Recovering is about living my life, as it evolves: perspectives of stroke survivors in remote northwest Queensland.

PURPOSE: Recovering from stroke in remote Australia has rarely been considered, even though rehabilitation services are generally scarce. The primary purpose of this study was to explore stroke recovery, from the perspective of stroke survivors in remote northwest Queensland (NWQ), to explicate the lens through which they view recovering. The secondary purpose was to explore the role of technology to support stroke survivors in remote locations along their recovery journey. METHODS: A qualitative study was undertaken using elements of constructivist grounded theory for data collection and analysis. Semi-structured interviews were conducted with fifteen stroke survivors and two partners living, working or travelling in remote NWQ. RESULTS: From the participants' perspective, recovering in a remote area after stroke is about living my life, as it evolves by endeavouring to recover my way and navigating my recovery in my world. Technology was only considered helpful when it supported participants to recover their way in their world. CONCLUSION: Recovering from stroke from the perspective of stroke survivors in remote NWQ is about living their life, as they want it to be, and as it unfolds within their own context. Technology only has a place when it can support them to recover their way in their world. These findings reinforce the importance of health professionals listening, learning about, and enabling stroke survivors along their recovery journey, within their remote context and support network.Implications for RehabilitationRecovering from the perspective of stroke survivors is about living their life as it evolves.To support stroke survivors from remote areas, health professionals need to listen to and learn from each stroke survivor about what matters to them, what works for them, and about their world; including the challenges (e.g., switching between services) and enablers (e.g., community support) as the stroke survivor perceives them.Finding ways to utilise the strengths within and around them, may improve the recovery process for the stroke survivor in a remote area, ensuring they can access care that meets their needs in their world.Working together with stroke survivors, health professionals need to consider how technology could help them to live their life, while recovering their way and in their world.

Filtration Markers, Cardiovascular Disease, Mortality, and Kidney Outcomes in Stable Kidney Transplant Recipients: The FAVORIT Trial.

Cystatin C and beta-2-microglobulin (B2M) are filtration markers associated with adverse outcomes in nontransplant populations, sometimes with stronger associations than for creatinine. We evaluated associations of estimated glomerular filtration rate from cystatin C (eGFRcys ), B2M (eGFRB2M ), and creatinine (eGFRcr ) with cardiovascular outcomes, mortality, and kidney failure in stable kidney transplant recipients using a case-cohort study nested within the Folic Acid for Vascular Outcome Reduction in Transplantation (FAVORIT) Trial. A random subcohort was selected (N = 508; mean age 51.6 years, median transplant vintage 4 years, 38% women, 23.6% nonwhite race) with enrichment for cardiovascular events (N = 306; 54 within the subcohort), mortality (N = 208; 68 within the subcohort), and kidney failure (N = 208; 52 within the subcohort). Mean eGFRcr , eGFRcys , and eGFRB2M were 46.0, 43.8, and 48.8 mL/min/1.73m2 , respectively. After multivariable adjustment, hazard ratios for eGFRcys and eGFRB2M <30 versus 60+ were 2.02 (95% confidence interval [CI] 1.09-3.76; p = 0.03) and 2.56 (1.35-4.88; p = 0.004) for cardiovascular events; 3.92 (2.11-7.31) and 4.09 (2.21-7.54; both p < 0.001) for mortality; and 9.49 (4.28-21.00) and 15.53 (6.99-34.51; both p < 0.001) for kidney failure. Associations persisted with additional adjustment for baseline eGFRcr . We conclude that cystatin C and B2M are strongly associated with cardiovascular events, mortality, and kidney failure in stable kidney transplant recipients.

Is a reduction in albuminuria associated with renal and cardiovascular protection? A post hoc analysis of the ALTITUDE trial.

AIMS: To investigate whether the degree of albuminuria reduction observed in the ALTITUDE trial is associated with renal and cardiovascular protection, and secondly, whether the reduction in albuminuria was too small to afford clinical benefit. METHODS: In a post hoc analysis of the ALTITUDE trial in 8561 patients with type 2 diabetes and chronic kidney disease or cardiovascular disease we examined the effect of albuminuria changes at 6 months on renal and cardiovascular outcomes using Cox proportional hazard regression. RESULTS: The median change in albuminuria in the first 6 months in the aliskiren arm of the trial was -12% (25th to 75th percentile: -48.7_to_ +41.9%) and 0.0% (25th to 75th percentile: -40.2_to_55%) in the placebo arm. Changes in albuminuria in the first 6 months were linearly associated with renal and cardiovascular endpoints: a >30% reduction in albuminuria in the first 6 months was associated with a 62% reduction in renal risk and a 25% reduction in cardiovascular risk compared with an increase in albuminuria. The association between changes at 6 months in albuminuria and renal or cardiovascular endpoints was similar in the two treatment groups (p for interaction >0.1 for both endpoints). CONCLUSIONS: The addition of aliskiren to angiotensin-converting enzyme inhibitor/angiotensin receptor blocker therapy resulted in albuminuria changes that were associated with renal and cardiovascular risk changes. This did not translate into renal or cardiovascular protection because the overall reduction in albuminuria in the aliskiren arm was too small and nearly similar to that in the placebo arm.

Pulse pressure is not an independent predictor of outcome in type 2 diabetes patients with chronic kidney disease and anemia--the Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT).

Pulse pressure (PP) remains an elusive cardiovascular risk factor with inconsistent findings. We clarified the prognostic value in patients with type 2 diabetes, chronic kidney disease (CKD) and anemia in the Trial to Reduce cardiovascular Events with Aranesp (darbepoetin alfa) Therapy. In 4038 type 2 diabetes patients, darbepoetin alfa treatment did not affect the primary outcome. Risk related to PP at randomization was evaluated in a multivariable model including age, gender, kidney function, cardiovascular disease (CVD) and other conventional risk factors. End points were myocardial infarction (MI), stroke, end stage renal disease (ESRD) and the composite of cardiovascular death, MI or hospitalization for myocardial ischemia, heart failure or stroke (CVD composite). Median (interquartile range) age, gender, eGFR and PP was 68 (60-75) years, 57.3% women, 33 (27-42) ml min(-1) per 1.73 m2 and 60 (50-74) mm Hg. During 29.1 months (median) follow-up, the number of events for composite CVD, MI, stroke and ESRD was 1010, 253, 154 and 668. In unadjusted analyses, higher quartiles of PP were associated with higher rates per 100 years of follow-up of all end points (P⩽0.04), except stroke (P=0.52). Adjusted hazard ratios (95% confidence interval) per one quartile increase in PP were 1.06 (0.99-1.26) for MI, 0.96 (0.83-1.11) for stroke, 1.01 (0.94-1.09) for ESRD and 1.01 (0.96-1.07) for CVD composite. Results were similar in continuous analyses of PP (per 10 mm Hg). In patients with type 2 diabetes, CKD and anemia, PP did not independently predict cardiovascular events or ESRD. This may reflect confounding by aggressive antihypertensive treatment, or PP may be too rough a risk marker in these high-risk patients.

First-in-class angiotensin receptor neprilysin inhibitor in heart failure.

Neprilysin inhibitors augment the natriuretic peptide system by preventing the breakdown of atrial natriuretic peptide and B-type natriuretic peptide. LCZ696, an angiotensin receptor neprilysin inhibitor composed of a neprilysin inhibitor prodrug and the angiotensin receptor antagonist valsartan, has proven effective in hypertension, has shown promise in a pilot trial of heart failure with preserved ejection fraction, and is being tested in a large outcomes trial of heart failure with reduced ejection fraction. A preserved ejection fraction outcomes trial is beginning.

Klinefelter's syndrome (mosaic) with chromosome 9 inv and schizophrenia.

Klinefelter's syndrome is a sex chromosome abnormality with low androgen level. The varied manifestations of the mental symptoms in some of them, that are inexplicable based on their genotype alone, has fascinated the researchers. We present here a case of Klinefelter's syndrome having a karyotype of mos 47, XXY, and also inversion in 9(th) chromosome, with schizophrenia. Despite the view that inv 9 is a normal variant, it is still worthwhile to explore whether it has any role in the etiology of schizophrenia especially when it occurs with other genotypic aberrations that are suspected to have relevance to psychiatric disorders including the Klinefelter's syndrome.

Barriers to advanced education for indigenous Australian health workers: an exploratory study.

INTRODUCTION: Aboriginal Health Workers (AHWs) play a crucial role in the delivery of primary health care services in underserved rural and remote communities throughout Australia. The Mount Isa Centre for Rural and Remote Health (MICRRH), in Northwest Queensland, Australia, has been involved in training AHWs since 2001. During this time, it has been observed that while there has been interest in pursuing further education in other health careers, the uptake for advanced study by AHWs has been minimal. This exploratory study was designed to assess the career aspirations of local AHWs (both qualified and students) as well as community stakeholder views to identify barriers experienced when undertaking advanced education. METHODS: The study used a descriptive and exploratory design. AHWs and key stakeholders were invited to participate. Open-ended interviews were undertaken with nine participants in two communities in the Mount Isa Health Service District in Northwest Queensland, Australia. FINDINGS: While there was some interest expressed in careers like medicine and nursing, the majority of participants indicated a preference for advancement to management or specialist areas as AHWs. In relation to the barriers faced by AHWs and students in continuing study or career advancement, three main themes emerged: support; infrastructure; and promotion.

A prospective evaluation of the angiotensin-converting enzyme D/I polymorphism and left ventricular remodeling in the 'Healing and Early Afterload Reducing Therapy' study.

The D/I (deletion, D, insertion, I) polymorphism of the angiotensin-converting enzyme (ACE) gene has been extensively studied for its association with a number of cardiovascular and other disease states. However, its potential association with differential clinical efficacy of ACE inhibitors (ACE-I) administered to patients who had suffered a myocardial infarction (MI), i.e. the prevention of left ventricular (LV) remodeling, has so far not been specifically studied. The aim of the study was to investigate whether the D/I polymorphism of the ACE gene is associated with the incidence of post-MI LV remodeling in patients drawn from the 'Healing and Early Afterload Reducing Therapy' (HEART) Study. The ACE D/I polymorphism was characterized by the polymerase chain reaction (PCR) in 265 subjects from the 'Healing and Early Afterload Reducing Therapy' Study, a double-blind, placebo-controlled trial with the objective of determining whether early or delayed administration of the ACE-I, ramipril, in patients with acute anterior wall MI would be optimal in reducing LV enlargement. Selected frequencies for the ACE D and I alleles were 0.59 and 0.41 (placebo-high dose group), 0.56 and 0.44 (low dose-low dose group), and, 0.60 and 0.40 (high dose-high dose group), respectively. All observed genotype frequencies were in Hardy-Weinberg equilibrium. There was no evidence for an association between genotype and outcome regarding LV size or function, nor with the initial blood pressure response after ACE-I administration (adjusted for covariates). Our data provide no evidence for an association of the ACE D/I polymorphism with the risk of LV remodeling post-MI in the presence of ACE-I therapy, and therefore do not suggest that differential clinical efficacy of ACE-inhibitors is related to this genetic marker.

Photodynamic therapy with verteporfin for choroidal neovascularization in patients with diabetic retinopathy.

PURPOSE: To report the use of photodynamic therapy (PDT) with verteporfin in three patients with choroidal neovascularization (CNV) from age-related macular degeneration and underlying diabetic retinopathy. The level of diabetic retinopathy would have excluded these patients from participation in previously reported randomized clinical trials evaluating PDT with verteporfin due to a theoretic concern of damage to the overlying retinal vasculature. DESIGN: Retrospective interventional case series. METHODS: Three patients from a referral practice with at least severe nonproliferative diabetic retinopathy and a history of clinically significant macular edema developed loss of vision from concurrent choroidal neovascularization evaluated with fundus photography and fluorescein angiography before and after PDT with verteporfin to identify adverse retinal vascular events. RESULTS: Four eyes in three patients had PDT using verteporfin. Three eyes received two treatments. With short follow-up, visual acuity remained stable in two eyes, improved from 20/400 to 20/320 in one eye, and decreased from 20/200 to 20/400 in one eye. Fluorescein angiograms at intervals from 2 weeks to 3 months after PDT showed no damage to the retinal vasculature or progression of the diabetic retinopathy, but did show a decreased area of fluorescein leakage from CNV. One eye that had new subretinal hemorrhage following treatment appeared to show new vasculopathy on initial evaluation of the post-treatment angiogram. Retrospective review suggested that the subretinal hemorrhage provided increased contrast to more easily visualize vasculopathy that was present before the PDT. CONCLUSIONS: Three patients with diabetic retinopathy undergoing a total of seven PDT treatments with verteporfin in four eyes had no new retinal vascular abnormalities develop. No other atypical responses of CNV to PDT were noted except new subretinal hemorrhage, providing increased contrast of the overlying vasculature, which gave the false impression of the development of new vasculopathy in one eye. Patients with diabetic retinopathy who have concurrent CNV for which PDT with verteporfin is recommended should be cautioned regarding the theoretical concerns of harming the retinal vasculature. Periodic surveillance for such concerns seems warranted until more experience is obtained.

Beyond remodeling: a new paradigm for angiotensin-converting enzyme inhibitors following myocardial infarction.

Angiotensin converting enzyme (ACE) inhibitors, originally designed to treat hypertension, were quickly demonstrated to confer hemodynamic and survival benefit to patients with congestive heart failure. Extending this paradigm to patients with left ventricular dysfunction (LVD) post-myocardial infarction (MI), ACE inhibitors were shown to attenuate ventricular remodeling and reduce mortality. An unexpected finding that ACE inhibitors could reduce the incidence of myocardial infarction, prompted enormous interest in their anti-ischemic potential. Indeed, a significant body of experimental literature supports the concept that ACE inhibitors have direct anti-atherosclerotic and anti-ischemic effect. Recent clinical trials have shown that ACE inhibitors confer significant protection from ischemic events.

Recovery of ventricular function after myocardial infarction in the reperfusion era: the healing and early afterload reducing therapy study.

BACKGROUND: Patients with reduced left ventricular function and ventricular enlargement after myocardial infarction are at significantly greater risk for congestive heart failure and death. Nevertheless, recovery of ventricular function occurs in a significant proportion of patients after myocardial infarction, and modern reperfusion strategies have been associated with increased recovery of function. OBJECTIVE: To determine the extent and predictors of recovery of ventricular function after anterior Q-wave myocardial infarction in the reperfusion era. DESIGN: Subgroup analysis of the Healing and Early Afterload Reducing Therapy study. SETTING: 35 medical centers in the United States and Canada. PATIENTS: 352 patients with Q-wave anterior myocardial infarction. INTERVENTION: Placebo for 14 days, followed by full-dose (10 mg) ramipril until day 90; low-dose (0.625 mg) ramipril for 90 days; or full-dose ramipril for 90 days. All patients underwent reperfusion therapy. MEASUREMENTS: Echocardiography was performed on day 1 (before randomization), day 14, and day 90 after myocardial infarction. Left ventricular volume and ejection fraction were measured and wall-motion analyses were performed at all three time points in 249 patients and at baseline in an additional 12 patients who died during follow-up. Echocardiographic and nonechocardiographic predictors of ventricular recovery were examined. RESULTS: By day 90, 55 of 252 (22%) patients who had abnormal ejection fraction and wall-motion abnormalities on day 1 demonstrated complete recovery of function (ejection fraction in the normal range and infarct segment length of 0%), and an additional 36% (91 of 252 patients) demonstrated partial recovery of function. At 90 days, 53% (132 of 249) of patients had greater than 5% improvement in ejection fraction, whereas only 16% (39 of 249) had a decrease in ejection fraction of more than 5%. The majority of functional improvement occurred by day 14 after infarction. Of various clinical and echocardiographic measures obtained on day 1, peak creatine kinase level was the strongest independent predictor of subsequent recovery of ventricular function in multivariate analysis. Each 100-unit increase in peak creatine kinase was associated with a 4.3% decreased odds of recovery (P < 0.001) after adjustment for ejection fraction on day 1, extent of akinesis or dyskinesis, treatment regimen, Killip class, age, and sex. CONCLUSION: Significant myocardial stunning with subsequent improvement of ventricular function occurred in the majority of patients after Q-wave anterior myocardial infarction. A lower peak level of creatine kinase, an estimate of the extent of necrosis, is independently predictive of recovery of function. Early functional assessment (day 1 after acute myocardial infarction) had limited ability to predict recovery of ventricular function.

Regional wall stress predicts ventricular remodeling after anteroseptal myocardial infarction in the Healing and Early Afterload Reducing Trial (HEART): an echocardiography-based structural analysis.

BACKGROUND: Increased left ventricular (LV) wall stress after myocardial infarction (MI) has been implicated in LV remodeling. However, the relationship between LV wall stress and LV remodeling is incompletely defined. METHOD: We prospectively studied the relationship between regional wall stress and LV remodeling by application of the finite element method to end-systolic LV models from patients enrolled in the Healing and Early Afterload Reducing Therapy (HEART) Trial. Individual LV models were constructed from orthogonal apical echocardiographic views obtained at day 14 after anteroseptal MI in 64 patients. Of these, 31 patients received low-dose (0.625 mg) ramipril and 33 patients received full-dose (10 mg) ramipril. LV wall stress was calculated by the finite element method and correlated with change in LV volume from day 14 to day 90 after MI. RESULTS: Among all patients, increases in apical regional wall stress were associated with LV volume changes (P -trend =.015). The relationship between apical regional wall stress and change in LV volume was strongest in the low-dose ramipril group (r = 0.53, P =.002) and remained significant after adjustment for end-diastolic volume, infarct size, ejection fraction, and systolic blood pressure yet was attenuated in the full-dose ramipril group. CONCLUSIONS: Apical regional wall stress is an independent predictor of subsequent LV remodeling after MI. The relationship between increased apical wall stress and LV dilatation appears to be attenuated by full-dose angiotensin-converting enzyme inhibition.

Temporal dissociation of left ventricular function and remodeling following experimental myocardial infarction in rats.

BACKGROUND: Left ventricular function early after myocardial infarction (MI) predicts subsequent clinical outcome. Nevertheless, the relationship between early changes in left ventricular function and subsequent left ventricular remodeling has not been well defined. METHODS AND RESULTS: To explore the temporal relationship between left ventricular function and remodeling after MI, rats (n = 63) underwent coronary artery ligation with and without reperfusion at 45 or 180 minutes or a sham operation. All animals were followed up by serial echocardiography preligation; 4, 24, and 48 hours; and 1, 2, 3, 4, 6, and 9 weeks after MI. Measures of global left ventricular size and function and regional wall motion were obtained at physiological heart rates. Histological infarct sizes (range, 0% to 52%) were determined in all animals. Within 4 hours of MI, fractional area change (FAC) decreased dramatically in association with an increase in left ventricular systolic cavity area, whereas diastolic area increased more gradually. Early FAC was related to infarct size (r = -0.82; P < .000), predicted the extent of left ventricular enlargement (P = .0001), and remained depressed throughout the duration of follow-up. Regional wall motion excursion and systolic wall thickness decreased in the infarcted and noninfarcted regions in animals with large infarctions. CONCLUSIONS: The rate of left ventricular dilatation after MI in rats is proportional to initial left ventricular function, although left ventricular function remains relatively constant as the ventricle progressively enlarges. Regional myocardial function after a large MI is abnormal in noninfarcted as well as infarcted regions.

Recovery of regional right ventricular function after thrombolysis for pulmonary embolism.

Abnormalities in right ventricular regional and global function can occur in the setting of acute pulmonary embolism. Treatment of acute pulmonary embolism with thrombolysis is associated with significant improvement in regional and global right ventricular function.

Echocardiography-derived left ventricular end-systolic regional wall stress and matrix remodeling after experimental myocardial infarction.

OBJECTIVES: We tested the hypothesis that regional end-systolic left ventricular (ESLV) wall stress is associated with extracellular matrix remodeling activity after myocardial infarction (MI). BACKGROUND: Increased left ventricular (LV) wall stress is a stimulus for LV enlargement, and echocardiography can be used to estimate regional wall stress. A powerful validation of a noninvasive method of estimating wall stress would be predicting cellular responses after a MI. METHODS: Echocardiographic images were obtained in rats 1, 7, 14 or 21 days after coronary ligation (n = 11) or sham surgery (n = 5). End-systolic left ventricular wall stress was calculated by finite element analysis in three regions (infarcted, noninfarcted and border) from short-axis images. Matrix metalloproteinase-9 (MMP-9) and macrophage density were determined by immunohistochemistry, and positive cells were counted in high power fields (hpf). RESULTS: Average ESLV wall stress was higher in rats with MI when compared to shams irrespective of time point (p < 0.01), and ESLV wall stress in the infarcted regions increased with time (25.1 +/- 5.9 vs. 69.9 +/- 4.4 kdyn/cm2, day 1 vs. 21; p < 0.01). Matrix metalloproteinase-9 expression was higher in infarcted and border regions when compared to noninfarcted regions (22.1 vs. 25.7 vs. 0.10 cells/hpf, respectively; p < 0.01). Over all regions, ESLV wall stress was associated with MMP-9 (r = 0.76; p < 0.001), macrophage density (r = 0.72; p < 0.001) and collagen content (r = 0.67; p < 0.001). End-systolic left ventricular wall stress was significantly higher when MMP-9 positive cell density was greater than 10 cells/hpf (45+/-20 vs. 14+/-10 kdyn/cm2; p < 0.001). CONCLUSIONS: Regional increases in ESLV wall stress determined by echocardiography-based structural analysis are associated with extracellular matrix degradation activity.

Ocular manifestations of systemic malignancies.

Ocular manifestations of systemic malignancy are important for both the ophthalmologist and the internist to recognize because they may precede the diagnosis of cancer. This review of the current literature discusses the clinical manifestations, etiology, and potential therapeutic interventions for a group of visual paraneoplastic syndromes, including carcinoma-associated retinopathy and melanoma-associated retinopathy. These conditions are characterized by elevated serum levels of autoantibodies directed against tumor antigen that cross-react with retinal proteins, resulting in rod and cone dysfunction. The clinical presentation, site of origin, frequency, and intraocular distribution of tumors metastatic to the eye are also reviewed.

The mechanism of decrease in dynamic mitral regurgitation during heart failure treatment: importance of reduction in the regurgitant orifice size.

OBJECTIVES: The purpose of this study was to quantify and characterize the regurgitant flow pattern and regurgitant orifice area in patients undergoing therapy for severe heart failure using contemporary echocardiographic techniques. BACKGROUND: Mitral regurgitation may be dynamic in patients with heart failure and ultimately correlate with outcome in a group of patients. METHODS: Fourteen patients with severe heart failure felt to require hemodynamic monitoring for the optimization of medical therapy were enrolled. Two-dimensional and Doppler echocardiograms were performed before and following invasively guided therapy. Hemodynamics and standard echocardiographic dimensions were determined as well as regurgitant volume and regurgitant orifice area derived from color M-mode and Doppler measurements. RESULTS: Invasively guided therapy for heart failure was associated with a reduction in weight, filling pressures of the left and right heart, systemic vascular resistance, and echocardiographic left atrial, left ventricular and mitral annular dimensions. The mitral regurgitant volume decreased from 47+/-27 ml before therapy to 14+/-14 ml after therapy; p < 0.001. While therapy for heart failure markedly attenuated the volume of regurgitation, the pattern of regurgitant flow across the mitral valve was not significantly altered. In contrast, there was no difference in the velocity time integral of the continuous-wave Doppler spectra of mitral regurgitation with therapy (128+/-23 cm to 123+/-25 cm, p = 0.23). In all patients, the regurgitant orifice area decreased with therapy from 0.55+/-0.38 cm2 to 0.21+/-0.20 cm2 (p < 0.001). CONCLUSIONS: Pharmacologic reduction in filling pressure and systemic vascular resistance leads to a reduction in the dynamic mitral regurgitation of heart failure through a reduction in the regurgitant orifice area but not through a change in the gradient across the mitral valve. Reduction of the regurgitant orifice area is likely related to decreased left ventricular volumes and decreased annular distention.