Lack of effectiveness of magnesium in chronic stable asthma. A prospective, randomized, double-blind, placebo-controlled, crossover trial in normal subjects and in patients with chronic stable asthma.

BACKGROUND: Magnesium sulfate has been helpful in the treatment of acute exacerbations of asthma. We hypothesized that magnesium would also be an effective bronchodilator in patients with chronic stable asthma. METHODS: We performed a prospective, randomized, double-blind, placebo-controlled, crossover trial in 15 patients with chronic, stable asthma and 10 nonasthmatics. On study day 1, spirometry and albuterol challenge were used to confirm the presence of asthma according to American Thoracic Society criteria. On study day 2, subjects received intravenous magnesium sulfate (2 g) or placebo (saline). On study day 3, subjects were crossed over to receive the other drug. Spirometry was performed before, during, and after drug or placebo administration. Circulating ionized magnesium concentrations were determined before and after intravenous magnesium or placebo administration. RESULTS: Magnesium infusion caused no statistically significant changes in forced expiratory volume in 1 second (mean +/- SEM, 1.92 +/- 0.13 L before, 1.98 +/- 0.12 L during, and 2.01 +/- 0.14 L after magnesium administration), forced vital capacity (mean +/- SEM, 3.44 +/- 0.25 L before, 3.60 +/- 0.26 L during, and 3.59 +/- 0.25 L after magnesium administration), or maximum forced expiratory flow rate (mean +/- SEM, 5.42 +/- 0.44 L/second before, 5.46 +/- 0.46 L/second during, and 5.57 +/- 0.49 L/second after magnesium administration). Placebo caused no changes in these three physiologic variables. CONCLUSION: Magnesium is not effective as a bronchodilator in chronic, stable asthmatics or in normal non-asthmatic adults.

Cardiac tamponade--an unusual presentation of lymphoma.

A rare instance of lymphoma in an adult presenting as cardiac tamponade is presented. Relevant literature is briefly reviewed.

Fibrosing mediastinitis--a rare cause of superior vena caval obstruction.

A rare case of fibrosing mediastinitis, possibly of tuberculous etiology, causing superior vena caval obstruction is presented. The diagnosis was based on clinical features of superior vena caval obstruction, chest radiography, phlebography and mediastinal calcification in absence of definite mass lesion on CT-scan of thorax. The disease followed a relatively benign non-progressive course over next nineteen months of follow-up.

Clinical, haemodynamic and echocardiographic study in chronic cor pulmonale.

Thirty patients of chronic cor pulmonale were studied clinically and by chest skiagram, electrocardiography, echocardiography, pulmonary function tests, arterial blood gas analysis and, wherever possible by right heart catheterization. Pulmonary arterial pressures (PAP) correlated significantly only with cardiomegaly on skiagram and with arterial oxygen tension (PaO2). There was no significant correlation between mean PA pressures and prominent pulmonary conus on RVH by ECG, FEV1, PaCO2 or right ventricular outflow tract dimensions by echocardiography. Left ventricular function, as assessed by pulmonary capillary wedge pressure on cardiac catheterization, by LV ejection fraction and fractional shortening on echocardiography was normal in all cases except two (6.67%). There was significant increase in left ventricular posterior wall thickness in the patients studied.

Sudden bradyarrhythmic death in patients with the implantable cardioverter-defibrillator: report of two cases.

Two cases of sudden bradyarrhythmic death necessitating cardiopulmonary resuscitation in patients with the automatic implantable cardioverter-defibrillator are described. One patient had sudden bradyarrhythmic death while being monitored in the hospital. This patient could not be resuscitated and represents the first reported sudden cardiac death secondary to bradyarrhythmia in a patient with the automatic implantable cardioverter-defibrillator. The second patient had an out-of-hospital sudden death followed by probable cardioverter-defibrillator discharge, leading to complete heart block with escape ventricular rhythm necessitating immediate temporary pacemaker insertion. These cases highlight the need for bradycardia back-up pacing and event monitoring in the newer tachyarrhythmia management devices.

Ventricular pacing threshold and time to capture postdefibrillation in patients undergoing implantable cardioverter-defibrillator implantation.

To assess the effect of defibrillation and amiodarone on ventricular pacing threshold and time to capture in patients undergoing automatic implantable cardioverter-defibrillator (AICD) implantation, 28 patients were prospectively evaluated. The patients were entered into one of two protocols: Ia--epicardial ventricular pacing threshold measured at baseline (preventricular fibrillation induction) and 10 and 60 seconds postdefibrillation with 20 J, or Ib--two fibrillation-defibrillation sequences were performed 3 minutes apart and ventricular pacing thresholds were measured for each sequence at baseline and at 10 and 60 seconds postdefibrillation with 20 J. Ten patients also underwent asynchronous pacing at 1.1 times baseline threshold during ventricular fibrillation with measurement of time to capture postdefibrillation. All patients were randomly assigned to receive either amiodarone or no antiarrhythmic drug therapy. Ventricular fibrillation was induced with AC (applied for 1-2 seconds), and standard epicardial bipolar and epicardial patch electrodes of the AICD were used for pacing and defibrillation, respectively. Ventricular pacing threshold at baseline, 10 seconds, 60 seconds, and 3 minutes postdefibrillation did not differ significantly. There were no significant differences in patients with or without amiodarone therapy. Furthermore, there was no transient loss of ventricular capture postdefibrillation or significant difference in time to capture with amiodarone (less than or equal to 2 seconds). We conclude that following internal defibrillation with 20 J: (1) ventricular pacing threshold at 10 seconds, 60 seconds, and 3 minutes were not significantly different from baseline with one or two fibrillation-defibrillation sequences, (2) time to capture was short, and (3) there was no significant difference in no drug versus amiodarone. These findings have direct clinical importance in considering device therapy with both pacing and defibrillating capabilities.

The use and clinical importance of a substrate-specific electrode for rapid determination of blood lactate concentrations.

OBJECTIVE: To determine the validity and clinical importance of a newly developed amperometric, enzymatic, substrate-specific electrode for the rapid measurement of circulating lactate concentrations. DESIGN: A prospective multiexperiment study. SETTING: The critical care medicine research laboratory, intensive care unit (ICU), emergency department (ED), and general wards of a university-affiliated hospital. PATIENTS: A total of 1218 patients and control subjects were studied on one or more occasions. INTERVENTIONS: Blood lactate concentrations, descriptive data, physiological parameters, and outcome results were determined in various patient populations. MAIN OUTCOME MEASURES AND RESULTS: Experiment 1: Lactate determinations performed with the new substrate-specific electrode were compared with two laboratory reference methods. Blood samples from 80 ICU patients and 165 ED patients formed the basis of this first experiment. There was excellent agreement between the test instrument and the two reference methods as reflected by bias (with reference method 1, 0.19 mmol/L; reference method 2, 0.09 mmol/L), precision (with reference method 1, +/- 0.47 mmol/L; reference method 2, +/- 0.34 mmol/L), and correlation data (with reference method 1, r = .92; reference method 2, r = .98). Experiment 2: The new test microchemistry instrument was used to analyze blood samples from 927 patients. The mean (SE) blood lactate concentrations in the various patient populations were 1.26 (0.04) mmol/L for control subjects (n = 85), 1.52 (0.03) mmol/L for general ward patients (n = 489; P < .001 vs normal subjects), 2.34 (0.15) mmol/L for ICU patients (n = 180; P < .001 vs normal subjects and general ward patients), and 2.44 (0.15) mmol/L for ED patients (n = 173; P < .001 vs normal subjects and general ward patients). None of the normal subjects and only one (0.2%) of 489 nonhypotensive general ward patients had a blood lactate value greater than 4 mmol/L. Circulating lactate concentrations greater than 4 mmol/L were 98.2% specific in predicting the need for hospital admission in patients presenting to the ED. Furthermore, lactate concentrations greater than 4 mmol/L were 96% specific in predicting mortality in hospitalized nonhypotensive patients. Experiment 3: Blood samples from 46 hypotensive ICU and ED patients and from 353 nonhypotensive ICU and ED patients (the latter samples were derived from experiment 2) were analyzed. A statistically significant difference was noted between the mean (SE) lactate concentration in hypotensive patients in the ICU and ED (4.75 [0.75] mmol/L) when compared with nonhypotensive ICU and ED patients (2.28 [0.10] mmol/L; P < .001). Furthermore, blood lactate values greater than 4 mmol/L were 87.5% specific in predicting mortality in hypotensive patients. CONCLUSIONS: Lactate determinations performed using the new test instrument are precise and accurate. Blood lactate concentrations greater than 4 mmol/L are unusual in normal and noncritically ill hospitalized patients and warrant concern. In hospitalized (non-ICU) nonhypotensive subjects, as well as in critically ill patients, a blood lactate concentration greater than 4 mmol/L may portend a poor prognosis.

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success.

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.