Peripheral cholesterol embolism in a percutaneous coronary angioplasty procedure. A case report

Cholesterol embolism is a rare but potentially serious complication of cardiac catheterization. We report the case of a patient who presented a cholesterol embolism in the lower extremities after percutaneous angioplasty and the elective implantation of a stent. Clinical evolution was favourable. The appearance of cholesterol embolism could have been precipitated, in this case, by anticoagulation treatment with heparin and intense antiaggregation.     

LDL apheresis for cholesterol embolism following coronary artery bypass graft surgery--a case report

A 76-year-old man without any prior history of abnormal urinalysis findings or renal insufficiency demonstrated mild renal dysfunction after coronary bypass graft surgery (CABG). Two months after CABG, pain and blueness in the toes (blue toe syndrome) appeared and, the serum creatinine level (S-Cr) increased from 1.2 to 2.0 mg/dL. On admission (3 months later), the urinary protein level was 0.5 g/day, white blood cell count 8,300/microL with eosinophils (Eo) 10.5%, S-Cr 2.1 mg/dL, and low-density lipoprotein (LDL) 106 mg/dL. Acute renal failure and blue toe syndrome due to a cholesterol embolism (CE) were diagnosed. Alprostadil 40 microg/day orally for 2 weeks and alprostadil 40 microg/day intravenously were used for 5 weeks, and Eo were 250/microL, S-Cr 2.5 mg/dL; however, blue toe syndrome gradually developed. At 8 weeks after admission, limaprost alfadex 30 microg/day orally was used for 3 weeks. However, the Eo gradually rose to 1,520/microL, S-Cr to 3.0 mg/dL, and LDL to 135 mg/dL, and LDL apheresis was therefore performed 20 times for CE. The data just after LDL apheresis was performed 10 times were as follows: Eo 1,120/microL, S-Cr 4.0 mg/dL, and LDL 89 mg/dL, and blue toe syndrome had disappeared. At 10 months after the first LDL apheresis, the Eo were 630/microL, S-Cr 2.9 mg/dL, and LDL 109 mg/dL. As a result, LDL apheresis was found to be beneficial for the treatment of CE with acute renal failure and blue toe syndrome after CABG.     

Cholesterol embolism after percutaneous transluminal coronary angioplasty procedure: a case report

A 68-year-old man with chest pain was treated under a diagnosis of angina pectoris based on coronary angiography by percutaneous transluminal coronary angioplasty including stent implantation performed by the femoral approach. About 1 month after intervention, his renal function deteriorated and purpura appeared on both feet, especially at the toe tips. He was treated under a tentative diagnosis of cholesterol embolism conservatively at the out-patient clinic. However, he was admitted by ambulance due to worsening renal failure 2 months later and died from multiple organ failure 2 weeks after admission. Autopsy examination identified cholesterol embolism due to crystal emboli in several organs. Cholesterol embolism rarely occurs after angiographic or interventional procedures, but is difficult to diagnose clinically and there is no established therapy. The number of intervention and angiography procedures is increasing, so the occurrence of embolism as a complication of these procedures might also increase.     

Surgery for massive pulmonary embolism following coronary angioplasty--a case report

A case of a 49-year-old female with acute coronary syndrome is presented. The patient underwent coronary angioplasty with stent implantation. Due to the recurrence of pain and dyspnea a repeated coronary angiography was performed 3 hours later which confirmed good result of angioplasty. For the next 48 hours a local compression on both femoral arteries was maintained and the patient received full anticoagulant and antiplatelet treatment. However, clinical condition of the patient continued to deteriorate. Echocardiography and spiral computerised tomography revealed the presence of a massive pulmonary embolism. The patient underwent surgery and fully recovered.     

Accordion effect--a rare pseudocomplication of coronary angioplasty. A case report

Accordion effect is a rare pseudocomplication of coronary angioplasty created by straightening of tortuous coronary artery with a guidewire. Its morphology is nearly identical with vessel dissection, spasm or thrombosis but no special treatment is needed. Immediate and correct diagnosis of accordion effect prevents consequences of unnecessary dilatation of normal coronary segment.     

Percutaneous transluminal coronary angioplasty of coronary artery embolism.

A 35-yr-old woman with known valvular heart disease presented with acute myocardial infarction. Angiography demonstrated a totally occluded distal left anterior descending coronary artery. Though initially successful, angioplasty ultimately failed to maintain arterial patency, leaving a more distal total occlusion after several balloon inflations. In spite of this, PTCA possibly provided a more localized infarction via a peripheral mobilization of the embolus.     

Cholesterol embolization following coronary angioplasty.

Cholesterol emboli syndrome is an uncommon complication seen after an invasive vascular procedure or surgery in a patient with atherosclerotic disease. The obstruction of small arteries by cholesterol crystals may be responsible for its clinical features, such as livedo reticularis, "purple toe" syndrome, renal failure, involvement of the gastrointestinal tract, coronary arteries, central nervous system or the multiple cholesterol emboli syndrome. Certain laboratory abnormalities are frequently associated: an elevated erythrocyte sedimentation rate and eosinophilia, BUN and creatinine increase in the cases with renal failure and creatine phosphokines augmentation suggesting muscle involvement. Disseminated microemboli composed mainly of cholesterol crystals are the usual pathological findings. A case of cholesterol embolism occurring after left heart catheterization and percutaneous transluminal coronary angioplasty is reported. Twenty-four hours after the procedure, the patient developed purplish discoloration of toes and soles, livedo reticularis on lumbar region, buttocks and limbs, and renal failure. Patient did well two months after anticoagulant therapy. Prognosis of these cases is related to the extent of systemic involvement and the most significant impact on this syndrome can be made by its prevention.     

Percutaneous transluminal coronary angioplasty in a patient with Kawasaki disease. A case report of an unsuccessful angioplasty.

A 13-year-old boy with severe coronary stenosis due to Kawasaki disease underwent percutaneous transluminal coronary angioplasty (PTCA). The guide wire and the balloon catheter easily passed through the stenosis in the left anterior descending artery. However, effective dilatation could not be achieved even when the balloon size was increased to 2.5 mm in diameter. We discontinued further inflation of the balloon because serious resistance was encountered on withdrawal of the balloon catheter. In patients with Kawasaki disease, the value of PTCA as a treatment for coronary stenosis is questionable.     

How long can a coronary reperfusion catheter be placed in acute coronary occlusion following failed transluminal coronary angioplasty? A case report

A coronary reperfusion catheter (CRC) is designed to preserve antegrade coronary flow when abrupt coronary closure occurs during percutaneous transluminal coronary angioplasty (PTCA). Insertion of the catheter to an occluded coronary artery for a few hours has been reported to be effective for myocardial salvage: however, it is unknown how long the catheter can be kept in place without causing extension of myocardial ischemia. The authors experienced a case in which the CRC was kept in place for twenty-four hours for anticoagulant therapy of an occluded coronary artery following failure of PTCA. This case suggests that adequate anticoagulant therapy can prolong the period during which a CRC can be kept in place if emergency coronary bypass surgery cannot be performed immediately after failure of coronary angioplasty.     

Coronary air embolism during coronary angioplasty

A case is described in which the use of the Hartzler microcatheter during coronary angioplasty resulted in coronary air embolism. The recognition, prevention, and mechanism of this occurrence are discussed.     

Percutaneous transluminal coronary angioplasty of coronary artery embolism

A 35-yr-old woman with known valvular heart disease presented with acute myocardial infarction. Angiography demonstrated a totally occluded distal left anterior descending coronary artery. Though initially successful, angioplasty ultimately failed to maintain arterial patency, leaving a more distal total occlusion after several balloon inflations. In spite of this, PTCA possibly provided a more localized infarction via a peripheral mobilization of the embolus.     

Restenosis following coronary angioplasty

Summary The assessment of restenosis following angioplasty has become increasingly important in determining the clinical value of the procedure. Despite this there has been no uniformly accepted methodology for assessing the procedure and consequently the published results have often been misleading with little concensus. In this paper some of the irregularities are documented and practical ways for adapting methodology proposed.     

Restenosis following coronary angioplasty

Restenosis is the most important problem limiting the success of coronary angioplasty. Clinically, restenosis is seen in approximately one-third of patients undergoing percutaneous transluminal coronary angioplasty. Several clinical and angiographic risk factors have been identified which may contribute to the development of restenosis. Histopathologic studies indicate that restenosis is characterized by intimal proliferation of smooth muscle cells in a loose connective tissue matrix. These intimal lesions are associated predominantly with the nonatheromatous portion of the vessel wall. Thinning of the media of the plaque-free wall and marked fragmentation of the internal elastic lamina are also seen. Traumatic injury of the vessel wall during angioplasty probably triggers a series of cellular and subcellular events which may ultimately lead to myointimal proliferation and restenosis. Although the exact mechanism by which this occurs is unknown, several factors may enhance smooth muscle cell growth and therefore may play a role in the development of restenosis. These include platelet deposition, mechanical stretching of the media, inflammation of the vessel wall, the activity of growth factors, and alterations in vessel geometry. These possible mechanisms of restenosis suggest several potential ways to limit the proliferative response to vascular injury. Anticoagulants and platelet antagonists, direct inhibitors of smooth muscle proliferation, anti-inflammatory agents, growth factor inhibitors, and new devices which improve final vessel geometry are currently being tested as methods to curb restenosis. Unfortunately, no treatment has yet been shown to reduce significantly the rate of restenosis following angioplasty. The problem of restenosis will most likely be solved by better understanding of the basic molecular and biologic phenomena involved in vascular injury and repair.     

Left main coronary artery embolism: a case report

A 27-year-old man had recurrent myocardial infarction found to be due to coronary embolism to the left main coronary artery with downstream embolization. The presumed etiology of thromboembolism was idiopathic cardiomyopathy. A unique method of treatment with Fogarty catheter retrieval was used.     

Percutaneous transluminal coronary angioplasty. A report of 100 cases

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 100 coronary heart patients with 122 vessels and 138 lesions dilated. Among these 100 cases, there were 39 complex PTCA performed. The primary success rate was 93% (93/100), was 94.3% (115/122) according to vessel dilated and was 92.1% (127/138) according to lesion dilated. In 4 cases whose lesions were located at the bifurcation of the vessel, kissing balloon technique via a single guiding catheter was applied with success. In 5 cases of total occlusion PTCA was performed with success in 4. PTCA with stent in 1. PTCA was performed in 1 cases of high risk whose LVEF was only 30% and coronary hemoperfusion pump was used during the procedure. Emergency PTCA was performed in 3 AMI patients during the acute phase and elective PTCA in 8 AMI cases after successful thrombolytic therapy. There were complications in 9 cases (9%). Among these 9 cases, 2 developed O-wave MI which recovered after medicinal therapy. One AMI complicated with heart failure was treated by emergency PTCA with success, but the patient died 10 days after PTCA due to pump failure and pulmonary infection. There were no deaths due to PTCA, nor was emergency coronary artery bypass graft (CABG) performed. These cases were followed for 1-30 months on an average of 13 months. Clinical success rate was 91.3%. The clinical success rate was 93.1% by 201Tl perfusion study. Restenosis in 7 cases was confirmed by coronary angiography. For these restenotic cases, PTCA was repeated with success in 4, CABG performed in 1, coronary atherectomy in 1, and medicinal therapy employed in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Staphylococcal pericarditis following percutaneous transluminal coronary angioplasty.

Infectious complications occurring after percutaneous transluminal coronary angioplasty are uncommon. We are reporting a case of bacterial pericarditis developing 1 week after coronary angioplasty and stent implantation. Treatment with appropriate antibiotics and drainage of the infected pericardial effusion was followed by a protracted hospital course and eventual control of infection and discharge of the patient.     

Death from coronary air embolism during percutaneous transluminal coronary angioplasty

A patient undergoing percutaneous transluminal angioplasty of a critical proximal stenosis of his anterior descending coronary artery died as a result of coronary air embolism from a defective dilatation catheter. The probable mechanism responsible for this lethal complication is discussed. Simple precautions are described that will prevent its future occurrence.