Standardisierte Kontrastmittelsonographie (CEUS) in der klinischen Akut- und Notfallmedizin sowie Intensivmedizin (CEUS-Akut)

Die Anaesthesiologie -     

Doppler echocardiography imaging of construction-induced regurgitation of technical heart valve prostheses]

The normal leakage flow in modern technical heart valve prostheses can be visualized by color-coded Doppler-echocardiography, provided that an adequate ultrasonic image quality can be achieved. Sometimes it may be difficult, however, to distinguish such a normal leakage flow from pathological regurgitation. We therefore mounted new specimens of five different types of prostheses (Bj?rk-Shiley monostrut, Medtronic-Hall, Omnicarbon, Saint Jude Medical, Duromedics) into an invitro model, where the leakage flows could directly be visualized as emerging water jets. When the system was completely filled, the jets could also be registered by two-dimensional Doppler-echocardiography. For each valve, characteristic patterns for the localization of the principal jets were found. Besides the relative broad central jet in the Medtronic-Hall valve, all other jets arose mainly at the ring. They were detected at the hinges or the basis of the larger struts, respectively, and with asymmetrical mono-disc valves at the side of the smaller opening. The length and the orientation of the jets were found to change significantly with minimal variations of the position of the closing discs. This variability could be confirmed, when in a separate model the overall leakage flows were repeatedly measured. For patient examinations it seems useful to refer mainly to the localization of the jet origins. The comparison with reference values of jet-dimensions in Doppler images will rarely enable the examiner to distinguish between normal and pathological jets.     

Medikamentöse Therapie des Vorhofflimmerns in speziellen Situationen

The treatment of atrial fibrillation has to take into account the underlying cardiac and extracardiac diseases. A successful treatment of the underlying disease will only be sufficient treatment of atrial fibrillation in very rare situations. Therefore, this review focuses on the consequences of underlying heart disease, the hemodynamics and concomitant clinical situations on the treatment of atrial fibrillation.     

Relation between symptoms and profiles of coronary artery blood flow velocities in patients with aortic valve stenosis: a study using transoesophageal Doppler echocardiography.

OBJECTIVE: To analyse profiles of coronary artery flow velocity at rest in patients with aortic stenosis and to determine whether changes of the coronary artery flow velocities are related to symptoms in patients with aortic stenosis. DESIGN: A prospective study investigating the significance of aortic valve area, pressure gradient across the aortic valve, systolic left ventricular wall stress index, ejection fraction, and left ventricular mass index in the coronary flow velocity profile of aortic stenosis; and comparing flow velocity profiles between symptomatic and asymptomatic patients with aortic stenosis using transoesophageal Doppler echocardiography to obtain coronary artery flow velocities of the left anterior descending coronary artery. SETTING: Tertiary referral cardiac centre. PATIENTS: Fifty eight patients with aortic stenosis and 15 controls with normal coronary arteries. RESULTS: Adequate recordings of the profile of coronary artery flow velocities were obtained in 46 patients (79%). Left ventricular wall stress was the only significant haemodynamic variable for determining peak systolic velocity (r = -0.83, F = 88.5, P < 0.001). The pressure gradient across the aortic valve was the only contributor for explaining peak diastolic velocity (r = 0.56, F = 20.9, P < 0.001). Controls and asymptomatic patients with aortic stenosis (n = 12) did not differ for peak systolic velocity [32.8 (SEM 9.7) v 27.0 (8.7) cm/s, NS] and peak diastolic velocity [58.3 (18.7) v 61.9 (13.5) cm/s, NS]. In contrast, patients with angina (n = 12) or syncope (n = 8) had lower peak systolic velocities and higher peak diastolic velocities than asymptomatic patients (P < 0.01). Peak systolic and diastolic velocities were -7.7 (22.5) cm/s and 81.7 (17.6) cm/s for patients with angina, and -19.5 (22.3) cm/s and 94.0 (20.9) cm/s for patients with syncope. Asymptomatic patients and patients with dyspnoea (n = 14) did not differ. CONCLUSIONS: Increased pressure gradient across the aortic valve and enhanced systolic wall stress result in characteristic changes of the profile of coronary flow velocities in patients with aortic stenosis. Decreased or reversed systolic flow velocities are compensated by enhanced diastolic flow velocities, particularly in patients with angina and syncope. This characteristic pattern of the profile of coronary artery flow velocities in patients with angina or syncope may be useful for differentiating those patients from asymptomatic patients.     

Electrophysiological characterization of connexin 40 deficient hearts--in vivo studies in mice

Intercellular communication is not only mediated by extracellular transmitters, but also directly by gap junction channels. One channel is composed of two hexameric hemichannels which consist of six polypeptide subunits called connexines (Cx). In the mammalian heart the following connexines have been documented: Cx37, Cx40, Cx43, Cx45, Cx46, Cx50 and Cx57. The labeling by number represents the rounded, molecular mass of the amino acid sequences given in kD. If identical connexin-isotypes form both connexons of a gap junction channel, homotypic coupling exists and a homomeric gap junction channel is formed. Different connexin-isotypes within both connexons cause form heterotypic coupling and heteromeric gap junction channels. Each channel type has specific properties regarding permeability and electrical conductance. Beside a typical age-dependent alignment of gap junction channels on the surface of the cardiac myocytes, regional distribution of the different connexins is different at distinct parts of the mouse heart. Cx40 is not found in the ventricular working myocardium of mice. In the atria as well as in the conduction system, Cx40 is the most frequently expressed. In line with the localization and the conduction properties of distinct homotypic gap junction channels, the Cx40 deficient mouse is suitable for analysis of atrial arrhythmias. Cx40-deficiency in the mouse heart results in characteristic ECG changes like first degree atrioventricular block and prolongation of the QRS duration. Thus, an impairment of the sinuatrial, intraatrial and atrioventricular conduction properties is documented in Cx40 deficient mice. These observations are associated with an increased atrial vulnerability. The Cx40 deficient mouse provides a good example of the relevance of transgenic mouse models to clarify the mechanisms of arrhythmogenesis. The clinical impact of future transgenic mouse models depends on the cooperation of geneticists, basic researchers and clinicians.     

Herzrhythmusst?rungen bei gezielt Connexin-defizienten M?usen: Bedeutung für die Rhythmologie

Gap-Junction-Kan?le erm?glichen eine direkte Kommunikation zwischen benachbarten Zellen. Sie sind aus jeweils zwei Halbkan?len, den Connexonen aufgebaut, welche ihrerseits aus sechs Proteinuntereinheiten, den Connexinen (Cx) bestehen. In den Herzmuskelzellen wurden bisher drei Connexin-Proteine nachgewiesen: Cx40, Cx43 und Cx45. Die Zahlen-Bezeichnung entspricht der aus der Aminos?uren-Sequenz errechneten, abgerundeten Molekülmasse in kilo Daltons. Sind beide Connexone aus identischen Connexin-Isotypen aufgebaut, spricht man von homotypischer Koppelung, wenn alle 12 Connexine den gleichen Isotyp besitzen, liegt ein homomerer Kanal vor. Darüberhinaus ist auch die Bildung funktioneller heterotypischer Kan?le zwischen Halbkan?len unterschiedlicher Connexin-Zusammensetzung m?glich. Die unterschiedlichen Connexin-Isotypen verleihen den Gap-Junction-Kan?len spezifische Eigenschaften im Hinblick auf Permeabilit?t und elektrische Leitf?higkeit. Neben einer typischen Membranlokalisation der Gap-Junction-Kan?le in der Myokardzelle bestehen zus?tzlich noch regionale Unterschiede der Connexine innerhalb einzelner Herzstrukturen. Für das Arbeitsmyokard des Ventrikels ist Cx43 charakteristisch; dagegen wurden Cx40 nicht und Cx45 nur in geringen Mengen in dieser Region bei der Maus nachgewiesen. Im Vorhofmyokard und im Erregungsleitungssystem ist das Cx40 vorherrschend. Cx45 bildet eine funktionell leitungsverz?gernde Grenzschicht zwischen Erregungsleitungssystem und umgebender Muskulatur. Entsprechend der Lokalisation und der Leitungseigenschaften der einzelnen Gap-Junction-Kan?le eignet sich die Cx43-defiziente Maus zur Analyse von Kammerrhythmusst?rungen, die Cx40-defiziente Maus prim?r zur Analyse von Vorhofrhythmusst?rungen. Eine Abnahme der ventrikul?ren Leitungsgeschwindigkeiten und eine gesteigerte ventrikul?re Vulnerabilit?t wurde bei Abnahme der Anzahl und Dichte von Cx43-Gap-Junction-Kan?len beobachtet. Dies wird in der Literatur jedoch kontrovers diskutiert. Cx40-Defizienz verursacht sinuatriale, intraatriale und atrioventrikul?re Leitungsverz?gerungen und eine gesteigerte atriale Vulnerabilit?t.? Transgene Mausmodelle und neue Mapping-Verfahren der Ausbreitung der elektrischen Erregungswelle tragen wesentlich zum besseren Verst?ndnis der Arrhythmogenese bei. Genetiker, Kliniker und Grundlagenforscher sind zur Zusammenarbeit aufgerufen, um die klinische Relevanz dieser Modelle und damit ihre Bedeutung in der modernen Medizin zu untersuchen.     

Effects of hypertonic versus isotonic infusion therapy on regional cerebral blood flow after experimental cardiac arrest cardiopulmonary resuscitation in pigs

OBJECTIVE: To evaluate the effects of hypertonic, isooncotic, and isotonic infusion therapy on cerebral blood flow (CBF) during and after cardiopulmonary resuscitation (CPR) from experimental cardiac arrest (CA). METHODS: In 32 domestic swine (13-23 kg) open chest CPR was initiated after 8 min of ventricular fibrillation. With the onset of CPR animals randomly received 2 ml/kg per 10 min of either hypertonic saline (HS: 7.2% NaCl), hypertonic-isooncotic HES-saline (HHS: 7.2% NaCl in 6% HES 200,000/0.5), isooncotic HES (6% HES 200,000/0.5), or isotonic (normal) saline (NS: 0.9% NaCl). Haemodynamic variables were monitored continuously, and coloured microspheres were used to measure CBF quantitatively before CA, during CPR, and 20, 90 and 240 min after restoration of spontaneous circulation (ROSC). RESULTS: In HES/NaCl treated animals, CBF significantly decreased during CPR compared to the prearrest level (P < 0.01, respectively; MANOVA). In contrast, CBF was sustained during CPR in HS/HHS treated animals and significantly higher compared to animals receiving NS (P < 0.05, respectively). During recirculation severe postischaemic hypoperfusion as indicated by a decrease of CBF below the prearrest level, was present only in animals receiving HES and NS. CONCLUSIONS: Hypertonic solutions (HS/HHS) applied during internal cardiac massage enhanced CBF during CPR and after ROSC.     

Time course of myocardial and cerebral blood flow during stable but hemodynamically compromising ventricular tachycardias

Myocardial and cerebral blood flow were determined with radiolabeled microspheres in 20 Sprague-Dawley rats during sinus rhythm and during stable but hemodynamically compromising ventricular tachycardias. In addition, in 10 animals the measurements were performed at hypotension induced by exsanguination. In controls (n=10), myocardial and cerebral blood flow were 5.14±0.6 and 1.03±0.3 ml/g per minute, respectively. The range of myocardial blood flow values was markedly enlarged after onset of tachycardia induced by epicardial pacing. The mean values of myocardial blood flow were 5.80±1.9 ml/g per minute (n.s.) after 1 min and 7.46±3.9 ml/g per minute (n.s.) after 5 min. Cerebral blood flow, however, significantly decreased after 1 min (0.57±0.1 ml/g per minute,P<0.01) and after 5 min (0.71±0.3 ml/per minute,P<0.05). In contrast, 1 min after exsanguination myocardial blood flow signifcantly decreased (4.03±1.5 ml/g per minute,P<0.05) and recovered after 5 min (6.06±1.2 ml/g per minute, n.s.) Cerebral blood flow was below control levels 1 min (0.70±0.2 ml/g per minute,P<0.05) after onset of hypotension due to exsanguination and returned to normal values with the next 4 min (0.90±1 ml/g per minute, n.s.). The results suggest that stable but hemodynamically compromising ventricular tachycardias markedly affect cerebral blood flow, whereas in most cases myocardial blood flow is maintained within normal ranges, or even increases. An augmented myocardial autoregulation can be concluded from the autoregulatory index. This maintainance of regulatory ability might be due to the increase of myocardial oxygen consumption at decreased coronary perfusion pressures during tachycardias. In contrast, during hypovolemic hypotension, myocardial as well as cerebral blood flow decreased. During stable but hemodynamically compromising ventricular tachycardias, cerebral blood flow initially drops drastically and recovers slowly over the next 5 min. This finding contrasts with the results of hypovolemic and drug-induced hypotension models.