[Intracoronary diagnosis in coronary angioplasty. Extended information with new techniques].
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Biomedical subjects
Publications and source records attributed to S R Johansson.
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An inexpensive approach to stratification of patients admitted for arterial surgery into groups of high and low cardiac risk has been prospectively evaluated in 235 consecutive patients. The Goldman and Detsky indices, assessed by a nurse the day before surgery, both identified patient groups with increased risk of lethal or potentially lethal (myocardial infarction, pulmonary oedema) cardiac events within 30 days after peripheral vascular surgery. The Goldman index was the more sensitive predictor of cardiac death (overall frequency 3.1 per cent) while the Detsky index was superior for prediction of non-lethal cardiac events (overall frequency 5.9 per cent). The simplest and yet most effective stratification into high and low cardiac risk was achieved using a Detsky score of 10 as the cut-off. It is concluded that multifactorial risk index-based preoperative screening can identify low-risk patients (Detsky score < or = 10), who may be accepted for vascular surgery (aortic aneurysm surgery excluded) without additional cardiac testing.
Arterial surgical patients have a poor long-term survival and suffer significant risks of experiencing perioperative cardiac events, mainly due to a high incidence of coronary atherosclerosis impairing left ventricular function. The perioperative cardiac risk can be assessed by use of clinical cardiac risk indices, which are inexpensive but may have suboptimal sensitivity, or by more extensive cardiac tests. In this study the efficacy of a combined, non-invasive and inexpensive technique of risk assessment was prospectively evaluated in 195 patients undergoing peripheral arterial surgery (aortic aneurysms not included). All patients were preoperatively examined by a nurse registering the Detsky cardiac risk index score (DRI) and performing resting computerised bioimpedance cardiodynamic measurements (CM). Cardiac deaths (CD, n = 6), potentially lethal cardiac complications (PLC, n = 11) within 30 days and long-term survival during 20 +/- 12 (S.D.) months of follow-up were identified. CD was best predicted by combining CM and DRI, while PLC was best predicted by combining DRI and the haemoglobin concentration of the blood (Hb). A group without CD containing 88% of the cases was identified. Furthermore, the combination of DRI < or = 10 and Hb > 120 g/l identified a low risk group (57% of all cases) with no PLC or CD. Using CM, DRI and Hb in combination, patient groups with long-term survival from 0-90% were identified. We conclude that this inexpensive cardiac risk screening both identifies low risk vascular surgical patients, for whom more sophisticated preoperative cardiac testing can be omitted, and predicts long-term survival.
The aim of this study was to assess the plasma mitogenic activity in connection with percutaneous transluminal coronary angioplasty (PTCA) and the relation to restenosis. Plasma samples were taken on the morning before, 1 and 24 h after, 2 weeks after and 6 months after elective PTCA in 50 patients. Follow-up coronary angiography was carried out after 6 months or earlier if clinically warranted. Samples were also taken from 17 patients undergoing coronary angiography without PTCA. The mitogenic activity, expressed as the fraction of labelled nuclei after incubation of arterial smooth muscle cells with plasma in the presence of 3H-thymidine, was higher 1 h after PTCA than before (53.1 +/- 7.4 vs 26.8 +/- 7.3, P < 0.001). Later values were not elevated and no increase was seen after coronary angiography. The groups with (n = 19) and without (n = 31) restenosis did not differ in mitogenic activity. These results indicate that the plasma level of mitogenic activity increases immediately after PTCA. The pathophysiological significance of this increase for the development of restenosis is unclear, since the magnitude of the increase does not seem to be related to restenosis.
Restenosis after coronary angioplasty (PTCA) is a major problem, limiting the long-term efficacy of the procedure. Lipoprotein levels are associated with the development of atherosclerosis and may also be associated with restenosis. In this study the serum levels of cholesterol (CH), triglycerides (TG), high density lipoprotein (HDL) and low density lipoprotein (LDL) were analysed in 157 patients undergoing 161 PTCA procedures. Follow-up coronary angiograms were performed after 6.0 +/- 4.3 months. The restenosis rate was 33%. Treatment with aspirin and a residual stenosis of 25-49% immediately after successful PTCA were the only variables associated with restenosis (P less than 0.05), otherwise the clinical and angiographic characteristics were similar with and without restenosis. There was no relationship between restenosis and the levels of CH, TG, HDL or LDL (P greater than 0.05). In univariate and multivariate analysis of males (n = 121) and females (n = 40) separately, restenosis was associated with low HDL in men and high HDL in women (P less than 0.05), but not with CH, TG or LDL (P greater than 0.05). We conclude that the serum levels of CH, TG and LDL do not seem to be related to restenosis after PTCA. It is suggested that low HDL in males and high HDL in females is related to restenosis.
PURPOSE: Recurrent stenosis after percutaneous transluminal coronary angioplasty (PTCA) is a significant problem, requiring repeat dilation in about one-third of all treated patients. Various clinical and procedure-related predictors have been proposed. Between 1983 and 1987, 257 patients underwent 322 procedures, where 380 stenoses were attempted. Indications were: stable angina pectoris 73%, unstable angina pectoris 22%, other indication 5%. The primary success rate was defined as a less than 50% remaining postprocedure stenosis. FINDINGS: Repeat angiograms were done for 88% of the initially successful cases, either six months after PTCA or if there was a clinical recurrence. Restenosis was defined as a recurrence of a more than 50% diameter stenosis. The restenosis rate was 33% and was significantly higher (p less than 0.05) for unstable (46%) than for stable angina pectoris (29%). There was a nonsignificant tendency to a higher restenosis rate in the left anterior descending artery than in the other coronary vessels. IMPLICATIONS: The increased restenosis rate seen after PTCA for unstable angina pectoris could be caused by a higher activity in systems affecting the proliferative processes in the smooth muscle cells of the arterial wall, which is thought to form the pathophysiologic basis for restenosis after PTCA.
PURPOSE: Revascularizing procedures like percutaneous transluminal coronary angioplasty (PTCA) aim at reducing the incidence and severity of myocardial ischemia. To evaluate this, continuous Holter ST analysis is a possible method. DESIGN: 41 patients (35 men, 6 women) with stable angina pectoris had continuous twenty-four-hour two-channel Holter registration (V5/aVF-analogous leads) recorded before and after PTCA. Transient myocardial ischemia (TM) was defined as 0.1 mV ST depression or more 80 msec after the J point for one minute or more. FINDINGS: PTCA was successful for 37 patients (90%). Eleven of these had a total of 53 episodes of TM, 36 (68%) before and 17 (32%) after PTCA (p less than 0.05). Fifteen episodes (28%) were symptomatic, and 38 (72%) were asymptomatic. Six patients had TM after successful PTCA, 5 of whom had one-vessel disease and a clinically uncomplicated course. One patient had multivessel disease, with only one vessel dilated. Follow-up angiograms for 9 of the 11 patients with TM revealed 5 restenoses. There was no significant correlation between TM after PTCA and subsequent restenosis (p greater than 0.05). IMPLICATIONS: TM is common in patients with stable angina pectoris. The incidence significantly decreases after successful PTCA, but TM is seen also with a clinically uncomplicated course. In multivessel disease this is consistent with incomplete revascularization, whereas in single-vessel disease the most likely cause is intermittent spasm or thrombosis. TM after successful PTCA does not seem to be a predictor of restenosis.
Restenosis after percutaneous transluminal coronary angioplasty (PTCA) cannot currently be prevented. Different medical regimens have been largely unsuccessful. Experimental studies suggest roles for beta-adrenergic blockers and calcium antagonists. Controlled clinical studies have failed to show any decrease in restenosis rate for calcium antagonists. Corresponding studies for beta blockers are lacking. This study evaluates 541 consecutive PTCA procedures, 455 (86%) in patients treated with beta blockers after PTCA (76% metoprolol, 14% atenolol, 4% sotalol, 6% others) and 86 (14%) in patients without beta blockers. Angiographic success was achieved in 483 of 620 lesions (78%), and was not significantly different with or without beta blockers (79 vs 73%, p greater than 0.05). The procedure success rate and the complication rates (myocardial infarction, emergency coronary artery bypass grafting, death) did not differ with or without beta blockers (p greater than 0.05). Follow-up angiograms for 426 of the 483 successfully dilated lesions (88%) revealed that a total of 155 stenoses had recurred (36%). The restenosis rate was not significantly different with (368) or without (58) beta blockers (36 vs 38%, p greater than 0.05). For beta blockers with calcium antagonists (84% nifedipine, 13% diltiazem, 2% verapamil, 1% others), the restenosis rate was 97 of 250 (39%) vs 36 of 118 (31%) (p greater than 0.05). This retrospective study indicates that treatment with beta-adrenergic blockers after PTCA, alone or in combination with calcium antagonists, does not influence either the success rate or the restenosis rate and can be continued if indicated from an antiischemic viewpoint.
Nitroglycerin (NTG) has the potential to reduce myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). Buccal administration of NTG offers practical advantages compared to intravenous or intracoronary administration. In a double-blind, randomized, placebo-controlled study, 100 patients were given 5 mg of buccal NTG or placebo during PTCA. A scoring system for ischemic pain during balloon inflation was defined as pain intensity (0 to 5) multiplied by duration of pain after balloon deflation (1 = 0 to 30 seconds, 2 = 30 to 60 seconds, 3 = 60 to 120 seconds, 4 = greater than 120 seconds but subsiding, and 5 = until next inflation). Fourteen patients were excluded: 12 for vagal reaction (eight NTG and four placebo; p greater than 0.05) requiring atropine, making buccal absorption unreliable, and two for inability to dilate. Eighteen patients (nine NTG and nine placebo) had no pain during balloon inflation. Sixty-eight patients (32 NTG and 36 placebo) had ischemic pain with a pain score (mean +/- SD) of 4.8 +/- 3.8 for the NTG group versus 7.1 +/- 4.8 for the placebo group (p = 0.03). We conclude that buccal NTG significantly decreases myocardial ischemia during PTCA.
The time course of resensitization of the down-regulated beta-adrenoceptor system of rat myometrium was studied. The isoprenaline-induced decrease of myometrial cAMP reversed rather rapidly and after 4 and 8 days no significant change of the cAMP level was demonstrated, however, the cAMP level was higher than in the control myometrium after 12 days. The elevated phosphodiesterase activity decreased to 80% of control activity after 4 days, but returned to control activity after 8 days. The decreased number of beta-adrenoceptors increased gradually after discontinuing the treatment and reached the number of the controls after 12 days. Our results suggest that the resensitization of the beta-adrenoceptor-cAMP-system is rather complex, the normalization of the cAMP content and the phosphodiesterase activity is more rapid than the normalization of the beta-adrenoceptor number which is a rather slow process in myometrial tissue.
The dimension, contractility, and regional wall motion of the right and left ventricles were scored on the angiograms of 13 patients with arrhythmogenic right ventricular dysplasia. In 10 patients the right ventricle was enlarged, in eight the contractility of the right ventricle was reduced, and in all but one patient there were regional wall motion abnormalities of the right ventricle. The most common abnormality of regional wall motion was mild hypokinesia. There were bulging or dyskinetic areas in seven patients. Regional wall motion abnormalities of the left ventricle were found in five patients, two of whom also had bulging or dyskinetic areas. The reproducibility of right ventricular dimension, contractility, and regional wall motion scores was generally fair but varied unexpectedly both within and between two observers (Kendall's Tau 0.38-0.92). The score values of regional wall motion for some of the segments differed considerably within and between observers. One of the observers consistently gave higher scores than the other. These data suggest that a more objective approach is needed for evaluating angiographic changes in arrhythmogenic right ventricular dysplasia.
Dose-response curves for intravenous bolus injections of isoprenaline were carried out in 40 normal subjects, in four groups of 10 comprising young and middle-aged males and females. The isoprenaline dose required to raise the heart rate by 50 beats/min, the CD50 (chronotropic dose 50 beats/min), was calculated individually and taken as a measure of the beta-adrenergic responsiveness. Females had significantly higher sensitivity to isoprenaline than males, i.e. lower CD50 values (95% confidence interval 0.07-0.11 versus 0.12-0.17 micrograms/kg body weight, p less than 0.001), and young subjects had higher sensitivity than middle-aged subjects (95% confidence interval for CD50 0.07-0.10 versus 0.12-0.18 microgram/kg body weight, p less than 0.001). Dose-response curves were also carried out for intravenous prenalterol, a partial beta 1-adrenergic agonist. The maximal heart-rate response to prenalterol (delta HRP) showed a significant inverse linear relationship with the CD50 (delta HRP = 44.8-0.11 x CD50, r = -0.53, rs = -0.69, p less than 0.001). A mental stress programme and isometric exercise gave significant increases in heart rate and blood pressure for all groups, but there was no significant relationship between the CD50 and the heart-rate response. By applying a theoretical model, developed by Kenakin and Beek [13], to the isoprenaline-prenalterol data, it is suggested that the observed age and sex differences in beta-adrenergic responsiveness are caused by a tissue-related difference in the stimulus-response mechanism.
Traditional paleodemographic methods of estimating mortality have been based on unrealistic assumptions about the prevalence of closed and stationary populations. When a living closed population was growing, the mean age at death of its skeletal survivors will be shifted below its true life expectancy. For declining populations, the mean age at death will be higher than true underlying life expectancy at birth. The faster the rate of growth, the larger and more curvilinear is the displacement. Mortality estimates can only be extracted from skeletal populations via an independent estimate of the growth rate. Fertility levels, however, can be estimated directly. The empirical importance of growth rate-dependent mortality estimates is demonstrated by reinterpreting mean-age-at-death data from several populations before and after the agricultural revolution; with detailed consideration given to the Old World populations of Acsadi and Nemeskeri and a New World population from central Illinois.
Diazoxide significantly decreased the blood pressure and relaxed the uterine muscle in anaesthetized normotensive rats. A marked elevation of blood glucose followed the intravenous injection of diazoxide. The hyperglycemic and the uterine relaxing response could be significantly decreased by injection of propranolol prior to diazoxide. The hypotensive effect was not diminished by propranolol, however. In liver and uterus the content of cAMP was increased following diazoxide treatment in vivo. The rise in cAMP could be completely inhibited by propranolol, indicating a beta-receptor stimulation being the cause of the cAMP elevation.
This study was performed in order to elucidate the mechanism behind the decreased responsiveness to beta-adrenergic stimulation occurring in uterine muscle after prolonged treatment with isoprenaline. Pretreatment of rats with isoprenaline, 20 nmol/kg, three times daily during four days, significantly decreased the myometrial relaxing effect of the beta-agonist. There was also a significant decrease of the beta-receptor binding capacity of the myometrial membranes measured by the (--)-(3H) DHA binding technique. In the animals pretreated with isoprenaline no significant increase of the adenylate cyclase activity could be observed after isoprenaline stimulation in vitro. The uterine cAMP level was diminished in the desensitized rats. The phosphodiesterase activity was increased. Thus both decreased production and increased degradation contribute to the lower level of uterine cAMP content. The activity of cAMP dependent protein kinase was also depressed. In this work, where low concentrations of isoprenaline have been administered in vivo, several biochemical parameters have been shown to contribute to the beta-adrenergic desensitization in myometrial tissue.
Three randomized, placebo-controlled, crossover experimental designs were used to define a suitable interdose interval and to study the adequacy of once-daily administration for applications in preventive trials on manifest or latent ischemic patients. Suppression of exercise tachycardia was used as the major effect variable. All measurements were made at different intervals after the last dose when the healthy subjects had been treated for at least 1 wk. Reductions of exercise tachycardia were found 24 hr after the last dose for atenolol, metoprolol, penbutolol, pindolol, propranolol, sotalol, and timolol. Penbutolol and propranolol induced equal reduction of exercise tachycardia at the end of the dose interval regardless of whether the total daily dose was given once daily or divided in 2 daily doses. Atenolol and sotalol, both with long half-lifes (t1/2s), were not superior to other beta blockers. Neither were slow-release preparations of metoprolol and propranolol markedly more effective 24 hr after the preparation than after ordinary tablets. Plasma concentration-time patterns after slow-release preparations may be important in patients with adverse experiences during peak plasma levels after conventional tablets.
Intravenous injection of isoprenaline and salbutamol into rats caused an inhibition of the spontaneous contractions of uterus and increased the uterine cAMP level in a dose-dependent manner. The effects of isoprenaline (0.036 nmol/kg) were diminished or completely prevented by propranolol (0.07-7 mumol/kg). Intravenous infusion of the beta-adrenergic agonists during one hour increased the uterine cAMP level. The highest level of cAMP measured was at 3 min. after start of infusion, thereafter it declined first rather fast but later more slowly. This time pattern of cAMP was very similar to what was seen during incubation of uterine tissue with isoprenaline in vitro. Pretreatment with isoprenaline three times daily 4-7 days before the experiments, decreased both the degree of inhibition and the increase of cAMP in uterus caused by an intravenous injection of isoprenaline. A slight effect on the cAMP rise was detectable after one day of pretreatment, and it seemed to have reached its maximal effect after 4 days, since no further decline in the cAMP response was seen when the pretreatment was prolonged. A dessensibilization to beta-adrenergic agonists was thus seen in uterus after excessive stimulation of isoprenaline in vivo.