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Biomedical subjects

H E Bøtker

Publications and source records attributed to H E Bøtker.

At least 19 recordsLinked to original sources
PubMed2006

Abnormalities of whole body protein turnover, muscle metabolism and levels of metabolic hormones in patients with chronic heart failure.

OBJECTIVE: It is well known that chronic heart failure (CHF) is associated with insulin resistance and cachexia, but little is known about the underlying substrate metabolism. The present study was undertaken to identify disturbances of basal glucose, lipid and protein metabolism. DESIGN: We studied eight nondiabetic patients with CHF (ejection fraction 30 +/- 4%) and eight healthy controls. Protein metabolism (whole body and regional muscle fluxes) and total glucose turnover were isotopically assayed. Substrate oxidation were obtained by indirect calorimetry. The metabolic response to exercise was studied by bicycle ergometry exercise. RESULTS: Our data confirm that CHF patients have a decreased lean body mass. CHF patients are characterised by (i) decreased glucose oxidation [glucose oxidation (mg kg(-1) min(-1)): 1.25 +/- 0.09 (patients) vs. 1.55 +/- 0.09 (controls), P < 0.01] and muscle glucose uptake [a - v diff(glucose) (micromol L(-1)): -10 +/- 25 (patients) vs. 70 +/- 22 (controls), P < 0.01], (ii) elevated levels of free fatty acids (FFA) [FFA (mmol L(-1)): 0.72 +/- 0.05 (patients) vs. 0.48 +/- 0.03 (controls), P < 0.01] and 3-hydroxybutyrate and signs of elevated fat oxidation and muscle fat utilization [a - v diff(FFA) (mmol L(-1)): 0.12 +/- 0.02 (patients) vs. 0.05 +/- 0.01 (controls), P < 0.05] and (iii) elevated protein turnover and protein breakdown [phenylalanine flux (micromol kg(-1) h(-1)): 36.4 +/- 1.5 (patients) vs. 29.6 +/- 1.3 (controls), P < 0.01]. Patients had high circulating levels of noradrenaline, glucagon, and adiponectin, and low levels of ghrelin. We failed to observe any differences in metabolic responses between controls and patients during short-term exercise. CONCLUSIONS: In the basal fasting state patients with CHF are characterized by several metabolic abnormalities which may contribute to CHF pathophysiology and may provide a basis for targeted intervention.

Aged↗
PubMed2005

Percutaneous coronary intervention in diabetic patients: a problem?

Pharmacological and technological advances in surgical and interventional coronary treatment modalities have shown reduced cardiovascular mortality in non-diabetic patients, but diabetic patients have not gained the same benefit of invasive treatment as non-diabetics. Although early studies suggest a poorer outcome after angioplasty than after coronary by-pass grafting (CABG) in diabetic patients, more recent studies including improved pharmacological therapy and stent implantation seem to justify increased use of revascularization by percutaneous coronary intervention (PCI) in diabetics with stable and unstable coronary syndromes as the relative benefit in long-term survival, non-fatal myocardial infarction and cerebrovascular accidents is similar. However, diabetic patients are still subject to higher morbidity and mortality after revascularization with CABG and PCI. This is related to increased co-morbidity, metabolic dysregulation, difficulties in obtaining complete revascularization, and more frequent appearance of new lesions as well as restenosis and hemostatic abnormalities. Drug-eluting stents appear to reduce the risk of restenosis, and aggressive antithrombotics also tend to improve the outcome. Unsolved problems are the significance of incomplete revascularization and whether a PCI strategy is associated with a procedure induced progression of the native diabetic vascular disease in treated or untreated vessels. Trials addressing adjunctive treatment and long-term clinical outcome specifically in diabetic patients should clarify these questions.

Angioplasty, Balloon, Coronary↗
PubMed2005

Myocardial infarction centres: the way forward.

In the era of primary PCI, a strategy of admitting patients to the nearest hospital should be obsolete. Instead, a prehospital diagnostic strategy should be implemented in order to: (1) refer patients directly to interventional centres, thereby eliminating delay at local hospitals; (2) alert the interventional centre, thereby reducing door to balloon times; (3) initiate adjunctive medication in the prehospital phase.

Coronary Care Units↗
PubMed2004

Ischaemic preconditioning does not protect the heart in obese and lean animal models of type 2 diabetes.

AIMS/HYPOTHESIS: The prevalence of type 2 diabetes mellitus is increasing worldwide with obese diabetic patients constituting the majority of this population. Type 2 diabetes is associated with increased morbidity and mortality after acute myocardial infarction. Previous experimental studies of ischaemia-reperfusion tolerance in diabetes have only been performed in animal models of type 1 diabetes mellitus, yielding conflicting data. The aim of the present study was to characterise and compare the tolerance to ischaemia and effects of ischaemic preconditioning (IPC) in hearts from obese Zucker diabetic fatty (ZDF) and lean Goto-Kakizaki (GK) type 2 diabetic rats, using non-obese Zucker and Wistar rats as respective controls. METHODS: The two rat strains were divided into 8 groups. The ZDF study (n=47) consisted of: Control -IPC, Control +IPC, ZDF -IPC and ZDF +IPC. The GK study (n=38) consisted of: Control -IPC, Control +IPC, GK -IPC and GK +IPC. Hearts, which were studied in a Langendorff preparation perfused with Krebs-Henseleit buffer, were subjected or not to IPC (+IPC, -IPC) before 50 minutes of regional ischaemia and 120 minutes reperfusion. RESULTS: Ischaemic reperfusion injury was smaller in obese (p<0.05) and lean (p<0.05) type 2 diabetic animals than in their respective control animals. IPC reduced ischaemic reperfusion injury during reperfusion in non-diabetic control rats (p<0.01), but failed to protect hearts from both diabetic animal models. Post-ischaemic haemodynamic recovery was impaired in the ZDF rats compared to both control and GK rats (p<0.05). CONCLUSIONS/INTERPRETATION: Ischaemic preconditioning does not protect hearts from obese or lean type 2 diabetic animals. However, the susceptibility of the type 2 diabetic myocardium to ischaemic damage is lower than in non-diabetic hearts. The method described here could be used as a tool to study the pathogenesis of increased cardiovascular morbidity and mortality in type 2 diabetes.

Animals↗
PubMed2004

Maternal hyperglycemia improves fetal cardiac function during tachycardia-induced heart failure in pigs.

BACKGROUND: Fetal tachycardia often leads to cardiac failure, which in experimental settings can be prevented by direct fetal glucose-insulin administration. In this study, we hypothesize that similar effects can be obtained indirectly by inducing maternal hyperglycemia. METHODS AND RESULTS: Systolic and diastolic indices (dP/dt(max) and tau) of left ventricular function were measured by use of high-fidelity catheters during 180 minutes of aggressive atrial pacing ( approximately 300 bpm) in 12 preterm porcine fetuses. In 6 fetuses, maternal hyperglycemia (15 mmol/L) was induced for the last 120 minutes of pacing. The remaining fetuses served as controls. Glucose, insulin, and free fatty acid levels were determined, as was fetal myocardial glycogen content. Maternal glucose infusion led to significant fetal hyperglycemia and hyperinsulinemia but did not change the inherently low fetal levels of free fatty acids. There were no differences between groups with regard to dP/dt(max) (1025+/-226 and 1037+/-207 mm Hg, P=NS) and tau (20.6+/-2.0 and 21.4+/-1.6 ms, P=NS) at baseline (100%). During the 180 minutes of pacing, systolic function (dP/dt(max)) and diastolic function (tau) deteriorated more in the control group than in the hyperglycemic group (P<0.001 for both). At 180 minutes, dP/dt(max) was 62+/-18% of baseline in controls and 85+/-11% in hyperglycemic fetuses (P=0.03), and tau was 117+/-12% and 98+/-4%, respectively (P=0.004). CONCLUSIONS: Induced maternal hyperglycemia improves fetal cardiac function during fetal tachycardia and suggests a possible additional therapeutic option to improve the function of the failing fetal heart before or during antiarrhythmic therapy. The findings may be relevant in fetal heart failure in general.

Animals↗
PubMed2001

Electromechanical mapping for detection of myocardial viability in patients with ischemic cardiomyopathy.

BACKGROUND: We evaluated the ability of electromechanical mapping of the left ventricle to distinguish between nonviable and viable myocardium in patients with ischemic cardiomyopathy. METHODS AND RESULTS: Unipolar voltage amplitudes and local endocardial shortening were measured in 31 patients (mean+/-SD age, 62+/-8 years) with ischemic cardiomyopathy (ejection fraction, 30+/-9%). Dysfunctional regions, identified by 3D echocardiography, were characterized as nonviable when PET revealed matched reduction of perfusion and metabolism and as viable when perfusion was reduced or normal and metabolism was preserved. Mean unipolar voltage amplitudes and local shortening differed among normal, nonviable, and viable dysfunctional segments. Coefficient of variation for local shortening exceeded differences between groups and did not allow distinction between normal and dysfunctional myocardium. Optimum nominal discriminatory unipolar voltage amplitude between nonviable and viable dysfunctional myocardium was 6.5 mV, but we observed a great overlap between groups. Individual cutoff levels calculated as a percentage of electrical activity in normal segments were more accurate in the detection of viable dysfunctional myocardium than a general nominal cutoff level. The optimum normalized discriminatory value was 68%. Sensitivity and specificity were 78% for the normalized discriminatory value compared with 69% for the nominal value (P:<0.02). CONCLUSIONS: Endocardial ECG amplitudes in patients with ischemic cardiomyopathy display a wide scatter, complicating the establishment of exact nominal values that allow distinction between viable and nonviable areas. Individual normalization of unipolar voltage amplitudes improves diagnostic accuracy. Electroanatomic mapping may enable identification of myocardial viability.

Body Surface Potential Mapping↗
PubMed2001

[Sexual activity in ischemic heart disease. Risk and therapeutic possibilities].

A major concern of patients with ischaemic heart disease is whether sexual activity is safe. In addition, patients are often reluctant to discuss sexual problems, including erectile dysfunction. Fear of sexual failure or fear of an acute ischaemic cardiac event as a result of sexual activity may create anxiety and lead to avoidance of sexual activity, which can significantly affect quality of life. In patients with a recent acute myocardial infarction the participation in a cardiac rehabilitation program should be strongly encouraged. The results are an improvement in physical capacity and self confidence. The performance of an exercise test at the time of hospital discharge following acute myocardial infarction is mandatory, and can be used in both risk stratification and cardiac rehabilitation. Patients who can manage a work capacity of at least 100 Watt without evidence of myocardial ischaemia or arrhythmias may without concerns take part in an active sexual life. Comprehensive information and appropriate use of pharmacologic agents for erectile dysfunction can add significantly to quality of life.

Coitus↗
PubMed2001

Energy stores and metabolites in chronic reversibly and irreversibly dysfunctional myocardium in humans.

OBJECTIVES: Our goal was to study metabolic energy stores and lactate content in chronic reversibly and irreversibly dysfunctional myocardium. BACKGROUND: It is unknown whether metabolism is deranged in chronic reversibly and irreversibly dysfunctional myocardium in humans. Semiquantitative histological examinations have shown altered mitochondrial morphology and glycogen accumulation in dysfunctional regions. METHODS: We studied 25 patients with a mean ejection fraction of 38 +/- 9% scheduled for coronary artery bypass surgery. Regional perfusion and metabolism were assessed by positron emission tomography, and regional function was assessed by echocardiography. Perioperative myocardial biopsies were obtained from a control region and from a dysfunctional region. We analyzed biopsies for contents of noncollagen protein (NCP), ATP, ADP, AMP, glycogen and lactate. Six months after surgery we assessed wall motion by echocardiography to group patients in those with (n = 11) and without (n = 14) functional improvement. RESULTS: Reversibly dysfunctional myocardium had reduced perfusion (0.59 +/- 0.16 vs. 0.69 +/- 0.20 ml/g/min, p < 0.05), similar glucose-tracer uptake (92 +/- 12 and 95 +/- 14%), ATP/ADP ratio (2.4 +/- 1.1 and 2.4 +/- 0.7), glycogen content (631 +/- 174 and 632 +/- 148 nmol/microg NCP) and lactate levels (59 +/- 27 and 52 +/- 29 nmol/microg NCP) compared with control regions. Irreversibly dysfunctional regions (n = 14) had severely reduced perfusion (0.48 +/- 0.15 vs. 0.72 +/- 0.12 ml/g/min, p < 0.001) and glucose-tracer uptake (52 +/- 16 vs. 94 +/- 15%, p < 0.001), reduced ATP/ADP ratio (1.5 +/- 0.9 vs. 2.3 +/- 0.9, p < 0.05), similar glycogen content (579 +/- 265 vs. 593 +/- 127 nmol/microg NCP) and increased lactate levels (114 +/- 52 vs. 89 +/- 24 nmol/microg NCP, p < 0.01) compared with control regions. CONCLUSIONS: Contents of metabolic energy stores and lactate in chronic reversibly dysfunctional myocardium were preserved. In contrast, energy stores were depleted in myocardium without functional recovery after revascularization.

Adenosine Diphosphate↗
PubMed2001

Prediction of reversible myocardial dysfunction by positron emission tomography, low-dose dobutamine echocardiography, resting ECG, and exercise testing.

We studied different algorithms to identify patients with heart failure who could potentially benefit from revascularization. Thirty-five coronary artery bypass (graft) patients with an ejection fraction of 35 +/- 7% underwent preoperative 18F-fluoro-2-deoxyglucose positron emission tomography (PET), low-dose dobutamine echocardiography (LDDE), and exercise testing. Follow-up by echocardiography and coronary angiography was performed 6 months after coronary artery bypass grafting. The sensitivity for prediction of reversible myocardial dysfunction was highest for PET and for ST depression or angina pectoris during exercise testing (100 and 93%, p = NS), 71% for LDDE (p < 0.05 vs. PET), and 50% for resting ECG (p < 0.02 vs. PET and exercise test). The specificity did not differ between LDDE (81%), PET (67%), and resting ECG (71%), but was lowest for exercise testing (33%; p < 0.02 vs. PET, LDDE, and resting ECG). Accuracies were: PET 80%, LDDE 77%, exercise testing 62%, and resting ECG 58% (p < 0.05 vs. PET). In patients with a negative exercise test, recovery was unlikely, and further viability testing may not be needed. In patients with a positive test, recovery may occur, and additional PET or LDDE should be performed. In these cases, PET with an 18F-fluoro-deoxyglucose uptake of > or =70% as the criterion for viability yields optimum diagnostic characteristics. This strategy awaits further evaluation in larger patient populations with heart failure.

Aged↗
PubMed2000

Positron emission tomography and low-dose dobutamine echocardiography in the prediction of postrevascularization improvement in left ventricular function and exercise parameters.

BACKGROUND: We studied the value of low-dose dobutamine echocardiography (LDDE) and positron emission tomography (PET) in predicting improvement of left ventricular function and exercise parameters after revascularization. METHODS: Forty-six consecutive patients with ischemic heart disease and an ejection fraction (EF) of 35% +/- 7% were included. Before revascularization, the patients underwent exercise testing and myocardial viability testing by LDDE and fluoride 18-fluoro-2-deoxyglucose PET. Six months after revascularization they underwent coronary angiography to study graft patency, and echocardiographic examination and the exercise test were repeated. RESULTS: In the prediction of the presence or absence of improved postrevascularization function in left ventricular regions with patent grafts, PET was more sensitive than LDDE (42/52 regions [81%] vs 27/52 regions [51%], P <.01), whereas LDDE was more specific than PET (187/209 regions [89%] vs 118/209 regions [56%], P <.001). Improvement of regional myocardial dysfunction was found in 19 patients, but their global left ventricular function did not improve significantly (EF 34% +/- 6% and 36% +/- 7%). In the remaining 27 patients with irreversible dysfunction, EF decreased (EF 36% +/- 7% vs 32% +/- 8%, P <.05). Among patients with reversible myocardial dysfunction, the rate pressure product (RPP) increased after revascularization (19,522 +/- 5474 vs 26,190 +/- 5610 mm Hg/min, P <.01), whereas the RPP did not change in patients with irreversible myocardial dysfunction (21,546 +/- 5450 and 22,774 +/- 8249 mm Hg/min). The number of PET viable segments was a predictor of the postoperative increase in the RPP in univariate (P <.04) and multivariate analyses (P <.001). In contrast, LDDE did not bear any prognostic information about improvement in the RPP. CONCLUSIONS: This study confirms earlier findings of higher sensitivity and lower specificity of PET compared with LDDE in predicting improvement of regional left ventricular function after revascularization. However, the feasibility of predicting postrevascularization improvement of exercise parameters seems unique for PET. The potential prognostic value of this finding needs further investigation.

Cardiotonic Agents↗
PubMed2000

Captopril improves oxygen and glucose extraction in pig hearts during reperfusion after cold cardioplegic storage.

The purpose of this study was to evaluate the haemodynamic and metabolic effects of captopril during reperfusion of pig hearts following 360 min global hypothermic cardioplegia and storage (HCS). The hearts were perfused with one litre of cold crystalloid cardioplegia (Bretschneider solution no. 3), excised and stored in saline at 4 degrees C for 360 min. The hearts were then reperfused with blood in a modified Langendorff model for 60 min. Left ventricular function, myocardial blood flow, and arteriovenous differences in oxygen, glucose and lactate were monitored intraoperatively and during reperfusion. Two groups of hearts were studied. Group I (captopril treated, n = 9): the pigs were pre-medicated with increasing oral doses of captopril for 3 weeks (12.5 mg-150 mg daily) and an intravenous dose (25 mg) upon arrival at the laboratory. Captopril was added to the cardioplegia (1000 microg/l) and to the reperfusion media (1000 microg/l). Group II (controls, n = 8): the pigs were given no premedication, captopril-free cardioplegia and the hearts were reperfused with captopril-free blood. Captopril increased myocardial oxygen and glucose extraction during reperfusion (p < 0.05 for both) while lactate remained unchanged after 360 min HCS. Treatments with captopril increased developed left ventricular pressure (DLVP) and relaxation (-dP/dtmax) during reperfusion (p < 0.05 for both), while contractility (+dP/dtmax) was unchanged. Heart rate was reduced in captopril-treated hearts (p < 0.05) while myocardial blood flow (MBF) was similar in the two groups. Captopril administration prior to and during HCS and postcardioplegic reperfusion improves oxygen and glucose extraction in large spontaneously beating porcine hearts during reperfusion. The underlying mechanisms seem to involve metabolic modulation, since myocardial uptake of oxygen and glucose was increased in the absence of changes in myocardial blood flow.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Short-term effects of growth hormone on myocardial glucose uptake in healthy humans.

Cardiac muscle is characterized by insulin resistance in specific heart diseases such as coronary artery disease and congestive heart failure, but not in generalized disorders like diabetes mellitus and essential hypertension when cardiac manifestations are absent. To examine whether the insulin antagonistic effect of growth hormone (GH) acts upon the heart, we compared insulin-stimulated whole body and myocardial glucose uptake with and without GH administration during a 3.5-h euglycemic-hyperinsulinemic clamp in eight healthy males. Myocardial 2-deoxy-2-[(18)F]fluoro-D-glucose uptake was measured with positron emission tomography. The data were converted to myocardial glucose uptake by tracer kinetic analysis. GH did not change the rate-pressure product. GH decreased whole body insulin-stimulated glucose disposal by 26% (48.0 +/- 12.1 vs. control 62.8 +/- 6.1 micromol. kg(-1). min(-1), P < 0.02). Free fatty acids were suppressed to a similar extent with and without GH during the insulin clamp. Insulin-stimulated myocardial glucose uptake was similar in the presence and in the absence of GH (0.34 +/- 0.05 and 0.31 +/- 0.03 micromol. g(-1). min(-1), P = 0.18). In conclusion, GH does not impair insulin-stimulated myocardial glucose uptake despite a considerable whole body insulin antagonistic effect. Myocardial insulin resistance is not an inherent consequence of whole body insulin resistance.

Adult↗
PubMed1999

[Cardiac scanning with positron emission tomography--PET. Clinical use and research aspect].

Assessment of regional myocardial glucose metabolism and regional myocardial perfusion has become possible with positron emission tomography (PET). These parameters are of importance in distinguishing viable from fibrotic myocardium in patients with ischaemic heart disease. PET scanning appears to be the method of choice in these patients, which has led to an increased clinical application of PET as a method usable to select patients with severe heart disease before potential revascularisation. In the present review, PET technology is briefly described, together with an overview of the scientific evidence supporting the clinical application of cardiac PET. Finally, its applications in the fields of pathophysiology and pharmacology are briefly described.

Denmark↗
PubMed1999

Enhanced exercise-induced hyperkalemia in patients with syndrome X.

OBJECTIVES: The purpose of this study was to determine whether patients with syndrome X have altered potassium metabolism. BACKGROUND: Patients with syndrome X have angina pectoris and exercise induced ST segment depression on the electrocardiogram despite normal coronary angiograms. Increasing evidence suggests that myocardial ischemia is uncommon in these patients. Altered potassium metabolism causing interstitial potassium accumulation in the myocardium may be an alternative mechanism for chest pain and ST segment depression in syndrome X. METHODS: We compared the magnitude of exercise-induced hyperkalemia in 16 patients with syndrome X (12 female and four male, mean +/- SD age 53 +/- 6 years) and 15 matched healthy control subjects. The participants underwent a bicycle test at a fixed load of 75 W for 10 min, and blood samples were taken for analysis of potassium, catecholamines and lactate before, during and in the recovery period after exercise. In five patients with syndrome X, the test was repeated during alpha1 adrenoceptor blockade. RESULTS: Baseline concentrations of serum potassium, plasma catecholamines and plasma lactate were similar in patients and control subjects. The rate of exercise-induced increment of serum potassium was increased in the patients (70 +/- 29 vs. 30 +/- 21 micromol/liter/min in control subjects, p < 0.001). Six patients, who stopped before 10 min of exercise, showed very rapid increments in serum potassium concentration. Compared to the control subjects, patients also demonstrated larger increments in rate-pressure product, plasma norepinephrine and lactate concentrations during exercise. The rate of serum potassium increment correlated with the rate of plasma norepinephrine increment in the patients (r = 0.63, p < 0.02), but not in the control subjects (r = 0.01, p = 0.97). Blockade of alpha1 adrenoceptors decreased systolic blood pressure at baseline, but did not influence the increment of serum potassium, plasma catecholamines and lactate. CONCLUSIONS: Patients with syndrome X have enhanced exercise induced hyperkalemia in parallel with augmented increases of circulating norepinephrine and lactate. The prevailing mechanisms behind the abnormal potassium handling comprise sources distinct from alpha1-adrenoceptor activation.

Exercise Test↗
PubMed1999

Myocardial adenine nucleotides, glycogen, and Na, K-ATPase in patients with idiopathic dilated cardiomyopathy requiring mechanical circulatory support.

Acute decompensation leading to progressive pump failure is a main cause of death in patients with congestive heart failure. To find possible metabolic defects associated with the onset of this fatal occurrence, we measured myocardial adenine nucleotides, glycogen, and Na,K-ATPase in patients with end-stage idiopathic dilated cardiomyopathy. The biopsy specimens were obtained from the right ventricle of beating hearts during implantation of a biventricular assistance device in 23 patients (group I) suffering from irreversible cardiogenic shock and during heart transplantation in 20 patients (group II) in compensated heart failure. Left ventricular ejection fraction (LVEF) was determined preoperatively by echocardiography. Left ventricular function in group I was more severely impaired than in group II (LVEF 16.8%+/-4.6% vs 22.1%+/-5.1 %; p <0.01). Myocardial adenosine triphosphate (ATP) in group I was significantly reduced in comparison with group II (119.4+/-10.2 vs 27.7+/-7.4 nmol/mg noncollagen protein; p <0.01). There was no difference in glycogen levels. Na,K-ATPase concentration in group I (n = 8) was lower than that of group II (n = 20) (425+/-80 vs 498+/-75 pmol/g wet weight; p <0.05). Linear regression analyses showed a significant correlation between adenosine triphosphate (ATP) and LVEF (r = 0.41, p <0.01) and between Na,K-ATPase and LVEF (r = 0.55, p <0.01). These results indicate that loss of myocardial ATP and Na,K-ATPase could partially contribute to the development of spontaneous deterioration of the chronically overloaded heart.

Adenine Nucleotides↗