Atrial overdrive pacing compared to CPAP in patients with obstructive sleep apnoea syndrome.

AIMS: Obstructive sleep apnoea (OSA) is associated with oxygen desaturation, blood pressure increase, and neurohumoral activation, resulting in possible detrimental effects on the cardiovascular system. Continuous positive airway pressure (CPAP) is the therapy of choice for OSA. In a recent study, nocturnal atrial overdrive pacing (pacing) reduced the severity of sleep apnoea in pacemaker patients. We compared the effects of CPAP with those of pacing in patients with OSA but without pacemaker indication or clinical signs of heart failure. METHODS AND RESULTS: Ten patients with OSA on CPAP therapy were studied for three nights by polysomnography. During the nights that followed a night without any treatment (baseline), the patients were treated with CPAP or pacing in a random order. Pacing was performed with a temporary pacing lead. The pacing frequency was 15 b.p.m. higher than the baseline heart rate. The apnoea-hypopnoea index was 41.0 h(-1) (12.0-66.6) at baseline and was significantly lower during CPAP [2.2 h(-1) (0.3-12.4)] compared with pacing [39.1 h(-1) (8.2-78.5)]. Furthermore, duration and quality of sleep were significantly improved during CPAP when compared with pacing. CONCLUSION: Nocturnal atrial overdrive pacing is no alternative therapeutic strategy to CPAP for the treatment of OSA in patients without clinical signs of heart failure and without conventional indication for anti-bradycardia pacing.     

Does the mechanism of action of biatrial pacing for atrial fibrillation involve changes in cardiac haemodynamics? Assessment by Doppler echocardiography and natriuretic peptide measurements.

AIMS: The antifibrillatory mechanism of biatrial (BI) pacing has not been fully elucidated. We investigated the role of a haemodynamic mechanism in eight patients implanted with a BI pacemaker (Chorus RM) by comparing changes in mitral Doppler flow and atrial and B-type natriuretic peptide levels (ANP, BNP) with BI pacing compared with sinus rhythm and right atrial (RA) pacing. METHODS AND RESULTS: Measurements were taken after 60 min in the supine position in each of two pairs of randomized pacing modes: (a) AAI40 beats x min(-1), (allows sinus rhythm mean rate 56 beats x min(-1), SR) vs AAI 40 beats x min(-1) with synchronized left atrial pacing (SRSync); (b) overdrive AAI RA pacing (89 beats x min(-1) (n = 6) or 70 beats x min(-1) (n = 2)) vs overdrive AAI BI pacing. Within each pair there was significant earlier activation of the left atrial Doppler signal in relation to the surface ECG P wave with BI pacing (SR 163 +/- 10 ms vs SRSync 144 +/- 21 ms (P = 0.02), and RA 232 +/- 14 ms vs BI 196 +/- 16 ms (P = 0.001)), and significant shortening of the P-R interval (SR 163 +/- 29 ms vs SRSync 148 +/- 20 (P = 0.007) and RA 261 +/- 27 ms vs BI 232 +/- 23 (P = 0.001)). The net observed effect was of no change in the atrioventricular timing sequence (delay of peak E or A to QRS/ mitral valve closure) and no change in other Doppler echo parameters. Levels of the cardiac peptides ANP and BNP were raised compared with healthy controls, but did not significantly change during the study. CONCLUSION: Acute BI pacing shortens the P-R interval and causes earlier left atrial contraction in relation to the surface electrocardiogram P wave. It does not alter the atrioventricular timing cycle, any other Doppler measurements or change cardiac peptide levels. This suggests that BI pacing does not cause haemodynamic changes that could account for any antifibrillatory properties.     

Daytime sleepiness and polysomnographic variables in sleep apnoea patients.

Excessive daytime sleepiness (EDS) is not invariably present in patients with obstructive sleep apnoea syndrome (OSAS). The aim of the present study was to investigate polysomnographic determinants of EDS in patients with OSAS. EDS was assessed using the Epworth Sleepiness Scale (ESS) and the multiple sleep latency test (MSLT). Patients showed EDS whenever the ESS score was >10 and the MSLT score <5 min. Absence of EDS was defined as having an ESS score of <10 and an MSLT score of >10 min. In total, 23 male patients with EDS (mean+/-sd ESS and MSLT score 17+/-3 and 4+/-1 min, respectively) and 17 without EDS (ESS and MSLT score 5+/-2 and 16+/-3 min, respectively), were studied. Both groups exhibited a similar apnoea/hypopnoea index (62+/-18 versus 60+/-20 events.h(-1)). Patients with EDS exhibited shorter sleep latency (11+/-16 versus 18+/-18 min) and greater sleep efficiency (90+/-7 versus 82+/-13%) than those without EDS. Patients with EDS showed lower oxygenation (lowest arterial oxygen saturation 69+/-12 versus 79+/-8%; mean arterial oxygen saturation 87+/-6 versus 90+/-5%). Sleep stage distribution and arousal index did not differ between the groups. Patients with obstructive sleep apnoea syndrome and excessive daytime sleepiness are characterised by shorter sleep latency, increased sleep efficiency and worse nocturnal oxygenation than those without excessive daytime sleepiness. Nocturnal hypoxaemia can be a major determinant of excessive daytime sleepiness in patients with obstructive sleep apnoea syndrome.     

Response of atrial flutter to overdrive atrial pacing and intravenous disopyramide phosphate, singly and in combination.

Ten patients who suffered spontaneous paroxysms of atrial flutter were investigated by electrophysiological techniques. Two had overt Wolff-Parkinson-White syndrome; three Lown-Ganong-Levine syndrome; and one a concealed accessory atrioventricular connection. Atrial flutter was initiated, at study, by right atrial pacing and electrograms from the right atrium and coronary sinus were observed for at least five minutes to ensure stable flutter in both atria. Atrial flutter was terminated by 2.5 s or 5 s bursts of atrial pacing at rates 10, 50, or 100 beats/min faster than the intrinsic flutter rate in only two patients. Atrial flutter, which was reinitiated in two patients, was then treated with intravenous disopyramide phosphate, 2 mg/kg body weight, infused over five minutes. In all 10 patients the atrial rate slowed from a mean of 310 +/- 39 beats/min to 217 +/- 27 beats/min and atrial flutter terminated in one case. Though the mean ventricular rate fell from 161 +/- 52 beats/min to 156 +/- 45 beats/min the atrioventricular conduction ratio fell from 2.17 +/- 0.86 to 1.55 +/- 0.59 and four patients were left with symptomatically significant increases of ventricular rate. In seven of nine patients overdrive atrial pacing, repeated after disopryamide, resulted in the conversion of atrial flutter to sinus rhythm. In this study, overdrive atrial pacing and intravenous disopyramide, singly and in combination, terminated atrial flutter in nine of the 10 patients and it is suggested that this method may provide an effective alternative to direct current cardioversion.     

Driving simulator and neuropsychological [corrected] testing in OSAS before and under CPAP therapy.

Patients with obstructive sleep apnoea syndrome (OSAS) have an increased car accident rate. Investigations on accident frequency are based on case history, insurance reports and driving simulator studies. The present study combines neuropsychological testing of different attention aspects engaged in driving a car and driving simulation to evaluate a suitable instrument for assessing therapeutic effects of continuous positive airway pressure (CPAP). Driving simulator investigation and neuropsychological testing of alertness, vigilance and divided attention were performed in 31 patients with polysomnographically confirmed OSAS (apnoea-hypopnoea index 24.8+/-21.5.h(-1)) before, and 2 and 42 days after initiation of CPAP. Divided attention and alertness improved significantly during CPAP, whereas vigilance remained unchanged. However, accident frequency (OSAS before therapy: 2.7+/-2.0; 2 days after CPAP: 1.5+/-1.4; 42 days after CPAP: 0.9+/-1.3) and frequency of concentration faults (OSAS before therapy: 12.4+/-5.1; 2 days after CPAP: 6.5+/-3.9; 42 days after CPAP: 4.9+/-3.3) decreased in the simulated driving situation after 2 and 42 days of therapy. There was no relation between accident frequency, concentration faults and daytime sleepiness, as measured by the Epworth Sleepiness Scale, and polysomnographic or neuropsychological findings, respectively. In conclusion, the present results suggest that driving simulation is a possible benchmark parameter of driving performance in obstructive sleep apnoea syndrome patients.     

Atrial overdrive pacing in patients with sleep apnea with implanted pacemaker

RATIONALE: Atrial overdrive pacing markedly improved sleep-disordered breathing in a recent study. OBJECTIVES: Using a single-blind, randomized, crossover design, we aimed to reproduce these findings and investigate the possible underlying mechanisms. METHODS: Twenty ambulatory patients with an implanted pacemaker or cardioverter defibrillator were studied by polysomnography on 3 consecutive nights in a randomized, single-blind, crossover study in which devices were programmed for nonpacing or for overdrive pacing at 7 or 15 beats/minute faster than the mean nocturnal heart rate. Ventilation and biomarkers (urinary norepinephrine excretion, amino-terminal portion of the precursor of brain natriuretic peptide, or NT-proBNP, were also evaluated. MEASUREMENTS AND MAIN RESULTS: Neither the primary endpoint apnea-hypopnea index, nor the apnea index, oxygen desaturation, ventilation, or biomarkers were affected by the nocturnal atrial overdrive pacing. A small, clinically insignificant, rate-dependent reduction in the hypopnea index was evoked by pacing (nonpacing, 13.4 +/- 1.4; pacing 7, 12.9 +/- 1.4; pacing 15, 10.9 +/- 1.0; p < 0.01, analysis of variance). CONCLUSIONS: The lack of effect on the apnea-hypopnea index means that atrial overdrive pacing is inappropriate for treating sleep-disordered breathing.     

Influence of heart rate and atrial transport on left ventricular volume and function: relation to hemodynamic changes produced by supraventricular arrhythmia

The response of the left ventricle to pacing-induced changes in heart rate and the atrioventricular (A-V) relation was examined with equilibrium gated radionuclide ventriculography in 20 patients who had normal ventricular function after surgery for recurrent supraventricular tachycardia. In 10 patients count-derived left ventricular ejection fraction, end-diastolic volume and stroke volume were measured during sinus rhythm and during atrial pacing at 120, 140 and 160 beats/min. In the other 10 patients similar determinations were made during sequential A-V and simultaneous ventricular and atrial (V/A) pacing, both at rates of 100 and 160 beats/min. Left ventricular ejection fraction did not change significantly with atrial pacing (from 0.65 +/- 0.02 [mean +/- standard error of the mean] at a baseline sinus rate of 91 +/- 3 beats/min to 0.62 +/- 0.03 at 160 beats/min) despite a progressive decrease in end-diastolic volume. The percent reduction in end-diastolic volume (% delta EDV) and stroke volume (+ delta SV) from the baseline values was linear and related to change in heart rate (delta HR) as % delta EDV = -0.60 delta HR + 5.19 (r = 0.71; p less than 0.01) and % delta SV = -0.62 delta HR + 5.03 (r = 0.76; p less than 0.001). Left ventricular ejection fraction with baseline sequential A-V pacing at 100 beats/min was 0.67 +/- 0.03 and not significantly altered by either sequential A-V or simultaneous V/A pacing at 160 beats/min. At 100 beats/min, loss of atrial transport with simultaneous V/A pacing resulted in a small reduction in end-diastolic volume from a baseline value of -9.0 +/- 1.9 percent (p less than 0.01) and a nonsignificant reduction in stroke volume of -3.7 +/- 1.6 percent. During simultaneous V/A pacing at 160 beats/min, the reduction in end-diastolic and stroke volumes from the baseline value was -26.6 +/- 3.8 percent and -28.8 +/- 4.3 percent, respectively (both p less than 0.01), but was significantly smaller (-16.1 +/- 3.6 percent and -19.2 +/- 4.1 percent, respectively [p less than 0.05]) when atrial transport was maintained during sequential A-V pacing at the same heart rate. During simultaneous V/A pacing at 160 beats/min, two thirds of the reduction in end-diastolic and stroke volumes from the baseline value was due to the increment in heart rate as assessed from sequential A-V pacing and the other third was due to loss of atrial transport. The data indicate that the hemodynamic consequences of supraventricular tachyarrhythmias in patients with normal ventricular function are due primarily to decreases in ventricular volume as heart rate is increased and atrial contribution is lost rather than to any changes in left ventricular ejection fraction.     

Physiologic pacing in patients with obstructive sleep apnea: a prospective, randomized crossover trial.

OBJECTIVES: This study was designed to assess the impact of prevention of bradycardia with physiologic pacing on the severity of obstructive sleep apnea. BACKGROUND: Apneic episodes during sleep are associated with slowing of the heart rate during apnea and tachycardia with subsequent arousal. Patients with permanent pacemakers may have reduced episodes of sleep apnea when their pacemaker rate is set faster than their spontaneous nocturnal heart rate. METHODS: We conducted a prospective, randomized, single-blind crossover trial of temporary atrial pacing in obstructive sleep apnea to reduce the apnea hypopnea index (AHI). Fifteen patients (age 60 +/- 13 years, 12 men) with moderate to severe obstructive sleep apnea (AHI 34 +/- 14) underwent insertion of an externalized atrial permanent pacing system via the left subclavian vein. Patients underwent overnight respiratory sleep studies in hospital, during atrial pacing at 75 beats/min, and with pacing turned off. The order of pacing mode was randomized, with crossover the subsequent night to the other mode. Patients were blinded to pacing mode, and the analysis of sleep recordings was blind to pacing mode. RESULTS: Pacing was tolerated without complications in all patients. Overnight physiologic pacing did not affect the AHI (pacing 39 +/- 21/h vs. control 42 +/- 21/h, p = 0.23, 95% confidence interval -9.3 to 2.5 for difference), desaturation time (pacing 3.8 +/- 6.0% vs. control 3.5 +/- 4.3%, p = 0.70), or the minimum SaO(2) (pacing 75 +/- 10% vs. control 77 +/- 11%, p = 0.38). There was a borderline significant reduction in circulatory time with pacing (pacing 23.4 +/- 3.2 s vs. control 25.5 +/- 4.4 s, p = 0.09). CONCLUSIONS: Temporary atrial pacing does not appear to improve respiratory manifestations of obstructive sleep apnea. Permanent atrial pacing in this patient population does not appear to be justified.     

Importance of the "atrial kick" in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 +/- 0.9 vs 5.2 +/- 0.8 liters/min at 110 beats/min, 4.2 +/- 0.9 vs 5.1 +/- 0.9 liters/min at 140 beats/min; p less than 0.05) and LV end-diastolic volume (77 +/- 27 vs 93 +/- 29 ml at 110 beats/min, 54 +/- 17 vs 65 +/- 19 ml at 140 beats/min; p less than 0.05), an increase in left atrial pressure (28 +/- 3 vs 20 +/- 5 mm Hg at 110 beats/min, 30 +/- 4 vs 25 +/- 5 mm Hg at 140 beats/min; p less than 0.05), and a decrease in mitral valve area (1.2 +/- 0.4 vs 1.4 +/- 0.5 cm2 at 110 beats/min, 1.2 +/- 0.4 vs 1.4 +/- 0.4 cm2 at 140 beats/min; p less than 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.     

Does atrial overdrive pacing prevent paroxysmal atrial fibrillation in paced patients?

The role of atrial overdrive pacing for the suppression of paroxysmal atrial fibrillation remains unclear. To investigate this we have performed a randomised study evaluating the role of an increased atrial base rate in suppressing this arrhythmia in patients implanted with a permanent pacemaker (Chorum ELA) for sick sinus syndrome with previous documented paroxysmal atrial fibrillation. Twenty-seven patients (mean age, 69; 15 female) were randomised to two 3-month single-blinded crossover periods of DDDR pacing. The pacemaker was set with a base rate of 60 bpm (normal) during one period and at 10 bpm (overdrive) above the average heart rate during the other, mean (S.D.) 75+/-7 beats/min (range, 70-96). The fallback algorithm of the pacemaker was activated to record the number and duration of paroxysmal atrial fibrillation episodes. During the overdrive period there was a significant increase in the total duration of atrial pacing (normal 60+/-26% vs. overdrive 72+/-28%, P<0.001). However there was no significant difference in the number of paroxysmal atrial fibrillation episodes (normal 43+/-109 vs. overdrive 43+/-106, P=ns), or their total duration (normal 42+/-108 h vs. overdrive 99+/-254 h, P=ns). In conclusion, atrial overdrive pacing, achieved by increasing the atrial base rate, has no incremental benefit in the suppression of paroxysmal atrial fibrillation when compared to rate responsive pacing with a base rate of 60 bpm.     

Effects of altered site of electrical activation on myocardial performance during inotropic stimulation

The effects of altering the site of electrical activation on responses to isoproterenol (ISO) and treadmill exercise were examined in mongrel dogs instrumented for long-term measurement of left ventricular pressure, left ventricular dP/dt, coronary blood flow, cardiac output, left ventricular diameters, and mean arterial pressure and O2 content in the coronary sinus and aorta. During spontaneous rhythm, 0.2 micrograms/kg/min ISO increased heart rate by 90 +/- 7 beats/min, left ventricular dP/dt by 2479 +/- 301 mm Hg/sec, cardiac output by 3.5 +/- 0.9 liters/min, coronary blood flow by 30.4 +/- 3.9 ml/min, and myocardial oxygen consumption (MVO2) by 3.91 +/- 0.84 ml/min. During right atrial pacing at 193 +/- 7 beats/min, the effects of ISO were not different from the effects during spontaneous rhythm, with the exception of a lesser increase in coronary blood flow and lesser reductions in coronary resistance and left ventricular end-diastolic diameter and pressure. During right ventricular pacing at an identical rate, ISO increased left ventricular dP/dt (1140 +/- 158 mm Hg/sec) and cardiac output (2.2 +/- 0.5 liters/min) significantly less (p less than .025) than during either sinus rhythm or right atrial pacing, while MVO2 rose to a higher value. During right ventricular pacing the changes in mean arterial pressure and left ventricular end-diastolic diameters with ISO were not significantly different from those during right atrial pacing. Treadmill exercise induced significantly smaller (p less than .025) increases in left ventricular dP/dt during right ventricular pacing as compared with during either right atrial pacing or sinus rhythm, while MVO2 rose to a higher value.(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormal lipid peroxidation in patients with sleep apnoea.

The prevalence of cardiovascular diseases is increased in patients with the obstructive sleep apnoea syndrome (OSAS). The fall and rise of arterial oxygenation that follows each apnoea may increase lipid peroxidation and contributes to explaining this association. In the present study, the authors determined lipid peroxidation in patients with OSAS and the effect of treatment with continuous positive airway pressure (CPAP). Fourteen male patients with severe OSAS (59+/-5 apnoea x h(-1)) (+/-SEM) and 13 healthy nonsmoking, male volunteers of similar age were studied. Patients were studied at diagnosis and after treatment with CPAP for more than 1 yr (>4 h x night(-1)). A venous blood sample was obtained early in the morning after fasting all night. In patients with OSAS, a sample before and during sleep was also obtained. Low density lipoprotein (LDL) particles were isolated by sequential ultracentrifugation. Their level of oxidation was determined by the thiobarbituric acid assay (TBARs), and their susceptibility to oxidation by the lag phase measurement. Patients with OSAS showed higher TBARs (28.1+/-2.8 versus 20.0+/-1.8 nmol x malondialdehyde x mgLDL protein(-1), p=0.02) and shorter lag phase values (83.8+/-3.4 versus 99.7+/-3.4 min, p=0.005) than controls. These differences were not due to the smoking status of the patient. Likewise, these values did not change significantly throughout the night yet, the lag phase value was significantly improved by treatment with CPAP (124.9+/-8.5 min; p<0.001). These results indicate that obstructive sleep apnoea syndrome is associated with abnormal lipid peroxidation and that this is improved by chronic use of Continuous positive airway pressure. These results can contribute towards explaining the high prevalence of cardiovascular diseases seen in Obstructive sleep apnoea syndrome.     

Impact of obstructive sleep apnoea on left ventricular mass and global function.

Obstructive sleep apnoea syndrome (OSAS) might be a cause of heart failure. The present study aimed to assess left ventricular mass and myocardial performance index (MPI) in OSAS patients. A total of 67 subjects without any cardiac or pulmonary disease, referred for evaluation of OSAS, had overnight polysomnography and echocardiography. According to apnoea-hypopnoea index (AHI), subjects were classified into three groups: mild OSAS (AHI: 5-14; n = 16), moderate OSAS (AHI: 15-29; n = 18), and severe OSAS (AHI: > or = 30; n = 33). Thickness of interventricular septum (IVS) and posterior wall (LVPW) were measured by M-mode, along with left ventricular mass (LVM) and LVM index (LVMI). Left ventricular MPI was calculated as (isovolumic contraction time+isovolumic relaxation time)/aortic ejection time by D?ppler echocardiography. There were no differences in age or body mass index among the groups, but blood pressures were higher in severe OSAS compared with moderate and mild OSAS. In severe OSAS, thickness of IVS (11.2+/-1.1 mm), LVPW (11.4+/-0.9 mm), LVM (298.8+/-83.1 g) and LVMI (144.7+/-39.8 g x m(-2)) were higher than in moderate OSAS (10.9+/-1.3 mm; 10.8+/-0.9 mm; 287.3+/-74.6 g; 126.5+/-41.2 g x m(-2), respectively) and mild OSAS (9.9+/-0.9 mm; 9.8+/-0.8 mm; 225.6+/-84.3 g; 100.5+/-42.3 g x m(-2), respectively). In severe OSAS, MPI (0.64+/-0.14) was significantly higher than in mild OSAS (0.50+/-0.09), but not significantly higher than moderate OSAS (0.60+/-0.10). In conclusion, severe and moderate obstructive sleep apnoea syndrome patients had higher left ventricular mass and left ventricular mass index, and also left ventricular global dysfunction.     

Subjective efficacy of nasal CPAP therapy in obstructive sleep apnoea syndrome: a prospective controlled study.

The response to nasal continuous positive airways pressure (nCPAP) of a wide variety of symptoms recognized to be associated with obstructive sleep apnoea syndrome (OSAS) was examined. Fifty-six consecutive patients with OSAS, confirmed by polysomnography (mean (SD) apnoea-hypopnoea index (AHI) 49.6 (22.6) events x h(-1), Epworth score 15.4 (5.0)), were asked to complete paired symptom evaluation questionnaires, before treatment and again after 4 months of nCPAP. The response rate was 80%. A control group of 21 consecutive OSAS patients of similar age, body mass index (BMI), AHI and Epworth score to the treated group but managed with conservative measures, completed the same questionnaires on two occasions, 4 months apart. The nCPAP-treated group showed significant reductions (Wilcoxon matched pairs test) in the symptoms of daytime sleepiness, restless sleep, heartburn, nocturia, enuresis, headache and nocturnal sweating, whereas controls showed no significant changes in these symptoms. There were no changes in BMI, smoking, alcohol consumption or exercise habits in either group. It was concluded that, in addition to improvements in symptoms of daytime sleepiness and restless sleep, a wide range of other symptoms may improve significantly with nasal continuous positive airways pressure therapy.     

Atrial rate-responsive pacing in sinus node disease

Patients with sinus node disease (SND) who are unable to achieve an adequate increase in heart rate during exercise are candidates for atrial rate-responsive pacing (AAI-R). We have implanted 40 AAI-R systems in SND patients with an average follow-up of 12.5 +/- 8 (range 3-30) months. All the patients received an activity-sensing pulse generator (Activitrax, Medtronic or Sensolog, Siemens-Pacesetter) with a single atrial lead. Only patients with an intraoperative AV nodal block cycle-length above 100 beats min-1 were included. During follow-up, one patient was observed to have transient asymptomatic 2:1 AV-block during sleep. No patient developed persistent AV-block or chronic atrial fibrillation. Twelve patients with persistent chronotropic incompetence were assigned for a randomized double-blind crossover study, comparing exercise treadmill capacity in AAI-R with conventional atrial inhibited pacing (AAI). During AAI-R pacing the maximum heart rate during exercise was 120 +/- 1 beats min-1 compared with 97 +/- 21 beats min-1 during AAI pacing (P less than 0.01). The average exercise time increased from 11.2 +/- 2 min during AAI-pacing to 13.4 +/- 3 min during AAI-R pacing (P less than 0.01). AAI pacing should be considered for patients with SND and chronotropic incompetence.     

Electrocardiographic signal-averaging during atrial pacing and effect of cycle length on the terminal QRS in patients with and without inducible ventricular tachycardia

Electrocardiographic signal-averaging during sinus rhythm (61 to 99 beats/min) and atrial pacing (100 to 171 beats/min) were performed to determine the effect of heart rate on late potentials in 15 patients without (group 1) and 7 patients with (group 2) inducible sustained ventricular tachycardia (VT). In sinus rhythm (79 +/- 12 vs 77 +/- 12 beats/min, difference not significant), the duration of the low-amplitude signal less than 40 microV was longer in group 2 than group 1 (43 +/- 21 vs 26 +/- 8 ms, p = 0.034) and more patients had late potentials (57 vs 7%, p = 0.021), but QRS duration (121 +/- 32 vs 98 +/- 19 ms) and terminal voltage (33 +/- 33 vs 50 +/- 26 ms) were not significantly different. With atrial pacing in group 1 (128 +/- 16 beats/min), 3 patients developed a simultaneous decrease in terminal voltage and an increase in terminal QRS duration consistent with a late potential, but mean total and terminal durations were unchanged. Terminal voltage increased (50 +/- 26 to 59 +/- 40) but not significantly. With atrial pacing in group 2 (119 +/- 12 beats/min) all patients either had a late potential or developed a simultaneous decrease in terminal voltage and an increase in terminal QRS duration (p = 0.001 vs group 1). Root mean square (p = 0.001 vs group 1). Root mean square voltage decreased (33 +/- 23 to 22 +/- 23) and became significantly different from group 1 (p = 0.017). Mean QRS duration, root mean square terminal voltage and low-amplitude terminal QRS duration, however, were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Total energy expenditure in children with obstructive sleep apnoea syndrome.

Childhood obstructive sleep apnoea syndrome (OSAS) acts as a check on growth and nutritional status. An increase in sleeping energy expenditure has been proposed as a possible mechanism, but to date, no studies have determined whether energy requirements (total energy expenditure; TEE) are raised in OSAS. The aim of this study was to test the hypothesis that OSAS is associated with increased TEE. Eleven children (mean+/-SD 5.8+/-2.2 yrs of age) with OSAS confirmed by nocturnal polysomnography were each matched with a pair of healthy controls (n=22) of the same age and sex. TEE was measured using the doubly-labelled water method in all subjects. In 10/11 patients TEE was also measured after adenotonsillectomy and changes in TEE assessed. There was no significant difference in TEE between patients (mean+/-SD 325+/-44 kJ x kg(-1) x day(-1)) and controls (339+/-48 kJ x kg(-1) x day(-1)), nor between patients and age- and sex-specific literature data on TEE, using the doubly-labelled water method. Differences in TEE within patients, before versus after surgery, were minor and not statistically significant. This study does not support the hypothesis that obstructive sleep apnoea syndrome in childhood is associated with increased energy requirements, and suggests that alternative explanations for the effect of this syndrome on growth and energy balance should be sought.     

Prevention of immediate reinitiation of atrial tachyarrhythmias by high-rate overdrive pacing: results from a prospective randomized trial

INTRODUCTION: Immediate reinitiation of atrial tachyarrhythmia (IRAT) is an important cause of failure to maintain sinus rhythm. IRAT prevention by overdrive pacing has not been evaluated in a prospective randomized trial. METHODS AND RESULTS: Patients with a DDDRP pacemaker offering temporary atrial overdrive pacing after AT termination (Post Mode Switching Overdrive Pacing [PMOP]) were enrolled into the prospective PIRAT (Prevention of IRAT) trial if paroxysmal AT episodes occurred after implantation. PMOP was randomly activated (120 beats/min for 2 min) or inactive. After 3 months, device memory was interrogated, symptoms and quality of life assessed, and patients crossed over to the alternative treatment arm for another 3 months. Primary study endpoint was the number of AT episodes; secondary endpoints were the cumulative time in AT (AT burden), percentage of AT episodes with IRAT, symptoms, and quality of life with PMOP active versus inactive. In 37 patients (21 men; 69 +/- 9 years), there was no difference in the median number of AT episodes (0.37 vs 0.34 per day), AT burden (both 1%), percentage of episodes with IRAT (30%vs 28%), symptoms, and quality of life during PMOP off versus on. With PMOP active, 29% of 439 ATs restarted during and 18% before PMOP intervention. The PMOP-induced rate increase appeared to be associated with IRAT in 9% of AT episodes. CONCLUSION: Automatic overdrive pacing after AT termination did not prevent IRAT, mainly due to insufficient overdrive suppression even at 120 beats/min and the delay between AT termination and PMOP intervention.     

Nocturnal blood pressure during apnoeic and ventilatory periods in patients with obstructive sleep apnoea.

The exact nature of asleep blood pressure in relation to awake blood pressure is still unclear in patients with obstructive sleep apnoea. This study aimed: 1) to investigate the asleep blood pressure in both apnoeic and ventilatory periods; 2) to determine the diurnal and nocturnal factors correlated with the changes in blood pressure from apnoea to ventilatory periods during sleep. Thirty-two patients, newly diagnosed as moderate to severe obstructive sleep apnoea with a standard nocturnal polysomnography, were enrolled. The blood pressure was monitored by using the noninvasive continuous monitoring method during polysomnographic study. The mean blood pressures in ventilatory periods during nonrapid eye movement (NREM) and rapid eye movement (REM) sleep were 117.5+/-17.9 mm Hg and 128.8+/-21.9 mm Hg, and those in apnoea periods were 94.5+/-15.4 mm Hg and 102.7+/-19.0 mm Hg. The average blood pressure during NREM sleep (103.0+/-16.1 mm Hg) was higher than the awake blood pressure (97.0+/-15.7 mm Hg). The blood pressure during REM sleep was greater than that during NREM sleep. The changes in the nocturnal blood pressure from apnoea to ventilatory periods were inversely correlated with the age and nocturnal mean nadir saturation. In conclusion, patients with obstructive sleep apnoea have higher asleep blood pressure than awake blood pressure.     

Effect of moderate alcohol upon obstructive sleep apnoea.

Moderate-to-large quantities of alcohol are known to aggravate severe obstructive sleep apnoea (OSA), however, the reported effects of moderate alcohol consumption upon mild-to-moderate OSA are inconsistent. Given the reported benefits of moderate alcohol consumption on cardiovascular mortality, recommendations regarding the management of patients with OSA are difficult to formulate. The aim of this study was to evaluate the effects of moderate alcohol on sleep and breathing in subjects with mild-to-moderate OSA. Twenty-one male volunteers, who snored habitually, underwent polysomnography with and without 0.5 g alcohol x kg body weight (BW)(-1) consumed 90 min prior to sleep time, in random order. The mean blood alcohol concentration (BAC) following alcohol at the time of lights out was 0.07 g x dL(-1). The distribution amongst the various sleep stages was not significantly altered by alcohol. The mean apnoea/hypopnoea index rose from 7.1+/-1.9 to 9.7+/-2.1 events x h(-1) (mean+/-SEM, p=0.017); however, there was no significant change in the minimum arterial oxygen saturation measured by pulse oximetry Sp,O2, apnoea length or snoring intensity. Mean sleep cardiac frequency rose significantly from 53.9+/-1.4 to 59.9+/-1.9 beats x min(-1) (P<0.001) and overnight urinary noradrenalin increased from 14.9+/-2.3 to 18.8+/-2.3 nmol x mmol creatinine(-1) (p=0.061) on the alcohol night compared to the nonalcohol night. To conclude, modest alcohol consumption, giving a mean blood alcohol concentration of 0.07 g x dL(-1), significantly increases both obstructive sleep apnoea frequency and mean sleep cardiac frequency.