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O Gøtzsche

Publications and source records attributed to O Gøtzsche.

At least 19 recordsLinked to original sources
PubMed1998

Time course of myocardial viability after acute myocardial infarction: an echocardiographic study.

The recognition of dysfunctional but viable myocardium after acute myocardial infarction (MI) may be of importance for both patient prognostication and the decision for revascularization. Low-dose dobutamine echocardiography (LDDE) has been shown to be a reliable technique in detecting reversibility of dysfunctional myocardium. The aim of the present study was to assess by LDDE possible time-dependent changes in myocardial viability and to evaluate the value of LDDE used in the postinfarction period. Twenty-seven patients with acute MI underwent LDDE on day 6, 30, and 90. At LDDE day 6, 41% of the affected segments showed a positive response to LDDE. At later examination on day 30 and 90, only 32% and 18%, respectively, of the dysfunctioning segments responded to dobutamine stimulation, with a significant decline in response (p < 0.0001), indicating loss of viability. Spontaneous segmental outcome was significantly better for LDDE-responding segments than for nonresponding segments (p = 0.0001). This study indicated that myocardial viability may be temporary and that a time-dependent loss of viability may take place during the first months after MI.

Dobutamine↗
PubMed1997

Evaluation and prognostic significance of left ventricular diastolic function assessed by Doppler echocardiography in the early phase of a first acute myocardial infarction.

AIM: To study the prognostic significance of left ventricular diastolic function evaluated by transmitral and pulmonary venous flow velocities obtained in the early phase of a first acute myocardial infarction in relation to later development of congestive heart failure. METHODS: Pulsed Doppler echocardiography of transmitral and pulmonary venous flow was assessed in 65 consecutive patients with a first myocardial infarction within 1 h of arrival in the coronary care unit. RESULTS: A univariate regression analysis identified age, left ventricular ejection fraction < or = 45%, mitral E deceleration time < or = 130 ms, E/A ratio > 1.5, peak pulmonary venous atrial flow velocity > or = 30 cm.s-1 and a difference between mitral and pulmonary venous atrial flow duration < 0 ms as variables significantly related to the development of congestive heart failure. However, in a multivariate analysis only mitral E deceleration time < or = 130 ms and age were significant independent variables related to the development of congestive heart failure during the first week following a first acute myocardial infarction. CONCLUSION: Assessment of left ventricular diastolic function complements measurements of systolic function in the evaluation of cardiac function, and mitral deceleration < or = 130 ms best identifies patients at risk of development of congestive heart failure following acute myocardial infarction.

Aged↗
PubMed1996

[Left ventricular diastolic function assessment by transthoracic Doppler echocardiography].

Left ventricular diastolic dysfunction is currently recognized in patients with different heart diseases. Three abnormal filling patterns of the left ventricle detected by pulsed-Doppler echocardiography are observed in patients with heart disease. Each filling pattern is characterised by different symptoms, and by differences in function and dimension of the left atrium and filling pressures. Mitral and pulmonary venous flow velocities and durations obtained by pulsed Doppler technique can be used to evaluate left ventricular diastolic function in patients with different heart diseases. However, several factors affect the transmitral and pulmonary venous flow such as age, heart rate, positioning of the sample volume and aortic- and mitral valve insufficiency. These factors must be taken into consideration when the diastolic function is evaluated by pulsed Doppler technique.

Diastole↗
PubMed1996

Incipient cardiomyopathy in young insulin-dependent diabetic patients: a seven-year prospective Doppler echocardiographic study.

Two echo-Doppler cardiographic investigations were performed 7 years apart in 17 insulin-dependent diabetic children without hypertension or nephropathy in order to detect early signs of cardiac abnormalities in this group without ischaemic heart disease. Relative to two matched control groups, the patients had reduced increase in left ventricular size (p < 0.01) and stroke volume (p < 0.05). An initially reduced end systolic wall stress and increased fractional shortening (p < 0.003) was normalized during the 7 years. Concomitant with early signs of autonomic neuropathy and aortic stiffening, left ventricular filling changed with increased velocity during atrial contraction (p < 0.01) correlating to the decreased stroke volumes (r = -0.57, p = 0.016). These early changes could suggest left ventricular restriction but could also reflect a changed sympathetic/parasympathetic balance in diabetic children. A reduced left ventricular cavity size and increased atrial ejection has thus been described in these insulin-dependent children without hypertension, nephropathy or evidence for ischaemic heart disease, suggesting the existence of a metabolically-induced cardiomyopathy.

Adolescent↗
PubMed1996

Increased number of myocardial voltage-gated Ca2+ channels and unchanged total beta-receptor number in long-term streptozotocin-diabetic rats.

In order to elucidate further the abnormal myocardial Ca2+ metabolism in diabetes mellitus, voltage-gated Ca2+ channels and beta-receptors were quantified in myocardial membranes of short- and long-term diabetic rats. Diabetes was induced by an injection of streptozotocin (STZ). Animals were killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were treated with insulin for 20 days following 180 days of untreated diabetes. Diabetic animals developed low triiodothyronine syndrome. During short-term diabetes, the maximum binding capacity (MBC) for Ca2+ channels was reduced by 25% at day 4 (p < 0.05) and the beta-receptor MBC was reduced by 48% (p < 0.05). A normalizing tendency was observed at day 7 for both receptor types; insulin-treated rats did not differ from controls at that time. After 90 and 200 days of untreated diabetes the Ca2+ channel MBC had increased by 36% and 27%, respectively (p < 0.05). Twenty days of strictly regulated blood glucose following 180 days of untreated diabetes totally normalized the Ca2+ channel MBC. This is in contrast to a previous report where insulin treatment did not normalize the Ca2+ channel MBC. Total beta-receptor MBCs did not differ from control values 90 and 200 days after STZ. In conclusion, an increase in rat myocardial Ca2+ channel MBC during long-term diabetes was fully normalized by short-term insulin treatment. The increase in sarcolemmal Ca2+ channels could serve to compensate for a defect coupling of the beta-receptor to adenylate cyclase. An elevated Ca2+ channel number may, at least theoretically, lead to increased Ca2+ flow across the cardiac sarcolemma and in this way contribute to the diabetic cardiomyopathy by increasing the intracellular Ca2+ concentration.

Animals↗
PubMed1995

Abnormal left ventricular diastolic function during cold pressor test in uncomplicated insulin-dependent diabetes mellitus.

1. Insulin-dependent diabetes mellitus is a known risk factor for congestive heart failure and an early diastolic dysfunction has been described. In order to see if diabetes itself and not complications like hypertension, nephropathy or ischaemic heart disease can be considered responsible for the abnormal diastolic function of the left ventricle, 17 young patients with uncomplicated insulin-dependent diabetes mellitus and 12 control subjects were exposed to a cold pressor test. 2. Blinded echo-Doppler examination was performed before and during the test. During basal conditions, left ventricular dimensions and volumes were smaller in diabetes and atrial contributions to left ventricular filling were increased. 3. During the cold pressor test, isovolumic relaxation time increased, peak early filling velocity (E) decreased, E deceleration time decreased and atrial contribution (A) increased significantly in diabetes, while only A increased in the control group. A marked increase in left atrial ejection force was seen in diabetes only (P < 0.002). This difference was seen in spite of comparable reductions in mitral area and atrioventricular compliance in the two groups. 4. The hyperfunction of the left atrium in diabetes is hypothesized to be due to reduce size of the left ventricle combined with incipient autonomic neuropathy.

Adolescent↗
PubMed1994

[Allergic myocarditis in clozapine treatment].

Clozapine is a high-dose neuroleptic, which is recommended only for those cases in which patients have failed to respond adequately to standard antipsychotic drugs. This report describes a 45 year old man with ischaemic heart disease who died of cardiogenic shock 11 days after starting treatment with clozapine. Autopsy showed apart from coronary atherosclerosis and interstitial fibrosis a considerable infiltration of eosinophilic granulocytes in the myocardium suggesting myocarditis as the cause of death.

Clozapine↗
PubMed1993

Abnormal changes in transmitral flow after acute exposure to nitroglycerin and nifedipine in uncomplicated insulin-dependent diabetes mellitus: a Doppler echocardiographic study.

To study the left ventricular (LV) diastolic function in uncomplicated insulin-dependent diabetic patients without hypertension (n = 25) and comparable controls (n = 15), the effect of acute administration of nitroglycerin and nifedipine on cavity dimensions and transmitral flow pattern was investigated by Doppler echocardiography. At baseline no significant differences in any of the LV Doppler echocardiographic parameters were seen in the two groups. Only in diabetics did nitroglycerin diminish LV diastolic and systolic diameter significantly (p < 0.0002 and 0.004, respectively), reducing the stroke volume from 70 +/- 16 to 64 +/- 20 ml, p < 0.01. The decrease in stroke volume correlated significantly to hemoglobin (Hb) A1c level (r = 0.42, p = 0.036). An excessive preload reducing effect on venous capacitance vessels is assumed in diabetes, and this preload reducing effect was also reflected in transmitral flow pattern where E-wave/A-wave ratio decreased significantly only in the diabetic subjects (p < 0.0005). Nifedipine induced the same degree of sympathetic activation in the two groups, but an increase in LV early peak filling rate (E wave) was seen in diabetes only (63.3 +/- 13.5 to 66.8 +/- 13.5 mm, p < 0.01). The atrial filling of LV (A wave) was increased significantly in both groups. Thus an abnormal LV diastolic function can be disclosed by these pharmacologic challenges. Regulation of preload and its influence on transmitral flow pattern in diabetes deserves further investigation, as does the influence of calcium antagonists on early relaxation in the diabetic myocardium.

Adult↗
PubMed1991

Reduced left ventricular afterload and increased contractility in children with insulin-dependent diabetes mellitus: an M-mode and Doppler-echocardiographic evaluation of left ventricular diastolic and systolic function.

Twenty-three children with diabetes mellitus, their ages ranging from 0.2-9.8 years, but with no sign of diabetic microvascular disease were investigated by M-mode and Doppler echocardiography, along with a comparable group of control subjects. In the diabetics, the fractional shortening and the mean velocity of fractional shortening were 14 and 18% higher, respectively, whereas the left ventricular end-systolic wall stress, an indicator of left ventricular afterload, was markedly reduced (22%). Assuming an unchanged preload in the two groups, this indicates a reduced afterload in these children. Systolic and diastolic time intervals, heart rate, and blood pressure were similar in diabetics and controls. Doppler-derived transmitral left ventricular filling indices were also similar. Thus, in these diabetic children no signs of left ventricular diastolic abnormality were detected. The state of hypercontractility of the left ventricle is considered to be due to a reduced afterload in early insulin-dependent diabetes.

Child↗
PubMed1990

[Atypical meningococcal disease diagnosed with meningococcal antibody test].

The case histories of three patients with atypical meningococcal disease in whom the diagnosis was established by means of a meningococcal antibody test (MAT) are presented. One patient had clinically atypical, but bacteriologically verified meningococcal disease; the other two patients were primarily suspected of having viral infections. The usefulness of investigation for meningococcal antibodies in serum from patients with assumed meningococcal disease or with fever of unknown origin is stressed.

Adolescent↗
PubMed1990

Early changes in thyroid hormone metabolism in the heart, liver, and brown adipose tissue during the induction of low T3 syndrome in streptozotocin-diabetic rats.

In order to elucidate the day-by-day development of low T3 syndrome, we made rats diabetic by an injection of streptozotocin. Untreated controls killed at day 0 and rats treated for 8 days with insulin after they had received streptozotocin served as controls. Sub-groups of animals were killed 1, 2, 3, 4 and 8 days after streptozotocin. In serum, heart and liver, T3 was depressed to less than 50% of controls at day 4, whereas the insulin-treated rats differed from controls only as to heart T3. Heart iodothyronine 5'-deiodinase activity was depressed to a minimum at day 3 and depression was not prevented by insulin. Liver iodothyronine 5'-deiodinase activity had not reached a minimum at day 8, and again, insulin treatment did not normalize this parameter. T3 contents and iodothyronine 5'-deiodinase activity in brown adipose tissue did not differ from values in controls at any point of time. Thus, in the rats with low T3 syndrome induced by streptozotocin-diabetes, a lowered iodothyronine 5'-deiodinase activity is not fully inhibited by insulin treatment, whereas the T3 content in the liver is re-established during an observation period of 8 days. A direct toxic effect of streptozotocin seems unlikely as an in vitro study showed no influence of streptozotocin on iodothyronine 5'-deiodinase activity in the liver. The study thus indicates that iodothyronine 5'-deiodinase activity in the heart and liver is depressed in experimental diabetes, despite near optimal regulation of blood glucose, and we suggest that lowered intracellular T3 production could, after some time, result in a hypothyroid state in different tissues.

Adipose Tissue, Brown↗
PubMed1988

Regression of glycogen nephrosis in experimental diabetes after pancreatic islet transplantation.

Glycogen nephrosis, i.e. the Armanni-Ebstein lesion which manifests itself by intracellular accumulation of beta-glycogen has been studied in two groups of streptozotocin diabetic rats and compared to controls. One diabetic group was left untreated and the other diabetic group received pancreatic islet transplantation after 4 weeks duration of diabetes. The kidneys were studied after another 4 week period with normoglycemia. In the non-transplanted diabetic animals glycogen containing tubules comprised 43% of the distal tubule length in the cortex but in the transplanted animals no abnormal, glycogen containing cells could be recovered at the light microscope level. Measurements of the total distal tubule length in the non-transplanted diabetic animals showed that the distal tubules increased in length by 24%. In the transplanted diabetic animals distal tubule length remained the same as in the non-transplanted diabetic animals in spite of normalization of the tubular morphology. This finding could possibly be responsible for the incomplete normalization of kidney weight after treatment.

Animals↗
PubMed1986

Myocardial cell dysfunction in diabetes mellitus. A review of clinical and experimental studies.

Evidence for an abnormal myocardial cell function in diabetes mellitus, influenced by acute metabolic changes, has appeared within recent years. Few but interesting clinical studies focus on this aspect of diabetic cardiopathy, and experimental studies have delivered possible explanations at the cellular level. These are concerned with the intracellular calcium homeostasis and transsarcolemmal receptor signaling. Because these changes are reversible by short-term insulin treatment, a new aspect for the study of diabetic heart disease has appeared.

Animals↗
PubMed1985

Acute insulin treatment normalizes the resistance to the cardiotoxic effect of isoproterenol in streptozotocin diabetic rats. A morphometric study of isoproterenol induced myocardial fibrosis.

The acute effect of insulin treatment on the earlier reported protective effect of streptozotocin diabetes against the cardiotoxic effect of high doses of isoproterenol (ISO) was investigated in rats. Thirty to 135 min after the injection of crystalline insulin, ISO was given subcutaneously and when ISO induced fibrosis in the myocardium was morphometrically analyzed 7 days later, a highly significant correlation (r = 0.83, 2 p = 0.006) to the slope of the fall in blood glucose after insulin treatment appeared. The myocardial content of catecholamines was estimated in these 8 day diabetic rats. The norepinephrine content was significantly increased while epinephrine remained unchanged. An enhanced sympathetic nervous system activity with a consequent down regulation of the myocardial beta-adrenergic receptors could, therefore, explain this catecholamine resistance. The rapid reversion after insulin treatment excludes the possibility that streptozotocin in itself causes the ISO resistance and points towards a direct insulin effect on myocardial catecholamine sensitivity in diabetic rats. The phenomenon described might elucidate pathogenetic mechanisms behind toxic myocardial cell degeneration and may possibly have relevance for acute cardiovascular complications in diabetic patients.

Animals↗
PubMed1985

Myocardial calcium uptake in streptozotocin diabetic and control rats after dibutyryl-cAMP; alpha-adrenergic stimulation and calcium deprivation.

Previous studies have shown a decreased myocardial calcium uptake after beta-adrenergic stimulation with isoproterenol in isolated perfused hearts from streptozotocin diabetic rats. Abnormalities in the beta-receptor-adenylate cyclase system could explain this but in order to circumvene the receptor we studied the effect of the permeable cAMP analogue, dibutyryl-cAMP on this calcium uptake. A marked increase was seen in control hearts while no increase could be registered in diabetic hearts. Defects in the protein kinase phosphorylation system or in the protein kinase substrate in the sarcolemma are suggested. alpha-Adrenergic stimulation with phenylephrine, being a cAMP independent positive inotropic agent, was also tested but no increase in calcium uptake was seen in either control or diabetic hearts. This could be due to a different effect on calcium currents during action potential after alpha-stimulation compared to the beta-adrenergic effect. Reexposure to calcium after calcium deprivation leads to excessive myocardial calcium uptake (calcium paradox), but the increase was significantly smaller in diabetic hearts, suggesting a differential responsiveness to the damage induced by this procedure. Early biochemical abnormalities in the basement membrane or in the composition and calcium binding ability of the sarcolemma could possibly constitute a common final site for the defect myocardial calcium uptake after isoproterenol, db-cAMP and calcium deprivation in streptozotocin diabetic rats.

Animals↗
PubMed1985

Abnormal myocardial calcium uptake in streptozocin-diabetic rats. Evidence for a direct insulin effect on catecholamine sensitivity.

Myocardial calcium uptake after isoproterenol (ISO) in the isolated, perfused heart was investigated at 24-h intervals after the injection of streptozocin (STZ) in rats. After 4 days, when hyperglycemia had persisted for 3 days, myocardial calcium uptake in response to this strong beta-adrenergic agonist fell significantly to the level of unstimulated hearts, which also was the level of propranolol-pretreated hearts exposed to ISO. Insulin, when given in vivo 60-90 min before perfusion, led to a complete normalization of this ISO response in diabetic rats (duration 8 days), while in vitro addition of insulin to the perfusate (0.1 U/ml) significantly increased, while not completely normalizing, the ISO-induced myocardial calcium uptake. Insulin, therefore, has a direct effect on this beta-adrenergic response in diabetic rats and streptozocin in itself does not cause the desensitization. Considering the essential role of this calcium transport for the electromechanical coupling in the heart, such metabolically induced changes in catecholamine sensitivity might hypothetically have relevance for the increased incidence of heart failure in diabetes.

Animals↗