[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.
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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.
It has become commonplace to observe that as mortality falls, morbidity levels rise. The question is why? The explanation offered here stresses the multidimensional nature of morbidity, and the important role that diverse cultural forces have on the patterns of behaviour which underlie reporting behaviour during modernization. These forces involve rising health expectations on the part of ordinary people, including their ability to perceive illness and their willingness to seek professional help, and institutional pressures on medical professionals which reward them for discovering and treating an ever-growing set of non-fatal diseases. Since non-Western developing countries are training physicians to practice scientific medicine, are educating their citizens to think about disease along modern lines, and measure morbidity as developed countries do, there is every reason to suppose that as mortality falls in these countries, morbidity will rise, just as it has done in the developed world.
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.
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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.
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