Biomedical subjects

B M Sanner

Publications and source records attributed to B M Sanner.

23 records · Page 2Linked to original sources

PubMed1997

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.

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PubMed1997

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.

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PubMed1997

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.

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PubMed1997

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.

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PubMed1996

[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].

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.

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