No abstract available.
Choriocarcinoma* ; Female ; Lung Neoplasms* ; Lung* ; Pregnancy

A variety of clinical conditions are known to result in a giant T wave and a marked QT prolongation. We report a case of a giant T wave and a QT prolongation after the resolution of an acute cardiogenic but nonischemic pulmonary edema.
Heart Failure ; Pulmonary Edema*

No abstract available.
Foreign Bodies* ; Pulmonary Artery*

BACKGROUND: In patients with myocardial infarction (MI) and chronic stable angina, the coronary flow reserve (CFR) is reduced not only in the region of myocardium perfused by the ischemia-related artery but also in the regions supplied by angiographically normal coronary arteries. The effect of myocardial stunning on the remote CFR is unknown, however. METHODS: In ten open-chest anesthetized dogs, left circumflex coronary artery was occluded for 15 minutes (myocardial stunning group, n=5) or for 30 minutes (MI group, n=5) and was followed by a reperfusion for 60 minutes. Before coronary occlusion and at 30 minutes and at 60 minutes after reperfusion, resting coronary blood flow (CBF) and maximal CBF after IV injection of each of adenosine (ADE) and acetylcholine (Ach) was measured with electromagnetic flow probe located in the proximal left anterior descending coronary artery. CFR was calculated as the ratio of maximal and resting CBF. RESULTS: At 30 minutes and 60 minutes after reperfusion, the remote resting CBF were significantly increased in both groups and the remote CFR was significantly decreased in both groups. The CFR of the MI group was lower than myocardial stunning group. The coronary vasodilator response to Ach was significantly lower than the response to ADE in both groups. CONCLUSION: After MI and myocardial stunning, there was severe coronary vasodilator abnormality in the remote myocardium and that was more marked after MI. The coronary vasodilator response to Ach was significantly lower than the response to ADE in both groups, suggesting endothelial dysfunction in remote myocardium.
Acetylcholine ; Adenosine ; Angina, Stable ; Animals ; Arteries ; Coronary Occlusion ; Coronary Vessels ; Dogs ; Humans ; Magnets ; Myocardial Infarction ; Myocardial Stunning* ; Myocardium ; Reperfusion

One of the authors' names was misprinted.

The Noonan syndrome is a rate clinical syndrome associated with similar congenital abnormalities, that is characteristics of Turner syndrome, such as short stature, webbed neck, low posterior hairline, cubitus valgus, shield chest or funnel chest, congenital features similar to Turner syndrome but with a normal karyotype, and Opitz et al. proposed the name "Noonan syndrome" for this condition in 1965. We experienced a 31-year old man with Noonan syndrome combined with valvular and infundibular pulmonic stenosis who had short stature, webbed neck and normal karyotype. So we report a case Noonan syndrome with a review of literature.
Adult ; Congenital Abnormalities ; Funnel Chest ; Humans ; Karyotype ; Neck ; Noonan Syndrome* ; Pulmonary Valve Stenosis* ; Thorax ; Turner Syndrome

No abstract available.
Echocardiography ; Heart Atria

BACKGROUND AND OBJECTIVES: The objective of this study was to assess the in-hospital clinical outcome and 6 months follow-up angiographic results after flexible balloon expandable MultiLink coronary stenting. The impact of post-stenting excessive high pressure balloon dilation on late outcome is controversial. The other purpose was to investigate the impact of post-stenting high pressure balloon dilation (HPD group > or =14 atm) on clinical and angiographic outcome in comparison to moderate pressure dilation (MPD group < 14 atm). MATERIALS AND METHOD: The MultiLink stents were implanted in 124 patients (mean age 58+/-9, M/F=94/30) with 128 lesions. Post-stenting high pressure balloon dilation was performed to have less than 10% of residual stenosis and smooth in-stent lumen without IVUS guidance. RESULTS: The indications for stenting were elective in 88 lesions (69%), suboptimal angioplasty results in 27 lesions (21%), and bail-out in 13 lesions (10%). The incidence of in-hospital major adverse cardiac events was 1.6% and major vascular complication rate was 3.2%. The follow-up angiography was performed in 86 patients (69%) at 7.9+/-2.6 months. The angiographic restenosis rate was 22.7%. The acute gain of HPD group had a tendency to be higher than MPD group (HPD:MPD=2.33+/-0.51 mm:2.22+/-0.44 mm, p=0.08) and the late loss of MPD group had a tendency to be lower than HPD group (MPD:HPD=0.86+/-0.73 mm:0.95+/-0.84 mm, p=0.09). And the net gain and restenosis rate of both groups were similar respectively (HPD:MPD=1.38+/-0.94 mm:1.36+/-0.83 mm, p=ns, HPD:MPD=22.5%:22.9%, p=ns). CONCLUSION: The MultiLink coronary stent system is a safe and effective device with high procedural success rate and also has the acceptable angiographic restenosis rate for the treatment of coronary artery disease. The post-stenting excessive high pressure balloon dilation might not be necessary during the deployment of MultiLink stent.
Angiography ; Angioplasty ; Constriction, Pathologic ; Coronary Artery Disease ; Follow-Up Studies* ; Humans ; Incidence ; Stents*

BACKGROUND: little is known about the mechanisms responsible for ventricular tachycardia during myocardial ischemia and reperfusion. The purpose of this study was to evaluate the effects of the autonomic nervous system on ventricular tachycardia in dogs. METHODS: Four groups of eight dogs were studied. The control group had intact autonomic neural innervation:the stellectomy group had bilateral transection of stellate ganglia:the vagotomy group had bilateral transection of cervical vagi; and the autonomic denervation group underwent bilateral transection of stellate ganglia and cervical vagi. Open-chest dogs anesthetized with ketamine were studied in 3 sequential steps: denervation, ischemia, and reperfusion stage. At the end of each step, we estimated effective refractory period (ERP) at four sites : the apex of non-ischemic area, the base of non-ischemic area, the apex of ischemic area, and the base of ischemic area. We observed early afterdepolarization (EAD) through recording monophasic action potential on the ischemic epicardium during ischemia and reperfusion stages. RESULTS: In ischemia stage, deltaERPs(ERPmax.-ERPmin.) were significantly prolonged, compared to deltaERPs at denervation stage, and deltaERPs of the vagotomy group tended to be prolonged to 60 minutes after myocardial ischemia, as compared to those of the stellectomy group and the autonomic denervation group. The incidence of ventricular tachycardia during ischemia presented a significant increase in the vagotomy group, compared to the control group. However, there was no difference in incidence of ventricular tachycardia between the stellectomy group and the control group. deltaERP at the group with the occurrence of ventricular tachycardia were significantly prolonged , compared to the other group without the occurrence of ventricular tachycardia. In terms of the incidence of EAD, there was no difference between the groups and it was not associated with ventricular tachycardia. deltaERP was significantly decreased to 30 minutes after reperfusion, at which point there was no significant difference between the groups. There was no correlation between EAD and ventricular tachycardia. However, deltaERP with ventricular tachycardia indicated much more significant increase than deltaERP without ventricular tachycardia. CONCLUSIONS: Sympathetic nerve may be related to prolongation of deltaERP and incidence of ventricular tachycardia in the ischemic period. However, EAD is not related to ventricular tachycardia during ischemia and reperfusion. These findings suggest that the major mechanism of ventricular tachycardia may be a reentry in ischemia and reperfusion period.
Action Potentials ; Animals ; Autonomic Denervation* ; Autonomic Nervous System ; Denervation ; Dogs ; Heart* ; Incidence ; Ischemia* ; Ketamine ; Myocardial Ischemia ; Pericardium ; Reperfusion* ; Stellate Ganglion ; Tachycardia* ; Tachycardia, Ventricular ; Vagotomy

Antithrombin III deficiency is an autosomal dominant disorder, which is manifested by recurrent venous thromboembolisms, such as: deep vein thrombosis and/or pulmonary embolism, but arterial embolisms are very rare. We report a case of a patient with hereditary antithrombin III deficiency, manifested by myocardial infarction and deep vein thrombosis.
Antithrombin III Deficiency* ; Antithrombin III* ; Embolism ; Humans ; Myocardial Infarction* ; Pulmonary Embolism ; Thromboembolism ; Venous Thrombosis*