Biomechanical hearts: muscular blood pumps, performed in a 1-step operation, and trained under support of clenbuterol.

BACKGROUND: As shown previously in goats, clenbuterol increased the power of electrically conditioned skeletal muscle ventricles (SMVs) of clinically relevant size (150 mL), which were constructed around a mock system. They pumped against a pressure of 60 to 70 mm Hg immediately during surgery and up to several months after, finally at >1 L/min. SMVs without clenbuterol administration failed. Thus, we expected that clenbuterol-supported SMVs might become integrated into the circulation by a 1-step operation instead of the 2-step procedure required up to now. METHODS AND RESULTS: In adult Boer goats (n=5), latissimus dorsi muscle was wrapped around a polyurethane chamber of 150 mL that was connected to the descending aorta. This muscular flow-through pumping chamber containing a stabilizing inner layer (called a biomechanical heart [BMH]) was formed and immediately made to work against a systemic load with the support of clenbuterol (5x150 microg/wk). During surgery, the mean stroke volume of BMHs was 53.8+/-22.4 mL. One month after surgery, in peripheral arterial pressure, the mean diastolic (P(MD)) and minimal diastolic (P(min)) pressures of BMH-supported heart cycles differed significantly from unsupported ones (P(MD)=+2.9+/-1.1 mm Hg [P<0.04], P(min)=-2.4+/-0.9 mm Hg [P<0.04]). After BMH-supported heart contractions, the subsequent maximal rate of pressure generation, dP/dt(max), increased by 20.5+/-8.1% (P<0.02). One BMH, catheterized 132 days after surgery, shifted a volume of 34.8 mL per beat and 1.4 L/min with a latissimus dorsi muscle of 330 g. Depending on duration of training, the percentage of myosin heavy chain type 1 ranged between 31% and 100%. CONCLUSIONS: Under support of clenbuterol, BMHs of a clinically relevant size can be trained effectively in the systemic circulation after a 1-step operation and offer the prospect of a sufficient volume shift and probably unloading of the left ventricle.

Cardiac release and kinetics of endothelin after severe short-lasting myocardial ischemia.

OBJECTIVES: The aim of this study was to investigate the release kinetics of endothelin after induced short-lasting myocardial ischemia. BACKGROUND: Endothelin is an endothelium-derived vasoactive peptide. Unequivocal proof of its cardiac release in ischemic syndromes has not yet been demonstrated. METHODS: A coronary sinus study with atrial pacing was performed in 23 patients with coronary artery disease. Endothelin (ET), cardiac troponin-T (TnT), myoglobin (Mb) and creatine kinase (CK) samples were withdrawn from the coronary sinus and a peripheral vein before and 1, 5, 10, 30 and 45 min and 1, 2, 3 and 6 h after pacing. The appearance of angina pectoris, abnormal cardiac lactate metabolism and ST segment depression were further criteria for myocardial ischemia. RESULTS: In the study group, pacing stress induced severe ischemia (mean duration +/- SD 6.1 +/- 1.2 min), with a maximum of 0.34 +/- 0.12-mV ST segment depression in 21 of 23 patients and angina pectoris in 22 of 23. The maximal cardiac lactate production was 42.8 +/- 17.3% (p < 0.03). TnT and CK levels in the total group were normal; in 14 of 23 patients a transient elevation of Mb with a maximum after 3 h was detected (86.4 +/- 27.1 micrograms/liter, p < 0.03). The ET concentrations increased significantly (p < 0.001) in the coronary sinus (from 4.6 +/- 0.8 [baseline] to 12.9 +/- 2.7 pg/ml at 1 min after cessation of pacing) and the peripheral vein, respectively (from 4.7 +/- 0.7 [baseline] to 8.3 +/- 2.1 pg/ml at 1 min). ET further remained elevated for 1 h with persisting higher coronary sinus than peripheral venous concentrations, indicating cardiac ET release. In a control group of 18 patients without heart disease, all variables were unchanged. CONCLUSIONS: Short-lasting severe myocardial ischemia was associated with significant ET release of cardiac origin that lasted up to 1 h.

Aortic atherosclerotic plaques as a source of systemic embolism.

OBJECTIVES: Our study was designed to determined the significance of aortogenic embolism in an unselected autopsy collective. BACKGROUND: Although embolism arising from atherosclerotic plaques in the aorta has been acknowledged, the role of aortic atheromatosis among other well known sources of embolism remains to be further clarified. METHODS: We examined the proximal part of the arterial system with regard to the presence of atherosclerotic lesions as well as cardiac changes in 120 consecutive necropsy studies. Pathologic evidence of embolic events was recorded. Clinical and neuropathologic data were also surveyed in all patients. RESULTS: Among atherosclerotic lesions, fibrous plaques (p < 0.05) and calcified (p < 0.0001) and ulcerated lesions (p < 0.0001) as well as thrombi (p < 0.005) were observed significantly more frequently in the aortic arch and in the descending aorta than in the ascending aorta, whereas fatty streaks were distributed uniformly. In 40 (33%) of the 120 patients, we found pathologic evidence of arterial embolization. Multiple logistic regression analysis revealed a significant correlation between embolism and complicated atherosclerotic plaques in the aortic arch (odds ratio [OR] 5.8, 95% confidence interval [CI] 1.1 to 31.7, p < 0.05), severe ipsilateral carotid artery disease (OR 3.1, 95% CI 3.1 to 45.3, p < 0.001) and atrial fibrillation (OR 3.5, 95% CI 1.1 to 9.9, p < 0.05). CONCLUSIONS: Complicated atherosclerotic plaques in the aortic arch represent an independent risk factor for systemic embolism similar to atrial fibrillation and severe atherosclerosis of the carotid arteries.

Exercise-induced myocardial ischemia in isolated coronary artery ectasias and aneurysms ("dilated coronopathy").

OBJECTIVES: The purpose of our study was to evaluate the clinical significance of isolated coronary artery ectasias or aneurysms (CEA). BACKGROUND: It has been postulated that altered coronary blood flow in CEA predisposes patients to the development of myocardial ischemia (CI) and infarction. METHODS: Sixty-seven patients with bilateral nonobstructive CEA without associated cardiac defects ("dilated coronaropathy") were derived from 16,341 cardiac catheterizations between 1986 and 1997. Ectasias were defined as luminal dilation of 1.5- to 2.0-fold, aneurysms of >2.0-fold of normal limits. Eleven of 25 patients presented with myocardial infarction due to an occlusion of the infarct vessel. In 42 patients without infarction (study group), exercise-induced CI was investigated. RESULTS: A corresponding CI was documented in 32 of 42 patients in a coronary sinus lactate study (reduced lactate extraction 5.6 +/- 4.1%) and in 29 of 40 patients in an ergometry (0.25 +/- 0.06 mV ST depressions). The results differed significantly from a control group of 29 patients without heart disease (p < 0.001). Nitroglycerin (0.8 mg) provoked a further significant deterioration of CI in the 32 of 42 developing a frank cardiac lactate production (-2.6 +/- 6.8%, p < 0.001). The metabolic extent of CI was significantly correlated to the coronary diameters of the proximal and middle segments of left anterior descending artery and the middle segment of left circumflex artery (r = 0.87, p < 0.001). Stigmata of an impaired coronary blood flow such as delayed antegrade filling, segmental backflow phenomenon and local deposition of dye were found significantly more often with increasing coronary diameters (p < 0.04). CONCLUSIONS: "Dilated coronaropathy" is an entity of nonobstructive, ischemic coronary artery disease. Nitroglycerin is of no therapeutic benefit but leads to an aggravation of exercise-induced CI.

Detection of a hypercoagulable state in nonvalvular atrial fibrillation and the effect of anticoagulant therapy.

The purpose of the study was to evaluate alterations of the hemostatic system and the effect of anticoagulant therapy in nonvalvular atrial fibrillation. A set of molecular hematologic markers was measured prospectively in 69 patients with atrial fibrillation and 28 age-matched patients in sinus rhythm. Significantly elevated levels of thrombin-antithrombin III complex (8.5 +/- 1.6 vs. 2.5 +/- 0.3 micrograms/l; p < 0.001), fibrin monomers (27.1 +/- 3.2 vs. 13.4 +/- 3.7 nM; p < 0.001), D-dimers (788 +/- 76 vs. 405 +/- 46 micrograms/l; p < 0.005), and tissue-type plasminogen activator (9.6 +/- 0.5 vs. 7.2 +/- 0.5 micrograms/l; p < 0.05) were observed in patients with atrial fibrillation compared to those in sinus rhythm. In a subgroup of patients in whom anticoagulant therapy with oral coumadin or standard intravenous heparin was established after the initial study, hemostatic activation decreased significantly. In conclusion, molecular hematologic markers indicate a hypercoagulable state in atrial fibrillation which may characterized a group of patients at elevated risk of thromboembolic disease.

Cardiac release and kinetics of endothelin after uncomplicated percutaneous transluminal coronary angioplasty.

This study was designed to assess the release kinetics of endothelin after percutaneous transluminal coronary angioplasty (PTCA) and to prove the coronary endothelium as the source of the endothelin release. Twenty-seven patients with single-vessel coronary artery disease underwent PTCA. Endothelin, troponin T, myoglobin, and creatine phosphokinase paired blood samples were withdrawn from the coronary sinus and a peripheral vein before the balloon maneuver and at 1, 5, 10, 30, 45 minute(s), and at 1, 2, 3, 6, 12, and 24 hour(s) after the last balloon maneuver. Myocardial ischemia was monitored by means of cardiac lactate metabolism and 12-lead electrocardiogram. Thirteen patients who underwent a diagnostic cardiac catheterization served as a control group. In the left coronary artery, PTCA (n = 19) endothelin concentrations increased from 4.1 pg/ml as a common mean baseline level before intervention to 13.9 +/- 2.6 pg/ml (mean +/- SD) in the coronary sinus and 7.9 +/- 2.2 pg/ml (mean +/- SD) in the peripheral vein at 1 minute after the intervention (p <0.001). The levels remained elevated for 3 hours with higher coronary sinus than peripheral venous concentrations due to persistent cardiac endothelin release. PTCA of the right coronary artery (n = 8) also led to an instantaneous endothelin increase from a mean concentration of 4.4 before intervention to 8.3 pg/ml after intervention with identical coronary sinus and peripheral venous levels (p <0.001). Endothelin levels gradually decreased to normal within 6 hours. No patient developed a measurable myocardial ischemia or a myocardial infarction. In the control group all parameters remained unchanged. Uncomplicated PTCA was followed by a significant cardiac endothelin release that seems to indicate endothelial injury and not myocardial ischemia.

Relation between QT dispersion and the extent of myocardial ischemia in patients with three-vessel coronary artery disease.

The aim of the study was to examine the relation between the extent of myocardial ischemia and changes in QT interval dispersion in patients with obstructive coronary artery disease and in patients with normal coronary arteries. QT interval dispersion reflects regional variations in ventricular repolarization and cardiac electrical instability. Previous studies showed QT interval dispersion changes during episodes of myocardial ischemia in patients with coronary artery disease, but no data on the relation between extent of myocardial ischemia and degree of QT interval dispersion changes are available. To assess the effects of myocardial ischemia on myocardial repolarization by analyzing the change in QT dispersion during incremental atrial pacing, we studied 33 patients (7 women and 26 men, mean age 60.1 +/- 5.1 years, 18 patients with normal coronary arteries, 15 patients with coronary 3-vessel disease). QT dispersion was measured at baseline, after each pacing period, within 30 seconds after cessation of pacing ("peak ischemic stress"), and at 1-minute intervals for up to 5 minutes. Paired blood samples for determination of serum lactate were withdrawn from the coronary sinus and radial artery to determine the cardiac lactate extraction ratio at each point of electrocardiographic registration. In patients with coronary artery disease, QT dispersion increased from a baseline value of 39 +/- 7 ms to a peak ischemic stress value of 63 +/- 10 ms (p <0.0001). Patients with normal coronary arteries showed almost unchanged values of QT dispersion (41 +/- 9 vs 42 +/- 7 ms). There was a significant relation between the pacing-induced change in QT dispersion and the induced change in myocardial lactate extraction ratio (r = 0.76, p <0.0001). The change in QT dispersion (baseline vs peak pacing stress) was related to the extent of the cardiac lactate extraction ratio (r = -0.79, p <0.0001). These data indicate that the severity or extent of induced myocardial ischemia was related to the degree of induced changes of the variability in the timing of the ventricular recovery pattern.

Cardiomyopathic lentiginosis/LEOPARD syndrome presenting as sudden cardiac arrest.

A 26-year-old apparently healthy man with numerous pigmented skin lesions collapsed during an evening party and was resuscitated from ventricular fibrillation. Hypertrophic cardiomyopathy and subaortic tunnel were disclosed by angiocardiography. A diagnosis of cardiomyopathic lentiginosis/lentigines (multiple), electrocardiographic abnormalities, ocular hypertelorism, pulmonary stenosis, abnormalities of the genitalia, retardation of growth, and deafness (sensorineural) syndrome was made. The patient then underwent treatment with an implantable pacer-cardioverter-defibrillator device. Further evaluation revealed several well-established features of the disorder. This is the first reported case of survival from ventricular fibrillation associated with this rare and little known multifaceted syndrome. Disseminated lentiginosis must prompt clinicians to evaluate such cases further since underlying disorders may be associated with considerable morbidity and, apparently, sudden death.

Impact of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarcted vessel in patients with acute right ventricular infarction.

OBJECTIVE: To assess the efficacy of early accelerated dose tissue plasminogen activator on in-hospital patency of the infarct related artery in patients with inferior myocardial infarction with and without right ventricular involvement. DESIGN: Single centre prospective assessment before discharge of infarct related vessel patency after early thrombolysis. SETTING: Tertiary cardiac referral centre at a university hospital. PATIENTS AND METHODS: 90 consecutive unselected patients with acute myocardial infarction, of whom 35 (39%) had electro-cardiographic evidence of right ventricular involvement (ST segment elevation greater than 0.1 mV in right precordial lead V4R), were studied. All patients received accelerated dose tissue plasminogen activator 100 mg within six hours from the onset of symptoms and had control angiography before discharge. MAIN OUTCOME MEASURES: Infarct related coronary artery patency using the Thrombolysis in Myocardial Infarction (TIMI) grading system before discharge. Incidence of prolonged systemic hypotension, sinus bradycardia, complete atrioventricular block, and ventricular tachyarrhythmia during early hospitalisation. RESULTS: Despite aspirin and bolus heparinisation before thrombolysis and high dose heparinisation thereafter for at least 48 hours the infarct related artery was more likely to be occluded (TIMI 0 or 1 flow) in patients with right ventricular involvement than in those without (69 v 29%, P < 0.001), as shown by control angiography performed a mean of 12.8 days after thrombolysis. These findings may be explained, at least in part, by predominant involvement of the proximal right coronary artery (66 v 31%, P < 0.05) and a low cardiac output syndrome, being indirectly reflected by a high incidence of prolonged hypotension (26 v 7%, P = 0.02), bradycardia (34 v 14%, P = 0.03), and complete atrioventricular block (37 v 5%, P = 0.0001). CONCLUSION: Primary angioplasty should be considered as the treatment of choice in patients with acute inferior infarction with right ventricular involvement because of the high failure rate of thrombolysis.

Embolism from the aortic arch in patients with cerebral ischemia.

The pathogenic role of aortic arch atherosclerosis (AAA) in embolic stroke is not well understood. We investigated, prospectively, the prevalence and severity of AAA in patients with embolic stroke to ascertain its role as a risk factor for cerebral ischemia. We examined 100 consecutive patients who had experienced acute symptoms due to cerebral ischemia. Clinical examination, electrocardiogram, x-ray, ultrasound examination of craniocervical arteries, transesophageal echocardiography (TEE), cranial computerized tomography, and magnetic resonance imaging were undertaken. Seventy-five patients showed evidence of AAA; 34 patients had moderate to severe (> 5 mm thickening) AAA. Age was positively related to the severity of AAA, as were smoking, coronary heart disease, diabetes mellitus, internal carotid artery (ICA) occlusive disease, and embologenic heart disease. Hypertension, which was evident in 52 patients, did not distinguish those cases showing AAA. Twelve patients showed evidence of high-degree ICA stenosis on the symptomatic side, although the extent of ICA stenosis and AAA were unrelated. A cardiac source of emboli was found in 28 patients. AAA was found to be the probable source for embolic stroke in 14 patients. These data indicate that aortic arch atherosclerosis is an important source of cerebral emboli which may increase the risk for ischemic stroke. Furthermore, we suggest that TEE examination of the aortic arch may be important for the diagnosis of AAA and ultimately for the prophylactic treatment of severe cerebral ischemia.

Myocardial ischemia in generalized coronary artery-left ventricular microfistulae.

Generalized (multiple) arterio-systemic fistulae are fistulae arising from all three major coronary arteries and drain into the left ventricle are rare and the clinical and hemodynamic sequelae are incompletely understood. This communication is based on the clinical and hemodynamic data of a series of patients (eight cases out of 7262 consecutive patients) incidentally identified at coronary angiography combined with data from cases previously reported in literature. The aim was to assess the role of generalized coronary artery fistulae as a non-atherosclerotic cause of myocardial ischemia by means of a coronary sinus lactate study. Coronary sinus lactate study demonstrated myocardial ischemia in 6/7 patients. Mean arterio-coronary venous lactate difference decreased from 0.31+/-0.18 mmol/l (lactate extraction ratio, LER, 29.4+/-13.9%) at rest to 0.04+/-0.13 mmol/l (LER -4.0+/-13.3%) at peak exercise. Five minutes after cessation of pacing, lactate difference increased to 0.22+/-0.21 mmol/l (LER -20.7+/- 13.2%). At peak pacing stress, 4/7 patients showed frank lactate production, and two patients presented with a reduced cardiac lactate extraction rate also indicating myocardial ischemia metabolically. In the present study, we demonstrated a possible role of a coronary steal mechanism due to microfistulae pathways in the pathogenesis of myocardial ischemia in patients with generalized coronary artery-left ventricular microfistulae.

Acquired thromboatheromatous coarctation of the aorta: acquired coarctation of the aorta.

BACKGROUND: Atheromatosis of the thoracic aorta and aortic arch is a well established source of systemic embolism. Acquired atheromatous coarctation of the aortic arch is a rare finding and not well documentated so far. CASE REPORT AND FINDINGS: Two patients presenting with intermittent claudication of the lower extremities were identified as having thromboatheromatous coarctation of the aortic arch as visualized by magnetic resonance tomography, fast CT scan, transesophageal echocardiography, cardiac catheterization and aortography. All findings including invasive hemodynamics resembled congenital coarctation of the aorta. One patient was treated surgically, while the other refused surgery and received long-term anticoagulation. CONCLUSION: Atheromatosis of the thoracic aorta and aortic arch not only cause systemic embolism, but may lead to the clinical and hemodynamic picture of coarctation of the aortic arch.

Priming of neutrophils after elective percutaneous transluminal coronary angioplasty is unrelated to accompanying brief myocardial ischemia.

OBJECTIVE: The purpose of this study was to investigate the effect of brief myocardial ischemia and vascular trauma induced by elective percutaneous transluminal coronary angioplasty on in vivo 'priming' and activation of neutrophils. PATIENTS AND METHODS: We studied 16 patients undergoing elective coronary angioplasty for symptomatic coronary artery disease and a control group of seven patients undergoing diagnostic cardiac catheterization. Free radical production from purified neutrophils (Ficoll-Hypaque density gradient method) was measured indirectly by the chemiluminescence method. Myocardial ischemia during balloon inflation was assessed by serial lactate determinations from coronary sinus and arterial blood. The degree of transient angioplasty-related myocardial ischemia was related to the oxidative response of activated neutrophils. RESULTS: Mean (+/-S.E.M.) oxidative response, i.e. the lucigenin- and luminol-enhanced-chemiluminescence (counts per minute) of neutrophils sampled from the coronary sinus increased significantly after percutaneous transluminal coronary angioplasty (Lucigenin-chemiluminescence: pre-angioplasty 3.69+/-0.64x10(5) vs. post-angioplasty 7.08+/-1.2x10(5), P<0.01; Luminol-chemiluminescence: pre-angioplasty 2.81+/-0.67x10(6) vs. post-angioplasty 5.2+/-0.92x10(6), P<0.01). Twelve of 16 patients developed transient cardiac lactate production (mean coronary sinus lactate excess: +0.12 mmol/l) and three disclosed a lactate extraction ratio <10%, both suggestive of myocardial ischemia. However, there was no correlation between the cardiac lactate production and the increased oxidative response after coronary angioplasty (r2 (Lucigenin-chemiluminescence)=0.02, n.s.; r2 (Luminol-chemiluminescence)=0.06, n.s.). CONCLUSION: 'Priming' of neutrophils, as reflected by increased oxidative response, is likely to occur after coronary angioplasty, but not after the angiographic procedure itself. However, 'priming' seems to be unrelated to the transient brief period of myocardial ischemia and rather depends on an alternative mechanism.

Prothrombin fragments F1+2, thrombin-antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis.

We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. Blood was collected from the antecubital vein through atraumatic venipuncture prior to the angiographic procedure. Plasma levels of hemostatic markers were related to the presence and graded severity of CAD. The levels of prothrombin fragment F1+2 (1.74+/-0.11 vs. 1.0+/-0.07 nmol/l, P<0.001), FM (41.6+/-5.5 vs. 7.42+/-3.05 nmol/l, P<0.001), TAT (15.6+/-2.7 vs. 2.96+/-0.32 microg/l, P<0.001) and fibrinogen (3.64+/-1.3 vs. 3.08+/-0.33 g/l, P<0.01) were significantly higher in patients with CAD compared to controls, while there was no difference regarding the fibrinolytic system represented by DD (441.6+/-58.9 vs. 337.4+/-42.05 microg/l, n.s.). Within the CAD group, patients with extensive coronary atherosclerosis (> or =2 vessel disease) had significantly higher values for prothrombin fragment F1+2 (1.89 vs. 1.57 nmol/l, P = 0.04), FM (50.7 vs. 29.8 nmol/l, P = 0.03), and a trend to significance was noted for fibrinogen (3.9 vs. 3.3 g/l, P = 0.07) suggesting that blood coagulability was related to the severity of the disease and that hemostatic markers of thrombin activity represent a useful tool to identify patients with a latent hypercoagulable state with a higher susceptibility to sustain coronary thrombosis.

The relationship of torque, velocity, and power with constant resistive load during sagittal trunk movement.

Strength and fitness studies have been used to determine the predictability of back pain episodes. Tests have demonstrated that isometric strength displays little prognostic value in the development of low-back pain. Static isometric tests have achieved widespread usage due to the simplicity and safety of protocols, the readily available technology, and the low administrative costs. Dynamic lifting models have, however, predicted significantly higher spinal loads than those derived from static models. The objectives of this study were twofold: to investigate the relationship of the torque, velocity, and power to the resistive load during trunk flexion and extension, and to develop predictive models for these relationships for the subject's performance of the 10th, 50th, and 90th percentile distribution. The results of the study found that the flexion/extension torque had a positive linear correlation with the set resistance; the velocity displayed a negative linear correlation, while power had a quadratic relationship with the resistance.

Effects of spinal flexion and extension exercises on low-back pain and spinal mobility in chronic mechanical low-back pain patients.

It has been estimated that one fourth to one half of all patients treated in physical therapy clinics suffer from low-back pain. The purpose of this study was to compare the effects of spinal flexion (Group I) and extension (Group II) exercises on low-back pain severity and thoracolumbar spinal mobility in chronic mechanical low-back pain patients. Both groups had significantly less low-back pain after treatment (P less than .10). There was no significant difference, however, between the spinal flexion and extension exercises in reduction of low-back pain severity. The results indicated a significant difference between the groups in increasing the sagittal mobility (P less than .10). The results did not indicate any significant difference between and within groups in increasing the coronal and transverse mobility of the thoracolumbar spine. Either the spinal flexion or extension exercises could be used to reduce chronic mechanical low-back pain severity, but the flexion exercises had an advantage in increasing the sagittal mobility within a short period of time.

Quantification of trunk muscle performance in standing, semistanding and sitting postures in healthy men.

The purpose of this study was to determine trunk muscle performance in the sitting, semistanding, and standing postures during isometric and dynamic extension and flexion movements. Twenty-five male subject volunteers, with no previous history of back pain participated in the study. A triaxial dynamometer that measures torque, angular position, and velocity was used to measure isometric and dynamic motor output. The dynamometer allows testing in the sitting and standing postures. A custom-designed module also allowed testing in the semistanding posture. Each subject was tested in two sessions. The first session included the physical examination and three trials of isometric maximum voluntary contractions in the three postures. The second session included the dynamic performance against a resistance equal to 50% of the effort, as measured in the first session. Subjects were instructed to perform five repetitive flexion and extension cycles as fast and accurately as possible with maximum effort. An analysis of variance with repeated measures design was used to investigate the effects of the postures (standing, semistanding and sitting), the direction of exertion (flexion and extension), and the interaction effects of the isometric and dynamic parameters (maximum and average torque, velocity, power, and range of motion). The effects of direction (F = 98, P < 0.0001) and the interaction of posture and direction (F = 7.9, P < 0.001) were significant. The maximum isometric flexion strength was significantly higher in the standing posture than in semistanding and sitting. The maximum isometric extension was not affected by the posture (sitting, semistanding and standing).(ABSTRACT TRUNCATED AT 250 WORDS)

Recovery of severe sciatica.

STUDY DESIGN: A prospective study of patients with acute severe sciatica. OBJECTIVES: To 1) describe the characteristics of patients with acute severe sciatica and the agreement among different diagnostic tests, 2) describe overall recovery during 1 year in terms of perceived disability, and pain, and 3) explore acute-phase predictors of failure to recover at 1 year. SUMMARY OF BACKGROUND DATA: The development of imaging techniques has been very impressive during recent decades. However, different authors have highlighted the prevalence of abnormal images among asymptomatic subjects. These findings increase the difficulty of interpreting the results from the diagnostic techniques used with each individual patient. Furthermore, other clinical and biopsychosocial variables need to be explored for their associations with recovery or failure to recover. This study aimed to explore those associations. METHODS: Consecutive patients admitted to the hospital for conservative management of severe acute sciatica were eligible for inclusion in the study. Patients were evaluated at admission, discharge, and 3, 6, and 12 months. All the visits included a standardized clinical examination and the completion of questionnaires that included items on demographics, pain, perceived disability, and quality of life. Imaging and blood samples were collected at the first visit, and an electromyogram was taken for sciatica lasting at least 3 weeks. RESULTS: The study included 82 consecutive patients (66% men) with a mean age of 43 +/- 10.3 years. The mean intensity of pain, on a visual analog scale of 0 to 100 (VAS) at Visit 1, was 73. The straight leg raising test was positive in 78% of the patients, with a mean value of 59 degrees +/- 18 degrees. The contralateral straight leg raising test was positive in 20% of the patients. Imaging was positive for disc herniation in 74% and electromyogram was positive in 62% of cases. These two diagnostic tests showed a good to excellent total agreement (58-87%) with the straight leg raising tests and the presence of radiating pain below the knee. The recovery of clinical symptoms and signs was observed mainly within the first 3 months. However, clinical recovery and perceived recovery was not complete in most cases. CONCLUSIONS: In most cases, there was good to excellent agreement among the different diagnostic tests. None of the tests was predictive of recovery. The presence of blood antibodies against 3'LM1 (IgM + IgG) and GD1a (IgM) was significantly associated (P < 0.023) with neurologic symptoms and signs. However, the meaning of these antibodies remains unclear. Only a minority of the patients (29%) had fully recovered after 12 months. Within the 1-year follow-up, one third of the patients had surgery.

Obstructive cardiomyopathy in a male dwarf with cryptorchidism.

Obstructive cardiomyopathy has been reported in cases of male and female Turner phenotype with normal chromosomes. We report here a case of a male dwarf with bilateral undescended testes and biventricular obstructive cardiomyopathy. Clinical features included choreoathetoid movements, chorioretinitis, bilateral nystagmus, and unusual red color of the hair, associated with some features of Turner phenotype. Endocrine studies were normal except for a lack of thyrotrophic stimulating hormone (TSH) stimulation. Propranolol removed the gradient during cardiac catheterization and relieved the exertional chest pain clinically.

Unusual cardiovascular manifestations in a case of pheochromocytoma.

A case of proven pheochromocytoma is reported of a patient who presented with attacks of apparent hypotension, pulmonary edema, and myocardial injury with typical ECG and enzyme change. In spite of unmeasurably low peripheral blood pressure recordings during the attack, central aortic pressure was well above 240/140 mmHg. A clinical shocklike state was in effect due to severe arterial vasoconstriction. The pulmonary artery pressure was 48/26 mmHg during attacks, wedge pressure was 26 mmHg, and cardiac index 1.8 liters/min/m2. The coronary angiogram showed abnormal pooling of dye in the myocardial capillary network. It is concluded that: (1) Apparent hypotensive episodes in pheochromocytoma may be misleading and central arterial measurements may be needed to demonstrate the hypertensive crisis. (2) The abnormal coronary angiogram in our patient may be due to myocardial necrosis and damage to the intact arteriolar and microvascular system of the myocardium.