Short- and long-term benefits of drug-eluting stents compared to bare metal stents even in treatment for large coronary arteries.

Although drug-eluting stents (DES) for percutaneous coronary intervention (PCI) have dramatically reduced the incidence of in-stent restenosis, their deployment for large-size coronary lesions is still controversial because of problems such as late in-stent thrombosis and late catch-up in DES. We aimed to evaluate the long-term outcome beyond 2 years of bare metal stents (BMS) as compared with DES in large vessels. Consecutive 228 patients who underwent PCI with large-size stents (>3.5 mm in diameter) in our hospital were enrolled in this study. The end points of this study are target lesion revascularization (TLR) and occurrence of major adverse cardiac events (MACE) for subject patients. We analyzed 183 patients (152 men, mean age 65.8 ± 10.5 years) whose outcome could be followed up for at least 2 years. At the first 8-month follow-up, clinically driven TLR rate was significantly higher in patients who received BMS than those who received DES (17.2 vs. 2.2 %, p < 0.05), although the rate of TLR was not different between the 2 groups beyond 8 months. Thus, overall rate of TLR was higher in BMS than in DES (22.7 vs. 5.4 %, p < 0.05). Under these conditions, the higher rate of TLR for BMS was observed in simple as well as complex lesions with or without diabetes, although there were no significant differences in MACE between BMS and DES. Multivariate analysis showed that BMS was an only independent factor of TLR at the 8 month follow-up period [p = 0.004, odds ratio 9.58, 95 % confidence interval (2.10-43.8)]. These results demonstrate that the rate of in-stent restenosis in large-size coronary lesions was transiently higher in the first 8 months for patients implanted with BMS compared with DES in which no in-stent thrombosis and TLR beyond 2 years were observed. We suggest using the DES even in large-size coronary lesions in terms of short- and long-term outcomes.

Related polymorphic F-box protein genes between haplotypes clustering in the BAC contig sequences around the S-RNase of Japanese pear.

Most fruit trees in the Rosaceae exhibit self-incompatibility, which is controlled by the pistil S gene, encoding a ribonuclease (S-RNase), and the pollen S gene at the S-locus. The pollen S in Prunus is an F-box protein gene (SLF/SFB) located near the S-RNase, but it has not been identified in Pyrus and Malus. In the Japanese pear, various F-box protein genes (PpSFBB(-α-γ)) linked to the S-RNase are proposed as the pollen S candidate. Two bacterial artificial chromosome (BAC) contigs around the S-RNase genes of Japanese pear were constructed, and 649 kb around S(4)-RNase and 378 kb around S(2)-RNase were sequenced. Six and 10 pollen-specific F-box protein genes (designated as PpSFBB(4-u1-u4, 4-d1-d2) and PpSFBB(2-u1-u5,) (2-d1-d5), respectively) were found, but PpSFBB(4-α-γ) and PpSFBB(2-γ) were absent. The PpSFBB(4) genes showed 66.2-93.1% amino acid identity with the PpSFBB(2) genes, which indicated clustering of related polymorphic F-box protein genes between haplotypes near the S-RNase of the Japanese pear. Phylogenetic analysis classified 36 F-box protein genes of Pyrus and Malus into two major groups (I and II), and also generated gene pairs of PpSFBB genes and PpSFBB/Malus F-box protein genes. Group I consisted of gene pairs with 76.3-94.9% identity, while group II consisted of gene pairs with higher identities (>92%) than group I. This grouping suggests that less polymorphic PpSFBB genes in group II are non-S pollen genes and that the pollen S candidates are included in the group I PpSFBB genes.

Life-threatening ventricular arrhythmia due to silent coronary artery spasm: usefulness of I-123 metaiodobenzylguanidine scintigraphy for detecting coronary artery spasm in the era of automated external defibrillators: a case report.

INTRODUCTION: Cardiac arrhythmia is sometimes life-threatening, and automated external defibrillators are presently used in some countries. Coronary artery spasm is one of the primary causes of life-threatening arrhythmia. In general, chest symptoms are key indicators of possible coronary artery spasm; however, if chest symptoms are not present, clinicians may not suspect this disease. We encountered a patient who had recovered from ventricular fibrillation treated by using an automated external defibrillator, and silent coronary artery spasm was considered to be the cause of this life-threatening arrhythmia. In this case, I-123 metaiodobenzylguanidine scintigraphy was a useful screening tool for a silent coronary artery spasm. CASE PRESENTATION: A 72-year-old Japanese man was transferred to our hospital after recovering from ventricular fibrillation treated by using an automated external defibrillator. He had never complained of chest symptoms previously. Decreased uptake of I-123 metaiodobenzylguanidine was observed in the inferolateral and anteroseptal walls of the left ventricle. A spasm provocation test of the coronary artery was performed, and silent coronary artery spasm was diagnosed as the underlying disease. CONCLUSION: Non-invasive I-123 metaiodobenzylguanidine scintigraphy was a useful screening tool for silent coronary artery spasm as a possible cause of cardiopulmonary arrest in a patient with no chest symptoms.

Coronary artery stenting in a patient with factor XI deficiency.

Factor XI deficiency is a rare inherited coagulopathy first described in Ashkenazi Jews. In Japanese populations, factor XI deficiency is thought to be very rare. This disorder causes unique problems during percutaneous coronary intervention (PCI). During PCI, prevention of thrombosis is important and heparin is usually used for anticoagulation. However, care must also be taken to avoid serious complications of bleeding. These two situations are contradictory and anticoagulation with heparin might increase severe bleeding in patients with factor XI deficiency. An 84-year-old Japanese woman was admitted to our hospital for the treatment of worsening effort angina pectoris. A coronary angiography revealed severe stenotic lesions at the left main trunk (LMT) and the right coronary artery (RCA). While performing PCI of the LMT, 8,000 U of heparin were used and the patient underwent successful drug-eluting stent implantation. At this point, the patient's activated coagulation time was over 1,500 s and there was a marked decrease of factor XI activity (<3%: normal range 75-145%). After the diagnosis of factor XI deficiency, PCI for the RCA was scheduled without anticoagulation and fresh frozen plasma instead of dual antiplatelet therapy by aspirin and clopidogrel. Two drug-eluting stents were deployed and dilation using the kissing balloon technique was performed. The procedure was uneventful without stent thrombosis or distal embolization or bleeding. Because the literature on stenting for patients with factor XI deficiency is very limited, this case provides additional clinical information.

Rapid changes in plaque composition and morphology after intensive lipid lowering therapy: study with serial coronary CT angiography.

Although intensive lipid lowering by statins can enhance plaque stability, few data exist regarding how early statins change plaque composition and morphology in clinical setting. Therefore, to examine early changes in plaque composition and morphology by intensive lipid lowering with statins, we evaluate coronary plaques from acute coronary syndrome (ACS) before and 3 weeks after lipid lowering by coronary CT angiography. We enrolled 110 patients with suspected ACS and underwent coronary CT. We defined plaque as unstable when CT number of plaque< 50HU and remodeling index (lesion diameter/reference diameter) >1.10. Rosuvastatin (5 mg/day) or atorvastatin (20 mg/day) were introduced to reduce low density lipoprotein cholesterol (LDL-C). Then, CT was again performed by the same condition 3 weeks after lipid lowering therapy. Total 10 patients (8 men, mean age 72.0 years), in whom informed consent regarding serial CT examination was obtained, were analyzed. Among them, 4 patients who denied to have intensive lipid lowering were served as controls. In remaining 6 patients, LDL-C reduced from 129.5±26.9 mg/dl to 68.5±11.1 mg/dl after statin treatment. Under these conditions, CT number of the targeted plaque significantly increased from 16.0±15.9 to 50.8±35.0 HU (p<0.05) and remodeling index decreased from 1.22±0.11 to 1.11±0.06 (p<0.05), although these values substantially unchanged in controls. These results demonstrate that MDCT-determined plaque composition as well as volume could be changed within 3 weeks after intensive lipid lowering. This may explain acute effects of statins in treatment of acute coronary syndrome.

A case of acute myocardial infarction with repetitive stent thrombosis during emergent percutaneous coronary intervention. Transient decrease in antithrombin III activity and heparin resistance.

A 59-year-old woman was admitted to our hospital for the treatment of an acute anterior myocardial infarction. She had a history of uncontrolled diabetes mellitus, hypertension, hyperlipidemia, obesity, and smoking. Coronary angiography revealed 90% stenosis with spontaneous dissection in the proximal portion of the left anterior descending artery. At this time, heparin was initiated for the first time. Although direct stenting (Be-stent, 3.0-18 mm) was performed for the culprit lesion, coronary dissection occurred at the left main trunk and additional stenting (Multi Link ZETA stent 3.5-15mm) was performed for the left main trunk. Soon after stenting, repetitive stent thrombosis occurred. Aspiration of the thrombus using an aspiration catheter was ineffective and repetitive angioplasty and intraaortic balloon pumping were required. Although we used 17,000 units of unfractionated heparin during the intervention, the activated coagulation time (ACT) was not prolonged (157 seconds). In the coronary care unit, the ACT and activated partial prothrombin time (aPTT) were not prolonged despite the use of large amounts of heparin (69,000 units in 2 days). Protein-S, protein-C, and hepaplastin testing were within normal limits and heparin-platelet factor IV complex antibody was not detected. In the acute phase, a decrease in the antithrombin III activity (65%) was noted and with administration of argatroban, prolongation of the aPTT was achieved. In the chronic phase, the decrease in antithrombin III activity and heparin resistance had improved spontaneously. It is important to recognize the existence of transient decreases in antithrombin III activity in the acute phase of myocardial infarction.

Persistent left bundle branch block in a patient with dilated cardiomyopathy that improved with low dose carvedilol therapy.

A 43-year-old Japanese woman with dilated cardiomyopathy had complete left ventricular bundle branch block (CLBBB), which had persisted for at least two years. At the time of admission, the serum brain natriuretic peptide (BNP) concentration was 502 pg/mL (normal range, 0-18 pg/mL), the left ventricular diastolic dimension (LVDd) was 59 mm, the left ventricular systolic dimension (LVDs) was 54 mm, the %fractional shortening (FS) was 8%, and the left ventricular ejection fraction (LVEF) was 19.7% by echocardiography. Low dose carvedilol was initiated for the treatment of heart failure. Adverse effects, such as progression of cardiac conduction disturbances, did not occur after initiation of carvedilol therapy. About one year after initiation of carvedilol therapy, the CLBBB disappeared and a significant improvement in left ventricular function was noted. The LVDd was 44 mm, the LVDs was 30 mm, the %FS was 33%, and the LVEF was 61%, and the serum BNP concentration was decreased to 18.5 pg/mL. We describe a case in which low dose carvedilol was effective for treating both CLBBB and left ventricular function.

Coronary artery multistenting in the treatment of life-threatening refractory coronary spasm after coronary artery bypass grafting.

A 74-year-old man had undergone on-pump coronary artery bypass grafting (CABG) for effort-induced angina pectoris. Soon after CABG using the left internal thoracic artery for the left anterior descending artery and saphenous vein for the left circumflex artery, ST elevation was found in the inferior leads and complete atrioventricular block, ventricular tachycardia, and circulatory collapse occurred. Emergent coronary angiography revealed diffuse severe spasm of the right coronary artery (RCA). Despite the intravenous and intracoronary administration of massive doses of vasodilators and intra-aortic balloon pumping, the coronary spasm did not resolve. Five stents were deployed from the distal to the proximal portion of the RCA. After multistenting, coronary flow was dramatically improved and the ST elevations in the inferior leads were also improved. Coronary artery spasm after CABG is relatively rare, but when it occurs, it can be fatal. Multistenting is a useful treatment for life-threatening refractory coronary spasm after CABG.