Biomedical subjects
Publications and source records attributed to P Mathes.
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UNLABELLED: The CIS was undertaken with the aim to evaluate the effects of lipid modifications on angiographic progression and regression of CAD in patients with CAD and hypercholesterolemia. The design included a multicenter randomized, double-blind, parallel, placebo-controlled comparison, with target and safety limits for adjusting the trial medication depending on the LDL cholesterol level (LDL-C) achieved, i.e., up to 40 mg of simvastatin (S) or placebo (P) daily, add-on medication (up to 3 x 4 g Colestyramin), and diet counselling. Male patients, average age 49 (< or = 56) years, were included with angiographic CAD and a screening total cholesterol of 207-350 mg/dl, who were not due to undergo coronary bypass surgery or PTCA, who did not suffer from serious other disease (e.g., diabetes mellitus), and who had not undergone coronary bypass surgery previously. RESULTS: All baseline variables were comparable in the treatment groups, with 129 patients taking S and 125 taking P. Of these 254 patients 217 had their final study visit and 207 underwent a second angiography after an average treatment time of 2.3 years under an average daily dose of 37 mg S. 205 pairs of films were available for analysis. Vital information was obtained of all patients until closure of the data bank, half a year after the last study angiography. Five deaths occurred within the study period, 12 through March 15, 1995 (S: 1/6, P: 4/6). 37 patients (S: 18, P: 19) discontinued trial drug and protocol. Concomitant CAD medication was comparable in both groups, except lipid-lowering add-on medication which was significantly higher in the P group (38% versus 13%). Significant changes in lipid levels, on treatment, were observed in the S group amounting to a mean difference in LDL-C of -35%, in Apo-Protein B (ApoB) of -30%, in VLDL-C of -37%, and in triglycerides (TG) of -27%, and in HDL-C of +6%, in comparison to the control group; these differences were even greater in 137 fully compliant patients: -41, -36, -39, -31, and +7%, respectively. Progression in the S group was significantly less, as defined by the two primary target criteria: 1) the minimum obstruction diameter (MOD), determined by quantitative coronary angiography (QCA), decreased about five times less in comparison to the control group (S: by -0.017; P: -0.0954 mm), and 2) the standardized visual global change score (GCS) deteriorated almost three times less in the S group (by +0.20) than in the P group (+0.58). Of the secondary target criteria, the mean lumen diameter (QCA) also developed a significant difference (S: -0.20; P: +0.23 mm; p = 0.0006) with a trend toward regression in the S group. The QCA-%-stenosis deteriorated three- to four-times less in the S group as compared to the control group (S: by 0.69%; P: by 2.73%; p = 0.0022), and the number of patients with angiographic progression was nearly halved (S: 30%; P: 56%; p < 0.0000). These differences were determined by intention to treat analysis (ITT), and they were obtained in spite of lipid lowering add-on medication in 38% of the P patients; they turned out to be more pronounced in 137 fully compliant patients, in an analysis "as treated". The mean decrease in LDL-C serum level caused by S was significantly correlated to the decrease in progression, and multivariate regression analysis of both treatment groups identified LDL-C (or ApoB) and TG as independent predictors of progression. Progression appeared to be most pronounced in low and medium sized lesions, and the beneficial effect of lipid intervention dominated in lesions with 12-56% QCA stenosis severity. A small fraction of patients who suffered from exercise-induced angina, with ST-segment-depression at the beginning of the study, experienced a significant improvement under S as compared to P treatment. Although the study was not designed to show differences in clinical events, the combined number of all major cardiovascular events tended to be less frequent in the S than in the C gr
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In April 1996 the Munich Rehabilitation Center was founded by the Social Security Agency as a "satellite center" of the "Klinik Höhenried for Cardiovascular Diseases", which is located 50 km south of Munich near the lake Starnberg and performs in-patient rehabilitation since 1967. The Munich Rehabilitation Center is exclusively designated for outpatient rehabilitation for patients in the Munich area. Monday to Friday from 9 a.m. to 4 p.m. up to 50 patients are treated according to the same standards as in residential centers. About 40% of patients treated are in WHO phase II, e.g. after coronary artery bypass grafting, acute myocardial infarction or a percutaneous transluminal coronary angioplasty. 60% have a chronic stable cardiac disease or risk factors for arteriosclerosis. After almost 3 years of experience we see some specific advantages in outpatient compared to the in-patient setting. Ambulatory treatment seems to be more than the residential center "minus a bed". For example: a "holiday feeling" can be avoided by the location in a city area, so the patients are focusing on medical rehabilitation. Outpatient rehabilitation makes an easy transition from a cardiological center to every day life possible. Some patients would refuse any further treatment far away from home because of personal or occupational reasons. Anxiety can be reduced and self-confidence increased by the outpatient setting. There is a daily feedback about the ability to transfer therapeutic advices home. We learned to appreciate outpatient rehabilitation as a cost-effective supplement to the proven in-patient setting for patients in municipal areas.
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BACKGROUND: In several angiographic trials, HMG-CoA reductase inhibitors have shown a beneficial effect on the progression of coronary artery disease. Using 20 mg simvastatin, day-1, a treatment period of up to 4 years was necessary to show a significant reduction in coronary artery disease progression. The question remains however whether higher dosages of simvastatin would be more advantageous in respect to the magnitude of the effect and the required time interval to demonstrate treatment efficacy. METHODS AND RESULTS: In the Coronary Intervention Study (CIS), a multicentre randomized double-blind placebo-controlled study, the effects of lipid-lowering therapy with simvastatin on progression of coronary artery disease in 254 men with documented coronary artery disease and hypercholesterolaemia were investigated. Following a period of lipid-lowering diet, treatment with 40 mg simvastatin or placebo was maintained for an average of 2.3 years. Two primary angiographic endpoints were chosen: the global change score (visual evaluation according to the method of Blankenhorn) and the per patient mean change of minimum lumen diameter (evaluated by the CAAS I system). The mean simvastatin dose was 34.5 mg day-1. In the placebo group, the serum lipids remained unchanged; in comparison to the placebo group the simvastatin group showed a 35% LDL-cholesterol decrease. Coronary angiography was repeated in 205 patients (81%) and 203 film pairs (80%,) were evaluable by quantitative coronary angiography. In the simvastatin and placebo groups, the mean global change scores were +0.20 and +0.58 respectively, demonstrating a significantly slower progression of coronary artery disease in the treatment group (P = 0.02). The change in minimum lumen diameter assessed by computer-assisted quantitative evaluation with the CAAS I system was -0.02 mm in the simvastatin group and -0.10 mm in the placebo group (P = 0.002). In the simvastatin group, there was a significant correlation between the LDL cholesterol levels achieved therapeutically and the per patient mean loss of minimum lumen diameter (r = 0.29; P = 0.003). During the study period, there was no significant difference in the incidence of serious cardiac events (15 of 129 patients in the simvastatin group and 19 of 125 patients in the placebo group, ns). CONCLUSION: Treatment with 40 mg simvastatin day-1 reduces serum cholesterol and slows the progression of coronary artery disease significantly within a short period of treatment time. In the treatment group, retardation of progression is inversely correlated to the LDL-cholesterol levels achieved.
1. Trimetazidine has a direct anti-ischaemic effect on the myocardium without altering the rate x pressure product or coronary blood flow. 2. The effects of trimetazidine (20 mg three times daily) were compared with those of propranolol (40 mg three times daily) in a double-blind parallel group multicentre study in 149 men with stable angina. 3. Reproducibility of exercise performance was verified during a 3 week run-in placebo washout period. All patients had > 1 mm ST-depression on exercise test. 4. After 3 months, similar anti-anginal efficacy was observed between the trimetazidine (n = 71) and propranolol (n = 78) groups. No significant differences were observed between trimetazidine and propranolol as regards anginal attack rate per week (mean difference P-TMZ: 2; 95% CI: -4.4, 0.5) and exercise duration (mean difference P-TMZ: 0 s; 95% CI: -33, 34) or time to 1 mm ST segment depression (mean difference P-TMZ: 13 s; 95% CI: -24, 51). Heart rate and rate x pressure product at rest and at peak exercise remained unchanged in the trimetazidine group but significantly decreased with propranolol (P < 0.001 in all cases). With both drugs there was a trend to decreased ischaemic episodes in the 46% patients who experienced ambulatory ischaemia on Holter monitoring. Six patients stopped trimetazidine and 12 propranolol. Of these, five in each group were withdrawn because of deterioration in cardiovascular status. 5. The results suggest that trimetazidine and propranolol at the doses studied have similar efficacy in patients with stable angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of three-week standardized physical training on exercise-induced ischaemia was investigated in patients with silent ischaemia after myocardial infarction. 24-hour monitoring and exercise ECGs before and after the period of physical training, were undertaken in 32 men (mean age 53.6 +/- 8.1 years) with angiographically proven coronary heart disease. The protocol of the standardized exercise included bicycle ergometry, gymnastics, breathing and movement exercises, as well as nonstandardized walking or hiking. Following the training period the number of ischaemic episodes fell from 90 to 72 for the group as a whole and that of the asymptomatic episodes from 79 to 64. The number and severity of ventricular arrhythmias were similar during silent and symptomatic ischaemia. There was a significant increase in duration of exercise until reaching the ischaemia threshold (mean exercise duration 4.7 +/- 2.1 vs 5.9 +/- 2.5 min; P = 0.0007). There was no increased risk concerning ventricular arrhythmias.
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Between January 1980 and December 1983 the medical and social status of 423 patients who were considered candidates for aortocoronary bypass surgery (ACBS) was assessed by a questionnaire, at a mean of 16 months after coronary angiography. Of these patients 54 had refused surgery, 15 were re-operated, 23 had angioplasty and seven had died on the waiting list. After exclusion of these 117 patients, 306 remained, who form the basis of this report. Fifty three patients (17%) had retired before surgery, four (1.3%) had died perioperatively and 19 were on sick-leave for less than three months. Of those who were still employed pre-operatively, 102 (44.3%) went back to work, 85 (37%) had retired and 42 (18%) were on sick-leave for longer than three months. Significant differences were noted between the 102 working and the 85 retired patients as far as medical and social factors are concerned. Of the medical factors, post-operative freedom of symptoms (P less than 0.0001), postoperative exercise tolerance (P less than 0.0001) and completeness of revascularization (P less than 0.05) seemed to have influence on return to work. Of the social factors, age (P less than 0.0001), type of occupation (P less than 0.0002), duration of preoperative absence from work (P less than 0.001) and heavy manual work (P less than 0.05) showed significant differences between the groups. Since duration of preoperative absence from work is the only preoperative factor that can be modified, strategies for improving the return-to-work rate should aim at the shortening of waiting times for coronary angiography and ACBS.
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In order to determine the value of cardiokymography in detecting left ventricular (LV) anterior wall asynergies, 80 consecutive patients had a cardiokymogram (CKG) and an electrocardiogram (ECG) on the day prior to coronary angiography. Technically adequate CKGs were obtained in 72 patients (67 men and 5 women, mean age 53 +/- 6.5 years). For validation of regional contraction abnormalities, quantitative LV angiography was used. Stepwise linear discriminant analysis was applied to investigate the diagnostic power of CKG. Sensitivity of the CKG for LV anterior wall asynergy was 67.9% (ECG: 39.6%) and specificity was 68.4% (ECG: 94.7%) on the basis of 1 SD of the mean values of the radial axis shortening of a control group. For 2 SD, the sensitivity was 65.6% (ECG: 56.3%) and the specificity 47.5% (ECG: 90%). By combined testing, the specificity increased to 98.3%, whereas the sensitivity dropped to 26.9%. The improvement of the post-test likelihood for a positive ECG by a positive CKG is especially pronounced in the intermediate prevalence range, whereas for a negative ECG the post-test likelihood can be further decreased by a negative CKG in the intermediate and high prevalence range. The ECG as a single test seems to be the more appropriate noninvasive method for detecting LV anterior wall asynergies; however, the combined use of both ECG and CKG may considerably improve the diagnostic accuracy.
From the data available so far it is apparent that in patients with stable angina, bypass graft surgery is not associated with any change in ventricular premature complexes or complex ventricular arrhythmias at rest or during exercise over a 1-5 year follow-up period despite the evidence of a substantial relief of exercise-induced ischaemia persisting for 5 years. In addition, ventricular arrhythmias are not predictive of sudden death except in a few patients, in whom ventricular tachycardia or ventricular fibrillation during exercise-induced ischaemia could be documented. Such exercise-induced arrhythmias appear to have a poor prognosis, unless the ischaemia is relieved by bypass surgery. The available literature suggests that ventricular arrhythmias at rest or during exercise in patients following bypass surgery are not related to ischaemia but to other unknown factors. Electrical instability during exercise may be caused by other factors rather than by ischaemia, and this phenomenon should be further investigated.
In a series of 300 patients following transmural infarction undergoing coronary angiography because of ischaemia in the surviving myocardium, 17 demonstrated an exercise response indicative of myocardial ischaemia in the absence of angina pectoris. The presence of ischaemia in the region of the myocardium under scrutiny was proven by: (1) ST-segment depression during bicycle-ergometry of at least 2 mm in leads without any QRS or ST-T changes at rest. (2) greater than 75% stenosis of vessels supplying the area under investigation, in addition to the vessel supplying the region of the infarction. (3) A reversible Thallium-perfusion defect on exercise. We compared those 17 patients with silent myocardial ischaemia with 21 patients with typical angina pectoris on exertion. All patients underwent 24-hour Holter monitoring, treadmill exercise testing at a target heart rate previously determined as inducing signs of myocardial ischaemia, and swimming and calisthenic programs with telemetric ECG recording. There was no close relationship between myocardial ischaemia and the occurrence of complex ventricular arrhythmias. In silent ischaemia complex ventricular arrhythmias do not occur at a higher rate than in patients with angina pectoris.
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Immunological, immunofluorescence and electromicroscopic studies were performed in a case of atypical myeloma. The 77-year-old patient presented with skeletal pain, multiple osteolytic lesions and bone marrow infiltration by atypical plasma cells. Monoclonal light chains kappa were confined to the plasma cells, as shown by immunofluorescence. No monoclonal immunoglobulin or fragments were detected in plasma or concentrated urine, even by highly sensitive immunological methods. The concentration of the immunoglobulins G, A and M in the plasma was markedly reduced. The plasma cells contained very little sarcoplasmatic reticulum. The simultaneous occurrence of monoclonal light chains kappa in the plasma cells and the absence of monoclonal immunoglobulins or fragments in plasma and urine suggest a non-secretory myeloma.