Biomedical subjects
Publications and source records attributed to G Louridas.
Hibernoma is a rare hypervascular tumour originating from brown fat. A case report of a thigh hibernoma with computed tomographic and angiographic findings is presented. An attempt to differentiate this tumour from the white fatty tumours, i.e., lipoma, angiolipoma, angiomyolipoma, and liposarcoma, is discussed.
In 11 asthmatic subjects the relative magnitude and the site of airway bronchoconstriction were compared after the oral administration of 40 mg of propranolol and 2.5 mg of pindolol and the magnitude and site of bronchodilation produced by 0.5 mg subcutaneous terbutaline were tested after pretreatment with propranolol and pindolol. Specific airway conductance (sGaw) and peak expiratory flow rate (PEFR), both believed to reflect changes in large airways, and capacity isoflow (Ciso-v) and delta Vmax50, both believed to reflect changes in small airways, were determined before and after administration of placebo, pindolol, and propranolol. Treatments were given double blind and in random order. After the administration of propranolol we noted a significant bronchoconstrictive effect in the large airways (mean values of PEFR and sGaw, expressed as percentages of control values, decreased by 87.4% +/- 13.2% and 43.3% +/- 8.9%) and in the small airways (mean value of Ciso-v increased by 20.6% +/- 4.7% and that of delta Vmax50 decreased by 50% +/- 11.9% of control). By contrast, pindolol produced no significant effect on sGaw or PEFR but the tests of small airway function showed significant bronchoconstriction (mean values of Ciso-v increased by 12.9% +/- 2.6% and those of delta Vmax50 decreased by 47.2% +/- 9.2%). This action makes pindolol potentially dangerous in asthmatic patients. The bronchodilator action of terbutaline on large airways is diminished after the use of both propranolol and pindolol.
The bronchodilator effect of salbutamol inhalation was compared with the oral administration of the drug in 10 patients with bronchial asthma. The study consisted of treating each patient for 4 consecutive days with: (1) a combined regimen consisting of a 2-mg tablet of salbutamol and 10 puffs of salbutamol inhalation (100 micrograms in each puff) given in pairs of two puffs every 20 min (regimen 1); (2) salbutamol inhalation (regimen 2); (3) salbutamol tablet (regimen 3), and (4) placebo, tablet and inhalation (regimen 4). The bronchodilator effect was assessed measuring the forced expiratory volume in 1 s, the forced vital capacity and the peak expiratory flow rate. The bronchodilator response was significantly greater on the inhalation alone and the combined regimen than on the oral and placebo regimens. The combined regimen showed a better although not significant bronchodilatory response than the inhalation regimen. We conclude that the inhalation treatment with salbutamol is superior to the oral route of administration in treating bronchial asthma and that the oral treatment has an added effect.
Baroreceptor sensitivity, reflected by the slope of the linear regression of the electrocardiographic R-R interval on the rise of systolic blood pressure after injection of phenylephrine, was significantly lower in 27 patients with chronic obstructive pulmonary disease (4.67 +/- 2.67) than in 10 normal subjects (12.07 +/- 3.3) of comparable age (p less than 0.001). In 20 patients in whom right heart catheterisation was performed, pulmonary artery pressure was inversely related to baroreflex sensitivity (r = - 0.603, p less than 0.01). Independent variables such as arterial Po2, Pco2, and mean pulmonary artery pressure were examined in order to assess their ability to predict baroreflex sensitivity. The independent variable that made the most significant contribution was mean pulmonary artery pressure. It seems that the attenuation of baroreflex response in patients with chronic obstructive pulmonary disease is caused mainly by pulmonary hypertension and partly by the central effects of hypoxia and hypercapnia.
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Vectorcardiograms in 34 patients with chronic obstructive pulmonary disease and 30 normal people were analyzed with the aim of developing sensitive criteria for the detection of pulmonary artery hypertension. The pulmonary artery pressure was correlated with the known vectorcardiographic measurements of the area of the QRS loop and with two new linear measurements which reflect the QRS loop displacement of the right ventricular hypertrophy. The proposed linear vector-cardiographic and the QRS loop area criteria provided a sensitive means for the noninvasive approximate estimation of mean pulmonary artery pressure in patients with chronic obstructive pulmonary disease. Their sensitivity and specificity were proved to be considerable.
The ECGs of 72 patients with an unequivocal vectorcardiographic diagnosis of either left anterior hemiblock (LAH) or inferior myocardial infarction (IMI) or both were reviewed. Our intention was to identify definite electrocardiographic criteria for the diagnosis of the left anterior hemiblock and of inferior myocardial infarction when both were present vectorcardiographically. All patients with left anterior hemiblock, accompanied or not by IMI, had a left axis deviation, a negative terminal deflection (S wave) in leads II, III and a VF; the majority of them also had a terminal r wave in lead a VR (50 of 52, 96%). The diagnosis of LAH was therefore always possible in the concomitant presence of both entities. A negative initial deflection (Q wave) significant in size or not significant was present in a minority of patients with both LAH and IMI (9 of 24, 37.5% in lead II; 7 of 24, 25% in lead III; and 12 of 24, 50% in lead aVF). In the patients with insignificant Q waves, as well as in the rest of the patients with rS configuration, the electrocardiographic diagnosis of IMI was not possible due to the concomitant presence of LAH.
We assessed the left ventricle function in 24 patients with severe (forced expiratory volume in 1 sec less than 50% of predicted) chronic obstructive pulmonary disease (COPD) and in 21 normal people. We measured the left ventricular systolic time intervals (STI) and echocardiographic left ventricular diameters, volumes, cardiac index, stroke volume index, echo ejection fraction and functional mean rate of circumferential fiber shortening (Vcf). In 13 of the 24 patients with COPD the mean pulmonary artery pressure and pulmonary artery wedge pressure were recorded. The STI in the patients with COPD were found abnormal while the echocardiographic parameters and pulmonary wedge pressure were normal. 1 patient had a high pulmonary arterial wedge pressure and a low Vcf. 2 patients had an ejection fraction less than 60%, but in only 1 of these the Vcf was low. No patient had all three parameters abnormal. We conclude that in patients with COPD the increased right ventricular afterload and the interaction between left and right ventricles are responsible for the abnormal left ventricular STI, while the left ventricular function is normal.
The systolic time intervals (STI) were used to study the left ventricular performance in 51 patients with chronic obstructive pulmonary disease (COPD), in 24 normal subjects and in 13 patients with both COPD and coronary heart disease (CHD). Our study shows that resting spine STI are abnormal in patients with COPD and that the STI in the sitting position and after exercise in these patients are changing in a similar way to those of normal subjects. In patients with both COPD and CHD we found the resting supine STI and the postexercise left ventricular ejection time index (LVETI) to differ from both normals and patients with COPD alone. When these same patients were sitting the STI failed to change, in striking contrast to the normal subjects and to the patients with COPD alone. The similar responses of normal subjects and of patients with COPD in the two stress conditions as well as the different postural and postexercise responses of patients with both COPD and CHD suggest a normal left ventricular function in patients with COPD.
Ventilatory response to CO2 (delta VE/delta PCO2), respiratory drive (delta P0.1/delta PCO2), breath-holding time (BHT) on 100% O2 and log BHT/PCO2 slope during CO2 rebreathing was assessed, in 19 control subjects and in 22 patients with chronic obstructive pulmonary disease (COPD) with hypercapnia (PCO2 greater than 50 mm Hg). The log BHT/PCO2 slope was expressed as the PCO2 increment to half the BHT. We found no correlation between BHT on 100% O2 and delta VE/delta PCO2 or delta P0.1/delta PCO2 in controls and COPD subjects. delta PCO2 halving BHT had an inverse statistical significant correlation with delta VE/delta PCO2 and delta P0.1 delta PCO2 in controls and patients. In contrast to delta P0.1/delta PCO2, the delta PCO2 halving BHT increased in COPD patients and there are patients with normal respiratory drive but prolonged delta PCO2 halving BHT. The delta PCO2 halving BHT as delta VE/delta PCO2 cannot be substituted for delta P0.1/delta PCO2 in the clinical assessment of respiratory chemosensitivity in COPD patients.
An echocardiographic (echo), vectorcardiographic (VCG) and electrocardiographic (ECG) study of the right ventricle was carried out in 27 patients with chronic obstructive pulmonary disease and cor pulmonale. The subxiphoid echocardiographic approach was applied in all patients. The right ventricular internal diameter index (RVIDd), anterior right ventricular wall thickness (RVWT) and the ratio (R) intraventricular septum thickness/anterior right ventricular wall thickness were statistically different in the 27 patients compared to the 33 normals. All 27 patients had a RVIDd greater than 1.33 cm while in only 17 (63%, P less than 0.01) of these was right ventricular hypertrophy (RVH) detected with VCG or ECg criteria. In 20 patients the RVWT was measured and in 19 of these the RVWT was greater than 0.56 cm. In only one patient was the RVWT less than 0.56 cm. VCG or ECG criteria showed RVH in only 14 (70%) of these patients. The R was measured in 18 patients. All patients had R less than 1.99 and in only 12 (67%, P less than 0.01) of these was RVH diagnosed with VCG or ECG criteria. It seems that the RVIDd, the RVWT and the R are useful indexes for the detection of right ventricular dilatation and hypertrophy. Therefore echocardiography is superior to the conventional ECG and VCG in the recognition of right ventricular hypertrophy and dilatation.
Coronary angiography was performed in 95 patients 3 months to 3 years after a single myocardial infarction. The patients were categorized into 4 groups according to coronary angiography findings: group I with three or four vessels diseased; group II with two vessels diseased; group III with one vessel diseased, and group IV with normal arteries. Vessel disease was considered present if 50% of the lumen was narrowed. The patient population was almost equally distributed among group I (26), group II (26), group II (33) and group III (34). Group IV included only 3 patients in this retrospective study.
Respiratory drive in a patient with central alveolar hypoventilation was assessed by mouth occlusion pressure method. Respiratory drive was almost abolished in this patient.
Respiratory drive (deltaP 0.1/deltaPCO2) and ventilatory response (deltaVE/deltaPCO2) to CO2 has been estimated in 20 normal subjects and 28 patients with chronic obstructive pulmonary disease (COPD). In patients with COPD, drive and ventilatory response to CO2 were diminished, but no statistical correlation with FEV1, MBC, TLC, FRC, RV/TLC was found. A statistically negative correlation was found between blood bicarbonate and drive or ventilatory response to CO2. Patients with emphysema and normal PaCO2 demonstrated normal deltaP 0.1/deltaPCO2. In contrast, patients with chronic bronchitis with the same pulmonary function abnormalities and hypercapnia had significant diminution of the deltaP 0.1/deltaPCO2. Therefore, we feel that pulmonary function abnormalities alone cannot explain the deltaP 0.1/deltaPCO2 decrease; in most cases there sould coexist a diminished respiratory sensitivity.
Two patients with a prolapse and cleft posterior mitral leaflet were studied. The first case had an associated ostium secundum type atrial septal defect. In both cases, the pansystolic regurgitation of contrast material during angiography corresponded to the pansystolic configuration of the murmur. In each instance, the systolic murmurs displayed a late systolic accentuation during the maximal prolapse of the mitral valve. The echocardiographic studies demonstrated only a late systolic prolapse which in both patients corresponded angiocardiographically to the maximum buckling of the pansystolic prolapse. Echocardiographic and angiocardiographic features of cleft posterior mitral valve leaflet are discussed.
In order to determine the incidence of bronchopulmonary aspergillosis in patients with other types of pulmonary pathology, 586 in-patients, out-patients and controls were examined during the period 1968-1970 in Baguley Hospital, Manchester, England. It was found that from the 344 in-patients and out-patients with other pulmonary pathology, 6 had a definite diagnosis of allergic aspergillosis. 1 had pulmonary aspergilloma while 53 other patients demonstrated some evidence of bronchopulmonary aspergillosis. These 53 patients had insufficient criteria to be classified in one of the recognised forms of aspergillosis. The number of controls examined was 242, none of whom were found to have allergic or other forms of aspergillosis. Eleven of these had a positive immediate skin test the other test being negative. In addition to the above groups 534 patients with bronchial asthma attending the out-patient department, were investigated with multiple intradermal tests, including Aspergillus fumigatus. Positive intradermal Aspergillus test was found in 130 of the patients with bronchial asthma. This investigation showed that the bronchopulmonary asperigillosis is more prevalent in patients with a pulmonary disease than in persons without this pathology.
The present report describes a patient with a whooping murmur secondary to tricuspid insufficiency. The main features of this tricuspid whoop were as follows: variable in time, moving from mid to late systole; unpredictably associated with normal respiratory phases; after deep inspiratory apnea was almost constantly present.
A case is reported showing a tachycardia dependent Wenckebach phenomenon in both the A-V node and the left bundle branch system. Pacing from the His bundle region induced manifest (direct) and imcompletely concealed (indirect) types of Wenckebach phenomenon within the left bundle branch system.