Assessment of the calcification of the nuchal ligament and osteophytes of the cervical spine in obstructive sleep apnoea subjects and snorers.

The previous reports suggest that obstructive sleep apnoea (OSA) is related to metabolic syndrome, mineral metabolism disorders and cardiovascular disease. In addition, a possible relationship between obesity and the calcification of ligaments has been implied. However, the potential link between OSA and the calcification of ligaments has not been directly studied. In this present study, to investigate the potential link between OSA and the calcification of ligaments, we examined the prevalence of the calcification of ligaments in OSA patients and the relationship between these findings and OSA severity. Eighty consecutive patients (60 males, 20 females) diagnosed as OSA or a heavy snorer based on full-night polyso-mnography were retrospectively recruited from May 2006 to July 2008. Each patient underwent cephalometric imaging examination before the arrangement of an oral appliance. One calibrated observer (YS) reviewed the cephalometric images for the presence of calcification of the nuchal ligament and osteophytes of the cervical spine. The prevalence of calcification of the nuchal ligament in OSA patients and snorers was 46.3% (males: 52%, females: 30%) There was a significant positive correlation between the severity of OSA (AHI) and the calcification of the nuchal ligament before and after adjusting for BMI. The prevalence of the calcification of the nuchal ligament in OSA subjects and snorers was higher than in previous studies with non-OSA subjects. In addition, it is suggested that the severity of OSA correlates with the presence of calcification of the nuchal ligament.

A case of obstructive sleep apnoea with anterior cervical osteophytes.

Osteophytes of the cervical spine are usually seen in elderly adults. When prominent, they have been blamed for dysphagia, cough, dysphonia and dyspnoea. This paper reports on an obstructive sleep apnoea (OSA) patient with cervical spinal osteophytes, one cause of airway obstruction. A 75-year-old male complained of pronounced snoring. The diagnosis was mild OSA, apnoea hypopnoea index was 9.4. Patient reported no restrictions in neck movements, experiences of neck pain or neck trauma. Previously, patient underwent a tonsillectomy due to discomfort in the pharyngeal region. A lateral cephalometric image was taken to observe airway before oral appliance therapy. The image revealed the presence of large osteophytes or sclerotic enthesopathy, lying on anterior surfaces from the fourth to seventh cervical vertebrae. A computed tomography (CT) image revealed the relationship of airway position to the spine. In the reconstructed three-dimensional (3D) image, the airway appeared displaced to the right of the craniomandiblar bone, with the hyoid bone similarly displaced in a manner to that of the airway. The spine also appeared displaced to the left side ofcraniomandiblar bone. Additionally, the 3D image revealed calcification of the stylohyoideum ligament and ligamentum nuchae. This present case highlights the necessity of CT examination for OSA patients. There were several ligament calcifications in the head and neck region. Cervical spine osteophytes, as a component of Forestier's or cervical spine disease, have been associated with dysphagia and dysphonia. It was reported that bilateral vocal cord paralysis was caused by osteophytes compressing the post-cricoid area of larynx.

Ehlers-Danlos syndrome type IV with a unique point mutation in COL3A1 and familial phenotype of myocardial infarction without organic coronary stenosis.

We report on a 43-year-old male patient with Ehlers-Danlos syndrome (EDS) type IV with acute myocardial infarction (MI) without organic coronary stenosis. The disease was complicated with pneumothorax, subcutaneous and mediastinal emphysema, and splenic artery rupture. Three of the patient's family members suffered sudden cardiac death or MI. A diagnosis of EDS type IV was confirmed by decreased production of type III collagen by 86%. Mutation analysis revealed a point mutation in the COL3A1 gene that substituted glycine for aspartate at amino acid position 877. This mutation had not been reported as pathogenic for EDS type IV. These findings suggest close linkage between the mutation and the phenotype with familial MI.

Increased serum concentrations of advanced glycation end products: a marker of coronary artery disease activity in type 2 diabetic patients.

OBJECTIVE: To assess whether the concentrations of serum advanced glycation end products (AGE) in diabetic patients with obstructive coronary artery disease differ from those in type 2 diabetic patients without obstructive coronary artery disease. DESIGN: Serum AGE concentrations were measured in type 2 diabetic patients and in non-diabetic patients, both with and without obstructive coronary artery disease, and the relation between these values and coronary disease severity was evaluated. RESULTS: Mean (SD) serum AGE concentrations were higher (p < 0.0125) in type 2 diabetic patients with obstructive coronary artery disease (5.5 (2.5) mU/ml, n = 30) than in patients without obstructive coronary artery disease (2.8 (0. 5) mU/ml, n = 12), and higher than in non-diabetic patients with (3. 4 (1.0) mU/ml, n = 28) and without (3.2 (0.4) mU/ml, n = 13) obstructive coronary artery disease. Serum AGE was associated with the degree of coronary arteriosclerosis in type 2 diabetic patients with obstructive coronary artery disease (single vessel: n = 13, 3.4 (0.9) mU/m; two vessel: n = 6, 5.7 (1.6) mU/m; three vessel: n = 11, 7.2 (2.5) mU/ml). Serum AGE was positively correlated with serum mean four year HbA(1C) (r = 0.46, p < 0.01), but not with recent serum HbA(1C) (r = 0.24). The four groups did not differ in the other coronary risk factors. CONCLUSIONS: Serum AGE concentrations may be associated with long term poor glycaemic control and reflect the severity of coronary arteriosclerosis in type 2 diabetic patients.

Expression of endothelin-1 after endothelial denudation of thoracic aortas in experimental hypercholesterolemic rats.

Although endothelin-1 (ET-1) is involved in balloon-induced neointima formation, the role of ET-1 in balloon-induced neointima formation in hypercholesterolemia is unclear. In addition, it remains to be determined whether ET-1 is produced by endothelial cells or vascular smooth muscle cells, or both. We investigated tissue immunoreactive ET-1 levels by immunoblot analysis, localization of ET-1 immunoreactivity by immunohistochemistry, and expression of preproET-1 mRNA by in situ hybridization in balloon-induced neointima formation in experimental hypercholesterolemic rats. Serum total cholesterol levels were significantly higher (p< 0.01) in the 5%cholesterol-diet group (194 +/- 17 mg/dl, n=20) than in the normal-diet group (64 +/- 2 mg/dl, n=20). Before and after endothelial denudation, plasma ET-1 levels and tissue immunoreactive ET-1 levels were significantly higher in cholesterol-diet rats. The expression of preproET-1 mRNA by in situ hybridization was observed in the nuclei of endothelial cells, but not medial smooth muscle cells in normal- or cholesterol diet rats. After endothelial denudation, plasma ET-1 levels and serum total cholesterol levels did not change in either the normal- or the cholesterol-diet rats. Tissue level of ET-1 tended to increase at 3 days after denudation in normal-diet rats (1.0 +/- 0.1 vs 2.6 +/- 0. 2 density ratio, p< 0.05), although endothelial cells had not yet regenerated. The expression of preproET-1 mRNA by in situ hybridization was not observed at 3 days after endothelial denudation in either endothelial or medial smooth muscle cells in normal-diet rats. Four weeks after denudation, regeneration of endothelial cells was almost complete, and an intimal hyperplasia was observed. Tissue ET-1 levels were significantly elevated 4 weeks after endothelial denudation in normal-diet rats (1.0 +/- 0.1 vs 7.6 +/- 0.2 density ratio, p< 0.05). The expression of preproET-1 mRNA by in situ hybridization was observed in the nuclei of regenerated endothelial cells after endothelial denudation, and in smooth muscle cells migrating into the intima, but was not observed in medial smooth muscle cells in normal-diet rats. A similar pattern was observed in cholesterol-diet rats. We concluded that ET-1 was involved in neointima formation and that ET-1 was produced by both endothelial and neointimal smooth muscle cells, but not medial smooth muscle cells after endothelial denudation in experimental hypercholesterolemic rats.

Alpha-human atrial natriuretic peptide, carperitide, reduces infarct size but not arrhythmias after coronary occlusion/reperfusion in dogs.

Carperitide, a recombinant form of alpha-hANP, possesses potent diuretic, natriuretic, and vasodilatory activity, and inhibits the renin-aldosterone system and sympathetic nervous activity. However, its beneficial effects on ischemic myocardium have not been studied fully. We examined carperitide's effects on infarct size, hemodynamics, and arrhythmia frequency in anesthetized dogs (n = 20) subjected to a 90-min coronary artery occlusion/6-h reperfusion protocol. Intravenous infusion of carperitide (0.2 microg/kg/min) commenced 15 min after occlusion and continued during occlusion/reperfusion. Ventricular fibrillation developed in two of 10 control versus three of 10 treated dogs (p = NS). Hemodynamics, collateral blood flow to the ischemic wall measured 10 min after occlusion, and extent of area at risk were comparable for the two groups. Infarct size/area at risk was smaller in treated than in control dogs (4.5 +/- 2.1% vs. 27.8 +/- 7.8%, respectively; p < 0.05). During occlusion, carperitide tended to increase collateral blood flow (+39%) and significantly decreased left ventricular systolic pressure (-13%) and end-diastolic pressure (-40%) compared with baseline. In control dogs, collateral blood flow tended to decrease (-8.3%), whereas most hemodynamic parameters did not change significantly with respect to baseline. The number of arrhythmias recorded during occlusion/reperfusion was similar in the two groups. Intravenous administration of carperitide limited infarct size, but did not reduce incidence of ventricular arrhythmias after 90-min coronary occlusion/6-h reperfusion in anesthetized dogs. Although the beneficial effects of carperitide may be attributable to concomitant changes in hemodynamics and collateral blood flow, the precise mechanisms require further investigation.

Left coronary artery-left ventricular fistula with acute myocardial infarction, representing the coronary steal phenomenon: a case report.

A 59-year-old man presented with a left anterior descending coronary artery to left ventricular fistula manifesting as myocardial infarction, representing the coronary steal phenomenon. Electrocardiography showed poor R progression in leads V1 through V3. The biochemical markers of myocardial injury were elevated. Creatine kinase level was 509 IU/l, creatine kinase MB isoenzyme (CK-MB)47 IU/l, cardiac troponin T 0.62 ng/ml, myosin light chain 6.1 ng/ml, and myoglobin 142 ng/ml. Thallium-201 myocardial perfusion imaging with dobutamine stress showed a dobutamine-induced perfusion deficit of the anteroseptal wall of the left ventricle with 0.1 mV ST-segment depression in II, III, aVF, V5, and V6. The mean left anterior descending blood flow measured with the Doppler guidewire was increased from 211 to 378 ml/min. Selective coronary arteriography showed dominant left coronary artery with the contrast medium streaming into the left ventricle via a maze of fine vessels from the distal left anterior descending coronary artery. No critical stenosis of the left anterior descending coronary artery was observed. Administration of acetylcholine 100 micrograms into the left coronary artery did not induce vasoconstriction of that artery. The fistula terminating in the left ventricle was ligated surgically and the patient became free of chest pain. Thallium-201 myocardial perfusion imaging with dobutamine stress revealed no perfusion deficit of the anteroseptal wall of the left ventricle. The presence of coronary steal phenomenon was detected by dobutamine stress myocardial imaging.

Long-term treatment with antipsychotic drugs in conventional doses prolonged QTc dispersion, but did not increase ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease.

OBJECTIVE: The aim of this study was to examine the hypothesis that long-term treatment with antipsychotic drugs in conventional doses prolongs QTc dispersion and increases ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease. METHODS: We measured QTc and QTc dispersion and ventricular tachyarrhythmias in 64 patients with schizophrenia, including 59 patients who received psychiatric medications, and five patients who did not receive psychiatric medications, and 45 healthy volunteers. None of the subjects had a history of cardiac disease or showed any abnormality in chest radiograph and transthoracic echocardiographic studies. None of the subjects had electrolyte abnormality. None of the subjects were taking drugs known to influence the QT interval, other than psychiatric medications. RESULTS: QTc and QTc dispersion were significantly (P < 0.017) increased in patients who received psychiatric medications compared with patients who did not receive psychiatric medications, or with healthy volunteers [QTc: 0.442 (0.029), 0.418 (0.029), 0.417 (0.028) s, QTc dispersion: 0.054 (0.013), 0.038 (0.017), 0.038 (0.009) s]. Daily ventricular premature beats were 183 (689), 77 (23), and 86 (149), respectively. No ventricular tachycardia was observed. There were no correlation between QTc and QTc dispersion and ventricular premature beats. CONCLUSION: Long-term treatment with antipsychotic drugs in conventional doses prolonged both QTc and QTc dispersion in patients with schizophrenia, but did not increase ventricular tachyarrhythmias in patients with schizophrenia in the absence of cardiac disease. However, despite the negative findings, ventricular tachyarrhythmias may occur as a rare side-effect of antipsychotic drugs, particularly if a patient has additional risk factors.

[Potential role of primary hypercoagulability and antiphospholipid antibody as a risk factor of acute pulmonary thromboembolism].

To examine whether primary hypercoagulable states, such as protein C and protein S deficiencies and antiphospholipid antibody, are associated with an increased risk, severity and recurrence of acute pulmonary thromboembolism, the blood levels of antithrombin III, protein C, protein S, lupus anticoagulant, anticardiolipin antibodies were measured in 23 patients with acute pulmonary thromboembolism, 7 men and 16 women (mean age +/- SD, 52 +/- 5 years), admitted to Nippon Medical School Hospital from January, 1990 through December, 1997. Four patients (17.4%) had protein C deficiency, one had protein S deficiency (4.3%), 10 had lupus anticoagulant (43.5%), and 2 had anticardiolipin antibodies (8.7%). Hemodynamic evaluation by Swan-Ganz catheter and venography of the lower extremity to detect deep venous thrombi were carried out in 20 and 21 patients, respectively. There were no differences between the patients with and without primary hypercoagulable states in age (52 +/- 14 vs 52 +/- 19 years), gender, or percentage of patients with deep venous thrombi in the lower extremity (91.7% vs 88.9%). Mean pulmonary arterial pressure (38 +/- 9 vs 26 +/- 4 mmHg, p < 0.05) and total pulmonary vascular resistance (10 +/- 5 vs 6 +/- 2 Wood unit, p < 0.1) were higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states. Recurrence of pulmonary thromboembolism tended to be higher in the 13 patients with primary hypercoagulable states compared with the 10 patients without primary hypercoagulable states (46.2% vs 10.0%, p < 0.1). These findings suggest that primary hypercoagulable states, such as protein C and S deficiencies and antiphospholipid antibody, are associated with the severity and increased risk and recurrence of acute pulmonary thromboembolism.

Effect of nasal continuous positive airway pressure on pulmonary edema complicating acute myocardial infarction.

Cardiogenic pulmonary edema is a frequent cause of reparatory failure. We investigated the effects of nasal continuous positive airway pressure (CPAP) in patients with severe pulmonary edema associated with acute myocardial infarction. Twenty-nine consecutive patients were divided into 3 groups: firstly, 7 intubated patients who received mechanical ventilation at study entry comprised the intubation group. The rest of the patients were randomly assigned to either of the following 2 groups: 11 patients who received oxygen plus CPAP delivered by a nasal mask (CPAP group), and 11 patients who received oxygen only via face mask (oxygen group). All patients in the intubation group had cardiogenic shock. Two patients (18%) in the CPAP group and 8 patients (73%) in the oxygen group required mechanical ventilation with endotracheal intubation (p=0.03). The hospital mortality rate in the CPAP group (9%) was significantly lower than the oxygen group (64%, p=0.02). The pulmonary artery wedge pressure and heart rate were significantly lower in the CPAP group than in the oxygen group 24 h after study entry (p<0.05 and p<0.01). The mean pulmonary artery pressure 48 h after study entry was 18+/-5 mmHg in the CPAP group and 25+/-8 mmHg in the oxygen group (p<0.05). The PaO2/FiO2 ratio increased in the intubation group (168+/-69 to 240+/-57, p<0.05) and the CPAP group (137+/-17 to 253+/-67, p<0.01) 24 h after study entry. Arterial plasma endothelin-1 concentrations decreased significantly earlier in the CPAP group than in the oxygen group (p<0.05). In patients without cardiogenic shock, nasal CPAP lead to an early improvement in oxygenation and hemodynamics, and decreased the mortality rate. Early and active respiratory management is recommended in patients with pulmonary edema associated with acute myocardial infarction.

[Evaluation of whole blood rapid troponin T assay: cooperative study of general practitioners and office cardiologists in Tokyo].

The recently developed whole blood rapid assay for cardiac troponin T (TROP T) was evaluated by a cooperative study of general practitioners and office cardiologists in the Tokyo area (Tokyo TROP T Trial). Seventy patients with suspected acute myocardial infarction treated at 14 medical clinics were enrolled in this study. The diagnostic efficacy of troponin T was compared with that of electrocardiographic evaluations and clinical standards for diagnosis of acute myocardial infarction. Twelve of the 70 patients (17.1%) had final diagnoses of acute myocardial infarction or severe unstable angina necessitating emergency coronary intervention. Troponin T was judged as positive when simultaneously measured serum troponin T was more than 0.25 ng/ml. Sensitivity, specificity, positive predictive value, and negative predictive value were 100%, 58.6%, 33.3%, and 100% for electrocardiographic evaluation, and 58.3%, 100%, 100%, and 92.1% for troponin T, respectively. Presence of bundle branch block (11/70 cases) or previous myocardial infarction (14/70 cases) caused false positive readings on electrocardiography, and resulted in the lower positive predictive value. In contrast, troponin T was false in patients admitted within 4 hours after the onset, or patients with smaller infarct. The Tokyo TROP T Trial by general practitioners and office cardiologists concluded that the combination of electrocardiographic evaluation and use of troponin T is a rapid and efficient diagnostic method for the evaluation of patients with suspected acute myocardial infarction.

Purulent pericarditis with tamponade caused by Salmonella enteritidis.

The incidence of purulent pericarditis has declined. However, mortality remains high. We describe a case of purulent pericarditis with tamponade caused by Salmonella enteritidis, and emphasize the importance of early recognition, prompt institution of appropriate antibiotic therapy, and early surgical drainage for survival.

External high-frequency oscillation for hypercapnia after upper abdominal surgery.

The purpose of this study was to evaluate the efficacy of external high-frequency oscillation (EHFO) in patients with hypercapnia following upper abdominal surgery. Seven patients were ventilated with EHFO for 2 hr at 60 oscillations/min, with cuirass pressures of 36 cm H2O (-26 to +10), and an inspiratory to expiratory ratio of 1:1. Blood gases and cardiac functional parameters were examined during the 2 hr on EHFO. Pulmonary functional parameters were analyzed prior to the institution and after the termination of EHFO. PaCO2 significantly decreased from 61 +/- 8 mmHg to 48 +/- 7 mmHg after 10 min on EHFO (p < 0.01). PaO2 significantly increased from 74 +/- 10 mmHg 95 +/- 26 mmHg after 1 hr on EHFO (p < 0.01). The heart rate decreased significantly from 108 +/- 27 beats/min to 101 +/- 24 beats/min after 30 min on EHFO (p < 0.05). The FEV1 and FVC significantly increased from 1.09 +/- 0.54 L to 1.50 +/- 0.46 L (p < 0.01) and from 1.90 +/- 0.74 L to 2.18 +/- 0.60 L (p < 0.05), respectively. The other parameters of lung function also significantly improved after the termination of EHFO. The significant changes in all of the pulmonary functional parameters continued for 1 hr after the termination of EHFO. EHFO is an effective method of gas exchange which is associated with earlier return to preoperative lung function.

Study of regional cerebral oxygen saturation during percutaneous cardiopulmonary support.

The purpose of this study was to evaluate the change of regional cerebral oxygen saturation (rSO2) during percutaneous cardiopulmonary support (PCPS) in patients with cardiogenic shock. Fifteen patients with cardiogenic shock were evaluated during PCPS by continuous monitoring of rSO2, systemic venous oxygen saturation (Svo2), and hemodynamics. The brain damage of these patients was also evaluated during and after PCPS. There were 10 males and 5 females. Their ages ranged from 57 to 79 years old (average: 60.0 +/- 14). Two patients were unconscious before PCPS, and 11 received intraaortic balloon pumping (IABP) before PCPS. The change of rSO2 was significantly correlated with the change of Svo2. The average of rSO2 was 64 +/- 3% at the stable hemodynamic condition. The rSO2 with pulsatile PCPS was higher than that with nonpulsatile PCPS. There was no correlation between brain damage and rSO2. The patients with low rSO2 (< 50%) that resulted in poor LV function could not be weaned from PCPS. In conclusion, the continuous monitoring of rSO2 during PCPS could be a useful tool.

The combination of external high-frequency oscillation and pressure support ventilation in acute respiratory failure.

BACKGROUND: Effective gas exchange can be maintained in animals by using external high-frequency oscillation (EHFO). The present study evaluates the effect of relatively long-term duration EHFO combined with pressure support ventilation (PSV) in patients with acute respiratory failure. METHODS: Twelve patients were ventilated with EHFO combined with PSV for 8 h at 60 oscillations.min-1, with a cuirass pressure of 36 cm H2O: -26 to +10 cm H2O (27 mm Hg: -19.5 to +7.5 mm Hg) and an inspiratory-to-expiratory ratio of 1:1. Blood gas values and hemodynamic parameters were measured. RESULTS: Significant increases were noted in cardiac index (3.0 +/- 0.7 to 3.2 +/- 0.7 1.min-1.m-2, P < 0.05) and stroke volume index (32 +/- 14 to 35 +/- 13 ml.m-2, P < 0.05) without changes in pulmonary artery wedge pressure at 1 h after EHFO. PaO2 (kPa)/FiO2 and PaCO2 improved from 21.9 +/- 7.5 to 26.8 +/- 8.0 (P < 0.05) at 2 h and from 6.9 +/- 1.7 to 6.1 +/- 0.9 (P < 0.01) at 30 min after EHFO, respectively. Breath sounds could be heard well throughout the lung fields after institution of EHFO. The mucous rales also decreased. CONCLUSIONS: As a method of ventilation for patients with acute respiratory failure, EHFO combined with PSV may have potential advantages over conventional mechanical ventilation when drainage of secretions if facilitated. Beneficial effects of EHFO may appear after several hours.

Amrinone improves lung compliance in patients receiving mechanical ventilation for cardiogenic pulmonary edema.

BACKGROUND: Decrease in lung compliance is one of the major causes of respiratory failure. We investigated whether amrinone could improve lung compliance. METHODS: We selected 20 consecutive patients with respiratory failure due to severe cardiogenic pulmonary edema to receive mechanical ventilation. Patients were administered a bolus injection (1 mg.kg-1) over 10 min followed by continuous intravenous infusion (10 micrograms.kg-1.min-1) of amrinone. Lung compliance, blood gas values, hemodynamic parameters, and sample plasma amrinone levels were assessed over a 120-min period after the onset of the continuous infusion of amrinone. RESULTS: Ten min following amrinone infusion, dynamic compliance (Cdyn) and static compliance (Cst) increased from 30 +/- 11 to 36 +/- 12 ml/cm H2O and from 37 +/- 12 to 42 +/- 13 ml/cm H2O, respectively (P < 0.01). Plasma amrinone levels reached a therapeutic level as vasodilator and positive inotropic effects at 10 min after amrinone infusion. The significant change in mean pulmonary artery pressure and pulmonary artery wedge pressure occurred later than the change in compliance of respiratory system. However, there were significant correlations between the mean pulmonary artery pressure and Cdyn (r = 0.36, P < 0.01) and Cst (r = 0.44, P < 0.01), as well as between plasma amrinone levels and Cdyn (r = 0.30, P < 0.05) and Cst (r = 0.41, P < 0.01). CONCLUSIONS: Amrinone-induced improvement in lung compliance was considered mainly to be due to an increase in the number of functioning lung units by improvement of the hemodynamics and a direct positive effect of amrinone on respiratory muscle contraction.

Origin and pathophysiological role of increased plasma endothelin-1 in patients with acute myocardial infarction.

To investigate the origin and pathophysiological role of increased plasma endothelin-1 (endothelin-1) concentration in patients with acute myocardial infarction (AMI), the authors measured plasma endothelin-1 sequentially after the onset of AMI and analyzed the origin by the simultaneously obtained blood samples from the radial artery, right atrium, and pulmonary artery in 28 patients with AMI. The data were correlated with cardiovascular hemodynamics, infarct size, and coronary arteriographic findings. Arterial endothelin-1 at twenty-four and seventy-two hours significantly correlated with mean pulmonary arterial pressure (r = 0.48, r = 0.46, P < 0.05, respectively), central venous pressure (r = 0.42 and 0.51, P < 0.05, respectively), and pulmonary vascular resistance (r = 0.42, r = 0.42, P < 0.05), and endothelin-1 at one hundred twenty hour significantly correlated with peak creatine kinase (r = 0.53, P < 0.05) and creatine kinase isozyme MB (r = 0.58, P < 0.01). Simultaneous blood samples showed no significant difference in endothelin-1 concentrations among them. However, a subgroup of patients with endothelin-1 concenration higher in the radial artery than that in the right atrium showed a significantly higher mean pulmonary arterial pressure (25.2 +/- 6.5 vs 17.0 +/- 1.6 mmHg, P < 0.05), peak creatine kinase (3594 +/- 1597 vs 865 +/- 495 IU/L, P < 0.05), and peak creatine kinase MB (214 +/- 91 vs 69 +/- 22 IU/L, P < 0.05) as compared with those in patients in whom endothelin-1 was higher in the right atrium than in the radial artery. Increased plasma endothelin-1 concentration in the early stage of AMI reflects higher pulmonary artery pressure and elevated pulmonary vascular resistance, while that in the later stage is related to the infarct size. The production of endothelin-1 in patients with severe pump failure may be accerelated in the pulmonary vascular bed, left ventricle, or systemic arterial trees, and the main origin in the later stage is possibly coronary vasculature in the infarcted area.