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Biomedical subjects

J W Mason

Publications and source records attributed to J W Mason.

At least 19 recordsLinked to original sources
PubMed1995

A clinical trial of immunosuppressive therapy for myocarditis. The Myocarditis Treatment Trial Investigators.

BACKGROUND: Myocarditis is a serious disorder, and treatment options are limited. This trial was designed to determine whether immunosuppressive therapy improves left ventricular function in patients with myocarditis and to examine measures of the immune response as predictors of the severity and outcome of disease. METHODS: We randomly assigned 111 patients with a histopathological diagnosis of myocarditis and a left ventricular ejection fraction of less than 0.45 to receive conventional therapy alone or combined with a 24-week regimen of immunosuppressive therapy. Immunosuppressive therapy consisted of prednisone with either cyclosporine or azathioprine. The primary outcome measure was a change in the left ventricular ejection fraction at 28 weeks. RESULTS: In the group as a whole, the mean (+/- SE) left ventricular ejection fraction improved from 0.25 +/- 0.01 at base line to 0.34 +/- 0.02 at 28 weeks (P < 0.001). The mean change in the left ventricular ejection fraction at 28 weeks did not differ significantly between the group of patients who received immunosuppressive therapy (a gain of 0.10; 95 percent confidence interval, 0.07 to 0.12) and the control group (a gain of 0.07; 95 percent confidence interval, 0.03 to 0.12). A higher left ventricular ejection fraction at base line, less intensive conventional drug therapy at base line, and a shorter duration of disease, but not the treatment assignment, were positive independent predictors of the left ventricular ejection fraction at week 28. There was no significant difference in survival between the two groups (P = 0.96). The mortality rate for the entire group was 20 percent at 1 year and 56 percent at 4.3 years. Features suggesting an effective inflammatory response were associated with less severe initial disease. CONCLUSIONS: Our results do not support routine treatment of myocarditis with immunosuppressive drugs. Ventricular function improved regardless of whether patients received immunosuppressive therapy, but long-term mortality was high. Patients with a vigorous inflammatory response had less severe disease.

Adult↗
PubMed1995

Cost of initial therapy in the Electrophysiological Study Versus ECG Monitoring trial (ESVEM).

BACKGROUND: Patients randomized to either serial electrophysiological testing (EPS) or serial Holter monitoring (HM) to guide antiarrhythmic therapy for life-threatening ventricular arrhythmias had equivalent rates of mortality and arrhythmia recurrence in the ESVEM study. This report analyzes the effects of EPS, HM, and clinical factors on the charges for initial evaluation and management of patients with life-threatening ventricular arrhythmias. METHODS AND RESULTS: Ten of 14 clinical centers participating in ESVEM provided bills from the initial hospitalization for randomized patients. Predictors of charges (1991 dollars) were analyzed by linear regression after logarithmic transformation. Initial hospital charge data were obtained for 286 patients randomized in ESVEM (88% of patients eligible for this substudy, 59% of all ESVEM patients). Patients with charge data were somewhat more likely to be older, to be female, and to have failed previous antiarrhythmic drug therapy at study entry and were less likely to have a drug predicted effective after randomization. Mean overall hospital charges were $35,986 (SD, $32,628) with a median of $24,532 (interquartile range, $16,126 to $43,593). Prerandomization patient characteristics generally had insignificant effects on charges, with the exception of presentation with resuscitated sudden death (28% increase in charges, P = .01) and heart failure (26% increase in charges, P = .02). Patients randomized to EPS had higher mean charges for evaluation ($42,002 versus $29,970, P = .0015) as well as more drug trials (3.0 versus 2.1, P = .0001) and a longer hospital stay (19.6 versus 13.9 days, P = .0007). In a multivariate regression model, failure to find an effective drug (P = .0001), the number of drug trials (P = .0001), and resuscitated sudden death as the presenting arrhythmia (P = .0001) were the only independent predictors of higher initial charges. CONCLUSIONS: (1) Initial hospital charges are significantly higher for EPS-guided than HM-guided therapy. (2) The higher charges for EPS-guided therapy were due to a greater number of drug trials and a lower probability of finding an effective drug. (3) Failure to find an effective drug, a larger number of drug trials, and a history of resuscitated sudden death independently predict higher charges.

Aged↗
PubMed1995

Pharmacokinetics and regional electrophysiological effects of intracoronary amiodarone administration.

BACKGROUND: The reason for the delay in onset of the electrophysiological effects and antiarrhythmic efficacy of amiodarone is not clear. The relation between the development of the electrophysiological effects of amiodarone and its myocardial concentration is unknown. We therefore examined the time course of development of electrophysiological effects during intracoronary infusion of amiodarone and related these changes to myocardial concentrations. METHODS AND RESULTS: Amiodarone (0.139 mg/min) or normal saline was infused for 10 hours into the proximal left anterior descending coronary artery of 24 open-chest dogs. Nineteen animals received intracoronary amiodarone and 5 received normal saline (control group). Ten of the 19 that received amiodarone underwent electrophysiological study (amio-EPS group). Sixteen of the 19, including 7 from the amio-EPS group, underwent pharmacological study (PS group). In the amio-EPS group during pacing at a cycle length of 300 ms, changes in conduction velocities in drug-exposed myocardium referenced to nonexposed myocardium at 1 hour of infusion were -3.7% in the longitudinal direction (P = NS) and -7.2% in the transverse direction (P < .05); at 3 hours, -12.9% (P < .05) and -9.1% (P < .05); and at 9 hours, -32.9% (P < .02) and -31.7% (P < .01). These changes were dependent on amiodarone concentration (R2 = .83). There was also an obvious rate-dependent effect that was more pronounced for transverse conduction velocities. This effect was also dependent on amiodarone concentration. In the PS group, amiodarone levels in the drug-exposed myocardium increased from a mean of 5.95 microgram/g at 15 minutes of infusion to 188.88 microgram/g at the 10th hour. This increase was time dependent (R2 = .91). In the nonexposed myocardium, amiodarone levels were always low and increased minimally over time from a mean of 2.68 to 14.45 microgram/g. This increase was also time dependent (R2 = .97). CONCLUSIONS: Selective intracoronary amiodarone infusion resulted in selective drug accumulation and concomitant time-dependent reduction of myocardial conduction velocity. There was a significant correlation between the extent of reduction of conduction velocity and myocardial amiodarone concentration but not coronary arterial or systemic concentration. Repolarization was not significantly altered.

Amiodarone↗
PubMed1995

Low urinary cortisol excretion in Holocaust survivors with posttraumatic stress disorder.

OBJECTIVE: The authors' objective was to compare the urinary cortisol excretion of Holocaust survivors with posttraumatic stress disorder (PTSD) (N = 22) to that of Holocaust survivors without PTSD (N = 25) and comparison subjects not exposed to the Holocaust (N = 15). METHOD: Twenty-four-hour urine samples were collected, and the following day, subjects were evaluated for the presence and severity of past and current PTSD and other psychiatric conditions. RESULTS: Holocaust survivors with PTSD showed significantly lower mean 24-hour urinary cortisol excretion than the two groups of subjects without PTSD. Multiple correlation analysis revealed a significant relationship between cortisol levels and severity of PTSD that was due to a substantial association with scores on the avoidance subscale. CONCLUSIONS: The present findings replicate the authors' previous observation of low urinary cortisol excretion in combat veterans with PTSD and extend these findings to a non-treatment-seeking civilian group. The results also demonstrate that low cortisol levels are associated with PTSD symptoms of a clinically significant nature, rather than occurring as a result of exposure to trauma per se, and that low cortisol levels may persist for decades following exposure to trauma among individuals with chronic PTSD.

Age Factors↗
PubMed1994

Predicting antiarrhythmic drug efficacy.

For years, electrophysiologic testing was regarded as the best way to select effective pharmacologic therapy. But now it appears that Holter monitoring is just as accurate--as well as simpler, safer, and cheaper. Nevertheless, most patients eventually will need an electrophysiologic study because of the high rate of arrhythmia recurrence.

Anti-Arrhythmia Agents↗
PubMed1992

Comparison of ST depression recorded by Holter monitors and 12-lead ECGs during coronary angiography and exercise testing.

Data from previous studies are debatable regarding whether Holter monitors are a reliable electrocardiographic indicator of ischemia, for which the 12-lead electrocardiogram (ECG) is the standard. Simultaneous 12-lead and Holter ECGs were performed on 30 patients with typical angina pectoris during coronary angiography or exercise testing. ST depression recorded by both methods was directly compared, using the 12-lead ECG as the reference. The Holter tapes were also scanned by two automated ST analysis programs and the results were compared to 12-lead ECGs. Only 66 of the 178 12-lead ECG ST depression events were also present on the Holter recordings (37.1% Holter sensitivity). ST depression was underestimated by the Holter recordings compared to the 12-lead ECGs (p < 0.0001). The majority (67.0%) of ST depression events identified by one computer program were false positive events. The degree of ST depression was overestimated compared to 12-lead ECGs by the second program (p = 0.0033). Holter-detected ST depression may not be a reliable ECG indicator of myocardial ischemia.

Adult↗
PubMed1992

Urinary catecholamine excretion and severity of PTSD symptoms in Vietnam combat veterans.

In the present study, we replicated and extended our previous findings of increased 24-hour urinary catecholamine excretion in posttraumatic stress disorder (PTSD). Dopamine, norepinephrine, and epinephrine concentrations were measured in 22 male patients with PTSD (14 inpatients and eight outpatients) and in 16 nonpsychiatric normal males. The PTSD inpatients showed significantly higher excretion of all three catecholamines compared with both outpatients with PTSD and normal controls. Dopamine and norepinephrine, but not epinephrine, levels were significantly correlated with severity of PTSD symptoms in the PTSD group as a whole. In particular, these catecholamines seemed related to intrusive symptoms. None of the catecholamines were correlated with severity of depression. The findings support the hypothesis of an enhanced sympathetic nervous system activation in PTSD, and suggest that increased sympathetic arousal may be closely linked to severity of certain PTSD symptom clusters.

Ambulatory Care↗
PubMed1991

Hypothalamic-pituitary-adrenal dysfunction in posttraumatic stress disorder.

Neuroendocrine studies examining the hypothalamic-pituitary-adrenal (HPA) axis under baseline conditions and in response to neuroendocrine challenges have supported the hypothesis of altered HPA functioning in posttraumatic stress disorder (PTSD). However, to date, there is much debate concerning the nature of HPA changes in PTSD. Furthermore, in studies showing parallel findings in PTSD and major depressive disorder there is controversy regarding whether the HPA alterations suggest a specific pathophysiology of PTSD, or, rather, reflect comorbid major depressive disorder. This review summarizes findings of HPA axis dysfunction in both PTSD and major depressive disorder, and shows distinct patterns of HPA changes, which are probably due to different mechanisms of action for cortisol and its regulatory factors.

Adrenocorticotropic Hormone↗
PubMed1991

Multidimensional hormonal discrimination of paranoid schizophrenic from bipolar manic patients.

The search for biological markers of psychiatric disorders has traditionally involved univariate approaches, usually focusing upon one measure at a time, and to date has been primarily directed towards the assessment of depressive rather than psychotic illnesses. The present study explores a multidimensional psychoendocrine strategy, using a profile of five hormones, including cortisol, epinephrine, norepinephrine, testosterone, and free thyroxine, and is directed at the differentiation of two major psychotic illnesses, bipolar manic disorder and paranoid schizophrenia. When the levels of these hormones were assessed at admission and biweekly during hospitalization, the mean values for all five hormones were found to differ markedly between the two diagnostic groups. There was, however, always a zone of overlap in levels between the two groups when each of the five hormones were viewed individually, so that at best only about 70% of patients were correctly separated by diagnostic group using any single hormone alone. By contrast, multivariate approaches combining mean values of three or more hormones, using either stepwise discriminant analysis or multidimensional scaling, yielded 95% correct classification of the two diagnostic groups. Similar but not quite as great accuracy of classification was achieved with only the initial hormone sample obtained at the time of hospital admission. These preliminary findings provide encouragement for further exploration of multidimensional hormonal strategies in the search for useful biological criteria to assist in the diagnosis of psychiatric disorders.

Adult↗
PubMed1991

Spontaneous variability of ventricular arrhythmias in patients with chronic heart failure.

Spontaneous variability of ventricular arrhythmia in patients with chronic heart failure is not well described. We measured this variability in 23 consecutive patients with chronic heart failure who were prospectively enrolled in the placebo limb of a trial concerned with treatment of heart failure. Patients underwent from one to three periods of ambulatory monitoring separated by 1 to 3 months while they were not receiving antiarrhythmic drug treatment. The variability in frequency of premature ventricular complexes (PVCs) was determined at interrecording intervals of 1, 2, and 3 months. The percentage reductions in total PVCs required to exceed the 95% confidence limits of spontaneous variability at these intervals were 91%, 90%, and 97%, respectively. Corresponding values for repetitive beats (beats in couplets and beats in ventricular tachycardia events) were 98%, 80%, and 97% and for ventricular tachycardia events 98%, 83%, and 98%, respectively. The percentage increases in total PVCs, repetitive beats, and ventricular tachycardia events required to identify aggravation of arrhythmia in this study population were 1301%, 4050%, and 6147%, respectively, at 1-month intervals and 2950%, 2868%, and 5938%, respectively, at 3-month intervals. The percentage reductions required to show a true drug effect at 2- and 3-month intervals were 63% and 84% for patients with an ejection fraction less than 0.22 and 89% and 98% for those with an ejection fraction greater than or equal to 0.22 (p less than 0.05 for both). Ventricular arrhythmia would have been missed in 6 (26%) of the 23 patients if only one screening ambulatory recording was available. Thus marked variability in PVCs occurs in patients with chronic heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Low urinary cortisol excretion in patients with posttraumatic stress disorder.

In the present study, we replicated and extended our previous findings of low urinary free-cortisol levels in PTSD. Cortisol was measured in 16 male patients (nine inpatients, seven outpatients) with posttraumatic stress disorder (PTSD) and in 16 nonpsychiatric control subjects. The mean cortisol level in the PTSD group was significantly lower, and the range narrower, than that observed in control subjects. Low cortisol in PTSD did not seem to be related to the presence or absence of major depressive disorder or to overall psychiatric symptomatology as assessed by the sum Brief Psychiatric Rating Scale score. In the outpatient group, there was a relationship between PTSD symptomatology and cortisol levels. The findings suggests a physiological adaptation of the hypothalamic-pituitary-adrenal axis to chronic stress.

Adult↗
PubMed1989

Possible subtypes of affective disorder suggested by differences in cerebral laterality and testosterone. A preliminary report.

Two language-related dichotic listening tests of cerebral laterality were used to divide a group of 18 hospitalized patients with affective disorder into two subgroups of nine. The groups proved to differ in serum testosterone levels at the time of admission and in mean serum testosterone levels throughout hospitalization. Moreover, there was a positive correlation between testosterone level and symptom severity in one of the laterality-defined subgroups and a negative correlation in the other. These data (1) provide new evidence of pathophysiological heterogeneity within a single general diagnostic group; (2) suggest that noninvasive, inexpensive, and easily administered dichotic listening tests may be able to define pathophysiologically meaningful subgroups; and (3) suggest a role for testosterone-related alterations in left hemisphere function in the pathogeneses of some affective disorders.

Adult↗