Interventionelle Therapie des akuten Herzinfarktes

Durch Einführung der thrombolytischen Therapie sowie einer Begleitmedikation mit Heparin und Acetylsalicyls?ure konnte die Therapie des akuten Myokardinfarktes (AMI) in den 1980er Jahren erheblich verbessert werden. Dieser Therapieform wurde zu Beginn der 90er Jahre die direkte Revaskularisation mittels akuter perkutaner transluminaler koronarer Angioplastie (PTCA) gegenübergestellt. Nachfolgend konnte die Erfolgsrate der interventionellen Therapie von Patienten mit akutem Myokardinfarkt durch die Einführung von Stents weiter gesteigert werden. Parallel wurde durch eine spezifischere antithrombotische Therapie die Sicherheit und Effektivit?t der perkutanen koronaren Intervention (PCI) deutlich verbessert. Derzeit befinden sich weitere neue Therapiestrategien zum Erhalt der linksventrikul?ren Funktion w?hrend der Reperfusion in der überprüfung. Diese umfassen systemische und lokale Medikamentenapplikation zur Verminderung des Reperfusionsschaden sowie kathetertechnische Ans?tze zur Begrenzung der Mikroembolisation und Schutz der nachgeschalteten Mikrozirkulation. Im folgenden Beitrag wird die interventionelle Therapie nach AMI unter Berücksichtigung dieser Neuentwicklungen dargestellt und der Stellenwert der prim?ren PCI in der Therapie des AMI bewertet.     

Improvement of respiratory compromise through abductor reinnervation and pacing in a patient with bilateral vocal fold impairment

Objectives/Hypothesis.

To determine whether respiratory compromise from bilateral vocal fold impairment (paralysis) can be objectively alleviated by reinnervation and pacing.

Methods.

A patient with paramedian vocal folds and synkinesis had a tracheotomy for stridor after bilateral laryngeal nerve injury and Miller Fisher syndrome. One posterior cricoarytenoideus (PCA) received a nerve‐muscle pedicle fitted with a perineural electrode for pacemaker stimulation. The airway was evaluated endoscopically and by spirometry for up to 1 year.

Results.

Bilateral vocal fold patency during quiet breathing was reversed to active vocal fold adduction during tracheal occlusion. Peak inspiratory flows (PIFs) were significantly higher (P < .001) after reinnervation. PIFs and glottic apertures increased further under stimulation (42 Hz, 1–4 mA, 42–400 μsec). although the differences were not significant.

Conclusions.

Based on our preliminary data, PCA reinnervation and pacing offer promise for amelioration of respiratory compromise after paradoxical adduction in bilateral vocal fold impairment. Laryngoscope, 2010     

Atrial Arrhythmias in Long-QT Syndrome under Daily Life Conditions: A Nested Case Control Study

Background: The long-QT syndromes (LQTS) are inherited electrical cardiomyopathies characterized by prolonged ventricular repolarization and ventricular arrhythmias. Several genetic reports have associated defects in LQTS-causing genes with atrial fibrillation (AF). We therefore studied whether atrial arrhythmias occur in patients with LQTS under daily-life conditions.
Methods: We systematically assessed atrial arrhythmias in LQTS patients and matched controls using implanted defibrillators or pacemakers as monitors of atrial rhythm in a nested case-control study. Twenty-one LQTS patients (3 male; 39 ± 18 years old; 18 on β blocker, ICD therapy duration 6.3 ± 2.7 years; 4 LQT1, 6 LQT2, 2 LQT3) were matched to 21 control subjects (13 male; 50 ± 19 years old; 3 on β blocker; pacemaker therapy duration 8.5 ± 5.5 years; 19 higher-degree AV block, 2 others). LQTS patients were identified by a systematic search of the LQTS patient databases in Münster and Munich.
Results: One-third (7 of 21) of the LQTS patients developed self-terminating atrial arrhythmias (atrial cycle lengths <250 ms). Only one control patient developed a single episode of postoperative AF (P < 0.05 vs LQTS).
Conclusions: LQTS patients at high risk for ventricular arrhythmias may develop short-lasting atrial arrhythmias under daily-life conditions, suggesting that prolonged atrial repolarization may contribute to the initiation of AF.     

Gro?es Pseudoaneurysma des linken Ventrikels nach Posterolateralwandinfarkt

Zusammenfassung Pseudoaneurysmen des linken Ventrikels sind eine sehr seltene Komplikation nach akutem Myokardinfarkt. Wir berichten über einen 69jährigen Patienten mit ausgedehnten posterolateral gelegenem Pseudoaneurysma, welches durch eine reanimationspflichtige Linksherzdekompensation klinisch manifest wurde. Lokalisation und Ausdehnung des Aneurysmas konnten echokardiographisch und angiographisch sicher quantifiziert werden; koronarangiographisch bestand korrespondierend zur Lokalisation des Aneurysmas ein proximaler Abbruch des Ramus circumflexus. Auf Grund der hohen Rupturgefahr von Pseudoaneurysmen wurde der Patient einer raschen chirurgischen Therapie zugeführt. Summary Pseudoaneurysmus of the left ventricle are rare complications after acute myocardial infarction. We report on a 69 year old patient with a large false aneurysm located in the posterolateral ventricular wall. It became clinically apparent during an episode of severe left heart failure. Echocardiography and left ventriculography allowed an accurate determination of localization and dimension of the pseudoaneurysm; coronary angiography revealed a proximal occlusion of the left circumflex coronary artery. Because of the high risk of rupture, a rapid surgical repair of the false aneurysm was indicated.     

Wallerian degeneration after cerebral infarction: evaluation with sequential MR imaging

The dynamic signal intensity changes at magnetic resonance (MR) imaging in active and chronic wallerian degeneration in the corticospinal tract were evaluated. Forty-three patients with wallerian degeneration seen on MR images after cerebral infarction were studied. When possible, patients with acute stroke were examined with MR imaging prospectively at the onset of symptoms and then at weekly intervals for several months. Focal infarction without distal axonal degeneration is demonstrated for the 1st month following onset of clinical symptoms. At 4 weeks, a well-defined band of hypointense signal appears on T2-weighted images in the topographic distribution of the corticospinal tract. After 10-14 weeks, the signal becomes permanently hyperintense. Over several years, accompanying ipsilateral brain stem shrinkage occurs. The dark signal intensity observed on T2-weighted images between 4 and 14 weeks is believed to result primarily from transitory increased lipid-protein ratio.