Paradoxical gas embolism by transpulmonary passage of venous emboli during hysteroscopic surgery: a case report and discussion.

After an episode of apparent venous gas embolism in a patient undergoing surgical hysteroscopy, transoesophageal echocardiography revealed air in the left but not in the right heart. Contrast echocardiography failed to demonstrate anatomical right-to-left shunts, making it likely that venous emboli overwhelmed the capacity of lungs to filter emboli, resulting in paradoxical embolization.

An unusual presentation and way to diagnose hepatocellular carcinoma.

A 67-year-old man with a history of chronic obstructive pulmonary disease (COPD) was admitted with acute progression of dyspnoea, productive cough, fever, elevated central venous pressure, oedema and liver enzyme abnormalities. Pneumonia with secondary right-sided congestive heart failure was considered. Additional abdominal ultrasound examination confirmed by a CT scan showed a mass in the inferior vena cava (VCI) extending into the right atrium. The central liver location and impaired haemostasis rendered liver biopsy impossible. An alternative approach was discussed and guided by two-dimensional transoesophageal electrocardiography accessing the right internal jugular vein, biopsies were taken from the atrial mass with histology suggesting the presence of a hepatocellular carcinoma as the cause of acute dyspnoea.

[Dyspnea after pneumonectomy due to atrial septum defect]. / Dyspnoe na pneumonectomie door een atriumseptumdefect.

A 55-year-old woman presented with complaints of recurrent dyspnoea one year after pneumonectomy carried out as treatment for a tumour of the left lung. During several months her symptoms progressed and eventually mechanical ventilation became necessary. On admission a patent foramen ovale was found with transoesophageal ultrasound but this was judged not to be the cause of her symptoms. The pulmonary angiogram showed a intracardiac shunt with no intrapulmonary shunts. After repeated transoesophageal ultrasound a second defect was found of a sinus venosus type. This large defect was proven to be clinically significant during catherisation of the heart, when occlusion with a balloon was performed. After surgical repair of these defects with an artificial patch, the patient recovered well. Since then she has been without complaints.

Premature ventricular contractions during triggered imaging with ultrasound contrast.

BACKGROUND: Premature ventricular contractions (PVCs) were observed during triggered second harmonic imaging of a contrast agent for myocardial perfusion assessment, with continuous infusion of the contrast agent. Further investigation into the relation of this phenomenon to both ultrasound energy and the contrast agent was carried out during a subsequent bolus-versus-infusion study. METHODS AND RESULTS: Two open-label studies in healthy male volunteers were performed. The initial study was a dose-response study in 10 subjects, which compared 3 infusion rates. Each volunteer received 3 continuous infusions with different infusion rates of the contrast agent for either 10 (n = 6) or 20 (n = 4) minutes. End-systolic triggered imaging with a mechanical index (MI) of 1.5 was used throughout this part of the study. The second study compared bolus injection with a continuous infusion in 9 volunteers, with a single-dose level but different imaging modalities: end-systolic and end-diastolic triggered imaging at MIs of both 1.1 and 1.5. Spontaneous baseline PVCs were uncommon: 10 in 344 minutes (0.03 PVC/min, maximal 1 PVC/min) of baseline imaging. During end-diastolic triggering, no increase in PVCs was seen, irrespective of MI. A significant increase to 1.06 PVC/min (P <.001) was seen during end-systolic imaging with an MI of 1.5, but not with an MI of 1.1. The increase in PVC rate was dose-dependent in the initial study. CONCLUSION: Imaging of contrast agents with high acoustic pressures can cause PVCs if end-systolic triggering is used. This effect is related to both the dose of contrast agent and acoustic pressure. It does not occur during end-diastolic triggered imaging. Precautionary measures would include using lower MIs or end-diastolic triggering.

Cardiac involvement in carriers of Duchenne and Becker muscular dystrophy.

A cross-sectional study in a cohort of DNA proven carriers of Duchenne (DMD) and Becker (BMD) muscular dystrophy was undertaken with the following objectives: (1) to estimate the frequency of electrocardiographic (ECG) and echocardiographic abnormalities; (2) to establish the proportion of carriers with dilated cardiomyopathy and (3) to assess possible associations between dilated cardiomyopathy and genotype. One hundred and twenty nine DMD and BMD carriers, aged 18-60 years, were traced through the files of the central register kept at the department of Human Genetics in Leiden. Investigations included full medical history, physical examination, ECG and two-dimensional and M-mode echocardiographic examination. Forty-seven percent had ECG changes. Thirty-six percent (DMD 41%, BMD 27%) had at least one abnormality as is usually found in the male patients. Echocardiographic examination was abnormal in 36% (DMD 38%, BMD 34%). Dilated cardiomyopathy was found in seven DMD carriers (8%), and in none of BMD carriers. In addition, 18% had left ventricle dilatation (DMD 19%, BMD 16%). Only 38% had a completely normal investigation of the heart. We found no association between genotype and cardiac manifestations. Our study underlines that cardiac involvement is part of the dystrophinopathies. Carriers should be told about the increased risk of this complication when asking genetic advice. It also implicates that a complete cardiological evaluation should be performed at least once in all carriers. If left ventricle dilatation or dilated cardiomyopathy is present a yearly follow up is needed, in order to start timely therapy.

Signs and symptoms of Duchenne muscular dystrophy and Becker muscular dystrophy among carriers in The Netherlands: a cohort study.

BACKGROUND: Carriers of Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) may show muscle weakness or dilated cardiomyopathy. Studies focusing on skeletal-muscle involvement were done before DNA analysis was possible. We undertook a cross-sectional study in a population of definite carriers to estimate the proportion and to assess the clinical profile of carriers with symptoms. We also assessed a possible correlation between genotype and phenotype. METHODS: Carriers of DMD and BMD, aged 18-60 years, were traced through the files of the central register kept at the Department of Human Genetics in Leiden, Netherlands. For each carrier who agreed to participate a medical history was taken, and muscle-strength assessment by hand-held dynamometry and manual muscle testing and cardiological assessment were done. FINDINGS: 129 carriers of muscular dystrophy (85 DMD, 44 BMD) participated in the study. In 90 women from 52 (70%) families, 37 different mutations were found. 28 (22%) women had symptoms. 22 (17%) had muscle weakness, varying from mild to moderately severe. Muscle weakness was found in carriers of DMD and BMD, but dilated cardiomyopathy was found only in seven (8%) carriers of DMD, of whom one had concomitant muscle weakness. There was an unexpectedly high proportion of left-ventricle dilation (18%). No genotype-phenotype correlation was found. INTERPRETATION: Clinical manifestation of muscle weakness, dilated cardiomyopathy, or both can be found in about a fifth of carriers of DMD and BMD. If left-ventricle dilation is taken into account, the proportion of carriers with symptoms is even higher, amounting to 40%.

In-hospital cardiopulmonary resuscitation: prearrest morbidity and outcome.

BACKGROUND: Considerations about the application of cardiopulmonary resuscitation (CPR) should include the expected probability of survival. The survival probability after CPR may be more accurately estimated by the occurrence in time of the prearrest morbidity of patients. OBJECTIVE: To identify risk factors for poor survival after CPR in relation to the dynamics of prearrest morbidity. METHODS: Medical records of CPR patients were reviewed. Prearrest morbidity was established by categorizing the medical diagnoses according to 3 functional time frames: before hospital admission, on hospital admission, and during hospital admission. Indicators of poor survival after CPR were identified through a logistic regression model. RESULTS: Included in the study were 553 CPR patients with a median age of 68 years (age range, 18-98 years); 21.7% survived to hospital discharge. Independent indicators of poor outcome were an age of 70 years or older (odds ratio [OR]=0.6, 95% confidence interval [CI]=0.4-0.9), stroke (OR=0.3, 95% CI=0.1-0.7) or renal failure (OR=0.3, 95% CI=0.1-0.8) before hospital admission, and congestive heart failure during hospital admission (OR=0.4, 95% CI=0.2-0.9). Indicators of good survival were angina pectoris before hospital admission (OR=2.1, 95% CI=1.3-.3.3) or ventricular dysrhythmia as the diagnosis on hospital admission (OR=11.0, 95% CI=4.1-33.7). Based on a logistic regression model, 17.4% of our CPR patients (n= 96) were identified as having a high risk for a poor outcome (< 10% survival). CONCLUSIONS: Time of prearrest morbidity has a prognostic value for survival after CPR. Patients at risk for poor survival can be identified on or during hospital admission, but the reliability and validity of the model needs further research. Although decisions will not be made by the model, its information can be useful for physicians in discussions about patient prognoses and to make decisions about CPR with more confidence.

Transmyocardial laser channels.

We present 2-dimensional echocardiographic images of laser-made channels in the myocardium in an experimental model and in a patient treated with transmyocardial laser revascularization.

Evolution of cardiac abnormalities in Becker muscular dystrophy over a 13-year period.

We evaluated the course of cardiac involvement in 27 previously reported patients with Becker muscular dystrophy (BMD) originating from nine kindreds. Since almost all affected individuals of each kindred were included, intrafamilial variability could be studied. We also attempted to identify associations between cardiac involvement, functional ability and mutations at DNA level. The mean follow-up period was 12.5 years. The number of patients with electrocardiographic abnormalities progressed from 44% to 71%. Dilated cardiomyopathy (DCM) with or without congestive heart failure was now present in 33% as compared with 15% in the previous study. In addition, 22% developed borderline echocardiographic abnormalities. Six patients (22%) became symptomatic and four patients died of congestive heart failure. In all families cardiac abnormalities were found. There was no association between DCM and mutation type. Despite equal functional motor ability, there was a considerable intrafamilial variation in cardiac involvement, even in brother pairs. We conclude that cardiac abnormalities are the rule and not the exception in BMD and are progressive over time. Left ventricular dilatation may begin at any moment in the course of BMD and the rate of progression is unpredictable. A substantial proportion of patients will develop an incapacitating and life-threatening DCM.

Diagnostic accuracy of transesophageal echocardiography during cardiopulmonary resuscitation.

OBJECTIVES: We sought to establish the diagnostic accuracy of transesophageal echocardiography (TEE) during cardiopulmonary resuscitation. BACKGROUND: Because of its bedside diagnostic capabilities, excellent cardiac images and lack of interference with resuscitation efforts, TEE is ideally suited to determine the cause of a circulatory arrest that is not due to severe arrhythmia. However, the diagnostic accuracy of TEE during resuscitation is unknown. METHODS: TEE was performed in patients with prolonged circulatory arrest. The TEE diagnoses were compared with diagnoses from autopsy, surgery and clinical follow-up. RESULTS: Of the 48 study patients (29 male, 19 female, mean age +/- SD 61 +/- 20 years), 28 had an in-hospital cardiac arrest and 20 an out-of-hospital onset of arrest. Forty-four patients eventually died; four survived to discharge. The diagnoses made with TEE were cardiac tamponade (n = 6), myocardial infarction (n = 21), pulmonary embolism (n = 6), ruptured aorta (n = 1), aortic dissection (n = 4), papillary muscle rupture (n = 1), other diagnosis (n = 2) and absence of structural cardiac abnormalities (n = 7). A definite diagnosis from a reference standard was available in 31 patients. The TEE diagnosis was confirmed in 27 of the 31-by postmortem examination (n = 19), operation (n = 2), angiography (n = 2) or clinical course (n = 4). In the other four patients the TEE diagnosis proved incorrect by postmortem examination. The sensitivity, specificity and positive predictive value of TEE were 93%, 50% and 87%, respectively. In 15 patients (31%), major therapeutic decisions were based on TEE findings. CONCLUSIONS: TEE can reliably establish the cause of a circulatory arrest during cardiopulmonary resuscitation.

Cardiac sympathetic neuronal function in left ventricular volume and pressure overload.

OBJECTIVES: In heart failure cardiac sympathetic neuronal function and activity appear to be altered. Although these changes are widely accepted, controversy exists concerning the neurohormonal changes occurring in pressure and volume overloaded hearts. The present study in rabbits was performed to assess the effects of mechanical overload on cardiac sympathetic neuronal function and beta-adrenoceptor density, in relation to left ventricular function. METHODS: In nine rabbits the aortic valve was perforated to induce left ventricular volume overload. Pressure overload was induced by suprarenal banding of the aorta abdominalis (group 1). Five animals were sham operated (group 2). Subanalysis of group 1 was performed for non-failing (n = 5) and failing (n = 4) hearts. Heart failure was defined as any reduction in left ventricular fractional shortening 2 weeks after the second operation compared to baseline. RESULTS: In animals with cardiac overload, left ventricular weight was higher compared with the control animals, 7.99 +/- 1.13 vs. 6.16 +/- 0.86 g (P < 0.02). Left ventricular end diastolic diameter increased from 1.35 +/- 0.16 to 1.57 +/- 0.15 cm (P < 0.005) after surgically induced overload. Left ventricular end systolic diameter and fractional shortening did not change significantly. Myocardial noradrenaline (NA) concentration and beta-adrenoceptor density were significantly lower in group 1 than in group 2, 1005 +/- 393 vs. 1643 +/- 109 ng/g (P < 0.02) and 167 +/- 36 vs. 224 +/- 36 fmol/mg protein (P < 0.03), respectively. Myocardial [123I]-MIBG uptake did not significantly differ between group 1 and 2, 2.1 +/- 0.58 vs. 1.8 +/- 0.44 (%ID/g x kg). A significant positive correlation between myocardial NA concentration and beta-adrenoceptor density was found (r = 0.66, P < 0.02). Myocardial NA concentration was inversely related to left ventricular weight (r =-0.75, P < 0.003). CONCLUSION: The present data indicate that in a condition of cardiac volume and pressure overload, sympathetic activity is enhanced as shown by myocardial noradrenaline depletion and beta-adrenoceptor downregulation. In contrast, no cardiac neuronal dysfunction is observed, even in the stage of early heart failure.

Pharmacokinetics and pharmacodynamics of saruplase, an unglycosylated single-chain urokinase-type plasminogen activator, in patients with acute myocardial infarction.

We examined in patients with acute myocardial infarction (AMI) the pharmacokinetics of saruplase, an unglycosylated, single chain, urokinase-type plasminogen activator (rscu-PA) by measuring urokinase-type plasminogen activator (u-PA) antigen and total u-PA activity, its conversion to active two-chain urokinase-type plasminogen activator (tcu-PA) and evaluated its effect on haemostatic parameters. Twelve patients were studied during and after administration of 20 mg bolus plus 60 mg continuous 1 h i.v. infusion of saruplase. For u-PA antigen and total u-PA activity (expressed as protein equivalents), where 234 U corresponds to 1 microgram, respectively, steady state plasma concentrations were 2.75 +/- 8.3 and 2.50 +/- 7.0 micrograms/ml (mean +/- standard deviation) and were reached within 20 min, t1/2 lambda 1 was 9.1 +/- 1.8 and 7.8 +/- 1.3 min, t1/2 lambda 2 1.2 +/- 0.2 and 1.9 +/- 0.5 h, and the total clearance was 393 +/- 110 and 427 +/- 113 ml/min. Inactivation of saruplase in plasma was negligible. After 15 min, tcu-PA was detected in plasma. From the ratio of the areas under the curve of tcu-PA and total u-PA activities it was calculated that 28 +/- 9.3% of the saruplase dose is converted into active tcu-PA. Systemic plasminaemia occurs as shown by a decrease in alpha 2-antiplasmin and fibrinogen and an increase in fibrinogen degradation products. Thrombin-antithrombin complex formation indicated activation of the clotting system. Saruplase is eliminated rapidly from plasma in AMI patients.(ABSTRACT TRUNCATED AT 250 WORDS)

The plasma concentration of soluble Fc-gamma RIII is related to production of neutrophils.

Fc gamma RIII (the CD16-antigen), a low-affinity receptor for IgG, is expressed by neutrophils, natural killer lymphocytes and macrophages. A soluble form of Fc gamma RIII has been identified in human plasma. This soluble form of Fc gamma RIII (sFc gamma RIII) originates from release by neutrophils. In the present study we show by transfusions of plasma that contains sFc gamma RIII of one allotype (NA1-Fc gamma RIII) in recipients homozygous for the other allotype (NA2-Fc gamma RIII) that the clearance of sFc gamma RIII is about 0.7 ml/min. Because the concentration of sFc gamma RIII was found to be constant in a small cohort of donors followed for about 1.5 years, the half-life of NA1-sFc gamma RIII is about 1.8 d, assuming a one-compartment model. The plasma concentration of sFc gamma RIII depended mainly on the production of neutrophils in the bone marrow, and was not influenced by shifts of neutrophils from one pool to another (storage, marginating or circulating pool). Because Fc gamma RIII is only expressed on mature neutrophils, this implies that the concentration of sFc gamma RIII depends on production of mature neutrophils.

The pharmacokinetics of recombinant double-chain t-PA (duteplase): effects of bolus injection, infusions, and administration by weight in patients with myocardial infarction.

The current mode of administration of recombinant tissue-type plasminogen activator (rt-PA) in acute myocardial infarction is rather complex, although the rationale for the different components of this scheme is not clearly established. We compared pharmacokinetics of a continuous infusion of 38.5 MU of Burroughs Wellcome t-PA (duteplase) over 90 minutes in nine patients (phase I) with a scheme including a 0.04 MU/kg bolus, a 60-minute 0.36 MU/kg lytic infusion and a 180-minute 0.21 MU/kg maintenance infusion in 15 patients with acute myocardial infarction (Phase II). t-PA activity and antigen were fitted in a one-compartment model from which model-dependent and model-independent parameters were derived. Clearance of t-PA activity was 1020 +/- 465 (mean +/- SD) ml/min in phase I and 1359 +/- 590 ml/min in phase II. Clearance of t-PA antigen was 666 +/- 230 ml/min in phase I and 704 +/- 199 ml/min in phase II. Clearance of activity was significantly (p less than 0.01) higher than of antigen. Clearance and steady-state plasma levels showed a large interindividual variability (coefficient of variation, 56.4%), but this was significantly reduced by dosing by weight (coefficient of variation, 28.9%; p = 0.031). A 10% bolus in phase II shortened the time to reach 75% and 90% of the steady-state plasma level by 4 and 5 minutes, respectively, not significantly different from phase I. A simulation study showed that a bolus should be approximately 15% of the lytic dose to achieve a maximal level in the shortest period.