Effect of Cuff Design on Auscultatory and Oscillometric Blood Pressure Measurements

Two-piece blood pressure (BP) cuffs are the historical cuff standard. Use of 1-piece cuffs is increasing. Substituting 1-piece for 2-piece cuffs has an unknown effect on measurement accuracy. We compared these cuff types in a 2-phase study using auscultatory and oscillometric techniques. METHODS Consenting subjects (aged ≥18 years) with BP levels between 80 and 220mm Hg/50 and 120mm Hg and arm circumferences between 25 and 43cm were studied using the International Standards Organization (ISO) 2013 protocol (modified). A Baum 2-piece cuff was used as the refer ence standard. A 1-piece Welch Allyn cuff was the comparator. In phase 1 (2-observer auscultation with a mercury sphygmomanometer), 88 sub jects were required to obtain 255 paired BP determinations. In phase 2 (oscillometric measurement with a Spacelabs 90207 device), 85 subjects were studied. Each phase was analyzed separately using paired t-tests. RESULTS Phase 1 mean age was 54.2±20.5 years, mean arm circumference was 29.9±3.7cm, 60% were female, and 32% had hypertension. One-piece cuff mean BPs were lower than the 2-piece cuff means (115.5±15.5/66.4±9.3 vs. 117.8±15.2/67.9±9.2; difference of −2.4±3.6/−1.5±2.4; P values <0.0001 for systolic and diastolic com parisons). Phase 2 mean age was 52.8±20.8 years, mean arm circumfer ence was 29.4±3.9cm, 67% were female, and 38% had hypertension. Mean BPs were lower for the 1-piece compared to the 2-piece cuff (116.5±12.8/67.1±8.1 vs. 120.8±13.5/70.4±8.5; difference of −4.4±3.6/−3.3±2.7; P values <0.0001 for both). CONCLUSIONS Mean BP is lower with 1-piece cuffs vs. 2-piece cuffs. Differences are greater with oscillometry. When performing validation studies and measurements for clinical purposes, cuff type should be taken into account.Scopu

Dilated cardiomyopathy-mediated heart failure induces a unique skeletal muscle myopathy with inflammation

Abstract Background Skeletal muscle myopathy and exercise intolerance are diagnostic hallmarks of heart failure (HF). However, the molecular adaptations of skeletal muscles during dilated cardiomyopathy (DCM)-mediated HF are not completely understood. Methods Skeletal muscle structure and function were compared in wild-type (WT) and cardiac myosin binding protein-C null mice (t/t), which develop DCM-induced HF. Cardiac function was examined by echocardiography. Exercise tolerance was measured using a graded maximum treadmill running test. Hindlimb muscle function was assessed in vivo from measurements of plantar flexor strength. Inflammatory status was evaluated from the expression of inflammatory markers and the presence of specific immune cell types in gastrocnemius muscles. Muscle regenerative capacityat days 3, 7, and 14 after eccentric contraction-induced injury was determined from the number of phenotypically new and adult fibers in the gastrocnemius, and functional recovery of plantar flexion torque. Results t/t mice developed DCM-induced HF in association with profound exercise intolerance, consistent with previous reports. Compared to WT, t/t mouse hearts show significant hypertrophy of the atria and ventricles and reduced fractional shortening, both systolic and diastolic. In parallel, the skeletal muscles of t/t mice exhibit weakness and myopathy. Compared to WT, plantar flexor muscles of t/t null mice produce less peak isometric plantar torque (Po), develop torque more slowly (+ dF/dt), and relax more slowly (− dF/dt, longer half-relaxation times,1/2RT). Gastrocnemius muscles of t/t mice have a greater number of fibers with smaller diameters and central nuclei. Oxidative fibers, both type I and type IIa, show significantly smaller cross-sectional areas and more central nuclei. These fiber phenotypes suggest ongoing repair and regeneration under homeostatic conditions. In addition, the ability of muscles to recover and regenerate after acute injury is impaired in t/t mice. Conclusions Our studies concluded that DCM-induced HF induces a unique skeletal myopathy characterized by decreased muscle strength, atrophy of oxidative fiber types, ongoing inflammation and damage under homeostasis, and impaired regeneration after acute muscle injury. Furthermore, this unique myopathy in DCM-induced HF likely contributes to and exacerbates exercise intolerance. Therefore, efforts to develop therapeutic interventions to treat skeletal myopathy during DCM-induced HF should be considered