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Biomedical subjects

J Neuzner

Publications and source records attributed to J Neuzner.

At least 73 records · Page 4Linked to original sources
PubMed1994

[Subtypes of muscarinic receptors--aspects of their physiologic significance for controlling heart rate in the human].

The cDNAs for five different muscarinic cholinoceptors have been cloned. The biochemical and physiological relevance of the m1, m2 and m3 receptors is understood in many aspects. The pharmacological defined M1, M2 and M3 related to antagonists binding studies closely correspond with those cloned. We compared effects of atropine and of the subtype selective M-cholinoceptor antagonists pirenzepine and AF-DX 116 in humans. Dose- or time-response curves have been established for heart rate. Plasma samples were drawn in parallel with the effect measurements and analysed for drug concentrations. Subtype-selective radioceptor assays of the samples served to estimate the respective receptor occupancy in vivo. After low dosis of pirenzepine (M1-selective blockade) a negative chronotropic effect on heart rate could be observed. After high doses of pirenzepine or atropine (M-unselective blockade) the wellknown tachycardia appeared in parallel with occupancy of both the M2 and M3 subtypes. AF-DX 116 induced a tachycardia without a decrease of salivary flow in agreement with its selectivity profile (M2 > M1 > M3). Gastric emptying was only slightly inhibited by AF-DX 116 but nearly completely by a very high dose of pirenzepine blocking M1-, M2- and M3-cholinoceptors. The negative chronotropic effect on heart rate of a low dose of pirenzepine (M1 selective) was multi-folded by pretreatment with isoprenaline but disappeared during bicycle exercise. The implications of the functional M cholinoceptor heterogeneity in humans revealed by antagonists are discussed according to its possible importance for the control of autonomous nerve system.

Atropine↗
PubMed1994

[Indications and contraindications for therapy with implantable cardioverters/defibrillators].

Despite all advances in the diagnostic and therapy of cardiovascular diseases the mortality from malignant ventricular tachyarrhythmias is still a major health problem. In addition to established therapeutic strategies in the prevention of sudden cardiac death such as antiarrhythmic drug treatment, catheter ablation or antiarrhythmic surgery the implantable cardioverter/defibrillator was introduced to clinical practice in 1980. The number of 50,000 overall implants reflects the current clinical status of the therapy with implantable cardioverters/defibrillators. Significant technical improvements in the defibrillator therapy may contribute to an increase in therapy acceptance. These advances include the introduction of nonthoracotomy lead systems, enhanced defibrillation efficacy, full programmable devices providing tiered electrical therapy, improved diagnostic Holter functions and enhanced arrhythmia detection algorithms. The major present goals of defibrillator therapy are, detection and termination of malignant ventricular tachyarrhythmias, reduction of sudden cardiac death, reduction in patient's mortality and improvement in quality of life. The efficacy and safety of defibrillator therapy to prevent sudden arrhythmic death has been proven in several large clinical investigations. The annual sudden cardiac death mortality is < 2% even in high-risk patient populations. Compared to sudden cardiac death rate there is a much higher rate of overall cardiac mortality because a defibrillator is not able to prevent nonarrhythmic cardiovascular deaths. There is a clinical impression that cardiovascular mortality is lower in patients treated with an implantable cardioverter/defibrillator compared to patients treated with other therapies. However there are no results from controlled studies providing scientific evidence that defribillator therapy can reduce overall cardiovascular mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Contraindications↗
PubMed1994

[Neurohumoral and hemodynamic effects in combination therapy of enoximone and dopamine].

Twelve patients with severe heart failure (NYHA class III-IV) were investigated by intraindividual comparison for the hemodynamic and neurohumoral effects of dopamine (3 and 6 micrograms/kg/min), enoximone (8 micrograms/kg/min), and the combination of both medications (dopamine 3 micrograms/kg/min+enoximone 8 micrograms/kg/min) using right heart catheterization. The duration of active treatment was 8 h for each substance with a subsequent washout time of 16 h. Dopamine led to a dose-dependent increase in cardiac index of 10-13% and 18-37% under 3 and 6 micrograms/kg/min, respectively (p < 0.001). Enoximone monotherapy produced a comparable increase in cardiac index between 27 and 32% (p < 0.001). Enoximone, but not dopamine, resulted in a significant decrease in mean pulmonary artery pressure (21-26%; p < 0.01), pulmonary capillary wedge pressure (24-30%; p < 0.01), and right atrial mean pressure (26-28%; p < 0.001). The systemic vascular resistance was without significant changes at low-dose dopamine therapy, decreased by 10-19% insignificantly at a dose of 6 micrograms/kg/min, and reached the level of significance with enoximone therapy (-20 to -25%; p < 0.001). There was a highly significant decrease by 49-55% in systemic vascular resistance with enoximone (p < 0.001), in contrast to dopamine. Heart rate and blood pressure remained without significant changes at low-dose dopamine, with the heart rate increasing significantly by 25% at a dose of 6 micrograms/kg/min within the first 2 h (p < 0.01). Enoximone produced a heart rate increase by 8-13% (being significant after 2 h; p < 0.05) with no changes in blood pressure. The combination therapy with dopamine and enoximone led to an additive increase in cardiac index by 35-43% (p < 0.001), a decrease in right atrial mean pressure by 28-36% (p < 0.01), a decrease in systemic vascular resistance by 27-30% (p < 0.01) and in pulmonary vascular resistance by 46-51%. An additive effect on heart rate was not observed. The respective monotherapies with low-dose dopamine and enoximone had no remarkable effect on plasma catecholamines, while dopamine at a dose of 6 micrograms/kg/min and combination therapy led to a significant increase in noradrenaline levels. There was a highly significant decrease in the plasma concentration of the atrial natriuretic factor under enoximone and combination therapy (p < 0.001) as well as a significant decrease in aldosterone (0 < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

Tedisamil (KC 8857) is a new specific bradycardic drug: does it also influence myocardial contractility? Analysis by the conductance (volume) technique in coronary artery disease.

To determine whether inotropism influences the bradycardic action of tedisamil, hemodynamic assessment was performed in 13 patients with ischemic coronary artery disease including analysis of end-systolic pressure-volume relationships after an infusion of tedisamil, 0.3 mg/kg, at rest, and during paced tachycardia stress. Slope Emax fell by 14% at rest (13 patients) and by 10% during tachycardia (6/13 patients), whereas loops of end-systolic pressure-volume relationships moved rightward; all parameter changes indicated a lack of significant inotropism loss with tedisamil (p > 0.05). Although the mean heart rate decreased from 77.5 to 64.7 beats/min and QTc duration increased by 14% (p < 0.05), filling pressure and dp/dtmin remained unchanged and vascular resistance increased by 30%. Parameters of left ventricular pump function (ejection fraction, stroke volume, left ventricular efficiency) decreased slightly (between 3% and 13%), whereas left ventricular volumes increased (end-diastolic volume by 6%, end-systolic volume by 23%). The respective parameter changes during tachycardia were comparable in tendency, and angina could no longer be induced during postdrug pacing stress. We concluded that the bradycardic effects of tedisamil are selectively generated without impairing either ventricular pump function or contractility in a clinically relevant fashion, whereas the postdrug anginal threshold appears elevated. Thus tedisamil can be used safely in ischemic coronary artery disease.

Aged↗
PubMed1993

123I-metaiodobenzylguanidine scintigraphy in the detection of irregular regional sympathetic innervation in long QT syndrome.

Twelve patients with the long QT syndrome were studied to determine the usefulness of 123I-metaiodobenzylguanidine (MIBG) single-photon emission tomography (SPECT) at 2 h and 6 h after injection; the results were compared to 10 healthy volunteers (controls). Uptake of MIBG in the left ventricle at 2 h after injection was significantly reduced in patients with the long QT syndrome (1.43 +/- 0.13 vs 1.66 +/- 0.15 in controls, heart-to-mediastinum ratio, P < 0.002) and washout after 6 h was faster on a planar view image. Decreased MIBG uptake could be observed preferentially in the anterior and lateral walls near the apex. The half-time values of MIBG washout from the left ventricle were significantly reduced in the long QT syndrome (6.4 +/- 1.5 h) compared to controls (16.7 +/- 15.3 h, P < 0.002). In three cases, the same pattern of disturbed activity distribution was maintained even after surgical left cardiac sympathetic denervation. The present results strongly support the hypothesis that an inhomogenous regional distribution of sympathetic nerve terminals accompanied by an overall reduction in their absolute number may play an important role in the pathogenesis of the long QT syndrome. Additional functional disturbances, possibly related to the uptake of catecholamines in the left ventricle may coexist with regional inhomogeneity of nerve terminals. The differences observed from one case to the other may be related to the variation in severity of the disease. MIBG SPECT imaging seems an interesting new tool for the quantitative assessment of presynaptic sympathetic nerve terminal disturbances in the left ventricle of patients with the long QT syndrome.

3-Iodobenzylguanidine↗
PubMed1993

Intracardiac emergency defibrillation for refractory ventricular fibrillation during implantation of cardioverter defibrillators with nonthoracotomy lead systems.

Implantable cardioverter defibrillators (ICDs) are being implanted in increasing numbers. At intraoperative defibrillation threshold tests refractory ventricular fibrillation (VF) requiring emergency open chest resuscitation is a major concern during implantation of nonthoracotomy ICD lead systems. A new method of high energy endocardial/extrathoracic defibrillation via the implanted ICD transvenous defibrillation electrode (TDE) was used to terminate refractory VF. During implantation of ICD with TDE in 20 patients refractory VF occurred in two patients. The arrhythmia was terminated with endocardial/extrathoracic defibrillation in both cases, and no complications were observed.

Aged↗
PubMed1993

[Stored intracardiac electrograms: accuracy of arrhythmia classification in patients with cardioverter/defibrillator system].

A cardioverter/defibrillator that is capable of storing endocardial electrograms before and after electrical device therapy was implanted in 29 patients presenting drug refractory ventricular arrhythmias. During a follow-up period of 7.5 +/- 4.6 months 15/29 patients (51%) experienced a total number of 112 pulse generator discharges. In 104 arrhythmia episodes the stored electrogram was analyzed. Morphological criterias of the stored electrogram as detectable P-waves and changes in the QRS-morphology during tachycardia compared to sinus rhythm served for classification of the documented arrhythmia. The analysis of the stored electrogram established a definitive diagnosis of the arrhythmia and allows to distinguish supraventricular arrhythmias from ventricular arrhythmias in every episode. 72/104 (69.2%) of the discharges were classified as appropriate, 32/104 (30.8%) of the device discharges were not appropriate and caused by atrial fibrillation and flutter, sinustachycardia and AV-nodal reentrant tachycardia. In two patients device discharges caused by a sensing malfunction ot the pulse generator was detected by the analysis of the stored electrogram. The new diagnostic feature of stored electrogram shows a high accuracy of rhythm classification and represents a major advance in the treatment with cardioverter/defibrillators.

Aged↗
PubMed1993

[Transvenous ablation of recurrent ventricular tachycardia in arrhythmogenic right ventricular dysplasia].

Catheter ablation was used to cure refractory ventricular tachycardias (VT) in a 20-years old lady with arrhythmogenic right ventricular dysplasia. Antiarrhythmic drugs (procainamide, amiodarone, gilurytmal, flecainide and beta-blockers) used in monotherapy or combination didn't prevent recurrence of sustained VT. During electrophysiological study 3 different morphologies of tachycardia were induced, indicating multiple sites of arrhythmia. One of them was typical for right ventricular outflow tract and similar to the VT recorded in clinical conditions. Endocardial mapping in that region showed pathological low amplitude, fragmented potentials. They preceded by 35 ms the onset of QRS complexes during VT. This area was suggested as a presumed origin of the VT and chosen for transvenous ablation. 11 direct current shock of 200-250 joules (total energy 2400 j) were delivered. No complications were seen during and after ablation. The procedure was terminated when only non sustained VT can be induced by programmed stimulation. The same results were obtained during the control study one month later. However, the patient was taking sotalol and mexiletine. During 6 months period of ambulatory observation the patient was doing well, free of arrhythmias.

Adult↗
PubMed1993

[Cardioverter-defibrillator implantations without thoracotomy: clinical experience with various electrode configurations and defibrillation wave forms of an endocardial/subcutaneous defibrillator system].

Twenty-seven consecutive patients with refractory ventricular arrhythmias were investigated for implantation of an nonthoracotomy cardioverter-defibrillator lead system. Supply with a nonthoracotomy lead system could be achieved in 25 of 27 patients (92.5%), while implantation proved impossible in two patients due to elevated defibrillation thresholds. After implantation of an endocardial defibrillation electrode no differences were found compared to the implantation of an endocardial defibrillation electrode with a subcutaneous chest wall defibrillation patch with regard to the defibrillation thresholds obtained for monophasic defibrillation waveform. Supply with an endocardial defibrillation lead system was successful in 18 of 25 patients (72%). Ten consecutive patients with implantation of an endocardial defibrillation lead system alone were compared for defibrillation efficacy following monophasic and biphasic defibrillation waveforms. Defibrillation with biphasic waveforms led to a decrease in the necessary defibrillation energy from 19 J (4.6 J) to 10 J (4.0 J). There was occurrence of refractory ventricular fibrillation that could not be controlled by endocardial and transthoracic defibrillation in two patients during the intraoperative testing of defibrillation thresholds. In both cases these arrhythmias could be terminated by the described method of endocardial/extrathoracic defibrillation (200 J). Further perioperative complications were not observed. Over a mean follow-up of 6.8 (1-17) months all patients demonstrated regular functioning of the cardioverter-defibrillator. Dislocation of defibrillation electrodes did not occur. Implantation of a cardioverter-defibrillator can be performed without thoracotomy in the majority of cases. The use of defibrillator systems with biphasic waveform widens the scope for implantation of nonthoracotomy defibrillating lead systems.

Adult↗
PubMed1991

Antiischemic and hemodynamic effects of an oral single dose of 150 mg of the phosphodiesterase inhibitor enoximone in patients with coronary artery disease--relation to plasma concentration.

The hemodynamic and antiischemic effects of a 150-mg single oral dose of the PDE inhibitor enoximone were correlated with the plasma levels of enoximone and its sulfoxide metabolite. Twenty-one patients with angiographically documented coronary artery disease were investigated by exercise testing 1 and 2 hours after drug administration. The control group consisted of 15 patients with proven coronary artery disease and stable reproducible angina pectoris on exercise. The enoximone group included 14 responders with therapeutic plasma concentrations 2 hours after drug intake and significantly reduced mean pulmonary artery pressures on exercise (from 42.4 +/- 8.6 to 30.9 +/- 11.2 mmHg, p less than 0.05). Compared to basal exercise values, responders showed a reduced ST-segment depression by 1 hour after drug intake (2.1 +/- 1.2 vs. 1.3 +/- 3 mm, p less than 0.05) and minimal values after 2 hours (0.9 +/- 1.0 mm, p less than 0.01) at comparable workloads. There were no significant changes in heart rate, blood pressure, cardiac output, and systemic vascular resistance. No significant improvement in the hemodynamic parameters and ST-segment depression was found in nonresponders with plasma concentrations below 100 ng/ml and 500 mg/ml for enoximone and its metabolite, respectively. In summary, oral administration of enoximone in patients with coronary artery disease led to favorable acute hemodynamic and antiischemic effects at sufficiently high plasma levels of enoximone and its sulfoxide metabolite.

Administration, Oral↗
PubMed1991

[Continuous enoximone infusion in patients with severe heart failure in dilated cardiomyopathy, hemodynamic, neurohumoral, chemical laboratory and clinical results].

UNLABELLED: The hemodynamic, clinical, and neurohumeral effects of a prolonged (6-days) intravenous enoximone-infusion therapy were evaluated in 12 patients suffering from severe cardiac failure due to dilated cardiomyopathy. The loading dose of enoximone was 1.5 mg/kg. The maintenance dose during the two phases of constant intravenous infusion were 4 and 8 mcg/kg/min, respectively. The enoximone infusion therapy produced sustained salutary effects on cardiac hemodynamics and on clinical status in every patient. The enoximone infusion therapy caused a decrease in mean pulmonary artery pressure by 38%, an increase in cardiac index by 60%, the pulmonary and systemic vascular resistance decreased by 61% and 37%, respectively. Side effects and therapy-related cardiac arrhythmias were not observed. CONCLUSION: Enoximone infusion therapy provides sustained salutary hemodynamic and clinical effects in patients with severe cardiac failure.

Aldosterone↗
PubMed1989

Hemodynamic, antiischemic, and neurohumoral effects of enoximone in patients with coronary artery disease.

To evaluate the risk of ischemia in 17 patients with significant coronary artery disease, the influence of enoximone was analyzed under the following conditions: (1) at rest (RC) and during exercise (ExC) under control conditions and (2) at rest (RE) and during exercise (ExE) after administration of enoximone (0.75 mg/kg, intravenously). During ExC all patients had ischemia (angina, and ST segment alterations); metabolic markers of ischemia (MMI) increased, as did the mean pulmonary artery pressure, from 19 to 41 mm Hg. However, during ExE ischemia was abolished (no angina, decrease in mean pulmonary artery pressure to 24 mm Hg, and improvement in MMI) and there was some improvement in left ventricular pump function, whereas pre- and afterload decreased (pulmonary artery pressure by 40%, systemic vascular resistance by 10%), and heart rate, arterial pressure, and myocardial oxygen consumption (MVO2) were all unchanged (p greater than 0.05). Comparative hemodynamics at RE vs RC showed a decrease in pulmonary artery pressure (by 25%) and pulmonary vascular resistance (by 19%) and an increase in heart rate (by 11%), whereas arterial pressure and MVO2 were unchanged (p greater than 0.05). Enoximone did not induce changes in plasma catecholamine, prostaglandin, or thromboxane levels (p greater than 0.05), whereas the atrial natriuretic factor decreased (by 15%), probably because of unloading of the atria during exercise. We concluded that enoximone induces beneficial hemodynamic effects in coronary artery disease without causing ischemia, probably by enhancing myocardial contractility, vasodilation, and improved diastolic properties.

Atrial Natriuretic Factor↗
PubMed1989

The influence of various degrees of cardiac failure, chronic medical treatment, and acute additional enoximone application on the parameters of the vasopressor system.

The characteristics of norepinephrine and epinephrine as well as plasma renin activity, angiotensin II, aldosterone, vasopressin, and atrial natriuretic factor (ANF) were examined in 64 patients (mean age of 52 +/- 16 years) with dilated cardiomyopathy. The findings were grouped according to the NYHA classification and compared with a normal cohort of 38 patients (mean age of 42 +/- 10 years). Furthermore, the influence of different cardioactive substances used in the treatment of cardiac failure was analyzed in more detail. Patients in NYHA class II already demonstrated an increased activity of the sympathicoadrenal, renin-angiotensin-aldosterone system (RAAS), vasopressin, and ANF system. The highest values were found in patients of NYHA class IV. In these patients, norepinephrine was enhanced by a factor of 7, epinephrine by a factor of 2, plasma renin activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 compared with those in normal subjects. The highest correlation coefficient was found for norepinephrine (r = 0.84). The acute application of 1-2 mg/kg of body weight of enoximone in patients with dilated cardiomyopathy (n = 15) resulted only in a significant lowering of the atrial natriuretic factor as an indicator for drug-induced unloading effects (venous pooling). All the parameters showed only a tendency; in none could statistical significance be established. Application of 0.75 mg/kg of body weight of enoximone i.v. in patients with coronary artery disease (n = 17) has no direct influence either on the sympathoadrenal, the ANF, or the prostaglandin systems. It could be demonstrated that the mode of medical treatment influences the parameters of vasoconstrictor systems in different ways.

Adult↗
PubMed1988

[Hemodynamic, anti-ischemic, metabolic and neurohumoral effects of enoximone (MDL 17,043) in patients with coronary disease].

The hemodynamic, anti-ischemic, metabolic, and neurohumoral effects of the phosphodiesterase inhibitor enoximone were investigated in 17 patients (mean age 58 +/- 2 years) with coronary heart disease as established by coronary angiography and positive exercise tests after i.v. application of 0.75 mg/kg body weight. Whereas administration of enoximone resulted in a significant increase in heart rate from 75 +/- 17 to 83 +/- 14 per minute (p less than 0.01), exercise heart rate, blood pressure and myocardial oxygen consumption did not change significantly (p greater than 0.05). At rest, enoximone led to a significant decrease of mean right atrial pressure from 5.7 +/- 2.3 to 3.8 +/- 1.2 mm Hg (p less than 0.01). During exercise there was a significant fall in pulmonary pressure (PAm from 40 +/- 7 to 24 +/- 7 mm Hg, p less than 0.001; PCm from 24 +/- 7 to 14 +/- 6 mm Hg, p less than 0.001) caused by preload reduction and concomitant inotropic increase; there was also a significant rise in cardiac output from 12.7 +/- 5 to 13.8 +/- 5 mm Hg (p less than 0.01) and a decrease of ST-segment depression from 1.97 +/- 0.76 to 0.53 +/- 0.51 mm (p less than 0.001). With improved peripheral and probably coronary blood flow, a concomitant decrease of the metabolic ischemic markers was detected during exercise (potassium 4.44 +/- 0.29 vs. 4.31 +/- 0.30 mval, p less than 0.05; lactate 19 +/- 9 vs. 18 +/- 7 mg/dl; pH 7.28 +/- 0.27 vs. 7.36 +/- 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

[Dipyridamole thallium-201 myocardial scintigraphy in coronary diagnosis; a comparison of methods with thallium-201 myocardial scintigraphy after ergometer stress].

Two scintigraphic methods, resting dipyridamole and exercise thallium-201 myocardial perfusion imaging, to detect and localize coronary artery stenosis were compared in 32 patients suffering from coronary artery disease. The sensitivity of detecting a greater than 50% coronary stenosis was 94% for exercise thallium-201 perfusion imaging and 88% for dipyridamole thallium-201 perfusion imaging. The overall sensitivity and specificity of localizing a greater than 50% coronary stenosis by the two methods were also not significantly different. The results of the two scintigraphic methods were independent of the severity of coronary artery disease. Dipyridamole thallium-201 myocardial perfusion imaging provides a useful and safe alternative test for detecting and localizing coronary artery stenosis in patients unable to perform maximal exercise.

Coronary Disease↗
PubMed1985

Lack of efficacy of high-dose intravenous immunoglobulin in autoimmune haemolytic anaemia: a clue to its mechanism.

5 patients with autoimmune haemolytic anaemia (AIHA) of warm type (4 idiopathic, 1 associated with systemic lupus erythematosus and thrombocytopenia) were treated with high doses of i.v. immunoglobulin (IgG; Sandoglobulin; 2.0 g/kg body weight). IgG therapy was ineffective in all 5 cases as indicated by a lack of clinical improvement, continuous signs of accelerated red blood cell (RBC) destruction, and an unchanged survival rate of 51Cr-labelled autologous RBC in 4 patients studied. IgG infused at equivalent doses into 5 healthy volunteers led to an increase of IgG coating of autologous RBC (irrespective of the ABO blood groups) without concomitant changes of haemoglobin, haematocrit or reticulocytes, increase of serum IgM in 3/5, a decrease of serum C4 in 5/5, and a decrease of serum haptoglobin in 2/5 individuals. We conclude that IgG at a dose of 2.0 g/kg body weight is ineffective in AIHA. This may be caused by an increased, though clinically inapparent, interaction of IgG-coated autologous RBC with the mononuclear phagocyte system.

ABO Blood-Group System↗
PubMed1985

Continuous subcutaneous insulin infusion therapy (CSII) influences cardiovascular responses to graded exercise in patients with autonomic diabetic neuropathy of the cardiovascular system (ADNCS).

We have demonstrated previously the effect of CSII on diabetics with ADNCS. In this study 16 Type-1-diabetics with ADNCS, 20 diabetics without ADNCS and 20 non diabetic controls were examined. Mean age and mean diabetes duration were similar in all groups. Graded exercise was performed in all patients using an ergometer cycle. In patients with ADNCS resting heart rate was significantly higher. The increase in heart rate during exercise was significantly lower, maximal tolerated work load was significantly reduced, and blood pressure-heart-rate multiplication as indirect measurement of oxygen uptake was significantly reduced too. The 16 diabetics with ADNCS were divided into 2 groups: 6 patients got CSII (12 months), 10 patients continued conventional s.c. therapy. After 6 and after 12 months graded exercise was performed again. The patients on s.c. therapy showed no improvement. 3 of the 6 CSII treated patients showed a significant improvement of the above mentioned parameters. Thus, in diabetics with ADNCS, CSII might not only influence the cardiovascular reflex tests, but might also have an effect on cardiovascular responses to graded exercise.

Autonomic Nervous System Diseases↗