Biomedical subjects

J Niebauer

Publications and source records attributed to J Niebauer.

47 records · Page 3Linked to original sources

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↗

PubMed1994

Verapamil treatment after coronary angioplasty in patients at high risk of recurrent stenosis.

OBJECTIVE: To evaluate the efficacy of high-dose verapamil treatment (240 mg twice daily) in the prevention of angiographic restenosis after primary successful coronary angioplasty in patients at high risk of recurrent obstruction. DESIGN: A placebo controlled, double blind trial in which patients with stable angina pectoris and patients with unstable angina or non-Q wave infarction treated with 330 mg aspirin and 75 mg dipyridamole twice daily were randomised to a verapamil group or a control group. Follow up angiography was performed 6 months after angioplasty or sooner if signs of recurrent ischaemia developed. SETTING: University department of cardiology. PATIENTS: 196 consecutive patients undergoing coronary angioplasty from the beginning of April 1987 to the end of March 1989 and meeting the selection criteria that included the presence of at least one of six predefined risk factors for restenosis. At the time of coronary angioplasty 113 patients had unstable angina or non-Q wave infarction and 83 had stable angina pectoris. RESULTS: In 89 (91%) patients in the verapamil group and in 83 (85%) control patients follow up angiograms were available. The restenosis rate was lower in the verapamil group (48.3%) than in the placebo group (62.7%) (odds ratio 0.56, 95% confidence interval (CI) 0.303 to 1.025 p = 0.059). Of the 172 patients in whom follow up angiograms were available, 24 (13 taking verapamil and 11 taking placebo) did not comply with the trial for more than 40 (34) days (mean (1 SD)). For the remaining 148 patients the restenosis rate was 47.4% in the verapamil group and 63.9% in the placebo group (odds ratio 0.52, 95% CI 0.271 to 0.993, p = 0.046). In the 97 patients with unstable angina or non-Q wave infarction the restenosis rate was not significantly influenced by verapamil (55.8% with verapamil v 62.2% with placebo, odds ratio 0.77, 95% CI 0.339 to 1.728, p = 0.520). In the 75 patients with stable angina pectoris the restenosis rate dropped from 63.2% with placebo to 37.8% with verapamil (odds ratio 0.36, 95% CI 0.137 to 0.917, p = 0.038). CONCLUSION: The observed beneficial effect of high-dose verapamil treatment on the angiographic restenosis rate in patients with stable angina pectoris and at increased risk of recurrent obstruction requires confirmation in further prospective studies.

Aged↗

PubMed1994

[Cost/benefit relations: evaluation of inpatient and ambulatory rehabilitation].

Three different forms of rehabilitation in patients after myocardial infarction are discussed on the basis of cost-effectiveness: 1) outpatient rehabilitation as performed in North America and other developed countries, 2) inpatient rehabilitation in Germany, and 3) outpatient rehabilitation in Germany. Parameters compared are mortality, coronary risk factor profile, and return to work. A metaanalysis of international studies on outpatient rehabilitation demonstrated a significant reduction of total and cardiovascular mortality. Similar data are not available for inpatient rehabilitation in Germany. However, data of 6 years of outpatient rehabilitation as performed in the "Heidelberg Study" demonstrate a continuous significant improvement in coronary risk factor profile and cardiopulmonary fitness. On the other hand, 4 weeks of inpatient rehabilitation exhibited only short-term and no long-lasting effects (4 years) on coronary risk factor profile. The economic benefit can be based on return to work, which is only marginally affected by rehabilitation in the USA, where more than 80% of the patients are back to work 6 months after myocardial infarction. In Germany, about 5 months after myocardial infarction 50% of the patients are retired, despite 4-6 weeks inpatient rehabilitation; i.e., the patients which are back to work can be assumed to be less than 50%. The costs of 8 weeks outpatient rehabilitation in North America has been calculated to be 804 DM per patient, 4 weeks of inpatient rehabilitation amounts to about 5320-5600 DM, and 1 year ambulatory treatment in the "Heidelberg Study" accounts for 2270 DM per patient. It can be concluded: outpatient rehabilitation as performed in North America has been shown to significantly reduce total and cardiovascular mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Ambulatory Care↗

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↗

PubMed1992

Greater diagnostic sensitivity of treadmill versus cycle exercise testing of asymptomatic men with coronary artery disease.

Maximal hemodynamic and ventilatory responses using cycle and treadmill ergometer were compared in 52 asymptomatic patients with angiographically proved coronary artery disease. Moreover, test sensitivity with respect to ST-segment depression and typical angina pectoris were compared between exercise modes used. Exercise tests were performed on different days in randomized order. In 42 patients, exercise-induced myocardial ischemia, expressed as a fraction of left ventricular circumference, was assessed by thallium-201 scintigraphy. The main finding of this study was a significantly higher maximal oxygen uptake (1.87 +/- 0.4 vs 2.2 +/- 0.5 liters/min; p less than 0.001), heart rate (148 +/- 19 vs 158 +/- 18 beats/min; p less than 0.001) and rate-pressure product (28.3 +/- 5 x 10(3) vs 30.7 +/- 5 x 10(3); p less than 0.001) during treadmill walking than during cycling. Therefore, stress-induced myocardial ischemia was significantly more extensive after treadmill walking (31 +/- 37 degrees vs 45 +/- 40 degrees; p less than 0.001). Moreover, there were significantly more patients with signs of myocardial ischemia (ST-segment depression or typical angina pectoris, or both) during treadmill than during cycle ergometry (35 vs 25 patients; p less than 0.05). However, lactate levels measured at peak exercise (4.07 +/- 2.0 vs 4.38 +/- 1.9 mmol/liter) and 3 minutes into the recovery period (5.60 +/- 2.2 vs 5.80 +/- 2.2 mmol/liter) were comparable between both methods, indicating no significant difference in anaerobic energy production. These findings suggest that walking on a treadmill represents an exercise method with a greater ability than cycling to detect coronary artery disease.

Coronary Disease↗

PubMed1992

Regular physical exercise and low-fat diet. Effects on progression of coronary artery disease.

BACKGROUND: Significant regression of coronary and femoral atherosclerotic lesions has been documented by angiographic studies using aggressive lipid-lowering treatment. This study tested the applicability and effects of intensive physical exercise and low-fat diet on coronary morphology and myocardial perfusion in nonselected patients with stable angina pectoris. METHODS AND RESULTS: Patients were recruited after routine coronary angiography for stable angina pectoris; they were randomized to an intervention group (n = 56) and a control group on "usual care" (n = 57). Treatment comprised intensive physical exercise in group training sessions (minimum, 2 hr/wk), daily home exercise periods (20 min/d), and low-fat, low-cholesterol diet (American Heart Association recommendation, phase 3). No lipid-lowering agents were prescribed. After 12 months of participation, repeat coronary angiography was performed; relative and minimal diameter reductions of coronary lesions were measured by digital image processing. Change in myocardial perfusion was assessed by 201Tl scintigraphy. In patients participating in the intervention group, body weight decreased by 5% (p less than 0.001), total cholesterol by 10% (p less than 0.001), and triglycerides by 24% (p less than 0.001); high density lipoproteins increased by 3% (p = NS). Physical work capacity improved by 23% (p less than 0.0001), and myocardial oxygen consumption, as estimated from maximal rate-pressure product, by 10% (p less than 0.05). Stress-induced myocardial ischemia decreased concurrently, indicating improvement of myocardial perfusion. Based on minimal lesion diameter, progression of coronary lesions was noted in nine patients (23%), no change in 18 patients (45%), and regression in 13 patients (32%). In the control group, metabolic and hemodynamic variables remained essentially unchanged, whereas progression of coronary lesions was noted in 25 patients (48%), no change in 18 patients (35%), and regression in nine patients (17%). These changes were significantly different from the intervention group (p less than 0.05). CONCLUSIONS: In patients participating in regular physical exercise and low-fat diet, coronary artery disease progresses at a slower pace compared with a control group on usual care.

Adult↗

PubMed1989

Frequency-dependent effects of activation and inhibition of protein kinase C on neurohypophysial release of oxytocin and vasopressin.

Isolated rat neurohypophyses were superfused in vitro and the release of vasopressin and oxytocin into the medium was determined by specific radioimmunoassays. Hormone secretion was increased by electrical stimulation of the pituitary stalk at different frequencies. The effects of several phorbol esters, known to activate phorbol 12,13-dibutyrate, PDB) or not to affect (4 alpha-phorbol 12,13-dideconate and phorbol 12-monoacetate) protein kinase C, and of the direct protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7) were tested. Electrical stimulation with 450 pulses caused the release of about 45 microU vasopressin and 55 microU oxytocin, when a frequency of 3 Hz was applied, and of about 500 microU vasopressin and oxytocin, when a frequency of 15 Hz was used. PDB (1 mumol/l) increased the release of vasopressin evoked by 15 Hz stimulation maximally by about 40-50% and that evoked by 3 Hz stimulation by about 150%. The release of oxytocin evoked by 15 Hz stimulation was increased by about 150% and that evoked by 3 Hz stimulation by about 400-500% in the presence of PDB. Both inactive phorbol esters had no effects on the evoked release of vasopressin or oxytocin. The effect of PDB on the release of vasopressin and oxytocin was blocked by H7 (10-30 mumol/l). H7 (30 mumol/l) alone reduced the release of vasopressin evoked by stimulation at 15 Hz by 50%. The release of oxytocin was not significantly affected by H7. In the presence of naloxone (1 mumol/l) the release of oxytocin evoked by 3 and 15 Hz stimulation was increased by about 175 and 105%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Inflammatory cytokines and the possible immunological role for lipoproteins in chronic heart failure.

AIMS: We studied the clinical and immunological importance of fasting cholesterol, HDL, LDL and triglycerides in patients with chronic heart failure in relation to plasma concentrations of tumor necrosis factor-alpha (TNFalpha), soluble TNF receptor-1 and -2 (sTNF-R1 and -R2), and a ratio potentially indicating recent endotoxin bioactivity (soluble [s] CD14/total cholesterol). METHODS AND RESULTS: Fifty-eight stable, non-oedematous patients with established heart failure and 19 controls were studied prospectively. Concentrations of sTNF-R1 and sCD14 were higher in patients than in controls (1238+/-96 vs. 632+/-72 pg/ml, P=0.005 and 3401+/-120 vs. 2775+/-139 pg/ml, P=0.007, respectively), whereas those of TNFalpha (9.3+/-1.1 vs. 6.7+/-0.6 pg/ml) and sTNF-R2 (2464+/-145 vs. 1920+/-303 pg/ml) were not. Cholesterol (5.6+/-0.1 vs. 5.5+/-0.2 mmol/l) and LDL (3.5+/-0.1 vs. 3.6+/-0.2 mmol/l) were not different (both P>0.75). Patients had lower HDL (1.10+/-0.04 vs. 1.4+/-0.06 mmol/l, P=0.0004) and higher triglycerides (2.1+/-0.1 vs. 1.1+/-0.1 mmol/l, P=0.0006). Aetiology and the presence of cardiac cachexia did not influence the lipid profile. Correlations in patients: cholesterol vs. TNFalpha (r=-0.40, P=0.003), vs. sTNF-R1 (r=-0.24, P=0.08), vs. sTNF-R2 (r=-0.29, P<0.04); sCD14 vs. TNFalpha (r=0.44, P=0.005), vs. sTNF-R1: (r=0.65, P<0.0001), vs. sTNF-R2 (r=0.59, P<0. 0001). The sCD14/cholesterol ratio related powerfully to TNFalpha (r=0.60), sTNF-R1 (r=0.74), and sTNF-R2 (r=0.65, all P<0.0001). This sCD14/cholesterol ratio emerged as the strongest predictor of TNFalpha, sTNF-R1 and -R2 (all P<0.01), independently of renal and hepatic function, and conventional measures of disease severity. A cholesterol level <5.2 mmol/l (n=18) significantly predicted a poor clinical outcome (P<0.04, RR 3.5, 95% CI 1.1-11.0) independently of peak VO(2) (P=0.07), NYHA class (P=0.08), aetiology (P=0.14), and age, body wasting, sodium, LVEF, heart rate, and blood pressure (all P>0.20, follow-up 12 months, event rate 26%). CONCLUSION: Our data supports previous findings that lower, rather than higher cholesterol levels are associated with poor clinical outcome in patients with chronic heart failure. This relationship is unrelated to heart failure aetiology, and suggests that the classic risk profile is not longer relevant in established heart failure. The little-recognised ability of all lipoprotein fractions to bind endotoxin and to serve as natural buffer substances may explain this relationship between lower lipoprotein levels, higher cytokine concentrations and impaired prognosis.

Analysis of Variance↗

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↗