bluuebunny/crossref_metadata_2025 huggingface dataset:
Relation between Ventricular Arrhythmias and Psychological Profile
Authors: Orth‐Gomér Kristina , Edwards Mary E. , Erhardt Leif , Sjögren Andreas , Theorell Töres
Published: August 2010

ABSTRACT. The association between psychological characteristics and ventricular arrhythmias was investigated in 150 men (50 with manifest IHD, 50 with risk indicators of IHD and 50 healthy men). Arrhythmias were recorded with 24‐hour Holter monitoring. Psychological characteristics were assessed by the Emotions Profile Index and the Structured Interview for pattern A behaviour. A depressive emotional state was associated with prognostically severe ventricular arrhythmia in healthy men, but not in men with overt IHD or risk indicators of IHD. When clinical characteristics and age were taken into account, depressiveness was—among healthy men—the second most important factor after high age. The results suggest that—in absence of IHD or other cardiovascular disease—a depressive emotional state may participate in the formation of ventricular arrhythmia.
Prognostication in Acute Cerebrovascular Disease
Authors: Britton Mona , de Faire Ulf , Helmers Claes , Miah Kashem
Published: August 2010

ABSTRACT. Subjective assessment of the short‐term outcome and functional state at discharge was made shortly after admission in 200 consecutive patients with acute cerebrovascular disease (CVD) treated in a stroke unit. The assessments proved correct in 59% of the patients. The accuracy of the predictions was not significantly better in patients with a correct preliminary diagnosis than in those with a false. When a known prognostic score for prediction of hospital mortality was tested on 179 of the patients with cerebral haemorrhage or infarction, a correct trend was noted. The score was best applicable in patients with serious symptoms and those with only minor deficit on admission. A high sensitivity of the score was combined with a relatively low specificity. A true comparison between the predictive value of the score and the quality of the subjective assessments was difficult as the latter, in addition to prediction of mortality, also included prediction of the patient's functional state at discharge. The degree of neurological deficit rather than the type of cerebrovascular lesion seemed associated with the short‐term outcome. Improvement of the quality of prognostic assessments in CVD is warranted.
Serum Magnesium in Acute Myocardial Infarction
Authors: Dyckner Thomas
Published: August 2010

ABSTRACT.During 1 1/2 years, 768 patients—905 admissions, 342 with acute myocardial infarction (AMI), 563 with other diagnoses—were treated in the CCU at Serafimerlasarettet. On admission, both the AMI and the non‐AMI group had significantly lower serum magnesium levels than a reference group. The incidence of serious VEBs, VT and VF on admission was significantly higher in the hypomagnesemic patients with AMI. AV blocks and SVB were more frequently observed in the hypermagnesemic patients, both in the AMI and in the non‐AMI group. The incidence of AF and SVT was higher in the hypomagnesemic patients.
Familial Occurrence of the Haemolytic Uraemic Syndrome
Authors: Hogewind Barend L. , de la Rivière Guy Brutel , van Es Leendert A. , Veltkamp Jan J.
Published: August 2010

ABSTRACT. A family is described in which the haemolytic uraemic syndrome (HUS) occurred in two generations. Both juvenile and adult onset of this syndrome were observed in this family. Those affected were all women, three developed HUS in the postpartum period, one towards the end of pregnancy and one as a five‐year old child. Because five cases were observed over a period of 16 years, exposure to the same infectious agent is highly unlikely. Although the transmission of a “dormant” virus cannot be excluded, the occurrence of HUS in two generations of one and the same family seems compatible with the hypothesis that susceptibility to the disease is transmitted as an autosomal dominant characteristic. This observation suggests a genetic influence on the development of HUS, possibly in conjunction with other factors, such as infectious agents, pregnancy and/or delivery.
The Effect of Renal Transplantation on Basal Serum Gastrin Concentration
Authors: Nielsen H. E. , Christensen C. K. , Brandsborg M. , Brandsborg O.
Published: August 2010

ABSTRACT. Basal serum gastrin concentration was measured before and every week during the initial 5 weeks after renal transplantation in 9 of 20 patients with chronic renal failure who obtained a well functioning renal transplant. Furthermore, calcium and phosphorus metabolism in relation to serum gastrin was investigated in all 20 patients 5 weeks after transplantation. Before renal transplantation, serum gastrin was markedly elevated as compared with the levels in normal controls. During the first 3–5 weeks after renal transplantation, serum gastrin decreased towards normal values. A slight but significant increase in serum gastrin persisted 5 weeks after transplantation. No significant relation between changes in serum gastrin concentration and in calcium and phosphorus metabolism was observed.
30 Min ACTH Stimulation Test as Predictor of Hypothalamic‐Pituitary‐Adrenocortical Function
Authors: Blichert‐Toft M. , Lindholm J. , Kehlet H.
Published: August 2010

ABSTRACT. In 32 subjects the hypothalamic‐pituitary‐adrenocortical (HPA) response to metyrapone was found to correlate significantly with the adrenocortical response to exogenous ACTH. This report provides additional evidence suggesting that a 30 min exogenous ACTH stimulation test accurately predicts the integrated responsiveness of the HPA system to various stimuli.
Marked Decrease in Serum HDL Cholesterol Level during Acute Myocardial Infarction
Authors: Rönnemaa T. , Viikari J. , Irjala K. , Peltola O.
Published: August 2010

ABSTRACT. The concentrations of serum total and HDL cholesterol and triglycerides were determined in 57 patients during the course of AMI. In seven days the concentration of serum cholesterol decreased by 24% and that of HDL cholesterol by 31%. The mean HDL/total cholesterol ratio decreased significantly (p<0.01) from 0.163 to 0.145. The magnitude of the change in both HDL and total cholesterol showed a positive correlation with infarction size. The concentration of triglycerides decreased in seven days on the average by 31% but there was great individual variation, which was not dependent on infarction size. Four months after infarction both HDL and total cholesterol as well as triglyceride concentrations had returned to the initial levels. There was a significant negative correlation between the concentrations of HDL cholesterol and triglycerides on admission (r = –0.66) and after four months (r = –0.53) but no correlation after seven days. The results indicate that the determination of serum lipids, including HDL cholesterol, in patients with AMI can, and should be performed on admission to hospital and not at the time of discharge, in order to get reliable estimates of these cardiovascular risk factors.
Alprenolol‐Induced Thrombocytopenia
Authors: Magnusson Bengt , Rödjer Stig
Published: August 2010

ABSTRACT. A case of alprenolol‐induced thrombocytopenia in a 65‐year‐old woman is reported. She was admitted to the hospital twice with platelet counts below 10 times 109/1. The platelet count rapidly returned to normal after discontinuation of alprenolol. The reason for the thrombocytopenia was increased platelet destruction.
Failure of Excessive Doses of Ampieillin to Prevent Bacterial Relapse in the Treatment of Acute. Pyelonephritis
Authors: Ode Bjöm , Bröms Margareta , Walder Mats , Cronberg Stig
Published: August 2010

ABSTRACT. In order to evaluate whether very high doses of ampicillin might be more effective than conventional therapy in eradicating bacteria in patients with acute pyelonephritis, 34 affected patients were randomly assigned into two treatment groups. One group was given ampicillin in a daily dose of 30 g for three days and 20 g for four days without further treatment. The other group was given ampicillin in moderate doses for one month. Out of 13 patients treated with excessive doses for one week, only three were completely cured whereas conventional therapy cured 9 out of 21. Thus, excessive doses of ampicillin given for one week were not more effective but more expensive and possibly less beneficial than conventional therapy.
The Preleukemic Syndrome
Authors: Weber R. F. A. , Geraedts J. P. M. , Kerkhofs H. , Leeksma C. H. W.
Published: August 2010

ABSTRACT.A long‐term prospective study including 151 patients with preleukemia was performed in 1958–79. The series comprised 78 women and 73 men with a mean age of 79 and 72 years, respectively. Acute leukemia was the cause of death in 35 patients, 61 died of infections and/or hemorrhage or of unrelated causes. The mean interval between the initial diagnosis and death from acute non‐lymphocytic leukemia was 36 months (range 2–121). Pitfalls in diagnosis are extensively discussed. The most striking was the advanced age of the patients. The presence of pancytopenia at the time of diagnosis was not predictive for subsequent blastic transformation.
Acquired Pancytopenia in Relatives of Patients with Aplastic Anaemia
Authors: Sleijfer Dirk Th. , Mulder Nanno H. , Nieweg Hendrik O. , Anders Georges J. P. A. , Gouw Wie‐Lie
Published: August 2010

ABSTRACT. We studied relatives of adult patients with acquired aplastic anaemia. Eight patients were found to have 11 family members with peripheral blood pancytopenia. Six of the 11 affected relatives had diminished and four normal cellularity and one had hypercellularity of the bone marrow. Thus, 19 persons in these eight families were affected. In two families, father and son were affected, in four families brother and/or sister, in one family a brother and an aunt and in one a nephew of the index patient. None of the patients or family members had congenital defects. All patients were diagnosed at an adult age and, furthermore, also the mode of inheritance in some of the families seems to exclude Fanconi's syndrome. It is concluded that relatives of patients with aplastic anaemia should be screened for manifestations of this syndrome of familial acquired blood pancytopenias.
The Preleukemic Syndrome
Authors: Geraedts J. P. M. , Weber R. F. A. , Kerkhofs H. , Leeksma C. H. W.
Published: August 2010

ABSTRACT. Out of 151 patients with preleukemic syndrome, bone marrow chromosome studies were carried out in 88 during the preleukemic phase and in 10 after blastic transformation. Out of 54 cases studied without banding techniques, 13 (24%) were abnormal, while 17 (50%) out of 34 banded cases showed abnormalities. This highly significant increase in yield of aberrations was not restricted to structural abnormalities. During the preleukemic phase of the disease, only 5 of the abnormal patients had no normal metaphases in their bone marrow. Four types of chromosome aberrations were observed more than once: –Y, +8, del 5q and del F or del 20q. They are all frequently observed in myeloproliferative disorders. After blastic transformation, 15 out of 19 patients were abnormal and the abnormalities were more complex. It seems, therefore, that a qualitative and quantitative difference exists between this group of patients and the published series of patients with ANLL. Small abnormal cell lines with the same chromosome abnormalities as in the bone marrow were observed in PHA‐stimulated blood cultures of 9 patients. Unstimulated cultures of the same blood sample did not show any mitosis. It is suggested that small subpopulations of lymphocytes arose from the same pluripotent stem cell as the leukemic myelogenous cells, although there may be other explanations.
Noise as a Contributory Factor in the Development of Elevated Arterial Pressure
Authors: Andrén Lennart , Hansson Lennart , Björkman Martin , Jonsson Anders
Published: August 2010

ABSTRACT.Arterial pressure and other hemodynamic variables (stroke volume (SV), cardiac output and total peripheral resistance) were studied in 18 healthy males before and during exposure to recorded industrial noise. All measurements took place under strictly standardized conditions in a noise laboratory. The frequency distribution and level of noise used for stimulation were continuously monitored and kept constant within close limits throughout the experiments. SV was measured with impedance cardiography. Indirect blood pressure (BP) in the brachial artery was measured with an automatic device and the derived parameters, cardiac output and total peripheral resistance, were calculated from these measurements. Compared with resting conditions at 40 dBA, stimulation with industrial noise at 95 dBA caused significant increases in diastolic BP, mean arterial pressure and total peripheral resistance. Minor but statistically significant reductions of SV and cardiac output were seen. Heart rate and systolic BP did not change. These alterations of the hemodynamic variables persisted throughout 20 min of noise stimulation and were maintained for 5 min following cessation of noise stimulation. All variables had returned to their initial levels 10 min after discontinuation of noise stimulation. This study suggests that exposure to industrial noise at levels prevailing during several industrial processes may cause acute elevations of arterial BP and peripheral vascular resistance. In animal studies, repeated elevations of BP due to exposure to noise have been shown to cause a permanent elevation of BP. Therefore, we suggest that noise may be one of several external stimuli contributing to the development of arterial hypertension in man.
Thyrotoxic Hypercalcemia Treated with Corticosteroids
Authors: Aanderud Sylvi , Bassøc Hans H.
Published: August 2010

ABSTRACT. A 42‐year‐old man presenting with symptomatic hypercalcemia was successfully treated with corticosteroids. Initially he was thought to suffer from Addison's disease. A thyrotoxic state was, however, disclosed during the treatment. Evidence suggests that the hypercalcemia was caused by thyrotoxicosis. The effects of thyroid and adrenocortical hormones on calcium metabolism are discussed. Corticosteroids seem valuable in differentiating thyrotoxic hypercalcemia from coincidental hyperparathyroidism.
Effect of Various Agents on Prostaglandin Biosynthesis and the Anti‐Aggregatory Effect
Authors: Förster W.
Published: August 2010

ABSTRACT. In view of the supposed importance of prostacyclin (PGI2) and thromboxane A2 (TXA2) in coronary regulation and platelet aggregation, the hypothesis has been proposed that anti‐anginal drugs might increase the blood supply to the heart not only by vasodilation and diminution of cardiac work but also by inhibition of formation or dissolution of platelet aggregates. Anti‐anginal drugs, especially dipyridamole and nitroglycerin were investigated to establish whether they increase the biosynthesis or anti‐platelet effect of PGI2 and inhibit TXA2 synthesis. In various in vitro models, dipyridamole showed an enhancement of PGI2, synthetase and cyclo‐oxygenase activity and increased PGI2, release, whereas it had only a weak inhibiting effect on TXA2 synthesis. There was a stimulating effect on PGI2, formation by some other anti‐anginal drugs. In contrast, nitroglycerin did not stimulate the biosynthesis of PGI2, in rabbits or guinea pigs, but strongly inhibited TXA2, formation in platelets. It showed an additional inhibiting effect on platelet aggregation and increased additively or more than additively the antiplatelet effect of small doses of PGI2, in ADP‐induced, arachidonic acid‐induced, and thrombin‐induced platelet aggregation. A hypothesis is discussed in which the action of nitroglycerin could be brought about by a vasodilating effect, as well as by its antiplatelet action on reversible platelet aggregates.
Metabolic Responses to Hypoglycemia in Juvenile Diabetics
Authors: Hilsted J. , Madsbad S. , Krarup T. , Heding L. G. , Sestoft L.
Published: August 2010

ABSTRACT. Glucagon and metabolic responses to insulin‐induced hypoglycemia were studied in seven juvenile diabetics, age 31±2 years (mean and S.E.M.), duration of diabetes 17±3 years, with diabetic autonomic neuropathy (decreased beat‐to beat variation in heart rate during hyperventilation and/or orthostatic hypotension) and in seven control patients of similar age and duration of diabetes without neuropathy. Before the hypoglycaemic episode, normoglycemia had been maintained for at least 10 hours. Following hypoglycemia, a slight but significant and similar increase in plasma glucagon was found in both patient groups. Metabolic responses to hypoglycemia were also similar in the two patient groups. In conclusion, diabetic autonomic neuropathy has no effect on glucagon and metabolic responses to hypoglycemia in juvenile, insulin‐treated diabetics.
Experience with Pancreatic Transplantation in Stockholm
Authors: Groth Carl‐Gustav , Lundgren Göran , Gunnarsson Rolf , Berg Bengt , Arner Peter , Östman Jan
Published: August 2010

ABSTRACT. Eight attempts at segmental pancreatic transplantation were made in 6 diabetic patients. While the indications for transplantation differed all the patients were severely incapacitated by the disease. None was uremic. The body and tail of the pancreas from cadaveric donors was used, the grafts were revascularized to the recipient's iliac vessels. Six of the grafts provided control of blood glucose for 7–51 days. Five of the grafts then failed owing to rejection, and one had to be removed while still functioning, because of arterial bleeding. Important lessons have been learned concerning both surgical and immunological aspects of this form of treatment: 1) Ducto‐jejunostomy should be used to provide exocrine pancreatic drainage. 2) HLA‐DR typing for donor‐recipient selection and thoracic‐duct drainage as an adjunctive immunosuppressive measure should be used to reduce the incidence of graft rejection. 3) An elevation of the postprandial blood glucose concentration is a first sign of rejection and should cause treatment. 4) Graft rejection can be reversed by conventional steroid medication.
BLOOD PRESSURE AND PULSE RESPONSE TO INSULIN‐INDUCED HYPOGLYCEMIA DURING NON‐SELECTIVE AND SELECTIVE β‐BLOCKADE
Authors: Pape J. , Jervell J. , Anker E. , Bergrem H. , Dahle K. , Leivestad T. , Lippe A. vd. , Myrseth L. , Thaulow E. , Urving H.
Published: August 2010

Hypoglycemia was induced in ten healty male volunteers during medication with atenolol, metoprolol and propranolol. The β‐blockers abolished the tachycardia during hypoglycemia. In some subjects bradycardia, and in two nodal bradycardia was observed on propranol. The physiologic blood pressure responses were dam‐pend during the β1‐selective blockade. With propranolol a rise in blood pressure was recorded, in two subjects up to 160/105. The blockers had no effect on degree of hypoglycemia or glucose recovery.
Cholesterol, High Density Lipoprotein‐Cholesterol (HDL) and Cholesterol/HDL‐ratio Versus Arterial Blood Pressure.
Authors: Ager E. , Møck H. I. , Brendstrup T. , Hollnagel H. , Schroll M. , Gyntelberg F.
Published: August 2010

Abstract: In a cardiovascular survey of 928 men and women aged exactly 30, 40, 50 & 60 years, a correlation between serum cholesterol, cholesterol/HDL‐ratio and arterial blood pressure was found. This correlation was indirectly caused by mutual correlations to relative weight and age as a final result found after multiple rank correlation analysis in each sex. HDL was not correlated to arterial blood pressure at all.
Thiazide diuretics, Hypokalemia and Cardiac Arrhythmias
Authors: Hollifield John W. , Slaton Paul E.
Published: August 2010

Thiazide diuretics are widely accepted as the cornerstone of antihypertensive treatment programs. Hypokalemia is a commonly encountered metabolic consequence of chronic thiazide therapy. We treated 38 patients (22 low renin, 16 normal renin) with moderate diastolic hypertension with hydrochlorothiazide (HCTC) administered on a twice daily schedule. Initial dose was 50 mg and the dose was increased at monthly intervals to 100 mg, 150 mg and 200 mg daily until blood pressure normalized. The serum K during the control period was 4.5 ± 0.2 mEq/I an on 50, 100, 150 and 200 mg HCTZ daily 3.9 ± 0.3, 3.4 ± 0.2, 2.9 ± 0.2, and 2.4 ± 0.3 mEq/I, respectively. Corresponding figures for whole body K were 4107 ± 208, 3722 ± 319, 3628 ± 257, 3551 ± 336, and 3269 ± 380 mEq, respectively.

In 13 patients we observed the effects of HCTZ therapy (100 mg daily) on the occurrence of PVC's during rest as well as during static and dynamic exercise. During rest we observed 0.6 ± 0.08 PVC beats/min ± SEM and during static and dynamic exercise 0.6 ± 0.06 and 0.8 ± 0.15, respectively. Corresponding figures during HCTZ therapy 100 mg daily were 1.4 ± 0.1, 3.6 ± 0.7 and 5.7 ± 0.8, respectively.

The occurrence of PVC's correlated significantly with the fall in serum K+ observed r = 0.72, p < 0.001.

In conclusion we found that thiazide diuretics cause hypokalemia and depletion of body potassium. The more profound hypokalemia, the greater the propensity for the occurrence of PVC's.
Potassium Maintenance Potassium Supplements or Potassium Sparing Agents
Authors: Morgan Trefor , Myers John
Published: August 2010

This paper reviews and presents data from a series of studies evaluating the extent of potassium depletion that occurs in various disease states and a comparison of the efficacy of potassium supplementation or potassium sparing diuretics in its correction. Changes in serum potassium levels are common after diuretics but are relatively minor in most people if small doses of diuretics are used. Total body potassium deficit is uncommon in people treated with a diuretic for hypertension and the fall in serum potassium results from alkalosis and a shift of potassium into the cell. Potassium sparing diuretics correct the potassium abnormality more readily than potassium supplements. Evidence is also presented that suggests that a high salt, low potassium diet may be an important cause of hypokalaemia in people given diuretics.
CHEST PAIN AND INVAGINATION OF GASTRIC FOLDS INTO THE OESOPHAGUS. A CASE REPORT
Authors: Aggestrup Søren
Published: August 2010

ABSTRACT. A patient with invagination into the oesophagus of gastric mucosal folds is described. He was referred with chest pain and was evaluated by cinematographic x‐ray examination, endoscopy and pressure‐ and pH‐probe investigations. After medical treatment he was operated on with a modified Belsey procedure and got painfree.
ANGINA PECTORIS SYMPTOMS CAUSED BY THORACIC SPINE DISORDERS. NEURO‐ANATOMICAL CONSIDERATIONS
Authors: Lindahl Olov , Hamberg Jern
Published: August 2010

ABSTRACT. The pain conducting systems in the thorax will be described. The diagnosis angina pectoris is a symptom diagnosis. The common medical assumption is that these symptoms are caused by decreased circulation in the coronary vessels. The truth is that exactly the same symptoms can be the results of pathological changes in for example the oesophagus, the mediastinum and the thoracic spine. Our knowledge of referred pain and the pathways for pain conduction permits us nowadays to understand how pain symptoms can have different origins and still be experienced as identical.
PROTECTION OF ISCHEMIC MYOCARDIUM FROM METABOLIC PRODUCTS
Authors: Ichihara Kazuo , Robishaw Janet D. , Vary Thomas C. , Neely James R.
Published: August 2010

Myocardial ischemia results in two major alterations in cellular metabolism that eventually may affect every cellular function. The primary and major alteration is a decrease in oxidative production of ATP and consequently a decrease in all ATP dependent processes as cellular ATP declines to very low levels. The second alteration is accumulation of metabolic products secondary to both decreased coronary flow (washout) and decreased oxidative metabolism. High levels of metabolic products result in inhibition of several enzymatic reactions. Glycolytic inhibition by high NADH results in the loss of anaerobic ATP production. Inhibition of β‐oxidation by high levels of NADH and FADH2 results in a accumulation of long‐chain acyl CoA and acylcarnitine esters and free fatty acids. These compounds are very active detergents and may alter several membrane functions such as Na+ K+ ATPase, and sarcoplasmic reticular, Ca++‐stimulated ATPase. Inaddition, the structure and function of mitochondria may be disrupted. Long‐chain acyl CoA is an effective inhibitor of lipolysis which may contribute to triglyceride accumulation in ischemic hearts.

It is well known that K+ arrest and hypothermia prevents many of the detrimental effects of ischemia. Tissue levels of high energy phosphates and the ability of the heart to recover mechanical function with reperfusion are preserved for much longer periods during hypothermic than during normothermic, hypoxic arrest. Other metabolic consequences of hypothermia and K+ arrest were studied in isolated rat hearts. Hypothermia (10°C) without ischemia completely inhibited glycolysis and reduced fatty acid oxidation to about 7% of the normothermic rate. This suggests that attempts to improve energy production by ischemic tissue during hypothermia will not be successful. Hypothermia (10°C) with ischemia not only preserved ATP levels but reduced tissue levels of lactate, acyl CoA and acylcarnitine and increased tissue glycogen. These observations suggest that hypothermia decreases energy production to the same extent as energy utilization and tissue stores of high‐energy phosphates are preserved. In addition, the lack of accumulation of metabolic products decreases the potential for damage to membranes and metabolic pathways. Low levels of lactate and NADH coupled with high levels of glycogen provides a condition for rapid glycolytic rates with reperfusion and rewarming.
THE MULTIFACTORIAL APPROACH TO MYOCARDIAL SALVAGE THE EXPERIENCE FROM DIVING SEALS
Authors: Kjekshus J.K. , Blix A.S. , Elsner R. , Millard R. , Hol. R.
Published: August 2010

The survival of ischemic myocardium is critically dependent on effective adjustments between myocardial residual flow and energy requirement in the ischemic regions. The quantitative and qualitative changes for optimal adjustments may be studied in diving animals, normally exposed to long periods of hypoxemia and anaerobiosis.

A series of studies have therefore been performed in seals in order to examine the regulations of myocardial blood flow, metabolism and left ventricular mechanics during diving asphyxia.

Unanesthetized animals instrumented with catheters in the left ventricle and in the coronary sinus were submerged for periods of 10 to 16 minutes. The heart rate decreased from 135 to 12 beats/minute. End diastolic and systolic ventricular pressures were almost unchanged while LVdP/dt was reduced by 25%. Myocardial distance gauges implanted in the left ventricular wall showed that left ventricular dimensions during diastole and systole remained essentially constant. Consequently dilatation of the heart and developed wall tension were strictly controlled during diving asphyxia. Average myocardial blood flow, determined by microsphere injections, decreased to 10% of predive values and remained constant during the dive.

Animals instrumented with mineature flow probes on the left circumflex coronary artery demonstrated that blood flow during diving ceases abruptly after the animal is submerged.

Small bursts of flow are periodically observed in steadily increasing magnitude at 30 to 45 second intervals throughout dives lasting up to 15 minutes. The progressive reduction in arterial oxygen content was associated with a time dependent increase in myocardial lactate and hydrogen ion production. Glucose extraction was reduced while free fatty acid extraction remained unchanged. Following restoration of breathing a reactive myocardial hyperemia was observed along with an immediate return to myocardial uptake of lactate. Arterial lactate concentration increased temporarily after emergence. Despite increased glycolytic activity throughout the dive, coronary flow distribution was fully controlled and no evidence of ischemic dilatation of the left ventricle or ST‐segment elevation in the electrocardiogram was observed. Thus, coronary flow during diving was regulated jointly by a marked reduction in myocardial oxygen requirement (metabolic) and vasoconstrictor control (neurogenic).

Glycolytic energy production became increasingly important througout the dive and was not associated with depressed myocardial function. These adaptations to diving asphyxia in the seal myocardium permit a reduction of coronary blood flow which is comparable to that in the infarcted dog myocardium, and therefore have relevance for therapeutic approaches to reduction of myocardial ischemic injury in man.
ELECTROPHYSIOLOGICAL AND BIOCHEMICAL DERANGEMENTS IN ISCHEMIC MYOCARDIUM: INTERACTIONS INVOLVING THE CELL MEMBRANE
Authors: Corr Peter B. , Lee Benjamin I. , Sobel Burton E.
Published: August 2010

Several lines of evidence indicate that metabolites accumulating in ischemic tissue may have a profound influence on membrane function and may thereby mediate many of the electrophysiological derangements characteristic of ischemic tissue in vivo. Recently, we have detected the accumulation of lysophosphoglycerides (LPG), intermediate metabolites of membrane phospholipids, in ischemic tissue in vivo, in effluents from ischemic isolated hearts and in venular effluents from ischemic regions in vivo. Furthermore, LPG, at comparable concentrations, induces reversible electrophysiological alterations in normoxic Purkinje fibers and ventricular muscle in vitro closely analogous to those changes characteristic of ischemic tissue in vivo. Concentration‐dependent changes seen include a reduction in resting potential, Vmax of phase 0, action potential duration and amplitude, with profound decreases in conduction velocity, heterogenous phase 0 depolarization, enhanced automaticity at reduced membrane potentials, and post‐repolarization refractoriness. Experiments utilizing 14C‐lysophosphatidyl choline (14C‐LPG) indicated that incorporation by LPC to a level of less than 1% of total cellular phospholipid is sufficient to induce electrophysiological derangements in isolated ventricular muscle. Based on the observations that venular effluents from ischemic regions in vivo exert deleterious electrophysiological effects in vitro, we have recently demonstrated a two‐fold increase in LPC in venular effluents from ischemic regions in vitro. at Although this two‐fold increase did not produce significant electrophysiological effects in vitro at normal pH, concomitant acidosis (pH = 6.7) comparable to that seen during ischemia in vivo, resulted in dramatic electrophysiological derangements after exposure to LPC. Subsequent experiments indicated that acidosis alone had modest electrophysiological effects but decreased the LPC concentrations three‐fold required to induce membrane effects but did not enhance the incorporation of 14C‐LPC into the cellular phospholipid fraction. Since long‐chain acyl carnitine also accumulate in ischemic myocardium and are also amphiphilic metabolites with many structural similarities to LPC, the effects of these compounds were also assessed in vitro. Palmitoyl carnitine at concentrations identical to LPC, induced electrophysiological derangements similar to LPC. In addition, the effects of the two compounds were additive and as with LPC, acidosis (pH = 6.7) decreased three‐fold the concentration of palmitoyl carnitine required to induce membrane derangements. The additive nature of the effects of these two different amphiphiles suggests that
THE IMMEDIATE ANTECEDENTS OF SUDDEN DEATH
Authors: Hinkle Lawrence E.
Published: August 2010

A 5 yr prospective survey of 1839 coronary heart disease (CHD) deaths, in 260.000 employed men aged 20–65 – and a detailed study of 142 deaths of all causes in 1020 men aged 40–65 who were observed for 5 yrs with repeated examinations and 24 hr ECG recordings shows the following:

60.4% of CHD deaths were «sudden» (SD) in <1 hr; 42.5% of SDs were in men not previously known to have heart disease. The cardiac phenomena of all deaths could be classified as «arrhythmic» (ARD) or «circulatory failture» (CFD). 91% of SDs in <1 hr and 85% of SDs in <24 hrs were ARDs. ARDs and CFDs occurred under different conditions with different precipitating causes and different predictive «risk factors».

At time of death 85% of ARDs were asleep, 88% awake and 42% active. 92.5% had myocardial disease: occlusions of major coronary vessels, scarring or fibrosis; recent acute MI or CO; hypertrophy 400 gms 80%; congestive heart failure 45%; cardiac dilatation 23%. 25% had severe anemia or anoxemia. 85% had major chronic disorders of rhythm or conduction (VPCs 10/1000 36%; pairs of PVC 15%; EC VPCs 23%; QRS . 11 sec 28 %).

At time of death 100% of CFDs were comatose and not arousable. 48% had no clinical evidence of heart disease. 57% had myocardial disease: definite CHD 26%; hypertrophy 400 gms 47%; chronic CHF 29%; cardiac dilatation 13%. 27% had major disorders of rhythm or conduction (VPC 10/1000 20%; pairs of PVC 10%; EC VPCs none; QRS. 11 sec 10%).

ARDs were precipitated by activities known to be associated with vagal effects on heart in 17.1% of the men; by activities known to be associated with sympathetic effects of heart in 34.1%, episodes of acute myocardial ischemia in 14.6%; or occurred during no apparent precipitating event in 34.1%. CFDs were precipitated by hemorrhage, trauma, infection, stroke, or other cause of peripheral vascular failure (87%), and by myocardial failure (13%).

Risk factors at age 55 for ARD in 5 years are confounded and interact. Men with combinations have higher risk. A risk factor for CFD is the presence of potentially fatal non‐cardiac disease likely to cause coma or peripheral vascular collapse.
EFFECT OF TIMOLOL ON LATE VENTRICULAR ARRHYTHMIAS AFTER ACUTE MYOCARDIAL INFARCTION
Authors: von der Lippe G. , Lund‐Johansen P. , Kjekshus J.
Published: August 2010

This is a subproject of the Norwegian timolol myocardial infarction study carried out at one of the clinical centers. High risk patients surviving either a reinfarction or large initial infarction were randomized to placebo (44 pts) or timolol (37 pts). A 24 hour ECG was obtained the day before randomization (at baseline, 7–28 days after the acute attack) then 3 days, 1 month and 6 months after start of therapy. During this period the number of patients with one or more of ventricular couplets, bigemini, ventricular tachycardia or early cycle premature ventricular contractions (PVC) (i.e. complex ventricular arrhythmias) and the average number of PVC per hour increased significantly in the placebo group but not in the timolol group.

The results indicate that there is an increased severity and incidence of ventricular arrhythmias in the first 6 months after myocardial infarction. Timolol effectively inhibited this trend. The importance of timolol as an antiarrhythmic agent may therefore be to prevent subclinical infarct extension and secondary ventricular arrhythmias related to the size of the myocardial damage.
QT Interval in Relation to Ventricular Arrhythmias and Sudden Cardiac Death in Postmyocardial Infarction Patients
Authors: Møller Mogens
Published: August 2010

ABSTRACT. Ninety‐one consecutive patients below the age of 70 years were subjected to a 60‐second resting ECG and 24‐hour ambulatory ECG monitoring two weeks and one, three and six months after an acute myocardial infarction. The corrected QT (QTC) interval decreased from the late hospital phase to the investigations three and six months after the infarction (p<0.01, <0.05). ECG monitorings showing complicated ventricular ectopic beats (multiform, repetitive, R‐on‐T) were associated with an insignificantly longer QTC than other recordings. Eleven patients suffered a sudden cardiac death during a median follow‐up period of 24 months (range 22–27). The QTC intervals in patients who died suddenly were insignificantly longer than in the survivors. Only four patients, who all survived, had a constantly prolonged QTC. After exclusion of tracings during quinidine therapy, a QTC longer than 440 msec was found in 7 (23%) of 31 recordings from patients who suffered a sudden cardiac death compared to 29 (10%) of 287 recordings from the survivors (p<0.05). A combination of complicated ventricular ectopic beats and a QTC longer than 440 msec was demonstrated in 5 (16%) of 31 and 14 (5%) of 287 recordings from the two groups of patients (p<0.05). A trend towards longer QTC intervals was observed in patients with complicated ventricular arrhythmias and in those who died suddenly, but no well defined high‐risk groups could be identified.
Health Consequences of Giving up Smoking in a Prospective Population Study of Middle‐Aged Swedish Men
Authors: Hjalmarsson Agneta , Svärdsudd Kurt
Published: August 2010

ABSTRACT. The effect when persons quit smoking was studied in a prospective study of 855 50‐year‐old men randomly selected from the general population of Gothenburg, Sweden. These men have been followed since 1963. For this report, data from the first ten years of follow‐up were used. The survivors from this period were divided into three groups: those who had never smoked, those who were smokers at the first examination but not since (ex‐smokers), and those who were smokers at all three examinations. Compared to ex‐smokers, the smokers had a steeper decrease of bronchial peak flow, more days of sick leave, more complaints and poorer self‐assessed life situation score. After adjusting for possible confounding factors and differences in moribidity prevalence between the groups at the start of the study, the smokers still had a more unfavorable health course than the ex‐smokers.
Blood Pressure and Heart Rate Recordings at Home and at the Clinic
Authors: Beckman M. , Panfilov V. , Sivertsson R. , Sannerstedt R. , Andersson O.
Published: August 2010

ABSTRACT. In 41 apparently healthy men, aged 22–25 years, with mild blood pressure elevation (MBPE) and 19 age‐ and sex‐matched normotensive controls (NC), blood pressure (BP) and heart rate (HR) readings at the clinic were compared to self‐determined morning and afternoon values at home. The criteria for inclusion in the MBPE group were auscultatory BP ≥ 150 mmHg systolic and/or ≥ 90 mmHg diastolic at the military enlistment center from which the subjects were recruited, and systolic BP ≥ 140 mmHg on two subsequent occasions at the clinic. The BPs of the controls, who were mainly recruited from the same center, did not exceed 130/80 mmHg either at the enlistment center or at the clinic. The magnitude of the difference in systolic BP between home and clinic readings in the MBPE group (+ 15.3 mmHg) differed significantly from that in the NC group (+ 1.8 mmHg) (p<0.001). In both groups the systolic BP increased slightly but significantly during the day and was higher at home in the afternoon than in the morning. HR showed the same type of variation as BP in both groups with higher values at the clinic. The rise tended to be more pronounced (p<0.1) in patients with MBPE. Surprisingly, resting HR at home in the morning was significantly lower in the MBPE than in the NC group. Normokinetic and hyperkinetic subgroups of patients with MBPE did not differ from each other with respect to the variations in HR and BP studied.
The Antidiabetic Effect and Pharmacokinetic Properties of Glipizide
Authors: Östman J. , Christenson I. , Jansson B. , Weiner L.
Published: August 2010

ABSTRACT. In 13 patients with maturity‐onset diabetes mellitus which did not respond to diet therapy alone, serum concentration of glipizide, blood glucose (B‐G) concentration, serum immunoreactive insulin (S‐IRI) and plasma glycerol (P‐G) were monitored hourly over 12 hours after placebo, an initial dose of glipizide (5 mg p.o.) and long‐term treatment with glipizide (range 7.5–20 mg, mean 10.4), which produced fasting B‐G of less than 8 mmol/1. During the long‐term treatment, glipizide was given in a random, cross‐over pattern, either as a single dose in the morning or as a three‐part divided dose regime, in the same total daily amount. The duration of the immediate effects of glipizide on B‐G, S‐IRI and S‐IRI/B‐G was 9, 4.5 and 6.5 hours, respectively. The mean apparent half‐life of glipizide was 4.1 hours, the mean distribution volume 0.13 l/kg and the mean plasma clearance 0.023 l/kg × h. The area under the concentration curve from 7.30 a.m. to 7.30 p.m. was 15% higher after the single dose regime. The serum levels of glipizide at 10 hours were only 30% lower than after the three‐part divided dose regime. There were no significant differences between the single and divided dose regimes as regards B‐G, S‐IRI and S‐IRI/B‐G, although the mean B‐G for the 12‐hour period was somewhat lower after the former than after the latter (7.0 against 8.7 mmol/l).
Improved Results of Closed Commissurotomy for Mitral Stenosis Using Ultracardiography as Selection Ground
Authors: Dernevik L. , Brorsson L. , Wallentin I. , William‐Olsson G.
Published: August 2010

ABSTRACT. The outcome was analysed in 122 of 124 patients with mitral stenosis subjected to closed commissurotomy 1967‐77. The follow‐up time was 1–11 years. Postoperative improvement was seen in 79% of the patients, but after about 5 years, 15% of them had started to decline. A mitral prosthesis has been inserted in 13 patients reoperated so far.
Familial Myeloproliferative Disease
Authors: Slee P. H. Th. J. , van Everdingen J. J. E. , Geraedts J. P. M. , te Veldey J. , den Ottolander G. J.
Published: August 2010

ABSTRACT. A family is described in which a form of myeloproliferative disease involving the megakaryocytic cell line occurs in three generations, resulting in thrombocytosis in several members. An autosomal dominant transmission with variable penetrance is proposed, based on the distribution of involved members in the pedigree. Two family members appeared to have an abnormal chromosome 7, which is frequently observed in patients with hematological disorders. It is our opinion that the chromosomal aberration is primarily related to the mutagenicity of the cytostatic treatment, although a primary defect cannot be fully excluded.
Busulfan, Antimetabolites, Radiotherapy, and Cost of Treatment in Chronic Myelocytic Leukemia
Authors: Ogier Claudio , Reizenstein Peter
Published: August 2010

ABSTRACT.The possibilities were studied of achieving remission more quickly, of preventing conceivably alkyiator‐induced blastic transformation, and of prolonging survival in chronic myelocytic leukemia (CML) by replacing busulfan induction of remission by antimetabolite induction. The promise of the project was not considered to merit a prospective, controlled, randomized multicenter study, and therefore a retrospective, non‐controlled, non‐randomized pilot study was elected. One antimetabolite‐treated group (cytosine arabinoside and thioguanine) and two busulfan‐treated patient groups were studied. One of the latter two groups received splenic irradiation in addition to busulfan. No statistically significant differences between the busulfan groups were found in the time to achieve remission, the length of the first, unmaintained remission, the frequency of blastic metamorphosis or the cost of treatment. The actuarial survival curves of all three groups were similar. The antimetabolite induction was well tolerated and led to a statistically significantly more rapid remission than busulfan. However, the remission was significantly shorter, and no significant difference in the frequency of blastic metamorphosis was found between the groups. The median cost (from diagnosis to death) of hospitalization, visits, treatment, and part of the loss of production was approximately 106 000 Sw. cr. in the busulfan + radiotherapy group, 116 000 in the busulfan group, and 178 000 in the antimetabolite group. It is suggested that a prospective, randomized, controlled study could confirm that the present antimetabolite induction may lead to a more rapid remission induction in CML without more side‐effects. However, to prevent early relapse, antimetabolite induction should be combined with busulfan maintenance treatment.
Cyclofenil‐Induced Hemolytic Anemia in Scleroderma
Authors: Russell M. Lynn , Schachter Ricky K.
Published: August 2010

ABSTRACT. Cyclofenil, a weak anti‐estrogen, has recently been undergoing clinical trials in the treatment of scleroderma. We report a patient who developed autoimmune hemolytic anemia as a possible complication of cyclofenil treatment.
Familial Lecithin‐Cholesterol Acyltransferase Deficiency in Four Norwegian Families
Authors: Albers J. J. , Gjone E. , Adolphson J. L. , Chen C.‐H. , Teisberg P. , Torsvik H.
Published: August 2010

ABSTRACT.Lecithin‐cholesterol acyltransferase (LCATase) mass was measured by radioimmunoassay in four Norwegian families with LCATase deficiency. LCATase activity was measured in some family members by the Glomset‐Wright method (G‐W method) and the Stokke‐Norum radioassay technique (S‐N method). It was also measured in one of the families by a sensitive common synthetic substrate method using apoprotein A–I‐containing proteolipo‐somes. The ten obligate heterozygotes had LCATase levels of 3.4±0.5 μg/ml (range 2.8–4.0), approximately 55–80% of the mean value of eight control subjects sampled at the same time (5.0±0.7 μg/ml, range 4.2–5.8). Six presumed heterozygotes deduced from the linkage of LCATase deficient gene with the α‐haptoglobin gene, had LCATase levels of 3.2±0.6, approximately 50–80% of control values. The eight subjects with LCATase deficiency had LCATase mass of 1.0±0.2 μg/ml (range 0.5–1.3), approximately 10–25% of control levels. The single LCATase deficient subject whose enzyme activity was measured by the synthetic substrate method had LCATase activity of 3.6 nmol/(ml·h), less than 4% of the activity level of normal subjects, 100 nmol/(ml·h), whereas the three obligate heterozygotes had LCATase activities of 48, 54, and 64 nmol/(ml·h), approximately 50–60% of the normal level. LCATase activity measured in heterozygotes by the G‐W method (mean 64, range 55–77 nmol/(ml·h),n= 6) or by the S‐N method (mean 44, range 34–67,n= 11) was significantly lower than in 30 control subjects (G‐W method: mean 120, range 91–163, S‐N method: mean 64, range 47–93). Previous studies have indicated that the seven other LCATase‐deficient subjects had no detectable LCATase activity. We conclude that familial LCATase deficiency in these four Norwegian kindreds is due to the presence of low levels of a functionally defective enzyme.
Individualization of Oral Theophylline Dosage in Elderly Patients
Authors: Talseth Tore , Kornstad Stig , Boye Nils P. , Bredesen Jan E.
Published: August 2010

ABSTRACT. The present study is a prospective evaluation of a dosing nomogram for oral theophylline in 69 middle‐aged and elderly patients (mean age 58.5 ± 15.4 years) with obstructive lung disease. The main features of the nomogram were that the theophylline dose was increased in middle‐aged as compared to old patients, and that smokers were always prescribed a higher dose than non‐smokers of a similar age. The target theophylline concentration is presently defined as a trough level at steady state of 50 μmol/l. Approximately 50 % of the patients achieved theophylline levels within ±20 % of the target concentration, and none had theophylline levels exceeding 110 μmol/l. We conclude that the nomogram represents a useful guide in establishing a safe initial theophylline dose in this patient group.