Reappraisal of the vasodepressor reflex in carotid sinus syndrome.
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BACKGROUND: The evaluation of the vasodepressor (VD) reflex of the carotid sinus syndrome is usually inaccurate, due to the difficulty in blood pressure measurement. AIM: To study the VD reflex with a beat-to-beat not invasive technique. METHODS: We investigated 68 patients (49 males, 19 females; mean age 70 +/- 11 years) affected by carotid sinus syndrome: cardioinhibitory (CI) form was present in 47 patients, mixed (M) form in 10 patients and VD form in 11 patients. The control group consisted of 9 patients (6 male, mean age 71 +/- 8 years) affected by third degree atrioventricular block who had received the implant of a permanent pacemaker and were pacemaker-dependent with a prolonged asystole at time of temporary inhibition of the pacemaker itself. The study of the VD reflex was performed in the supine position; beat-to-beat arterial systolic pressure was monitored by a photoplethysmographic method using a finger cuff (Finapres technique). RESULTS: In all the patients the carotid sinus massage caused a marked fall in systolic blood pressure which was greatest at the end of the massage: from 143 +/- 25 mm Hg to 74 +/- 20 mm Hg in the patients with CI form, from 144 +/- 14 mm Hg to 76 +/- 18 mm Hg in those with M form and from 125 +/- 26 mm Hg to 65 +/- 13 mm Hg in those with VD form. A decrease in systolic blood pressure > or = 50 mm Hg occurred in 84% of cases. Afterwards, the patients with CI form had a progressive increase of systolic blood pressure that reached the initial value after a mean of 27 seconds. In the patients with VD form systolic blood pressure was significantly (p < or = 0.5) lower than that observed in all the other groups, beginning from the third second after the end of the massage; mean systolic blood pressure value remained significantly lower than the initial value for more than 27 seconds. The patients with M form showed an intermediate pattern. Also control group patients showed a fall in systolic blood pressure immediately after pacemaker inhibition (from 152 +/- 29 mm Hg to 87 +/- 25 mm Hg) that was of similar extent than that observed in carotid sinus syndrome patients, but pressure returned to initial value within 9 seconds. CONCLUSIONS: An important VD reflex is present in most patients with carotid sinus syndrome. It lasts more than the CI reflex and it persists for several seconds after the end of the massage. The initial fall of systolic blood pressure is of similar extent in all the forms of carotid sinus syndrome, but the patients with the VD form are characterized by a longer duration and greater entity of the decrease. These results point out the importance of the VD reflex in patients with the carotid sinus syndrome.
The purpose of this study was to evaluate the effects of atrioventricular junction radiofrequency ablation on the quality of life, exercise performance, and echocardiographic parameters in 23 patients with chronic, severely symptomatic, drug-refractory atrial fibrillation or flutter. Initially, patients were randomized to receive ablation plus pacemaker therapy (n = 12) or pacemaker therapy alone (n = 11). After 15 days, palpitations decreased by 92% and 37% (p = 0.004), rest dyspnea by 79% and 40% (p = NS), effort dyspnea by 65% and 30% (p = 0.03), exercise intolerance by 54% and 17% (p = 0.005), and asthenia by 67% and 31% (p = 0.02) in the 2 groups, respectively. At the end of this short-term study, control patients also underwent ablation therapy, and a 3-month intrapatient follow-up study was performed in 22 patients. New York Heart Association functional class > or = 3 was present in 14 patients (64%) before, but in only 3 patients (14%) after ablation therapy (p = 0.002); specific activity scale functional class > or = 3 was present in 9 patients (41%) before, but in only 5 (23%) after ablation therapy (p = NS). Exercise duration during standardized stress testing increased by a mean of 63 +/- 93 seconds (15% increase) (p = 0.001). In the 9 patients with depressed left ventricular systolic function, echocardiographic fractional shortening increased by 34% (from 23 +/- 5% to 31 +/- 9%) (p = 0.003). In the remaining 13 patients with normal systolic function, fractional shortening decreased by 10% (from 40 +/- 5% to 36 +/- 6%) (p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Atrial fibrillation is a relative contraindication to atrial synchronous pacing because of the risk of the tracking of rapid atrial rhythms by the pacemaker. In this study, we describe the clinical results of an AV synchronous rate responsive pacemaker with an original algorithm, which is able to sense pathological increments in atrial rate and automatically to switch into a non-AV synchronous mode of pacing. This pacemaker was implanted in 12 patients who had undergone radiofrequency ablation of the AV junction in order to cure severely symptomatic, drug refractory, paroxysmal atrial fibrillation. In an acute, intrapatient comparison between the standard AV synchronous mode and the automatic switching mode, ventricular tracking of atrial fibrillation occurred in 35% and 4% of total beats at rest and in 24% and 2% of total beats during exercise, respectively (P < 0.001). During 5 +/- 4 months of follow-up, no further tachyarrhythmia related symptoms occurred. In conclusion, the standard DDDR mode is unable to eliminate ventricular tracking of atrial fibrillation, thus undermining the efficacy of AV junction ablation therapy. The automatic switching mode eliminates this adverse effect of dual chamber pacing.
We attempted radiofrequency ablation of the AV junction with a sequential right- and left-sided approach in 78 patients affected by severely symptomatic, drug refractory atrial fibrillation. Stable third-degree AV block was obtained in 99% of cases and, after 3 months, persisted in 92% of cases. Single session, stepwise, radiofrequency modulation of the AV node was attempted in 13 patients with paroxysmal atrial fibrillation. During sinus rhythm, ablation of the slow and fast AV node pathways was performed in order to increase the nodal refractory period or to slow conduction. Clinically successful modulation of AV conduction was achieved in 15% of cases and persisted during a 3-month follow-up. In conclusion, AV junction ablation is a well-established means of treating atrial fibrillation, but implies the implant of a permanent pacemaker. AV node modulation avoids the pacemaker implant, but is efficacious only in a minority of patients. Thus, in patients affected by paroxysmal atrial fibrillation, AV modulation should be attempted first; if this is ineffective, AV ablation can be performed during the same session.
The effects of a 20-mg i.v., bolus of adenosine 5' triphosphate (ATP) on the heart rhythm was studied in 79 patients affected by neurally-mediated syncope (26 cases) or sick sinus syndrome (22 cases) or both syndromes (31 cases) and in 31 healthy control subjects in order to examine the sensitivity of cardiac purinoceptors in such circumstances. During ATP infusion, the sinus cycle lengthened to > 2 seconds in no control, in 1 (4%) patient with neurally-mediated syncope, in 5 (23%) patients with sick sinus syndrome, and in 13 (42%) patients with both neurally-mediated and sick sinus syndromes (P = 0.01). Atrioventricular block occurred in 14 (45%) of controls, in 10 (38%) patients with neurally-mediated syncope, in 4 (18%) patients with sick sinus syndrome, and in 13 (42%) patients with both neurally-mediated syncope and sick sinus syndrome (n.s.). Thus, exogenous ATP exerts different effects on patients with neurally-mediated syncope and patients with sick sinus syndrome. In fact, intrisic disease of the sinus node is necessary to modulate an abnormal adenosine-mediated sinus arrest, whereas patients affected by neurally-mediated syncope alone show a normal sensitivity to the drug administration. The effect of ATP on atrioventricular conduction is greater than that on sinus node and is of similar magnitude in patients and controls; thus the clinical meaning of ATP induced atrioventricular block remains uncertain.
BACKGROUND: Patients with bundle branch block and syncope, especially those with abnormal electrophysiologic study, are at high risk of progression to second-or third-degree atrioventricular block and therefore they often receive a permanent back-up pacemaker. The aim of this study was to evaluate of the incidence of bundle branch block progression to second or third-degree atrioventricular block during long-term follow-up. METHODS: A retrospective study was performed on 60 patients (49 males, age 77 +/- 9 years) with bundle branch block and permanent back-up pacemaker. The patients were subdivided into 3 groups: 13 patients, at pre-implant electrophysiologic study had HV interval > or = 100 msec and/or second- or third-degree atrioventricular block induced by ajmaline i.v. administration (Group 1); 20 patients with HV interval of 70-100 msec and/or HV > or = 120 msec after ajmaline administration (Group 2); 27 patients who had received a permanent pacemaker because of carotid sinus syndrome or sick sinus syndrome (22 patients) or because of recurrent syncopes and negative electrophysiologic study (5 patients) (Group 3). RESULTS: During a mean follow-up of 62 +/- 41 months, 17/60 patients (28%) had progression to second- (n = 4) or third-degree (n = 13) atrioventricular block: atrioventricular block occurred in 54% of Group 1 patients in 25% of Group 2 patients and in 19% of Group 3 patients. The actuarial rate of progression to atrioventricular block for the overall population was, at 5 and 10 years, 25% and 58% respectively; in Group 1 it was 46% and 62%; in Group 2 it was 22% and 55% and in Group 3 it was 21% and 59% (p = 0.06). The patients with right bundle branch block and left anterior hemiblock were at higher risk of progression to atrioventricular block than those with right bundle branch block or left bundle branch block (risk 42% vs 14%, p = 0.06). The presence of an abnormal electrophysiologic study did not increase the progression rate either in the patients with right bundle branch block and left anterior hemiblock (risk of 43%), nor did it in those patients with other types of bundle branch block (risk of 18%). Moreover, the induction of second- or third-degree atrioventricular block during ajmaline administration was associated with a higher risk of block during the follow-up (60% vs 25%, p = 0.06). CONCLUSIONS: Patients treated with pacemaker because of symptomatic bundle branch block have a high risk of progression to second- or third-degree atrioventricular block in the long-term follow-up. The results argue against the practical usefulness of electrophysiological study since a risk stratification could be obtained by the simpler surface electrocardiogram; moreover, risk of block was also present in the patients affected by carotid sinus syndrome or sick sinus syndrome, and in those affected by unexplained syncope with negative electrophysiologic study.
The occurrence rate of spontaneous asystolic episodes during long-term follow-up in patients with abnormal asystolic responses induced by means of vasovagal maneuvers was evaluated. The heart rate of 23 patients (mean age 64 +/- 12 years; 6 women and 17 men) affected by neurally mediated syncope (mean 4.3 +/- 4.9 episodes) was continuously monitored by a specially designed implanted pacemaker able to detect and store in its memory all asystolic episodes lasting 3 to 6 or > 6 seconds. Asystolic, neurally mediated syncope was diagnosed when a reflex asystole of > 3 seconds was induced during carotid sinus massage (n = 22), eyeball compression test (n = 3) or head-up tilt test (n = 2). During a total of 357 months (mean 15 +/- 7) of monitoring, asystolic episodes occurred in 17 patients (74%): 1,765 episodes of 3- to 6-second (median 3) duration occurred in 14 patients, and 47 episodes of > 6-second (median 2) duration occurred in 11. The actuarial estimates of occurrence of asystolic episodes of > 3 and > 6 seconds were 82 and 53%, respectively, after 2 years of follow-up. Only 12 episodes of 3 to 6 seconds (0.7%), and 20 episodes of > 6 seconds (43%) resulted in presyncopal or syncopal symptoms. Thus, an asystolic response to vasovagal maneuvers predicts the occurrence of spontaneous asystolic episodes during follow-up. With few exceptions, spontaneous episodes are asymptomatic and their incidence is low.
OBJECTIVES: The purpose of this study was to evaluate the role of autonomic reflexes in the genesis of syncope associated with the onset of paroxysmal atrial fibrillation. BACKGROUND: Syncope associated with paroxysmal atrial fibrillation has been interpreted as an ominous finding predictive of rapid ventricular rates. However, various mechanisms may be involved when heart rate is not particularly high. METHODS: Forty patients (age 60 +/- 14 years, 20 men, 20 women) with syncope and atrial fibrillation were compared with atrial fibrillation without syncope. Carotid sinus massage and head-up tilt testing (at 60 degrees for 60 min at baseline and during isoproterenol infusion) were performed during sinus rhythm. A positive response was defined as the induction of syncope. Atrial fibrillation was also induced on a tilt table at 60 degrees by means of short bursts of atrial pacing. RESULTS: Results of carotid sinus massage were positive in 15 (37%) of 40 patients but in no control subjects (p = 0.002). Head-up tilt test findings were positive in 25 (66%) of 38 patients and in 2 (12%) of 16 control subjects (p = 0.0004). The induction of atrial fibrillation in the upright position elicited syncope in 16 (42%) of 38 patients but in none of 16 control subjects (p = 0.001). At the beginning of atrial fibrillation, systolic blood pressure was lower in patients than in control subjects (88 +/- 32 vs. 127 +/- 32 mm Hg), whereas mean heart rate was similar (142 +/- 35 vs. 134 +/- 25 beats/min). The correlation between heart rate and systolic blood pressure was weak (r = 0.35), and in five patients syncope occurred at a heart rate < or = 130 beats/min. At the time of syncope, heart rate decreased (-12 +/- 21 beats/min) in patients with induced syncope, whereas it remained unchanged in patients without induced syncope (+1 +/- 17 beats/min, p = 0.04) or slightly increased in control subjects (+9 +/- 21 beats/min, p = 0.009). CONCLUSIONS: Patients with syncope associated with paroxysmal atrial fibrillation are predisposed to an abnormal neural response during both sinus rhythm and arrhythmia. In some patients the onset of atrial fibrillation triggers vasovagal syncope.
OBJECTIVES: This study investigates the role of an abnormal neural reflex in causing syncope in patients with sinus bradycardia. BACKGROUND: Syncope is commonly considered an indication of severity in sinus bradycardia. However, the occurrence of syncope is unpredictable, and the prognosis appears to be similar in patients with and without syncope. METHODS: Head-up tilt testing (60 degrees for 60 min), carotid sinus massage in the supine and standing positions, 24-h Holter ambulatory electrocardiographic (ECG) recording and electrophysiologic study before and after pharmacologic autonomic blockade were performed in 25 patients with sinus bradycardia and syncope (group I, sinus rate < 50 beats/min, age 71 +/- 12 years) and 25 patients with sinus bradycardia and no neurologic symptoms (group II, sinus rate < 50 beats/min, age 67 +/- 16 years). RESULTS: Clinical characteristics and ambulatory ECG monitoring data were similar in the two study groups. A positive response (induction of syncope or presyncope with hypotension and/or bradycardia) was obtained by head-up tilt testing in 15 group I (60%) and in 3 group II (12%) patients (p < 0.001) and by carotid sinus massage in 11 group I (44%) and 6 group II (24%) patients (p = NS). Results of at least one test (head-up tilt testing or carotid sinus massage, or both) were positive in 19 group I (76%) and 9 group II (36%) patients (p < 0.01). Basal and intrinsic corrected sinus node recovery time did not differ significantly between the two groups. An abnormal intrinsic heart rate was present in 66% of group I and 26% of group II patients (p < 0.01). The different percentage of positive findings on head-up tilt testing and carotid sinus massage in the two groups was independent of the presence of intrinsic sinus node dysfunction. CONCLUSIONS: These results indicate that an abnormal neural reflex plays a role in causing syncope in patients with sinus bradycardia. This reflex seems to be unrelated to the severity of sinus node dysfunction, even if the latter could enhance the cardioinhibitory response.
To study the efficacy of medical treatment for preventing syncopal recurrences in patients affected by tilt-induced neurally mediated syncope, a randomized placebo-treatment prospective study was performed in 30 patients (10 men and 20 women, mean age 42 +/- 21 years) who had syncope reproduced in 2 consecutive head-up tilt-table tests without pharmacologic intervention (n = 20) or during isoproterenol infusion (n = 10). Patients were randomly assigned to 2 groups: 15 to placebo, and 15 to drug therapy (determined on the basis of serial pharmacologic tilting tests). Therapy was either atenolol (n = 7), dihydroergotamine (n = 2), domperidone (n = 2), cafedrine (n = 1), or elastic compression stockings, alone or in association with drugs (n = 3). During a mean of 10 +/- 7 months of follow-up, syncope recurred in 3 patients (20%) in the treatment group and in 4 (27%) in the placebo group; actuarial rates of absence of syncopal recurrences after 20 months were 70 and 67%, respectively. Thus, the outcome of either treated or untreated patients was favorable (with a low recurrence rate of syncope), and the usefulness of tilting-guided medical therapy remains uncertain.
The natural history of patients with severe carotid sinus syndrome, and the efficacy of permanent pacemaker treatment are not clearly known. A randomized treatment/nontreatment prospective study was performed in 60 patients affected by carotid sinus syndrome whose symptoms were judged to involve risk of major trauma or interfered with their daily activity. They were randomly assigned to 2 groups: 28 patients to no therapy (nonpacing group), and 32 to VVI (n = 18) or DDD (n = 14) pacemaker implant (pacing group). Syncope recurred in 16 patients (57%) of the nopacing group (mean follow-up 36 +/- 10 months) and in only 3 (9%) of the pacing group (mean follow-up 34 +/- 10 months) (p = 0.0002); moreover, 19 (68%) in the nonpacing group needed a secondary pacemaker implant because of the severity of symptoms. The actuarial rate of absence of syncopal recurrence after 1, 2, 3 and 4 years was 64, 54, 38 and 38%, respectively, for the nonpacing group, and 100, 97, 93 and 84%, respectively, for the pacing group (p = 0.0001). The actuarial rate of absence of minor symptoms after 1, 2, 3 and 4 years was 21, 14, 7 and 7%, respectively, for the nonpacing group and 66, 43, 27 and 27%, respectively, for the pacing group (p = 0.002). Reproducibility of carotid sinus reflex was tested after 15 +/- 8 months in 54 patients; an abnormal response to carotid sinus massage persisted in all 54. In conclusion, symptoms recur in most patients with untreated carotid sinus syndrome, and pacing is a useful therapy for preventing recurrences.
We have studied the electrophysiology of the sinus node and the role of the autonomic nervous system on sinus node function in 8 thyrotoxic patients of both sexes, 37.5 +/- 4.3 (mean +/- SE) yr old. The resting heart rate (RHR), the sino-atrial conduction time (SACT), and the sinus node recovery time (SNRT) were measured in the untreated condition (basal), after sympathetic blockade with propranolol 0.2 mg/kg body weight (BW) i.v. infusion, and after complete autonomic blockade with the additional administration of atropine 0.04 mg/kg BW i.v. bolus. 1) In the thyrotoxic patients the RHR was higher [117 +/- 6 beats per min (bpm)] than in 20 normal subjects (73 +/- 1 bpm, P less than 0.001), whereas the SACT and SNRT values were not different. 2) After sympathetic blockade with propranolol, the RHR decrement and SACT increase were greater in the hyperthyroid patients than in normal subjects, whereas there was no difference in SNRT values between the two groups. 3) In the thyrotoxic patients the complete autonomic blockade reestablished the electrophysiological parameters to values similar to those observed in basal condition. In conclusion, in thyrotoxic patients the intrinsic activity of the sinus node is increased. It appears that this is a direct consequence of thyroid hormone excess, rather than an effect of extrinsic influences exerted by the autonomic nervous system on sinus node activity.
It is generally accepted that a positive response to carotid sinus massage (CSM) or head-up tilt (HUT) in patients affected by syncope suggests a reflex cause of the syncope. To study the role of the autonomic nervous system in causing syncope in the sick sinus syndrome (SSS), CSM and HUT were performed in 35 consecutive patients (20 men, mean age 70 +/- 9 years) with syncope and SSS. Results were compared with those in 35 patients affected by syncope that, despite careful cardiovascular and neurologic examination, were of uncertain origin (21 men; mean age 68 +/- 9 years) and with those of 35 subjects without syncope (20 men; mean age 69 +/- 10). All patients underwent CSM in the supine and standing positions for 10 seconds and HUT to 60 degrees for 60 minutes. In the patients with SSS, the full reproduction of spontaneous symptoms by CSM occurred in 21 (60%) and by HUT, in 19 (54%). At least 1 test was positive in 28 patients (80%): cardioinhibitory or mixed responses in 69%, vasodepressor responses in 11%. The percentages of positive tests in the patients with syncope of uncertain origin were similar to or slightly less than those of patients with SSS (CSM 63%, HUT 26%, overall 74%) with cardioinhibitory or mixed responses in 54% and vasodepressor in 20% (p less than 0.05). In control subjects, syncope was induced by CSM in 1 (3%) and by HUT in 2 (6%); overall positivity was 9%. In conclusion, in most patients affected by syncope and SSS, an abnormal neural reflex probably plays a major role in causing syncope.(ABSTRACT TRUNCATED AT 250 WORDS)
To verify the role of abnormal neural mechanisms in unexplained syncopes, we evaluated the results of carotid sinus massage (CSM), eyeball compression (EBC), and head-up tilt test (HUT) in the basal state (B) and during isoproterenol infusion (ISO) in: (1) 100 consecutive patients affected by syncope which, despite careful cardiovascular and neurologic examination, was of uncertain origin (age 60 +/- 18 years; 54 men) and (2) 25 healthy subjects matched 4:1 with the patients of the previous group. All the patients underwent CSM and EBC in the supine and standing position for 10 seconds and HUT at 60 degrees for 60 minutes; if HUT-B was negative (68 cases), it was repeated during ISO (1 to 5 micrograms/min) infusion. In the patients with uncertain syncope, spontaneous symptoms were fully reproduced in 49%, 16%, 32%, and 16% of cases respectively by means of CSM, EBC, HUT, and HUT-ISO; overall positivity for at least one test was observed in 79% of cases. The results of CSM, EBC, or HUT-ISO were linked to age, sex, and underlying heart disease. In the healthy subjects, syncope was induced by CSM, EBC, HUT, and HUT-ISO in one case each; overall positivity was 16%. In conclusion, neural reflex induction tests reproduced spontaneous symptoms in most patients affected by uncertain syncope, while they evoked normal responses in most healthy subjects. Therefore on the basis of results of induction tests, the diagnosis of neurally mediated syncope can be ascribed to most patients affected by syncope of uncertain origin.
ECG recording of spontaneous, neurally-mediated syncope is rare. We have observed ten patients who sustained 70 syncopal episodes in whom: (1) ECG monitoring recorded syncope caused by ventricular asystole (AV block, three patients; sinus arrest; seven patients); (2) syncope and the spontaneously observed arrhythmias were reproducible by carotid sinus massage, upright tilt test, or eyeball pressure; and (3) no discernable cause of precipitating factors were detected. Two patients had a history of cardiac disease and four patients had only mild nonclinical ECG or echocardiographic abnormalities. Syncopal episodes recorded during Holter monitoring were of sudden onset in four patients and preceded by prodromal symptoms in six patients. The maximum RR pause was 9.4 +/- 3.7 seconds (range 4.5-15). Electrophysiological evaluation was normal in seven patients. Slight sinus node dysfunction or atrioventricular conduction abnormalities were noted in three others. The clinical characteristics of spontaneous and induced episodes strongly suggest that increased vagal tone played a role in causing the spontaneous events. Vagal stimulation tests are useful for the diagnosis of syncope of unknown origin.
A new method for selection of the pacing mode in 60 consecutive patients with severe cardioinhibitory or mixed carotid sinus syndrome was prospectively validated. DDD pacing was preferred for 26 patients with: (1) the cardioinhibitory form and who had symptomatic pacemaker effect; (2) mixed type I form, (cardioinhibitory and vasodepressor) with symptomatic pacemaker effect, ventriculoatrial conduction or orthostatic hypotension; (3) mixed type II; or (4) severe bradycardia. VVI pacing was selected in the remaining 34 patients without these symptoms. During a 32 +/- 10 month follow-up period syncope and severe dizziness persisted in five patients in the VVI group (15%) and in three patients in the DDD group (12%). Symptomatic relief occurred in 87% (52/60) of patients. Minor symptoms persisted in 47% of the VVI group and 42% of the DDD group. No patient developed cardiac insufficiency or intolerance to pacing. During a 2-month duration a single-blind, randomized, cross-over study compared VVI and DDD pacing, 69% of the patients programmed from DDD to VVI suffered more frequent, severe, and intolerable symptoms. (1) Thirty four of 60 patients (57% of the entire group) in whom VVI pacing was satisfactory were identified prior to pacemaker implant. In the remainder, VVI pacing was contraindicated as it produced frequent side effects. (2) The preimplant predictive value that VVI pacing would be successful was 85% for those eventually receiving VVI pacemakers and the preimplant predictive value that VVI pacing would fail was 69% for those who underwent DDD implant.
In patients affected by high degree AV block without preexisting congestive heart failure there is no definite demonstration that DDD pacing gives real clinical advantages in respect to VVIR pacing. We performed an intrapatient, long-term study between the two pacing modes in 14 high degree AV block patients, using the Medtronic Synergyst 7027 dual chamber pacemaker, who could be programmed alternatively in DDD or VVIR mode. After a 4-week run-in period following the pacemaker implant, patients completed a randomized, double-blind, cross-over study to compare the effect of 6-week period VVIR and DDD pacing on symptoms and cardiovascular parameters. A semiquantitative score scale was used to quantify the symptoms of general well-being, palpitations, dizziness, pulsating sensation in the neck or abdomen, shortness of breath at rest and during effort, chest pain, and NYHA classification. The sum of symptom scores was 10.4 +/- 6.7 in VVIR period and 4.6 +/- 2.7 in DDD period (P less than 0.001); five patients (36%) crossed over early from VVIR to DDD because of intolerable symptoms; overall, eight patients preferred the DDD mode and no one preferred the VVIR. Cardiac output at rest (echo-Doppler method) was 4.7 +/- 1.4 versus 5.7 +/- 1.6 liter/min (P less than 0.01), body weight was 65.9 +/- 6.6 versus 64.9 +/- 6.1 kg (P less than 0.02), atrial natriuretic peptide was 236 +/- 112 versus 198 +/- 110 pg/mL (P less than 0.01), respectively, during VVIR and DDD modes. Effort tolerance was similar with the two modes of pacing (68 +/- 15 vs 70 +/- 18 watts/min).(ABSTRACT TRUNCATED AT 250 WORDS)