Management of Spinal Cord Stimulators in Patients with Cardiac Pacemakers

We report a case of spinal cord stimulation (neurostimulation) as treatment for angina pectoris pain in a patient with a demand pacemaker. The precautions to avoid inhibition of the demand pacemaker by the neurostimulator are discussed.     

Regional and systemic effects of short-term intense muscular work on plasma concentration and content of total and ionized calcium

Isokinetic work with one leg was carried out with maximal force for 2 min by five healthy subjects. The concentrations of plasma total calcium and of ionized calcium in the effluent from the leg increased by a mean of 13.6 +/- 1.8% (SD) and 16.2 +/- 2.0%, respectively. The corresponding rises in the resting arm were 7.7 +/- 4.3% and 8.1 +/- 3.0%. There was a close correlation (r = 0.86; P less than 0.001) between the degree of exercise-induced acidosis and the rise in plasma ionized calcium. However, the calcium values normalized both in the leg and in the arm within 5 min after the exercise and were similar at the two measuring sites despite a lower pH in the leg sample. During work there was a reduction of the plasma volume of 11.2 +/- 6.0% in the regional (femoral) and 12.4 +/- 4.2% in the systemic (antecubital) sample (P less than 0.001 compared to baseline values for both measurements). When adjustments were made for the reduction in plasma volume as well as for acidosis it was evident that, despite the apparent increases in the calcium concentrations, there was a net reduction of the plasma ionized calcium content (the total amount of plasma ionized calcium). This decrease was significantly (P less than 0.05) more pronounced in the exercising leg than in the systemic circulation but the difference could largely be explained by higher calcium-lactate complex formation in the leg.     

The Paclitaxel‐Eluting Coroflex™ Stent Study II (PECOPS II) Acute and 6‐Month Clinical and Angiographic Follow‐Up, 1‐Year Clinical Follow‐Up

Background and Objectives: Paclitaxel‐coated stents have proven their efficacy for reducing restenosis in de novo coronary artery lesions and in‐stent restenoses with superiority compared to bare metal stents. This study was performed to evaluate the procedural and 1 year results of the Paclitaxel‐eluting Coroflex? Please stent in coronary artery lesions. Methods: One‐hundred and twenty‐nine patients (66.2 ± 8.2 years, 31.0% diabetics, 20.2% unstable angina, 41.8% multivessel disease) were enrolled per protocol for elective single stent deployment into native de novo or post‐PTCA restenotic coronary lesions.The mean reference diameter was 2.84 ± 0.43 mm, the lesion length 12.51 ± 4.6 mm, and the minimal lumen diameter 0.75 ± 0.29 mm. Follow‐up was performed clinically in 129/129 (100%) after 6 and 12 months and angiographically in 120/129 (93%) patients after 6 months. Results: The success rates of the procedure and deployment were 100% and 95.3%, respectively. The in‐stent late loss and the late‐loss index were 0.27 ± 0.59 mm and 0.17 ± 0.40 resulting in binary in‐stent restenoses in 16/120 (13.3%) subjects and in‐segment restenoses in 20/120 (16.7%) subjects. Major adverse cardiac events occurred in 23/129 (17.8%) during the first 6 months of follow‐up with 3/129 (2.3%) myocardial infarctions, 1/129 (0.8%) secondary to stent thrombosis. From 6 to 12 months, 2/129 (1.6%) nonlesion related PCI were performed. Conclusion: The data of the Paclitaxel‐eluting Coroflex? Please stent evaluated in PECOPS II are within the range of the other currently available Paclitaxel‐eluting stent. (J Interven Cardiol 2010;23:160‐166)     

DIURNAL VARIATIONS IN PLASMA PROLACTIN, GROWTH HORMONE, CORTISOL AND BLOOD GLUCOSE IN LABILE DIABETES MELLITUS

In labile diabetes mellitus wihout ketoacidosis we have studied plasma prolactin levels and a possible causal connection between fluctuation in blood glucose concentration and plasma prolactin, growth hormone and cortisol levels. The hormone concentrations in plasma and blood glucose concentration were determined at 20 min intervals for a 24 h period in six male patients with insulin treated diabetes mellitus. Prolactin varied within the normal range but without any significant rise in relation to sleep in five out of the six patients. Growth hormone levels were low with superimposed secretory peaks. Plasma cortisol showed a normal diurnal rhythm. Blood glucose fluctuated as expected, but the variations and especially the falls in blood glucose to non-hypoglycaemic levels were not followed by increases in plasma hormone concentrations. No relationship could be demonstrated between the changes in the plasma concentration of prolactin, growth hormone and cortisol.     

Effect of vein pump activation upon muscle blood flow and venous pressure in the human leg

The effect of vein pump activation upon superficial venous pressure and blood flow in human skeletal muscle tissue was studied in 7 healthy subjects. Blood flow was measured in the anterior tibia muscle by the local ¹³³Xe washout technique. The subjects were placed on a steeply tilted couch in nearly erect position. The vein pump in gastroenemius-soleus muscles was activated by heel-raisings. and the anterior tibial muscle remained relaxed during this procedure. Blood flow in the resting anterior tibial muscle was constant before, during and after 20 heel-raisings per min. A more heavy exercise with 40 heel-raisings per min increased blood flow about 100%. This increase in blood flow was absent during venous stasis (40 mmHg), and in areas infiltrated with lidocaine. It is concluded, that intense dynamic exercise in gastrocnemius-soleus muscles, in erect humans, increased blood flow considerably in another crural muscle remaining in the resting state. The present study strongly suggests, that the observed increase in blood flow, was associated with a decrease in regional subfascial venous pressure to below the threshold level of the local sympathetic veno-arteriolar reflex.     

Transport of glucose across the blood-brain barrier: Reevaluation of the accelerative exchange diffusion

In an earlier study of glucose transport across the blood-brain barrier it was concluded that the kinetic transport constants increase as the brain glucose concentration increases, a finding that was attributed to accelerative exchange diffusion (Betz et al. 1975). The conclusion, however, relied upon application of a commonly used simplified treatment of tracer extraction data. In this study it is demonstrated that the simplified treatment is applicable only in the case of zero brain glucose concentration, and a more general model for determination of the kinetic constants is developed. Re-analysis by this model of the data of Betz et al. (1975)—comprising a range of brain glucose concentrations—gave kinetic constants which did not vary significantly over a wide range of brain glucose concentrations. For brain glucose concentrations up to about 12 mmol l^-1, the kinetic constants obtained for glucose transport across the blood-brain barrier are Km =6.18±0.38mmol l^-1 V_max= 1.65±0.06 μmol g-¹ min^-1     

Posture-Dependent Chronotropic Effect of Carotid Sinus Massage

The hypertensive carotid sinus can be divided into cardioinhibitory (chronotropic) and vasodepressor components; the former can be evaluated by carotid sinus massage performed in the supine position. We present the case of a patient in whom the abnormal cardioinhibitory response could only be demonstrated while in the sitting position.     

QUANTITATION OF THE ACCELERATING EFFECT OF METYRAPONE ON CORTISOL METABOLISM

Quantitation of the accelerating effect of metyrapone on cortisol metabolism has been made by determination of the metabolic clearance rate (MCR) of exogenous cortisol during a metyrapone load. Six adrenalectomized patients were studied. The slope of cortisol concentrations in plasma was determined after intravenous administration of 0.3 mg cortisol/kg b. w. with or without metyrapone 17.5 mg/kg b. w./h. In all six patients studied, the MCR of cortisol increased during metyrapone load from an average of 12.3 ± 5.0 (SD) 1/h to 29.6 ± 15.7 (SD) 1/h or corrected for body weight 3.0 ± 1.1 (SD) ml/kg b.w./min to 7.1 ± 2.5 (SD) ml/kg b.w./min The discrepancy discovered in clinical practice between the relatively small rise in plasma total corticosteroid concentration and the greater increase in urinary excretion of corticosteroid metabolites during the metyrapone test may be explained by the findings in this study.