Background. Optimal timing of cardiac transplantation in ambulatory patients with severe left ventricular dysfunction is often difficult. To determine whether measurement of peak oxygen consumption (Vo2) during maximal exercise testing can be used to identify patients in whom transplantation can be safely deferred, we prospectively performed exercise testing on all ambulatory patients referred for transplant between October 1986 and December 1989. Methods and Results. Patients were assigned into one of three groups on the basis of exercise data: Group 1 (n=35) comprised patients accepted for transplant (Vo2<14 ml/kg/min); group 2 (n=52) comprised patients considered too well for transplant (Vo2>14 ml/kg/min); and group 3 (n=27) comprised patients with low Vo2 rejected for transplant due to noncardiac problems. All three groups were comparable in New York Heart Association functional class, ejection fraction, and cardiac index (p=NS). Pulmonary capillary wedge pressure was significantly lower in group 2 than in either group 1 or 3 (p<0.05), although there was wide overlap. Patients with preserved exercise capacity (group 2) had cumulative 1-and 2-year survival rates of 94% and 84%, which are equal to survival levels after transplantation. In contrast, patients rejected for transplant (group 3) had survival rates of only 47% at 1 year and 32% at 2 years, whereas patients awaiting transplantation (group 1) had a survival rate of 790% at 1 year (both p <0.005 versus patients with Vo2> 14 ml/kg/min). All deaths in group 2 were sudden. By univariate and multivariate analyses, peak Vo2 was the best predictor of survival, with only pulmonary capillary wedge pressure providing additional prognostic information.Conclusions. These data suggest that cardiac transplantation can be safely deferred in ambulatory patients with severe left ventricular dysfunction and peak exercise Vo2 of more than 14 ml/min/kg. (Circulation 1991;83:778-786)

These findings indicate that patients with chronic HF frequently develop significant skeletal muscle atrophy and metabolic abnormalities. Atrophy contributes modestly to both the reduced exercise capacity and altered muscle metabolism.

Carpal tunnel syndrome (CTS) is a common clinical problem and frequently requires surgical therapy. The results of electrodiagnostic (EDX) studies have been found to be highly sensitive and specific for the diagnosis of CTS. This document defines the standards, guidelines, and options for EDX studies of CTS based on a critical review of the literature published in 1993 1 and recently updated by a review of the literature through the year 2000.2 The reader is referred to the updated review 2 for a detailed discussion of the literature and the EDX techniques for the assessment of CTS that are summarized here. Both reviews addressed the following key clinical questions:

Patients with heart failure frequently exhibit abnormal skeletal muscle metabolic responses to exercise, as assessed with 31P NMR. To investigate whether these metabolic abnormalities are due to intrinsic skeletal muscle changes, we performed gastrocnemius muscle biopsies on 22 patients with heart failure (peak Vo2, 15.4±4.7 ml/kg/min; ejection fraction, 20±7%) and on eight normal subjects. Biopsies were analyzed for fiber type and area, capillarity, citrate synthase, phosphofructokinase, lactate dehydrogenase, and ,B-hydroxyacyl CoA dehydrogenase activity. All patients with heart failure also underwent 31P NMR studies of their calf muscle during plantarflexion at three workloads. Muscle pH responses and the relation of the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) to systemic Vo2 were then evaluated.Compared with normal subjects, patients with heart failure exhibited a shift in fiber distribution with increased percentage of the fast twitch, glycolytic, easily fatigable type Ilb fibers (normal subjects, 22.7± 10.1; heart failure, 33.1 ± 1. 1%; p <0.05), atrophy of type lla (normal subjects, 5,477±1,109; heart failure, 4,239±1,247 ALm2; p<0.05) and type lIb fibers (normal subjects, 5,957±1,388; heart failure, 4,144±945 um2; p<0.01), and decreased activity of j-hydroxyacyl CoA dehydrogenase (normal subjects, 5.17±1.44; heart failure, 3.67±1.68 mol/kg protein/hr; p<0.05). No significant linear correlation could be identified between the slope of the Pi/PCr to Vo2 relation and muscle histochemistry or enzyme activities. Similarly, no linear relation was found between intracellular pH at peak exercise and any muscle variable. These data suggest that patients with heart failure develop intrinsic skeletal muscle changes but that these intrinsic muscle changes do not contribute significantly to the abnormal skeletal muscle 31P NMR metabolic responses observed in such patients. (Circulation 1989;80:1338-1346 E xertional fatigue in patients with heart failure has traditionally been attributed to skeletal muscle underperfusion. However, recent investigations suggest that intrinsic skeletal muscle abnormalities may be operative, as well. Abnormal forearm 31P NMR responses to forearm exercise in patients with heart failure have been

SUMMARY End-systolic left ventricular (LV) meridional wall stress is a quantitative index of true myocardial afterload that can be plotted against LV end-systolic diameter to give an index of contractility independent of loading conditions. We developed a noninvasive method for estimating end-systolic LV meridional wall stress based on M-mode LV echographic end-systolic diameter (LVID) and posterior wall thickness (PWT) and cuff systolic arterial pressure and compared it to simultaneous invasive LV wall stress derived from micromanometer LV pressure recordings and continuously digitized echograms in 12 subjects (four with atypical chest pain, six with severe aortic regurgitation (AR) and two with congestive cardiomyopathy), before and after load manipulation with nitroprusside, nitroglycerin, phenylephrine or saline. Cuff systolic pressure correlated well with end-systolic LV micromanometer pressure (r = 0.89, n = 31, range 96-160 mm Hg) and noninvasive end-systolic stress (0.334 P(LVID)/PWT [1 + PWT/LVID]) correlated extremely well with invasive stress (r = 0.97, n = 31, range 36-213 X 109 dyn/cm2). Invasive and noninvasive slopes (r = 0.91, n = 7) and LVID intercepts (r 0.89, n = 7) of the stress-diameter plots also correlated well. Noninvasive stressdiameter plots in nine normal subjects showed a range of slopes of 50-93 X 101 dyn/cm and intercepts of 1.8-2.8 cm. Mean basal end-systolic noninvasive stress in 22 normal subjects (64.8 ± 19.5 X 10W dyn/cm2) and 14 treated hypertensives (56.3 ± 26.7 X 103 dyn/cm2) was significantly lower than in nine patients with symptomatic aortic regurgitation who had reduced ejection fraction (142.2 ± 53.2 X 10o dyn/cm2,p < 0.01) or four patients with congestive cardiomyopathy (187.3 ± 49.8 X 103 dyn/cm2, p < 0.01), while a mild elevation of stress in symptomatic aortic regurgitation with normal ejection fraction was not statistically significant (91.1 ± 20.7 X 103 dyn/cm2, n = 6). Thus, afterload excess contributed to ejection fraction reduction. We conclude that end-systolic stress may be determined noninvasively and may be a useful approach to quantitation of LV afterload and contractility.LEFT VENTRICULAR (LV) systolic function is the product of the interaction of four variables: myocardial contractile state, end-diastolic myocardial length, afterload and LV myocardial mass.1 Clinical ejection phase indexes, such as ejection fraction or velocity of circumferential fiber shortening, cannot determine the relative contribution of each of these variables to LV pump dysfunction in a given heart. Therefore, methods are needed to quantitate each of the fundamental variables using noninvasive techniques. There are well-characterized noninvasive methods for estimating LV diameter, wall thickness, chamber volume and myocardial mass,2 6 but quantitation of afterload and contractility remain a challenge.Recent studies have examined the use of the endsystolic force-length relationship to characterize myocardial contractility.7-' This relationship can be plotted using LV end-systolic p...