Activity Participation and Perceived Health Status in Patients with Severe Mental Illness: a Prospective Study.

OBJECTIVE: To examine associations between severe mental illness (SMI), general health symptoms, mental wellbeing, and different activity levels in patients with SMI. METHOD: Consecutive patients with SMI referred for occupational therapy were prospectively included. Their hours of activities per day during hospital stay were recorded as <1 hour, 1-3 hours, and >3 hours in three categories: basic self-care activities, interest-based activities, and role-specific activities. Patients were free to join or decline any activities. Patients' somatic and mental health were measured at admission, discharge, and 1 month after discharge using the Brief Psychiatric Rating Scale (BPRS), Patient Health Questionnaire-15 (PHQ-15), Pittsburgh Sleep Quality Index (PSQI), Chinese version of Short Warwick Edinburgh Mental Wellbeing Scale (C-SWEMWBS), and Chinese version of General Activity Motivation Measure (GAMM). RESULTS: 84 patients (35 men and 49 women) aged 16 to 63 years were assessed at the three timepoints. The mean length of hospital stay of current admission was 74.73 days. The most common diagnosis was schizophrenia (n=35), followed by depression (n=15), psychosis (n=14), bipolar affective disorder (n=10), others (n=8), and delusional disorder (n=2). The hours of activities per day was <1 hour in 32 (38.1%) patients, 1-3 hours in 34 (40%) patients, and >3 hours in 18 (21.2%) patients. Improvement in somatic and mental health was positively associated with hours of activities per day. Activities were associated with reduced psychiatric symptoms (measured by BPRS) at discharge (Z = 5.978, p < 0.01). Activities were associated with less somatic complaints (measured by PHQ-15) [χ2 = 23.478, p < 0.01], better sleep quality (measured by PSQI) [χ2 = 14.762, p < 0.01]. The BPRS score for psychiatric symptoms at discharge was inversely associated with C-SWEMWBS score for mental wellbeing (r = -0.233, p = 0.033) and C-GAMM score for activity motivation (r = -0.258, p = 0.018). Basic self-care activities were a predictor for psychiatric symptoms (measured by BPRS) at discharge (adjusted R2 = 0.091, F = 8.496, p = 0.005), whereas a combined group of badminton and Tai Chi was a predictor for general activity motivation (measured by GAMM) at 1 month after discharge (adjusted R2 = 0.047, F = 4.697, p < 0.05), and soccer alone was a predictor for somatic health (measured by PHQ-15) at 1 month after discharge (adjusted R2 = 0.06, F = 5.784, p < 0.05). CONCLUSION: Participating in activities of patients' own choice and interests is positively associated with patients' psychiatric and somatic health and subjective wellbeing. Outdoor soccer has added effect on patients' somatic health. The beneficial effects are maintained at 1 month after discharge. Daily participation of activity meaningful to patients can be a non-pharmacological treatment for patients with SMI to improve somatic and mental health.

[Pulmonary artery rupture with Swan-Ganz catheter during cardiac surgery: management and decision-making]. / Rupture de l'artère pulmonaire par cathéter de Swan-Ganz au cours de la chirurgie cardiaque: conduite à tenir et stratégie.

Pulmonary artery catheterization is almost uniformly used nowadays in cardiac surgery. Although rare, rupture of the pulmonary artery following catheterization is highly lethal. This review examines ways of avoiding its occurrence and means of improving outcomes in case of rupture.

Identification of the site of non-enzymatic glycation of glutathione peroxidase: rationalization of the glycation-related catalytic alterations on the basis of three-dimensional protein structure.

Bovine erythrocyte glutathione peroxidase has been glycated in vitro by incubation in 0.05 M glucose at pH 7.4. Upon glycation the estimated KM for t-butylhydroperoxide reduction increased by approx. 3-fold in comparison to non-glycated glutathione peroxidase. The glycated protein fraction was stabilized by NaBH4 reduction and subjected to tryptic cleavage. Affinity chromatography of the tryptic digest on m-aminophenylboronate-Agarose resulted in the isolation of a single glycated peptide. The peptide was identified as T94-K117 by amino-acid composition comparison to the published amino-acid sequence for this enzyme. The glycation site has been identified as the epsilon-NH2 group of K110. Examination of the three-dimensional structure of bovine erythrocyte glutathione peroxidase indicates that K110 lies on the surface of the protein approximately 15 A away from the active site selenocysteine (SEC 45). Modeling studies indicate that K110 can communicate via H-bonded interactions with the alpha-helix containing the active site residues (SEC-45 and R50). The observed elevation of KM upon glycation of bovine glutathione peroxidase is discussed in terms of the disruption of the long range H-bonded interaction.

Promotion of atrial fibrillation by heart failure in dogs: atrial remodeling of a different sort.

BACKGROUND: Studies of atrial fibrillation (AF) due to atrial tachycardia have provided insights into the remodeling mechanisms by which "AF begets AF" but have not elucidated the substrate that initially supports AF before remodeling occurs. We studied the effects of congestive heart failure (CHF), an entity strongly associated with clinical AF, on atrial electrophysiology in the dog and compared the results with those in dogs subjected to rapid atrial pacing (RAP; 400 bpm) with a controlled ventricular rate (AV block plus ventricular pacemaker at 80 bpm). METHODS AND RESULTS: CHF induced by 5 weeks of rapid ventricular pacing (220 to 240 bpm) increased the duration of AF induced by burst pacing (from 8+/-4 seconds in control dogs to 535+/-82 seconds; P<0.01), similar to the effect of 1 week of RAP (713+/-300 seconds). In contrast to RAP, CHF did not alter atrial refractory period, refractoriness heterogeneity, or conduction velocity at a cycle length of 360 ms; however, CHF dogs had a substantial increase in the heterogeneity of conduction during atrial pacing (heterogeneity index in CHF dogs, 2. 76+/-0.16 versus 1.46+/-0.10 for control and 1.51+/-0.06 for RAP dogs; P<0.01) owing to discrete regions of slow conduction. Histological examination revealed extensive interstitial fibrosis (connective tissue occupying 12.8+/-1.9% of the cross-sectional area) in CHF dogs compared with control (0.8+/-0.3%) and RAP (0. 9+/-0.2%) dogs. CONCLUSIONS: Experimental CHF strongly promotes the induction of sustained AF by causing interstitial fibrosis that interferes with local conduction. The substrates of AF in CHF are very different from those of atrial tachycardia-related AF, with important potential implications for understanding, treating, and preventing AF related to CHF.

Effects of angiotensin-converting enzyme inhibition on the development of the atrial fibrillation substrate in dogs with ventricular tachypacing-induced congestive heart failure.

BACKGROUND: Atrial structural remodeling creates a substrate for atrial fibrillation (AF), but the underlying signal transduction mechanisms are unknown. This study assessed the effects of ACE inhibition on arrhythmogenic atrial remodeling and associated mitogen-activated protein kinase (MAPK) changes in a dog model of congestive heart failure (CHF). METHODS AND RESULTS: Dogs were subjected to various durations of ventricular tachypacing (VTP, 220 to 240 bpm) in the presence or absence of oral enalapril 2 mg. kg(-1). d(-1). VTP for 5 weeks induced CHF, local atrial conduction slowing, and interstitial fibrosis and prolonged atrial burst pacing-induced AF. Atrial angiotensin II concentrations and MAPK expression were increased by tachypacing, with substantial changes in phosphorylated forms of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38-kinase. Enalapril significantly reduced tachypacing-induced changes in atrial angiotensin II concentrations and ERK expression. Enalapril also attenuated the effects of CHF on atrial conduction (conduction heterogeneity index reduced from 3.1+/-0.4 to 1.9+/-0.2 ms/mm, P<0.05), atrial fibrosis (from 11.9+/-1.1% to 7.5+/-0.4%, P<0.01), and mean AF duration (from 651+/-164 to 218+/-75 seconds, P<0.05). Vasodilator therapy of a separate group of VTP dogs with hydralazine and isosorbide mononitrate did not alter CHF-induced fibrosis or AF promotion. CONCLUSIONS: CHF-induced increases in angiotensin II content and MAPK activation contribute to arrhythmogenic atrial structural remodeling. ACE inhibition interferes with signal transduction leading to the AF substrate in CHF and may represent a useful new component to AF therapy.

Mouse monoclonal antibody 5-21-3 recognizes a contiguous, conformation-dependent epitope and maps to a hydrophilic region in HIV-1 gp41.

Mouse monoclonal antibody 5-21-3 is mapped to an epitope within a hydrophilic region of HIV-1 gp41 between amino acids 642 and 665 (numbering by Meyers et al. based on HXB2 isolate). The epitope is formed from amino acids within the sequence IHSLIEESQNQQEKNEQELLELDK; however, antibody 5-21-3 is unable to recognize the epitope-forming sequence when it is presented to the antibody in the form of a short (642-665) synthetic polypeptide. The epitope apparently is partially formed when additional native sequence of varying length is added to the amino and/or carboxy ends of the epitope-forming sequence, and 5-21-3 binds these larger synthetic polypeptides to varying degrees depending on the position and length of the flanking sequences. The 5-21-3 epitope apparently is formed from contiguous amino acids which require a specific, conformation-dependent, secondary structure for proper epitope formation. Binding preferences exhibited by 5-21-3 toward synthetic polypeptides and recombinant proteins may reflect the conformational nature of the epitope in disrupted HIV which elicited formation of the monoclonal.

Right ventricular rupture. A complication of postoperative mediastinitis.

Mediastinitis-related right ventricular rupture is an unusual but potentially life-threatening complication of cardiac operations. Between January 1981 and December 1990, a total of 10,182 patients underwent heart operations for ischemic, valvular, and congenital heart disease at the Montreal Heart Institute. Forty-eight patients (0.5%) had postoperative mediastinitis necessitating surgical exploration and sternal debridement. The mediastinum was left open for daily irrigation with povidone-iodine and chest reconstruction was postponed. During treatment, seven patients (0.07%) had right ventricular rupture necessitating immediate surgical repair. All had ischemic heart disease before the operation. There were five women and two men, ages ranging from 52 to 65 years (mean 58 +/- 5 years). Surgical repair consisted of autologous patch covered with omentoplasty assisted with cardiopulmonary bypass. Two patients died, one during the operation of massive hemorrhage and the other 10 days after the operation of uncontrolled sepsis. Five patients survived 2 to 29 months (mean 23 +/- 10 months) after right ventricular rupture, with an overall survival of 71%. Obesity was more frequent in the patients with right ventricular rupture and was found to be a significant risk factor (multivariate analysis, p < 0.05, relative risk 3.22). Histologic examination of the right ventricle in the patient who died after a successful repair revealed fatty infiltration of the right ventricular wall. This may have predisposed the patient toward ventricular rupture. In conclusion, right ventricular rupture, an unusual event in heart surgery, is related to open sternal debridement. Favorable outcome of this complication depends on immediate surgical management, autologous repair, and the use of omentoplasty.

Receptor-specific effects of acute rejection after heart transplantation on endothelium-dependent coronary relaxation in dogs.

To establish the effects of acute rejection on coronary artery endothelial reactivity in a canine model of heart transplantation, we submitted seven mongrel dogs to heterotopic heart transplantation without immunosuppression for a period of 7 days. At harvesting, all transplanted hearts displayed a grade IV histologic rejection. Compared with native heart, the endothelium-dependent relaxation of the coronary arteries from the graft displayed an increased sensitivity to serotonin, a decreased sensitivity to thrombin, and no change in the response to acetylcholine and adenosine diphosphate; endothelium-independent relaxation to sodium nitroprusside was not affected. Therefore, in the canine heterotopic heart transplant model, acute rejection has no effect on endothelium-independent relaxation of coronary arteries but affects endothelium-dependent relaxation in a receptor-specific manner.

Clinical trial of retrograde warm blood reperfusion versus standard cold topical irrigation of transplanted hearts.

BACKGROUND: A prospective, randomized clinical study involving 34 patients undergoing heart transplantation compared myocardial preservation of donor hearts maintained with continuous reperfusion with retrograde warm blood cardioplegia during surgical implantation versus the standard cold topical irrigation. METHODS: Hearts in both groups were arrested with a standard crystalloid solution and maintained in a cold saline solution during transportation. In the retrograde group, cardioplegia was administered through a catheter in the coronary sinus during surgical implantation. An average of 471 +/- 30 mL of hyperkalemic crystalloid solution diluted 1:4 in warm blood from the oxygenator was infused. In the standard group, the heart was kept cold by topical irrigation of cold saline solution and was reperfused only when the ascending aorta was unclamped. RESULTS: Preoperative characteristics of donors and recipients were similar in the two cohorts. Ischemic time average 139 +/- 12 minutes in the retrograde group compared with 130 +/- 11 minutes in the standard group (p = 0.57). Cardiopulmonary bypass time averaged 89 +/- 4 minutes in the retrograde group and 110 +/- 12 minutes in the standard group (p = 0.12). Defibrillation at reperfusion was performed in 4 patients (4/17, 24%) in the retrograde group and 12 patients (12/18, 67%) in the standard group (p = 0.01). There were no deaths in the retrograde group (0/17), whereas in the standard group, 3 patients (3/17) died of early graft failure (p = 0.11). Four early graft failures occurred in the standard group (p = 0.06). Two patients (2/17, 12%) were weaned from bypass with ventricular assist devices in the standard group. The number of subendocardial necrotic cells in the first two weekly endomyocardial biopsy specimens averaged 2.7 +/- 0.8 cells/mm2 in the retrograde group and 5.9 +/- 2.4 cells/mm2 in the standard group (p = 0.12). CONCLUSIONS: Retrograde warm blood reperfusion appears to improve the initial recovery of transplanted hearts. The technique is easy to use and may be a useful approach to graft protection during surgical implantation.

First cytogenetic evidence of homozygosity for the retinoblastoma deletion in chromosome 13.

Retinoblastoma (Rb) provided the first model in which both normal alleles of a recessive gene had to be lost as a prerequisite for tumorigenicity. However, region q14 of chromosome 13 appears cytogenetically normal in the majority of Rb tumors, and no homozygotic deletion had previously been observed. High-resolution cytogenetics of an Rb tumor revealed a homozygotic deletion in bands q13.3-14.2 of chromosomes 13 in 35% of the cells and a heterozygotic deletion, involving the same region, in 17%. In one third of the cells, although random chromosome loss occasionally occurred, no specific anomaly was detected. The remaining cells showed either monosomy 13, tetraploidy, or an i(1p). Revealing a homozygotic deletion in subbands 14.1 and 14.2 of chromosomes 13 provides the first cytogenetic evidence of the two somatic mutations considered essential to inactivate the Rb gene. These results allow insight into the succession of events necessary for tumor development.

The expression of proteins and activities of metabolic enzymes in transplanted brain tissue.

The middle three-fifths of the forebrains of 14-day-old embryos were obtained and transplanted into the cortical cavities of adult rats made 7 days prior to the transplantation. The expression of proteins, as revealed by 2-dimensional gel electrophoresis studies, and the activities of energy metabolizing enzymes in the mature allografts were compared with those in the 14-day-old embryonic forebrains and corresponding areas in the contralateral cerebral hemispheres of the hosts. They were shown to approach adult pattern and adult values after 10-12 weeks of growth. The biochemical findings were discussed and correlated with some of the anatomical observations.

Aortopulmonary fistula detected by echocardiography 12 years after aortoplasty for correction of ascending aorta aneurysm.

We describe a case of aortopulmonary fistula in which the correct diagnosis was made by transthoracic echocardiography. The transesophageal approach, because of severe aortic dilatation, failed to provide the correct diagnosis, underlining the importance of complete transthoracic and transesophageal studies in the evaluation of aortic aneurysms.

Obstruction of left ventricular outflow tract by vegetation and periaortic abscess.

Echocardiography is the modality of choice for the noninvasive recognition of vegetations and abscesses that complicate endocarditis. Vegetation size is highly variable, and it has been suggested that large vegetations are related to a more complicated course. The case we present is unusual in that the echocardiographically detected vegetation was very large, highly mobile, and caused severe obstruction of the left ventricular outflow tract, which led to impaction and cardiac arrest.

Angiosarcomas of the interatrial septum mimicking atrial myxomas.

Angiosarcoma of the heart is a rare tumor. This tumor is most frequently located in the right atrium and pericardium. Localization of a tumor in the interatrial septum usually suggests atrial myxoma. We report two cases of angiosarcoma originating from the interatrial septum, one extending into the right atrium and the other into the left atrium, mimicking atrial myxomas. Transesophageal echocardiography allowed the diagnosis and comprehensive assessment of compromised structures.

Differences in the neurotoxic effects of manganese during development and aging: some observations on brain regional neurotransmitter and non-neurotransmitter metabolism in a developmental rat model of chronic manganese encephalopathy.

The effects of chronic and life-span (i.e. over 2 years) treatment with manganese (1 mg MnCl2.4H2O per ml of drinking water) on a number of neurochemical parameters were studied. In development Mn-treatment led to transient but age-dependent decreases in synaptosomal dopamine uptake in hypothalamus, striatum and mid-brain and decreases in synaptosomal choline uptake in hypothalamus but increase in synaptosomal choline uptake in striatum. However, synaptosomal noradrenaline and serotonin uptake in these brain regions remained unaltered. Mn-treatment in development led to small decreases in choline acetyltransferase activities in cerebellum and mid-brain of 2 month old rats but did not affect the regional distribution of glutamic acid decarboxylase or acetylcholinesterase. The same treatment did not alter regional distribution of NAD-linked isocitric dehydrogenase although treatment with a high dose (10 mg MnCl2.4H2O per ml) resulted in transient but age-dependent decreases in the activities of this enzyme but not those of glucose-6-phosphate dehydrogenase in cerebral cortex and mid-brain. Lifespan Mn-treatment (1 mg MnCl2.4H2O per ml) exerted antagonistic effects on the age-related changes in activities of several enzymes. These results suggest that chronic Mn toxicity selectively affects several neurochemical paradigms and the long-term effects of Mn toxicity on brain development and aging are different.

Manganese mineral interactions in brain.

Manganese (Mn) is an essential mineral but is toxic when taken in excess. However, whether its interactions with other minerals in organs and cells are involved in mechanisms underlying Mn toxicity is poorly understood. We designed a developmental rat model of chronic Mn treatment (Group A: 1 mg MnCl2.4H2O per ml of drinking water; Group B: 10 mg MnCl2.4H2O per ml of drinking water; Group C: 20 mg MnCl2.4H2O per ml of drinking water; Control Group given water without manganese addition). Employing the model and instrumental neutron activation analysis, we investigated two hypotheses: (i) chronic manganese treatment alters the brain regional distribution of manganese and this altered manganese distribution also leads to region-specific changes of other metals; (ii) chronic manganese treatment induces differential changes in subcellular distributions of metals and electrolytes. In the treated rats, brain Mn level showed dose-related increases, the most pronounced being noted in striatum, hypothalamus, and hippocampus: these increases also led to alterations in regional distribution pattern of Mn. In the treated rats, Fe level was increased in hypothalamus, cerebellum, hippocampus, pons and medulla, and striatum. Cu level was increased in pons and medulla, hippocampus, midbrain, and striatum. Se level was increased in cerebellum, striatum, midbrain, hypothalamus, and pons and medulla. Zn level was increased in hypothalamus and striatum. Ca level was increased in midbrain but decreased in cerebellum; however, Mg and Al levels were not markedly affected. In brains of Mn-treated rats, Mn levels in subcellular fractions were all increased, being especially marked in nuclei, mitochondria, and synaptosomes; the subcellular distributions of Fe, Cu, Zn, and Mg were differentially altered although those of Al and Ca were minimally affected. These results are consistent with our hypotheses and may have implications in manganese neurotoxicity. The cellular and molecular mechanisms underlying manganese-mineral interactions in brain are still poorly defined and merit further investigation.

Feasibility of cardiac cryoablation using a transvenous steerable electrode catheter.

We investigated the feasibility of using cryogenic technology in an electrode catheter for percutaneous ablation of cardiac tissue. Despite its high success rate, radiofrequency catheter ablation has important limitations especially with regards to the treatment of ventricular arrhythmias associated with a chronic scar. Arrhythmia surgery experience has shown that freezing with a hand held probe can permanently ablate the arrhythmogenic substrate of ventricular tachycardia associated with an old scar. Moreover, cryosurgery also allows for reversible "ice mapping," in which the area likely responsible for the arrhythmia can be evaluated by suppressing its electrophysiologic properties prior to the creation of an irreversible state. A new steerable cryoablation catheter using Halocarbon 502 as a refrigerant was utilized in six dogs. Serial cryoapplications were performed in the right and left ventricles. In two dogs, we attempted reversible ice mapping of the AV node. Pathological evaluation of the lesions was done acutely in all the animals. Forty-two cryoapplications were delivered at a mean temperature of -45 +/- 9.8 degrees C. No lesion was found at pathological evaluation for 16 cryoapplications which did not achieve a temperature of less (colder) than -30 degrees C. The remaining applications resulted in 26 lesions which were hemorrhagic and sharply demarcated from normal myocardium. Histological evaluation revealed contraction band necrosis. Reversible ice mapping of the AV node was successfully achieved in two animals. Cryoablation is feasible using an electrode catheter with multiple electrodes. This technology has the potential to allow for reversible ice mapping to confirm a successful ablation target before definitive ablation.

Successful treatment of severe heart failure caused by idiopathic giant cell myocarditis.

A 53-year-old woman presented with increasing dyspnea over one month and signs of severe heart failure. A right ventricular biopsy revealed giant cell myocarditis. She was treated with a combination of cyclosporine, imuran and prednisone and improved dramatically--left ventricular ejection fraction increased from 13 to 66%. That such a response is possible has important implications with respect to both the etiology and treatment of this rare disorder.

Hypercalcemic cardiomyopathy associated with primary hyperparathyroidism mimicking primary obstructive hypertrophic cardiomyopathy.

A 72-year-old woman presented to hospital with rapidly progressive dyspnea and chest pain on exertion. Physical findings included a grade 3/6 systolic murmur increased by the Valsalva manoeuvre. Transthoracic echocardiography revealed concentric left ventricular hypertrophy, systolic anterior motion of the mitral valve and critical dynamic outflow tract obstruction. The myocardium was strikingly heterogeneous with hyperdynamic left ventricular systolic function. Laboratory findings included severe hypercalcemia secondary to primary hyperparathyroidism. The patient's outcome was unfavourable with nephrogenic diabetes insipidus, pancreatitis, shock, severe acidosis and death. Postmortem examination confirmed the presence of severe concentric left ventricular hypertrophy, a narrowed left ventricular outflow tract and localized endocardial fibrosis of the left interventricular septum. Microscopic findings showed diffuse calcium deposits of the myocardium, coronary arteries, kidneys and lungs. This appears to be the first report of two-dimensional and Doppler echocardiographic findings in hypercalcemic cardiomyopathy mimicking obstructive hypertrophic cardiomyopathy.