OBJECTIVES: To investigate the role of ATP-sensitive potassium channel (KATP) during sustained ventricular fibrillation (VF), the effects of gliburide, a specific blocker of KATP channel and PCO400, an KATP opener, were studied in isolated and perfused swine right ventricular free walls (n=). METHODS: Recording of single cell transmembrane potentials was performed and constructed action potential duration restitution (APDR) curve by plotting APD 90%(APD90) versus preceding diastolic interval (DI). RESULTS: All isolated tissues fibrillated spontaneously. In this preparation, stable VF could persist over a 4-hour period if it was allowed to continue undisturbed (n=). Gliburide (1-5 uM) increased DI without significant changes in APD90 during VF, resulting in more regularization of VF. Higher concentration (10-20 uM) increased both APD90 and DI, and converted to monomorphic ventricular tachycardia (MVT) through the transitional period characterized by APD alternans. PCO400 (1-2.5 uM) caused a significant shortening of APD during MVT and a period of APD alternans became more evident before conversion from MVT to VF. Gliburide eliminated profibrillatory effect of PCO400. This antifibrillatory action of gliburide was accompanied by gradual decrease in the maximum slope of APDR curve during VF. CONCLUSION: KATP channel blockade causes a transition from VF to MVT via lengthening of DI and APD alternans, concomitantly with a reduction of the slope of APD restitution curve.
Action Potentials ; Membrane Potentials ; Potassium Channels ; Swine ; Tachycardia, Ventricular ; Ventricular Fibrillation*

Chondroid syringoma is a sweat gland tumor that is composed of a mixture of epithelial cells and mesenchymal tissue. It is most frequently located on the head and neck. Chondroid syringoma is a firm intradermal or subcutaneous nodule. Histologically, the epithelial component consists of tubulocystic structures and aggregates of epithelial cells as well as single scattered epithelial cells throughout the stroma. It rarely contains osteoid stroma, and there are only a few reports of cases associated with ossification. We describe here an unusual chondroid syringoma associated with marked ossification.
Adenoma, Pleomorphic* ; Epithelial Cells ; Head ; Neck ; Sweat Glands

No abstract available.
Brugada Syndrome* ; Bundle-Branch Block* ; Death, Sudden, Cardiac*

BACKGROUND: Arterial stiffening may affect regional myocardial function in hypertensive patients with normal ejection fraction (EF). METHODS: Brachial-ankle pulse wave velocity (PWV) was measured in 70 patients, of mean age 48 +/- 14 years, with untreated hypertension and EF > 55%. Using two-dimensional-speckle tracking echocardiography, we measured longitudinal and circumferential strain (epsilon) and strain rate (SR). Basal and apical rotations were measured using short axis views. RESULTS: The mean systolic and diastolic blood pressure in these patients was 152 +/- 15 mmHg and 92 +/- 11 mmHg, respectively. The mean value of PWV was 1578 +/- 274 cm/s. PWV significantly correlated with age (r = 0.682, p < 0.001), body mass index (r = -0.330, p = 0.005), systolic blood pressure (r = 0.386, p = 0.001) and pulse pressure (r = 0.509, p < 0.001). PWV also significantly correlated with septal E' velocity (r = -0.570, p < 0.001), E/A ratio (r = -0.414, p < 0.001), E/E' ratio (r = 0.589, p < 0.001), systolic global longitudinal epsilon (r = 0.300, p = 0.012) and early diastolic SR (SRE) (r = -0.479, p < 0.001) suggesting impaired abnormal relaxation. PWV was also correlated with basal rotation (r = -0.301, p = 0.011) and basal-to-apical twist (r = -0.256, p = 0.032). The increases in apical rotation and basal-to-apical twist were attenuated in patients with PWV > 1700 cm/s compared to those with PWV < or = 1400 cm/s or those with PWV 1400-1700 cm/s. CONCLUSION: In hypertensive patients with normal ejection fraction, arterial stiffening contributes to impaired systolic and diastolic function of the regional myocardium. Compensatory increases in ventricular twist were diminished in patients with advanced stage of vascular stiffening.
Axis, Cervical Vertebra ; Blood Pressure ; Body Mass Index ; Echocardiography ; Humans ; Hypertension ; Myocardium ; Pulse Wave Analysis ; Relaxation ; Sprains and Strains ; Track and Field ; Vascular Stiffness

A 34-year-old man, who had been treated with an endoscopic injection of a mixture of n-butyl-2-cyanoacrylate (Histoacryl) and Lipiodol for control of variceal bleeding 6 months previously, presented with an intracardiac mass in the right atrium (RA). Two-dimensional echocardiography revealed an intracardiac mass in the RA that appeared to extend from the inferior vena cava. The origin of the sclerosant was traced by computed tomography (CT). This is a very rare case in which the sclerosant migration route was demonstrated by CT scan. The findings of this case suggest that the systemic migration of sclerosant into an intracardiac chamber should be considered in patients with an intracardiac mass, especially with a history of previous sclerotherapy for variceal bleeding.
Adult ; Echocardiography ; Embolism ; Enbucrilate ; Esophageal and Gastric Varices ; Esophagus ; Ethiodized Oil ; Heart Atria ; Hemorrhage ; Humans ; Sclerotherapy ; Vena Cava, Inferior

Neurogenic pulmonary edema (NPE) leading to cardiopulmonary dysfunction is a potentially life-threatening complication in patients with central nervous system lesions. This case report describes a 28-yr woman with life-threatening fulminant NPE, which was refractory to conventional respiratory treatment, following the rupture of an aneurysm. She was treated successfully with extracorporeal membrane oxygenation (ECMO), although ECMO therapy is generally contraindicated in neurological injuries such as brain trauma and diseases that are likely to require surgical intervention. The success of this treatment suggests that ECMO therapy should not be withheld from patients with life-threatening fulminant NPE after subarachnoid hemorrhage.
Adult ; Brain/radiography ; Decompressive Craniectomy ; Extracorporeal Membrane Oxygenation ; Female ; Humans ; Intracranial Aneurysm/complications/*diagnosis ; Pulmonary Edema/*diagnosis/etiology/therapy ; Subarachnoid Hemorrhage/etiology ; Tomography, X-Ray Computed

BACKGROUND AND OBJECTIVES: Circulating B-type natriuretic peptide (BNP) has been used as a marker of left ventricular hypertrophy and heart failure, and known to be increased after exercise in healthy men as well as patients with left ventricular dysfunction. However, the relationship between exercise duration and BNP level, and the determinants of circulating BNP concentration during exercise have not been fully elucidated. For these reason, we measured circulating BNP level during exercise, and exercise-induced changes of cardiac function by echocardiography in healthy men. MATERIALS AND METHODS: Ten healthy male volunteers (mean age 27+/-3 year-old) underwent symptom-limited bicycle ergometer in supine position for 30 min. The workload started at 25 W for 6 min with increment of 50 W every 3 min. Blood samples for BNP were obtained at baseline, every 1 min for first 3 min, 25 W, 75 W, 125 W, peak exercise and 10 min after resting. RESULTS: BNP level was increased only at peak exercise (mean:5.3+/-0.5 vs 7.7+/-4.1 pg/ml, median:5.0 vs 6.3 pg/ml, p<0.05), not during submaximal exercise, and sustained 10 minutes after exercise (190+/-25 watt, 14.9+/-12 min). Peak BNP level was significantly correlated with baseline BNP level (r=0.723, p<0.05), E' (0.18+/-0.04 vs 0.29+/-0.08 m/sec, r=-0.649, p<0.05) and E/E' (4.18+/- 0.87 vs 5.66+/-2.31, r=0.769 p<0.01) by bivariate correlation analysis, but correlated with only baseline BNP level by multiple linear regression analysis (p<0.05). CONCLUSION: Circulating BNP concentration was minimally increased only after peak exercise in young healthy men, not increased at submaximal exercise The BNP concentration after exercise is only determined by baseline BNP level, not by duration and workload of exercise.
Echocardiography ; Echocardiography, Stress ; Heart Failure ; Humans ; Hypertrophy, Left Ventricular ; Linear Models ; Male ; Natriuretic Peptide, Brain* ; Supine Position ; Ventricular Dysfunction, Left ; Volunteers

BACKGROUND: In acute myocardial infarction, left ventricular remodeling, which was influenced by infarct size, location, and patency of infarct related artery(IRA), is a important prognostic factor for chronic heart failure and survival. Recently, several reports suggested that patent IRA does not always mean true myocardial reperfusion, and myocardial contrast echocardiography(MCE) may be a useful tool for assessing infarct size and viability of infarcted myocardium. So, we investigated the association between the degree of myocardial reperfusion assessed by MCE and long term change of left ventricular volume in acute anterior wall myocardial infarction patients who had patent IRA. METHODS: The study population was consisted of 17 patients with first acute anterior wall myocardial infarction patients who had patent left anterior descending artery by thrombolytic therapy or rescue PTCA. MCE was done immediately after coronary angiography within two weeks of myocardial infarction onset and analyzed by semiquantitative method to get opacification index. For analysis of left ventricular ejection fraction, wall motion abnormality and left ventricular volume, echocardiogram was taken within 2 weeks of myocardial infarction oneset and 9 months later in each case. Wall motion abnormality was quantified as wall motion index. According to serial changes of left ventricular volume, patients were divided into two groups ; group 1(less than 10% increase of LV volume at follow-up compared to intial echocardiographic exam) and group 2(more than 10% increase of left ventricular volume). We compared the opacification index of infarcted myocardium, wall motion abnormality, and ejection fraction between the two groups. RESULTS: Initial left ventricular volume and ejection fraction were not different between group 1 and group 2, but the opacification index was lower and initial wall motion index higher in group 2 than group 1. Opacification index, wall motion index, ejection fraction and left ventricular volume were closely correlated in the whole cases. By multivariate ananlysis, opacification index was the only significant factor predicting left ventricular volume increment. CONCLUSION: Myocardial reperfusion, which is closely correlated with ejection fraction and wall motion abnormality, acts as a independent predictor of left ventricular dilatation after acute anterior wall myocardial infarction. This result suggests that assessment of microvascular integrity with myocardial contrast echocardiography may be a valuable indicator to predict long-term change of left ventricular volume, although this is suggestive result in a limited number of patients.
Anterior Wall Myocardial Infarction* ; Arteries ; Coronary Angiography ; Dilatation ; Echocardiography ; Follow-Up Studies ; Heart Failure ; Humans ; Myocardial Infarction ; Myocardial Reperfusion* ; Myocardium ; Stroke Volume ; Thrombolytic Therapy ; Ventricular Remodeling

BACKGROUND AND OBJECTIVES: The mechanism responsible for lethal ventricular arrhythmia (LVA) after acute myocardial infarction (AMI) remains unclear. SUBJECTS AND METHODS: The corrected QT interval (QTc) and interval from the peak to the end of the T wave (TpTe) were measured, which indicated myocardial transmural dispersion of repolarization (TDR) in 72 patients with AMI. TpTe was also expressed as a corrected value, [TpTe/QTe]x100% and TpTe/√RR. These parameters were obtained from all the 12-leads of electrocardiography after arrival at the hospital, just before and after percutaneous coronary intervention (PCI), and at 4, 24, and 48 hours and 5 days after PCI. RESULTS: Analyzing with repeated measures analysis of variance, the TpTe, [TpTe/QTe]x100% and TpTe/√RR after AMI showed significant changes in time variance. The patients were divided into LVA (17 patients, 24%) and non-LVA group (55 patients, 76%). The [TpTe/ QTe]×100% (V₂: 25±7% vs. 22±5%, p=0.036) and TpTe/√RR (V₂: 109 ± 42 ms vs. 88 ± 22 ms, p=0.05, V₃: 108±39 ms vs. 91±27 ms, p=0.048) in V₂ and V₃ leads were prolonged in the LVA group after PCI. The [TpTe/QTe]×100% (28±9 % vs. 22±5%, p=0.025) and TpTe/√RR (129±53 ms vs. 99±41 ms, p=0.05) in V₃ lead were prolonged in the LVA group 24 hours after PCI. CONCLUSION: The mechanisms responsible for LVA after AMI may be associated with increased TDR, and PCI may have an important role in reducing LVA.
Arrhythmias, Cardiac ; Electrocardiography* ; Humans ; Myocardial Infarction* ; Percutaneous Coronary Intervention

BACKGROUND: Atrial fibrillation (AF) has a tendency to become persistent over time and is known to induce atrial electrical, mechanical and ionic remodeling. However, the underlying mechanisms by which AF persists were not fully determined. The present study was carried out to assess alterations in the gene expression, including the oxidative stress-related genes of atrial myocardial cells in patients with persistent AF, and ultrastructural remodeling, as assessed by electron microscopy (EM) in pacing-induced sustained AF canine models. METHODS: cDNA microarray technique and Western blot studies were performed, with tissue samples (right atrial appendage) from 10 patients, 4 with persistent AF and 6 used as controls, which had undergone coronary artery bypass surgery. Four dogs were subjected to continuous left atrial pacing at 400 bpm for at least 12 weeks to induce AF. One dog in sinus rhythm was used as a control sham operation. Tissue samples (1 mm3) were obtained from 4 sites of both atria for EM examination. RESULTS: Thirty up-regulated and 25 down-regulated gene expressions were observed in the patients with AF. Eight of the up-regulated and 6 of the down-regulated genes were oxidative stress-related, which were confirmed by Western blot analyses. The characteristics of ultrastructural remodeling by persistent AF were: 1) an increased number of minimitochondria, 2) disarrayed myofilaments, 3) rarefaction of myofilaments, 4) disintegrated cristae and alignment in mitochondria and 5) vacuolization. CONCLUSIONS: Persistent AF leads to alterations in the gene expression related to oxidative stress in the atrium, and also results in ultrastructural changes similar to those of an ischemia-reperfusion injury.
Animals ; Atrial Fibrillation* ; Blotting, Western ; Coronary Artery Bypass ; Dogs ; Gene Expression* ; Humans ; Microscopy, Electron ; Mitochondria ; Muscle Cells ; Myofibrils ; Oligonucleotide Array Sequence Analysis ; Oxidative Stress ; Reperfusion Injury