Azithromycin, Chlamydia pneumoniae, and intimal thickening.
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Biomedical subjects
Publications and source records attributed to B Lüderitz.
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BACKGROUND: During atrial fibrillation, electrophysiological changes occur in atrial tissue that favor the maintenance of the arrhythmia and facilitate recurrence after conversion to sinus rhythm. An implantable defibrillator connected to right atrial and coronary sinus defibrillation leads allows prompt restoration of sinus rhythm by a low-energy shock. The safety and efficacy of this system, called the Atrioverter, were evaluated in a prospective, multicenter study. METHODS AND RESULTS: The study included 51 patients with recurrent atrial fibrillation who had not responded to antiarrhythmic drugs, were in New York Heart Association Heart failure class I or II, and were at low risk for ventricular arrhythmias. The atrial defibrillation threshold had to be </=240 V during preimplant testing. Atrial fibrillation detection, R-wave shock synchronization, and defibrillation threshold were tested at implantation and during follow-up. Shock termination of spontaneous episodes of atrial fibrillation was performed under physician observation. Results are given after a minimum of 3 months of follow-up. During a follow-up of 72 to 613 days (mean, 259+/-138 days), 96% of 227 spontaneous episodes of atrial fibrillation in 41 patients were successfully converted to sinus rhythm by the Atrioverter. In 27% of episodes, several shocks were required because of early recurrence of atrial fibrillation. Shocks did not induce ventricular arrhythmias. Most patients received antiarrhythmic medication during follow-up. In 4 patients, the Atrioverter was removed: in 1 because of infection, in 1 because of cardiac tamponade, and in 1 because of frequent episodes of atrial fibrillation requiring His bundle ablation. CONCLUSIONS: With the Atrioverter, prompt and safe restoration of sinus rhythm is possible in patients with recurrent atrial fibrillation.
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Atrial fibrillation (AF) is an arrhythmia resulting in loss of atrial contribution to ventricular filling, an irregular ventricular contraction, and an inappropriately rapid ventricular rate. An uncontrolled ventricular response may result in various changes of ventricular function and structure referred to as tachycardia-related cardiomyopathy. However, the effects of tachycardia may be reversible with adequate pharmacologic or nonpharmacologic interventional rate control. The purpose of this review article is to discuss the present knowledge regarding tachycardia-related cardiomyopathy and therapy for rate control.
BASIC PROBLEM AND OBJECTIVE: Untreated patients with obstructive sleep apnoea (OSA) have an increased risk of death from cardiovascular (cv) disease. This study was undertaken to determine the disease spectrum in patients with sonographically proven OSA (apnoea-hypopnoea index > or = 5), with special reference to cv risk factors and accompanying diseases in relation to the severity of their respiratory abnormalities. The study's aim was to clarify what risk factors and accompanying diseases were associated with different degrees of OSA. PATIENTS AND METHODS: A systematic recording of cv risk factors and accompanying diseases as well as their association to the severity of nocturnal respiratory disorders was made for 175 patients (165 men, 10 women, mean age 54 +/- 10.2 years) with sonographically proven OSA (mean apnoea-hypopnoea index 37 +/- 24.4). RESULTS: The body mass index (BMI) was significantly related to the severity of the respiratory disorder (apnoea-hypopnoea index, AHI, P < 0.05, odds ratio [OR]: 1.95; 95% confidence interval [CI]: 1.15-3.31). In a multivariate analysis, nocturnal breathing pause (P < 0.05; OR: 3.8; 95% CI: 1.3-11.1), left ventricular hypertrophy (P < 0.01; OR: 3.9; 95% CI: 1.5-10.3) and diabetes mellitus (P < 0.05; OR: 4.2, 95% CI: 1.2-14.7) were independently associated with a high-grade breathing disorder (AHI > or = 20). The incidence of left ventricular hypertrophy rose with an increasing severity of nocturnal OSA. CONCLUSION: These data indicate that in patients with high-grade OSA (AHI > or = 20) there is a further grouping together of cardiovascular risk factors, namely increasing body weight, diabetes mellitus, arterial hypertension and left ventricular hypertrophy; they explain the increased mortality rate among these patients from vascular complications.
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Chronic atrial fibrillation (AF), which is refractory to external electrical direct current shock and/or pharmacologic cardioversion, may be successfully cardioverted using internal atrial defibrillation. To avoid unnecessary procedures, it is important to be able to predict which patients will revert to AF. Thirty-eight patients with chronic AF underwent successful internal atrial defibrillation and were followed for 6 months after restoration of sinus rhythm. Left atrial (LA) diameter, left ventricular ejection fraction, maximum LA appendage area, and peak emptying velocities of the LA appendage were analyzed to determine which of these factors were associated with recurrence of AF. Forty-nine percent of patients had a recurrence of AF within 6 months following internal atrial defibrillation. The preprocedural ejection fraction (mean +/- SD 59 + 14% vs 57 + 13%, p = 0.63), LA diameter (4.2 +/- 0.6 cm vs 4.5 +/- 0.6 cm, p = 0.16), and LA appendage area (5.0 +/- 1.5 cm2 vs 5.8 +/- 1.5 cm2, p = 0.13) did not differ significantly between patients who maintained sinus rhythm and those who had recurrence of AF. Peak emptying velocities of the LA appendage before cardioversion were significantly lower in patients with recurrence of AF compared with patients who maintained sinus rhythm (0.26 +/- 0.1 m/s vs 0.49 +/- 0.17 m/s, p = 0.001). A peak emptying velocity <0.36 had a sensitivity of 82% and a specificity of 83% for predicting recurrence of AF.
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HISTORY AND CLINICAL FINDING: A 69-year-old man with severe haemophilia A sustained an acute myocardial infarction (MI) after self-administration of 3000 units factor VIII over 10 min. On admission he had no signs of heart failure. INVESTIGATIONS: The ECG showed an acute posterior wall MI. Creatinekinase rose to a maximum of 321 U/l with a significant MB proportion. The echocardiogram demonstrated hypokinesia of the posterior wall. TREATMENT AND COURSE: After initial thrombolysis treatment with a total of 100 mg rtPA according to an accelerated scheme coronary angiography, performed because the symptoms persisted, revealed two-vessel disease. A subtotal stenosis of the right coronary artery was balloon-dilated with good primary results. Regular factor VIII substitution was temporarily administered with the aim of initially achieving high normal levels of factor VIII activity. CONCLUSION: Factor VIII substitution in haemophilia A may promote thrombotic complications. Thrombolytic treatment and balloon angioplasty of acute MI can be successfully performed even in patients with severe haemophilia A.
Quantitative cultures of respiratory secretions represent a valid technique for the diagnosis of ventilator-associated pneumonia. Contamination, colonization and true infection can be differentiated with a reasonable specificity using established cut-offs of bacterial colony counts. Quantitative investigations provide local epidemiological databases as a framework for empirical antimicrobial policies and may also prove helpful in the guidance of individual antimicrobial therapy. Another reasonable indication is HIV-associated pneumonia. However, the use of this technique in routine practice is hampered by the high expertise and experience that will be necessary to be successfully used. Nevertheless, in view of the need to identify bacterial susceptibility patterns, at least large treatment centers should routinely use this most powerful diagnostic technique.
BACKGROUND AND OBJECTIVE: Epidemiological studies have demonstrated a circadian distribution of sudden cardiac death (SD) and acute myocardial infarction (AMI), with a maximum frequency of events during the morning hours. Recently an analysis of computer recordings of implanted cardioverter/defibrillators has confirmed these findings with respect to SD. The majority of these studies concerned patients with coronary heart disease. In a prospective study we evaluated the circadian and weekly distribution of malignant ventricular tachyarrhythmias (VTA) in patients with a nonischaemic cardiac disease, namely dilated cardiomyopathy (CMP), and those with coronary heart disease (CHD). PATIENTS AND METHODS: Over a mean period of 25 +/- 9 months computer-stored data and cardiac electrograms recorded from the implanted cardioverter/defibrillators (ICD) were analysed in 28 patients with CHD and 11 with DCMP. The circadian and weekly distribution of VTA was obtained, using customary arrhythmia classification and the stored and timed events. RESULTS: Patients with CHD had a maximal frequency of VTA or ventricular fibrillation (VF) during the morning, with a peak between 9 and 10 o/c, while those with DCMP were at a higher risk of VTA or VF in the later afternoon and early evening. Regarding the frequency of events during the week, a significantly higher incidence of VTA was recorded on Saturdays in those with CHD, but on Mondays and Wednesdays in those with DCMP. INTERPRETATION: The circadian and weekly distribution of VTA differs significantly between patients with CHD and those with DCMP. A possible reason for this difference may be different trigger mechanisms in the two types of cardiac disease, since transient ischaemia is unlikely to be the cause in patients with nonischaemic DCMP.
Arterial hypotension can cause cerebral ischemia when the autoregulation of the cerebral circulation is exhausted. We hypothesized that sudden cerebral vasoconstriction induced by moderate hypotensive, but hemodynamically stable, sustained ventricular tachycardias (MHT-VT) further compromises cerebral blood flow (CBF) and induces an ischemic stress response of the brain. CBF-measurements and morphological studies were performed without and with blockade of alpha-adrenergic receptors in order to determine the impact of MHT-VF on brain perfusion and brain tissue. Using a model of MHT-VT, CBF was measured with colored microspheres in 71 rats during control conditions. after the onset of MHT-VT, after the onset of moderate hypotensive hypovolemia (MHH), and after additional non- selective (alpha-blockade with phentolamine and selective alpha1-blockade with prazosin, respectively (0.2-0.4 mg/kg body weight). Plasma catecholamine concentrations were measured in 18 additional rats during control conditions. during MHT-VT and during MHH. The occurrence of heat shock protein (hsp) 72 and activated microglia in the brain was analysed in 18 additional rats in controls, after MHT-VT and MHH. After 20 min of the respective induced hypotension, control conditions were restored for a period of 8 h, by stopping VT or by infusion of isotonic saline solution. CBF was 0.98+/-0.16 (mean+/-S.D.) ml/g/min during control conditions at an arterial pressure of 118+/-13 mmHg, 0.50+/-0.05 ml/g/min (P<0.05 v control) during MHT-VT (76+/-4 mm Hg) and 0.75+/-0.14 ml/g/min (P<0.05 v control and v MHT-VT ) during MHH (71 +/- 8 mm Hg). CBF was better preserved with non-selective alpha-blockade during MHT-VT (0.78+/-0.15 ml/g/min, P<0.05 v MHT-VT and control) as well as with selective alpha1-blockade (0.67+/-0.08 ml/g/min, P<0.05 v MHT-VT and control). Plasma catecholamines were elevated during MHT-VT (P<0.05 v control) but not during MHH (P = N.S. v control). hsp 72 and activated microglia were found in hippocampal regions only after MHT-VT (P<0.05 v control and MHH). These morphological changes were prevented by non-selective alpha-blockade. Stable sustained MHT-VT further reduce the already compromised CBF leading to morphological alterations in the brain which are characteristic of an early ischemic stress response. alpha-Blockade prevents alpha1-adrenergic vasoconstriction and attenuates cerebral hypoperfusion.
Atrial fibrillation (AF) is a frequent and costly health care problem representing the most common arrhythmia resulting in hospital admission. Total mortality and cardiovascular mortality are significantly increased in patients with AF compared to controls. In addition to symptoms of palpitations patients with AF have an increased risk of stroke and may also develop decreased exercise tolerance and left ventricular dysfunction. All of these problems may be reversed with restoration and maintenance of sinus rhythm. External electrical cardioversion has been a remarkably effective and safe method for termination of this arrhythmia. Originally described by Lown et al. in 1963, it has been a well accepted mode of acute therapy. However, this technique requires general anesthesia or heavy sedation. Internal atrial defibrillation has been evaluated as an alternative approach to the external technique for over 2 decades. Recent studies have shown that low-energy internal atrial defibrillation using biphasic shocks is an effective and safe means in restoring sinus rhythm in patients with AF and should be considered especially in patients in whom external cardioversion attempts have failed. IMPLANTABLE ATRIAL DEFIBRILLATOR: Recently, a stand alone IAD, the Metrix System (model 3000 and 3020), has entered clinical investigation. Atrial defibrillation is accomplished by a shock delivered between electrodes in the right atrium and the coronary sinus. The right atrium lead has an active fixation in the right atrium. The coronary sinus lead has a natural spiral configuration for retention in the coronary sinus, and can be straightened with a stylet. Both leads are 7 French in diameter and the defibrillation coils are each 6 cm in length. The electrodes may be placed using separate leads, or very soon by using a single bipolar lead. A separate bipolar right ventricular lead is used for R wave synchronization and post shock pacing. The Metrix defibrillator can be used to induce AF by using R wave synchronous shocks and can store intracardiac electrograms (EGMs) for up to 2 minutes from the most recent 6 AF episodes. The device can be programmed into one of the following operating modes: fully automatic, patient activated, monitor mode, bradycardia pacing only, and off. As AF is not life-threatening, in the automatic mode the device is only intermittently active in detecting and treating AF, and this "sleep wake-up" cycle interval is programmable. The device employs extensive processing both for detection and R wave synchronization. In April 1996, the phase I Metrix multicenter clinical trial was started. As of May 1997, a total of 51 Metrix systems had been implanted as part of the phase I multicenter clinical trial. Preliminary data suggest that both defibrillation thresholds and electrograms are stable over time (implant to 3 months). Detection accuracy has been excellent (100% specificity, 92.3% sensitivity) and there have been no errors of R wave selection for synchronization. No proarrhythmias have resulted from over 3700 shocks delivered. The device is effective in electrically converting 96% of the spontaneous episodes of AF. In 27% of episodes several shocks were required because of early recurrence of AF. In 5 patients, the atrial defibrillator was removed: 2 infections, 1 cardiac tamponade, 1 permanent loss of telemetry, 1 patient required His-Bundle ablation because of frequent episodes of drug refractory AF with rapid ventricular response. Initial clinical experience under controlled conditions with the Metrix system suggests that the implantable atrial defibrillator may offer a therapeutic alternative for a subgroup of patients with drug refractory, symptomatic, long lasting, and infrequent episodes of AF. Further efforts must be undertaken to reduce the patient discomfort associated with internal atrial defibrillation in an attempt to make this new therapy acceptable to a larger patient population with AF. (ABSTRACT TRUNCATED)
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