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Dive into the research topics where Per Henningsen is active.

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Featured researches published by Per Henningsen.


American Heart Journal | 1995

Randomized double-blind Scandinavian trial of angiopeptin versus placebo for the prevention of clinical events and restenosis after coronary balloon angioplasty

Ulrik Hedegaard Eriksen; Ole Amtorp; Jens Peder Bagger; Haakan Emanuelsson; Marie L. Foegh; Per Henningsen; Kari Saunamäki; Mark Schaeffer; Per Thayssen; Hans Ørskov; Richard E. Kuntz; Jeffrey J. Popma

Angiopeptin, a somatostatin analogue, inhibits intimal hyperplasia after percutaneous transluminal coronary artery balloon angioplasty (PTCA) in several animal models. This pilot study sought to determine the effect of subcutaneous infusion of angiopeptin on clinical events and restenosis in patients undergoing successful PTCA. One hundred twelve patients were randomized to receive continuous subcutaneous angiopeptin (750 micrograms/day) or placebo infusion from the day before PTCA and for the following 4 days in a double-blind study. An additional subcutaneous injection of 375 micrograms of angiopeptin or saline was given immediately before PTCA. Eighty patients had a successful PTCA, and 75 of these patients with 94 lesions underwent angiography 6 +/- 2 months after PTCA. All 112 patients underwent a 12-month clinical follow-up examination. Age, sex, smoking, diabetes, hypertension, hyperlipidemia, and morphologic features of stenosis were similar in both groups. The hierarchical 12-month event rate (death, myocardial infarction, coronary artery bypass grafting, and repeated PTCA) was reduced from 34% to 25% (p = 0.30) by angiopeptin by intention-to-treat analysis. Restenosis (> or = 50% diameter stenosis) was significantly reduced in lesions treated with angiopeptin (12% vs 40%; p = 0.003). Late lumen loss also was significantly reduced after angiopeptin treatment (0.12 +/- 0.46 mm vs 0.52 +/- 0.64 mm; p = 0.003). In conclusion, continuous subcutaneous angiopeptin infusion for 5 days tended to decrease clinical events and restenosis after PTCA.


Clinical Endocrinology | 1989

THE CARDIOVASCULAR EFFECTS OF OCTREOTIDE TREATMENT IN ACROMEGALY: AN ECHOCARDIOGRAPHIC STUDY

Leif Thuesen; Stig Engkjær Christensen; Jørgen Weeke; Hans Ørskov; Per Henningsen

Nine acromegalic patients were treated by the somatostatin analogue SMS 201–995 octreotide (Sandostatin (octreotide), Sandoz, Basle, Switzerland)) 250 μg/ day in 4 divided s.c. injections (50 + 50 + 50 +100 μg) for 1 month, 250 μg/24 h as continuous s.c. infusions for another month and thereafter 200 μg three times daily as s.c. injections. Echocardiography was performed before the treatment, following 1 month of octreotide s.c. infusion/injection and after 6 and after 12 months of octreotide treatment. No differences in serum growth hormone, heart rate, blood pressure, cardiac contractility or left ventricular wall mass or wall thickness were found between the infusion and the injection periods. As compared to the pretreatment levels serum growth hormone decreased by 62 and 66%, respectively following 6 and 12 months octreotide treatment. The heart rate per minute (± SD) decreased from the pretreatment level of 75 ± 12 to 63·13 (P> 0.007) at month 12. The systolic and the diastolic blood pressure decreased from the pretreatment level of 121 ± 8 and 79 ± 5 mmHg respectively to 108 ± 7 (P> 0.0007) and 71 ± 7 mmHg (P> 0.0001) respectively at month 12. The left ventricular wall thickness was reduced from 26 ± 3 mm before treatment to 24 ± 3 mm (P> 0.05) at month 6 and to 24 ± 4 mm (P> 0.04) at month 12. The left ventricular wall mass was 168 ± 48 g/m2 before octreotide treatment, 156 ± 46 g/m2 (NS) after 6 months and 157 ± 52 g/m2 after 12 months (P> 0.08) of octreotide treatment. In age and sex‐matched normal control subjects the left ventricular wall thickness was 20 ± 2 mm, and the left ventricular wall mass was 122 ± 26 g/m2. The wall thickness and the wall mass were increased in the acromegalic patients as compared to the controls before and following the octreotide treatment periods. We suggest that reduction of serum growth hormone levels by octreotide in acromegalic patients is associated with a decrease of the left ventricular wall thickness, but the wall thickness is not reduced to levels of normal control subjects.


Diabetologia | 1985

Increased myocardial contractility in short-term Type 1 diabetic patients: an echocardiographic study

Leif Thuesen; J. Sandahl Christiansen; N. Falstie-Jensen; C.K. Christensen; K. Hermansen; C. E. Mogensen; Per Henningsen

SummaryCardiac function was investigated by echocardiography in 24 short-term Type 1 diabetic patients with a mean diabetes duration of 7 years (range 4–14 years) during conditions of ordinary metabolic control. Compared to 24 age and sex matched normal control subjects, measurements of myocardial contractility as left ventricular fractional shortening and mean circumferential shortening velocity were increased by 12% and 20% respectively. Another 8 Type 1 diabetic patients were examined during conditions of poor (hyperglycaemia and ketosis) and good metabolic control. Following improved glycaemic control, left ventricular fractional shortening and mean circumferential shortening velocity decreased by 16% and 24% respectively. Our findings show that short-term Type 1 diabetes is associated with increased myocardial contractility. Furthermore, this condition is related to the state of metabolic control.


Diabetes | 1988

Cardiac Hyperfunction in Insulin-Dependent Diabetic Patients Developing Microvascular Complications

Leif Thuesen; Jens Sandahl Christiansen; Carl Erik Mogensen; Per Henningsen

Cardiac function was studied by echocardiography in 80 insulin-dependent diabetic patients with no signs of ischemie heart disease and in 40 healthy control subjects. Echocardiographic findings were related to the urinary albumin excretion rate (UAE). In the diabetes group, fractional shortening of the left ventricle (FS) was 37.3% versus 34.3% (P < .01) in the control group, whereas indices of preload and afterload were at the same levels as in control subjects. In diabetic patients with preclinical nephropathy (UAE 20–200 μm/min), FS was 41.1% compared to 37.0% (P < .002) in patients with no signs of nephropathy (UAE <20 μ/min) and 34.8% (P < .001) in patients with clinical nephropathy (UAE <200 μg/min). Furthermore, in patients with preclinical nephropathy, afterload was significantly decreased, whereas preload was at the same level as in the other two groups of UAE. In conclusion, a condition of cardiac hyperfunction has been found in diabetic patients with no signs of ischemie heart disease and seems pronounced in diabetic patients developing microvascular disease (patients with preclinical nephropathy), probably secondarily to a condition of hyperperfusion in these patients.


American Journal of Cardiology | 1988

Altered global myocardial substrate preference at rest and during pacing in coronary artery disease with stable angina pectoris

Anne Thomassen; Jens Peder Bagger; Torsten Toftegaard Nielsen; Per Henningsen

In 21 control subjects with atypical chest pains and normal coronary arteries and in 64 patients with stable angina and coronary artery disease (CAD), myocardial exchanges of free fatty acids, glucose, lactate, citrate, glutamate, alanine and oxygen were determined before, during and after pacing. At rest, myocardial uptake of fatty acids was 50% lower in CAD patients than in the control subjects (p less than 0.001), whereas uptakes of glucose and lactate were twice as high (p less than 0.01). CAD patients showed increased myocardial glutamate uptake (p less than 0.001) and alanine release (p less than 0.001). In control subjects, myocardial fatty acid uptake was directly related (r = 0.54, p less than 0.01), whereas uptakes of glucose (r = -0.42, p less than 0.05) and lactate (r = -0.46, p less than 0.05) were inversely related to arterial fatty acid levels. Citrate release was inversely related to glucose uptake (R = 0.44, p less than 0.05). These relations were absent in CAD patients. Glutamate consumption correlated only with glucose uptake in CAD patients (p less than 0.001) but did so with lactate uptake and alanine release in all individuals (p less than 0.001). Pacing caused angina in the CAD patients but not in the control subjects. Pacing induced no metabolic changes among control subjects but provoked myocardial lactate release in 40 CAD patients, including an additional decrease of fatty acid uptake (p less than 0.05) and increase of glucose uptake (p less than 0.05) compared with resting levels.(ABSTRACT TRUNCATED AT 250 WORDS)


Metabolism-clinical and Experimental | 1991

Effects of intravenous glutamate on substrate availability and utilization across the human heart and leg

Anne Thomassen; Torsten Toftegaard Nielsen; Jens Peder Bagger; Per Henningsen

To study the effect of monosodium glutamate on hemodynamics and on substrate metabolism in cardiac and skeletal muscle, an intravenous (IV) dose of 1.2, 2.5, or 5.0 mg/kg body weight was administered to 27 patients during arterial-coronary sinus catheterization (15 patients) or arterial-femoral vein catheterization (13 patients). Data were obtained for 25 minutes after the injection. Arterial glutamate concentrations increased 2.5-5 fold in a dose-related manner. Glutamate administration reduced arterial levels of free fatty acids by 25% (P less than .001), of lactate by 13% (P less than .05), and of alanine by 6% (P less than .05). Arterial glucose increased by 10% (P less than .001) and arterial insulin was increased threefold (P less than .01). Myocardial uptake of free fatty acids decreased by 25% (P less than .001), whereas uptakes of glutamate and glucose increased by 60% (P less than .001) and 100% (P less than .001), respectively. Cardiac release of citrate increased transiently (P less than .05), whereas consumption of lactate and releases of alanine were unchanged by the glutamate. Across the leg, the arteriovenous differences of glutamate were elevated threefold to eightfold (dose-related) (P less than .001), and that of glucose was doubled (P less than .01). The release of citrate increased (P less than .01). Arterial-femoral vein gradients of free fatty acids, lactate, and alanine remained unchanged. Heart rate, blood pressure, coronary sinus flow, coronary vascular resistance, and cardiac oxygen uptake were unmodified by glutamate. Six patients complained of short-lasting burning sensations after the highest glutamate doses. In conclusion, glutamate administration stimulates insulin secretion and changes substrate availability and utilization in human cardiac and skeletal muscle from free fatty acids toward glucose and glutamate.


Diabetes | 1989

Cardiac Metabolic and Hemodynamic Effects of Insulin in Patients With Coronary Artery Disease

Anne Thomassen; Torsten Toftegaard Nielsen; Jens Peder Bagger; Per Henningsen

To assess the effects of insulin in stable coronary artery disease (CAD), 2 U i.v. insulin was given to 9 control and 10 CAD patients during coronary sinus catheterization. Hemodynamic and metabolic data were obtained before and for 90 min after insulin injection. Insulin induced no changes in heart rate, mean aortic pressure, rate-pressure product, coronary sinus flow, or coronary resistance. Metabolic changes were similar in both groups and included 1) 30% decrease of arterial glucose (P < .001) and 3-fold increase of myocardial glucose uptake (P < .001), 2) 1.5- to 2.5-fold elevation of arterial lactate (P < .001) and myocardial lactate usage (P < .001), respectively, 3) 50–70% suppression of arterial levels (P < .001) and myocardial uptake of free fatty acids (P < .01), and 4) 10% reduction of myocardial net oxygen consumption (P < .05). Myocardial citrate efflux increased in the CAD patients (P < .05), whereas alanine release rose only in control patients (P < .01), suggesting that glucose enters glycogen production in the CAD patients and pyruvate production in the control patients to a high degree. Myocardial glutamate uptake remained unchanged. In conclusion, insulin sensitivity was not altered in CAD. The insulin-induced shift from myocardial free fatty acid to carbohydrate usage may be beneficial to the ischemie heart by increasing glycogen stores, saving oxygen, and inhibiting an excess free-fatty acid concentration, which may be toxic during ischemia.


American Journal of Cardiology | 1991

Antiischemic and metabolic effects of glutamate during pacing in patients with stable angina pectoris secondary to either coronary artery disease or syndrome X

Anne Thomassen; Torsten Toftegaard Nielsen; Jens Peder Bagger; Anders Kirstein Pedersen; Per Henningsen

The effects of glutamate on anginal threshold, cardiac metabolism and hemodynamics were studied in 11 patients with stable angina pectoris, positive stress test results, and pacing-induced myocardial lactate release due to coronary artery disease (CAD) (n = 9) or syndrome X (n = 2). Data were obtained before, during and after 2 identical periods of coronary sinus pacing, the second being preceded by an intravenous injection of monosodium glutamate 1.2 (n = 7) or 2.5 (n = 4) mg/kg body weight. After glutamate administration, pacing time to onset of angina increased from mean +/- standard deviation 103 +/- 53 to 166 +/- 71 seconds (p less than 0.01) and ST-segment depression after pacing decreased from 2.3 +/- 1.0 to 1.6 +/- 1.1 mm (p less than 0.01). Arterial glutamate concentration increased 60% (p less than 0.01) after the low dose and 150% (p less than 0.01) after the high dose of glutamate. Regardless of dose, myocardial glutamate uptake increased by 25% (p less than 0.01). Pacing-induced cardiac release of lactate diminished 50% (p less than 0.05), whereas the releases of xanthine and hypoxanthine were unchanged by glutamate. Arterial free fatty acids decreased 20% (p less than 0.01). Circulating levels and cardiac exchanges of alanine, glucose and citrate were unchanged. Glutamate did not influence heart rate, arterial blood pressure, coronary blood flow, coronary vascular resistance or myocardial oxygen consumption. One patient complained of short-lasting burning sensations after receiving the high glutamate dose. In conclusion, augmented provision of glutamate enhances pacing tolerance in stable angina, presumably by a metabolic improvement of cardiac energy production during ischemia.


American Journal of Cardiology | 1987

Metabolic and hemodynamic effects of nicardipine during pacing-induced angina pectoris

Anne Thomassen; Jens Peder Bagger; Torsten Toftegaard Nielsen; Per Henningsen

During repeat exercise testing in 10 patients with stable angina, individual optimal doses of nicardipine were determined. Hemodynamic values and cardiac metabolism were studied during 2 pacing periods carried out before and after this dose (mean 5.3 mg). Postpacing ST-segment depression diminished (1 mm) after nicardipine administration (p less than 0.05), whereas pacing time to onset of angina did not change. Nicardipine administration increased heart rate 16% (p less than 0.005) and reduced systolic (10%) and diastolic (8%) blood pressures (both p less than 0.005). Coronary blood flow increased 16% (p less than 0.05) and coronary vascular resistance decreased 24% (p less than 0.01). Myocardial oxygen consumption was unchanged despite an 11% decrease in rate-pressure product during pacing (p less than 0.02). In the control state before nicardipine administration, metabolic signs of ischemia included release of lactate across the heart in 7 patients, decreased mean free fatty acid and glutamate uptake and alanine release during pacing, together with increased glucose uptake and citrate release during recovery. After nicardipine lactate release decreased in 5 of the 7 patients, pacing no longer changed free fatty acid, glutamate and alanine uptake/release from the level at rest. During recovery glucose uptake was reduced and citrate release was unaffected. The hemodynamic data indicate that nicardipine is a systemic and coronary vasodilator, increasing oxygen supply to the ischemic myocardium. The metabolic results indicate a change in substrate utilization toward that of normal heart, suggesting improved aerobic energy supply.


American Journal of Cardiology | 1990

Effects of Glutamate on Exercise Tolerance and Circulating Substrate Levels in Stable Angina Pectoris

Anne Thomassen; Hans Erik Bøtker; Torsten Toftegaard Nielsen; Kristian Thygesen; Per Henningsen

The effects of glutamate on exercise tolerance, ischemic threshold and venous substrate concentrations were studied in 20 patients with stable angina pectoris and positive stress tests. Each patient underwent 4 upright bicycle exercise tests on consecutive days. The first and fourth tests were performed without medication while the second and third tests were preceded by a low and high bolus dose of monosodium glutamate, either 0.8 and 1.5 mg/kg body weight intravenously (10 patients) or 40 and 80 mg/kg orally (10 patients). Comparison of the first and fourth tests revealed good reproducibility of electrocardiographic, hemodynamic and metabolic data. Glutamate increased exercise duration (p less than 0.05) in a dose-related way when given intravenously (59 +/- 14 and 153 +/- 14 seconds) and when given orally (53 +/- 21 and 90 +/- 23 seconds; all data are mean +/- standard error of the mean). It also delayed the onset of ST-segment depression (p less than 0.05) by 73 +/- 19, 120 +/- 23, 62 +/- 27 and 80 +/- 30 seconds, respectively. Hemodynamics were not changed by glutamate at rest or at comparable workloads, but at onset of ST-segment depression the heart rate-blood pressure product was increased (p less than 0.05). Glutamate administration induced dose-related 1.5- to 10-fold elevations in plasma glutamate, 15 to 50% decreases in plasma free fatty acids (p less than 0.05) and 5 to 30% increases in plasma alanine contents. Circulating levels of glucose, lactate, citrate and albumin were not modified by glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)

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Leif Thuesen

Aarhus University Hospital

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Cramer Christensen

University of Southern Denmark

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J. Sandahl Christiansen

Memorial Hospital of South Bend

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