Usefulness of transesophageal echocardiography in identifying small left ventricular apical thrombus.

OBJECTIVES: The aim of this study was to determine whether transesophageal echocardiography could clarify the nature of equivocal echodense structures in the left ventricular apical region frequently found on transthoracic echocardiography by directing the ultrasound beam from the left ventricular base to the apex and achieving better image quality. BACKGROUND: Transthoracic echocardiography often reveals an echogenic structure suggesting thrombus in the left ventricular apical region because of limited near-field resolution and echo vibration artifact in apical views. METHODS: Thirty-six patients with coronary artery disease or dilated cardiomyopathy who had apical wall motion abnormalities and equivocal transthoracic echodense structures were studied with transesophageal echocardiography using special manipulation of the transesophageal probe for adequate imaging of the apical region. Left ventricular thrombus was defined when echogenic structures with a clearly delineated margin adjacent to but distinct from the endocardium were observed in at least two different tomographic views in the four-chamber and left ventricular long-axis views during both systole and diastole. RESULTS: Left ventricular thrombus (mean size 1.3 +/- 0.7 cm2) was defined by transesophageal echocardiography in 19 (53%) of 36 patients with suspected thrombus on transthoracic echocardiography in the four-chamber or left ventricular long-axis view. Heavy trabeculation or extremely high echo reflection, or both, was observed in the apical region in 12 patients (33%). No extra structures in the apical region were found in five patients. In 19 patients with transesophageal echocardiographically defined thrombus, 6 patients (31%) experienced arterial embolic events before the transesophageal procedure. In contrast, none of 17 patients without transesophageal echocardiographically defined thrombi had systemic embolism (p < 0.03). CONCLUSIONS: 1) Transesophageal echocardiography is useful in identifying left ventricular apical thrombus in patients with unclear echogenic structures on transthoracic apical images; and 2) the high incidence of arterial embolism in patients with transesophageal echocardiographically detected left ventricular thrombus indicates the clinical importance of such thrombus.

Biochemical evidence of platelet activation in patients with persistent unstable angina.

Thromboxane released from activated platelets and prostacyclin of the vessel wall may act as potent antagonistic modulators of platelet aggregability and coronary vascular tone. Therefore, urinary excretion of their major metabolites, 2,3-dinor-thromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1 alpha, was studied in 16 patients presenting with prolonged angina at rest. The 10 patients whose condition did not improve under vigorous antianginal treatment within 48 hours exhibited higher thromboxane metabolite excretion than did the 6 patients who responded to therapy (2,208 +/- 1,542 versus 609 +/- 312 ng/g creatinine; p less than 0.001). Elevated values were also found in four of eight patients with sustained postinfarction angina. Enhanced thromboxane metabolite excretion was frequently associated with angiographic evidence of thrombus formation. When nine patients were restudied in a stable phase after 11 +/- 5 months, thromboxane metabolite excretion was consistently normal or high normal. Excretion of prostacyclin metabolites was not depressed in any patient but correlated weakly with thromboxane (r = 0.41). Thus, enhanced thromboxane production as an index of platelet activation may identify patients with active thrombus formation who could benefit most from platelet inhibitory treatment.

Noninvasive estimation of regurgitant flow rate and volume in patients with mitral regurgitation by Doppler color mapping of accelerating flow field.

OBJECTIVES: This study was designed to examine the accuracy of proximal accelerating flow calculations in estimating regurgitant flow rate or volume in patients with different types of mitral valve disease. BACKGROUND: Flow acceleration proximal to a regurgitant orifice, observed with Doppler color flow mapping, is constituted by isovelocity surfaces centered at the orifice. By conservation of mass, the flow rate through each isovelocity surface equals the flow rate through the regurgitant orifice. METHODS: Forty-six adults with mitral regurgitation of angiographic grades I to IV were studied. The proximal accelerating flow rate (Q) was calculated by: Q = 2 pi r2.Vn, where pi r2 is the area of the hemisphere and Vn is the Nyquist velocity. Radius of the hemisphere (r) was measured from two-dimensional or M-mode Doppler color recording. From the M-mode color study, integration of accelerating flow rate throughout systole yielded stroke accelerating flow volume and mean flow rate. Mitral regurgitant flow rate and stroke regurgitant volume were measured by using a combination of pulsed wave Doppler and two-dimensional echocardiographic measurements of aortic forward flow and mitral inflow. RESULTS: The proximal accelerating flow region was observed in 42 of 46 patients. Maximal accelerating flow measured from either two-dimensional (372 +/- 389 ml/s) or M-mode (406 +/- 421 ml/s) Doppler color study tended to overestimate the mean regurgitant flow rate (306 +/- 253 ml/s, p < 0.05). Mean Doppler accelerating flow rate correlated well with mean regurgitant flow rate (r = 0.95, p < 0.001), although there was a tendency toward slight overestimation of mean regurgitant flow by mean accelerating flow in severe mitral regurgitation. However, there was no significant difference between the mean accelerating flow rate (318 +/- 304 ml/s) and the mean regurgitant flow rate (306 +/- 253 ml/s, p = NS) for all patients. A similar relation was found between accelerating flow stroke volume (78.27 +/- 62.72 ml) and regurgitant flow stroke volume (76.06 +/- 59.76 ml) (r = 0.95, p < 0.001). The etiology of mitral regurgitation did not appear to affect the relation between accelerating flow and regurgitant flow. CONCLUSIONS: Proximal accelerating flow rate calculated by the hemispheric model of the isovelocity surface was applicable and accurate in most patients with mitral regurgitation of a variety of causes. There was slight overestimation of regurgitant flow rate by accelerating flow rate when the regurgitant lesion was more severe.

Efficacy of high dose intravenous heparin for treatment of left ventricular thrombi with high embolic risk.

OBJECTIVES: This study was performed to assess the efficacy of high dose intravenous heparin to treat mobile or protruding left ventricular thrombi as detected by serial echocardiography. BACKGROUND: The presence of mobile and protruding left ventricular thrombi greatly increases the risk of arterial embolization, yet optimal therapy, be it thrombolysis, anticoagulation or surgical removal, has not been defined. METHODS: Full dose heparin, 31,291 +/- 7,980 (mean +/- SD) IU/day, to prolong partial thromboplastin time to at least twice normal, was administered intravenously to 23 consecutive patients with 25 mobile and protruding thrombi. Patients were prospectively evaluated for hemorrhagic complications and embolic events during therapy. The presence or absence of thrombi and their size and characteristics were assessed by serial echocardiography. RESULTS: In all 23 patients left ventricular thrombi decreased in size, with disappearance of the high risk features. The duration of high dose heparin infusion was 7 to 22 days (mean 14 +/- 4). Thrombus size was reduced from 3.9 +/- 2.6 to 0.16 +/- 0.38 cm2, and thrombus disappeared entirely in 19 (83%) of 23 patients. No embolic events were detected during treatment, and the only complication was an upper gastrointestinal hemorrhage that was successfully treated medically. CONCLUSION: High dose intravenous heparin is a highly effective and safe treatment for completely resolving left ventricular thrombi with high risk features for embolization. Most such thrombi disappear completely within 1 to 3 weeks of this treatment without embolic or hemorrhagic complications.

Treatment of 10 dogs with discospondylitis by fluoroscopy-guided percutaneous discectomy.

Ten dogs suffering from discospondylitis were treated by percutaneous discectomy and local and systemic antibiotic therapy. With fluoroscopic guidance, a cylinder 5 mm in diameter was removed from the centre of the intervertebral space, yielding a fenestration and decompressing the disc without producing any spinal instability. The causative bacteria were identified in nine of the 10 biopsy specimens, but in only three urine cultures and four blood cultures. In two cases, the antibiotics used initially had to be changed owing to the organisms' antibiotic resistance. The clinical signs of the dogs improved markedly after two to nine days (mean 4.2 days) and had resolved completely after five to 14 days (mean 9.1 days). In all the cases the disease could be classified histologically as either acute or chronic, and the disease was classified as chronic in one dog. No side effects were observed.

Partial percutaneous discectomy for treatment of thoracolumbar disc protrusion: retrospective study of 331 dogs.

OBJECTIVES: To determine retrospectively the prognosis and outcome for dogs diagnosed with thoracolumbar intervertebral disc disease treated with partial percutaneous discectomy (PPD). METHODS: Three hundred and thirty-one dogs presenting with symptoms of thoracolumbar intervertebral disc disease from 1998 to 2003 were treated with PPD. Diagnosis and location of intervertebral disc disease was confirmed by clinical examination, radiography, myelography and magnetic resonance imaging. PPD was performed via fluoroscopy-guided removal of a 5 mm bore cylinder out of the central intervertebral space. RESULTS: Clinical success after surgery was achieved in 159 (88.8 per cent) grade II to IV patients and 58 (38.2 per cent) grade V patients. The mean (sd) time from percutaneous discectomy to first improvement was 8.3 (13.2) days. CLINICAL SIGNIFICANCE: The PPD approach to the thoracolumbar spine involves minor trauma (yielding rapid recovery) and less pain, and produces results comparable with open fenestration. Consequently, this simple minimal invasive technique can be recommended as an alternative to the technique of fenestration and can be easily performed in addition to open surgical decompression techniques or prophylactically. However, it is not a replacement for surgical treatment in dogs with thoracolumbar disc disease that require removal of disc fragments causing spinal cord or nerve root compression.

Quantitation of coronary venous adenosine in patients: limitations evaluated by radioimmunoassay.

Experimental studies have shown that adenosine is rapidly released in response to myocardial ischaemia. To evaluate whether coronary venous adenosine release is a metabolic characteristic of myocardial ischaemia in patients, adenosine concentrations were measured by a highly sensitive and specific radioimmunoassay. In three patients with normal coronary arteries and in seven with obstructive coronary artery disease coronary venous adenosine content was measured at rest and during atrial pacing. When whole blood or plasma were extracted immediately with perchloric acid the adenosine content was found to be lower than that previously reported. Recovery studies showed that the importance of time and temperature at low adenosine concentrations had been underestimated in preceding studies. In patients with coronary artery disease coronary venous adenosine concentration increased from 106.3(48.8) nmol.litre-1 to 114.9(57.0) nmol.litre-1 (NS) during pacing and was 130.4(63.3) nmol.litre-1 (NS) 2 min after pacing. Even in the presence of lactate production enhanced adenosine release was not consistently evidenced. Furthermore, venous adenosine content did not increase in five patients undergoing coronary artery occlusion during angioplasty of the left anterior descending coronary artery. The extremely short half life of coronary venous adenosine appears to preclude its use as an index of myocardial ischaemia in patients.

Interrupting the adaptive changes in congestive heart failure.

Circulating plasma concentrations of norepinephrine, renin, angiotensin and vasopressin are increased in congestive heart failure. By increasing ventricular afterload, heart failure is further worsened, which in turn--in a vicious cycle--stimulates neurohumoral vasoconstrictor mechanisms. Furthermore, because of the compensatory but excessive stimulation of the sympathomimetic system, a down-regulation and desensitization particularly of the myocardial beta 1 receptors and depletion of myocardial catecholamine occurs in chronic heart failure. These defects may be restored toward normal by interventions that attenuate the activity of the sympathetic nervous system. A direct approach to modify the excessive vasoconstriction is to administer systemic vasodilator drugs, but despite favorable short-term effects, tolerance developed to most of these drugs during long-term treatment. One reason for the loss of effectiveness is the reflex activation of the sympathetic system, which increases vasoconstrictor hormone concentrations. Activation of the renin-angiotensin system can be modified effectively by angiotensin-converting enzyme inhibitors that have shown favorable responses in patients with chronic heart failure. Beta-blocking agents interfere with endogenous sympathetic activation and have produced beneficial effects in patients with congestive cardiomyopathy. Long-term treatment is associated with up-regulation of the number of beta receptors and an improved responsiveness to catecholamines. Owing to the negative inotropic effects of beta-blocking agents, some of the patients with severe heart failure deteriorated hemodynamically and clinically. Theoretically, it should be advantageous to have a substance that combines protection against excessive beta stimulation with a mild inotropic support to prevent cardiac decompensation. This may be achieved by a selective beta 1-partial agonist like xamoterol.

Left ventricular hemodynamics and function in acute myocardial infarction: studies during the acute phase, convalescence and late recovery.

The left ventricular hemodynamics of 70 patients with acute myocardial infarction were determined from measurements of pulmonary arterial end-diastolic pressure, cardiac index, mean arterial pressure and heart rate during the acute phase(first study, 5 hours after admission), 4 to 6 weeks later (second study, during convalescence) and in 35 percent of all subjects 6 to 12 months after the acute infarction (third study). Serial analysis of serum creatine kinase was carried out during the acute phase. The peak CK value normalized for body surface area was used as a rough index of the extent of the acute myocardial necrosis. The condition of all survivors of the acute stage improved. Patients with only slightly reduced left ventricular performance during the acute stage recovered to nearly normal during convalescence. The condition of patients with greatly reduced left ventricular function also improved but remained impaired during convalescence. In all patients the main changes in left ventricular hemodynamics occurred within the first 4 to 6 weeks; there was almost no further alteration during the following 9 months.

Recanalization of chronic, totally occluded coronary arteries by new angioplasty systems.

The benefit and safety of new angioplasty equipment as compared with the conventional guidewire approach was evaluated in 154 consecutive patients. with chronic, totally occluded coronary arteries. The protocol followed a stepwise design: first, conventional guidewires and low-profile balloons were used, followed by "balloon-on-the-wire" systems (Probe, Ace) or by a shaft-enforced, tip-deflecting catheter (Omniflex). In 97 patients with occlusions of 2 to 12 weeks' duration, recanalization was achieved in 51 patients (53%) with the conventional approach and in 29 patients with the new devices (balloon-on-the-wire [n = 5], Omniflex [n = 24]), thereby raising the success rate to 82%. In 57 occlusions of greater than 12 weeks' duration, the recanalization attempt was successful in 58%, mediated in 16 patients (28%) by the Omniflex catheter and in 5 patients by balloon-on-the-wire systems. There were no life-threatening complications and only 1 (0.6%) emergency bypass operation was necessary. New angioplasty devices are therefore of considerable value in the attempt to improve the results of coronary angioplasty in chronic total occlusions.

Influence of heat shock protein 70 and metallothionein induction by zinc-bis-(DL-hydrogenaspartate) on the release of inflammatory mediators in a porcine model of recurrent endotoxemia.

The manipulation of stress gene expression by heavy metals provides protection against the lethal effects of endotoxemia in murine models of septic shock. Recent in vitro studies with alveolar macrophages or monocytes show that induction of the stress response in these cells is followed by a decreased liberation of major cytokines [tumor necrosis factor-alpha (TNF alpha) and interleukin-1 (IL-1)] after endotoxin challenge. These findings suggest that the increased resistance to endotoxin in vivo after stress protein induction could be explained by an altered pattern of inflammatory mediator release. Therefore, we measured the time course of thromboxane-B2 (TxB2), 6-keto-PGF1 alpha, platelet activating factor (PAF), TNF alpha, interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) formation with and without induction of the stress response in an established porcine model of recurrent endotoxemia (Klosterhalfen et al., Biochem Pharmacol 43: 2103-2109, 1992). Induction of the stress response was done by a pretreatment with Zn2+ (25 mg/kg zinc-bis-(DL-hydrogenasparate = 5 mg/kg Zn2+). Pretreatment with Zn2+ prior to lipopolysaccharide (LPS) infusion induced an increased heat shock protein 70 and metallothionein expression in the lungs, liver, and kidneys and increased plasma levels of TNF alpha, IL-1 beta, IL-6, and TxB2 as opposed to untreated controls. After LPS infusion, however, pretreated animals showed significantly decreased peak plasma levels of all mediators as opposed to the untreated group. The time course of mediator release was identical with the decreasing and increasing three peak profiles described previously. Hemodynamic data presented significantly decreased peak pulmonary artery pressures and significantly altered hypodynamic/hyperdynamic cardiac output levels in the pretreated group. In conclusion, the data show that the induction of stress proteins by Zn2+ could be a practicable strategy to prevent sepsis.

The influence of heat shock protein 70 induction on hemodynamic variables in a porcine model of recurrent endotoxemia.

The manipulation of stress gene expression by heavy metals provides protection against the lethal effects of endotoxemia in murine models of septic shock. These findings suggest that the increased resistance to endotoxin in vivo after stress protein induction could be explained by an attenuation of hemodynamic alterations and an altered pattern of inflammatory mediator release. Therefore, we measured main hemodynamic variables such as systemic and pulmonary artery pressure, cardiac output, heart rate, central venous pressure, and pulmonary artery wedge pressure, as well as the time-course of thromboxane-B2, 6-keto-PGF1 alpha, and interleukin 6 formation with and without induction of the stress response in an established porcine model of recurrent endotoxemia (Circ Shock 35:237-244, 1991). Induction of the stress response was carried out by a pretreatment with Zn2+ (25 mg/kg zinc-bis-(DL-hydrogenaspartate) = 5 mg/kg Zn2+). Pretreatment with Zn2+ prior to lipopolysaccharide (LPS) infusion induced an increased heat shock protein 70 (HSP70) expression in the lungs, liver, and kidneys and significantly increased plasma levels of interleukin 6, 6-keto-PGF1 alpha, and thromboxane-B2, compared with untreated controls. After LPS infusion, however, pretreated animals showed significantly decreased peak plasma levels of all mediators compared with the untreated group. Hemodynamic data presented significantly decreased peak pulmonary artery pressure and pulmonary vascular resistance index values, significantly increased systemic artery pressure and systemic vascular resistance index values, and significantly altered hypodynamic/hyperdynamic cardiac output levels in the pretreated group. In conclusion, the data show that the induction of HSP70 by Zn2+ attenuates the liberation of inflammatory mediators, as well as the course of hemodynamic variables due to LPS.

Induction of heat shock protein 70 by zinc-bis-(DL-hydrogenaspartate) reduces cytokine liberation, apoptosis, and mortality rate in a rat model of LD100 endotoxemia.

A prospective, randomized model of LD100/24 h endotoxemia was performed in male Wistar rats (n = 26; 250-300 g). The animals were divided into four groups: Group I (n = 5; saline treatment only), Group II (n = 5; Zn2+ treatment only), Group III (n = 8; saline pretreatment, lipopolysaccharide (LPS) treatment), and Group IV (n = 8; Zn2+ pretreatment, LPS treatment). Zn2+ pretreatment was carried out by intraperitoneal injection of 50 mg/kg zinc-bis-(DL-hydrogenaspartate) (10 mg/kg Zn2+). LD100/24 h endotoxemia was induced by intraperitoneal administration of 20 mg/kg LPS of the Escherichia coli strain WO111:B4. Tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 were detected by enzyme-linked immunosorbent assay (ELISA). HSP70 expression in the lungs, the liver, and the kidneys was determined by immunohistochemistry, Western blotting, and an HSP70 ELISA. Apoptosis was also detected by an in situ apoptosis detection kit (TUNEL) and a cell death detection ELISA, respectively. This rat model of endotoxemia proves the close relationship between HSP70 expression, cytokine liberation, and development of apoptosis. The data demonstrate that: 1) Zn2+ is a potent inducer of HSP70 expression; 2) the application of Zn2+ leads to slightly increased cytokine plasma levels; and 3) the manipulation of the heat shock response by Zn2+ significantly increases the survival rate after LD100 endotoxemia. Enhanced survival rate in animals pretreated with Zn2+ may be explained by increased tissue levels of HSP70, a subsequent significantly decreased liberation of the proinflammatory cytokines after LPS challenge, and a significantly decreased rate of apoptosis.

The therapeutic effect of C1-inhibitor on gut-derived bacterial translocation after thermal injury.

To test the effects of C1-esterase inhibitor in scald burns on bacterial translocation and intestinal damage, standardized deep partial-thickness burns were inflicted on domestic pigs, scalding 30% of the skin surface for 25 s with 75 degrees C hot water. The animals (n = 17; weight 25-35 kg) were divided into three groups: I) the control group (n = 5) without scald burn; II) the group (n = 6) with scald burn; and III) the group with C1-inhibitor (n = 6): scald burn and treatment with C1-inhibitor (C1-INH; BERINERT, Behring, Marburg, Germany). Parameters measured and compared in this model were activity of complement system, hemodynamics, body weight, pathological organ alterations including intestinal lesions, bacterial translocation, and skin damage. C1-INH administration significantly decreased the plasma levels of the specific soluble membrane attack complex (SC5b-9), bacterial translocation, and the degree of intestinal ischemia in the postburn period compared with untreated animals. Moreover, animals treated with C1-INH exhibited a minor degree of organ alterations including damage of the skin and development of edema. The favorable effects of C1-INH may be explained by the protection of the intestinal and dermal microcirculation in the acute phase of thermal injury.

Differentiation of spontaneous canine breast tumors using dynamic magnetic resonance imaging with 24-Gadolinium-DTPA-cascade-polymer, a new blood-pool agent. Preliminary experience.

RATIONALE AND OBJECTIVES: The author assess the enhancement characteristics over time of spontaneous breast tumors in dogs comparing gadopentetate dimeglumine with a new blood-pool agent (24-gadolinium [Gd]-DTPA-cascade polymer). METHODS: Eighteen dogs with spontaneous breast tumors (5 carcinomas, 4 adenomas, and 9 benign mixed-tissue tumors) underwent dynamic magnetic resonance imaging after intravenous injection of gadopentetate dimeglumine and the blood-pool agent. Signal intensity time curves were followed up to 30 minutes after injection of both agents in the same animal. A nonlinear fitting routine enabled calculation of the delivery and clearance half lives of the contrast agent kinetics in each tumor. RESULTS: For gadopentetate dimeglumine, a fast signal increase was found immediately after intravenous injection, with a subsequent signal decay in all tumors. No difference was observed between the enhancement kinetics of different tumor types after gadopentetate dimeglumine application. Similar kinetics were found in benign lesions after injection of the blood-pool agent. However, in carcinomas the blood-pool agent displayed a slower delivery, delayed peak enhancement, and slower tumor tissue clearance or even a signal plateau of more than 30 minutes. CONCLUSIONS: Dynamic magnetic resonance imaging of breast neoplasms using a blood-pool agent may help to better differentiate between benign and malignant lesions because it demonstrates the enlarged interstitial space and increased capillary permeability in carcinomas.

Age, cardiovascular risk factors and coronary heart disease as determinants of platelet function in men. A multivariate approach.

Older age, the cardiovascular risk factors and arteriosclerosis have been reported to be associated with stimulated platelet function. To evaluate the relative importance of these factors in determining platelet function, a cross-sectional multivariate study in 191 men, 113 healthy subjects and 78 patients with angiographically documented coronary heart disease, was performed. In healthy subjects, stepwise multiple linear regression identified age to be a major determinant of platelet aggregability. After induction with both ADP and collagen the platelet aggregatory response markedly increased with age. In the patients, platelet function was not age dependent. In multivariate analysis of variance, neither smoking status nor hypercholesterolemia (greater than or equal to 240 mg/dl) were determinants of platelet function in either group. An increase in systolic blood pressure was associated with slightly more inhibited ADP induced aggregation in both healthy subjects and patients with coronary heart disease. In patients compared to healthy subjects, aggregation after induction with ADP and collagen was markedly enhanced and the in vitro formation of thromboxane after collagen stimulation increased. Thus, by multivariate analysis, age and the presence or absence of coronary heart disease were found to be major determinants of platelet function. In contrast, the cardiovascular risk factors smoking, hypercholesterolemia and hypertension were associated with only minor or no alterations of platelet function.

Biplane transesophageal color Doppler echocardiography for assessment of mitral valve area with mitral inflow jet widths.

Biplane transesophageal color Doppler echocardiography can image the mitral valve orifice in two orthogonal views. If the maximal stenotic jet width through the mitral valve obtained with the vertical transducer represents the major axis, the stenotic jet width dissected by the horizontal transducer should be the minor axis of the mitral orifice. Thus the mitral valve area can be calculated assuming an oval shape of mitral orifice. Nineteen patients with mitral stenosis were investigated. Maximal mitral stenotic jet width (JW1) was searched on a vertical plane and the jet width from the orthogonal view (JW2) was obtained on a horizontal plane. Mitral valve areas from the color Doppler jet widths were calculated by pi.JW1/2.JW2/2 and compared with those derived from Gorlin's formula. Adequate quality of echocardiographic images could be obtained in all patients for transesophageal color Doppler jet width measurements or Doppler pressure half-time determinations and in 16 of 19 patients for transthoracic planimetery of the mitral orifice at the parasternal short axis. Mitral valve areas derived from biplane transesophageal color Doppler imaging (1.31 +/- 0.53 cm2) were not different from those calculated according to Gorlin's formula from the catheterization data (1.25 +/- 0.50 cm2), those determined by transthoracic echocardiographic planimetery (1.38 +/- 0.5 cm2), or those calculated from the Doppler pressure half-time method (1.32 +/- 0.41 cm2) (difference not significant by analysis of variance). There was a very strong correlation between transesophageal echocardiographic mitral valve areas and those derived from catheterization data (r = 0.94; standard error of the estimate = 0.13 cm2). A similar correlation was obtained for the planimetric echocardiographic method (r = 0.94; standard error of the estimate = 0.14 cm2). A slightly less strong correlation was found between mitral valve areas derived from the Doppler pressure half-time method and those derived from Gorlin's formula (r = 0.83; standard error of the estimate = 0.24 cm2). The pressure half-time method accurately predicted the mitral valve area in most (15/19) patients, but it significantly (> 0.4 cm2) overestimated mitral valve area in two patients with aortic regurgitation and underestimated (< 0.4 cm2) mitral valve area in two patients with left ventricular hypertrophy. Determination of mitral valve area by color Doppler biplane transesophageal echocardiography is an alternative for accurate estimation of mitral valve area and may be most useful in intraoperative monitoring during surgical or balloon mitral commissurotomy or in the case of inadequate imaging quality of transthoracic echocardiography.

A fast low-noise line scan x-ray detector.

A fast, low-noise line scan detector (NIKOS) for digital radiography has been developed. It consists of an input x-ray phosphor screen that is coupled to a modified Reticon photodiode array by means of fiber optics with incorporated image intensifier. In its current version the detector can be operated with a maximum 500 Hz image acquisition rate for interlaced readout of two lines of 128 pixels each. Using a Gd2O2S:Tb x-ray input phosphor, an afterglow of 25% in the first subsequent readout was observed. We also conducted afterglow measurements on several other powder and single-crystal phosphors and the photodiode array. Using CdWO4, the afterglow of the detector is limited by the lag of the photodiode array of 4.5%. By modifying the readout electronics the noise of the photodiode array was reduced to below 1 Graylevel, corresponding to a signal-to-noise ratio of 5200. The detective quantum efficiency (DQE) of the detector ranged from 0.18 to 0.4 for typical signal levels. The sensitivity was 10% saturation per 1.9 mR entrance dose. The modular design of the NIKOS detector allows for individual selection of each component to optimize performance for a given application.

Exercise capacity, arrhythmias, humoral and chemical parameters during long-term therapy with xamoterol.

In order to assess potential harmful effects of the partial beta-1 agonist xamoterol during long-term therapy, we randomly assigned 30 patients with coronary arterial disease and heart failure in classes II and III of the classification of the New York Heart Association to 200 mg of xamoterol twice daily or placebo during a treatment period of 3 months. A supine bicycle exercise test was performed at baseline and after three months in order to assess changes of exercise capacity. Blood samples for determination of creatinine, electrolytes, renin and norepinephrine were withdrawn simultaneously. Twenty-four hour ambulatory Holter electrocardiograms were performed before study, at the end of the study and 72 hours after withdrawal of study medication. On xamoterol, exercise capacity increased from 21.9 +/- 9.7 to 27.8 +/- 14.8 kilojoule (P = 0.032) compared to baseline levels. Exercise duration increased from 340 +/- 115 to 400 +/- 144 seconds (P = 0.043). Heart rate decreased by 10% (P = 0.05) at the 50 watt level and by 10% (P = 0.024) on maximum exercise compared to the baseline values. The rate pressure product was unchanged at rest and dropped by 11% (P = 0.038) on maximum exercise. In contrast, on placebo no significant changes occurred. During xamoterol therapy no changes of blood pressure, electrolytes, renal function and the time-intervals of electrocardiogram were observed. Xamoterol did not enhance arrhythmias during 24-hour ambulatory Holter monitoring. No serious side effects were observed. Xamoterol would appear to be a suitable and safe drug in the therapy of mild to moderate heart failure.

[Transjugular puncture of the portal vein. Portography and selective phlebography of abdominal organs. An experimental study in dogs (author's transl)]. / Transjugulare Pfortaderpunktion, Portographie und selektive Phlebographie viszeraler Organe. Eine experimentelle Studie am Hund

Transjugular transhepatic portography is a new method for catheterising the portal vein and its tributaries. In order to gather experience of the method before applying it clinically, the transvenous approach was studied in six dogs. Transjugular portography has the following advantages as compared with umbilical vein catheterization and percutaneous, transhepatic portal vein catherterisation: 1. Because of the relative positions of the jugular veins, vena cava and portal vein, manipulation of the catheter for selective phlebography is simpler. 2. There is no risk of a haemoperitoneum or bile peritonitis if a correct technique is used since the liver capsule remains intact. 3. In the presence of portal hypertension, it may be possible in future to create an intrahepatic portocaval shunt by the transjugular approach without a major operation. Sclerosis of oesophageal varices is possible, as it is with the other procedures.