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C Marburger

Publications and source records attributed to C Marburger.

11 recordsLinked to original sources
PubMed2000

Myocardial ischemia during physical exercise in patients with stable coronary artery disease: predictability and prevention.

AIMS: We assessed whether exercise-induced myocardial ischemia during intensive group exercise sessions can be predicted in patients with coronary artery disease and stable angina pectoris. METHODS AND RESULTS: Twenty-three patients underwent cardiac catheterization, 201-thallium scintigraphy, and exercise testing prior to participation in group training sessions. Heart rates and myocardial ischemia were documented by Holter monitoring. The individual training heart rate was calculated as a percentage of the maximal heart rate achieved during symptom-limited exercise testing. Myocardial ischemia occurred significantly more often during group exercise sessions (15 of 23 patients) than during treadmill testing (4 of 23 patients, P<0.001). Maximal heart rate (145+/-23 vs. 134+/-21 beats/min, P<0.004) and maximal plasma lactate concentrations (6.0+/-2.9 vs. 4.3+/-2.0 mmol/l, P<0.05) were significantly higher than during symptom-limited exercise testing. Ischemic episodes occurred significantly more often during jogging than during competitive ball games or interval training. Myocardial ischemia occurred in patients who exceeded their individual target training heart rates (43 of 44 episodes; P<0.001). Duration of ischemic episodes did not correlate with any marker obtained at the beginning of the study. CONCLUSION: These data demonstrate that routine diagnostic procedures do not sufficiently identify patients at risk for exercise-induced myocardial ischemia. Ischemic events are only effectively prevented by choosing adequate types of exercise and, above all, by the strict adherence to individual target heart rates.

Coronary Angiography↗
PubMed1997

Attenuated progression of coronary artery disease after 6 years of multifactorial risk intervention: role of physical exercise.

BACKGROUND: It was the aim of this study to assess the long-term effects of physical exercise and low-fat diet on the progression of coronary artery disease. At the beginning of the study, 113 male patients with coronary artery disease were randomized to an intervention group (n=56) or a control group (n=57); 90 patients (80%) could be reevaluated after 6 years. METHODS AND RESULTS: Patients in the intervention group (n=40) showed a reduction in total serum cholesterol (6.03+/-1.03 versus 5.67+/-1.01 mmol/L; P<.03) and triglyceride levels (1.94+/-0.8 versus 1.6+/-0.89 mmol/L; P<.005) and maintained their initial body mass index (26+/-2 versus 27+/-2 kg/m2; P=NS), but results were not statistically different from the control group (n=50) (total serum cholesterol, 6.05+/-1.02 versus 5.79+/-0.88 mmol/L; triglycerides, 2.25+/-1.28 versus 1.85+/-0.96 mmol/L [both P=NS]; body mass index, 26+/-2 versus 28+/-3 kg/m2 [P<.0001]). In the intervention group, there was a significant 28% increase in physical work capacity (166+/-59 versus 212+/-89 W; P<.001), whereas values remained essentially unchanged in the control group (165+/-51 versus 170+/-60 W; P=NS; between groups, P<.05). In the intervention group, coronary stenoses progressed at a significantly slower rate than in the control group (P<.0001). Energy expenditure during exercise was assessed in a subgroup; patients with regression of coronary stenoses spent an average of 1784+/-384 kcal/wk (approximately 4 hours of moderate aerobic exercise per week). Multivariate regression analysis identified only physical work capacity as independently contributing to angiographic changes. CONCLUSIONS: After 6 years of multifactorial risk intervention, there is significant and persistent improvement in lipoprotein levels and physical work capacity, which results in a significant retardation of disease progression. These beneficial effects appear to be largely due to chronic physical exercise.

Adult↗
PubMed1997

[Secondary resistance to coumarin derivatives in a patient with a hypercoagulability syndrome].

HISTORY AND CLINICAL FINDINGS: A 23-year-old woman with deep (leg) vein thrombosis was hospitalised because the Quick value had not decreased despite administration of phenprocoumon. Two years previously she had sustained an anterior wall myocardial infarction and a scar on her right kidney had been an incidental sonographic finding. There was bluish, fine reticular discoloration over the toes of both legs. Physical examination was otherwise unremarkable except for obesity. INVESTIGATIONS: The concentration of creatine kinase was raised to 250 U/l and that of lactate dehydrogenase to 300 U/l. The platelet count was decreased to 75/nl. The level of IgG anti-cardiolipin antibodies was raised (204 U/l) and the test for lupus anticoagulant positive. A biopsy of the skin from a toe revealing livedoid vasculitis, primary antiphospholipid syndrome (PAPS) was diagnosed. TREATMENT AND COURSE: Noncompliance, excessive vitamin K ingestion, drug interaction and malabsorption were excluded as cause of the lacking action of phenprocoumon. Despite anti-coagulation with high-dosage low-molecular heparin and inhibition of platelet aggregation with ticlopidine and finally also immunosuppressive treatment with cyclophosphamide, skin necroses developed on the toes and she had recurrent pulmonary embolisms of which she died. CONCLUSION: Standard treatment of PAPS is effective anti-coagulation with coumarin derivatives. Secondary resistance to coumarin is a rare occurrence: its cause remains unknown.

Adult↗
PubMed1996

Predictive value of lipid profile for salutary coronary angiographic changes in patients on a low-fat diet and physical exercise program.

In this study, 113 patients with modestly elevated levels of low-density lipoprotein cholesterol (<210 mg/dl) and coronary artery disease were randomized to an intervention group (n=56) or a control group (n=57). The intervention program consisted of daily exercise and a low-fat diet according to the American Heart Association's recommendation phase III; patients in the control group received "usual care" rendered by their private physician. After 1 year, complete data were available for all 92 patients (intervention: n=40; control: n=52) who underwent repeat coronary angiography. During the study course, patients in the intervention group showed an increase in apolipoprotein A-I(123 +/- 18 vs 129 +/- 20 mg/dl; p < 0.02) and apolipoprotein A-I/B (1.3 +/- 0.4 vs 1.5 +/- 0.4; p <0.01) and a decrease in apolipoprotein B (99 +/- 20 vs 89 +/- 18 mg/dl; p < 0.01), while apolipoprotein A-II remained unchanged (38 +/- 6 vs 38 +/- 6 mg/dl; p=NS). In the control group, there were no significant changes (apolipoprotein A-I, 124 +/- 17 vs 128 +/- 13 mg/dl; apolipoprotein A-II, 38 +/- 6 vs 39 +/- 6 mg/dl; apolipoprotein B, 100 +/- 21 vs 99 +/- 16 mg/dl; apolipoprotein A-I/B, 1.3 +/- 0.3 vs 1.4 +/- 0.5; all p=NS). As previously reported, there was a significant retardation of progression in patients in the intervention group (progression 23%, no change 45%, regression 32%) compared with the control group (progression 48%, no change 35%, regression 17%) (p < 0.05). Although retardation of progression was significantly associated with an increase in apolipoprotein A-I/B and a decrease in apolipoprotein B (p < 0.05), these gave way in multivariate analysis to changes in total cholesterol/high-density lipoprotein cholesterol, absolute levels of low-density lipoprotein cholesterol, and, in a subgroup of patients, to leisure-time physical activity (all p < 0.05). These data demonstrate that an intervention based on a low-fat diet and intensive physical exercise is capable of improving apolipoprotein levels, associated with retardation of progression of coronary artery disease. However, total cholesterol/high-density lipoprotein cholesterol and low-density lipoprotein cholesterol appear superior to apolipoproteins as metabolic markers for effective treatment in patients with coronary artery disease.

Adult↗
PubMed1995

Impact of intensive physical exercise and low-fat diet on collateral vessel formation in stable angina pectoris and angiographically confirmed coronary artery disease.

This randomized study was performed to assess the effects of > 3 hours of physical exercise per week and low-fat diet on collateral formation in nonselected patients with coronary artery disease (intervention group, n = 56). Results were compared with those of patients in a control group (n = 57), who received usual care by their private physicians. Coronary lesions were assessed by quantitative coronary angiography at the beginning and after 1 year of study (n = 92). As previously reported, after 1 year there was a significant retardation of progression of coronary artery disease in the intervention group as compared with the control group. In this study, evaluation of collateral formation revealed no significant difference between both groups, and changes in hemodynamic and metabolic variables or leisure time physical activity were not related to changes in collateral formation. Although progression of the disease was significantly related to an increase in collateral formation, regression was significantly related to a decrease in collateral formation (p < 0.00001). Because patients in the intervention group exercised for > 3 hours/week, and patients with regression of coronary artery disease even dedicated 5 to 6 hours to leisure time physical activity per week, these findings question whether an exercise program within the safety tolerance of patients will be able to induce coronary collateralization in the presence of regression of coronary artery disease.

Activities of Daily Living↗
PubMed1994

Identification of patients at risk during swimming by Holter monitoring.

Cardiac arrest during swimming accounts for a considerable number of deaths during physical exercise in patients with coronary artery disease. A link between ST-segment depression and cardiac arrest has been observed in previous studies. In this study, exercise-induced myocardial ischemia was assessed in 23 patients with coronary artery disease by bipolar Holter monitoring during swimming, jogging, and treadmill testing. During treadmill testing, Holter monitoring and standard electrocardiograms were simultaneously recorded. Detection of ST-segment depression during swimming was standardized in a group of normal volunteers (n = 7). All patients with silent myocardial ischemia (n = 8) documented by thallium-201 scintigraphy had ST-segment depression during treadmill testing and swimming when recorded by Holter monitoring, whereas the standard electrocardiogram during treadmill testing was negative in 5 patients. Heart rate at 1 mm ST-segment depression was significantly lower during swimming (110 +/- 11 beats/min) than during treadmill testing (documented by standard electrocardiogram) (133 +/- 23 beats/min, p < 0.002) and jogging (125 +/- 21 beats/min, p < 0.03). However, there was no significant difference in heart rate at onset of angina pectoris in symptomatic patients, suggesting a delayed sensation of ischemic symptoms during swimming. The only clinical event in our group during 8 years of swimming occurred during this study. One patient with silent myocardial ischemia developed ST-segment depression during swimming that degenerated into ventricular fibrillation, requiring resuscitation. Therefore, Holter monitoring can be considered a valuable addition in identifying patients with silent myocardial ischemia during swimming, and thus identifying patients at risk for exertion-related life-threatening ventricular tachyarrhythmias.

Adult↗
PubMed1994

Association between lipoprotein(a) and progression of coronary artery disease in middle-aged men.

The association between lipoprotein(a) (Lp[a]) and progression of coronary artery disease (CAD) compared with other serum lipids was evaluated in 104 patients with angiographically proven coronary atherosclerosis. Patients were randomized to either an intervention or a control group. The 12-month intervention program consisted of a low-fat diet and daily physical exercise. Patients in the control group received "usual care" by their private physician. Eighty-three patients (36 in the intervention and 47 in the control group) underwent repeat angiography after 1 year. Angiographically documented net regression was seen in 13 patients (8 in the intervention and 5 in the control group), no change was seen in 40 patients (21 in the intervention and 19 in the control group) and progression was noted in 30 patients (7 in the intervention and 23 in the control group). No correlation could be shown between Lp(a) and angiographically documented progression of the disease. In a multivariate analysis including metabolic variables, group assignment, age and smoking habits, only assignment to the intervention group (p = 0.0075) and a decrease in total cholesterol (p = 0.0167) were independently associated with the course of the disease. Patients with or without previous myocardial infarction (70 vs 34) did not differ in Lp(a) levels (median 9.15 vs 14.25 mg/dl). Patients with Lp(a) > 25 mg/dl were younger than patients with Lp(a) < or = 25 mg/dl (52 vs 55 years; p < 0.03), indicating a connection between Lp(a) and the development of premature CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1994

[Low-fat diet and physical training in coronary heart disease. Long-term results of secondary prevention].

The long-term effect of a low-fat diet and physical training was investigated in 36 men (mean age 51 +/- 6 years) with coronary heart disease (one-vessel disease, n = 11; two vessel-disease: n = 18; three-vessel disease: n = 7). 18 patients (interventionist, group 1) undertook physical training within a coronary sport group (1 h twice weekly) and daily bicycle ergometry (30 min). They were held to a low-fat diet. In the remaining 18 patients (control, group 2), physical training and low-fat diet depended on own initiative after receiving advice. Over an observation period of 6 years total cholesterol concentration in the 17 patients of group 1 decreased significantly (243 +/- 33 vs. 219 +/- 28 mg/dl; P < 0.02). Physical performance in 12 patients (group 1) increased from 169 +/- 40 to 202 +/- 42 W in (P < 0.01). In contrast, total cholesterol increased slightly in group 2 (n = 16) from 245 +/- 31 at the beginning to 247 +/- 39 mg/dl (no significant change) at the end of the 6 years. Physical performance (n = 12) decreased slightly from 165 +/- 45 to 146 +/- 52 W (not significant). The difference between the two groups was significant after 6 years (P < 0.02 and P < 0.007, respectively). There seemed to be a tendency for progression of the coronary heart disease to be slower in the interventionist than the control group.

Body Mass Index↗
PubMed1993

Various intensities of leisure time physical activity in patients with coronary artery disease: effects on cardiorespiratory fitness and progression of coronary atherosclerotic lesions.

OBJECTIVES: This study was designed to define the effect of different levels of leisure time physical activity on cardiorespiratory fitness and progression of coronary atherosclerotic lesions in unselected patients with coronary artery disease. BACKGROUND: It has been shown in various studies that regression of coronary atherosclerotic lesions can be achieved by means of lipid-lowering drugs, reduction of fat consumption and physical exercise. METHODS: Patients were prospectively randomized either to an intervention group (n = 29) participating in regular physical exercise or to a control group (n = 33) receiving usual care. Energy expenditure in leisure time physical activity was estimated from standardized questionnaires and from participation in group exercise sessions. After 12 months of participation, repeat coronary angiography was performed; coronary lesions were measured by digital image processing. RESULTS: After 1 year, patients in the intervention group achieved an increase in oxygen uptake at a ventilatory threshold of 7% (p < 0.001) and peak exercise of 14% (p < 0.05), whereas a significant decrease was observed in patients in the control group. To achieve significant improvement in cardiorespiratory fitness, approximately 1,400 kcal/week had to be expended in the form of leisure time physical activity (p < 0.001). The mean energy expended in such activity was 1,876 +/- 163 kcal/week in the intervention group and 1,187 +/- 97 kcal/week in the control group (p < 0.001). In the intervention group, regression of coronary artery disease was noted in 8 patients (28%), progression of disease in 3 (10%) and no change in coronary morphology in 18 (62%). In contrast, coronary artery disease progressed at a significantly faster rate in patients in the control group (progression in 45%, no change in 49% and regression in 6%) (p < 0.001 vs. intervention). When the two groups were combined, the lowest level of leisure time physical activity was noted in patients with progression of disease (1,022 +/- 142 kcal/week) as opposed to patients with no change (1,533 +/- 122 kcal/week) or regression of disease (2,204 +/- 237 kcal/week) (p < 0.005). CONCLUSIONS: Measurable improvement in cardiorespiratory fitness requires approximately 1,400 kcal/week of leisure time physical activity; higher work loads are necessary to halt progression of coronary atherosclerotic lesions (1,533 +/- 122 kcal/week), whereas regression of coronary lesions is observed only in patients expending an average of 2,200 kcal/week in leisure time physical activity, amounting to approximately 5 to 6 h/week of regular physical exercise.

Coronary Angiography↗
PubMedDate not supplied

Five years of physical exercise and low fat diet: effects on progression of coronary artery disease.

PURPOSE: This study was designed to assess the long-term effects of low-fat diet and intensive physical exercise. METHODS: Long-term efficacy of exercise and diet was assessed in 18 nonselected, fully employed patients with symptomatic coronary artery disease. Results were compared to 18 patients on usual care. RESULTS: In the intervention group at 1 year, serum lipoproteins were brought to ideal levels, exercise-induced myocardial ischemia was significantly reduced, and progression in coronary atherosclerosis was retarded. After more than 5 years, patients in the intervention group showed a significant reduction in lipoprotein levels (total cholesterol, 248 [179-299] vs 214 [173-272] mg/dL, P < .01; low density lipoprotein, 146 [83-216], vs 152 [121-197] mg/dL, P < .005 vs control; triglycerides; 151 [80-303] mg/dl, vs 98 [46-182] mg/dL; P < .005) and body mass index (26 +/- 2.9 vs 25.4 +/- 3.3 kg/m2; P < .05). Exercise induced myocardial ischemia, measured by 201thallium scintigraphy, decreased by 29% (41 degrees +/- 36 degrees vs 29 degrees +/- 29 degrees, P = NS) and coronary atherosclerosis, assessed by angiography and digital image processing, progressed at a slower pace in light of a 21% increase in physical work capacity (169 +/- 40 vs 205 +/- 50, P < .01) and a 28% increase in maximal rate pressure product (25 +/- 6 vs 32 +/- 4, P < .004). In contrast, patients in the control group showed only poorly controlled coronary risk factors (total cholesterol, 243 [179-306] vs 26 [178-304] mg/dL, P = NS; low density lipoprotein, 151 [79-229] vs 196 [107-238] mg/dL, P < .0005 vs intervention; body mass index 25.7 +/- 2.5 vs 27.5 +/- 3.5 kg/m2, P < .01), whereas their physical work capacity tended to deteriorate (165 +/- 45 vs 142 +/- 62 Watts, P = not significant). CONCLUSIONS: These data demonstrate that current usual care is insufficient in controlling risk factors of coronary artery disease. However, intensive physical exercise and low-fat diet remain an effective form of treatment after more than 5 years.

Constriction, Pathologic↗