Enhanced American College of Cardiology/American Heart Association Strategy for Prevention of Sudden Cardiac Death in High-Risk Patients With Hypertrophic Cardiomyopathy.

Importance: Strategies for reliable selection of high-risk patients with hypertrophic cardiomyopathy (HCM) for prevention of sudden cardiac death (SCD) with implantable cardioverter/defibrillators (ICDs) are incompletely resolved. Objective: To assess the reliability of SCD prediction methods leading to prophylactic ICD recommendations to reduce the number of SCDs occurring in patients with HCM. Design, Setting, and Participants: In this observational longitudinal study, 2094 predominantly adult patients with HCM consecutively evaluated over 17 years in a large HCM clinical center were studied. All patients underwent prospective ICD decision making relying on individual major risk markers derived from the HCM literature and an enhanced American College of Cardiology/American Heart Association (ACC/AHA) guidelines-based risk factor algorithm with complete clinical outcome follow-up. Data were collected from June 2017 to February 2018, and data were analyzed from February to July 2018. Main Outcomes and Measures: Arrhythmic SCD or appropriate ICD intervention for ventricular tachycardia or ventricular fibrillation. Results: Of the 2094 study patients, 1313 (62.7%) were male, and the mean (SD) age was 51 (17) years. Of 527 patients with primary prevention ICDs implanted based on 1 or more major risk markers, 82 (15.6%) experienced device therapy-terminated ventricular tachycardia or ventricular fibrillation episodes, which exceeded the 5 HCM-related SCDs occurring among 1567 patients without ICDs (0.3%), including 2 who declined device therapy, by 49-fold (95% CI, 20-119; P = .001). Cumulative 5-year probability of an appropriate ICD intervention was 10.5% (95% CI, 8.0-13.5). The enhanced ACC/AHA clinical risk factor strategy was highly sensitive for predicting SCD events (range, 87%-95%) but less specific for identifying patients without SCD events (78%). The C statistic calculated for enhanced ACC/AHA guidelines was 0.81 (95% CI, 0.77-0.85), demonstrating good discrimination between patients who did or did not experience an SCD event. Compared with enhanced ACC/AHA risk factors, the European Society of Cardiology risk score retrospectively applied to the study patients was much less sensitive than the ACC/AHA criteria (34% [95% CI, 22-44] vs 95% [95% CI, 89-99]), consistent with recognizing fewer high-risk patients. Conclusions and Relevance: A systematic enhanced ACC/AHA guideline and practice-based risk factor strategy prospectively predicted SCD events in nearly all at-risk patients with HCM, resulting in prophylactically implanted ICDs that prevented many catastrophic arrhythmic events in this at-risk population.

Physiotherapists and Physiotherapy Student Placements across Regions in Ontario: A Descriptive Comparison.

PURPOSE: To describe the distribution and type of physiotherapy student placements in one year relative to the number of practising physiotherapists of Ontario. METHODS: Site information about physiotherapy students' clinical placements in Ontario in 2010 was obtained from Academic Coordinators of Clinical Education. Worksite information about physiotherapists who reported providing direct patient care at a primary employment site in Ontario and at least 600 practice hours in their annual renewal was obtained from the College of Physiotherapists of Ontario. Each placement and each physiotherapist was attributed to one of Ontario's 14 local health integration networks (LHINs). For each LHIN, a ratio of student placements to practising physiotherapists was calculated, using summed counts. Counts of placement types by setting, patient mix, and practice area were also calculated for each LHIN. RESULTS: The 5 LHINs in which the university programmes are located had high placement:physiotherapist ratios, from 0.92 to 0.38. The other 9 LHINs had lower ratios, the 3 lowest at approximately 0.15. There was a wide mix of clinical placement types across LHINs. CONCLUSION: Physiotherapists' participation in physiotherapy students' clinical education varied widely among Ontario regions. Future research could explore whether regional differences are persistent, why they occur, and whether they should be reduced.

Objectif : Mesurer la répartition et décrire le type de stages des étudiants en physiothérapie en une année, comparativement au nombre de physiothérapeutes en exercice en Ontario. Méthode : Les renseignements sur les lieux des stages des étudiants en physiothérapie en Ontario en 2010 ont été obtenus en faisant appel aux coordonnateurs de l'enseignement clinique des universités. Les renseignements sur les milieux de travail des physiothérapeutes qui ont dit offrir des soins directement aux patients dans un établissement de soins de santé primaires en Ontario et qui comptent au moins 600 heures de pratique lors de leur renouvellement annuel ont été obtenus auprès du College of Physiotherapists of Ontario. Chaque stage et chaque physiothérapeute ont été attribués à l'un des 14 Réseaux locaux d'intégration des soins de santé (RLISS) de l'Ontario. Pour chaque RLISS, un rapport entre le nombre de stages étudiants et le nombre de physiothérapeutes en exercice a été calculé à l'aide du total cumulé de chacun. Le nombre de stages d'un type précis par établissement, par type de patients et par domaine de pratique a aussi été calculé pour chaque RLISS. Résultats : Les cinq RLISS situés dans la même région où sont offerts les programmes universitaires affichaient un fort taux de stages: le rapport par physiothérapeute y variait de 0,92 à 0,38. Les neuf autres RLISS affichaient des rapports moins élevés, et les trois RLISS comportant le rapport le plus faible affichaient un coefficient de 0,15. On a dénombré un ensemble très varié de types de stages à travers les différents RLISS. Conclusion : En Ontario, la participation des physiothérapeutes à la formation clinique des étudiants en physiothérapie varie d'une région à l'autre. Des recherches futures pourraient se pencher sur les différences entre les régions et voir si ces différences sont persistantes, pourquoi elles surviennent et s'il serait important de les atténuer.

Effect of atenolol vs metoprolol succinate on vascular function in patients with hypertension.

BACKGROUND: We evaluated the effect of atenolol vs metoprolol succinate on vascular function in patients with essential hypertension. HYPOTHESIS: Given intrinsic differences between these agents, we hypothesized that atenolol and metoprolol succinate would have disparate effects on vascular function. METHODS: This study included 24 patients with hypertension (age 56 ± 2 years, 8 female, body mass index 28 ± 1) and featured a randomized, double-blind, crossover design. Each ß-blocker (atenolol or metoprolol succinate) was taken by patients once daily for a 4-week period. Measures of vascular function included peripheral augmentation index (AIx) and pulse wave amplitude reactive hyperemia index from peripheral arterial tonometry, and brachial artery flow-mediated dilation from ultrasound. RESULTS: There were similar reductions in mean arterial pressure following treatment with atenolol and metoprolol succinate. Compared with metoprolol succinate, there was a significant increase in peripheral AIx following atenolol therapy (P < 0.05). There were no changes in brachial artery flow-mediated dilation or pulse wave amplitude reactive hyperemia index following either drug treatment. CONCLUSIONS: Although atenolol and metoprolol succinate have similar effects on blood-pressure reduction, they have different effects on vascular function. Compared with metoprolol succinate, atenolol increases peripheral AIx. Neither drug has an effect on vascular endothelial function. These findings may have clinical implications, depending on the indication for treatment in an individual patient.

A developmental perspective on congenital muscular torticollis: a critical appraisal of the evidence.

PURPOSE: The aims of this review were to (1) identify and evaluate research evidence regarding the developmental outcomes of infants with congenital muscular torticollis (CMT) and (2) critically appraise and compare the outcomes of interventions targeting neck muscle extensibility and strength with those considering neck muscle function within the broader context of global infant development. SUMMARY: An association between CMT and early developmental delay is supported by levels 3B, 4, and 5 evidence; no evidence was found of longer-term influences of CMT on the development of perceptual, cognitive, and motor skills. The effectiveness of passive manual stretching is supported by levels 2A, 3B, 4, and 5 evidence; no clear evidence was found of the effectiveness of developmentally supportive interventions. CONCLUSION: Controlled studies are needed to clarify the developmental consequences of CMT.

Pulse wave amplitude is associated with brachial artery diameter: implications for gender differences in microvascular function.

The ratio of pulse wave amplitude (PWA) during reactive hyperemia compared to baseline as measured by peripheral arterial tonometry (PAT) is a non-invasive measure of microvascular endothelial function referred to as the pulse wave amplitude reactive hyperemia index (PWA-RHI). Whether upstream conduit vessel structure may affect downstream resistance vessel PWA has not been clearly examined. We tested the hypothesis that digital PWA is influenced by brachial artery diameter (BAD) and that this association would influence comparison of PWA-RHI between genders. Measures of vascular structure and microvascular function were carried out in 115 patients varying in cardiovascular risk profiles (average age 57 years, male n = 79, CAD n = 43). PWA was assessed using plethysmography at baseline and following 5 minutes of brachial artery occlusion. BAD was assessed using high-resolution ultrasonography. Results : There was a negative association between BAD and PWA-RHI ( r = -0.34, p < 0.05). Women had greater PWA-RHI and smaller BAD compared with men (p < 0.05). When co-varying for BAD, there were no longer gender differences in PWA-RHI. Moreover, when a sub-group of men and women without CAD (n = 40), matched for BAD, were examined, there were no gender differences in PWA-RHI. In conclusion, PWA-RHI obtained from PAT is associated with BAD. Studies examining gender differences in microvascular endothelial function with PAT may need to correct for BAD as a potential confounder.

Extended-release niacin reduces LDL particle number without changing total LDL cholesterol in patients with stable CAD.

BACKGROUND: The importance of the number of circulating low-density lipoprotein (LDL) cholesterol particles, in addition to total LDL level, has been increasingly recognized. The effects of extended-release niacin (ERN) on LDL particle numbers have not been studied. OBJECTIVE: To evaluate ERN's effects on LDL particle numbers. METHODS: Fifty-four patients with stable coronary artery disease (CAD) and well-controlled LDL levels were randomly assigned to 3 months of ERN (1 g/day) or placebo in addition to their baseline medications. Lipoprotein particle number was analyzed by proton nuclear magnetic resonance spectroscopy at baseline and after 3 months. RESULTS: Compared to baseline, the addition of ERN had no significant effect on total LDL cholesterol levels; however, ERN decreased the number of medium and small LDL particles (P < .005). After 3 months, ERN decreased the number of medium and small LDL particles compared to placebo-treated patients (P < .05). ERN raised HDL cholesterol levels by 2.7%, significantly increased the number of large HDL particles (P < .001), and decreased the number of small HDL particles (P = .027) compared to placebo. There were no significant changes in lipid values or particle numbers in the placebo-treated patients. In patients with stable coronary artery disease and well-controlled LDL cholesterol levels, ERN reduced the number of circulating particles of the more atherogenic subtypes of LDL, despite having no effect on total LDL cholesterol levels. ERN also favorably altered the number of HDL particles. CONCLUSION: ERN-induced alterations in lipoprotein particle numbers may contribute to its anti-atherosclerotic effects, and these effects may not be evident from the standard lipid profile.

Assessment of peripheral vascular endothelial function in the ambulatory setting.

Until now, peripheral vascular endothelial function testing has been performed in research laboratories under highly controlled conditions, thus limiting its clinical applicability. In this study, we evaluated endothelial function in two peripheral vascular beds before and during reactive hyperemia in an outpatient clinic setting. The brachial artery was imaged with a portable ultrasound device and changes in vessel diameter were expressed as percent flow-mediated dilation (%FMD). Pulse wave amplitude of the finger was detected by peripheral arterial tonometry (PAT) and PAT hyperemia was defined as the maximal plethysmographic recording compared to baseline. Sixty individuals (43 men) were enrolled with an average age 53 +/- 2 years (mean +/- SE). The 31 individuals with more than two cardiac risk factors (CRF) had lower FMD (7.0 +/- 1.1%) and PAT hyperemia (2.1 +/- 0.9) compared to the 29 individuals with 0-2 CRF (FMD 11.3 +/- 0.8%, PAT hyperemia 2.4 +/- 0.1; p < 0.05 for both). The 32 individuals with coronary artery disease (CAD) had lower FMD (6.8 +/- 1.1%) and PAT hyperemia (2.0 +/- 0.1) compared to the 28 individuals without CAD (FMD 11.5 +/- 0.8%, PAT hyperemia 2.4 +/- 0.1; p < 0.05 for both). Thus, peripheral vascular endothelial function testing in the ambulatory setting correlates with the extent of CAD risk and the presence or absence of CAD. In conclusion, these data suggest that peripheral vascular endothelial function testing is feasible in ambulatory patients, and this is an important next step in bringing this technology to clinical applicability.

Effects of extended-release niacin on lipoprotein particle size, distribution, and inflammatory markers in patients with coronary artery disease.

In this study, niacin was added to existing therapy for 3 months in 54 subjects with stable coronary artery disease. Average total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglyceride levels were similar between groups. Three months of niacin treatment increased total HDL by 7.5% and decreased triglycerides by 15% compared with baseline values (p <0.005 for each), whereas total cholesterol and LDL levels remained unchanged. Addition of niacin resulted in a 32% increase in large-particle HDL (p <0.001), an 8% decrease in small-particle HDL (p = 0.0032), an 82% increase in large-particle LDL (p = 0.09), and a 12% decrease in small-particle LDL (p = 0.008). Niacin decreased lipoprotein-associated phospholipase A2 and C-reactive protein levels (20% and 15%, respectively, p <0.05 for the 2 comparisons). No significant changes from baseline were seen in any tested parameter in subjects who received placebo. In conclusion, addition of niacin to existing medical regimens for patients with coronary artery disease and already well-controlled LDL levels favorably improves the distribution of lipoprotein particle sizes and inflammatory markers in a manner that would be expected to confer atheroprotection. The effect of altering lipoprotein particle distribution and inflammatory markers on surrogate markers of atherosclerosis and clinical cardiovascular events in this population remains unclear.