Removal of knotted intravascular devices. Case report and review of the literature.

OBJECTIVE: to review published reports on knotted intravascular devices/catheters. METHOD: report of two cases and systematic review of the literature. RESULTS: a total of 113 reported cases of knotted intravascular devices/catheters were located. Pulmonary artery catheters (Swan-Ganz) were responsible for more than two thirds of the total reported intravascular knots. In 62% (70/113) of the cases withdrawal of the knotted catheters was achieved successfully with different interventional radiological techniques, avoiding the need for surgical exploration. In 32% (36/113) of the patients surgical removal was favoured. Capture with one of the interventional techniques and pulling down the knot into an easily accessible vein to be removed through an open venotomy, was the most common surgical procedure. However, in five cases, an open cardiotomy was required. In seven cases the patient's condition was critical and precluded any surgical procedure, so the knotted catheter was left in situ. The mortality of this event was 8% (9/113). CONCLUSIONS: interventional radiological techniques have largely replaced open surgical removal. Knotted catheters may need to be surgically removed when (a) the knot is large in size with many loops, or (b) intracardiac fixing of the knot is encountered.

Comparative efficacy of primary angioplasty with stent implantation and thrombolysis in restoring basal coronary artery flow in acute ST segment elevation myocardial infarction: quantitative assessment using the corrected TIMI frame count.

Following thrombolysis and primary percutaneous transluminal coronary angioplasty (PTCA) for acute ST segment elevation myocardial infarction, basal flow in the culprit artery is known to influence prognosis. The purpose of this study was to determine if differences exist in basal flow in culprit and nonculprit coronary arteries in patients with acute ST segment elevation myocardial infarction who were treated with thrombolysis or primary PTCA with stent implantation. Twenty patients were randomized to thrombolysis (with recombinant tissue plasminogen activator) and 24 to primary PTCA with stent implantation within 3 hours of onset of acute ST segment elevation myocardial infarction. Coronary angiography was performed 90-120 minutes after thrombolysis or immediately after PTCA with stent implantation and again at 18-36 hours after intervention in both groups. Patients who failed to achieve thrombolysis in myocardial infarction (TIMI) grade 2 or 3 flow were excluded. The corrected TIMI frame count was used as the index of basal coronary artery flow. Early after intervention the mean corrected TIMI frame count in the culprit coronary artery was significantly lower in the primary PTCA with stent group (27.4 +/- 7.7 frames) than in the thrombolysis group (39.8 +/- 10 frames, p < 0.001). Eight thrombolysis patients (40%) and 20 primary PTCA patients (83%, p < 0.01) achieved TIMI grade 3 flow early after intervention. By 18-36 hours after intervention there were no significant differences in the mean correct TIMI frame count between the thrombolysis and primary PTCA with stent groups. There were no significant differences in the mean corrected TIMI frame count between these two groups in the nonculprit coronary artery, either early after intervention or at 18-36 hours. In successfully reperfused coronary arteries following acute ST segment elevation myocardial infarction, primary angioplasty with stent implantation reestablished TIMI grade 2 or 3 flow faster and more effectively than thrombolysis did.

Comparison of endothelin-1 levels at rest and during exercise between patients with cardiac syndrome-X and healthy people.

Several previous studies have shown that endothelin-1 (ET 1) plasma levels are raised in cases of endothelial abnormality and microvascular dysfunction. Syndrome-X constitutes an important clinical entity characterized by angina-like pain and normal coronary arteries which is believed to reflect microvascular dysfunction. The aim of the present study was to investigate the role of ET 1 in the pathophysiology of the above syndrome. For that purpose the plasma ET 1 concentrations, measured by radioimmunoassay, between 28 X-syndrome patients (group A) and 10 age-matched normal control subjects (group B) at rest and at the peak of the exercise testing were compared. We specify that all individuals of group A were referred to our Department for effort angina and were found to have normal coronary arteriograms, negative ergonovine and hyperventilation test and positive exercise test. Our results showed that while at rest ET 1 plasma concentrations did not differ significantly between the two groups, at the peak of the exercise test its levels were found to be significantly higher in syndrome-X patients as compared with those of normal subjects (p< 0.001). In addition, in healthy control subjects ET 1 levels decreased during exercise as compared with the baseline values and that difference was found to be statistically significant (p approximately 0.01). The above finding suggests opposite kinetics during exercise of ET 1 between the two groups studied, which could explain effort angina onset in patients with syndrome-X.

Origin of angina pectoris in patients with high-grade single-vessel coronary artery stenosis undergoing percutaneous transluminal coronary angioplasty.

This study shows that in patients with subtotal (95% to 99%) coronary artery stenosis, the presence of myocardial ischemia is dictated primarily by the presence and degree of coronary collateral flow, with anterograde flow participating little, if at all, in the origin of myocardial ischemia and angina pectoris. Conversely, in patients with severe but not subtotal coronary artery stenosis (70% to 94%), both reduced anterograde flow and coronary collateralization contribute to the evolution of myocardial ischemia and angina pectoris.

Symptomatic reinfarctation of a previously silent myocardial region four months after successful reperfusion--a case report.

Coronary collateral circulation helps to preserve myocardial perfusion distal to severely stenotic or totally obstructed coronary arteries. The presence or absence of angina pectoris and the state of myocardial function depend on the extent of collateralization and its functional contribution to myocardial blood flow. Clinical and experimental observations have suggested that newly developed collaterals usually remain even after successful revascularizaton. The authors present a case of a patient with extensive intercoronary collaterals and hibernating myocardium after an acute inferior wall myocardial infarction who underwent successful percutaneous transluminal coronary angioplasty of a totally obstructed, dominant right coronary artery and then experienced extensive reinfarction following reocclusion 4 months later. This case demonstrates failure of extensive collaterals to prevent acute myocardial infarction.