No abstract

oronary arteriovenous fistula (CAVF) is an abnormal communication between a coronary artery and a cardiac chamber, great vessel, or other vascular structure. Most of them are found incidentally during coronary angiography (CAG), and are identified as a cause of a continuous murmur, myocardial ischemia, congestive heart failure or, rarely, bacterial endocarditis. [1][2][3] However, cases with pericardial effusion (PE) caused by rupture of the aneurysmal coronary artery are quite rare; only 3 cases of cardiac tamponade caused by rupture of the CAVF have been previously reported. [4][5][6] We report a case of chronic PE caused by a CAVF. The PE was observed for 6 months, and finally developed into cardiac tamponade. Case ReportA 75-year-old woman was referred to hospital for investigation of recurrent PE. She had a history of pulmonary tuberculosis 50 years ago. In August 1998, she had been admitted to another hospital for further investigation of cardiomegaly (cardiothoracic ratio (CTR) 63%) and was the PE was diagnosed for the first time. However, she was free of symptoms and the laboratory examinations were normal, including thyroid function and tuberculin reaction. Chest computed tomography (CT) did not show any abnormal findings except for the PE and a scar from the pulmonary tuberculosis. She was treated with diuretics and the PE disappeared within 6 months. The CTR decreased Circulation Journal Vol.66, August 2002from 63% to 54% on the chest X-ray. In February 1999, she developed shortness of breath and general fatigue, and echocardiographic examination revealed that the PE had recurred.On the admission to hospital in February 1999, her vital signs were: blood pressure 148/70 mmHg, heart rate 92 beats/min, respiratory rate 20 breaths/min, and body temperature 36.5°C. Pulsus paradoxus was not detected. Chest auscultation revealed bilaterally normal respiratory sounds and a soft continuous murmur at the left sternal border of the 4th intercostal space. She had hepatomegaly, bilateral leg edema and a markedly expanded external jugular vein.Laboratory tests were as follows: leukocytes 7.2×10 3 / l; C-reactive protein 0.5 mg/dl; erythrocyte sedimentation rate of 24 mm/h; TSH 1.86 IU/ml; free T3 1.77 pg/ml; free T4 0.83 ng/ml; tuberculin reaction 10×10 mm. A chest Xray revealed cardiomegaly (CTR = 67%) without pulmonary infiltration. The electrocardiogram (ECG) on admission was normal except for flat T waves in leads V4-6 (Fig 1A). An enhanced CT scan revealed a dilated right coronary artery (RCA) and a dilated coronary sinus (CS) vein, an expanded inferior vena cava and a large, circumferential PE (Fig 2). However, leakage of contrast media into the pericardial space was not seen. A diagnostic pericardiocentesis yielded 20 ml of bloody fluid (Hct = 22%) that contained 5.7 mg/dl of protein, 56 mg/dl of glucose and 23.2 IU/L of adenosine deaminase. The culture for bacteria in the pericardial fluid was negative, and a polymerase chain reaction for the tuberculosis bacillus was not detected. There was no evidence of ...

An 81-year-old woman developed pilsicainide intoxication associated with dehydration. The patient had been taking pilsicainide (100 mg/day) for 1 year because of paroxysmal atrial fibrillation. Her renal function was within normal limits. One week before admission, she was suffering from pneumonia, and had appetite loss, fever, and severe fatigue. Physical examination revealed dehydration. The electrocardiogram (ECG) on admission showed atrioventricular dissociation, idioventricular rhythm with marked QRS widening and QTc prolongation. The plasma concentration of pilsicainide on admission was markedly elevated at 6.2 g/ml, approximately 6 times the therapeutic range (0.25-1.0 g/ml). Continuous saline infusion was initiated for the treatment of dehydration,which progressively improved. As a result, sinus rhythm was recovered 2 h after admission, and the QRS and JT intervals gradually normalized. This is an interesting case because the proarrhythmia of pilsicainide was induced by dehydration. (Jpn Circ J 1999; 63: 219 -222)

We studied the expression of PTH-related peptide (PTHrP) and its mRNA in rat gastric smooth muscle in relation to various gastric motility states. Male rats were divided into groups subjected to fasting, feeding ad libitum, cold restraint stress, pyloric ligation, and carbachol stimulation. Cold restraint stress induced abnormal contractions. Rhythmic and moderate contractions were produced by carbachol administration, and marked distension was induced by pyloric ligation. PTHrP mRNA expression was weak in the physiological fasting and feeding states, but was markedly increased by pyloric ligation and carbachol stimulation. PTHrP and its mRNA were localized to the proper muscle layer and muscularis mucosa, but not in the mucosa by immunohistochemistry and in situ hybridization. The gene expression of PTHrP receptor in the gastric tissue was confirmed by reverse transcription-polymerase chain reaction, but serum PTHrP levels did not increase in all groups. These findings suggest that PTHrP acts as an autocrine or paracrine factor in gastric smooth muscle that responds to muscle activity caused by distension and cholinergic stimulation. However, PTHrP gene expression was decreased by stress despite the presence of strong contractions, and the sufficient relaxation did not occur. PTHrP suppression by stress is caused by the increase in corticosterone, as pretreatment of metyrapone, an inhibitor of 11 beta-hydroxylation, enhanced PTHrP gene expression in association with serum corticosterone suppression. In conclusion, PTHrP might be an important gastrointestinal peptide that regulates gastric contractile activity and is influenced by the serum corticosterone level.

Proliferation of vascular smooth muscle cells (VSMCs) is considered to be one key event underlying the pathophysiology of restenosis after angioplasty. The parathyroid hormone-related peptide (PTHrP) and its receptor, a local autocrine and paracrine regulator of cellular growth in a variety of normal cell types, have been reported in the vicinity of VSMCs. To investigate how PTHrP might be involved in the process of neointimal formation after balloon angioplasty, we examined PTHrP expression in balloon-denuded rat carotid arteries and human coronary arteries that had been retrieved by directional atherectomy. In rat carotid arteries, the RNase protection assay and in situ hybridization demonstrated that PTHrP mRNA expression increased fourfold to sixfold 1 to 7 days after denudation and continued for 28 days, coincident with downregulation of PTH/PTHrP receptor mRNA expression. In situ hybridization and immunohistochemistry revealed that PTHrP expression in balloon-denuded carotid arteries was mainly localized to the neointima. To confirm the involvement of the PTHrP in human coronary artery restenotic lesions, immunohistochemical analysis of human coronary atherectomy specimens (23 primary and 10 restenotic lesions) was then performed. The number of intimal cells that expressed PTHrP protein was significantly higher in restenotic (407 +/- 53 cells/mm2; range, 143 to 739) than in stable angina (50 +/- 12 cells/mm2; range, 18 to 132; P<.05) or unstable angina (129 +/- 16 cells/mm2; range, 21 to 232; P<.05) specimens. These data demonstrate that PTHrP gene expression in VSMCs markedly increases during neointimal formation, supporting the hypothesis that PTHrP may play an important role in vascular stenosis as a regulator of VSMC proliferation.