion: In a large cohort study with over a decade of follow-up, AF was associated with an increased risk for MI. This association was more pronounced in women.

Background —The purpose of our study was to define the incidence and mechanisms of atypical right atrial flutter. Methods and Results —A total of 28 (8%) of 372 consecutive patients with atrial flutter (AFL) had 36 episodes of sustained atypical right AFL. Among 24 (67%) of 36 episodes of lower loop reentry (LLR), 13 (54%) of 24 episodes had early breakthrough at the lower lateral tricuspid annulus, whereas 11 (46%) of 24 episodes had early breakthrough at the high lateral tricuspid annulus, and 9 (38%) of 24 episodes showed multiple annular breaks. Bidirectional isthmus block resulted in elimination of LLR. A pattern of posterior breakthrough from the eustachian ridge to the septum was observed in 4 (14%) of 28 patients. Upper loop reentry was observed in 8 (22%) of 36 episodes and was defined as showing a clockwise orientation with early annular break and wave-front collision over the isthmus. Two patients had atypical right AFL around low voltage areas (“scars”) in the posterolateral right atrium. Conclusions —Atypical right AFL is most commonly associated with an isthmus-dependent mechanism (ie, LLR or subeustachian isthmus breaks). Non–isthmus-dependent circuits include upper loop reentry or scar-related circuits.

Background —Previous studies have shown the importance of the timing of atrial and ventricular systole on the hemodynamic response during supraventricular tachycardia (SVT). However, the reflex changes in autonomic tone during SVT remain poorly understood. Methods and Results —Eleven patients with permanent dual-chamber pacemakers were enrolled in the study. Arterial blood pressure (BP), central venous pressure (CVP), and peripheral muscle sympathetic nerve activity (SNA) were recorded during DDD pacing at a rate of 175 bpm (cycle length 343 ms) with an atrioventricular (AV) interval of 30, 200 and 110 ms, simulating tachycardia with near-simultaneous atrial and ventricular systole, short-RP tachycardia (RPPR). Each pacing run was performed for 3 minutes separated by a 5-minute recovery period. All patients demonstrated an abrupt fall in BP, an increase in CVP, and an increase in SNA regardless of the AV interval. The decreases in SBP, DBP, and MAP and the increase in CVP were significantly less during long-RP tachycardia (AV interval 110 ms) than during the other 2 pacing modes ( P P Conclusions —These data suggest that the superior maintenance of hemodynamic stability during long-RP tachycardia is accompanied by reduced sympathoexcitation, which is primarily mediated by the arterial baroreceptors, with a modest cardiopulmonary vasodepressor effect.

Background —Although there have been few studies in which the hemodynamic effects of right ventricular (RV) and left ventricular (LV) pacing were compared with those of biventricular (BV) pacing, the autonomic changes during these different pacing modes remain unknown. We hypothesized that BV pacing results in improved hemodynamics and a decrease in sympathetic nerve activity (SNA) compared with single-site pacing. Methods and Results —Thirteen men with a mean ejection fraction of 0.28±0.7 were enrolled in the study. Arterial blood pressure (BP), central venous pressure (CVP), and SNA were recorded during 3 minutes of right atrial (RA)-RV, RA-LV, and RA-BV pacing at a rate 10 beats faster than sinus rhythm. BP was greater during LV (151±7/85±3 mm Hg) and BV (151±6/85±3 mm Hg) pacing than during RV pacing (146±7/82±3 mm Hg) ( P P =0.27). SNA was significantly less ( P P P =0.08 to 0.14), there was a trend for patients with a narrow QRS to have a lower mean BP and higher SNA during LV pacing than during BV pacing ( r =0.42 to 0.49). Conclusions —LV-based pacing results in improved hemodynamics and a decrease in SNA compared with RV pacing in patients with LV dysfunction regardless of the QRS duration.

Background —Ventricular tachyarrhythmias present a unique set of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures and decreasing arterial pressure. The net effect on the control of sympathetic nerve activity (SNA) in humans is unknown. The purpose of this study was to determine the relative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure during ventricular pacing in humans. Methods and Results —Two experiments were performed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infusion (NTP) in 12 patients and studied with and without head-up tilt or phenylephrine to normalize the stimuli to either the arterial or cardiopulmonary baroreceptors in 9 patients. In experiment 1, the slope of the relation between SNA and mean arterial pressure was greater during NTP (−4.7±1.4 U/mm Hg) than during ventricular pacing (−3.4±1.1 U/mm Hg). Comparison of NTP doses and ventricular pacing rates that produced comparable hypotension showed that SNA increased more during NTP ( P =0.03). In experiment 2, normalization of arterial pressure during pacing resulted in SNA decreasing below baseline ( P P =0.04). Conclusions —These data demonstrate that in humans arterial baroreflex control predominates in mediating sympathoexcitation during ventricular tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulation.

Background —Despite similar degrees of left ventricular dysfunction and similar tachycardia or pacing rate, blood pressure (BP) response and symptoms vary greatly among patients. Sympathetic nerve activity (SNA) increases during sustained ventricular tachycardia (VT), and the magnitude of this sympathoexcitatory response appears to contribute to the net hemodynamic outcome. We hypothesize that the magnitude of sympathoexcitation and thus arterial baroreflex gain is an important determinant of the hemodynamic outcome of VT. Methods and Results —We evaluated the relation between arterial baroreflex sympathetic gain and BP recovery during rapid ventricular pacing (VP) in patients referred for electrophysiological study. Efferent postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients during nitroprusside infusion and during VP at 150 (n=12) or 120 (n=2) bpm. Arterial baroreflex gain was defined as the slope of the relationship of change in SNA to change in diastolic BP during nitroprusside infusion. Recovery of mean arterial pressure (MAP) during VP was measured as the increase in MAP from the nadir at the onset of pacing to the steady-state value during sustained VP. Arterial baroreflex gain correlated positively with recovery of MAP ( r =0.57, P =0.034). No significant correlation between ejection fraction and baroreflex gain ( r =0.48, P =0.08) or BP recovery ( r =0.41, P =0.15) was found. When patients were separated into high versus low baroreflex gain, the recovery of MAP during simulated VT was significantly greater in patients with high gain. Conclusions —These data strongly suggest that arterial baroreflex gain contributes significantly to hemodynamic stability during simulated VT. Knowledge of baroreflex gain in individual patients may help the clinician tailor therapy directed toward sustained VT.

A 53-year-old executive (6 ft 3 in tall; 327 lb) with a history of diabetes mellitus, hypertension, and coronary artery disease (coronary artery angioplasty in 1995) was traveling with his wife on vacation and ran to catch a connecting flight. The plane had closed the doors for takeoff when his wife noted that he was unresponsive. A flight attendant brought out the on-board automatic external defibrillator (AED; “ForeRunner,” Heartstream) and was assisted by a passenger with paramedic …