Biomedical subjects
Publications and source records attributed to N Cristal.
The energy expenditure in 23 healthy parturient women during spontaneous labor was assessed by continuous measurement of their O2 consumption and CO2 production. Due to the intermittent character of uterine contractions, normal labor and delivery did not impose high energy demands on the parturient, whereas a prolonged labor and delivery in which energy input was high led to maternal metabolic disturbances.
Hematocrit values, plasma fibrinogen levels, and erythrocyte deformability are well-recognized factors affecting blood viscosity. We studied the incidence of abnormalities in these factors among 17 patients suffering from thromboangiitis obliterans (Buerger's disease) compared with 14 normal age- and sex-matched control subjects. Hematocrit values and fibrinogen levels were higher, whereas the erythrocyte filterability index was lower among the patients with Buerger's disease (p less than 0.001). Incubation of washed erythrocytes from these patients with control plasma of blood type AB produced an improvement of the filterability index (p less than 0.005). Our findings suggest that patients suffering from Buerger's disease show, in addition to the well-recognized arterial lesions, an abnormality in the factors affecting blood viscosity. This may contribute to a worsening of the clinical manifestations. Evidence is presented suggesting that a plasmatic factor may be responsible for the impaired erythrocyte filterability.
We compared the effect of two exercise stress tests on blood pressure in normal and borderline populations. The aim of the trial was to determine if isometric exercise testing by handgrip can replace the isotonic exercise test in population screening for the detection of mild and latent hypertension. The study involved 150 subjects; 62 were normotensive and 88 were borderline hypertensive. No significant statistical difference was found in diastolic pressure between the tests. In normotensive subjects, the diastolic response after isotonic effort was 79.3 +/- 9.6 mm Hg and 89.0 +/- 9.7 mm Hg after the isometric test (p less than 0.05). However, both results did not pass 100 mm Hg. In borderline hypertensive patients the diastolic response to the isotonic test was 105.6 +/- 8.8 mm Hg and after the isometric test 107.7 +/- 10.6 mm Hg (NS). The results show that the handgrip isometric test can replace the complicated isotonic test for the screening detection and evaluation of hypertensives in the population.
An appreciation of the hemodynamic and biochemical changes induced by drugs is critical for a logical diagnostic interpretation of graded stress tests and the evaluation of the projected exercise prescription and exercise programs that a patient is asked to follow. Drug therapy is clearly not a contraindication to acute or chronic exercise as long as the potential benefits and complications of exercise and drug interaction are considered.
Worldwide clinical trial data concerning the pharmacokinetic and pharmacodynamic characteristics of the clonidine transdermal therapeutic system (TTS) are reviewed with reference to its antihypertensive efficacy. The amount of clonidine delivered to the systemic circulation is a direct function of TTS size. After initial patch application, there is a delay of 2 to 3 days before the onset of action, but after removal of the patch, plasma clonidine levels decline slowly, at an elimination half-life of about 20 hours. Evaluation in approximately 2000 patients with mild to moderate hypertension has shown that the bioavailability of transdermal clonidine is comparable to that of oral clonidine and that equivalent blood pressure reductions are achieved. The rate at which dose increases were found necessary to maintain adequate blood pressure control over extended periods reflects a low incidence of tolerance to this new once-a-week dosage form of clonidine, and there has been little evidence of rebound hypertension after discontinuation of TTS treatment.
Four cases of purulent complications in the heart following acute myocardial infarction are described. Fever occurred during the first week after coronary occlusion. In one case thrombophlebitis at an infusion site was followed by purulent pericarditis. One patient had an infected mural thrombus with peripheral septic embolic, and two suffered from streptococcal endocarditis. The association between these infections and recent acute myocardial infarction could be related to tissue necrosis and local thrombosis, but the increasing risk of bacteremia following invasive monitoring procedures in these patients is a risk factor that should not be ignored.
Serum amyloid A concentrations were determined in serial serum samples of 41 patients with confirmed acute myocardial infarction (10 with acute ischaemia and two with myocarditis). A sharp increase in serum amyloid A concentration was observed early at onset of infarct; it peaked on the third day (up to 2200 fold of normal values) and declined towards normal during the following days, if no complications occurred. Different patterns were observed in patients with acute ischaemia or myocarditis. Although serum amyloid A is not a specific marker, it may, because of its high sensitivity and characteristic patterns of change, represent an additional useful biochemical variable in the diagnosis, follow up, and prognosis of acute ischaemic heart disease.
Alpha 1-antitrypsin serum levels were measured in 48 patients with acute myocardial infarction and in 19 control patients either with coronary heart disease without necrosis, or with neither coronary disease nor inflammation. Alpha 1-antitrypsin was significantly raised in the group of patients with acute myocardial infarction. As some patients individually showed no change in alpha 1-antitrypsin levels, however, they were divided into two groups according to the maximum serum levels attained. Patients with non-increasing levels of alpha 1-antitrypsin showed increased mortality and a higher incidence of cardiogenic shock, whereas reinfarction occurred more frequently in the group with high alpha 1-antitrypsin levels. Our findings may suggest that the course of a myocardial infarction is determined not only by the severity of the ischaemic event, but also by the response of the "acute" phase reaction" mechanism. We conclude that a failure of alpha 1-antitrypsin levels to increase after myocardial infarction may be associated with a worse clinical course.
Plasma fibrinogen levels were followed from admission to the coronary care unit up to 3 months after an acute myocardial infarction (AMI) (51 patients at entry--49 patients at follow-up). Mean initial value as determined with 24 hours of onset of symptoms was 522 mg% +/- 205 S.D. Peak value 845 mg% +/- 215 S.D. was reached 3-5 days after onset of symptoms. Mean fibrinogen level on a later follow-up was similar to the initial value (521 mg% +/- 145 S.D.). Our data confirm that a rise in the plasma fibrinogen level is common after myocardial necrosis. No correlation was found between the maximum peak value and the clinical course of the disease. However, death, reinfarction and cardiogenic shock were more frequent among patients with an initial plasma fibrinogen level higher than 400 mg%. Our findings suggest that the acute increase in fibrinogen following necrosis is less significant to the clinical course than a chronically high plasma fibrinogen level.
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In the case described, necrosis of the atrial musculature led to rupture of the chamber. This was overlooked for 4 days until the patient died of ventricular rupture. This unusual complication of atrial infarction may be amenable to surgical repair if recognised in time. The high gain recording of P waves in the presence of AV block made it possible to evaluate the P wave changes during atrial infarction: (1) changes in the configuration and width of the P wave, probably resulting from intra-atrial conduction defect; (2) depression of the PR segment (0.04 to 0.07 mV); and (3) a previously unrecorded convexity in the first portion of the PR segment, in the leads in which the depression of the PR segment was observed.
The activity of dopamine beta-hydroxylase in the serum was measured in patients with acute cardiac disorders who were admitted to a coronary care unit. The activity of the enzyme on admission was similar in patients with acute myocardial infarction and in those with other conditions; on discharge, the activity was reduced significantly. Patients with myocardial infarction had the greatest fall in the activity of dopamine beta-hydroxylase. Patients with multiple signs of sympathetic hyperactivity had significantly higher values for the activity of dopamine beta-hydroxylase on admission. Pain was found to significantly increase the activity of the enzyme. These data confirm findings that the activity of dopamine beta-hydroxylase in the serum reflects the intensity of sympathetic activity. The factors contributing to the elevated sympathetic activity in some patients with acute myocardial infarction seem to be nonspecific, but because of the ominous nature of increased sympathetic tone in this condition, it could be advantageous to identify these patients.
Fibrinogen labeled with iodine 125 was used to detect deep vein thrombosis (DVT) in 35 patients during their course and convalescence from acute myocardial infarction. Clinical status was assessed and scored with the use of a modified coronary prognostic index. According to the prognostic scores, patients were allocated to one of two groups. Of 27 patients in good clinical condition, DVT developed in only one patient, whereas thromboembolic complications occurred in seven of eight patients who were severely ill--a highly significant difference. Prophylactic anticoagulation is advisable in patients at risk.
Atrial fibrillation was observed in 39 (11 percent) of 350 instances of acute myocardial infarction. The mortality among these patients was 41 percent (16/39). Atrial fibrillation was more common in patients with undetermined infarctions and in older people. As opposed to death rates close to 50 percent among patients with anterior, combined, and undetermined infarctions, the presence of atrial fibrillation did not affect the mortality among patients with inferior infarctions (10 percent, 1/10). Ventricular rates higher than 120 beats per minute and duration of the arrhythmia longer than six hours were not associated with increased mortality. Hemodynamic failure was present in almost all of the cases and preceded the arrhythmia in most of them. It is concluded that different mechanisms are responsible for the production of atrial fibrillation in the setting of acute myocardial infarction, and the prognosis of the patient is related to the mechanism of production and not to the arrhythmia itself.
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A case is presented in which transient left anterior hemiblock masked the electrocardiographic signs of old inferior wall infarction. The electrocardiographic features are correlated with the anatomopathological findings. This case re-emphasizes the need for careful evaluation of patients with chest pain and left anterior hemiblock.