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

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

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*

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: A reduction of the coronary flow reserve (CFR) following successful percutaneous coronary intervention (PCI) is related to microvascular impairment. Embolization of atherosclerotic debris during PCI is a possible explanation for the finding of abnormal coronary Doppler flow following PCI. SUBJECTS AND METHODS: The CFR and intravascular ultrasound (IVUS), both before and after PCI, were recorded in 69 lesions of 69 patients with coronary artery disease. An abnormal CFR was defined as one with no change or a decrease after successful PCI. RESULTS: The patients were divided into abnormal (n=17) and normal CFR (n=52) groups. After stenting, the hyperemic flow velocity was significantly lower in the abnormal CFR group (39.3+/-12.6 vs. 48.9+/-15.4 cm/s, p=0.022). 94 and 29% of the abnormal group had soft plaques and lipid cores, respectively, compared with 62 and 2% in the normal CFR group (soft plaque: p=0.029, lipid core: p=0.002). The abnormal CFR group had smaller post-procedural vessels (15.1+/-4.2 vs. 18.2+/-4.9 mm2, p=0.039) and plaque areas (6.8+/-2.7 vs. 9.9+/-3.8 mm2, p=0.006). Furthermore, the abnormal CFR group showed less vessel expansion (1.7+/-5.5 vs. 5.0+/-3.9 mm2, p=0.018) and greater plaque loss (4.1+/-5.3 vs. 0.7+/-3.4 mm2, p=0.009). The abnormal CFR group had an increased CK-MB following PCI (4 patients, 23.5% vs. 2 patients, 3.8%, p=0.029). In a multivariable analysis, the only predictor of an abnormal CFR was the presence of a lipid core within the plaque. CONCLUSION: Soft plaques, the presence of a lipid core and a large reduction in plaques increase the risk of microembolization during the PCI procedure.
Coronary Artery Disease ; Humans ; Percutaneous Coronary Intervention ; Stents* ; Ultrasonics ; Ultrasonography*

Absent right superior vena cava in visceroatrial situs solitus is rare. It has been known the absent right superior vena cava is usually accompanied with persistent left superior vena cava. And this anomaly could be combined witk additional congenital heart disease and rhythm disturbances. We experienced one case of absent right superior vena cava accompanied by persistent left superior vena cava, secundum type atrial septal defect, and transient post-operative sinus node dysfunction.
Heart Defects, Congenital ; Heart Septal Defects, Atrial ; Sick Sinus Syndrome ; Vena Cava, Superior*

BACKGROUND: The diagnostic and prognostic implication of exaggerated blood pressure response to exercise has not been well characterized. Endothelial dysfunction has been demonstrated in patients with atherosclerosis or with risk factors for coronary artery disease. However, whether the cause of exercise induced hypertension might be due to endothelial dysfunction has not been well elucidated. Therefore, we designed this study to evaluate the endothelial function in patients with exaggerated blood pressure response during exercise. METHODS: Exercise hypertension is defined as a systolic blood pressure >or= 210 mmHg in men and >or= 190 mmHg in female, during treadmill exercise test. The endothelial function of the brachial artery, in 35 patients with exercise hypertension and 35 control subjects (mean age of 45.5+/-8.1) were measured by a high resolution ultrasound technique. The concentrations of nitrite and cyclic-GMP were measured from exercise hypertension group and control subjects during, before and after treadmill exercise. RESULTS: There were no significant differences in the clinical variables between the control and exercise hypertension group. The LVH on ECG was detected more frequently in exercise hypertension group (14 % vs. 40 %, p<0.05) and LV mass/BSA (132+/-12 vs. 139+/-14 g/m2, p<0.05) was also higher in exercise hypetension group. Endothelial-dependent vasodilation was impaired in patients with exercise hypertension (6.5+/-0.8 vs. 3.1+/-0.6 %, p<0.05). On univariate analysis, the extent of vasodilation was significantly correlated with age (r=-0.28, p<0.05) and delta systolic blood pressure (r=-0.36, p<0.05). Both the levels of NO2-/NO3- and cyclic-GMP at the maximal exercise were significantly higher than those at rest and recovery in control and exercise hypertension group (p<0.05). Although there was no difference at the increment of NO2-/NO3- during the maximal exercise between the control and exercise hypertension group (55+/-17 vs. 56+/-12 mmHg, p>0.05), a significant difference of cyclic GMP level during the maximal exercise was noted between the groups (10+/-1.8 vs. 8.3+/-2.5 pmol/mL, p<0.05). CONCLSUION: Patients with exercise induced hypertension have impaired endothelium-dependent vasodilation. This study supports the concept that endothelial dysfunction may play a significant role in exercise induced hypertension.
Atherosclerosis ; Blood Pressure* ; Brachial Artery ; Coronary Artery Disease ; Cyclic GMP ; Electrocardiography ; Endothelium ; Exercise Test* ; Female ; Humans ; Hypertension ; Male ; Nitric Oxide ; Risk Factors ; Ultrasonography ; Vasodilation

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