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Biomedical subjects

C Lengyel

Publications and source records attributed to C Lengyel.

13 recordsLinked to original sources
PubMed2005

Coronary flow reserve, insulin resistance and blood pressure response to standing in patients with normoglycaemia: is there a relationship?

AIMS: To establish the relationships between coronary flow reserve, cardiovascular autonomic function, and insulin resistance characterized by the homeostasis model assessment insulin resistance score in patients with normal carbohydrate metabolism according to the World Health Organization (WHO) and American Diabetes Association (ADA) criteria, and with morphologically normal epicardial coronary arteries. METHODS: Twenty-five patients [12 women and 13 men, mean (sd) age: 53 +/- 11 years] with normal coronary angiography were enrolled into the study. Coronary flow reserve was measured during stress transoesophageal echocardiography. Autonomic dysfunction was assessed by means of five standard cardiovascular reflex tests. The fasting serum glucose and insulin levels were determined and the homeostasis assessment model insulin resistance score was calculated. RESULTS: In patients with normal carbohydrate metabolism, negative correlations were observed between the coronary flow reserve and both the serum insulin level (r = -0.445, P = 0.026) and the homeostasis assessment model insulin resistance score (r = -0.449, P = 0.024). The systolic blood pressure response to standing also correlated with the coronary flow reserve (r = -0.519, P = 0.011). The heart rate response to deep breathing, the Valsalva ratio, the 30/15 ratio and the sustained handgrip test results were not correlated with the coronary flow reserve. CONCLUSIONS: Our data suggest the possible role of insulin resistance and early sympathetic nerve dysfunction in the development of decreased coronary flow reserve in patients without diabetes mellitus or impaired glucose tolerance.

Adult↗
PubMed2004

Regional differences in the manifestation of gastrointestinal motor disorders in type 1 diabetic patients with autonomic neuropathy.

OBJECTIVE: The aim of this work was to establish the prevalence and severity of different gastrointestinal symptoms and their relationships to esophageal, gastric and recto-anal motor disturbances by manometry in patients with Type 1 diabetes mellitus and autonomic neuropathy. PATIENTS AND METHODS: Sixteen patients (mean age: 53.4 +/- 14.9 years) with long standing type 1 diabetes mellitus (mean diabetes duration: 22.1 +/- 14.7 years) and autonomic neuropathy (mean Ewing score: 5.73 +/- 2.34) were investigated. The gastrointestinal symptom scores were established by using the Talley dyspepsia questionnaire. The motor function of the digestive tract was tested in the esophagus, in the stomach, and in the ano-rectum by perfusion manometry. RESULTS: Manometric evaluation of the esophagus did not reveal significant abnormalities in the region of the upper sphincter in patients with diabetes mellitus. In contrast, diabetic patients had decreased peristaltic wave amplitude, prolonged duration, decreased wave propagation velocity, and increased number of simultaneous contractions in the esophageal body, and decreased lower esophageal sphincter pressures with prolonged relaxation compared to the age- and sex-matched controls. Symptom analysis showed correlations between reflux symptoms and LES relaxation times, and between dysphagia scores and esophageal body peristaltic wave duration, propagation velocity and the rate of simultaneous contractions. In the gastric antrum, frequent, and often severe, fasting motility disorders were observed, which had no correlation with dyspeptic symptoms. In the ano-rectal region the diabetic patients had a lower squeezing-resting pressure difference, and impaired fecal expulsive function. Motility disorders were simultaneously present at multiple parts of the gastrointestinal tract in 13/16 cases. CONCLUSIONS: In patients with type 1 diabetes mellitus and autonomic neuropathy gastrointestinal motility disorders were observed frequently, and in most of the cases simultaneously. While esophageal and ano-rectal symptoms correlated better with the manometric abnormalities, the lack of correlation between the impaired fasting gastric motility and dyspeptic symptoms shows that, on the basis of the clinical symptom analysis, the prevalence of such motor disorders could be underestimated. The early recognition of gastrointestinal motility disorders may be important for the better long-term management of patients with type 1 diabetes mellitus.

Adult↗
PubMed2001

Gallbladder hypomotility in diabetic polyneuropathy.

This study was performed to evaluate the gallbladder motility in long-standing diabetes mellitus. The gallbladder function of diabetic patients was measured by means of quantitative hepatobiliary scintigraphy, and the severity of the associated autonomic and sensory polyneuropathy was determined. The presence of a marked gallbladder hypomotility was established, and a positive correlation was observed between the severity of the autonomic disturbance and the contractile disorder. This study underlines the important role of the neuropathy in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.

Autonomic Nervous System↗
PubMed2001

Pharmacological block of the slow component of the outward delayed rectifier current (I(Ks)) fails to lengthen rabbit ventricular muscle QT(c) and action potential duration.

1. The effects of I(Ks) block by chromanol 293B and L-735,821 on rabbit QT-interval, action potential duration (APD), and membrane current were compared to those of E-4031, a recognized I(Kr) blocker. Measurements were made in rabbit Langendorff-perfused whole hearts, isolated papillary muscle, and single isolated ventricular myocytes. 2. Neither chromanol 293B (10 microM) nor L-735,821 (100 nM) had a significant effect on QTc interval in Langendorff-perfused hearts. E-4031 (100 nM), on the other hand, significantly increased QTc interval (35.6+/-3.9%, n=8, P<0.05). 3. Similarly both chromanol 293B (10 microM) and L-735,821 (100 nM) produced little increase in papillary muscle APD (less than 7%) while pacing at cycle lengths between 300 and 5000 ms. In contrast, E-4031 (100 nM) markedly increased (30 - 60%) APD in a reverse frequency-dependent manner. 4. In ventricular myocytes, the same concentrations of chromanol 293B (10 microM), L-735,821 (100 nM) and E-4031 (1 microM) markedly or totally blocked I(Ks) and I(Kr), respectively. 5. I(Ks) tail currents activated slowly (at +30 mV, tau=888.1+/-48.2 ms, n=21) and deactivated rapidly (at -40 mV, tau=157.1+/-4.7 ms, n=22), while I(Kr) tail currents activated rapidly (at +30 mV, tau=35.5+/-3.1 ms, n=26) and deactivated slowly (at -40 mV, tau(1)=641.5+/-29.0 ms, tau(2)=6531+/-343, n=35). I(Kr) was estimated to contribute substantially more to total current density during normal ventricular muscle action potentials (i.e., after a 150 ms square pulse to +30 mV) than does I(Ks). 6. These findings indicate that block of I(Ks) is not likely to provide antiarrhythmic benefit by lengthening normal ventricular muscle QTc, APD, and refractoriness over a wide range of frequencies.

Action Potentials↗
PubMed2001

Brainstem auditory-evoked potential examinations in diabetic patients.

Brainstem auditory-evoked potential (BAEP) examinations were performed in 15 patients with long-standing type-1 diabetes mellitus (DM). Cardiovascular reflex tests were applied for assessment of autonomic neuropathy. The aim of our investigation was to compare the BAEP results of this patient group with controls and to look for a possible correlation between the alteration of the auditory brainstem function and the cardiovascular autonomic neuropathy. Analysis of the latencies (waves I, II, III and V) and the inter-peak latencies (waves I-III and I-V) of BAEPs revealed a significant difference between diabetics and healthy controls. The amplitudes of waves I, III and V were definitely lower in comparison with those of healthy controls. A positive correlation was observed between the overall autonomic score and the latencies (waves III and V) and inter-peak latencies (waves I-III and I-V). These data support the hypothesis that long-standing DM and diabetic neuropathy might be related as a cause of certain dysfunctions of the central auditory pathways.

Adult↗
PubMed1998

Suppression of erythromycin-induced early afterdepolarizations and torsade de pointes ventricular tachycardia by mexiletine.

Erythromycin is a selective IKr-blocking, action potential duration (APD)-prolonging drug, which may induce early afterdepolarizations (EADs) and torsade de pointes ventricular tachycardia. The successful termination of an erythromycin-induced clinical torsades de pointes by the authors with mexiletine prompted them to investigate in vitro whether erythromycin is able to induce EADs in Purkinje fibers and, if so, whether EADs are suppressible or not by mexiletine. Electrically stimulated canine Purkinje fibers (n = 9) were superfused with erythromycin (200 mg/l) and action potentials were recorded by an intracellular microelectrode technique. Erythromycin induced a pronounced prolongation of APD and the appearance of EADs in all Purkinje preparations (9/9). After the addition of mexiletine (10 mM), a marked shortening of APD and the disappearance of EADs (7/9) were observed. Mexiletine, an inhibitor of the tetrodotoxin-sensitive window Na(+)-current, may prevent IKr-blocking drug-induced torsade de pointes ventricular tachycardia by abolishing APD prolongation and EADs.

Action Potentials↗
PubMed1997

[Gallbladder hypomotility in diabetic polyneuropathy].

A study was made of the pathogenic role of gallbladder hypomotility, which is presumably responsible for the high incidence of gallstone disease in long-standing diabetes mellitus. The gallbladder motility of diabetic patients (n = 10) was measured by means of quantitative hepatobiliary scintigraphy, and the severity of concomitant autonomic and sensory polyneuropathy was determined. The presence of marked gallbladder hypomotility was proven, and a positive correlation was observed between the severity of autonomic neuropathy and the contractile disorder. In this group of diabetic patients, a hypaesthetic sensory polyneuropathy too was recognized, the degree of which exhibited a positive correlation with the autonomic neuropathy score. This study underlines the important role of the autonomic neural dysfunction in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.

Diabetes Mellitus, Type 1↗
PubMed1997

[Erythrocyte-induced "torsade de pointes" ventricular tachycardia].

A case of erythromycin-induced acquired long QT syndrome and "torsades de pointes" ventricular tachycardia is reported. The peculiar ventricular tachyarrhythmia was evoked by orally administered erythromycin (1.5 g/die) in the presence of diuretic (clopamide)-induced hypokalaemia. The pause-dependent "torsades de pointes" was preceded by prolonged QTU interval (560 ms), "particular bigeminy" and "short-long-short" RR interval sequence. The recurrent ventricular tachycardia causing syncopal attacks was abolished by the discontinuation of erythromycin treatment, K+/Mg(2+)-supplementation and oral mexiletine therapy. It is emphasized that the macrolide antibiotic/prokinetic erythromycin, applied in therapeutic dosages, blocks the rapidly activating delayed rectifier potassium current (IKr), and as such, prolongs ventricular repolarization and may be "torsadogenic".

Clopamide↗
PubMed1997

[Increase of the QT interval dispersion in diabetes mellitus].

The QT dispersion, measured as the interlead variability of QT interval (QTd = QTmax-QTmin), reflects the spatial inhomogeneity of ventricular repolarization times. The authors studied QTd and heart rate-corrected QTd (QTc-d) in 81 patients with diabetes mellitus (IDDM: 39, NIDDM: 42) using Bazett's formula; 20 non-diabetic subjects acted as controls (means +/- SD). QTd (43 +/- 17 ms) and QT c-d (52 +/- 20 ms) were increased (p < 0.05) as compared to the control values (QTd = 32 +/- 17 and, QTc-d = 35 +/- 17 ms, respectively). A significant difference was also observed in QTc-d if the two diabetic groups were compared to the control separately (p < 0.05). Moreover, comparison of the diabetic groups (IDDM vs NIDDM) revealed that type I diabetes mellitus is accompanied by a more pronounced spatial dispersion of ventricular reporlarization (QTd = 49 +/- 16, and QTc-d = 59 +/- 19 ms) as compared to NIDDM (QTd = 38 +/- 16, QTc-d = 46 +/- 20 ms [p < 0.01]). The hypothesis that increased QTd/QTc-d is truly a predictive marker of sudden arrhythmic cardiac death in patients with diabetes mellitus needs further clinical investigation.

Adult↗
PubMed1996

[Amiodarone-induced pulmonary fibrosis].

The most feared side-effect of long-term amiodarone therapy is progressive alveolitis/pneumonitis leading to pulmonary fibrosis. The case history of a patient is presented who received amiodarone unnecessarily in a high dose (600 mg/day) for 4 years: drug-induced dermatopathy, hypothyroidism and lung fibrosis developed. After cessation of amiodarone treatment the pulmonary complication did not disappear therefore glucocorticoid therapy was introduced. New-onset improductive cough, dyspnea, fever and/or enhanced erythrocyte sedimentation rate may suggest the presence of amiodarone pulmonary toxicity and may form the basis of indication of high-resolution computed tomography (HRCT). Amiodarone-induced pulmonary involvement can be shown by HRCT early, before the appearance of any considerable abnormality of chest radiography.

Amiodarone↗