Preventing progression to first-episode psychosis in early initial prodromal states.

BACKGROUND: Young people with self-experienced cognitive thought and perception deficits (basic symptoms) may present with an early initial prodromal state (EIPS) of psychosis in which most of the disability and neurobiological deficits of schizophrenia have not yet occurred. AIMS: To investigate the effects of an integrated psychological intervention (IPI), combining individual cognitive-behavioural therapy, group skills training, cognitive remediation and multifamily psychoeducation, on the prevention of psychosis in the EIPS. METHOD: A randomised controlled, multicentre, parallel group trial of 12 months of IPI v. supportive counselling (trial registration number: NCT00204087). Primary outcome was progression to psychosis at 12- and 24-month follow-up. RESULTS: A total of 128 help-seeking out-patients in an EIPS were randomised. Integrated psychological intervention was superior to supportive counselling in preventing progression to psychosis at 12-month follow-up (3.2% v. 16.9%; P = 0.008) and at 24-month follow-up (6.3% v. 20.0%; P = 0.019). CONCLUSIONS: Integrated psychological intervention appears effective in delaying the onset of psychosis over a 24-month time period in people in an EIPS.

Treatment with humanized monoclonal antibody against CD154 prevents acute renal allograft rejection in nonhuman primates.

CD154 is the ligand for the receptor CD40. This ligand-receptor pair mediates endothelial and antigen-presenting cell activation, and facilitates the interaction of these cells with T cells and platelets. We demonstrate here that administration of a CD154-specific monoclonal antibody (hu5C8) allows for renal allotransplantation in outbred, MHC-mismatched rhesus monkeys without acute rejection. The effect persisted for more than 10 months after therapy termination, and no additional drug was required to achieve extended graft survival. Indeed, the use of tacrolimus or chronic steroids seemed to antagonize the anti-rejection effect. Monkeys treated with antibody against CD154 remained healthy during and after therapy. The mechanism of action does not require global depletion of T or B cells. Long-term survivors lost their mixed lymphocyte reactivity in a donor-specific manner, but still formed donor-specific antibody and generated T cells that infiltrated the grafted organ without any obvious effect on graft function. Thus, therapy with antibody against CD154 is a promising agent for clinical use in human allotransplantation.

Reduced subjective quality of life in persons at risk for psychosis.

OBJECTIVE: Subjective quality of life (sQoL) and potentially contributing factors were investigated in individuals putatively in an early (EIPS) or late initial prodromal state (LIPS) and healthy controls (HC). METHOD: Participants comprised 58 EIPS individuals, 157 LIPS individuals and 87 HC individuals. sQoL was assessed together with locus of control (LoC), coping, demography and psychopathology. RESULTS: Putatively prodromal groups exhibited markedly lower sQoL than HC (all domains P < 0.00001). EIPS and LIPS individuals did not differ significantly. Depression was the most consistent explaining variable of sQoL in EIPS and LIPS individuals. In EIPS individuals, LoC emerged as an additional predictor. CONCLUSION: Individuals at risk for psychosis experienced a marked impairment of sQoL across all domains. This was evident even in the early state, showed no significant further deterioration during the late state and was predominantly explained by non-specific symptoms.

Interactions between digoxin and potassium-sparing diuretics.

A kinetic and hemodynamic study of digoxin was performed in six healthy subjects and similar studies were performed during digoxin with spironolactone and with triamterene. Spironolactone reduced renal tubular secretion of digoxin and attenuated its positive inotropic effect (evaluated by systolic time intervals and echocardiography) and triamterene reduced the extrarenal elimination of digoxin, but induced no changes in digoxin-elicited inotrophy. It is suggested that the renal handling of digoxin is influenced by the intracellular potassium concentration in the renal tubular cell. The results indicate a drug-receptor interaction between spironolactone metabolites and digoxin at the hypothetical inotropic digitalis receptor. Amiloride has been reported to suppress digoxin inotropism, whereas spironolactone induces minor inhibition and triamterene does not affect digoxin inotropism.

Treatment with the humanized CD154-specific monoclonal antibody, hu5C8, prevents acute rejection of primary skin allografts in nonhuman primates.

BACKGROUND: Allogeneic skin transplantation remains a rigorous test of any immune intervention designed to prevent allograft rejection. To date, no single, clinically available immunosuppressant has been reported to induce long-term primary skin allograft survival in primates. We have previously shown that treatment with the humanized CD154-specific monoclonal antibody, humanized 5C8 (hu5C8), induces long-term renal allograft survival in nonhuman primates. In this study, we evaluated the efficacy of hu5C8 in preventing primary skin allograft rejection in rhesus monkeys. METHODS: Ten rhesus monkeys were transplanted with full-thickness skin allografts mismatched at both class I and class II major histocompatibility loci. Of these, two were given no treatment, five were treated with hu5C8 alone, and three received hu5C8 combined with whole blood donor-specific transfusion (DST). All recipients also received skin autografts for comparison. Animals were followed by inspection, serial biopsy, mixed lymphocyte culture, and alloantibody determination. RESULTS: Treatment with hu5C8 alone or hu5C8 plus DST greatly prolonged allograft survival. Rejection occurred in the untreated group within 7 days. Mean allograft survival in the monotherapy hu5C8 group was >236 days and in the DST group was >202 days; these differences were not significant. Rejection eventually occurred in most animals. Allograft survival was not correlated with the development of T cell hyporesponsiveness in mixed lymphocyte culture. Rejection was not predicted by the development of donor-specific alloantibody. CONCLUSION: These results show that treatment with the CD154-specific monoclonal antibody, hu5C8, greatly delays the onset of acute skin allograft rejection.

Induction therapy with monoclonal antibodies specific for CD80 and CD86 delays the onset of acute renal allograft rejection in non-human primates.

CD80 and CD86 (also known as B7-1 and B7-2, respectively) are both ligands for the T cell costimulatory receptors CD28 and CD152. Both CD80 and CD86 mediate T cell costimulation, and as such, have been studied for their role in promoting allograft rejection. In this study we demonstrate that administering monoclonal antibodies specific for these B7 ligands can delay the onset of acute renal allograft rejection in rhesus monkeys. The most durable effect results from simultaneous administration of both anti-B7 antibodies. The mechanism of action does not involve global depletion of T or B cells. Despite in vitro and in vivo evidence demonstrating the effectiveness of the anti-B7 antibodies in suppressing T cell responsiveness to alloantigen, their use does not result in durable tolerance. Prolonged therapy with murine anti-B7 antibodies is limited by the development of neutralizing antibodies, but that problem was avoided when humanized anti-B7 reagents are used. Most animals develop rejection and an alloantibody response although still on antibody therapy and before the development of a neutralizing antibody response. Anti-B7 antibody therapy may have use as an adjunctive agent for clinical allotransplantation, but using the dosing regimens we used, is not a tolerizing therapy in this non-human primate model.

Early estimation of risk by echocardiographic determination of wall motion index in an unselected population with acute myocardial infarction.

In a prospective series of 201 consecutive patients with creatine kinase-MB--documented acute myocardial infarction (AMI), postadmittance and predischarge echocardiographic wall motion indexes (WMI) were determined (median 45 hours vs 14 days after AMI). No significant change of left ventricular systolic performance was found between postadmittance and predischarge examinations in 179 survivors (WMI 1.3 +/- 0.4 vs 1.4 +/- 0.4, p greater than 0.05). Hospital mortality was 11% (22 of 201), cumulated 2-month mortality 15% (31 of 201) and cumulated 1-year mortality 26% (52 of 201). Mortality increased rapidly with decreasing left ventricular function as determined by WMI. When early WMI was less than 1.0, 1-year mortality was 51% (28 of 55) versus 8% (7 of 83) when WMI was greater than 1.3 (p less than 0.0001). Ventricular fibrillation (n = 24) and cardiogenic shock (n = 27) carried a much better prognosis when WMI showed good left ventricular function. When WMI was less than 1.0, 1-year mortality was 83% (10 of 12) versus 93% (13 of 14) in ventricular fibrillation and cardiogenic shock, respectively, whereas it was 0% (0 of 4) versus 33% (2 of 6) when WMI was greater than 1.3. In 15% of patients major discrepancies between early Killip class and WMI were noted. WMI showed much smaller fluctuations during the hospital course of AMI than did Killip class and appeared to be a more stable prognostic marker. Large-scale, early risk stratification by echocardiography has now become available and appears to facilitate a rational, individualized discharge policy in the coronary care unit and to provide an improved basis for randomization of patients in controlled studies aimed at tailoring new treatment in AMI.

Echocardiographic algorithms for admission and predischarge prediction of mortality in acute myocardial infarction.

To develop improved prognostic algorithms for routine bedside use in acute myocardial infarction (AMI), the prognostic value concerning 2- and 12-month mortality of an early (within 72 hours after AMI) resting echocardiogram was defined in 201 consecutive patients. The relation between (1) the clinical variables (age, sex, prior and repeat AMI, arrhythmias, cardiac arrest, early [less than 72 hours after AMI] and late heart failure, early and maximal in-hospital Killip class, and maximal creatine kinase-MB isoenzyme), (2) early myocardial performance by echocardiography, and (3) mortality was characterized by Kaplan-Meier survival curves and receiver-operating characteristic curves based on Cox regression model. Only age and clinical heart failure in terms of the maximal in-hospital Killip class had independent predictive value of death (p less than 0.05) when an early echocardiographic estimate of left ventricular ejection fraction (LVEF) was included in the multivariate statistical models. The following 2 optimized algorithms for admission and predischarge calculation of risk of mortality at 2 and 12 months were developed based on the Cox model, using combinations of age, maximal Killip class and early echocardiographic LVEF: mortality at 2 months = 1 - exp - [0.051 x exp [0.044 x (age -60) - (0.117 x (LVEF - 40)]]; and mortality at 1 year = 1 - exp - [0.101 x exp [0.408 x (maxKillip - 1) - (0.061 x (LVEF - 40)]]. Discriminative power for prediction of mortality of the predischarge algorithm in an independent population of 195 patients 5 days after AMI compared favorably with that obtained in the original population, confirming the validity of the proposed method of prognostication.

Characteristics and prognostic importance of ST-segment elevation on Holter monitoring early after acute myocardial infarction.

The correlation between episodes of ST-segment elevation on Holter monitoring, clinical characteristics, left ventricular function, exercise testing, and long-term prognosis was determined in 123 consecutive patients 55 +/- 8 years old (mean +/- SD) with a first acute myocardial infarction (AMI). During 36 hours of Holter recording 11 +/- 5 days after AMI, 11 patients (9%) had 91 episodes of ST-segment elevation (group 1), whereas 112 patients had no such episodes (group 2). Most episodes of ST-segment elevation occurred in leads with pathologic Q waves or small, indistinct R waves. Large, anterior Q-wave AMIs were more prevalent in group 1 than in group 2, and in-hospital heart failure also occurred more frequently in group 1 patients (82% vs 23%; p < 0.0005). Regional and global left ventricular function was reduced in group 1 compared with group 2: ejection fraction 33 +/- 11% vs 50 +/- 11% (p = 0.0001). All episodes of ST-segment elevation were asymptomatic and did not correlate with different indicators of myocardial ischemia. Indeed, exercise-induced ST-segment depression was more prevalent in group 2 than in group 1: 57 vs 18% (p < 0.035). Over a mean of 5 years (range 4 to 6) of follow-up, an association between episodes of ST-segment elevation on Holter monitoring and (1) cardiac death (Kaplan-Meier analysis; p < 0.005), and (2) cardiac death and nonfatal reinfarction (Kaplan-Meier analysis; p < 0.025) was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Transient myocardial ischemia after a first acute myocardial infarction and its relation to clinical characteristics, predischarge exercise testing and cardiac events at one-year follow-up.

The relation between early out-of-hospital ambulatory ST-segment monitoring, clinical characteristics, predischarge maximal exercise testing and cardiac events was determined in 123 consecutive men (age 55 +/- 8 years) with a first acute myocardial infarction (AMI). During 36 hours of ambulatory recording 11 +/- 5 days after AMI 23 patients (19%) had 123 ischemic episodes (group 1), whereas 100 patients demonstrated no ischemia (group 2). Exercise-induced ST-segment depression was more prevalent in group 1 (83%) than in group 2 (47%) (p < 0.005). Group 1 patients also had more severe ischemia as judged from a shorter exercise duration before significant ST-segment depression (5.5 +/- 2.4 vs 7.7 +/- 4.1 minutes; p < 0.03) and more pronounced ST-segment depression on exercise testing (4.1 +/- 2.6 vs 2.6 +/- 1.6 mm; p < 0.03). Furthermore, exercise test results revealed an impaired hemodynamic response in group 1 compared with group 2: systolic blood pressure at maximal work load 160 +/- 31 vs 176 +/- 28 mm Hg (p < 0.025) and systolic blood pressure increase during exercise 41 +/- 24 vs 56 +/- 22 mm Hg (p < 0.01). With-in 368 +/- 8 days of follow-up the frequency of cardiac events (cardiac death, nonfatal reinfarction, and severe angina including the need of revascularization) was 52% in group 1 compared with 22% in group 2 (p < 0.01). Exercise-induced ischemia did not predict an adverse outcome: event rate 30 vs 25% in patients without residual ischemia (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Attenuation of left ventricular dilatation after acute myocardial infarction by early initiation of enalapril therapy. CONSENSUS II Multi-Echo Study Group.

This trial investigated the effect of enalapril, administered early, on left ventricular (LV) volumes after myocardial infarction. Four hundred twenty-eight patients included in the Cooperative New Scandinavian Enalapril Survival Study (CONSENSUS II) were examined with echocardiography within 5 days, at 1 month and at 6 months after myocardial infarction. Enalaprilat (1 mg) or placebo infusion was initiated within 24 hours after infarction, followed by oral treatment to a target dose of 20 mg/day. A significant attenuation of LV dilatation was noted at 1 month in patients treated with enalapril compared with those receiving placebo. Changes in LV end-diastolic volume indexes during the first month were (mean +/- SEM) 5.7 +/- 1.0 ml/m2 for the placebo group and 1.9 +/- 0.8 ml/m2 for the enalapril group (p < 0.02). Changes in LV end-systolic volume indexes were 3.1 +/- 0.8 and 0.5 +/- 0.6 ml/m2, respectively (p < 0.02). The between-group difference was most marked in patients with anterior wall infarction (p < 0.005). Volume changes beyond the first month were similar in both groups but the differences observed at 1 month were maintained. The larger volumes in the placebo versus enalapril group were significant or borderline significant at 1 and 6 months. Thus, enalapril treatment initiated early after myocardial infarction and continued for 6 months can attenuate LV dilatation during the first month resulting in smaller LV volumes after 1 and 6 months.

Comparison of degrees of left ventricular dilation within three hours and up to six days after onset of first acute myocardial infarction.

Following an acute myocardial infarction (AMI) there is immediate deterioration of contractility in the infarcted left ventricular (LV) wall. This can be followed by regional dilation (expansion) as well as global remodeling. We examined 35 consecutive patients--with no history of myocardial ischemia--who were admitted to hospital within 3 hours after initial symptoms and with ST-segment changes on an electrocardiogram consistent with transmural ischemia. Echocardiography was performed at admission, and at 6 hours, 12 hours, 24 hours, 3 days, and 6 days after onset of the AMI. Within 3 hours after onset of symptoms an increase in both end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) was found in both anterior and inferior infarcts when compared with healthy controls (mean +/- SD EDVI: 99 +/- 13 ml/m2 [anterior], 69 +/- 17 ml/m2 [inferior], 51 +/- 15 ml/m2 [controls], p < or = 0.00001; ESVI: 62 +/- 12 ml/m2 [anterior], 38 +/- 11 ml/m2 [inferior], 17 +/- 6 ml/m2 [controls], p < or = 0.00001). At all points in time, volumes were larger in anterior infarcts than in inferior infarcts (p < 0.05). The volumes did not change during the 6 days (p > 0.1). Thus, major LV dilation is present within 3 hours after onset of symptoms of first AMI. The dilation is more pronounced in anterior versus inferior infarcts. From 3 hours until day 6 no further changes in LV volumes occurred.

Prognosis of late versus early ventricular fibrillation in acute myocardial infarction.

To determine the prognosis of late ventricular fibrillation (VF) after acute myocardial infarction (AMI), the length of the monitoring period after AMI was extended. All patients in this series were continuously monitored in a coronary care unit to ensure observation of all VF within 18 days of AMI. From 1977 to 1985, 4,269 patients were admitted with AMI and 413 (9.6%) had in-hospital VF. Of these 281 (6.8%) had early VF (less than 48 hours after AMI) and 132 (3.2%) had late VF (greater than or equal to 48 hours after AMI). In-hospital mortality was 50 and 54% for early and late VF, respectively (p = 0.31). Kaplan-Meier survival analysis showed better survival after discharge for patients with early versus late VF (p = 0.009) but this difference was fully explained by the presence of heart failure. Survival analysis showed the same prognosis after 1, 3 and 5 years for early and late VF, when VF was not associated with heart failure. When VF was associated with heart failure (secondary VF) early VF had a greater mortality than late VF after 2 and 5 years. Logistic regression analysis showed that heart failure (relative risk 1.9 [1.1 to 3.1]) and cardiogenic shock (relative risk 3.9 [1.8 to 8.5]) were significant risk factors for in-hospital death. Late VF compared to early VF had no prognostic implication (relative risk 1.0 [0.6 to 1.6]). For patients discharged from the hospital, risk factors were heart failure (1.8 [1.1 to 2.8]) and previous AMI (1.6 [1.3 to 2.1]).(ABSTRACT TRUNCATED AT 250 WORDS)

Interobserver agreement and accuracy of bedside estimation of right and left ventricular ejection fraction in acute myocardial infarction.

Ninety-eight patients with acute myocardial infarction were examined by 3 clinicians who, independently of each other, gave an estimate of left ventricular (LV) and right ventricular (RV) ejection fraction (EF) in each patient. Their estimates were based on physical examination, chest x-ray, electrocardiogram, patient history and clinical course during admission. Ejection fractions were estimated as belonging to 1 of 4 categories: normal (LVEF greater than or equal to 0.53, RVEF greater than or equal to 0.57), mildly reduced (LVEF 0.40 to 0.52, RVEF 0.45 to 0.56), moderately reduced (LVEF 0.30 to 0.39, RVEF 0.35 to 0.44) or severely reduced (LVEF less than 0.30, RVEF less than 0.35). Radionuclide ventriculography was carried out immediately after the physical examination. LVEF was correctly estimated in 43% of all examinations, deviated from radionuclide LVEF by 1 LVEF category in 45% and by 2 LVEF categories in 12%. The 3 clinicians agreed on estimated LVEF in only 32% of the patients. RVEF was correctly estimated in 67% of the examinations, but none of the clinicians identified greater than 43% of the relatively few patients with reduced radionuclide RVEF and they greatly disagreed as to who among the patients had a reduced RVEF. Previous myocardial infarction, electrocardiographic infarct location, Killip class, physical signs of left- and right-sided heart failure, radiographic pulmonary congestion and cardiomegaly were analyzed to determine which were the most helpful in predicting LVEF and RVEF. The results disclosed that several variables, traditionally believed to be reliable indexes of reduced ventricular function, were surprisingly poor predictors of LVEF and RVEF.

Impact of coronary artery disease on left ventricular systolic function and geometry in hypertensive patients with left ventricular hypertrophy (the LIFE study).

Hypertensive patients with left ventricular (LV) hypertrophy have a higher incidence of cardiovascular events than those without it. We hypothesized that a close relation exists between clinical evidence of coronary artery disease (CAD) and alterations in LV structure and function that contribute to their higher risk. Echocardiograms were recorded in 963 hypertensive patients (mean age 66 +/- 7 years, 41% women) with electrocardiographic LV hypertrophy, and divided into 149 with and 814 without clinical (prior myocardial infarction or angina pectoris) or electrocardiographic (Minnesota codes 1.1, 1.2) evidence of CAD. Patients with CAD had larger LV internal dimensions (5.5 +/- 0.6 vs 5.2 +/- 0.5 cm), increased LV mass (136 +/- 31 vs 122 +/- 24 g/m(2), and 62.4 +/- 19.4 vs 55.5 +/- 12.1 g/m(2.7)), lower ejection fraction (58 +/- 10% vs 62 +/- 8%), higher circumferential end-systolic wall stress (cESS) (198 +/- 59 vs 181 +/- 47 kdynes/cm(2), all p <0.001), and higher total peripheral resistances (2,088 +/- 628 vs 1,963 +/- 553 dynes x s x m(2)/cm(3), p = 0.02). Although eccentric LV hypertrophy predominated, the CAD group had a greater prevalence of this geometric pattern than the non-CAD group (56% vs 47%, p <0.02). An index of myocardial oxygen demand per beat--the LV mass x cESS x ejection time--was 20% higher in patients with CAD. In conclusion, clinical evidence of CAD in hypertensive patients with electrocardiographic evidence of LV hypertrophy identifies subjects with structural and functional abnormalities at high risk for cardiovascular events. LV mass. cESS. ejection time, a noninvasive index that parallels myocardial oxygen demand per beat, is especially high in hypertensive patients with CAD.

Progressive strength training in sedentary, older African American women.

PURPOSE: This study investigated effects of an 8-wk, low-frequency and low-volume, supervised, progressive strength training program emphasizing free weight, multijoint movements on the muscular power, strength, endurance, and flexibility of African American women 44 to 68 yr of age. METHODS: Nineteen sedentary African American women were randomly assigned to a strength training (ST) only group (N = 12; mean age, 51 yr) or a nonexercise control (C) group (N = 7; mean age, 52 yr). Maximal power, strength, absolute endurance, and flexibility were assessed before and after training. Subjects trained 2 d x wk(-1) using free weight (barbells and dumbbells) and machine (plate loaded) exercises for two to three sets of 8 to 10 repetitions on both primary and assistance exercises. RESULTS: Upper body power (medicine ball put distance) significantly increased statistically (P = 0.002), but gains possibly lacked practical significance because of measurement variation. Lower body power (peak watts on bicycle) experienced a small, nonsignificant increase in the ST group. Significant increases (P = 0.000) in 1RM muscle strength occurred in the ST group (leg press, +99.8%; bench press, +34.4%). Absolute endurance significantly increased (P = 0.000) in the ST group (leg press repetitions to failure at 70% pretest 1RM, +221%; bench press repetitions to failure at 50% pretest 1RM, +112%). Significant flexibility gains occurred in the ST group (sit-and-reach test, +8.2%; P = 0.017). No significant changes occurred in power, strength, absolute endurance, or flexibility in the C group. CONCLUSION: This study demonstrates that 8 wk of low-frequency, supervised, progressive strength training emphasizing free weight, multijoint movements can safely cause significant gains in muscle strength, absolute endurance, and flexibility in older African American women.

Effect of enalapril initiated early after acute myocardial infarction on heart failure parameters, with reference to clinical class and echocardiographic determinants. CONSENSUS II Multi-Echo Study Group.

BACKGROUND AND HYPOTHESIS: Although the angiotensin-converting enzyme inhibitor enalapril has recently been shown to reduce mortality and the need for hospitalization in patients with left ventricular dysfunction and congestive heart failure, this drug was found to have no significant impact on short-term mortality after acute myocardial infarction (AMI) in the CONSENSUS II trial. The effect of enalapril initiated early after AMI on clinical and echocardiographic determinants of left ventricular (LV) function was studied in a subset of patients from CONSENSUS II. METHODS: Symptoms and signs of heart failure were classified as NYHA and dyspnea classes. Echocardiography included LV end-systolic volumes (ESV) and end-diastolic volumes (EDV), as well as ejection fraction (EF), wall motion index (WMI), and mitral flow indices. In all, 428 patients were included and followed for an average of 5.1 months by serial examinations, starting 2-5 days after myocardial infarction (MI) and repeated after 1 month and at the completion of the study. RESULTS: There was no beneficial effect of enalapril on clinically determined function. Changes (i.e., changes in NYHA class) in the functional status remained correlated with changes in echocardiographic determinants throughout the study in patients belonging to the placebo group: EDV index (r = 0.36, p = 0.002, ESV index (r = 0.49, p < 0.001), EF (r = -0.41, p < 0.001), and WMI (r = 0.29, p = 0.008). In a stepwise logistic regression model, the best baseline parameters to predict NYHA class at final visit in all patients were age (p = 0.014) and ESV index (p = 0.001). CONCLUSION: Enalapril treatment for an average period of 5.1 months following MI resulted in no clinically significant beneficial effects on NYHA and dyspnea class. Changes in clinical function class were correlated with changes in echocardiographic determinants in placebo-treated patients, but not in patients given enalapril.

Mechanomyographic and electromyographic amplitude and frequency responses from the superficial quadriceps femoris muscles during maximal, eccentric isokinetic muscle actions.

The purposes of this study were to examine the effects of gender and muscle (vastus lateralis = VL, rectus femoris = RF, and vastus medialis = VM) on the velocity-related patterns for peak torque (PT), mean power output (MP), mechanomyographic (MMG) amplitude, electromyographic (EMG) amplitude, MMG mean power frequency (MPF), and EMG MPF during maximal, eccentric isokinetic muscle actions. Thirteen females (mean +/- SD age = 21 +/- 1 years) and eleven males (mean +/- SD age = 21 +/- 2 years) volunteered for this investigation. PT and MP were measured on a calibrated Cybex 6000 dynamometer at randomly ordered velocities of 60, 120, and 180 degrees.s-1, while MMG and EMG signals were recorded simultaneously from the VL, RF, and VM muscles. The results indicated no gender-related differences for the patterns of PT, MP, MMG amplitude, EMG amplitude, MMG MPF, or EMG MPF. Furthermore, no muscle-related differences were found for the patterns of MMG amplitude, EMG amplitude, or MMG MPF. The normalized values for MP and MMG amplitude increased from 60 to 180 degrees.s-1 (60 degrees.s-1 < 120 degrees.s-1 < 180 degrees.s-1). PT and EMG MPF remained unchanged across velocity, while EMG amplitude remained unchanged from 60 to 120 degrees.s-1, but decreased (approximately 10%) from 120 to 180 degrees.s-1. The findings indicated a close association between the patterns for MP and MMG amplitude, and a similarity between the patterns for PT, EMG amplitude, and EMG MPF across velocity. Therefore, the present findings suggested that motor unit recruitment (EMG amplitude), firing rate (MMG MPF), and muscle fiber action potential conduction velocity (EMG MPF) exhibited velocity-related patterns that were similar to PT production, while MMG amplitude was more closely associated with MP.

[Transesophageal echocardiography. A new cardiologic examination method]. / Transøsofageal ekkokardiografi. En ny kardiologisk undersøgelsesmetode.

Transoesophageal echocardiography is a new diagnostic method which uses the oesophagus as an ultrasonic window to the heart and central vessels. The images obtained are often of supreme quality compared to those obtained by conventional transthoracic echocardiography, because the distance between the transducer and the heart is reduced. The equipment, the examination technique, and preliminary experience after 80 examinations are described. It is concluded that the technique is particularly informative in patients with endocarditis or mitral valve disease and that the transoesophageal approach has become essential for the diagnosis of prosthetic valve dysfunction. Furthermore, the technique allows visualization of the descending aorta, which is often impossible to image from the precordial window, and the technique has proved useful in the emergency diagnostic elucidation of aneurysm of the thoracic aorta. So far a limited number of formal investigations comparing the results of transoesophageal echocardiography with the results of reference methods have been performed, however, practical clinical experience is already sufficiently extensive to state that transoesophageal echocardiography has come to stay. Disregarding coronary angiography it seems probable that combined transthoracic and transoesophageal echocardiography with time will eliminate the need for cardiac catheterization and angiography.

[Early discharge after acute myocardial infarction. Cost-effectiveness of early echocardiographic risk evaluation]. / Tidlig udskrivelse efter akut myokardieinfarkt. Cost-effectiveness af tidlig ekkokardiografisk risikobedømmelse.

A total of 195 consecutive patients with acute myocardial infarction were examined and risk classified (low or middle/high risk) on the fifth day by two physicians. These two physicians employed two different sets of criteria: conventional clinical examination compared with 2-D echocardiographic assessment of the wall motion of the left ventricle (wall motion index, WMI). Both physicians concluded their examination by determination of a theoretical time for discharge. By design this was on the 5th-7th days for low risk patients by echocardiography, while low risk patients by clinical criteria are normally discharged on the 7th to 8th days. The most sensitive method of identifying the low risk patients was achieved by combining the clinical examination with echocardiographic WMI determination. In this manner, a total of 104 (53%) low risk patients could be identified. A potential saving of 18% of the total duration of hospitalization could be calculated from the two theoretical times of discharge for the total population. All of the patients in this study could be assessed by echocardiography which provided valuable information and thus may be implemented in the routine treatment of acute myocardial infarction.