[A 67-year old man with epigastric pain]. / 67-jähriger Patient mit epigastrischen Schmerzen.

A 67-year-old man suffering from epigastric pain showed a phytobezoar in the endoscopy. Therapy with Coca Cola® and enzymes was initiated. The (partial) lysis led to a migration of the bezoar into the ileum, resulting in a small bowel obstruction. After removal of the remaining bezoar via ileotomy a secondary pneumatosis intestinalis occurred. As a rare finding the (phyto-)bezoar should be considered as a differential diagnosis of abdominal pain - especially considering the rising numbers of bariatric surgery, which is a potential risk factor. Furthermore, intestinal obstruction after migration has to be considered as a relevant complication of treatment.

Sleep-Disordered breathing in patients referred for angina evaluation--association with left ventricular dysfunction.

BACKGROUND: Clinical observations have linked sleep-disordered breathing to cardiovascular morbidity and mortality, and especially to coronary artery disease. HYPOTHESIS: The study was undertaken to determine the prevalence of sleep-disordered breathing in consecutive patients referred for angina evaluation, and analyzed the parameters influencing the severity of sleep-disordered breathing. METHODS: In all, 68 consecutive patients (53 men, 15 women, aged 63.4 +/- 10.0 years) referred for angina evaluation were studied. Coronary angiography, selective left ventriculography, and a polygraphic study with a validated six-channel monitoring device were performed. Full-night polysomnography was used to reevaluate patients with an apnea/hypopnea index > or = 10/h. RESULTS: Sleep-disordered breathing as defined by an apnea/hypopnea index > or = 10/h was found in 30.9% of patients; its prevalence was not increased in patients with and without coronary artery disease (26.5 vs. 42.1%). Multiple stepwise linear regression analysis revealed that the severity of sleep-disordered breathing was significantly and independently associated with left ventricular ejection fraction (r = -0.38; p = 0.002), but not with age, body mass index, gender, diabetes mellitus, hypertension, hyperuricemia, hypercholesterolemia, smoking habits, or coronary artery disease. In this group of patients, multiple logistic regression analysis could not demonstrate sleep-disordered breathing to be an independent predictor of coronary artery disease. CONCLUSIONS: Sleep-disordered breathing is common in patients referred for angina evaluation. The degree of sleep-disordered breathing is mainly determined by the extent of left ventricular dysfunction.

Platelet function in patients with obstructive sleep apnoea syndrome.

Patients with obstructive sleep apnoea syndrome (OSAS) are subject to an increased cardiovascular morbidity including myocardial infarction and stroke. Platelets play an important role in the pathogenesis and triggering of acute cardiovascular syndromes. So far, the influence of OSAS on platelet function is not fully understood. Platelet aggregability to epinephrine, collagen, arachidonic acid, and adenosine diphosphate in vitro was measured in 17 consecutive male patients (53.0+/-2.1 yrs) with polysomnographically verified OSAS and compared with that of 15 male controls (50.1+/-3.6 yrs) at 20:00 h, 24:00 h, and 06:00 h. In addition, the long-term effects of continuous positive airway pressure (CPAP) therapy on platelet aggregability was assessed after 6 months. Platelet aggregation in vitro induced by epinephrine showed a slight increase overnight in the untreated OSAS patients (NS) whereas it decreased slightly (NS) in the controls and in the treated OSAS patients. Pretherapeutic platelet aggregability was significantly lowered by CPAP therapy both at 24:00 h (64.0+/-6.5 versus 55.3+/-6.7%, p<0.05) and at 06:00 h (64.1+/-6.5 versus 45.8+/-7.6%; p=0.01). Platelet aggregability during sleep in the controls resembled that found in patients with OSAS during CPAP therapy. The results suggest that obstructive sleep apnoea syndrome contributes, at least in part, to platelet dysfunction and that long-term continuous positive airway pressure treatment may reduce platelet aggregability.

[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.

Influence of tissue affinity of angiotensin-converting enzyme inhibitors on left ventricular remodeling after myocardial infarction.

BACKGROUND: The demonstration of local renin-angiotension systems has raised the question of whether angiotensin-converting enzyme (ACE) inhibitors with different tissue affinities differ with regard to their effects on postinfarction remodeling. HYPOTHESIS: The study was undertaken to investigate the influence of ACE inhibitors with different tissue affinity on morphology and function of the infarcted left ventricle. METHODS: In all, 52 patients (17 women, 35 men, 38-73 years) with large acute myocardial infarction were randomized to receive either 25-75 mg/day captopril or 10-20 mg/day fosinopril beginning on the Day 7 after infarction. Of these, 28 had anterior and 24 had posterior wall infarctions. Infarct size was determined by the creatine kinase integral method. Fifty patients were examined by cinemagnetic resonance imaging (CMRI) 1 and 26 weeks after infarction. The following parameters were determined: left ventricular end-diastolic and end-systolic volume index (LVEDVI, LVESVI), ejection fraction (LVEF), infarct weight, and muscle mass (LVMM). The volume-to-mass ratio (VMR) was calculated and the clinical status according to the guidelines of the New York Heart Association (NYHA) was documented at each examination time. The results were compared with those of a historical sample without ACE-inhibitor therapy examined in an identical manner (n = 31, 10 women, 21 men, 36-75 years). RESULTS: LVEDVI and LVESVI increased in the first 6 months after infarction by 24.9 and 36.6%, respectively, in the historical sample; by 11.0 and 7.8%, respectively, under captopril; and by 13.1 and 10.7%, respectively, under fosinopril. LVEF decreased by 14.9% in the untreated sample, by 3.7% under captopril and by 5.0% under fosinopril. Infarct weight and LVMM increased by 12.7 and 15.3%, respectively, without ACE inhibition, by 5.7 and 10.1%, respectively, in patients treated with captopril, and by 6.1 and 9.3%, respectively, in patients treated with fosinopril. The VMR increased by 7.4% in the historical sample, by 3.5% in the captopril group, and by 1.8% in the fosinopril group. The NYHA clinical status improved by 18.2% without ACE inhibition, by 42.9% in the captopril group, and by 26.3% in the fosinopril group. The differences between the two ACE-inhibitor groups and the reference group were all significant, while the differences between the captopril group and the fosinopril group were significant only for VMR (p < 0.01) and NYHA class (p < 0.05). CONCLUSIONS: Both captopril and fosinopril have a comparable positive influence on postinfarction remodeling and on clinical status. Lipophilicity and tissue affinity do not seem to play a clinically important role in ACE-inhibitor therapy after infarction.

Use of conventional and self-adjusting nasal continuous positive airway pressure for treatment of severe obstructive sleep apnea syndrome: a comparative study.

STUDY OBJECTIVES: To compare conventional and self-adjusting nasal continuous positive airway pressure (nCPAP) therapy in patients with severe obstructive sleep apnea syndrome with respect to suppression of respiratory disturbances, quality of sleep, mean mask pressure, and patient compliance. DESIGN: Cohort study of consecutive patients with obstructive sleep apnea syndrome, single-blinded. SETTING: Clinical sleep laboratory in Germany. PATIENTS: Fifty patients (44 men, 6 women who ranged in age from 35 to 71 years) with polysomnographically confirmed severe obstructive sleep apnea syndrome (respiratory disturbance index [RDI], >20/h). MEASUREMENTS AND INTERVENTIONS: After baseline polysomnography, patients were randomly treated with nCPAP either in conventional (group 1) or in automatically adjusting (group 2) mode. Three to 6 months after adjustment, all patients underwent polysomnography again. They also were examined with a portable monitoring device and received a questionnaire on subjective well-being and device evaluation. RESULTS: Anthropometric and respiratory data were comparable in both groups; body mass index had not changed significantly in the follow-up. RDI dropped by 91.5% (from 38.3+/- 13.9/h to 3.6+/-4.4/h) in conventional and by 93.6% (from 35.5+/-9.6/h to 2.4+/-1.6/h) in self-adjusting mode (statistically not significant [NS]). Sleep efficiency decreased by 4.0% in conventional and increased by 2.0% in self-adjusting mode (NS). In both groups, normal sleep structure was largely restored. Mean mask pressure was 8.1+/-2.5 cm H2O in group 1 and 6.5+/-1.7 cm H2O in group 2 (p<0.01). Patient compliance in terms of nights per week of mask appliance was better in the self-adjusting mode (5.7+/-0.7 to 6.5+/-0.4; p<0.01). CONCLUSION: Self-adjusting nCPAP demonstrates the same reliability in suppression of respiratory disturbances as fixed-mask pressure therapy. Sleep quality is slightly superior, patient compliance is highly significantly better.

Pulmonary hypertension in patients with obstructive sleep apnea syndrome.

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is associated with an increased cardiovascular morbidity, including pulmonary hypertension. Little is known about factors influencing the degree of pulmonary hypertension and left ventricular dysfunction in patients with OSAS, especially in the absence of concomitant lung disease. METHODS: Right heart catheterization, arterial blood gas analysis, and pulmonary function tests were performed in 92 consecutive patients (81 men and 11 women; mean +/- SD age, 53.1 +/- 11.0 years) with polysomnographically verified OSAS, in whom clinically significant lung disease was excluded. RESULTS: Eighteen patients (20%) had mild pulmonary hypertension; 8 (44%) of them also had increased pulmonary capillary wedge pressures (Ppew). Left ventricular dysfunction was associated with arterial hypertension. Only Ppcw (r = 0.51; P < .001) and the percentage of time during sleep spent with an oxygen saturation below 90% (as an indicator of the severity of OSAS) (r = 0.34; P = .003) were significantly and independently associated with pulmonary artery pressure. CONCLUSIONS: Obstructive sleep apnea syndrome can cause mild pulmonary hypertension, even in the absence of pulmonary disease. In these patients, pulmonary hypertension is of the postcapillary type, or-in patients with normal left ventricular function-strongly related to the severity of OSAS. Our findings indicate that OSAS may constitute an important, and independent, risk factor for pulmonary hypertension.

Right ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

There is conclusive evidence that obstructive sleep apnoea syndrome (OSAS) influences right heart haemodynamics and can also induce pulmonary hypertension. It is not known, however, whether right ventricular dysfunction can occur in patients with OSAS in the absence of lung disease. We studied 107 patients (94 males, 13 females, mean age 55 +/- 11 yrs) with polysomnographically verified OSAS in whom clinically significant lung disease was excluded. Right ventricular ejection fraction (RVEF) was determined by radionuclide ventriculography. In addition, pulmonary function tests, arterial blood gas analysis and right heart catheterization were performed. RVEF was impaired in 19 patients (18%). Eighteen (95%) had signs or symptoms consistent with mild right ventricular failure. Patients with or without impaired RVEF did not differ with respect to body mass index, age or lung function. Stepwise multiple logistic regression analysis revealed that RVEF was significantly associated with the apnoea/hypopnoea index (r = -0.68; p = 0.0009) and the extent of nocturnal oxyhaemoglobin saturation (r = 0.42; p = 0.035), but not with age, body mass index, blood gas analysis, gender, lung function, pulmonary artery pressure and left ventricular ejection fraction. We conclude that in patients with otherwise unexplained right ventricular failure, obstructive sleep apnoea syndrome may underlie the right ventricular dysfunction.

[Pronounced hypersomnia in a 13-year-old patient with periodic leg movements]. / Ausgeprägte Hypersomnie einer 13jährigen bei periodic leg movement.

We report on a rare case of a thirteen-year old female with excessive daytime somnolence, which was caused by periodic leg movement. This underlines the necessity first to consider this diagnosis and second to record unconditionally the EMG derivation at minimum of the tibialis muscles in all patients with hypersomnolence. Even if carbamazepine is not the treatment of choice, in this case it was of remarkable effect.

Changes of the left ventricle after myocardial infarction--estimation with cine magnetic resonance imaging during the first six months.

BACKGROUND: In recent years, the interest of cardiologists has focused increasingly on the morphologic and functional changes of the left ventricle after myocardial infarction (MI), due to their great prognostic significance for the patient. HYPOTHESIS: The aim of this study was to evaluate changes in left ventricular morphology and function during the first 6 months following MI. METHODS: In all, 61 patients (17 women, 44 men, age 36-83 years) were examined with cine magnetic resonance imaging (CMRI) 1, 4, and 26 weeks after myocardial infarction. Thirty-two patients had anterior MI and 29 patients had posterior MI. According to enzyme-derived infarct weight, 15 patients had small infarcts (< 20 g), 19 had intermediate-sized infarcts (20-40 g), and 27 patients had large infarcts (> 40 g). CMRI was performed in the true short axis of the left ventricle. In each examination, left ventricular end-diastolic and end-systolic volume indices (LVEDVI, LVESVI), stroke volume index (LVSVI), ejection fraction (LVEF), and regional thickness, mass, and motility of the myocardial wall-diastolic thickness (IDdia), infarct mass (IM) and motility (IMOT) of the infarct area and diastolic and systolic thickness (VDdia, VDsys), muscular mass (VM), and motility (VMOT)-were determined. In addition, patients were divided into subgroups according to New York Heart Association (NYHA) functional status at baseline. RESULTS: In the total group, LVEDVI increased from 73.9 +/- 23.5 ml/m2 to 85.4 +/- 28.1 ml/m2 (p < 0.001) and LVESVI from 40.5 +/- 19.4 ml/m2 to 51.2 +/- 29.0 ml/m2 (p < 0.001). In the subgroups the development depended on infarct size and location. LVSVI and LVEF remained more or less constant except for large anterior infarctions. All changes of the myocardial wall depended on infarct size and location: In all patients IDdia decreased from 10.4 +/- 1.6 mm to 8.9 +/- 1.7 mm (p < 0.001), IMOT from 2.0 +/- 1.6 mm to 0.5 +/- 2.9 mm (p < 0.001). IM increased from 41 +/- 21 g to 45 +/- 25 g (p < 0.001). In the total group, VDdia increased from 11.9 +/- 1.6 mm to 12.4 +/- 1.8 mm (p < 0.05), VDsys from 16.6 +/- 2.5 mm to 17.2 +/- 3.1 mm (p < 0.05). In the subgroups changes varied: VDdia and VDsys decreased markedly in large anterior wall infarctions. VM increased in the total cohort from a mean of 246 +/- 66 g to 276 +/- 80 g (p < 0.001). VMOT decreased from 7.1 +/- 2.4 mm to 6.3 +/- 2.7 mm (p < 0.05). Loss of motility was most pronounced in anterior infarctions. The volume-mass ratio, a measure of the success of compensation of volume increase by myocardial hypertrophy, decreased in small infarcts, remained unchanged in intermediate infarcts, and increased in large infarcts. There was a trend toward improvement of the NYHA functional status during the observation period. CONCLUSIONS: Changes of the left ventricular chamber during the first 6 months following MI are dependent on its size and location, with large anterior infarctions having the worst course. Myocardial wall remodeling is also dependent on infarct size and location, and the volume-mass ratio increases in the presence of large areas of necrosis, indicating the non-compensatory effect of myocardial hypertrophy. However, these changes have no clinical effect during the first half year after MI.

[Effect of infarct size and site, patency of the infarct vessel and perfusion of vital myocardium on remodeling of the left ventricle--studies with cine-magnetic resonance tomography in the first 6 months following myocardial infarct]. / Einfluss von Infarktgrösse und -lokalisation, Offenheit des Infarktgefässes sowie Perfusion des vitalen Myokards auf das Remodeling des linken Ventrikels--Untersuchungen mit der Cine-Magnetresonanztomographie in den ersten 6 Monaten nach Myokardinfarkt.

BACKGROUND: Aim of the study was to evaluate the influence of infarct size and location and patency of the infarction and non-infarction vessels on left ventricular morphology and function in the first 6 months after myocardial infarction. METHODS: 61 patients (17 female, 44 male, 36-83 years) were examined with Cine Magnetic Resonance Imaging (CMRI) 1 and 26 weeks, and with coronary angiography 4 weeks after infarction. 32 patients had anterior, 29 patients posterior myocardial infarction. 15 patients had small infarcts (< 20 gm), 19 intermediate sized (20-40 gm) and 27 patients large infarcts (> 40 gm). CMRI was done in short axis of the left ventricle. Left ventricular enddiastolic and endsystolic volume indices (LVEDVI, LVESVI), ejection fraction (LVEF), muscle mass (VM) and motility (VMOT) of the vital myocardium, mass (IM) and area (IA) of the infarction zone, and volume-mass-ratio (VMR) of the left ventricle were determined on each examination. RESULTS: After 6 months large infarctions had 25% more LVEDVI, 41% more LVESVI, 20% less LVEF, 11% more VM, 13% less VMOT, 13% more IM, 47% more IA, and a 17% increased VMR compared to small infarcts. Anterior infarctions showed 11% more LVEDVI, 19% more LVESVI, 7% less LVEF, 4% more VM, the same VMOT, 5% more IM, 21% more IA, and 6% more VMR than posterior infarctions. If the infarction vessel was not perfused, after 6 months LVEDVI was 12% more, LVESVI 19% more, LVEF 7% smaller, VM 4% less, VMOT the same, IM 5% more, IA 17% more, and VMR 7% more increased than in the group with open infarction artery. When both non-infarction vessels were stenosed, LVEDVI rose 24% more, LVESVI 49% more, LVEF fell 25% more, VM rose 12% more, VMOT fell 26% more, and VMR rose 12% more than in patients with indisturbed perfusion of the vital myocardium. CONCLUSION: Perfusions of the vital myocardium and infarct size seem to be the most important factors for post infarction remodeling of the left ventricle. Infarct location and patency of the infarction vessel are of less influence.

[Coronary heart disease in patients with obstructive sleep apnea]. / Koronare Herzerkrankung bei Patienten mit obstruktiver Schlafapnoe.

OBJECTIVE: As patients with severe obstructive sleep apnoea (OSA) have increased cardiovascular morbidity and mortality rates, the prevalence of coronary heart disease (CHD) was investigated in patients with OSA proven by polysomnography (apnoea/hypopnea index > or = 10/h). PATIENTS AND METHODS: In 440 patients (400 men, 40 women; mean age 55.3 [16-80] years) with OSA proven by polysomnography, the possible diagnosis of CHD was assessed by history, physical examination, ECG at rest and on exercise, one- and two-dimensional echocardiography and, where indicated, myocardial scintigraphy and coronary angiography. RESULTS: CHD was demonstrated by angiography in 24.6% (men: 26.4%; women: 7.5%). Adding patients with CHD diagnosed noninvasively, but unconfirmed by angiography, positive correlation was found in 33.2% (men: 34.8%; women: 17.5%). CONCLUSION: There was a high prevalence of CHD in patients with OSA. This underlines the importance of careful cardiac diagnosis in patients with OSA.

[Modification of cardiopulmonary performance parameters in patients with obstructive sleep apnea treated with nCPAP therapy]. / Entwicklung kardiopulmonaler Leistungsparameter bei Patienten mit obstruktiver Schlafapnoe unter nCPAP-Therapie.

nCPAP influences cardiopulmonary hemodynamic function in patients with obstructive sleep apnea (OSA). It is known that systolic function of the right and left ventricle, systemic and pulmonary hypertension, arterial blood gases and lung function during the day may improve under this treatment. We prospectively followed 30 patients with severe OSA and determined diastolic left ventricular function (Doppler echocardiography), cardiovascular efficiency (steady state exercise stress testing); and individual assessment of performance (standardized psychometric questionnaire) before, and 2 weeks and 6 months after initiation of nCPAP treatment. The following results could be obtained (first value after 2 weeks, second value after 6 months): Doppler echocardiography: E/A rose by 9.3% (p < 0.05) and another 0.5% (n.s.). E/A integral increased by 13.8% (p < 0.01) and another 3.5% (n.s.). Deceleration period decreased by 22.7% (p < 0.01) and another 3.1% (n.s.). Steady state exercise stress testing: Maximum performance rose by 10% (p < 0.05) and another 17.5% (p < 0.01). Heart rate ratio 100 W/rest dropped by 13.5% (p < 0.001) and another 6.5% (p < 0.01), systolic blood pressure ratio 100 W/rest by 0.8% (n.s.) and another 14.9% (p < 0.001). Diastolic blood pressure ratio 100 W/rest did not change significantly. Questionnaire: Assessment of well-being increased by 44.5% (p < 0.05) and another 16.9% (n.s.). After an initial drop of 0.8% (n.s.), quality of life increased by 14.9% (p < 0.05). Assessment of performance rose by 21.7% (p < 0.05) and another 4.1% (n.s.). nCPAP therapy in patients with OSA improves diastolic function of the left ventricle, cardiovascular performance and individual assessment of performance.

[Obstructive sleep apnea in patients with coronary heart disease]. / Obstruktive Schlafapnoe bei Patienten mit koronarer Herzerkrankung.

Patients with obstructive sleep apnea have an increased cardiovascular morbidity and mortality, those with co-existent coronary artery disease being particularly at risk. The object of our study was to evaluate the prevalence of obstructive sleep apnea in patients with coronary artery disease. 153 patients (117 men, 36 women) with verified coronary artery disease were given a highly sensitive standardized questionnaire. The 59 patients with pathological results were then checked with a 6-channel non-laboratory monitoring system. 22.2% of all patients had a respiratory disturbance index (RDI) above 5/h. and 14.4% above 10/h. 13.3% had a pathological RDI and additionally suffered from excessive daytime sleepiness. Patients with coronary artery disease have a high prevalence of obstructive sleep apnea and should consequently be screened for this sleep-related breathing disorder.

Magnetic resonance angiography as a technique for the visualization of hemodialysis shunts.

In order to test the suitability of magnetic resonance angiography for the visualization of Brescia-Cimino hemodialysis shunts, 20 patients (8 women, 12 men, aged 24-69 years) were examined with this technique. The shunt arm was placed in an extremity coil. The time-of-flight method was applied. Examination time was less than 15 min. Arterial digital subtraction angiography (DSA) of the shunt arm was carried out additionally in 8 patients in whom pathological results had been obtained. Surgery was performed on 2 patients. In all cases, the feeding artery, anastomosis, and shunt were clearly visible. The results corresponded exactly to those of DSA and, in the patients who had undergone surgery, also to the situs. The patients stated that the examination technique was not very disturbing. Magnetic resonance angiography in the time-of-flight technique seems to be recommendable for the examination of Brescia-Cimino dialysis shunts. Compared to DSA, it has major advantages: it is noninvasive, and no ionizing radiation or contrast medium are associated with the procedure.