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Multiple stressors like alterations of water quality, hydrology and hydromorphology impact riverine ecosystems. To counteract its consequences, restoration measures are required, e.g. demanded by the EU Water Framework Directive. However, small-scale hydromorphological restoration measures often show little success. Besides overriding stressors, recolonization potential and insufficient time for development are often discussed as reasons for this lack of success. Over a period of 17 years a hydromorphological restoration measure in a German lowland stream reach was evaluated, excluding most of these confounding factors. The restoration measure was left to its self-dynamic development, i.e. there was no further intervention by water management, apart from some large wood installations after 8 years. In the accompanying studies, changes in hydromorphology and the organism groups’ macroinvertebrates (including both structural and functional diversities), fish and macrophytes were investigated. We proved a rapid and stable enhancement of ecological functions as indicated by a diverse and resilient macroinvertebrate biocoenosis. Both taxonomic and functional richness of macroinvertebrates significantly increased, but varied over time. Since the restoration measure allowed self-dynamic development, a taxonomic and functional endpoint was not achieved even after 17 years, even though near-reference conditions were attained after only 4 years. Deficits in fish communities were most probably due to their low recolonization potential. Our results underscore that small scale hydromorphological restoration can be successful if overriding stressors are absent. Furthermore, we proved the importance of self-dynamics in restoration measures, allowing hydromorphological and biological development.

The interaction forces between silicon oxide surfaces in the presence of surfactant solutions were studied. Based on the qualitative and quantitative analysis of these interaction forces the correlation with the structure of the aggregates on the surfaces is analyzed. A colloidal probe atomic force microscope (AFM) was used to measure the forces between two colloidal silica particles and between a colloidal particle and a silicon wafer in the presence of hexadecyltrimethylammonium bromide (CTAB) at concentrations between 0.005 mM and 1.2 mM. Different interaction forces were obtained for the silica particle–silica particle system when compared to those for the silica particle–silicon wafer system for the same studied concentration. This indicates that the silica particles and the silicon wafer have different aggregate morphologies on their surfaces. The point of zero charge (pzc) was obtained at 0.05 mM CTAB concentration for the silica particles and at 0.3 mM for the silica particle–silicon wafer system. This indicates a higher charge at the silicon wafer than at the silica particles. The observed long range attractions are explained by nanobubbles present at the silicon oxide surfaces and/or by attractive electrostatic interactions between the surfaces, induced by oppositely charged patches at the opposing Si oxide surfaces.

The German Cardiac Society is the oldest national cardiac society in Europe, founded on June 3, 1927, in Bad Nauheim by Dr. Bruno Kisch and Professor Arthur Weber. They were actively supported by Dr. Franz Groedel, who together with Kisch became co-founders of the American College of Cardiology in 1949. Both Groedel and Kisch would be proud to see the fulfillment of their visions and dreams, which was commemorated at the joint session of the two societies held during the 78th annual meeting of the German Cardiac Society in Mannheim, Germany. “It is ironic that their dreadful years in Germany and their loss to German Cardiology helped to contribute to advances in American and international Cardiology,” said Dr. Simon Dack, American College of Cardiology president in 1956 and 1957. The legacy of Groedel might be reflected by his own words: “We will meet the future not merely by dreams but by concerned action and inextinguishable enthusiasm.”

Large-scale restoration of streams and rivers is a mandatory prerequisite for the implementation of the European Water Framework Directive (WFD) to reach good ecological status of water bodies. This contribution analyzes the success of the largest river restoration in Germany at the Upper Main. Sections with a length of more than 18 km were restored between 1990 and 2008, including re-connection of former oxbow-lakes, multiple-channelling, and establishment of wide riparian buffer zones. Measuring the success of restoration by means of a multimetric assessment system, we found a clear success of restoration indicated by the status of hydromorphology and by the biological parameters, including macroinvertebrates, fishes, and macrophytes. Unlike non-restored reaches, the restored reaches attained a good ecological status. As such, the restoration of the Upper Main is shown to be a pilot project for the implementation of the WFD on a large scale.

Organophosphate poisoning is associated with a high mortality rate due to respiratory failure, dysrhythmias, and multi-organ failure. We report two cases of survival after "in-the field" antidote treatment of very severe organophosphate poisonings. Two patients orally ingested large amounts of the organophosphorous agent oxydemeton-methyl in suicide attempts, resulting in the hypercholinergic syndrome in both. Resuscitation included early administration of antidote by emergency medical personnel as well as high-dose atropine. Plasma levels of pseudo cholinesterase were initially very low in both patients. Long-term mechanical ventilation was necessary, and both patients developed aspiration pneumonia. At discharge, no major neurological deficits were present. Prompt antidote treatment and aggressive supportive emergency and intensive care unit therapy contribute to improved survival after acute organophosphate poisoning. We believe that in cases of mass poisonings--for example, terrorist activity--therapy must be available on the scene as soon as possible. This also may require decentralized antidote storage.

If compared to two-dimensional echocardiography (2DE), myocardial contrast echocardiography (MCE) improves detection of coronary artery disease (CAD) during pharmacological stress, but data on MCE vs. 2DE during supine bicycle stress is limited. Although previous myocardial infarction (MI) influences sensitivity of 2DE, its effect on MCE has not been evaluated.The study sought to determine the incremental benefit of MCE over 2DE for evaluation of CAD during supine bicycle stress and to assess the impact of previous MI on diagnostic values of both methods.We studied 103 consecutive patients scheduled for coronary angiography. Prior to coronary angiography, all patients underwent supine bicycle stress. 2DE and MCE were performed during this stress test. The diagnosis of obstructive CAD (or =50% stenosis) was based on the presence of inducible wall motion and perfusion abnormalities.Quantitative coronary angiography revealedor =50% stenosis in 53 of 77 patients without previous MI and in 21 of 26 patients with previous MI. If compared to 2DE, MCE was more sensitive (68% vs. 86%; p0.001) and more accurate (73% vs. 86%; p0.001) to detector =50% stenosis. In patients without previous MI, 2DE and MCE yielded sensitivity of 65% and 85% (p0.01) and accuracy of 71% and 85% (p0.01), whereas in patients with previous MI sensitivity was 79% and 90% (p=NS) and accuracy 79% and 88% (p = NS), respectively.MCE enhances sensitivity and accuracy of 2DE in detection of obstructive CAD during supine bicycle stress. The incremental benefit of MCE is especially present in patients without previous MI.

Background The population of patients likely to respond to selected pacing algorithms for maintenance of sinus rhythm is unknown. Objectives The purpose of this study was to identify patients with specific onset patterns of paroxysmal atrial fibrillation (AF). Methods Dual-chamber pacemakers with advanced diagnostic functions were implanted in 112 patients with conventional indications for antibradycardia pacing and a history of paroxysmal AF. Pacemaker diagnostic data were analyzed after 97.5 ± 40.9 days. According to the frequency of premature atrial contractions (PACs) during the 5 minutes before AF onset, patients were assigned to one of three groups: group A (high PAC activity), group B (moderate PAC activity), or group C (low PAC activity). Results AF burden was lower in group A (4.6% ± 2.4%) than group B (15.8% ± 3.0%, P = .003) and group C (15.5% ± 3.1%, P = .003). Fewer AF episodes occurred in group A (2.1 ± 1.3 per day) than group B (3.8 ± 1.2 per day, P = .006). Mean AF episode duration was shorter in group A (11.4 ± 10.2 hours) than group C (41.4 ± 27.5 hours, P = .03). Conclusion The coincidence of low PAC activity before AF onset, high AF burden, and extended arrhythmia episode duration appears to be the consequence of a high atrial substrate factor. In these "substrate fibrillators," the efficacy of pacing algorithms for maintenance of sinus rhythm may be limited. In contrast, "trigger fibrillators" exhibiting low AF burden despite high PAC incidence may represent the target population for specific PAC-suppressing pacing algorithms.

Study objectives To evaluate the impact of obstructive sleep apnea syndrome (OSAS) on serum creatine phosphokinase (CK) levels. Design Single-center prospective cross-sectional study. Setting Academic sleep disorder center. Patients Two hundred one consecutive patients (mean [± SD] age, 54.9 ± 11.0 years; 155 men and 46 women; mean body mass index, 31.3 ± 6.9 kg/m2) with suspected sleep-disordered breathing. Measurements and results OSAS was confirmed in182 patients (apnea-hypopnea index [AHI], > 5 events per hour) and was ruled out in 19 patients (control subjects) by standard polysomnography. Sixty-six OSAS patients and 1 control patient showed an unexplained CK elevation. The mean baseline CK level was significantly higher in patients with severe OSAS (AHI, > 30 event per hour; n = 89) compared to those with mild-to-moderate OSAS (AHI, 5 to 30 events per hour; n = 93) and control subjects (191.4 ± 12.9 vs 134.3 ± 7.5 vs 107.1 ± 7.9 U/L, respectively; p 148 U/L (r = 0.660) for CK, which yielded a positive predictive value of 99%, a sensitivity of 43%, and a specificity of 95% for the diagnosis of OSAS. The mean nocturnal oxyhemoglobin saturation was the main predictor of CK level (r = 0.47; p Conclusions One third of our study population showed a mild-to-moderate elevation in CK level, which was highly predictive of OSAS. The application of CPAP therapy in OSAS patients resulted in a significant decrease in CK level. We speculate that OSAS may account for a substantial number of cases of unexplained CK elevation (ie, hyperCKemia). Further studies should address the prevalence of OSAS in patients with mild-to-moderate hyperCKemia.

Several experimental and clinical studies have demonstrated that platelet size and function correlate since large platelets are hemostatically more reactive than platelets of normal size. Since platelets play a crucial role in vascular remodeling after percutaneous transluminal coronary angioplasty (PTCA), we investigated the influence of the mean platelet volume (MPV), a parameter of platelet size, on restenosis after PTCA.The retrospective study comprised 174 patients who underwent elective PTCA and follow-up angiography within 6 months thereafter. According to the follow-up angiograms, the patients were assigned to group A ("restenosis", n=74) or group B ("no restenosis", n=100). Both groups were compared in regard to pre-procedural hematological routine parameters including MPV, platelet count, hematocrit, white blood cell count and fibrinogen.MPV was significantly increased in group A, compared with that in group B (8.75+/-0.99 fl vs. 8.04+/-0.74 fl, p0.001). This difference in MPV was evident in patients with stable and unstable angina pectoris. In addition, MPV had an impact on the time-related incidence of angiographic restenosis, as early restenosis was associated with higher pre-procedural MPV values. Platelet count correlated inversely with MPV (r=-0.36, p0.01) and was significantly lower in group A than in group B. The remaining hematological parameters were not different in both groups.The MPV seems to be a marker of coronary restenosis in patients undergoing PTCA. Patients with high pre-procedural MPV values might benefit from an intensified antiplatelet therapy after coronary interventions.

Objective Patients with atrial fibrillation and echocardiographic risk factors have a relevant risk of cerebral embolism. However, there is little knowledge about the long-term fate and the rate of clinical silent cerebral embolism under continued oral anticoagulation. Our aims were to assess the prognosis of patients with atrial fibrillation and determine a high-risk group with an increased risk of cerebral embolism under oral anticoagulation. Methods A total of 173 consecutive patients with persistent or permanent atrial fibrillation and left atrial (LA) thrombi, dense spontaneous echocontrast, reduced LA appendage peak emptying velocities, or a combination of these were included in the study. In all, 169 patients with atrial fibrillation and without echocardiographic risk factors served as control patients. We performed serial and prospective transesophageal echocardiography, cranial magnetic resonance imaging, and clinical examinations during a period of 12 months. Results During the follow-up period 7 (4%) of the patients at high risk had cerebral embolism with neurologic deficits. A total of 4 (2%) patients died because of embolic events and 19 (11%) patients had silent embolism as documented on magnetic resonance imaging. In the control group, 10 (6%) patients had embolic events documented on magnetic resonance imaging; one was clinically apparent. Study patients with an event had more often previous thromboembolism ( P Conclusions Patients with persistent or permanent atrial fibrillation and LA thrombi, dense spontaneous echocontrast, or reduced LA appendage peak emptying velocities have an explicitly increased risk of cerebral embolism (17%) despite oral anticoagulation. Previous thromboembolic event is another important predictor for an event.

Since hydromorphology in about 80% of German streams and rivers is degraded to a high degree, increased efforts in hydromorphological renaturalization are necessary. A measurement of the success of the first realized projects shows that improvement in stream morphology has a remarkably positive influence on aquatic ecology. An example of a restored stretch of a lowland stream in Saxony-Anhalt is used to describe the possibilities of success measurement programs for improvement of poor renaturalization. Therefore, a combined morphological and hydrobiological approach was developed. An integrated ecological assessment is possible by using the multimetric index EQIM (Ecological Quality Index using benthic Macroinvertebrates) and the GFI (German Fauna Index). The latter represents a tolerance measure to evaluate the hydromorphological status of a site by using certain taxa that indicate either positive or negative physical attributes. To consider the special characteristics of the stream in its landscape unit, specific reference conditions (‘Leitbild’) were defined for macroinvertebrate communities by sampling comparable but undisturbed streams in the same landscape unit. Only the combination of biological indices, hydromorphological mapping and comparison to the reference status allows for an expressive evaluation of renaturalization measures and precise conclusions for their improvement.

OBJECTIVES We sought to evaluate: 1) the contribution of dendritic cells (DCs); and 2) the impact of B-cell lymphoma 2 protein (Bcl-2), a central anti-apoptotic protooncogene, and of heat shock protein 47 (HSP47), indicating subsequent collagen deposition, in neointima formation after angioplasty. BACKGROUND The origin of neointimal cells and the factors that promote their accumulation are still unclear. Previous studies reported intimal presence of DCs and suggested cells of primarily extravascular origin to contribute to arterial repair. METHODS Sprague-Dawley rats underwent carotid balloon angioplasty. At different times after angioplasty, tissue sections were analyzed by immunohistochemistry using OX-62 and S100 as DC markers and antibodies against Bcl-2 and HSP47, supplemented by electron microscopic analysis of cell type and apoptosis. RESULTS Four days after injury, DCs adhered along the internal elastic lamina and demonstrated intense Bcl-2 and HSP47 expression, consistent with low apoptosis. With ongoing neointima enlargement, luminal DCs remained prevalent and were colocalized with Bcl-2 and HSP47, while signaling decreased to basal regions. Media showed no DCs and only low Bcl-2 and HSP47 immunoreactivity. Adventitia transiently revealed a structural separation between day 4 and 7. Whereas the inner layer demonstrated sparse cellularity, apoptosis and no DC, Bcl-2, and HSP47 labeling, the outer layer was characterized by high myofibroblast density with strong Bcl-2 and HSP47 expression but absence of DCs. CONCLUSIONS We identify DCs as novel components in early neointima formation, promoted by coordinated anti-apoptotic Bcl-2 and HSP47 expression. Despite intense adventitial remodeling, there is no evidence of adventitial cell transmigration.

Background Although specific antiplatelet drugs are well-established and effective in atherosclerosis prevention, recent clinical trials have also shown that use of angiotensin-converting enzyme (ACE) inhibitors results in a decrease in cardiovascular events. Therefore, in this study, we sought to assess the coagulative activity of patients with cardiovascular disease grouped for treatment with either ACE inhibitors, aspirin, clopidogrel/aspirin, or none of these medications. Methods Blood samples from 303 patients with cardiovascular disease were analyzed with whole-blood aggregometry. Platelet aggregation was determined by the increase in impedance across paired electrodes in response to the aggregatory agents adenosine diphosphate (ADP) or collagen. Results As the central finding, platelet aggregation was attenuated by ACE inhibitors and by aspirin or clopidogrel/aspirin, which was indicated by a lower impedance increase compared with no medication. With ACE inhibition, platelet aggregation decreased by 33% ( P =.042) after ADP induction. No significant antithrombotic effect was seen with aspirin alone (17%, P = 1.0), whereas a decrease in ADP-induced platelet aggregation was extensive with clopidogrel/aspirin (85%, P =.001). After collagen induction, platelet aggregation was reduced by 16% ( P =.028) in the presence of ACE inhibitor therapy, whereas inhibition with aspirin and clopidogrel/aspirin was 23% ( P =.004) and 35% ( P =.026), respectively, compared with participants who were not treated. Conclusions These ex vivo data on whole-blood aggregometry provide direct evidence that ACE inhibitors decrease platelet aggregation, whereas aspirin and clopidogrel are confirmed as established antithrombotics. Pleiotropic effects of ACE inhibition on platelet function may contribute to the clinical benefit observed with this drug class on major cardiovascular end points. (Am Heart J 2003;145:343-8.)

OBJECTIVES The study was done to assess the prevalence of left atrial (LA) chamber and appendage thrombi in patients with atrial flutter (AFl) scheduled for electrophysiologic study (EPS), to evaluate the prevalence of thromboembolic complications after transesophageal echocardiographic (TEE)-guided restoration of sinus rhythm and to evaluate clinical risk factors for a thrombogenic milieu. BACKGROUND Recent studies showed controversial results on the prevalence of atrial thrombi and the risk of thromboembolism after restoring sinus rhythm in patients with AFl. METHODS Between 1995 and 1999, patients with AFl who were scheduled for EPS were included in the study. After transesophageal assessment of the left atrial appendage and exclusion of thrombi, an effective anticoagulation was initiated and patients underwent EPS within 24 h. RESULTS We performed 202 EPSs (radiofrequency catheter ablation, n = 122; overdrive stimulation, n = 64; electrical cardioversion, n = 16) in 139 consecutive patients with AFl. Fifteen patients with a thrombogenic milieu were identified. All of them had paroxysmal atrial fibrillation (AF). Transesophageal echocardiography revealed LA thrombi in two cases (1%). After EPS no thromboembolic complications were observed. Diabetes mellitus, arterial hypertension and a decreased left ventricular ejection fraction were found to be independent risk factors associated with a thrombogenic milieu. CONCLUSIONS The findings of a low prevalence of LA appendage thrombi (1%) in patients with AFl and a close correlation between a history of previous embolism and paroxysmal AF support the current guidelines that patients with pure AFl do not require anticoagulation therapy, whereas patients with AFl and paroxysmal AF should receive anticoagulation therapy. In addition, the presence of clinical risk factors should alert the physician to an increased likelihood for a thrombogenic milieu.

OBJECTIVESIn this study, the transverse conduction capabilities of the crista terminalis (CT) were determined during pacing in sinus rhythm in patients with atrial flutter and atrial fibrillation.BACKGROUNDIt has been demonstrated that the CT is a barrier to transverse conduction during typical atrial flutter. Mapping studies in animal models provide evidence that this is functional. The influence of transverse conduction capabilities of the CT on the development of atrial flutter remains unclear.METHODSThe CT was identified by intracardiac echocardiography. The atrial activation at the CT was determined during programmed stimulation with one extrastimulus at five pacing sites anteriorly to the CT in 10 patients with atrial flutter and 10 patients with atrial fibrillation before and after intravenous administration of 2 mg/kg disopyramide. Subsequently, atrial arrhythmias were reinduced.RESULTSAt baseline, pacing with longer coupling intervals resulted in a transverse pulse propagation across the CT. During shorter coupling intervals, split electrograms and a marked alteration of the activation sequence of its second component were found, indicating a functional conduction block. In patients with atrial flutter, the longest coupling interval that resulted in a complete transverse conduction block at the CT was significantly longer than that in patients with atrial fibrillation (285 ± 49 ms vs. 221 ± 28 ms; p < 0.05). After disopyramide administration, a transverse conduction block occurred at longer coupling intervals as compared with baseline (287 ± 68 ms vs. 250 ± 52 ms; p < 0.05). Subsequently, a sustained atrial arrhythmia was inducible in 15 of 20 patients. This was atrial flutter in three patients with previously documented atrial fibrillation and in eight patients with history of atrial flutter. Mapping revealed a conduction block at the CT in all of these patients.CONCLUSIONSIt was found that the CT provides transverse conduction capabilities and that the conduction block during atrial flutter is functional. Limited transverse conduction capabilities of the CT seem to contribute to the development of atrial flutter.

BACKGROUND: Metoprolol can improve haemodynamics in chronic heart failure, but survival benefit has not been proven. We investigated whether metoprolol controlled release/extended release (CR/XL) once daily, in addition to standard therapy, would lower mortality in patients with decreased ejection fraction and symptoms of heart failure. METHODS: We enrolled 3991 patients with chronic heart failure in New York Heart Association (NYHA) functional class II-IV and with ejection fraction of 0.40 or less, stabilised with optimum standard therapy, in a double-blind randomised controlled study. Randomisation was preceded by a 2-week single-blind placebo run-in period. 1990 patients were randomly assigned metoprolol CR/XL 12.5 mg (NYHA III-IV) or 25.0 mg once daily (NYHA II) and 2001 were assigned placebo. The target dose was 200 mg once daily and doses were up-titrated over 8 weeks. Our primary endpoint was all-cause mortality, analysed by intention to treat. FINDINGS: The study was stopped early on the recommendation of the independent safety committee. Mean follow-up time was 1 year. All-cause mortality was lower in the metoprolol CR/XL group than in the placebo group (145 [7.2%, per patient-year of follow-up]) vs 217 deaths [11.0%], relative risk 0.66 [95% CI 0.53-0.81]; p=0.00009 or adjusted for interim analyses p=0.0062). There were fewer sudden deaths in the metoprolol CR/XL group than in the placebo group (79 vs 132, 0.59 [0.45-0.78]; p=0.0002) and deaths from worsening heart failure (30 vs 58, 0.51 [0.33-0.79]; p=0.0023). INTERPRETATION: Metoprolol CR/XL once daily in addition to optimum standard therapy improved survival. The drug was well tolerated.

Internal atrial defibrillation (IAD) is able to restore sinus rhythm in patients with chronic atrial fibrillation (AF) and failed external electrical and/or pharmacologic cardioversion. To assess whether cardiorespiratory and hemodynamic function improve after IAD, 35 patients were prospectively investigated during constant workload exercise by spiroergometry and Doppler echocardiography before IAD, and 1 day and 1 month after IAD. Oxygen uptake kinetics, ventilation, left atrial mechanical function, and pulmonary artery pressure were determined simultaneously at rest and during steady state. During the serial follow-up, 20 patients maintained sinus rhythm. The time interval for achieving the steady state (146 +/- 53 vs 132 +/- 42 seconds; p = 0.5) and the oxygen deficit (645 +/- 190 vs 670 +/- 174 ml; p = 0.7) were not different before and 1 day after IAD, but decreased significantly after 1 month (98 +/- 16 seconds, p = 0.01 and 487 +/- 72 ml, p = 0.02). Exercise pulmonary artery systolic pressures were 38 +/- 13 mm Hg before IAD, increased significantly to 46 +/- 11 mm Hg on day 1 (p = 0.03), and decreased below baseline values at 1 month to 31 +/- 12 mm Hg (p = 0.07). Peak A-wave velocities increased from 0.51 +/- 0.1 m/s after 1 day to 0.67 +/- 0.2 m/s after 1 month (p = 0.03). Restoration of sinus rhythm in patients with AF resistant to external electrical and/or pharmacologic cardioversion improves hemodynamic and cardiorespiratory function at daily activity exercise levels.

In selected patients, atrial fibrillation (AF) converts to atrial flutter (AFI) due to treatment with class IC antiarrhythmic drugs. In this study, we prospectively investigated the effects of AFI ablation and continuation of drug therapy in patients with AF who developed AFI due to long-term administration of class IC antiarrhythmic drugs. The study population consisted of 187 patients from an AF registry with paroxysmal AF who were orally treated with flecainide (n = 96) or propafenone (n = 91). Twenty-four patients (12.8%) developed AFI during the course of treatment. In 20 of these patients (10.7%), electrophysiologic study revealed typical AFI. These patients underwent radiofrequency ablation of AFI. Ablation failed in 1 patient. All patients continued preexisting drug treatment. Recurrence of AF was assessed by ambulatory Holter monitoring and serial questionnaires. During a mean follow-up of 11 +/- 4 months, the incidence of AF episodes was significantly lower in patients with a combined therapy (2.7 +/- 3.6 per year) than in control subjects with a sole drug treatment (7.8 +/- 9.2 per year, p0.05) and than before therapy (10.2 +/- 5.4 per year, p0.001). Subgroup analysis revealed that 7 patients (36.8%) remained symptom free with no evidence of atrial tachyarrhythmia. Eight additional patients (42.1%) had ongoing paroxysmal AF, however, with a significantly lower incidence of AF episodes than before therapy (2.3 +/- 1.6 per year vs 11.5 +/- 5.0 per year, p0.001). In the remaining 4 patients (14.7%), no beneficial effect of AFI ablation was found. It is concluded that in patients with AF who develop typical AFI due to administration of class IC antiarrhythmic agents, a combined therapy with catheter ablation of AFI and continuation of drug treatment is highly effective in reducing occurrence and duration of atrial tachyarrhythmias.

Zusammenfassung Der zweite Entwurf der Deutschen Norm 1946/4 (Juni 2007) beinhaltet zahlreiche Verbesserungen im Vergleich zum Standard von 1999, welcher immer noch gultig ist. Er beinhaltet eine Beschreibung, wie das Luftungssystem von Operationssalen zu beurteilen ist, um eine moglichst niedrige Keimkonzentration in der Zuluft des Operationsgebiets sicherzustellen. Die hygienischen Abnahmeprufungen basieren auf der Bestimmung des Turbulenzgrades der Zuluft an 121 Punkten innerhalb des Schutzgebiets, 1,2 m uber dem Fusboden. Das Schutzgebiet ist wahrend der Messungen vollstandig von allen spater fest oder mobil installierten Geraten befreit (ohne OP-Tisch, OP-Lampen etc.). Das Ziel besteht darin, niedrige Turbulenzgradwerte zu erreichen. Die Autoren fuhrten verschiedene Untersuchungen durch, um festzustellen, ob dieses Untersuchungsprozedere als Qualifikationsmethode geeignet ist. Sie kamen allerdings zu dem Ergebnis, dass sich das dargestellte Konzept nicht bewahrt hat.

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 (P0.05 v control) during MHT-VT (76+/-4 mm Hg) and 0.75+/-0.14 ml/g/min (P0.05 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, P0.05 v MHT-VT and control) as well as with selective alpha1-blockade (0.67+/-0.08 ml/g/min, P0.05 v MHT-VT and control). Plasma catecholamines were elevated during MHT-VT (P0.05 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 (P0.05 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 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.

The aim of this study was to assess whether N-acetylcysteine (NAC) is able to prevent tolerance to a 48-hour infusion of nitroglycerin (NTG) in the setting of normal left ventricular function. In 16 patients, the hemodynamic response to 0.8 mg sublingual (s.l.) NTG was assessed by measuring mean arterial, pulmonary artery, pulmonary capillary wedge and right atrial pressures, cardiac output, and calculation of the systemic and pulmonary vascular resistances. The parameters were obtained at baseline and 1 to 10 minutes after the s.l. NTG application (day 1). NTG was started at 1.5 microg/kg/min; concomitantly, a bolus of 2,000 mg of NAC was administered, followed by an infusion of 5 mg/kg/hour. Both infusions were continued for 48 hours, and the hemodynamic study was repeated (day 3). The same measurements were obtained in a matched control group of 15 patients with NTG infusion alone. Plasma renin activity, aldosterone, and norepinephrine were measured before and after the infusion period. The first s.l. NTG infusion (day 1) caused a significant decrease in mean arterial (p0.01), pulmonary artery (p0.001), and right atrial pressures (p0.001), and in systemic (p0.01) and pulmonary vascular resistances (p0.001) in both groups. After the 48-hour infusion (day 3), there was a total loss of nitrate-mediated vasodilation (pressure values and vascular resistances day 3day 1) in 5 of 16 patients (NAC nonresponders), whereas in the other 11 of 16 patients (NAC responders), there was significant vasodilation throughout the infusion period. Tolerance had developed in 14 of 15 patients with NTG infusion alone. The same difference (responder vs nonresponder vs NTG alone) held true regarding the response to the second s.l. NTG infusion after 48 hours. The neurohormonal counter-regulation and intravascular volume expansion (increase in plasma renin activity, p0.001, and norepinephrine, p0.05; decrease in aldosterone, p0.01) did not differ between responders and nonresponders. We conclude that NAC attenuates tolerance development to a continuous NTG infusion in a specific patient subgroup and that this occurs despite the same amount of neurohormonal counter-regulation and intravascular volume expansion compared with patients with tolerance development.

We report a bronchopulmonary infection with Mycobacterium malmoense in a patient with severe immunosuppression due to insulin-dependent diabetes mellitus, humoral immunodeficiency after thymoma (Good's syndrome) and prolonged immunosuppressive treatment after myasthenic crisis. It presented as non-resolving pneumonia of the left lower lobe. Bronchoscopically, a bronchoesophageal fistula was detected. Numerous acid-fast organisms were found in the sputum specimen and in the bronchial biopsy around the fistula. M. malmoense was isolated from sputum, bronchoalveolar lavage and bronchial biopsy. Whereas conventional in vitro susceptibility testing revealed susceptibility only to ethambutol, multi-drug susceptibility testing confirmed susceptibility to rifampicin, ethambutol, clarithromycin and prothionamide. The clinical outcome after 12 months of therapy resulted in a stable remission and considerable suppression of the mycobacterial load, but not in complete eradication.

We investigated the physiologic heart rate (HR) to work rate (WR) relation throughout peak exercise in normal subjects as a guideline for rate-adaptive pacemaker slope programming. The study group consisted of 41 middle-aged subjects (22 men and 19 women) without evidence of cardiopulmonary disease. Peak-exercise stress tests were performed on a calibrated treadmill by using the symptom-limited "ramping incremental treadmill exercise" (RITE) protocol. The HR response, oxygen uptake, and treadmill workload increments were assessed simultaneously. The HR/WR slope, as determined using linear regression analysis, was 0.37 +/- 0.13 beats/min/W for the entire study group, which indicates an upper range increase of 5 beats/10 W increase of external treadmill work performed, using the mean value +/- 1 SD. Men generated an HR/WR slope of 0.32 +/- 0.09 beats/min/W, and women, 0.43 +/- 0.15 beats/min/W, indicating a significant sex-related difference in the HR/WR relation (p < 0.01). Thus, to achieve an appropriate matching of HR with patient effort, rate-adaptive pacemakers should generate an average increase of approximately 5 beats per increase in 10 W of external treadmill work. The HR/WR relation can easily be determined to provide the clinician with a minimal check system to avoid a hyper- or hypochronotropic paced response to exercise.

It is important to understand the potential interactions between the implantable cardioverter defibrillator (ICD) and antiarrhythmic therapy in patients who receive pharmacologic therapy as an adjunct to ICD therapy. In our cohort of 101 patients, antiarrhythmic agents were prescribed in 67% of the patients during long-term therapy for the following reasons: to suppress ventricular tachycardia/ventricular fibrillation episodes (50%), to lower the rate of ventricular tachycardia (19%), to prevent supraventricular tachyarrhythmia (21%), and for other reasons (10%). The potential influence of antiarrhythmic drugs on the defibrillation threshold (DFT) is the most important issue. In animal studies lidocaine increased the DFT in a dose-dependent manner. Quinidine, procainamide, propafenone, and flecainide did not affect the DFT or, in some cases, led to a small increase. Sotalol even decreased the energy requirements for internal defibrillation. In a prospective investigation we were able to document a significant increase of DFT (from 14.1 + 3.0 to 20.9 + 5.4 J, p < 0.001) by the use of amiodarone (400 mg/day), whereas this effect was not found in patients who received mexiletine (720 mg/day). In conclusion, the DFT or the safety margin for defibrillation should be known before antiarrhythmic agents are administered to patients with an ICD. In case of a small safety margin, the DFT should be reassessed after antiarrhythmic drug therapy is begun.

The objective of minute ventilation (MV)-controlled pacemaker algorithms is to simulate the physiologic relationship of the sensed signal and the sinus node response during exercise. In our study we determined the relationship between heart rate and MV in healthy middle-aged subjects by measuring breath-by-breath gas exchange throughout peak exercise. Regarding several clinical limitations of peak exercise testing, we additionally evaluated whether a 35 W low-intensity treadmill exercise (LITE) protocol can be used as a substitute for peak exercise testing to determine the physiologic heart rate to MV slope. The results demonstrated that the heart rate to MV relationship is not linear throughout peak exercise but is curvilinear with a smooth logarithmic-type profile. To simulate this relationship, MV-based rate adaptive pacemakers should generate a decreasing heart rate to MV slope during higher levels of work. The heart rate to MV slope determined during the early, dynamic phase of low-intensity exercise represents the same slope derived from peak exercise below the anaerobic threshold. The low-intensity treadmill exercise protocol, with minimal patient effort, can thus be used as a substitute for peak exercise to optimize rate adaptive slope programming of MV-controlled pacemakers.

The narrowest central flow region of a jet is defined as the vena contracta. This term is applied also to the contracted zone of the Doppler color flow image of a jet at its passage through an incompetent mitral valve. The clinical applicability of measuring the size of the vena contracta by transthoracic color-coded Doppler echocardiography for estimating the severity of mitral regurgitation (MR) was evaluated. In 78 of 82 patients with angiographically proved MR, a coherent flow image across the valve was visualized. The maximal diameter in the apical long-axis view was considered as a representative value for the size of the vena contracta. In comparison with the maximal left atrial velocity pixel area, this parameter revealed higher correlations to the angiographic degree of MR and to the regurgitant volume (r = 0.94 vs 0.72, and 0.83 vs 0.71, respectively). The highest positive and negative predictive accuracies for differentiating mild-to-moderate from severe MR were determined for a diameter of 6.5 mm (88 and 96%, respectively). Because the vena contracta is directly related to the severity of MR, it is concluded that it is helpful to use this parameter instead of the maximal velocity pixel area for semiquantitative grading.

I t is universally acknowledged that in 1899, Wenckebach first described type I second-degree atrioventricular (AV) block in humans.1 The centennial of this clinical landmark was recently publicized.2 Although Wenckebach called this process “Luciani periods” after the Italian physiologist who observed this phenomenon in the frog heart in 1872, this pattern is now widely known as the Wenckebach phenomenon or periodicity.3 A number of workers have attributed the discovery of both types I and II second-degree AV block solely to Wenckebach.4–6 As a result, types I and II second-degree AV block is sometimes incorrectly designated as Wenckebach type I and type II block.7 Others have claimed that type II block was described independently by Wenckebach and Hay both in 1906.8–13 There are also rare, unfounded claims by compatriots of John Hay that it was he who discovered both types I and II second-degree AV block.14 It was actually John Hay who discovered the form of second-degree AV block currently known as type II block15 (Figure 1). Information about John Hay can be found in the recent article by Upshaw and Silverman.16 Hay’s original contribution was cited by Thomas Lewis in his 1925 book17 and by Schamroth in his 1971 book.18 Yet, Burch in his monograph on the history of electrocardiography merely stated that “incomplete heart block was studied extensively in man by MacKenzie, Wenckebach and Hay, by means of the polygraph.” without citing Hay’s work nor his 1906 article.19 Katz and Pick of the famed Chicago School of Electrocardiography did not mention Hay’s contribution to the understanding of second-degreeAV block in their classic 1956 book.20 In fact, the Chicago electrocardiographers indicated in other publications that Wenckebach and Hay described type II seconddegree AV block independently.12 In 1906 John Hay from Liverpool, England, published a case report in the Lancet describing a new form of second-degree AV block distinct from that previously reported by Wenckebach.15 Hay documented his findings without the benefit of the electrocardiograph, which was introduced clinically years later. Hay analyzed simultaneous tracings from the radial (arterial) and jugular (venous) pulses in a 65year-old patient with lightheadedness. The recordings in Figures 2 and 3 were described as showing a-c intervals (as a measure of AV conduction corresponding to the PR interval of the electrocardiogram) essentially normal and constant in duration regardless of the number of missing ventricular beats. Figure 2 clearly shows what is now considered type II seconddegree AV block with constant a-c intervals before and after a single-blocked atrial impulse (“a” wave not followed by “c” deflection) in a sequence of at least 4:3 AV block. Hay correctly emphasized that no similar case had been recorded in the literature and dismissed the type of AV block described by Wenckebach because the a-c interval failed to vary. The purist will argue that Figure 2 cannot be interpreted as type II second-degree AV block because there are no PR intervals and the behavior of the a-c intervals cannot be determined accurately. However, the diagnosis of type II block can be made with certainty by looking at the heart rate in the arterial recording on top of Figure 2. Note that the duration of the pause between the fourth and fifth arterial beats is exactly double that of the cycle before the block (between the third and fourth arterial beats). This indicates that AV conduction before and after the blocked impulse was constant. This constitutes the hallmark of type II block when there are at least 2 consecutively conducted P waves and only a single nonconducted impulse. A vagal effect on the AV node can be ruled out because the cycle before the block (between the third and From the Broward General Hospital, Fort Lauderdale, Florida; and the University of Bonn, Bonn, Germany. Dr. Barold’s address is: 6237 NW 21st Court, Boca Raton, Florida 33496. E-mail: ssbarold@aol.com. Manuscript received November 24, 2000; revised manuscript received and accepted January17, 2001. FIGURE 1. John Hay 1873 to 1959. (Courtesy of Arthur Hollman MD., London England).

In a prospective and parallel, randomized study, the long-term stability of epicardial defibrillation threshold was evaluated in 22 patients, using a patch-patch lead configuration at the time of implantation and generator replacement. The concomitant antiarrhythmic drug treatment consisted of either mexiletine (720 mg/day) or amiodarone (400 mg/day) and was administered to patients in a randomized and parallel manner. During a mean follow-up of 24 +/- 6 months, the defibrillation threshold increased significantly from 14.3 +/- 2.8 to 17.9 +/- 5.3 J (p < 0.05) for the entire patient group. The increase in the chronic defibrillation threshold was due to a marked increase in defibrillation energy needs in the subgroup of patients receiving amiodarone. Whereas no significant change in the defibrillation threshold was documented in the subgroup of patients receiving mexiletine, the mean defibrillation threshold increased from 14.1 +/- 3.0 to 20.9 +/- 5.4 J (p < 0.001) in those receiving amiodarone. In all patients with increased defibrillation thresholds, reevaluation showed a reduction in the defibrillation threshold after discontinuation of antiarrhythmic drug therapy. The only variable associated with an increase in the chronic defibrillation threshold was amiodarone treatment. These findings suggest that the defibrillation threshold should be measured at each generator replacement and in case of a change in antiarrhythmic drug treatment. In particular, if amiodarone treatment is initiated, it is recommended that the defibrillation threshold should be reevaluated to ensure an adequate margin of safety.