The use of real-time ultrasound imaging for biofeedback of lumbar multifudus muscle contraction in healthy subjects

Study Design: Randomized controlled trial. Objective: To determine if the provision of visual biofeedback using real-time ultrasound imaging enhances the ability to activate the multifidus muscle. Background: Increasingly clinicians are using real-time ultrasound as a form of biofeedback when re-educating muscle activation. The effectiveness of this form of biofeedback for the multifidus muscle has not been reported. Methods and Measures: Healthy subjects were randomly divided into groups that received different forms of biofeedback. All subjects received clinical instruction on how to activate the multifidus muscle isometrically prior to testing and verbal feedback regarding the amount of multifidus contraction, which occurred during 10 repetitions (acquisition phase). In addition, 1 group received visual biofeedback (watched the multifidus muscle contract) using real-time ultrasound imaging. All subjects were reassessed a week later (retention phase). Results: Subjects from both groups improved their voluntary contraction of the multifidus muscle in the acquisition phase (P

Alterations in dihydropyridine receptors in dystrophin-deficient cardiac muscle

The deficiency of dystrophin, a critical membrane stabilizing protein, in the mdx mouse causes an elevation in intracellular calcium in myocytes. One mechanism that could elicit increases in intracellular calcium is enhanced influx via the L-type calcium channels. This study investigated the effects of the dihydropyridines BAY K 8644 and nifedipine and alterations in dihydropyridine receptors in dystrophin-deficient mdx hearts. A lower force of contraction and a reduced potency of extracellular calcium (P < 0.05) were evident in mdx left atria. The dihydropyridine agonist BAY K 8644 and antagonist nifedipine had 2.7- and 1.9-fold lower potencies in contracting left atria (P < 0.05). This corresponded with a 2.0-fold reduction in dihydropyridine receptor affinity evident from radioligand binding studies of mdx ventricular homogenates (P < 0.05). Increased ventricular dihydropyridine receptor protein was evident from both radioligand binding studies and Western blot analysis and was accompanied by increased mRNA levels (P < 0.05). Patch-clamp studies in isolated ventricular myocytes showed no change in L-type calcium current density but revealed delayed channel inactivation (P < 0.05). This study indicates that a deficiency of dystrophin leads to changes in dihydropyridine receptors and L-type calcium channel properties that may contribute to enhanced calcium influx. Increased influx is a potential mechanism for the calcium overload observed in dystrophin-deficient cardiac muscle.

Identification of a novel frameshift mutation in the giant muscle filament titin in a large Australian family with dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is an etiologically heterogeneous cardiac disease characterized by left ventricular dilation and systolic dysfunction. Approximately 25-30% of DCM patients show a family history of mainly autosomal dominant inheritance. We and others have previously demonstrated that mutations in the giant muscle filament titin (TTN) can cause DCM. However, the prevalence of titin mutations in familial DCM is unknown. In this paper, we report a novel heterozygous 1-bp deletion mutation (c.62890delG) in TTN that cosegregates with DCM in a large Australian pedigree (A3). The TTN deletion mutation c.62890delG causes a frameshift, thereby generating a truncated A-band titin due to a premature stop codon (p.E20963KfsX10) and the addition of ten novel amino acid residues. The clinical phenotype of DCM in kindred A3 demonstrates incomplete penetrance and variable expressivity. Finally, protein analysis of a skeletal muscle biopsy sample from an affected member did not reveal the predicted truncated titin isoform although the aberrant mRNA was present, suggesting posttranslational modification and degradation of the truncated protein. The identification of a novel disease-causing mutation in the giant titin gene in a third large family with DCM indicates that mutations in titin may account for a significant portion of the genetic etiology in familial DCM.

Prognostic value of intraventricular dyssynchrony according to clinical stage of left ventricular impairment

Intraventricular dyssynchrony has prognostic implications in patients who have severe functional limitation and decreased ejection fraction. Patients with less advanced cardiac disease often exhibit intraventricular dyssynchrony, but there is little available information about its prognostic relevance in such patients. We investigated the prognostic effect of intraventricular dyssynchrony on outcome in 318 patients with known or suspected coronary artery disease who were classified according to the presence or absence of left ventricular dysfunction and heart failure symptoms. Mortality was considered the primary end point over a median follow-up of 56 months, and a Cox proportional hazards model was used for survival analysis. Despite a low prevalence (8%) of left bundle branch block, there was a high prevalence of intraventricular dyssynchrony even in patients without symptomatic heart failure. The magnitude of intraventricular dyssynchrony correlated poorly with QRS duration (r = 0.25),end-systolic volume index (r = 0.27), and number of scar segments (r = 0.25). There,were 58 deaths during follow-up. Ventricular volume, ischemic burden, and magnitude of intraventricular dyssynchrony predicted outcome, but magnitude of intraventricular dyssynchrony was an independent predictor of survival only in patients with asymptomatic left ventricular dysfunction. In conclusion, patients with known or suspected coronary artery disease have a high prevalence of intraventricular dyssynchrony. Although ventricular volume, ischemic burden, and intraventricular dyssynchrony are potentially important prognostic markers, the relative importance of intraventricular dyssynchrony changes with the clinical setting and, may be greatest-in patients with preclinical disease. (c) 2006 Elsevier Inc. All rights reserved.

Prevalence of heart failure and systolic ventricular dysfunction in older Australians: the Canberra Heart Study

Objective: To estimate the prevalence of heart failure (HF) and left ventricular (LV) systolic dysfunction in a population-based sample of older Australians. Design, setting and participants: A cross-sectional survey of 2000 randomly selected residents of Canberra, aged 60-86 years, conducted between February 2002 and June 2003. Participants were assessed by history, physical examination by a cardiologist, and echocardiography. Main outcome measures: Age- and sex-specific prevalence rates of clinical HF and LV systolic dysfunction (defined as LV ejection fraction

Characteristics of left ventricular diastolic dysfunction in the community: an echocardiographic survey

Objective: To determine the prevalence and predictors of left ventricular (LV) diastolic dysfunction in older adults. Design, setting and participants: A cross-sectional survey of 1275 randomly selected residents of Canberra, aged 60 to 86 years (mean age 69.4; 50% men), conducted between February 2002 and June 2003. Main outcome measures: Prevalence of LV diastolic dysfunction as characterised by comprehensive Doppler echocardiography. Results: The prevalence of any diastolic dysfunction was 34.7% (95% CI 32.1% to 37.4%) and that of moderate to severe diastolic dysfunction was 7.3% (95% CI 5.9% to 8.9%). Of subjects with moderate to severe diastolic dysfunction, 77.4% had an LV ejection fraction (EF) > 50% and 76.3% were in a preclinical stage of disease. Predictors of diastolic dysfunction were higher age (p < 0.0001), reduced EF (p < 0.0001), obesity (p < 0.0001) and a history of hypertension (p < 0.0001), diabetes (p = 0.02) and myocardial infarction (p = 0.003). Moderate to severe diastolic dysfunction with normal EF, although predominantly preclinical, was independently associated with increased LV mass (p < 0.0001), left atrial volume (p < 0.0001), and circulating amino-terminal pro-B-type natriuretic peptide concentrations (p < 0.0001), and with decreased quality of life (p < 0.005). Conclusion: Diastolic dysfunction is common in the community and often unaccompanied by overt congestive heart failure. Despite the lack of symptoms, advanced diastolic dysfunction with normal EF is associated with reduced quality of life and structural abnormalities that reflect increased cardiovascular risk.

Association of subclinical right ventricular dysfunction with obesity

OBJECTIVES The purpose of this research was to identify the determinants of right ventricular (RV) dysfunction in overweight and obese subjects. BACKGROUND Right ventricular dysfunction in obese subjects is usually ascribed to comorbid diseases, especially obstructive sleep apnea. We used tissue Doppler imaging to identify the determinants of RV dysfunction in overweight and obese subjects. METHODS Standard and tissue Doppler echocardiography was performed in 112 overweight (body mass index [BMI] 25 to 29.9 kg/m(2)) or obese (BMI >30 kg/m(1)) subjects and 36 referents (BMI 35 kg/m(2) had reduced RV function compared with referent subjects, evidenced by reduced s(m) (6.5 +/- 2.4 cm/s vs. 10.2 +/- 1.5 cm/s, p < 0.001), peak strain (-21 +/- 4% vs. -28 +/- 4%, p < 0.001), peak strain rate (-1.4 +/- 0.4 s(-1) vs. -2.0 +/- 0.5 s(-1), p < 0.001), and e(m) (6.8 +/- 2.4 cm/s vs. -10.3 +/- 2.5 cm/s, p < 0.001), irrespective of the presence of sleep apnea. Similar but lesser degrees of reduced systolic function (p < 0.05) were present in overweight (BMI 25 to 29.9 kg/m(2)) and mildly obese (BMI 30 to 35 kg/m(2)) groups. Differences in RV e(m), s(m), and strain indexes were demonstrated between the severely versus overweight and mildly obese groups (p < 0.05). Body mass index remained independently related to RV changes after adjusting for age, log insulin, and mean arterial pressures. In obese patients, these changes were associated with reduced exercise capacity but not the duration of obesity and presence of sleep apnea or its severity. CONCLUSIONS Increasing BMI is associated with increasing severity of RV dysfunction in overweight and obese subjects without overt heart disease, independent of sleep apnea.

Measuring and predicting the dynamics of linear monodisperse entangled polymers in rapid flow through an abrupt contraction. A small angle neutron scattering study

Small-angle neutron scattering measurements on a series of monodisperse linear entangled polystyrene melts in nonlinear flow through an abrupt 4:1 contraction have been made. Clear signatures of melt deformation and subsequent relaxation can be observed in the scattering patterns, which were taken along the centerline. These data are compared with the predictions of a recently derived molecular theory. Two levels of molecular theory are used: a detailed equation describing the evolution of molecular structure over all length scales relevant to the scattering data and a simplified version of the model, which is suitable for finite element computations. The velocity field for the complex melt flow is computed using the simplified model and scattering predictions are made by feeding these flow histories into the detailed model. The modeling quantitatively captures the full scattering intensity patterns over a broad range of data with independent variation of position within the contraction geometry, bulk flow rate and melt molecular weight. The study provides a strong, quantitative validation of current theoretical ideas concerning the microscopic dynamics of entangled polymers which builds upon existing comparisons with nonlinear mechanical stress data. Furthermore, we are able to confirm the appreciable length scale dependence of relaxation in polymer melts and highlight some wider implications of this phenomenon.