Right-to-Left Shunting through a Patent Foramen Ovale as a Cause of Hypoxemia in a Patient with Acute Right Ventricular Infarction Diagnosed by Contrast Echocardiography

Right ventricular (RV) infarction is a well-recognized complication of acute inferior myocardial infarction. Rightto-Left shunt through a patent foramen ovale (PFO) is an unusual complication of acute RV myocardial infarction that can result in the development of severe hypoxemia. However, the diagnosis may not be easy without high index of suspicion and echocardiography combined with an echocardiographic contrast (agitated saline) is useful diagnostic imaging modality in this regard. We report a case of acute inferior myocardial infarction and RV infarction associated with unexplained hypoxemia. Contrast echocardiography detected a significant right to left shunt through patent foramen ovale, which considered as a cause of hypoxemia in this patient.

Isolated Bicuspid Pulmonic Valve

No abstract available.

A Case of Cardiac Lipoma

No abstract available.

A Case of Hepatoma extension to Right Atrium

No abstract available.

The role of transesophageal three-dimensional echocardiography in the measurement of dynamic changes of atrial septal defect

No abstract available.

Antiplatelet Effect of Hirudin in a Rabbit Carotid Artery Eversion Model

BACKGROUND AND OBJECTIVES: Thrombin and its interaction with platelets play a pivotal role in arterial thrombus formation. Hirudin, an anticoagulant agent derived from medicinal leeches(Hirudo medicinalis), is a unique and specific thrombin inhibitor with no effect on other serine protease. We investigated the inhibitory effect of hirudin on platelet deposition in a rabbit carotid artery eversion model of acute arterial thrombosis. MATERIALS AND METHODS: The everted arterial segments were perfused with 111 Indium-labeled human platelets only(control, n=8), and a mixed solution of 111 Indium-labeled human platelets and hirudin(30, 45, 60, 90 microgram/ml, n=3, respectively). Platelet deposition was calculated by a gamma-counter and confirmed by scanning electron microscopy. RESULTS: 1) Indium-111 labeling efficiency of platelets was 87.0+/-6.6%, and the aggregation of platelets was not changed after labeling. The number of platelets perfused through each arterial segment was 4.3 +/-0.2x10(8) platelets/ml. 2) The control group showed a platelet deposition rate of 23.9+/-7.0 % and a number of platelet deposition of 9.8+/-2.5x10(8) platelets/cm2 . 3) Platelet deposition of arteries perfused with hirudin(60 microgram/ml) was significantly decreased compared with that of the control group(2.9+/-0.6 vs 9.8+/-2.5x10(8)/cm2 , p<0.05). 4) The number of deposited platelets in hirudin-perfused arteries was dose-dependently decreased(30 microgram/ml:6.7+/-1.4x10(8) /cm2 , 45 microgram/ml: 4.8+/-1.7x10(8) /cm2 , 60 microgram/ml: 2.9+/-1.8x10(8)/cm2, 90 microgram/ml:2.9+/-1.4x10(8)/cm2: p<0.05 vs. control, respectively). 5) Scanning electron microscopic examination revealed significantly reduced platelet deposition in hirudin-perfused groups compared with control group. CONCLUSION: Hirudin inhibits effectively platelet deposition and arterial thrombus formation in a rabbit carotid artery eversion model. The antiplatelet effect of hirudin in this model suggests that hirudin may be an useful antithrombotic agent therapeutically useful in the prevention of acute arterial thrombus formation.

A Case Report of Primary Cardiac Lymphoma: Diagnosis by Transvenous Biopsy

Primary cardiac lymphomas diagnosed antemortem are extremely rare. We present a case of primary cardiac lymphma diagnosed antemortem by transvenous biopsy under transesophageal echocardiographic guidance. The patient who was a 62 years old male presented with facial edema, dyspnea on exertion and syncope. The chest X-ray film showed double contour at right cardiac border and the ECG showed marked sinus bradycardia. Transesophageal echocardiography (TEE), chest computed tomography (CT) and magnetic resonance imaging (MRI) showed intracardiac tumor of right atrium, invasing interatrial septum and inlets of superior and inferior vena cava and lateral wall of right atrium. Abdominopelvic CT and bone scan failed to show any extracardiac location. Transvenous biopsy confirmed the diagnosis of malignant lymphoma (diffuse large cell, B cell type). After chemotherapy was begun, the tumor makedly shrunk and symptoms resolved. Primary cardiac lymphoma is extremely rare and almost uniformly fatal, but this case showed that early diagnosis and intensive che-motherapy might contribute to a better prognosis for patients with malignant lymphoma of the heart.

Ultrastructural changes of the external elastic lamina in experimental hypercholesterolemic porcine coronary arteries

The external elastic lamina (EEL) serves as a barrier for cells and macromolecules between the media and adventitia in the vascular wall. We evaluated the morphological changes and quantitative assessments of the EEL architecture in the coronary circulation of pigs fed with a high cholesterol diet. Confocal microscopy analysis of the EEL from hypercholesterolemic coronary arteries revealed an altered pattern characterized by fragmentation and disorganization of the EEL associated with an increase in the thickness. Computerized digital analysis of the images obtained by confocal scanning microscopy demonstrated that compared to normal coronary arteries, the EEL of hypercholesterolemic coronary arteries decreased in the percentage of their elastin content (30.80 +/- 1.64% vs. 47.85 +/- 1.82%, p = 0.001). The percentage of elastin content was negatively correlated with the vessel wall area (r = -0.82, p = 0.001). The immunoreactivity for matrix metalloproteinase-3 (MMP-3) increased in cholesterol-fed coronary arteries, predominantly in the neointima and adventitia. This study demonstrates that experimental hypercholesterolemia induced ultrastructural changes of the EEL in coronary circulation. The EEL may also be an atherosclerosis-prone area compared with the intima. The EEL may play an important role in the development of structural changes which characterizes the early phase of coronary atherosclerosis and vascular remodeling.

A Clinical Study on Anti-Hypertensive Effect and Safety of Candesartan Cilexetil (Atacand) in Mild to Moderate Hypertensive Patients

BACKGROUND AND OBJECTIVES: Candesartan cilexetil (Atacand ), a selective type I angiotensin II receptor blocker, has recently been introduced as a new antihypertensive agent. We evaluated its anti-hypertensive effect and safety in mild to moderate hypertensive patients. MATERIALS AND METHODS: Candesartan cilexetil, 8 mg or 16 mg, was administered once a day over 8 weeks period in the patients with mild to moderate hypertension (25 male, 26 female, mean age: 53.5+/-1.2 years). For safety evaluation, laboratory tests were performed before and after treatment with candesartan cilexetil. Changes in blood pressure, heart rate and electrocardiogram were also observed. RESULTS: 1) The mean blood pressures in the sitting position were systolic 164.1+/-2.1 mmHg and diastolic 106.3+/-0.8 mmHg before treatment, which were lowered to 135.4+/-2.0 mmHg and 89.1+/-1.1 mmHg, repectively after 8 weeks of treatment (p0.05). 4) Laboratory tests revealed no significant abnormality by the treatment with candesartan cilexetil. 5) Left ventricular hypertrophy by ECG criteria detected in 3 cases disappeared after treatment with candesartan cilexetil. 6) No significant side effects were observed during the treatment period. CONCLUSION: Candesartan cilexetil, 8 mg or 16 mg, once a day is an effective and well tolerated antihypertensive treatment. It has a significant dose-dependent antihypertensive effect.

The Inhibitory Effect of Triflusal (Disgren)on the Platelet Aggregation in Healthy Volunteers: Impedance Method with the Whole Blood

BACKGROUND: Antiplatelet drugs play an important role in the prevention and treatment of coronary artery diseases. Triflusal, an antiplatelet drug structually related to acetylsalicylic acid, selectively inhibits the cyclooxygenase of platelet and thromboxane A2 formation. However there is a controversy about the clinical dosage and the quantitative evaluation of the platelet antiaggregatory effect of triflusal. In this study we have evaluated the platelet antiaggregatory effect and cost-effective dosage of triflusal in the whole blood of healthy volunteers. METHODS: Using the whole blood of 50 healthy people, we performed a baseline platelet aggregation function test induced by adenosine diphosphate (ADP) and collagen. The subjects were subdivided into 3 treated groups (300 mg, 600 mg, 900 mg). We compared the platelet aggregation effect between the baseline results and 2 weeks after triflusal administration. RESULTS: Triflusal inhibited the platelet aggregation induced by ADP and collagen in the 600 mg administration group most effectively. The platelet aggregation induced by collagen was inhibited dose-dependently. The definite inhibitory responders (% inhibition > or = 25) for platelet aggregation induced by collagen were more common than those induced by ADP (33% vs 27% in 300 mg, 71% vs 53% in 600 mg, 78% vs 39% in 900 mg). There were no serious clinical side-effects except gastrointestinal trouble. One volunteer in the 900 mg treated group discontinued the treatment due to epigastric pain. CONCLUSION: We conclude that triflusal has a dose-dependent inhibitory effect on platelet aggregation induced by collagen and that the most effective dosage for platelet antiaggregation effect is 600 mg per day.

The Inhibitory Effect of Triflusal (Disgren)on the Platelet Aggregation in Healthy Volunteers: Impedance Method with the Whole Blood

BACKGROUND: Antiplatelet drugs play an important role in the prevention and treatment of coronary artery diseases. Triflusal, an antiplatelet drug structually related to acetylsalicylic acid, selectively inhibits the cyclooxygenase of platelet and thromboxane A2 formation. However there is a controversy about the clinical dosage and the quantitative evaluation of the platelet antiaggregatory effect of triflusal. In this study we have evaluated the platelet antiaggregatory effect and cost-effective dosage of triflusal in the whole blood of healthy volunteers. METHODS: Using the whole blood of 50 healthy people, we performed a baseline platelet aggregation function test induced by adenosine diphosphate (ADP) and collagen. The subjects were subdivided into 3 treated groups (300 mg, 600 mg, 900 mg). We compared the platelet aggregation effect between the baseline results and 2 weeks after triflusal administration. RESULTS: Triflusal inhibited the platelet aggregation induced by ADP and collagen in the 600 mg administration group most effectively. The platelet aggregation induced by collagen was inhibited dose-dependently. The definite inhibitory responders (% inhibition > or = 25) for platelet aggregation induced by collagen were more common than those induced by ADP (33% vs 27% in 300 mg, 71% vs 53% in 600 mg, 78% vs 39% in 900 mg). There were no serious clinical side-effects except gastrointestinal trouble. One volunteer in the 900 mg treated group discontinued the treatment due to epigastric pain. CONCLUSION: We conclude that triflusal has a dose-dependent inhibitory effect on platelet aggregation induced by collagen and that the most effective dosage for platelet antiaggregation effect is 600 mg per day.