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Biomedical subjects

G Müller-Esch

Publications and source records attributed to G Müller-Esch.

At least 19 recordsLinked to original sources
PubMed2003

Angina intensity is not different in diabetic and non-diabetic patients with acute myocardial infarction.

BACKGROUND: Diabetic patients with acute myocardial infarction (AMI) may have diminished pain or a higher frequency of asymptomatic infarctions. This appears to be a common clinical perception. METHODS: Data from two registries of AMI patients presenting in hospital (MITRA PLUS with 18786 patients; North German Registry, NGR, 1042 patients with detailed symptom interviews) were analyzed concerning symptoms of acute myocardial infarction in patients with diabetes mellitus (DM) and without diabetes (non-DM). RESULTS: DM patients were significantly older and more often female than non-DM. There were no differences in the frequency of pre-infarction angina between DM and non-DM (Mitra Plus). In NGR, severe angina during AMI occurred in 49.8% of DM and 46.3% of non-DM (n. s.). No chest pain was reported in 16.9% of DM and 15.0% of non-DM (n. s.). Extra-thoracic pain, dizziness, nausea, sweating, palpitations, radiation of angina and localization of radiating pain was not different between DM and non-DM patients. Severe dyspnea occurred in 29.5% of DM and 19.5% of non-DM patients (p = 0.003). CONCLUSIONS: Apart from a higher frequency of severe dyspnea in diabetics, there appears to be no difference in the clinical symptoms of AMI patients with and without diabetes mellitus. AMI with little or no angina was also frequently found in non-diabetics. In the hospital, diabetics with suspected AMI do not appear to need a special judgement of symptoms. This could accelerate access of diabetics to standard therapeutic procedures.

Aged↗
PubMed2002

[Day-night variability of the prehospital phase of acute myocardial infarct].

While a circadian rhythm in the onset of acute myocardial infarction (AMI) is well established, little is known about the variability of prehospital delay and decision processes. Seven hundred and thirty-nine consecutive AMI patients (median age 65.3 years; 30.2% women) with a median decision time of 60 min and a total prehospital delay of 180 min were studied. In 30.9% of patients onset of AMI symptoms was at night (10.00 p.m.-06.00 a.m.). At night patient decision time was significantly longer than during daytime (120 vs 45 min, difference 75 min; p < 0.001), total prehospital delay was prolonged accordingly (240 vs 170 min, difference 70 min; p < 0.001). The relative risk (RR; 95% confidence interval, CI) for a late decision (> 1 h) to seek medical care at night was significantly increased in females (RR 1.96; CI 1.07-3.61, p = 0.028), non-smokers (RR 2.49; CI 1.42-4.39, p = 0.001) and patients with radiation of anginal pain (RR 2.34; CI 1.32-4.15; p = 0.003). Of all patients with a late decision to seek medical care at night, 95.6% belonged to one of these groups. These variables were not significant for early or late decisions during daytime. Decision processes of AMI patients may be different during daytime and at night. In conclusion, in AMI patients, decision time to seek medical help is prolonged at night. Simple clinical variables (female sex, non-smokers, radiation of anginal pain) identify patients at high risk for a late decision at night. This information should be included into public and individualized education campaigns.

Aged↗
PubMed2002

Emotional attitudes toward symptoms and inadequate coping strategies are major determinants of patient delay in acute myocardial infarction.

BACKGROUND: Early reperfusion treatment in acute myocardial infarction (AMI) preserves ventricular function and saves lives. After onset of AMI symptoms, patients often delay for hours until the decision to seek medical help. AIM: Of the MI-heart (Myocardial Infarction--HElp seeking And ReacTions) study was to identify factors determining patient decision delay. METHODS: 739 consecutive patients with confirmed AMI (median age 65.3 years, 30.2% females) were studied after transfer from the intensive care unit. A standardized interview covered AMI symptoms, attitudes toward symptoms, coping strategies, and clinical and sociodemographic variables. RESULTS: Of patients, 93.3% knew an AMI could be deadly. 43.9% of the patients who suspected an AMI, and knew it could be deadly, decided late (> 1 hour) to seek medical help. In univariate analyses, attitudes toward symptoms and coping strategies had the highest impact on a late decision. Stepwise logistic regression identified the following independent contributors to a late decision to seek medical help (relative risk, 95% confidence interval): wanting to wait and see (3.53; 2.32-5.39), not taking symptoms seriously (2.47; 1.64-3.72), not wanting to bother anybody (2.14; 1.29-3.57), symptoms improving at first (2.33; 1.52-3.56), asking others for advice (0.46; 0.30-0.71), taking pain medication (2.01; 1.01-4.03), age > 65 years (1.69; 1.17-2.44), very strong intensity of angina (0.60; 0.42-0.87). CONCLUSIONS: Emotional attitudes to AMI symptoms and inadequate coping strategies are the major determinants of patient decision delay. They should be considered as a key factor in patient and public education. Modification of these emotional factors might best be achieved by an individualized approach.

Adaptation, Psychological↗
PubMed2001

[Bradycardia despite hyperthyroidism].

Hyperthyroidism is usually associated with tachycardia, hypothyroidism with bradycardia. After observing clinically inapparent hyperthyroidism in patients requiring pacemaker implantation, we studied the occurrence of hyperthyroidism in patients receiving a first permanent pacemaker. Of 237 patients (age 71.4 +/- 8.9 years; 54.9% females), 16 (6.75%) had subclinical (TSH < 0.1 mE/l and fT3 < or = 9.0 pmol/l) and 4 (1.69%) overt hyperthyroidism (TSH < 0.1 mE/l and fT3 > 9.0 pmol/l). Prevalence of hyperthyroidism was similar to that in the general population. Compared to euthyroid patients, in the patients with subclinical or overt hyperthyroidism there were significantly more females (n = 16) than males (n = 4; p = 0.018). Hyperthyroid patients were older (75.0 +/- 9.6 vs. 70.7 +/- 8.9 years; p = 0.015). At follow-up, all patients had a relevant proportion of pacemacer-induced beats. Clinical signs of hyperthyroidism or cardiac symptoms were not different between groups. In conclusion, bradycardia does not exclude the presence of hyperthyroidism. Temporary pacing is recommended in thyreotoxicosis with bradycardia. In contrast, primary implantation of a permanent pacemaker appears to be adequate in patients with bradycardia, cardiovascular disease and an additional diagnosis of hyperthyroidism.

Age Factors↗
PubMed1998

[Renal urodilatin secretion is associated with diuresis and natriuresis after spontaneous, supraventricular tachycardia].

Patients with paroxysmal supraventricular tachycardia (SVT) may have a polyuria after termination of tachycardia. There is increasing evidence that the renal peptide urodilatin (ANP (95-126))--and not plasma ANP (ANP (99-126))--is the member of the natriuretic peptide family mediating natriuresis and diuresis in man. In patients with SVT we, therefore, analyzed the relationship between diuresis, natriuresis, plasma ANP, urinary urodilatin excretion and renal excretion of cyclic GMP, the second messenger in the ANP system. During and after clinical presentation with spontaneously occurring SVT, two patients with AV-nodal and one patient with atrioventricular reentry tachycardia (heart rate 160 to 200 bpm) were studied. Urinary urodilatin excretion was correlated to diuresis (r = 0.73) and natriuresis (r = 0.93); similarly urinary cyclic GMP excretion was related to diuresis (r = 0.80) and natriuresis (r = 0.87; p < 0.001, respectively). In contrast, there was no significant correlation between plasma ANP concentrations and diuresis (r = 0.28, n.s.) or natriuresis (r = 0.11, n.s.). As an explorative analysis, stepwise multiple linear regression identified urinary urodilatin as the most important contributor to diuresis and natriuresis after SVT. These data on polyuria after spontaneous SVT further support the view that in man urodilatin is the member of the natriuretic peptide family participating in kidney physiology.

Adult↗
PubMed1997

[Primary chylopericardium--stepwise diagnosis and therapy of a differential diagnostically important illness].

Primary chylopericardium is a rare disease with a highly variable clinical course. We report on a 24-year old female with chylopericardium detected during a pulmonary infection. Despite successful treatment of the infectious disease, the chylopericardium persisted and led to cardiac tamponade. From this case, as well as from the literature, it is intriguing to postulate an inflammatory injury of preexisting anomalous lymphatic vessels leading to onset or aggravation of primary chylopericardium. The clinical hallmark of chylopericardium is a milky white, but odorless pericardial fluid at pericardiocentesis. For cases where conservative treatment and pericardiocentesis fail, we newly introduced the method of pericardio-peritoneal shunting by a pericardial window. With postoperative reaccumulation of pericardial fluid, total parenteral nutrition followed by medium chain triglyceride diet was successfully reinitiated. This combined surgical and conservative approach was performed for the first time and may have helped to avoid the more aggressive treatment of thoracic duct ligation and resection. During 2 years of follow-up the patient was asymptomatic and had no recurrence of pericardial effusion.

Adult↗
PubMed1997

Transcranial power-mode duplex ultrasound in two patients with moyamoya syndrome.

Moyamoya syndrome is characterized by the reticulated collateralization of the intracranial vasculature distal to an occlusion of proximal intracranial vessels. In the present study this pathology was visualized in 2 patients, aged 29 and 32 years, using transcranial color Doppler imaging (TCDI). Digital subtraction angiography in both patients revealed stenosis of the intracranial portion of the internal carotid arteries, occlusion and stenosis of several cerebral arteries, and a bilateral reticulated collateral network particularly in the region of both basal ganglia, typical of moyamoya syndrome. TCDI with power-mode Doppler depicted parts of the intracranial collateral network, not possible using conventional color-flow Doppler. TCDI with power-mode Doppler permitted better visualization of intracranial vascular pathology in comparison to conventional color-flow Doppler, enabling a rapid and noninvasive diagnosis of rare cerebrovascular anomalies.

Adult↗
PubMed1996

Neutral endopeptidase 24.11 inhibition may not exhibit beneficial haemodynamic effects in patients with congestive heart failure.

OBJECTIVES: Inhibition of neutral endopeptidase 24.11 (NEP) prevents degradation of plasma atrial natriuretic peptide (ANP), a substance with vasodilatory and natriuretic properties. The aim of the study was to investigate the haemodynamic and endocrine effects of the NEP inhibitor candoxatril in patients with congestive heart failure (CHF). METHODS: In a randomized double-blind, parallel group study design, 24 patients with CHF received a 10-day oral drug treatment with candoxatril (25, 100 or 400 mg b.i.d.) or placebo. Invasive haemodynamics and laboratory parameters were measured on days 1 and 10. RESULTS: On the first treatment day, candoxatril produced a dose-dependent increase in plasma cyclic GMP, the second messenger of ANP. At doses of 100 and 400 mg, candoxatril induced an increase (!) in systemic vascular resistance (SVR) and a decrease in cardiac index (CI), which was not observed with placebo and the lower candoxatril dose. CONCLUSION: Despite significant activation of the ANP system, reflected by a dose-dependent increase in plasma cyclic GMP concentrations, high doses of candoxatril induced systemic vasoconstrictory rather than vasocilatory effects in patients with CHF. Therefore NEP inhibition by candoxatril may not exhibit beneficial haemodynamic effects in CHF.

Aldosterone↗
PubMed1995

The dihydropyridine calcium channel blocker BAY t 7207 attenuates the exercise induced increase in plasma ANF and cyclic GMP in patients with mildly impaired left ventricular function.

In man, chronic antihypertensive calcium antagonist treatment improves cardiac function and reduces plasma ANF concentrations. Physical exercise increases cardiac workload and plasma ANF levels. In the present study, we investigated the effects of acute administration of the dihydropyridine calcium antagonist BAY t 7207 (BAY) during bicycle exercise on plasma ANF and plasma cyclic GMP levels, on mean arterial pressure (MAP), heart rate (HR), and on natriuresis and urinary urodilatin excretion. In a randomized, double-blind placebo controlled cross-over trial, 8 patients (age 56.8 +/- 2.5 y) with documented coronary artery disease and mildly impaired left ventricular function (EF 50.0 +/- 1.3%), received oral BAY (20 mg) or placebo. Forty-five minutes after medication, patients underwent a standardised exercise bicycle test in the supine position (6 min 25 W, 6 min 50 W). Before exercise, MAP was lower after BAY (88.8 +/- 4.1 mmHg) than after placebo (95.7 +/- 3.5 mmHg; p = 0.024), and HR was higher after BAY (76.8 +/- 3.5 bpm) than after placebo (69.5 +/- 3.6 bpm; p = 0.049). Plasma ANF tended to be higher after BAY (31.2 +/- 5.6 pg/ml) than after placebo (26.7 +/- 5.0 pg/ml), and plasma cGMP was not different (BAY 3.4 +/- 0.3, placebo 3.8 +/- 0.3 pmol/ml). During exercise, the relative increases in HR (+43%) and MAP (+17%) were identical after BAY and placebo. In contrast, ANF levels during exercise increased by 130 +/- 28% after placebo but only by 36 +/- 11% after BAY (p = 0.011). In parallel, plasma cyclic GMP increased by 61 +/- 13% after placebo and by 20 +/- 8% after BAY (p = 0.013). At the end of exercise, the BAY-induced reduction in plasma cyclic GMP reflected the reduction in diastolic arterial pressure (r = 0.717; p = 0.045). Compared to placebo, BAY treatment increased the fractional excretion rate of sodium from 0.46 +/- 0.11 to 0.90 +/- 0.22% (p = 0.016), without relation to urinary urodilatin excretion. Thus, the calcium antagonist BAY t 7207 attenuated the exercise-induced increase in plasma ANF and cyclic GMP probably due to its vasodilator effect. The relationship between blood pressure and the ANF system during exercise, which parallels findings during chronic antihypertensive treatment, may open a perspective for early evaluation of long-term therapy with calcium channel blockers.

Atrial Natriuretic Factor↗
PubMed1995

Severe hypotension and bradycardia after continuous intravenous infusion of urodilatin (ANP 95-126) in a patient with congestive heart failure.

The effects of a continuous i.v. infusion of urodilatin at a dose of 30 ng kg-1 min-1 were studied in a patient with congestive heart failure. After 30 min, urodilatin had induced a marked stimulation of plasma cyclic GMP concentrations. In parallel haematocrit increased. No significant diuresis and no change of invasive haemodynamics was observed. After 2 h the patient developed a profuse perspiration. Eighty minutes later he suffered from dizziness due to hypotension (blood pressure 80/40 mmHg) and a sudden bradycardia (50 bpm). Urodilatin was discontinued and symptoms were relieved by bed tilt and rapid infusion of isotonic saline solution. Mechanisms contributing to these adverse effects may be fluid extravasation to the third space and sympathoinhibitory effects known to occur with natriuretic peptide infusion.

Atrial Natriuretic Factor↗
PubMed1992

Effects of atrial natriuretic factor on anterior pituitary hormone secretion in normal man.

The effects of intravenous human atrial natriuretic factor ANF(99-126) administration on anterior pituitary hormone secretion have not been extensively investigated in humans. We repeatedly studied 10 healthy volunteers (5 female, 5 male, aged 28 +/- 2 years) on 2 occasions, 3 days apart. In randomized, single blind order, subjects received pretreatment with either placebo or intravenous ANF(99-126) (bolus 100 micrograms/kg, 30-min infusion of 0.1 micrograms/kg.min). Subsequently on both occasions subjects received a combined intravenous bolus injection of pituitary releasing hormones (200 micrograms thyrotropin releasing hormone, 100 micrograms gonadotropin releasing hormone and 100 micrograms human adrenocorticotropin releasing hormone; Bissendorf, Hannover, FRG). Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), thyrotropin (TSH), prolactin, ANF and cyclic guanosine monophosphate (GMP) were determined by radioimmunoassay. ANF(99-126) treatment induced a significant reduction in basal ACTH plasma concentrations and tended to decrease basal plasma cortisol. The TSH response to combined releasing hormone administration was significantly diminished after ANF(99-126) pretreatment. In women, the releasing hormone induced prolactin increase was reduced after ANF(99-126) pretreatment. With the present study design, ANF(99-126) did not alter the basal or releasing hormone stimulated plasma concentrations of cortisol, LH, FSH and GH. Releasing hormone administration did not affect ANF and cyclic GMP plasma levels. In humans, effects of natriuretic peptides on anterior pituitary hormone secretion may have to be considered with investigational or therapeutic administration of ANF analogues or agents interfering with the ANF metabolism.

Adult↗
PubMed1992

Haemodynamic and renal effects of urodilatin bolus injections in patients with congestive heart failure.

Urodilatin (ANF(95-126)) is an analogue of the atrial natriuretic factor (ANF(99-126)), which has been isolated from human urine. Recently we have shown in healthy volunteers, that intravenous bolus injections of synthetic urodilatin produce more pronounced reductions of pulmonary arterial pressure than ANF(99-126). To compare haemodynamic and renal effects of synthetic urodilatin with those of ANF(99-126) in congestive heart failure (CHF), 12 patients (66.3 +/- 1.4 years) received either two high dose intravenous bolus injections of 4 micrograms kg-1 bw Urodilatin (URO) at a 30 min interval (n = 6) or the same doses of ANF(99-126) (n = 6). Prior to i.v. URO, no URO immunoreactivity was found in human plasma (specific RIA, no crossreactivity to ANF). Similar to ANF, the increase in diuresis (1.4 +/- 0.7 to 3.7 +/- 1.6 ml min-1) and natriuresis (169 +/- 114 to 430 +/- 197 mumol min-1) was moderate after URO in CHF. During the 90 min study period, mean plasma cyclic GMP levels increased much more after URO (by 53.4 +/- 15.1 nM) than after ANF (by 13.1 +/- 3.0 nM; P = 0.04). In contrast to ANF, i.v. bolus injections of URO produced sustained haemodynamic effects in CHF lasting up to 90 min: The average (0-90 min) reduction of systemic vascular resistance was more pronounced after URO (-578 +/- 148) than after ANF (-204 +/- 65 dyn*s*cm-5, P = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Haemodynamic and renal effects of urodilatin in healthy volunteers.

Urodilatin (ANF(95-126)), an analogue of the atrial natriuretic factor (ANF(99-126)), has recently been isolated from human urine. To study haemodynamic and renal effects of synthetic urodilatin, 18 healthy male volunteers (age 26.1 +/- 0.8 years; X +/- SEM) received i.v. bolus injections of urodilatin at doses of 1, 2 or 4 micrograms kg-1 body weight (bw) (n = 6 per dosage group). Urodilatin dose-dependently increased heart rate and cardiac index. A dose-dependent increase in plasma cyclic GMP levels was also observed. Urinary cyclic GMP excretion, urine flow and natriuresis increased 7-fold, 5-fold and 4-fold, respectively. Renal effects were not different between dosage groups. Compared with ANF(99-126), after urodilatin the reduction in mean pulmonary arterial pressure (PAP) was more pronounced (2 micrograms kg-1, n = 6; ANF -1.8 +/- 0.5, URO: -5.5 +/- 1.1 mmHg, P less than 0.05). Furthermore, after urodilatin the reduction of PAP lasted continuously from 2 up to 90 min after injection, while ANF(99-126) produced only a transient decrease of PAP. Similarly the reduction of pulmonary capillary wedge pressure (PCWP) by urodilatin from 9.3 +/- 1.2 to 3.8 +/- 0.9 mmHg (P less than 0.05) was also sustained up to 90 min post administration. These data in healthy volunteers suggest that, due to prolonged reduction of PAP and PCWP with increases of cardiac index and reduction of systemic vascular resistance, urodilatin might exhibit beneficial effects in cardiovascular disease.

Adult↗
PubMed1991

Osteoporosis in longstanding acromegaly: characteristic changes of vertebral trabecular architecture and bone matrix composition.

Although it is now 60 years after Erdheim's (1931) detailed description of vertebral alterations in severe acromegaly, it is still unclear whether osteoporosis is a consistent feature of acromegalic bone disease or not. We studied the vertebral trabecular bone of a 44-year-old woman who had suffered active acromegaly for more than 20 years, and compared it with 17 normal as well as 2 osteoporotic controls. Histomorphometry revealed a very low trabecular bone volume and thus documented the presence of osteoporosis. The mean trabecular plate thickness was strikingly increased in acromegaly (possibly caused in part by a low-dose fluoride treatment), whereas it was normal or reduced in the osteoporotic controls. The meticulous analysis showed islands of cartilaginous tissue in the core of the acromegalic trabeculae which were not present in any other sample. In these areas collagen II was detected by immunohistochemistry. Biochemical analysis revealed that collagen II accounted for 7% of the total collagenous matrix. The degree of hydroxylation of lysyl residues of collagen I was close to the average value of all control samples studied. Our data show that osteoporosis can occur in acromegaly and that it is characterized by unusual architectural and compositional features. These findings challenge the prevailing view that the matrix of osteoporotic bone always shows a normal composition.

Acromegaly↗
PubMed1990

Pituitary sarcoidosis.

A 66-year-old woman presenting with pituitary insufficiency was operated on for an intrasellar tumor. Surprisingly, this tumor, at first suspected to be a hormone-inactive pituitary adenoma, consisted in fact of sarcoid granulomatous tissue in the pituitary gland as found histologically. The morphological picture as seen in the cranial computed tomography was identical with that of an adenoma. This possibility had not previously been considered, although there had been an extracerebral manifestation of the sarcoidosis in the left ovary.

Adenoma↗