Risk factors related to infections of implanted pacemakers and cardioverter-defibrillators: results of a large prospective study.

BACKGROUND: The Prospective Evaluation of Pacemaker Lead Endocarditis study is a multicenter, prospective survey of the incidence and risk factors of infectious complications after implantation of pacemakers and cardioverter-defibrillators. METHODS AND RESULTS: Between January 1, 2000, and December 31, 2000, 6319 consecutive recipients of implantable systems were enrolled at 44 medical centers and followed up for 12 months. All infectious complications were recorded, and their occurrence was related to the baseline demographic, clinical, and procedural characteristics. Among 5866 pacing systems, 3789 included 2 and 117 had >2 leads; among 453 implantable cardioverter-defibrillators, 178 were dual-lead systems. A total of 4461 de novo implantations occurred and 1858 pulse generator or lead replacements. Reinterventions were performed before hospital discharge in 101 patients. Single- and multiple-variable logistic regression analyses were performed to identify risk factors; adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated. At 12 months, device-related infections were reported in 42 patients (0.68%; 95% CI, 0.47 to 0.89). The occurrence of infection was positively correlated with fever within 24 hours before the implantation procedure (aOR, 5.83; 95% CI, 2.00 to 16.98), use of temporary pacing before the implantation procedure (aOR, 2.46; 95% CI, 1.09 to 5.13), and early reinterventions (aOR, 15.04; 95% CI, 6.7 to 33.73). Implantation of a new system (aOR, 0.46; 95% CI, 0.24 to 0.87) and antibiotic prophylaxis (aOR, 0.4; 95% CI, 0.18 to 0.86) were negatively correlated with risk of infection. CONCLUSIONS: This study identified several factors of risk of device infection and confirmed the efficacy of antibiotic prophylaxis in recipients of new or replacement pacemakers or implantable cardioverter-defibrillators.

Cardiovascular variables do not predict head-up tilt test outcome better than body composition.

Reflex syncope is a well-recognized phenomenon, but the understanding of its underlying pathophysiology remains limited. We hypothesized that patients with a history of syncope and a positive head-up tilt test (HUTT) outcome are in a "not-yet defined" abnormal state even before the head-up position. We performed a 45 min HUTT on 86 patients with a history of syncope. We assessed 19 variables during the supine period before head-up position. Of these variables, 9 were cardiovascular variables (CV) while 8 were body composition variables (BC). The two remaining variables were age and sex. Forty-five patients (41 +/- 15 years, 22 males) have a positive HUTT outcome and 41 a negative one (46 +/- 15 years, 22 males). Statistical tests applied on each of the 19 variables individually did not discriminate patients with a positive and a negative outcome. We used neural networks to screen the sets of variables that allowed for the best predictions of HUTT outcomes. The sensitivity, specificity, positive and negative predictive values (PPV and NPV, respectively) were determined. The best set of predictive values determined from the 19 variables was 76, 81, 78 and 80% for sensitivity, sensibility, PPV, and NPV, respectively. Unexpectedly, the HUTT outcome prediction performed with cardiovascular variables was not better than the prediction performed with body composition variables only. Patients with a positive HUTT outcome are in an abnormal state that can be detected even before the head-up position. Body composition is an important contributor to this abnormal state.

Increased hydration alone does not improve orthostatic tolerance in patients with neurocardiogenic syncope.

In patients with neurocardiogenic syncope, the beneficial effects of increased daily fluid intake, without an accompanying high dose of salt, are unknown. Our aim was to (1) determine whether plasma volume was low in patients with recurrent neurocardiogenic syncope, and (2) determine how recommendation about increased daily fluid intake, without an accompanying high dose of sodium, effects plasma volume and if this potential therapy improves orthostatic tolerance. Eighty-six patients with neurocardiogenic syncope were recruited in a prospective randomized open study. After an initial head-up tilt test, patients were randomly assigned to either the hydration supplementation group (1500 ml of water + 1500 mg of NaCl/day) or the no treatment (control) group. After ten days a second head-up tilt test was performed. Plasma volume, osmolality, and total body water were measured at baseline, and heart rate, arterial blood pressure, and cardiac transthoracic impedance were monitored during tilting. Hydration treatment did not affect the number of positive tilt tests (52% initial day, 54% after treatment, NS). In both groups, the overall number of positive tilt tests decreased between the initial and final head-up tilt test. There was no association between low plasma volume and positive tilt test. Patients with the lowest plasma volume were equally distributed in both positive and negative tilt response groups. An increased daily intake of fluid, without an accompanying high dose of salt, had no measurable beneficial effect on tolerance to head-up tilting in patients with neurocardiogenic syncope. Moreover in this patient group there was no association between a low plasma volume and a reduced tolerance to orthostatic stress.

Do we need a reflex tachycardia to stand up?

BACKGROUND: Sophisticated atrio-ventricular pacing models are designed to integrate the pacemaker into cardiovascular autonomic control to react appropriately to the cardiovascular demands. Such an approach might be beneficial for patients with vasovagal responses to counterbalance the upright fall in arterial blood pressure by a pacing rate increase. We hypothesized that this approach would improve the cardiovascular response to standing in comparison with a regular pacing mode. METHODS: Two 5-minute tilt tests were performed in a random order in 5 patients with a pacemaker (CLS-INOS(2)) for sinus node disease and atrio-ventricular block. One tilt test was performed in fixed pacing rate (DDD), the other one was performed in close loop stimulation (CLS), which allowed an upright rate-rise pacing. Heart rate, systolic blood pressure, and cardiac output (modelflow) were recorded on a beat-by-beat basis. RESULTS: Changes of systolic blood pressure and cardiac output in response to upright posture were not significantly different between DDD and CLS modes (2.7 +/- 13.2 vs 10.1 +/- 12.9 mmHg and -0.8 +/- 0.3 vs -1.1 +/- 0.4 L/min, respectively). But upright posture led to a tachycardia of more than 30 bpm in 3 patients in CLS mode and to a fall in systolic blood pressure greater than 20 mmHg in 3 patients in CLS mode and only in one patient in DDD mode. CONCLUSION: Systolic blood pressure and cardiac output are not improved by the upright tachycardia and upright blood pressure response is actually worsened when an upright rate-rise pacing is used. Thus, it appears that tachycardia alone cannot compensate for an upright fall in blood pressure.

Fever as a precipitant of idiopathic ventricular fibrillation in patients with normal hearts.

INTRODUCTION: Ventricular fibrillation (VF) is the main mechanism of sudden cardiac death. The clinical precipitants of sudden cardiac death due to idiopathic VF are poorly characterized. Emerging evidence implicates triggers originating predominantly from the distal Purkinje arborization and the right ventricular outflow tract. METHODS AND RESULTS: We report three patients without structural heart disease or repolarization abnormalities in whom a febrile illness was the only concurrent disease associated with unexpected sudden cardiac death due to VF storm. An automated defibrillator was implanted in all three patients. In one patient with persistent recurrent VF episodes, mapping demonstrated the origin of these triggers was from the Purkinje arborization of the anterior wall of the right ventricle. Ablation at a site of earliest activation during ectopy, where pace mapping was concordant and Purkinje potential preceded the onset of ventriculogram, resulted in suppression of all arrhythmias. After follow-up of 22, 9, and 18 months in the three patients, no ventricular arrhythmias have been recorded. CONCLUSION: We present a series of patients in whom an apparently benign febrile illness was associated with malignant ventricular arrhythmias in the absence of cardiac disease or other factors known to precipitate sudden cardiac death. Physicians should be aware of this possible phenomenon in cases of febrile illness associated with syncope.

Changes in the transthoracic impedance signal predict the outcome of a 70 degrees head-up tilt test.

We determined whether early changes in central haemodynamics, as determined by transthoracic impedance, induced by a 70 degrees head-up tilt (HUT) test could predict syncope. Heart rate, arterial blood pressure and central haemodynamics [pre-ejection period and rapid left ventricular ejection time ( T (1)), slow ejection time ( T (2)) and d Z /d t (max) (where Z is thoracic impedance), assessed by the transthoracic impedance technique], were recorded during supine rest and during a 45 min 70 degrees HUT test in 68 patients (40+/-2 years) with a history of unexplained recurrent syncope. We found that 38 patients (42+/-3 years) had a symptomatic outcome to 70 degrees HUT (fainters) and 30 (39+/-2 years) had a negative outcome (non-fainters). When measured between 5 and 10 min of 70 degrees HUT, T (2) had increased significantly only in the fainters, and a change in T (2) of >40 ms from baseline predicted a positive outcome with a sensitivity of 68% and a specificity of 70%. During supine rest prior to 70 degrees HUT, the fainters exhibited a shorter T (2) than non-fainters (183+/-10 compared with 233+/-14 ms; P <0.01), and a T (2) of <199 ms predicted a positive outcome to 70 degrees HUT with a sensitivity of 68% and a specificity of 63%. Incorporation of the changes that occurred from rest to 70 degrees HUT in other haemodynamic variables (heart rate >11 beats/min, systolic pressure <2 mmHg, diastolic pressure <7 mmHg and pulse pressure <-3 mmHg) increased the specificity to 97% and the positive predictive value to 93%. Thus transthoracic impedance could detect differences in central haemodynamics between fainters and non-fainters during supine rest and during the initial period of 70 degrees HUT with a consistent sensitivity and specificity when combined with peripheral haemodynamic variables.

Holter changes resulting from right-sided and bilateral infrastellate upper thoracic sympathectomy.

BACKGROUND: We tested the hypothesis that no right-sided dominance exists after infrastellate surgical upper-thoracic sympathectomy. We aimed to confirm whether a significant bradycardia was constant and only dependent on the right side. METHODS: We performed 24-hour Holter electrocardiographic recordings in 12 patients referred for bilateral sympathectomy. Surgery was performed at two distinct times allowing for the study of the consequences of unilateral right and bilateral sympathectomy. RESULTS: Heart rate was 77 +/- 8 beats per minute before surgery on the 24-hour recording and significantly decreased after bilateral (67.8 +/- 6.5 beats per minute; p < 0.05) but not after unilateral right sympathectomy. Consistently spectral analysis variables significantly changed after bilateral surgery but showed no right-sided dominance. Little effect of sympathectomy was found on the QT interval, which tended to decrease after bilateral sympathectomy. CONCLUSIONS: Patients should be informed of the bradycardia resulting from sympathectomy. No right-sided dominance can be found consistently with the random distribution of substellate cardiac fibers reported in anatomic studies.