Biomedical subjects

W Otter

Publications and source records attributed to W Otter.

8 recordsLinked to original sources

PubMed2004

Hospital outcome of acute myocardial infarction in patients with and without diabetes mellitus.

AIMS: To assess hospital mortality and morbidity in diabetic and non-diabetic patients with acute myocardial infarction and to compare the results between the two groups. METHODS: All patients admitted in 1999 to the intensive care unit of the Schwabing City Hospital with diagnosis of acute myocardial infarction were assessed for hospital mortality and co-morbidity. RESULTS: Three hundred and thirty patients with acute myocardial infarction were admitted. Of those, 126 (38%) were diabetic and 204 (62%) were non-diabetic patients. Mortality within 24 h after admission was 13.5% in diabetic patients and 5.4% in non-diabetic patients (P<0.01). Mortality during entire hospitalization was higher in diabetic than in non-diabetic patients (29.4% vs. 16.2%; P=0.004). Diabetic patients were resuscitated more frequently than non-diabetic patients (24% vs. 11%, P<0.01). In diabetic patients, heart rate at admission was increased (91 +/- 27 vs. 82 +/- 23/min; P<0.01) and presence of angina pectoris was reported less frequently (59% (n=72) vs. 82% (n=167); P<0.001). Preceding myocardial infarction, microalbuminuria, peripheral artery disease and arterial hypertension were more frequent in diabetic than in non-diabetic patients. Diabetic patients demonstrated higher C-reactive protein (CRP) levels than non-diabetic patients (91.4 +/- 78.2 mg/l vs. 45.2 +/- 62.4 mg/l; P<0.001). CONCLUSIONS: In diabetic patients with acute myocardial infarction, early hospital mortality is increased and signs of cardiac autonomic dysfunction and microangiopathy are detected more frequently than in non-diabetic patients. The need for advanced treatment strategies early in the course of diabetic patients with myocardial infarction is emphasized.

Aged↗

PubMed2003

[Diagnosis of acute myocardial infarction in diabetes mellitus. Blood sugar to be tested].

Rapid and accurate establishment of the clinical symptoms and the initiation of appropriate treatment are essential prerequisites for starting therapeutic measures capable of improving the prognosis of diabetics suffering an acute myocardial infarction. Early diagnostic measures in suspected myocardial infarction include laboratory investigations such as myocardium-specific enzymes, blood glucose and, where indicated, HbA1c and hsCRP, as also an ECG, echocardiography, and possibly scintigraphy to investigate further potential risks. In diabetics with an acute coronary syndrome, early coronary angiography should also be considered. A multifactorial approach can significantly lower the cardiovascular complication rate.

Angina, Unstable↗

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↗

PubMed1999

Novel neurohormonal modulators in cardiovascular disorders. The therapeutic potential of endopeptidase inhibitors.

Since angiotensin II is an established target of pharmacological interventions, there is an increasing interest in the biological effects and metabolism of other vasoactive peptides like atrial natriuretic factor (ANF) and endothelin (ET). Exogenous administration of the vasodilatory and natriuretic ANF and of its analogues improved haemodynamics and renal function in cardiovascular disease, including congestive heart failure (CHF). Effects of natriuretic peptides appeared to be attenuated during prolonged infusion and in more severe disease. Promising results were obtained in animal experiments and initial patient studies concerning haemodynamics and kidney function with inhibition of ANF metabolism by inhibitors of the neutral endopeptidase 24.11 (NEP). With further clinical studies, moderately relevant effects of acute intravenous or oral NEP inhibition were observed, but these effects were blunted with prolonged drug administration. There is increasing evidence that NEP inhibitors such as candoxatril, expected to exhibit vasodilatory activity at least at certain doses and in certain clinical settings, even induce vasoconstriction. As well as natriuretic peptides, NEP also metabolises the vasoactive peptides ET, angiotensin II and bradykinin. It now appears to be evident, especially from human experiments on forearm blood flow after intra-arterial infusion of agents, that NEP inhibitor--induced vasoconstriction is mediated by increased ET-1 rather than by angiotensin II. The hypothesis that concurrent ACE inhibition would unmask the benefits of NEP inhibitors was not supported by a recent 10-week study in CHF; with ecadotril given to ACE inhibitor-pretreated patients, there were no clear hints towards improvement of symptoms but troublesome aspects on mortality. Future clinical studies on dual inhibitors of NEP and ACE will have to reveal the place of NEP inhibition in cardiovascular disease in the presence of established therapeutic standards. Remarkable haemodynamic and cardioprotective effects have been obtained with antagonists of the ET receptor. Specific inhibitors of the endothelin converting enzyme (ECE) have only recently been introduced, inhibiting ET generation from its precursor, big ET. If the results previously obtained with ET receptor antagonists can be reproduced with ECE inhibitors, and transferred to clinical medicine, endopeptidase inhibition might open new horizons in cardiovascular treatment strategies.

Animals↗

PubMed1997

Increased renal natriuretic peptide (urodilatin) excretion in heart failure patients.

Accumulating evidence suggests that urodilatin, a kidney-derived member of the natriuretic peptide family, contributes as a major mediator of sodium excretion to body fluid regulation in healthy men. In contrast to other members of the natriuretic peptide family, pathophysiological data for the renal natriuretic peptide have still been missing. The present study compares renal synthesis of urodilatin in patients with congestive heart failure (CHF) and healthy volunteers. Because urodilatin excretion, considerably increases with increasing nutritive sodium intake (p<0.004), the CHF patients (15 NYHA I/II, 8 NYHA III/IV) were kept on a 165 mmol/day sodium diet and 6 healthy volunteers on a identical nutritive sodium intake level were selected as proper controls. Although urodilatin excretion significantly increased (p<0.027) with increasing severity of CHF and was therefore significantly higher in mild CHF (40.7 +/- 2.5 fmol/min) and severe CHF (54.7 +/- 6.6 fmol/min) than in healthy controls (3.2 +/- 4.2 fmol/min), both groups of CHF patients retained sodium and had significantly lower sodium excretion rates (NYHA I/II 79.0 +/- 6.9 micromol/min, NYHA III/IV 97.9 +/- 12.7 micromol/min) than the healthy controls (139 +/- 3.4 micromol/min). Our data suggest that renal urodilatin synthesis, may not be involved in the etiology of sodium retention in CHF, but may rather be stimulated to counteract antinatriuresis during CHF.

Adolescent↗

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↗

PubMed1996

Cocaine or phenylephrine/lignocaine for nasal fibreoptic intubation?

In order to assess if a mixture of phenylephrine/lignocaine is as effective as cocaine for local analgesia and vasoconstriction during nasal fibreoptic intubation, 99 patients receiving topical nasal analgesia either with cocaine 10% or a mixture of phenylephrine 1% and lignocaine 4% were studied in a randomized double-blind investigation. After topical analgesia a flexible fibreoptic endoscope was advanced through a nostril. Larynx, glottis and trachea were endoscopically sprayed with lignocaine. Following induction of anaesthesia a nasotracheal tube was inserted fibreoptically. Pain intensity and amount of epistaxis during endoscopy were assessed. Blood pressure, heart rate and ECG-ST segment were determined before and after topical nasal analgesia, after induction of anaesthesia and after nasotracheal intubation. There were no significant differences in pain intensity of epistaxis between groups during endoscopy, nor significant alterations in haemodynamic parameters or ST-segment. It is concluded that the mixture of phenylephrine and lignocaine is a useful alternative to cocaine for local analgesia and vasoconstriction during nasal fibreoptic intubation.

Administration, Intranasal↗

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↗