Elevated plasma levels of soluble tumor necrosis factor receptor (sTNFRp60) reflect severity of acute pancreatitis.

OBJECTIVE: To investigate the role of activated leukocytes in acute pancreatitis, we measured soluble receptors of tumour necrosis factor alpha (sTNFR, p60 subtype) in plasma and evaluated the association of sTNFR with the clinical severity of the disease. DESIGN: Prospective, descriptive study. SETTING: A medical intensive care unit (ICU) in a university hospital. PATIENTS: 25 consecutive ICU admissions of adult patients with acute pancreatitis. MEASUREMENTS AND RESULTS: The clinical severity of the disease was assessed using weights for the worst 17 physiological abnormalities of the Acute Physiology and Chronic Health Evaluation III score over a 24-h period after admission. According to the sum of these weights (giving the Acute Physiology Score, APS) patients were divided into a group with mild pancreatitis (APS < 25) and into a group with severe pancreatitis (APS > or = 25). Soluble TNFR was determined in plasma using an enzyme-linked immunoadsorbent assay. In patients with clinically severe pancreatitis, plasma sTNFR concentrations of 8.8 (16) ng/ ml (median, interquartile range) were significantly higher when compared to patients with mild disease [2.7 (1.5) ng/ml; p < 0.0001]. The sensitivity and specificity of sTNFR plasma concentrations (cutoff point at 5 ng/ml) for the prediction of severe pancreatitis were 90 and 100%, respectively. A highly positive correlation between sTNFR and deviations of physiological parameters from normal (APS score) was demonstrated (r = 0.81). The development of multiple organ failure (MOF) and death was associated with significantly higher sTNFR levels when compared to patients without MOF and survivors [16.4 (17) vs 3.2 (2) ng/ml, p = 0.0014 and 16.0 (18) vs 3.3 (4) ng/ml, p = 0.016, respectively]. For evidence of necrotizing pancreatitis, plasma C-reactive protein concentrations were measured and a significant exponential regression was found with sTNFR (r = 0.77, p < 0.0001). Patients developing pancreatic necrosis, as demonstrated by contrast-enhanced computed tomography, had significantly higher sTNFR concentrations when compared to patients with edematous pancreatitis [9.1 (17) vs 3.2 (2) ng/ml, p = 0.0018). CONCLUSION: The p60 subtype of soluble TNFR is elevated in the plasma of patients with clinically severe acute pancreatitis. This elevation is positively correlated to abnormalities in physiological parameters, development of MOF, and mortality. The association with pancreatic necrosis suggests that, by mediating the effects of TNF, TNFRp60 reflects inflammatory tissue damage leading to severe systemic complications.

Q.E.D. Alcohol test: a simple and quick method to detect ethanol in saliva of patients in emergency departments. Comparison with the conventional determination in blood.

OBJECTIVE: The aim of this pilot study was to assess whether ethanol concentrations in saliva are comparable to those in blood and to evaluate whether this new non-invasive saliva alcohol test is suitable for use in emergency departments. DESIGN: Prospective, open, non-randomised study. SETTING: University hospital emergency department. PATIENTS AND METHODS: 100 consecutive patients who were admitted to the emergency department whose smell and/or behaviour indicated alcohol abuse. Fifteen patients participated as a control group after they were asked to abstain from alcohol consumption for 24 h before the study. INTERVENTIONS: Blood and saliva samples were obtained at the same time for ethanol measurement. The Q.E.D. Alcohol Test A350 was used in order to measure the concentration of ethanol in saliva. Blood samples were analysed by the alcohol dehydrogenase method. RESULTS: The mean difference between the ethanol levels in blood and saliva was -0.1 mg/dl, whereas the values measured in saliva were on average 0.1 mg/dl higher than those measured in blood (p = 0.002). CONCLUSION: The Q.E.D. Alcohol Test A 350, which uses saliva, is well suited for quantitative determination of alcohol levels. The levels measured in saliva correlate well with those measured in blood at both the lower and the upper end of the scale. Because this test is quick and easy to perform by emergency room personnel and the results are accurate enough for clinical purposes, it should prove valuable to determine whether impaired consciousness is related to alcohol intoxication or to other likely causes.

Aborted sudden death in a patient with a structurally normal heart: the Brugada syndrome.

We report a 37-year-old man with documented aborted sudden death. After resuscitation, the patient showed no structural heart disease but the ECG showed a right bundle-branch block with a descending ST segment elevation in leads V(1) and V(2). After transient normalization of the ECG, the administration of ajmaline led to spontaneous development of the distinct descending ST segment elevation in the right precordial leads and therefore to the diagnosis of Brugada syndrome. The incidence of sudden cardiac death among these patients is high. The only treatment is an implantable cardioverter-defibrillator (ICD). The Brugada syndrome should therefore be borne in mind in the differential diagnosis of sudden death.

Near fatal anticholinergic intoxication after routine fundoscopy.

We describe a case of severe anticholinergic intoxication following the topical instillation of tropicamide-containing eyedrops. Tropicamide is a short-acting atropine-like derivative and has been regarded as an effective and safe mydriatic. Half an hour after routine fundoscopy, a 62-year-old man experienced two generalized seizures with respiratory arrest and required intubation and mechanical ventilation. The patient was treated with physostigmine and made a full recovery.

Comparison of acute effects of anthracyclines on cardiac electrophysiological parameters of isolated guinea-pig hearts.

This study was performed to evaluate the acute effects of two anthracycline derivatives, doxorubicin and 4'O-tetrahydropyranyl-doxorubicin [(THP)-doxorubicin], on the conduction intervals, heart rate and refractoriness of isolated spontaneously beating guinea-pig hearts using a high-resolution ECG recording technique (SST-ECG). Doxorubicin as well as (THP)-doxorubicin were added to the perfusate in increasing concentrations of 0.1, 1 and 10 microM. Doxorubicin did not significantly alter the heart rate or conduction intervals. Only the rate-dependent QT interval was significantly shortened under the influence of 10 microM doxorubicin. In contrast, 10 microM (THP)-doxorubicin led to a significant reduction in the heart rate (-13% +/- 3%; P less than 0.01, n = 7) and to a prolongation of atrioventricular conduction time (24% +/- 10%; P less than 0.05, n = 7). The rate-dependent repolarization period (QT interval) was only insignificantly shortened in the presence of 10 microM (THP)-doxorubicin. The maximal following frequencies of each part of the conduction system were not changed by 10 microM doxorubicin. In the presence of (THP)-doxorubicin, the maximal following frequency of the ventricular myocardium was increased by as much as 36% +/- 8% (P less than 0.01, n = 7), indicating a shortening of the effective refractory period of the ventricular myocardium (V-ERP). These results show that the activation of (THP)-doxorubicin resembles the effects of Ca-antagonistic compounds on the heart (i.e. decrease in the spontaneous sinus rate and prolongation of the AV-nodal conduction interval). Changes in the QT interval exerted by doxorubicin and the shortening of the ventricular effective refractory period by (THP)-doxorubicin may indicate an alteration of the K(+)-conductance of the membrane. As the acute electrophysiological effects of doxorubicin and (THP)-doxorubicin are modest and occur only at excessive concentrations (10 microM), a direct influence on the generation of arrhythmias in healthy hearts is unlikely.

Influence of a novel amino acid solution (enriched with the dipeptide glycyl-tyrosine) on plasma amino acid concentration of patients with acute renal failure.

In this randomized, double-blind controlled study we compared the effect of parenteralnutrition with two different amino acid solutions on the plasma concentration of amino acids in 27 patients with acute renal failure. Fourteen patients received the new dipeptide-containing (glycyl-tyrosine) amino acid solution (AADI) in combination with glucose (60%) and fat (10%) as an 'all-in-one' solution over 120 h continuously via a central venous catheter. In the control group (AAST), parenteral nutrition with a standard amino acid solution in isonitrogenous and isocaloric form (0.7 g amino acids/kg BW/day and 25 kcal/kg BW/day) was administered to 13 patients over the same period of time. The administration of the dipeptide-containing amino acid solution caused a return to within the normal range of most of the amino acid concentrations which were decreased at the onset. A significant difference could be found between the AADI and AAST group for the achieved plasma concentrations of threonine (P < 0.01), phenylalanine (P<0.05), isoleucine (P<0.05), tryptophan (P<0.01) and ornithine (P<0.05), The phenylalanine/tyrosine ratio, did not change in the AADI group, while a marked increase was observed in the AAST group. (152.7 +/- 23.5 - 159.8 +/- 37.6 vs 172.6 +/- 24.6 - 310.6 +/- 136.7, respectively). The plasma concentration of glycyl-tyrosine was at the limit of detectability indicating rapid hydrolysis of the dipeptide in acute renal failure. These data suggest that the new dipeptide-containing amino acid solution offers a clear advantage over a standard amino acid formulation in correcting the amino acid imbalances in plasma of patients with ARF and is able to maintain normal tyrosine concentrations and phenylalanine/tyrosine ratio.

Antiarrhythmic effects of adenosine on ischemia-induced ventricular fibrillation.

PURPOSE: The antiarrhythmic efficacy of adenosine during states of AV-nodal reentrant tachycardias is well known and clinically established. Adenosine is also able to reduce ventricular arrhythmias when applied before coronary ligation in rats. Hypoxia or ischemia leads to an increased production of adenosine by cardiac myocytes. The purpose of this study was to evaluate if adenosine also has a direct antiarrhythmic effect on ischemia-induced ventricular fibrillation. MATERIALS AND METHODS: In this study, the antiarrhythmic effects of adenosine on ventricular fibrillation during global (low flow) ischemia were evaluated in isolated guinea pig hearts perfused by the method of Langendorff. RESULTS: Adenosine showed a dose-dependent prolongation of the peak to peak interval of the ventricular ECG signal during ventricular fibrillation until ventricular flutter or tachycardia occurred at a concentration of 2 mmol/L. At a concentration of 20 mmol/L, adenosine converted ventricular fibrillation into ventricular tachycardia with intermittent periods of asystole. This conversion of ventricular fibrillation to asystole was antagonised by 200 micromol/L theophylline. CONCLUSION: Adenosine appears to have an antiarrhythmogenic effect both in supraventricular and ventricular rhythm disturbances. During myocardial infarction, where huge amounts of adenosine are present in ischemic regions, asystole may respond to adenosine antagonists.

The evaluation of the no-independent vasodilatative effect of iloprost in isolated perfused Guinea pig hind limbs.

AIM: In critical limb ischemia vasodilatators play an important role in the treatment of the disease. Considering that the endothelium is seriously damaged in these patients, we wanted to evaluate if the vasodilatative effect of iloprost does or does not depend on the endothelium by using the model of the isolated perfused guinea pig hind limb. METHODS: A catheter was inserted via the distal aorta and common iliac artery. After stabilization, iloprost was administered at a dosage of 0.1 microM. In a subsequent series of experiments precontraction of the peripheral vascular bed was achieved with 40 mM KCl followed by 0.1 microM iloprost. In a 3rd series of experiments L-NAME (100 microM) was administered after the equilibration period for 30 minutes, followed by 0.1 microM iloprost. In the 4th series of experiments, after the administration of L-NAME (100 microM), KCl (40 mM) was administered to precontract the vascular bed and iloprost 0.1 microM was added. RESULTS: The administration of iloprost alone and after addition of KCL induced a significant decrease in vascular resistance(-49.6+/-14.1% [x+/-SEM, n=7]). The addition of L-NAME did not affect vascular resistance. The consecutive addition of iloprost reduced vascular resistance significantly (-4.2+/-0.7% [x+/-SEM, n=7]). After addition of L-NAME 100 microM and precontraction with KCl 40 mM, iloprost once again significantly reduced peripheral vascular resistance (-51.5+/-14.4% [x+/-SEM, n=6]). Reduction of peripheral vascular resistance by iloprost was comparable to that without L-NAME. CONCLUSION: Our data show that iloprost at a dosage of 0.1 microM achieves a significant reduction in peripheral vascular resistance and that the vasodilatative effect of iloprost is independent of NO. Iloprost therefore seems to be an ideal vasodilatative drug for the treatment of patients with impaired endothelial function.

[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. / Ketoazidotische diabetische Stoffwechselentgleisung: Pathophysiologie, Klinik, Diagnose und Therapie.

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Intensive care management of acute pancreatitis: recognition of patients at high risk of developing severe or fatal complications.

The clinical spectrum of acute pancreatitis ranges from mild, self-limiting disease of fulminant illness that may rapidly lead to multiple organ failure and death. To identify factors associated with a subsequent severe course and/or high mortality we investigated retrospectively 91 patients admitted to the medical intensive care unit (ICU) with acute pancreatitis during a 2 year period. 67% of the attacks were mild (< or = 1 complication). The overall mortality rate was 9%, whereby 3% of patients with alcoholic and 13% with biliary pancreatitis died. 75% of the patients in the group with a fatal outcome were aged over sixty and 30% in the group with a mild course (p < 0.05). Females with pancreatitis of biliary origin had a mild course in 57% and a severe (> or = 2 complications) or fatal outcome in 43%. In males with alcohol abuse we observed a mild form of pancreatitis in 79% and a severe or fatal course in 21%. The delay between onset of abdominal pain and commencement of treatment in hospital was greater than 12 hours in 70% of all patients studied and there was no association with severity and development of subsequent complications. The median of the acute physiology and chronic health evaluation scoring system (APACHE-III) on the day of admission was 19 in patients with mild disease, which was significantly lower than in patients with severe (40) or fatal acute pancreatitis (53) (p < 0.0001). Serial APACHE-III measurements over 5 days after admission provided further differentiation between mild and severe or fatal cases (p < 0.0001), but no significant difference was observed between survivors with severe course and fatal outcome. In addition, RANSON scores were calculated for comparison with APACHE-III at admission and after 48 hours: concerning the recognition between mild and severe/fatal pancreatitis both scoring systems exhibited similar significant differences on day 1 and day 2. The RANSON scoring system provided further a significant differentiation between survivors with a severe course of pancreatitis when compared to deaths on day 2, whereas the APACHE-III scoring system did not. Advanced age, female sex, biliary obstruction and elevated RANSON and APACHE-III scores are risk factors for an increased rate of life-threatening complications in acute pancreatitis. The daily assessment of such scoring systems may allow the recognition of such patients and may be helpful in the routine clinical management and monitoring of acute pancreatitis.

Analysis of single channel currents with a microprocessor based device.

Data evaluation of single channel currents obtained from artificial black lipid membranes and with the patch clamp method is an important part of every single channel study, but it is a time consuming part often exceeding the time for experimentation and recording by far. We describe here a microprocessor based device, which allows the experimentator to analyse in a simple way the distribution of current levels in a single channel trace (amplitude-histogram analysis of single channel currents) either online, or offline. Current levels are sampled at a constant frequency of 6 kHz and the relative frequencies of occurrence of these current levels are displayed as a histogram on the screen of an analog or digital storage oscilloscope. The data reducing algorithm of this analyser eliminates the requirement of large amounts of mass storage that normally is needed for digital amplitude-histogram analysis of single channel recordings. Examples of evaluation for both a voltage operated cation-channel and a blockage of a potassium channel by tetraethylammoniumchloride (TEA) are given.

[Further advances in the salt sensitivity hypothesis in man]. / Weitere Fortschritte bei der Salzsensitivitätshypothese beim Menschen.

The hypothesis, proposed by us since 1981, that genetically determined salt sensitivity exists in the normotensive population has been confirmed by other groups. We propose that in salt sensitive subjects an augmented upregulation of alpha-2 combined with simultaneous downregulation of beta-2 adrenoceptors by a high salt diet (resulting in an increase in the "operative" adrenoceptor ratio) is responsible for the rise of blood pressure. In salt resistant subjects the "operative alpha-2/beta-2 adrenoceptor ratio" does not increase on a high salt intake. The adrenoceptor changes in salt sensitive subjects probably lead to an increased central sympathetic outflow (through receptor changes in certain brain areas) and to simultaneous enhanced end-organ response in resistance vessels and in the kidney, causing enhanced vasoconstriction and enhanced sodium reabsorption. Long term follow up of salt sensitive normotensives will show, whether they develop "essential hypertension" in the future.

Osteomyelitis of the spine and abscess formation in the left thigh after stent-graft implantation in the superficial femoral artery.

PURPOSE: To present a rare case of abscess formation around a covered stent in the superficial femoral artery. METHODS AND RESULTS: Two weeks after balloon dilation of a left superficial femoral artery (SFA) occlusion, during which a Hemobahn covered stent had been placed to treat dissection, a 77-year-old nondiabetic male developed intolerable pain and swelling of his left thigh. An abscess had formed around the stent, which was patent; intravenous antibiotic therapy quelled the symptoms, and the patient discontinued his oral antibiotic regimen weeks after discharge. General septicemia ensued. Acute lower limb ischemia and excruciating back pain prompted readmission. The SFA stent-graft occlusion required femoropopliteal bypass; the abscess and spondylodiskitis that had developed in the T12 and L1 vertebrae responded to intravenous antibiotics. The patient is without signs of infection at 6 months. CONCLUSIONS: Local and systemic infections associated with intraluminal prostheses are rare, and prophylactic antibiotic therapy is not commonly employed. Balloon- or device-induced arterial injury may expose the arterial wall to bacterial colonization, suggesting that patients receiving lengthy stents or experiencing arterial injury during angioplasty should receive antibiotics as a precautionary measure.

Pulmonary embolism and intracardiac thrombi--individual therapeutic procedures.

Mobile right heart thrombus is a severe but rare presentation of thromboembolic disease and usually coexists with an already massive pulmonary embolism (PE). But looking at the literature there is no clear consensus on therapeutic management. We therefore tried to find possible therapeutic guidelines and to evaluate an optimal diagnostic procedure looking at three patients who presented at our department with mobile right heart thrombus in the last year. The first patient with a small (diameter = 1 cm) thrombus in the right ventricle and peripheral pulmonary embolism underwent successful thrombolytic therapy without any complications. Patients II and III showed large intracardiac masses, in patient III extending into the superior vena cava, with central PE. These two patients underwent pulmonary arteriotomy. The diagnostic line in each case was transthoracal echocardiography followed by a helix lung CT scan. Only patients with small intracardiac thrombi and thrombotic masses in the peripheral pulmonary arteries but with hemodynamically significant PE should be treated with thrombolytic agents.

[Marine toxins]. / Maritime Toxine.

The consumption of seafood, which is contaminated by toxines of red tides, is a common cause of disease in tropic regions. The most important diseases, which are caused by red tides are Paralytic Shellfish Poisoning (PSP), Diarrhetic Shellfish Poisoning (DSP), Neurotoxic Shellfish Poisoning (NSP), Amnesic Shellfish Poisoning (ASP), Ciguatera Fish Poisoning (CFP).

Aortic dissection due to discontinuation of beta-blocker therapy.

beta-Blockers are known to protect a vulnerable aorta from acute dissection, as well as reducing the risk of recurrent dissection. This case presentation reports the history of a 60-year-old male suffering from acute aortic dissection following discontinuation of beta-blocker therapy. The patient has shown arterial hypertension for about 20 years treated solely by beta-blockers. Two days after stopping the use of metoprolol, a nonselective beta 1-blocker without ISA, the patient developed severe chest pain during exercise. Diagnosis of type I-aortic dissection according to DeBakey was achieved by transthoracal echocardiography and computed tomography. Successful surgery by replacement of the ascending aorta was performed about 1 h following admission to the intensive care unit. During the procedure, tamponade of the left ventricle occurred followed by cardiogenic shock. Postoperative management was complicated by prolonged respiratory therapy and acute gastrointestinal bleeding; 1-year follow-up showed no evidence of disease. Thus, in this case acute dissection may be the consequence of discontinuing the use of metoprolol, possibly due to uncontrolled hypertension or specific response to the beta-blocker.

The effects of the propranolol enantiomers on the intracardiac electrophysiological activities of Langendorff perfused hearts.

The optical isomers of the beta blocking agent propranolol exert beta receptor blocking as well as membrane stabilizing effects. The latter is thought to be responsible for the antiarrhythmic effect of the drug. In this study we quantified the electrophysiological effects of both isomers of propranolol on the conduction and pacemaker system of the heart. The experiments were performed on isolated hearts using a special ECG recording and stimulation technique. To abolish isoproterenol's beta adrenergic stimulatory effect on heart rate, 30-times higher concentrations of (+)propranolol were necessary than of (-)propranolol in order to be consistent. Both isomers caused a similar and marked slowing of conduction velocity through the bundle of His and ventricular myocardium. Also, heart rate, as well as atrio-ventricular conduction velocity were significantly slowed by a concentration of 10 microM of either drug, (-)propranolol being slightly more effective. Only in the presence of (-)propranolol did significant changes of atrio-ventricular and His-bundle conduction occur at a concentration of 1 microM. During programmed stimulation sinus node recovery time was more prolonged by (-)propranolol than during perfusion with (+)propranolol. The highest rate of pacing with 1:1 conduction of the sino-atrial conduction, the atrial and ventricular myocardium was significantly depressed to a comparable degree by either isomers of propranolol. These effects appear to be primarily responsible for the antiarrhythmic effects of both isomers. Because of the minor effects of (+)propranolol on sinus- and AV-node activity, as well as on beta adrenergic receptors, this isomer may have potential clinical importance in the treatment of arrhythmias.

Effects of adenosine on electrical activity of isolated guinea pig hearts.

Negative chronotropic and dromotropic effects of adenosine seem to be responsible for its antiarrhythmic action on supraventricular tachyarrhythmias. To further characterize the effects of adenosine on supraventricular arrhythmias heart rate, conduction, refractoriness, the time to steady-state of AV-nodal conduction slowing and of sinus rate reduction were evaluated. Changes of heart rate, conduction intervals and effective refractory periods were determined by the use of a high-resolution ECG recording technique in isolated guinea pig hearts perfused by the method of Langendorff. Adenosine in concentrations of 3 and 10 microM reduced sinus rate and prolonged AV-nodal conduction significantly, while intraventricular and His bundle conduction were not altered. The maximal effect of adenosine on the sinus node and AV nodal conduction occurred after 636 +/- 109 and 111 +/- 35 (mean +/- SE) beats, respectively. During programmed stimulation at a cycle length of 250 ms, adenosine reduced atrial ERP in a dose-dependent manner. At cycle lengths of 170 and 200 ms, adenosine increased the atrial ERP at 3 microM, and then progressively shortened the ERP at higher doses. At all adenosine concentrations used, the usual rate-dependent adaption in ERP was suppressed. These observations explain the efficacy of adenosine against supraventricular tachyarrhythmias where the AV-node forms a part of a reentrant circuit. Adenosine shortened the atrial ERP, but at high pacing rates also led to a relative prolongation of the atrial ERP as the rate-dependent adaption was suppressed. These opposite effects of adenosine may explain earlier contradictory findings of its action on atrial arrhythmias.

A high-resolution esophageal electrocardiogram for monitoring atrial activity in the hypothermic potassium-arrested heart.

Atrial electrical activities during hypothermic, K(+)-induced cardioplegic arrest correlate with an increased incidence of postoperative supraventricular dysrhythmias in coronary artery bypass graft patients. Surface electrocardiogram (ECG) (S-ECG) may be insufficiently sensitive to detect such activity intraoperatively, and invasive methods are impractical and traumatic. From induction of anesthesia until the end of surgery, esophageal ECG signals were detected with a new bipolar esophageal probe and a new high-resolution preamplifier (frequency range 0.01-2000 Hz). The S-ECG and the esophageal ECG (E-ECG) were evaluated independently in 18 patients. Eight of 18 patients presented during cardioplegic arrest a mean of 483 +/- 119 high-amplitude, biphasic P components (mean amplitude 0.7 +/- 0.1 mV, range 0.35-1.15 mV) per patient (mean 36 +/- 6 [5-59] potentials/min) similar to those coinciding with the surface ECG P-waves during sinus rhythm. Six of these eight patients presented a mean of 29 +/- 11 low atrial activities (mean amplitude 0.14 +/- 0.023 mV; range 0.1-0.25 mV) per patient (mean 8.4 +/- 5.6 [2.3-48] potentials/min) in the E-ECG. In the S-ECG, one patient of these eight presented 26 P waves during cardioplegic arrest simultaneously with activities in the E-ECG. During the first 5 days, seven of eight (88%) patients with atrial activities in the E-ECG versus 3 of 10 (30%) patients without atrial activities developed supraventricular tachyarrhythmias postoperatively (P < 0.05). This new high-resolution E-ECG device detected in a beat-to-beat technique more atrial activity during cardioplegic arrest than a S-ECG and offered the advantages of artifact exclusion and better prediction of postoperative supraventricular dysrhythmias.