[Effect of ACE-inhibitors on left ventricular remodeling after acute anterior or posterior myocardial infarct. Cine- magnetic resonance tomography study]. / Einfluss von ACE-Hemmern auf das Remodeling des linken Ventrikels nach akutem Vorder- oder Hinterwandinfarkt. Untersuchungen mit der Cine-Magnetresonanztomographie.

The question whether patients with posterior infarctions (PMI) have a comparable benefit of an ACE-inhibitor therapy to those with anterior infarction (AMI) is still open. The study was undertaken to investigate the different influence of ACE inhibitors on the remodeling of the left ventricle after AMI or PMI. 52 patients (Pt.) (17 female, 38-73 years) were randomized to receive either 25-75 mg/day captopril (C) or 5-20 mg/day fosinopril (F) beginning on day 7 after acute myocardial infarction. 28 Pt. had AMI, 24 Pt. PMI. Infarct size was determined by the creatine kinase integral method. 50 Pt. were examined by cine magnetic resonance imaging 1 and 26 weeks after infarction. We determined: left ventricular end-diastolic (LVEDVI) and end-systolic (LVESVI) volume index, ejection fraction (EF), infarction weight (IW), left ventricular muscle mass (MM), systolic wall thickening (SWT) and motility (MOT) of the vital myocardium, and clinical behavior according to the guidelines of the New York Heart Association (NYHA). The results were compared with those of a sample (V) without ACE inhibitor therapy (10 females, 21 males, 36-75 years, 19 AMI, 12 PMI). There were no significant differences between C and F. Without ACE-inhibition therapy LVEDVI increased by 28.2% in AMI, by 18.4% in PMI (p < 0.001), with ACE-inhibition by 13.7% in AMI and by 9.9% in PMI (p < 0.001). LVESVI increased in V by 40.1% in AMI, by 28.5% in PMI (p < 0.001). With ACE-inhibitor we found an increase of 11.2% in AMI and 5.3% in PMI (p < 0.001). EF decreased without ACE-inhibitor by 18.7% in AMI and by 10.2% in PMI (p < 0.001), with ACE-inhibition increased by 4.3% in AMI and PMI, respectively (n. s.). NYHA got better in all groups, by 17.4% in AMI and 20.8% in PMI without ACE-inhibitor (n.s.), by 45.5% in AMI and 31.6% in PMI with ACE-inhibitor (p < 0.001). IG increased by 15.5% in AMI and 8.8% in PMI in V (p < 0.001), by 11.2% in AMI and 5.3% in PMI with C or F (p < 0.001). MM got bigger in V by 16.6% in AMI and 12.7% in PMI (p < 0.05), with ACE-inhibitor by 11.7% in AMI and 8.0% in PMI (p < 0.05). sWD increased by 12.9% in AMI and by 6.7% in PMI in V (p < 0.01), by 37.1% in AMI and 88.0% in PMI with C or F (p < 0.001). MOT decreased by 39.6% in AMI and 14.9% in PMI without ACE-inhibition (p < 0.001) and increased by 4.3% in AMI and by 5.0% in PMI with ACE-inhibitor (n. s.). All differences between V and the ACE-inhibitor groups were significant. Even patients with PMI clearly benefit from ACE-inhibitor therapy, but less than those with AMI. Captopril and fosinopril show no different effects after myocardial infarction.

[Effect of the long-acting beta-2 agonist inhalant formoterol on the quality of sleep of patients with bronchial asthma]. / Einfluss des inhalativen, langwirksamen Beta-2-Agonisten Formoterol auf die Schlafqualität von Patienten mit Asthma bronchiale.

BACKGROUND: Patients with asthma bronchiale often complain of exacerbations during the night. Some anti-asthmatic drugs are known to impair the quality of sleep. HYPOTHESIS: The study was undertaken to prove the effect of the long-acting, inhaled beta-2-agonist formoterol on the quality of sleep in patients with mild or moderate asthma bronchiale. METHODS: 20 patients with asthma bronchiale (15 female, 21-75 years, O 33.3 years) without sleep disorder were evaluated by polysomnography during 3 nights. After one adaptation night, the patients were randomly assigned 24 micrograms of formoterol during one and placebo during the other night. The frequency of respiratory disturbances, arousals, sleep latency, sleep stages, sleep efficiency, motoric activity, and subjective impression of sleep quality were compared in both groups. RESULTS: Respiratory disturbances were less, and the subjective impression of sleep quality was better with formoterol in 50% of the patients. The objective quality of sleep was slightly better with formoterol, but not significant (Tab. 1). CONCLUSIONS: In patients with mild or moderate asthma bronchiale, formoterol does not impair, probably slightly improves the quality of sleep.

Is the tissue affinity of ACE inhibitors of relevance for the remodeling of the left ventricular wall following myocardial infarction? Estimations with cine magnetic resonance imaging.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors have been shown to be of value in the treatment of postinfarction remodeling. The question whether substances with a greater tissue affinity are associated with advantages for the acute and the chronic course is, however, still unclear. AIM: The aim of the present study was to investigate the influence of ACE inhibitors with differing tissue affinities on the remodeling of the left ventricular wall in patients recovering from myocardial infarction. METHODS: 52 patients (17 women, aged 38-73 years) suffering their first acute myocardial infarction were randomized to receive a daily dose of either 25-75 mg captopril or 10-20 mg fosinopril, beginning on the 7th postinfarction day. 28 patients had an anterior wall infarction and 24 patients an inferior wall infarction. The size of the infarct was determined using the creatine kinase integral method. 50 patients were investigated by cine magnetic resonance imaging 1 and 26 weeks after the infarction. The following parameters were determined: infarct weight and diastolic diameter of the infarcted zone, systolic wall stress, muscle mass, diastolic and systolic diameters, systolic wall thickening, and motility of the noninfarcted myocardium. RESULTS: The infarct weight increased under captopril by 5.7% (p < 0.05) and under fosinopril by 6.1% (p < 0.05). The diastolic diameter of the infarcted zone decreased by 12% under captopril (p < 0.001) and by 11% under fosinopril (p < 0.001). The systolic wall thickness increased by 12.1% (p < 0.001) and the muscle mass by 12.7% (p < 0.001) under captopril and by 15.4% (p < 0.001) and 9.6% (p < 0.01), respectively, under fosinopril. Under captopril, the diastolic diameter increased by 2.3% (p < 0.05) and the systolic diameter by 17.8% (p < 0.01) and under fosinopril by 2.8% (n.s.) and 17.5% (p < 0.001), respectively. The systolic wall thickening increased by 73.9% under captopril (p < 0.001) and by 129.4% under fosinopril (p < 0.001). The motility decreased by 13.8% (p < 0.05) under captopril and by 6.0% (n.s.) under fosinopril. For all parameters, the results seen in anterior wall infarction were appreciably poorer than those seen in inferior wall infarction. All the differences between captopril and fosinopril were not significant. CONCLUSIONS: Captopril and fosinopril show no major differences in their influence on left ventricular wall remodeling following myocardial infarction. On the basis of the present results, the tissue affinity of an ACE inhibitor does not appear to be of a significant relevance for postinfarction treatment.

[Nocturnal gastroesophageal reflux as a cause of refractory chronic laryngitis--pathophysiology and management]. / Nächtlicher gastroösophagealer Reflux als Ursache der therapierefraktären chronischen Laryngitis--Mechanismen und Management.

Chronic laryngitis is a common disease with a multifactoral genesis. One of the known causal factors is gastrolaryngeal acid reflux as a consequence of gastroesophageal reflux disease (GERD). 10 to 30% of the patients do not show an adequate response to the standard treatment with proton pump inhibitors, which could not be well explained in the past. Our own observations indicate, that sleep related gastroesophageal reflux may play an important role. The special physiological conditions in sleep can impair the reflux, and an increased nocturnal breathing effort in snoring or sleep apnea induces an intensive gastrolaryngeal reflux. This paper explains the pathophysiological background and the diagnostics and differential treatment.

Ciguatera fish poisoning following travel to the tropics.

A 40-year-old man-as well as 15 more participants of the same meal-suddenly experienced vomiting and watery diarrhea four hours after having eaten a meal of grouper in the Dominican Republic. Symptoms persisted for four hours and were followed by a generalized pruritus and paresthesias of the lips, tongue, palms, and soles of the feet. Physical examination was normal with the exception of a pulse of 45 beats per minute, a blood pressure of 80/50 mmHg, and paradoxical temperature perception. Laboratory values were regular except for the erythrocyte sedimentation rate of 40 mm per hour. 24-hour Holter electrocardiogram showed a normal sinus rhythm with impaired heart rate variability (37-100 beats per minute). Due to the typical history and the clinical findings, ciguatera toxin ingestion was diagnosed. Pruritus decreased slightly with symptomatic therapy, but it took 16 weeks for all symptoms to resolve. Ciguatera fish poisoning is rare in temperate countries. Symptoms of this neurotoxic disease are gastrointestinal, neurologic, and cardiovascular manifestations with paresthesias, paradoxical sensor disturbances, and muscular weakness as well as bradycardia and hypotension. With travel to and from the tropics and increasing imports of tropical fish ciguatera will be of growing importance even in nontropical areas.