Annals of clinical research最新文献

To determine if multiple risk factor modification favorably alters the rate of progression of coronary atherosclerosis, 300 patients with established atherosclerosis have been randomized into a clinical trial; 155 to usual care and 145 to special intervention. All patients have medical/risk examinations at baseline and annually for 4 years. The special intervention patients undergo aggressive risk factor management with emphasis on lipoprotein modification, dietary management, smoking abatement, blood pressure control, weight loss and increased physical activity. To measure progression of atherosclerosis, a quantitative, computer-assisted coronary arteriographic system was developed to analyze the baseline and 4-year follow-up arteriograms. This procedure uses a catheter with a metallic calibration cylinder at its tip to determine absolute artery size and automated computer edge detection techniques to define the internal border of the artery. The analysis system detects artery borders using changes in cine film density and measures distances between these borders. For each segment the minimum, maximum and mean diameters are measured and percent stenosis and atheroma area calculated. This system provides precise and reproducible measures of coronary artery segment diameter. Using this technique, we estimate a 33% reduction in the rate of coronary artery progression over 4 years, defined as mean segment diameter, can be detected at a power of 0.80 and an alpha of 0.05 (one tailed test) with a sample size of 120 in each of 2 groups.

The association between measures of social connections and mortality from ischemic heart disease was studied using data from the Alameda County Study in California and the North Karelia Study in Eastern Finland. In both studies, there is a significant association between the extent of social connections and mortality from ischemic heart disease. Those who are socially isolated are at 2 to 3-fold increased risk of death over 5 to 9 years when compared to those most connected. These results are found when there is extensive adjustment for traditional cardiovascular risk factors. Analyses using a variety of techniques provide no evidence that this association is due to the impact of prevalent disease on the extent of social contacts. Furthermore, changes in social connections during one 9-year period are prospectively associated with increased risk of death from ischemic heart disease in a subsequent 9-year period. Finally, evidence is presented indicating that the level of social connections modifies the association between diastolic blood pressure and risk of death from ischemic heart disease.

The sauna induces changes in the secretion of hormones, some similar to changes induced in any other stress situation and others characteristic of exposure to the sauna. Noradrenaline is usually the only catecholamine raised by the sauna in people accustomed to it. The secretion of the antidiuretic hormone is increased and the renin-angiotensin-aldosterone system is activated. The concentrations of the growth hormone and prolactin, in particular, secreted from the anterior pituitary are increased in the circulation. The concentration of the immunoreactive beta-endorphin in blood may also increase which may reflect the feeling of pleasure or, on the other hand, discomfort induced by the sauna. The views on the effects of the sauna on the secretion of the ACTH and cortisol are partly contradictory, probably due to differing ways of taking the sauna bath. In Finnish sauna takers the concentration of cortisol in blood is not usually increased. The changes induced by the sauna in various hormone concentrations in the circulation are, however, normalized within a couple of hours after the heat stress.

In a retrospective study of four patients with paroxysmal ventricular tachycardia (VT) induced by silent ischaemia (SI) one case was related to transmural SI secondary to coronary artery spasm and the other cases to subendocardial SI related to non-dynamic coronary artery stenosis. In one patient it was possible simultaneously to document the presence of myocardial ischaemia preceding VT using two independent markers: ECG and thallium scintigraphy. The common feature was attacks of fast polymorphic VT with fainting and intermediate cardiac arrest as the sole clinical manifestation. Attacks at rest occurred in both types of patients, whereas exercise induced attacks were an inconstant feature of SI-VT in non-dynamic coronary artery stenosis. VT suppression was accomplished by anti-ischaemic intervention in three patients: by calcium antagonist medication in the patient with coronary artery spasm, by coronary artery surgery in two cases of non-dynamic artery stenosis. The risk of underdiagnosing SI-VT is discussed. Screening of patients with the aborted cardiac arrest syndrome by ambulatory ECG-monitoring and repeated symptom-limited exercise-ECG is recommended.

Hepatic bile flow and its bile acid composition were determined in a group of 23 rats receiving 20% (W/v) ethanol by daily intubations 5 times a week over a 10-12 week period and in a control group of 23 rats. The aim was to elucidate the well known role of alcohol in pancreatitis. Chronic ethanol administration resulted in a significant increase in 2-h bile production and bile secretion rates. Molar concentrations of total and individual bile acids were determined by the hydroxysteroid dehydrogenase method after thin layer separation. No significant differences in molar concentrations of total or separate bile acid were observed. Special attention was paid to free bile acids. A spot with a Rf value corresponding to cholic acid was found in 10 rats in each group. This was examined by mass spectrometry using direct inlet technique, but no free cholic acid could be identified. Thus it seems that the changes in the amounts of bile acids are not decisive for the origin of acute alcoholic pancreatitis but that increased bile flow caused by chronic alcohol ingestion may favour reflux of bile into the pancreas, resulting in pancreatitis.

A series of 181 patients (158 with obstructive uropathy) treated by percutaneous nephrostomy (PN) in 1978-1987 is evaluated. In 8.3% of the patients PN did not succeed. The success rate of PN was lower when done outside normal working hours and before ultrasound guidance was used. Major complications occurred in 5.5% and minor ones in 10.5%. There was no direct mortality. The complications and the possible avoidance of them are discussed. In 68% of patients nephrostomy improved their clinical condition. The benefit of PN was closely related to the existing renal recovery potential following the relief of obstruction; a problem that has not yet been fully solved.

Circulatory effects of bopindolol, a new nonselective beta blocking agent with intrinsic sympathomimetic activity and atenolol were compared. After baseline and first dose measurements atenolol 25 mg twice daily and bopindolol 1 mg daily were given to 10 healthy young subjects. Haemodynamic measurements were made noninvasively using echocardiography and systolic time intervals. Clinical and circulatory indices were measured at baseline, after initial dose and after one week of regular treatment at rest and at isometric handgrip exercise (IE) (HG). Atenol reduced the heart rate from 62 bpm to 49 and blunted totally the HR increase during IE (p less than 0.01). Bopindolol caused a 10% fall in heart rate (NS) at rest and a 15% fall (p less than 0.05) during IE. BP fell by 6% after atenol administration and 4% after bopindolol (NS) at rest and similarly during IE. In contrast to bopindolol, atenolol caused small increases initially in left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD). A 10% increase in FS was seen at rest after bopindolol administration (NS). With the fall in heart rate the estimated cardiac output (CO) also fell from 3.66 to 3.151/min (P less than 0.05) after atenolol but rose from 3.87 to 3.93 after bopindolol (NS) during chronic treatment. Consecutively the total peripheral resistance (TPR) was increased to some extent by atenolol, whereas bopindolol reduced it at rest and during IE. A similar response was also found in systolic time intervals PEP/LVET which were reduced during bopindolol administration.(ABSTRACT TRUNCATED AT 250 WORDS)