Lower muscle endurance in patients with alcoholic liver disease.

Patients with alcoholic liver disease often complain of restricted physical capacity, which could be due to decreased muscle endurance. The aim of this study was to assess the muscular endurance in patients with alcoholic liver disease. In a cross sectional study, 24 patients with alcoholic liver disease and 22 controls were evaluated using isometric dynamometry. Endurance was determined during contractions for 3 min elicited by intermittent external electrical stimuli to the femoral quadriceps muscle. Second, endurance was evaluated during voluntary contractions by performance of a maximal isometric knee extension maintained for 1.5 min. Although no difference between patients and controls was found for voluntary contractions, the patients did have lower involuntary muscular endurance. Muscular endurance was not related to lean body mass. Maximal voluntary isometric muscle strength and total work of knee extensors were almost halved in the patients and lower also after correction for differences in lean body mass. In addition to low-muscle strength, patients with alcoholic liver disease have lower involuntary isometric muscular endurance unrelated to lean body mass.

Magnesium supplementation and muscle function in patients with alcoholic liver disease: a randomized, placebo-controlled trial.

OBJECTIVE: The study was undertaken in order to evaluate the effect of magnesium (Mg) supplementation on muscle contents of Mg, muscle strength, muscle mass and sodium, potassium pumps (Na,K-pumps) in patients with alcoholic liver disease. Retrospectively, patients were also stratified according to spironolactone treatment. MATERIAL AND METHODS: The study comprised a placebo-controlled, randomized trial in which 59 consecutive patients with alcoholic liver disease were treated with Mg intravenously and orally (12.5 mmol daily) or placebo for 6 weeks. Muscle content of Mg, maximum isokinetic muscle strength, skeletal muscle mass and muscle content of Na,K-pumps were measured before and after Mg supplementation. RESULTS: Muscle Mg did not increase during the trial (paired t-test), but Mg supplementation and the duration of pre-study spironolactone treatment were independent predictors of muscle Mg (multiple regression). Muscle strength increased by 14% during the trial (p<0.001) and muscle mass increased by 11% (p=0.05), but with no difference between placebo and Mg treatment. Spironolactone treatment was associated with a 33% increase in the content of Na,K-pumps (p<0.001). CONCLUSIONS: Six weeks of Mg supplementation did not increase muscle Mg, although Mg supplementation and spironolactone treatment were independent predictors of muscle Mg. The intervention had no effect on muscle strength and mass, but both increased during the study, probably owing to the general care and attendance to the patients.

Hemodynamic function of the standard St. Jude bileaflet disc valve has no clinical impact 10 years after aortic valve replacement.

OBJECTIVES: Size mismatch and impaired left ventricular function have been shown to determine the hemodynamic function of the standard St. Jude bileaflet disc valve early after aortic valve replacement (AVR). We aimed to analyse St. Jude valve hemodynamic function and its clinical impact in the survivors of a prospective series 10 years after AVR for aortic stenosis. DESIGN: Forty-three survivors aged 32-90 years from a prospective series attended a follow-up study with Doppler echo and radionuclide cardiography 10 years after AVR for aortic stenosis. Six patients with significant left sided valve regurgitation were excluded from further analysis: they had significantly lower St. Jude valve gradient and left ventricular ejection fraction (LVEF) and larger mass index (LVMi) than 37 without. RESULTS: In the 37 patients without left sided valve regurgitation peak and mean gradients were inversely related to St. Jude valve geometric orifice area (GOA) indexed for either body surface area or left ventricular end-diastolic dimension (LVEDD). The gradients correlated directly with LVEDD but not with LVEF or LVMi. Eleven patients with hypertension had higher peak gradients (31+/-13 versus 22+/-8 mmHg, p<0.05), lower LVEF, and higher LVEDD and LVMi than 26 without. Peak gradient was greater than 35 mmHg in five hypertensive patients with normal LVEF but lesser than 30 mmHg in six with impaired LVEF. Supranormal LVEF and severe size mismatch identified the remaining patients (N=3) with peak gradient above 35 mmHg. In a multilinear regression analysis GOA indexed for LVEDD, hypertension, and LVEF were independently related to peak gradient. CONCLUSION: High gradients of the standard St. Jude bileaflet disc valve 10 years after AVR was primarily related to systemic hypertension and mismatch between valve and left ventricular cavity size. Hypertension and left sided valve regurgitation, but not St. Jude valve gradient or size mismatch, were the dominant determinants of left ventricular hypertrophy and impaired function.

Predictable changes in left ventricular mass and function during ten years after valve replacement for aortic stenosis.

BACKGROUND AND AIM OF THE STUDY: Left ventricular (LV) hypertrophy is the underlying basis for longevity after aortic valve replacement (AVR) for aortic stenosis (AS). However, a detailed account of changes in LV mass and function in the long term after AVR and identification of the determinants of such changes have not yet been presented. METHODS: Ninety-one unselected consecutive adult patients with AS underwent AVR and were followed up to 10 years, at which time 41 survivors without new mitral disease underwent repeat measurement of LV mass index (LVMi), ejection fraction (LVEF), fast filling fraction (LVFFF), and end-diastolic volume index (LVEDVi). A subgroup comprising 49 patients was also assessed at eight days, three months, and 1.5 years postoperatively. All measurements were analyzed in a longitudinal regression model for repeated measures. RESULTS: LVMi fell from 202 +/- 58 g/m2 (n = 91) via 150 +/- 45 g/m2 (n = 39) at 1.5 years to 139 +/- 40 g/m2 (n = 41) at 10 years in all patients, and to 124 +/- 31 g/m2 (n = 29) in non-hypertensive patients. The LVMi falls were paralleled by improvements in LVEF and LVEDVi. LVFFF was not correlated to LVMi before the 10-year study. The longitudinal model indicated progressive reduction of LVMi to 1.5 years, but no change thereafter. The predictor variables were preoperative LVMi and end-systolic dimension index (high values of both related to high postoperative LVMi), hypertension, and male gender. The model for LVEF indicated a rapid increase to three months, followed by a slight decrease to 1.5 years and further to 10 years, predicted by preoperative LVEF and LVFFF. LVFFF fell sharply by three months, had recovered somewhat at 1.5 years and fully at 10 years, positively related to preoperative LVFFF and inversely to end-systolic chamber radius:wall thickness ration and small-sized prosthetic valves. LVEDVi converged from extreme values over time predicted by preoperative LVEF, but rose with hypertension and coronary artery disease. Hemodynamic function of the prosthetic aortic valve at any of the measurement times had no impact. CONCLUSION: Changes in LV mass and function up to 10 years after AVR for AS were highly predictable. Poorer outcomes were related to preoperative excessive hypertrophy and indices of underlying irreversible myocardial disease and further compromised by hypertension and, to a lesser extent, coronary artery disease. The hemodynamic function of the aortic prosthetic valve did not seem to play a role.

Regression of left ventricular hypertrophy during 10 years after valve replacement for aortic stenosis is related to the preoperative risk profile.

BACKGROUND: Previous studies have suggested that regression of hypertrophy may be the underlying determinant of longevity and left ventricular function after valve replacement (AVR) for aortic stenosis (AS). The potential for hypertrophy regression could therefore be related to the preoperative risk profile. METHODS: Ninety-one consecutive patients with AS had a "project" Doppler-echo and radionuclide ventriculography in addition to the standard investigation programme prior to AVR with a disc valve (19-29mm, n=82), a caged ball valve (26-29mm, n=8), or a stented porcine valve (26mm, n=1); 49 (group A) were selected for a serial follow-up study while 42 served as controls (group B). Forty-two group A patients took part in a 1.5-year examination while 47 (26 group A, 21 group B) patients were studied at 10 years. RESULTS: Groups A and B were comparable as regards all pre- and intra-operative data including left ventricular mass index (LVMi). A previously developed preoperative prognostic index (PI) separated the patients into groups with low (n=23), intermediary (n=19) and high risk (n=49) with 10-year survivals of 87%, 58% and 43% (P<0.01). LVMi dropped from 202+/-58g/m(2)preoperatively to 152+/-45g/m(2)(P<0.0001) at 1.5 years, and 139+/-40g/m(2)(P<0.0001) at 10 years (three and six patients, respectively, with paravalvular leak or mitral regurgitation excluded). PI correlated with preoperative (r=0.51, P<0.001), 1.5-year (r=0.46, P<0.01), and 10-year LVMi (r=0.41, P<0.01). Also preoperative left ventricular ejection fraction correlated with the three LVMi measurements. Patients with systemic hypertension had higher LVMi at 1.5 years (193+/-42, n=6 vs 144+/-42, n=33, P<0.05) and 10 years (175+/-39, n=12 vs 124+/-31g/m(2), n=29, P<0.001). Patients with low, intermediary or high PI, excluding those with hypertension, had 1.5-year LVMi of 110+/-35 (n=8), 134+/-43 (n=9) and 164+/-33g/m(2)(n=16; P<0.01), respectively, and 10-year LVMi of 116+/-25 (n=17), 126+/-27 (n=6), and 146+/-41g/m(2)(n=6; P<0.05), respectively. There was no relation between LVMi at 1.5 or 10 years and peak or mean Doppler gradient, prosthetic valve size, or valve size index. CONCLUSIONS: Left ventricular hypertrophy regression for patients who survived up to 10 years after AVR for AS is dependent on the preoperative risk profile indicating that irreversible myocardial disease is the underlying factor. Systemic hypertension is an important factor in its own right.

Late anthracycline cardiotoxicity after childhood cancer: a prospective longitudinal study.

BACKGROUND: The objective of the current study was to examine the risk factors for progression in severity of anthracycline-induced cardiac dysfunction, thereby providing information that is useful in refining cancer treatment regimes and guiding follow-up. METHODS: Serial echocardiograms were performed on 101 acute lymphoblastic leukemia survivors and 83 Wilms tumor survivors after a mean interval of 6.2 years and 6.7 years since last anthracycline dose, respectively, at first study, and after 10.3 years and 11.1 years, respectively, at second study. The paired data were contrasted with data from 100 normal subjects, and potential correlations with follow-up interval, cumulative dose, cancer diagnosis, gender, age at diagnosis, and growth were explored using univariate and multiple regression techniques. RESULTS: The most important predictor of worsening cardiac performance was total anthracycline dose. As a group, patients receiving < 240 mg/m(2) showed no deterioration of left ventricular end systolic stress at > 10 years from the end of treatment. CONCLUSIONS: Survivors who have received low-dose anthracycline require cardiac surveillance infrequently. In good prognosis tumors, cumulative anthracycline dose should be maintained at < 250 mg/m(2).

Effect of oral nitroglycerin and cold stress on myocardial perfusion in areas subtended by stenosed and nonstenosed coronary arteries.

Physical obstruction and coronary vasoconstriction mediated by adrenergic stress are believed to be responsible for episodes of myocardial hypoperfusion and angina. Nitroglycerin relieves symptoms by reducing preload and dilating epicardial vessels. The net perfusion change and relation to stenosis severity of nitroglycerin and adrenergic stress have been debated. This study aimed to evaluate whether oral nitroglycerin and adrenergic stress alters perfusion in myocardial segments subtended by stenosed and nonstenosed coronary arteries. Myocardial perfusion was quantified (using N-13-ammonia positron emission tomography [PET]) at rest, after oral nitroglycerin 400 microg, and after cold stress in 25 patients with coronary artery disease (62 +/- 9 years, 21 men) and in 30 controls (34 +/- 9 years, 22 men). Myocardial perfusion was quantified in areas supplied by stenosed (>70%) and nonstenosed (<30%) coronary arteries. The cold pressor test did not significantly alter myocardial perfusion in any of the groups. However, when normalized for rate-pressure product, the response in stenosed areas showed a significantly more pronounced reduction compared with nonstenosed areas (0.78 +/- 0.18 vs 0.64 +/- 0.19 ml/g/min, p <0.005 and 0.86 +/- 0.19 vs 0.73 +/- 0.24 ml/g/min, p <0.05, p <0.05) for intergroup comparison. In both stenosed areas and nonstenosed areas nitroglycerin increased perfusion (0.51 +/- 0.14 vs 0.60 +/- 0.17 ml/g/min, p <0.05 and 0.56 +/- 0.14 vs 0.61 +/- 0.17 ml/g/min, p <0.05). Nitroglycerin did not alter myocardial perfusion in the control group. There was a negative correlation between the cold pressor test response and stenosis severity (r(2) = 0.17, p <0.046), whereas this was not the case for nitroglycerin. In patients with coronary artery disease, myocardial segments supplied by stenosed coronary arteries showed an altered perfusion response to adrenergic stress. Oral nitroglycerin increased myocardial perfusion irrespective of the presence of a stenosis.