A first trial in the clinical application of photodynamic therapy for the prevention of restenosis after coronary-stent placement.

BACKGROUND AND OBJECTIVES: The aim of this clinical study was to evaluate the safety of local delivery of a photosensitizer followed by photodynamic therapy (PDT), to determine its effectiveness in reducing in-stent restenosis. STUDY DESIGN/PATIENTS AND METHODS: Porfimer sodium was administered via a local delivery catheter to five coronary-stent implanted lesions followed by irradiation with a pulse laser. Coronary angiography (CAG) was performed at the baseline, after the procedure and at a 6-month follow-up. RESULTS: By the 18-month clinical follow-up, no adverse events such as photodermatosis, or myocardial ischemia had occurred. At the follow-up, no coronary embolization, dissection, or aneurysmal dilatation was observed in the CAG. In-stent diameter stenosis, late loss, and loss index were 19.16+/-8.20%, 0.37+/-0.18 mm, and 0.19+/-0.12, respectively. No in-stent restenosis was observed. CONCLUSIONS: This study suggests that PDT, with local delivery of Porfimer sodium, is safe and may be a feasible technique in preventing in-stent restenosis.

[Hypertrophic cardiomyopathy with mid-ventricular obstruction complicated by apical aneurysm appearing as delayed contrast hyperenhancement on magnetic resonance imaging: two case reports].

Case 1: A 52-year-old man presented with a chief complaint of palpitation. Diabetes mellitus was pointed out in 1992. Electrocardiography (ECG) revealed left ventricular hypertrophy in 1997. He visited our department in October 1997. Echocardiography showed increased wall thickness at the interventricular septum. The diagnosis was hypertrophic cardiomyopathy. Holter ECG revealed nonsustained ventricular tachycardia in December 1997. After this, he visited our outpatient clinic. Echocardiography indicated ventricular aneurysm in January 2002, so he was hospitalized in March 2002. Case 2: A 64-year-old woman was transferred to our hospital because of chest discomfort and tachycardial attack. She had been treated for hypertension and diabetes mellitus. She was taken to a hospital by ambulance. On admission, ECG showed wide QRS tachycardia. Cardiac magnetic resonance imaging in both patients disclosed almost complete obstruction of the mid-ventricle in the systolic phase on long- and short-axis cine images, and gadolinium delayed imaging revealed contrast hyperenhancement corresponding to an apical ventricular aneurysm on both long- and short-axis images. The final diagnosis was mid-ventricular obstructive hypertrophic cardiomyopathy with apical aneurysm characterized by delayed hyperenhancement on magnetic resonance imaging with gadolinium.

Enhanced expression of the apoptosis inducing ligand TRAIL in mononuclear cells after myocardial infarction.

Tumor necrosis factor (TNF) family proteins including TNF-alpha and Fas (CD95)-ligand have been implicated in the development of acute myocardial infarction (AMI). We studied whether AMI patients displayed up-regulation of another TNF family member, TNF-related-apoptosis-inducing ligand (TRAIL), on peripheral blood mononuclear cells (PBMCs). We compared expression of TRAIL on PBMCs from 26 patients in the acute phase of AMI with that on PBMCs from 16 healthy control subjects using flow cytometry and RT-PCR. In addition, expression of TRAIL protein on PBMCs from patients in the acute phase of AMI was also compared with that from the same patients 7 days later. Furthermore, we compared the expression of TRAIL protein on CD4+, CD8+, CD14+, and CD19+ cells from patients in the acute phase of AMI with that from control subjects using flow cytometry. Finally, expression of the TRAIL receptors (TRAILR)-1 and TRAILR-2 in human cardiomyocytes was examined immunohistochemically. Expression of TRAIL protein was significantly higher in the acute phase of AMI than in control subjects. Expression of TRAIL protein was significantly higher in the acute phase of AMI than 7 days later. TRAIL mRNA expression in the acute phase of AMI was higher than in control subjects. Expression of TRAIL protein on CD4+ and CD14+ cells from AMI patients was significantly higher than that from control subjects. Expression of TRAILR-1 and TRAILR-2 in human cardiomyocytes was confirmed immunohistochemically. TRAIL on infiltrating CD4 and CD146 cells may be involved in the induction of cardiomyocyte apoptosis after AMI.