[Incidence and clinical outcome of contrast-induced nephropathy in the elderly patients].

BACKGROUND: Aging is an established risk factor for contrast-induced nephropathy (CIN). However, little information is available on the incidence and clinical outcome of CIN for the elderly patients in Japan. OBJECTIVES: We determined the incidence and clinical outcome of CIN in the Japanese elderly patient. METHODS: We studied 292 patients who had mild renal dysfunction (estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m(2)) at baseline and underwent coronary angiography. Patients were divided into two groups base on their age: the elderly group (age ≥ 75, n=108) and the control group (age<75, n=184). CIN was defined as a 25% increase in serum creatinine or an increase in serum creatinine by>0.5 mg/dl above the baseline value at or within 2 days post procedure. RESULTS: Patients in the elderly group had a higher incidence of CIN (14%) than those in the control group (9%). In patients who developed CIN, there was no significant difference between the two groups in baseline GFR and GFR on days 1, 2, 7 and 30 after the procedure. However, the relative increase in GFR above baseline on day 7 (-4.0 ± 6.1 vs -8.3 ± 8.0 ml/min P=0.096) and day 30 (1.5 ± 9.4 vs -10.1 ± 9.6 ml/min P=0.0017) in the elderly group was higher than that in the control group. Furthermore, death occurred in 3 patients in the elderly group (20%) whereas no patient died in the control group (P=0.092). CONCLUSION: Aging (age ≥ 75) is a risk factor for CIN in Japanese. CIN in the elderly patients may be associated with prolonged renal dysfunction and poor prognosis.

Urinary liver-type fatty acid-binding protein level as a predictive biomarker of contrast-induced acute kidney injury.

BACKGROUND: Contrast-induced acute kidney injury (CI-AKI) is a well-known complication of contrast medium exposure in patients with chronic kidney disease. However, there are no biological markers to accurately predict the onset of CI-AKI. Liver-type fatty acid-binding protein (L-FABP), an intracellular carrier protein for free fatty acids, is markedly upregulated and abundantly expressed in the proximal tubules after renal ischaemia. We prospectively investigated whether urinary L-FABP is a suitable marker for the prediction of CI-AKI. METHODS: We performed a prospective study of 220 consecutive patients with chronic kidney disease who underwent elective catheterization [serum creatinine (Cr) ≥ 1.2 mg/dL (106 M)]. Serum Cr and L-FABP levels were measured immediately before and 1 and 2 days after the procedure. CI-AKI was defined as an increase in serum Cr level of ≥ 0.3 mg/dL within 48 h after the procedure. RESULTS: We observed the development of CI-AKI in 19 patients (8.6%). Urinary L-FABP levels were significantly higher in patients with CI-AKI than those without CI-AKI before contrast medium exposure. Receiver operating characteristic analysis showed that baseline urinary L-FABP level exhibited 82% sensitivity and 69% specificity, at a cut-off value of 24.5 µg/g Cr. Using multivariate analysis, we found that independent predictors of CI-AKI development were L-FABP level of ≥ 24.5 µg/g Cr [odds ratio (OR): 9.10; 95% confidence interval (CI), 3.20-28.9], and left ventricular ejection fraction ≤ 40% (OR, 3.42; 95% CI, 1.07-10.8). CONCLUSIONS: Urinary L-FABP level is useful for predicting the onset of CI-AKI before contrast medium exposure.

Radiofrequency catheter ablation of posterior paraseptal accessory pathway with atresia of the coronary sinus ostium.

A 42-year-old man was referred to our hospital for an electrophysiologic study because of recurrent episodes of palpitation. On coronary angiogram, an anomalous atresia of the coronary sinus (CS) ostium was discovered. The ablation catheter was inserted from the right femoral artery to the accessory pathway (AP) of posterior paraseptal area. The earliest retrograde atrial activation was recorded in the 5-6 o'clock region of the mitral annulus. Radiofrequency energy was delivered to this site, resulting in elimination of the AP. After this application, there was persistent ventriculoatrial dissociation and led to successful ablation of the AP.

Opposing effect of p38 MAP kinase and JNK inhibitors on the development of heart failure in the cardiomyopathic hamster.

OBJECTIVE: p38 MAP kinase (p38 MAPK) and c-Jun NH2-terminal kinase (JNK) have been implicated in the pathophysiology of heart failure. We investigated the effects of chronic treatment with p38 MAPK and JNK inhibitors on the development of heart failure in dilated cardiomyopathy (DCM) hamster heart. METHODS AND RESULTS: BIO14.6 hamster hearts showed markedly increased p38 MAPK and JNK activities at 6 weeks of age when there was no significant increase in the area of fibrosis, heart weight/body weight, left ventricular (LV) chamber dilation and LV dysfunction. p38 MAPK and JNK activities were attenuated at 26 weeks of age and abolished at 40 weeks of age in BIO14.6 hamster hearts. BIO14.6 hamsters and the control BIOF1B hamsters were chronically treated (i.p.) with the p38 MAPK inhibitors, SB203580 (1 mg/kg/day) and FR167653 (3 mg/kg/day), or the JNK inhibitor, SP600125 (1 mg/kg/day) or vehicle for 20 weeks starting from 6 weeks of age. Treatment of BIO14.6 hamster hearts with SB203580 and FR167653 reduced the number of TUNEL-positive myocytes, the area of fibrosis and heart weight/body weight associated with a significant decrease of LV dimension and an increase in LV ejection fraction and LV contractility compared to the vehicle-treated counterpart. In contrast, treatment with SP600125 increased the number of TUNEL-positive myocytes and the area of interstitial fibrosis associated with aggravation of LV chamber dilation and LV dysfunction. CONCLUSIONS: These results suggest that chronic treatment with p38 MAPK and JNK inhibitors produces opposing effects on the development of heart failure in the DCM hamster heart.

Dystrophin is a possible end-target of ischemic preconditioning against cardiomyocyte oncosis during the early phase of reperfusion.

OBJECTIVE: Dystrophin is a sarcolemmal membrane protein that prevents the myocyte from oncosis induced by physical stress. Because ischemic preconditioning (IPC) protects mitochondria and prevents oncosis during reperfusion, we hypothesized that dystrophin is an end-target of IPC distal to mitochondrial protection. METHODS AND RESULTS: Isolated rat hearts were subjected to 30 min ischemia followed by reperfusion. IPC was introduced by 3 cycles of 5 min ischemia and 5 min reperfusion. The loss of sarcolemmal dystrophin and myocardial ATP during ischemia was comparable between the control and the IPC heart. Similar changes in sarcolemmal dystrophin and myocardial ATP were observed when the heart was treated with 2,4-dinitrophenol (DNP), an uncoupler of mitochondrial respiration, or oligomycin, an inhibitor of mitochondrial F1F0-ATPase. However, the IPC heart increased sarcolemmal dystrophin during reperfusion associated with an increase in tetramethylrhodamine ethylester (TMRE) uptake, an indicator of mitochondrial membrane potential (DeltaPsim), and myocardial ATP and inhibited myocyte oncosis. The increase in myocardial ATP and relocalization of dystrophin to the sarcolemma mediated by IPC was inhibited by treatment with DNP or oligomycin during reperfusion. In vitro experiments demonstrated that mitochondria isolated from the ischemic IPC heart increased ATP generation and facilitated relocalization of dystrophin from the insoluble to the soluble fractions in a manner sensitive to DNP and oligomycin. CONCLUSIONS: These results suggest that enhanced relocalization of dystrophin to the sarcolemma during reperfusion may be a mechanistic link between IPC-mediated improvement of mitochondrial function and its protection against oncosis during the early phase of reperfusion.

Role of oxidative/nitrosative stress in the tolerance to ischemia/reperfusion injury in cardiomyopathic hamster heart.

We investigated the role of oxidative/nitrosative stress in the tolerance to ischemia/reperfusion (I/R) injury in BIO14.6 cardiomyopathy hamster hearts at 6 weeks of age. These hearts showed no significant morphologic change and left ventricular (LV) dysfunction. However, expression and activity of iNOS, nitrotyrosine (NT) formation, and protein kinase C (PKC)-epsilon activity were increased in these hearts. When the BIO14.6 hamster hearts were isolated and subjected to 40 min of global ischemia, they showed smaller myocardial necrosis and greater recovery of LV function during reperfusion compared with the control hamster heart. All of these effects were abrogated by prolonged treatment with the antioxidant, 2-mercaptopropionylglycine (MPG). Brief preischemic treatment with MPG or the iNOS inhibitor 1400W also abrogated NT formation and activation of PKC-epsilon and inhibited the tolerance to I/R injury in the BIO14.6 hamster heart. Brief preischemic treatment with the PKC inhibitor chelerythrine or the K(ATP) channel blockers, 5-hydroxydecanoate (5-HD) and glibenclamide, had no effect on iNOS activation and NT formation but inhibited the tolerance to I/R injury in the cardiomyopathic heart. These results suggest that oxidative/nitrosative stress plays a role in the tolerance to I/R injury in the cardiomyopathic heart through activation of PKC and the downstream effectors, K(ATP) channels.

Improvement of collateral perfusion and regional function by implantation of peripheral blood mononuclear cells into ischemic hibernating myocardium.

OBJECTIVE: This study was performed to evaluate the angiogenic effect of implantation of peripheral blood mononuclear cells (PB-MNCs) compared with bone marrow mononuclear cells (BM-MNCs) into ischemic hibernating myocardium. METHODS AND RESULTS: A NOGA electromechanical system was used to map the hibernating region and to inject cells. PB-MNCs and BM-MNCs contained similar levels of vascular endothelial growth factor and basic fibroblast growth factor, whereas contents of angiogenic cytokines (interleukin-1beta and tumor necrosis factor-alpha) were larger in PB-MNCs. Numbers of endothelial progenitors were approximately 500-fold higher in BM-MNCs. In BM-MNC-implanted myocardia of pigs, an increase in systolic function (ejection fraction from 33% to 52%) and regional blood flow (2.1-fold) and a reduction of the ischemic area (from 29% to 8%) were observed. PB-MNC implantation reduced the ischemic area (from 31% to 17%), the extent of which was less than that seen with BM-MNCs. In saline-implanted myocardium, the ischemic area expanded (from 28% to 38%), and systolic function deteriorated. Angiography revealed an increase in collateral vessel formation by PB-MNC or BM-MNC implantation. Capillary numbers were increased 2.6- and 1.7-fold by BM-MNC and PB-MNC implantation, respectively. BM-MNCs but not PB-MNCs were incorporated into neocapillaries. CONCLUSIONS: Catheter-based implantation of PB-MNCs can effectively improve collateral perfusion and regional function in hibernating ischemic myocardium by its ability to mainly supply angiogenic factors and cytokines.

Usefulness of strain rate imaging in detecting ischemic myocardium during dobutamine stress.

BACKGROUND: Tissue Doppler imaging-derived systolic myocardial velocity can detect subtle alterations in contractility during dobutamine stress. However, increased cardiac translation and tethering during dobutamine stress may affect measurements. METHODS: To examine the hypothesis that regional ischemic myocardium can be sensitively detected during dobutamine stress using myocardial strain rate, a new indicator of regional myocardial contraction that is independent of cardiac translation and tethering, we studied seven closed-chest pig confirmed chronic ischemic models produced by placing an ameroid constrictor on the left circumflex artery. Left ventricular short-axis tissue Doppler imaging was obtained at baseline and during dobutamine stress (10 and 30 microg/kg/min). Peak systolic myocardial velocity and peak systolic myocardial strain rate in anterior and posterior segments were derived offline at each stage. RESULTS: In peak systolic myocardial velocity and peak systolic myocardial strain rate, repeated-measures analysis of variance showed significant interaction between nonischemic and ischemic segments during dobutamine stress. Statistical significance between nonischemic and ischemic segments was reached at baseline, 10 microg/kg/min dobutamine, and 30 microg/kg/min dobutamine in peak systolic myocardial strain rate, and at 30 microg/kg/min dobutamine in peak systolic myocardial velocity. By receiver operating characteristic (ROC) analysis for predicting ischemic segments at 30 microg/kg/min dobutamine, a cutoff value of peak systolic myocardial strain rate was 4.84, with a sensitivity of 100% and a specificity of 100%. Peak systolic myocardial velocity was the less discriminating parameter (cutoff, 6.46; sensitivity, 86%; specificity, 86%). CONCLUSIONS: Myocardial strain rate imaging might represent an accurate parameter for clinical recognition of regional ischemic myocardium during dobutamine stress echocardiography.

Increased level of oxidized LDL-dependent monocyte-derived microparticles in acute coronary syndrome.

We measured and compared the levels of plasma soluble (s) P-selectin, sCD40L, platelet-derived microparticles (PDMP), monocyte-derived microparticles (MDMP), and anti-oxidized LDL antibody, to obtain a better understanding of their potential contribution to vascular complications in acute coronary syndrome (ACS). The concentrations of sP-selectin, sCD40L, PDMP, and MDMP in ACS patients were significantly higher than those in normal controls and patients with stable angina. When levels of these markers were compared with differences in concentration of anti-oxidized LDL antibody, all markers were significantly higher in ACS patients with a high level of anti-oxidized LDL antibody. Next, a monocytic cell line (THP-1) was incubated with high shear stress-induced platelet aggregates and PDMP. After incubation,THP-1 cells generated tissue factor-expressing MDMPs. This finding was particularly significant in the presence of oxidized LDL. These findings suggest that elevated levels of MDMPs may be a sign of atherosclerotic development in ACS patients, particularly those who exhibit anti-oxidized LDL antibodies.

High-performance liquid chromatographic method with column-switching and post-column reaction for determination of serotonin levels in platelet-poor plasma.

OBJECTIVES: Measurement of serotonin concentrations in blood is considered to be important for the clinical studies of diseases involving vascular endothelial injury. We have developed a high-performance liquid chromatographic (HPLC) method for measurement of serotonin level in platelet-poor plasma (PPP). METHODS: Venous blood samples were collected using vacuum tubes containing ethylenediaminetetraacetic acid (EDTA) dipotassium salt; the optimum concentration in blood was 7.4 mmol/l. Serotonin in samples was separated by HPLC with a column-switching system, and was specifically converted into a fluorescent derivative with benzylamine for convenient detection. RESULTS: The between-day assay coefficient of variation for a serotonin level (5.1 nmol/l) in PPP was 6.2%. The mean concentration of serotonin in PPP in healthy subjects was 5.7 +/- 3.0 nmol/l. The serotonin levels in PPP in patients with ischemic heart disease were significantly higher than those in healthy subjects (P = 0.001). CONCLUSIONS: The developed method had sufficient performance to determine serotonin levels in PPP from patients with ischemic heart disease.

Correlation of angiographic morphology immediately after coronary balloon angioplasty with coronary vasomotion late after angioplasty.

BACKGROUND: Various vasomotor responses to acetylcholine have been observed after coronary angioplasty. However, the relationship between the grade of vascular injury due to balloon angioplasty and vasomotor response to acetylcholine in the chronic stage is unknown. In this study we examined the correlation between the morphology immediately after coronary angioplasty and the vasomotor response to acetylcholine 1 year after angioplasty. METHODS: Thirty nine patients with a total of 45 coronary lesions without restenosis 1 year after angioplasty were studied. The 45 lesions were divided into two groups according to the morphology immediately after angioplasty. Group A comprised smooth-walled dilation and smooth-walled dilation with intraluminal haziness which were considered to be related to injury limited to the intima or the surface of the media. Group B comprised intraluminal and extraluminal haziness and extraluminal type dissection which were considered to be related to extensive medial injury. In the 39 patients, acetylcholine provocation test was performed. RESULTS: Transient total occlusion of angioplasty site was induced by acetylcholine in four lesions only in Group A. Percent change in coronary diameter after acetylcholine injection relative to that after injection of isosorbide dinitrate at the angioplasty site was larger in Group A than that of Group B. CONCLUSION: In the chronic stage, vessels with minor vascular injury exhibited a large vasomotor response to acetylcholine; conversely, the response was low in vessels with severe vascular injury by angioplasty. These observations suggest that severe vascular injury by balloon angioplasty may control coronary vasomotion in the chronic stage.

Association of platelet-derived microparticles with C-C chemokines on vascular complication in patients with acute myocardial infarction.

The levels of platelet-derived microparticles (PDMPs), platelet activation markers (P-selectin, CD63, and PAC-1 on activated platelets), and C-C chemokines (monocyte chemotactic peptide [MCP]-1 and regulated on activation normally T-cell expressed and secreted [RANTES] were measured and compared in patients with acute myocardial infarction (AMI) or stable pectoris angina. These substances are thought to paricipate in the development of complications in patients with AMI. The percentage binding of anti-P-selectin, CD63, and PAC-1 antibody to platelets, and the levels of PDMPs (per 10(4) platelets) were higher in the patients with AMI than in those with stable pectoris angina (P-selectin, 23.1% +/- 2.1% vs. 10.3% +/- 1.2%, p < 0.001; CD63, 24.6% +/- 3.3% vs. 11.2% +/- 3.1%, p < 0.01; PAC-1, 14.1% +/- 1.7% vs. 9.3% +/- 2.1%, p < 0.05; PDMPs, 613 +/- 71 vs. 413 +/- 55, p < 0.01). There were no differences in platelet levels of GPIIb/IIIa and GPIb between groups. Levels of MCP-1 and RANTES were higher in the patients with AMI than in patients with stable pectoris angina (MCP-1, 430 +/- 35 vs. 265 +/- 23, p<0.01; RANTES, 175 +/- 32 vs. 88 +/- 29, p<0.001). The effects of percutaneous transluminal coronary angioplasty (PTCA) on the levels of these agents in patients with AMI were studied. Platelet activation markers were significantly decreased in patients with AMI after PTCA. RANTES level was also significantly decreased after treatment, but MCP-1 level was not changed. In addition, this tendency was clearer in STENT patients. These findings suggest that in patients with AMI PTCA, particularly STENT, may prevent the development of complications in which activated platelet and RANTES participate.

Quadricuspid aortic valve associated with idiopathic dilated cardiomyopathy: A case report.

A patient without any known congenital cardiac abnormalities who suffered from ventricular tachycardia was taken to the emergency room following successful resuscitation. Transthoracic echocardiography showed diffuse left ventricle dysfunction and mild aortic regurgitation. Coronary angiography demonstrated intact coronary and suspected morphological abnormalities of the aortic valve. In addition, transesophageal echocardiography revealed a rare quadricuspid aortic valve malformation. After controlling ventricular tachycardia and congestive heart failure with optimal medical therapy, the patient had an uneventful course and was subsequently discharged 3 weeks after admission. To our knowledge, this is the first report of quadricuspid aortic valve associated with idiopathic dilated cardiomyopathy. .

Atypical morphology and myocardial perfusion of mid-ventricular ballooning: A case report.

Although some atypical types of transient left ventricular apical ballooning syndrome have been reported, only a few atypical types of transient mid-ventricular ballooning have been reported. A 70-year-old female underwent surgery for urothelial carcinoma. At day 5 after the surgery, she was admitted to our department without cardiac symptoms because of ST elevation in leads I, II, III, aVF and V1-V6 indicating acute coronary syndrome. She was diagnosed with stress induced cardiomyopathy based on an angiographically normal coronary artery, newly developed extensive wall motion abnormality (hyperbasal contraction and akinesis from the mid-left ventricle to the apex without hypercontraction of the small area adjacent to the apex) based on left ventriculography, and a small elevation of myocardial enzymes incongruous with the area of contraction abnormality. Myocardial scintigraphy with 99mTc-tetrofosmin showed a severely reduced myocardial perfusion in an extensive mid-ventricular area without a left ventricular base and top of apex, in accord with a wall motion abnormality different from typical apical ballooning or typical mid-ventricular ballooning previously diagnosed in our hospital. This is the first report presenting an atypical mid-ventricular ballooning based on the myocardial atypical perfusion findings.

A new protocol using sodium bicarbonate for the prevention of contrast-induced nephropathy in patients undergoing coronary angiography.

Contrast-induced nephropathy (CIN) is associated with increased morbidity and mortality rates. Although a previous study reported that pretreatment with sodium bicarbonate is more effective than sodium chloride for prophylaxis of CIN, this has not been a universal finding. We performed a prospective randomized trial to investigate whether CIN can be avoided using sodium bicarbonate. In total 155 patients with a glomerular filtration rate (GFR) <60 ml/min/1.73 m(2) who were undergoing coronary angiography were enrolled. We assigned patients to sodium chloride plus sodium bicarbonate (bicarbonate group, n = 78) or sodium chloride alone (chloride group, n = 77). Infusion of sodium bicarbonate at 1 ml/kg/hour continued from 3 hours before to 6 hours after coronary angiography. CIN was defined as a 25% increase in serum creatinine from baseline value or an absolute increase of ≥0.5 mg/dl, which appeared within 2 days of contrast. Baseline GFR was not significantly different between the 2 groups. Patients in the bicarbonate group had a higher GFR than those in the chloride group on day 2 (45.8 ± 13.4 vs 40.9 ± 14.6 ml/min/1.73 m(2), p = 0.031) and at 1 month (49.5 ± 14.7 vs 43.7 ± 15.5 ml/min/1.73 m(2), p = 0.019). CIN occurred in 10 patients (13%) in the chloride group but in only 2 patients (2.6%) in the bicarbonate group (p = 0.012). Sodium chloride plus sodium bicarbonate is more effective than sodium chloride alone for prophylaxis of CIN and can lead to retention of better long-term renal function.

Comparison of neointimal morphology of in-stent restenosis with sirolimus-eluting stents versus bare metal stents: virtual histology-intravascular ultrasound analysis.

Sirolimus-eluting stents (SES) have reduced the incidence of restenosis and target lesion revascularization compared to bare metal stents (BMS). However, inhibition of endothelialization and neointimal formation after SES implantation may produce vulnerable plaques. The present study compared the neointimal morphology of in-stent restenosis (ISR) between SES and BMS using virtual histology-intravascular ultrasound (VH-IVUS). Thirty ISR lesions (SES n = 15, BMS n = 15) demonstrated by coronary angiography in 30 patients with stable angina pectoris were analyzed with VH-IVUS between 6 months to 3 years after stent implantation. Tissue maps were reconstructed from radiofrequency data using VH-IVUS software. ISR lesions after SES implantation consisted of a significantly increased necrotic core (NC) compared to BMS (12.9 vs. 5.6% of neointimal volume, p < 0.01). However, the NC in ISR lesions after SES implantation was covered with a thick fibrous cap. An increase in the size of NC covered with a thick fibrous cap is a characteristic morphological feature of ISR after SES implantation. Further studies are needed to clarify whether such a morphological change is related to the attenuation of stent thrombosis after SES implantation.

Contrast-induced nephropathy in patients undergoing emergency percutaneous coronary intervention for acute coronary syndrome.

Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after coronary angiography and percutaneous coronary intervention (PCI). The aim of the present study was to assess the clinical features and in-hospital outcomes of CIN after emergency PCI. The serum creatinine (SCr) concentration was measured from days 0 to 30 in 338 consecutive patients with acute coronary syndrome undergoing emergency PCI. CIN was defined as an increase in SCr of >25% or >0.5 mg/dl within 2 days after PCI. Overall, 94 patients (28%) developed CIN. The mean SCr on admission was not significantly different between patients with CIN and those without CIN. The CIN group had significantly greater SCr at days 1, 2, and 30 than did the no CIN group. Multivariate analysis showed female gender (odds ratio [OR] 2.38, 95% confidence interval [CI] 1.12 to 5.07, p = 0.025), a culprit lesion in the left anterior descending artery (OR 2.37, 95% CI 1.31 to 4.27, p = 0.0042), contrast agent volume >200 ml (OR 3.60, 95% CI 1.96 to 6.62, p <0.001) and end-diastolic pulmonary arterial pressure >15 mm Hg (OR 2.03, 95% CI 1.02 to 4.04, p <0.01) to all correlate independently with CIN. The in-hospital mortality rate was greater in the CIN group than in the no CIN group (9.6% vs 3.3%, respectively; p = 0.025). In conclusion, CIN is a frequent complication of emergency PCI for acute coronary syndrome and is associated with a greater mortality rate and persistent renal dysfunction.

Prevention of contrast-induced nephropathy by chronic pravastatin treatment in patients with cardiovascular disease and renal insufficiency.

BACKGROUND: Contrast-induced nephropathy (CIN) is known to increase morbidity and mortality of cardiovascular disease. Recent studies have shown statins prevented CIN after contrast media exposure, but optimal statin type and dosage are still unknown. PURPOSE: The aims of the present study were to evaluate whether chronic pravastatin treatment before scheduled coronary angiography or percutaneous coronary intervention could reduce the incidence of CIN and to elucidate the factors related to CIN in patients with renal insufficiency. METHODS: We studied 431 consecutive patients with renal insufficiency. One hundred ninety-four patients were receiving pravastatin treatment as standard chronic treatment of hypercholesterolemia. Serum creatinine levels were measured at baseline (pre-procedure) and within 48 h after contrast media exposure (peak post-procedure). CIN was defined as an increase in the serum creatinine values of > or = 25% or > or = 0.5 mg/dl after contrast media exposure. Logistic regression analysis was performed to evaluate the important factors related to CIN using four variables: age, pravastatin, pre-procedure serum creatinine, and contrast volume. RESULTS: CIN was observed in 36 patients (8.4%). Patients without pravastatin (p<0.01), high level pre-procedure serum creatinine (p<0.01), and high contrast volume (p=0.034) had a significantly higher incidence of CIN. Logistic regression analysis revealed that pravastatin treatment (chi(2)=6.549, p=0.011, odds ratio=0.34), pre-procedure serum creatinine (chi(2)=6.294, p=0.009, odds ratio=2.78), and contrast volume (chi(2)=4.484, p=0.034, odds ratio=1.01) were independently related to the decreased risk of CIN. CONCLUSIONS: Chronic pravastatin treatment before contrast media exposure was important for preventing CIN in patients with renal insufficiency. Also, reducing the dose of contrast media was important for preventing CIN in patients with high-baseline serum creatinine levels.

Nicorandil suppressed myocardial injury after percutaneous coronary intervention.

BACKGROUND: Nicorandil exerts beneficial effects as an adjunctive therapy for patients with ischemic heart disease. This study was designed to assess the effects of nicorandil on the myocardial protective benefits of elective percutaneous coronary intervention (PCI). METHODS: We randomly divided 49 patients scheduled to undergo elective PCI into two groups, nicorandil and control. Before PCI, the former received an intravenous bolus injection of nicorandil (4 mg), followed by continuous infusion at 6 mg/h for 24 h after intervention. Oral administration of nicorandil was continued until follow-up coronary angiography (CAG). Serial venous blood samples, for measurement of creatine kinase (CK), creatine kinase MB isoform (CK-MB), troponin I (TnI) and myoglobin, were obtained before PCI, and at 0 h, 4 h, 24 h and 48 h after PCI. Left ventricular function and left ventricular wall motion were evaluated by means of contrast ventriculography before PCI and follow-up CAG. RESULTS: At 24 h after PCI, elevations of cardiac enzymes were significantly suppressed in the nicorandil as compared to the control group; CK (78.1+/-34.9 versus 117.4+/-137.9 U/l, P=0.0141), CK-MB (1.57+/-1.90 versus 2.67+/-4.50 U/l, P=0.0485) and TnI (0.37+/-0.55 versus 0.86+/-1.65 ng/ml, P=0.0101). Regional left ventricular wall motion was significantly improved at follow-up in the nicorandil as compared to the control group. CONCLUSIONS: Nicorandil suppressed elevations of cardiac enzymes after elective PCI and left ventricular wall motion was also significantly improved at follow-up, suggesting that nicorandil enhances the myocardial protective effect of PCI against angioplasty-related myocardial injury.

Success rate of implantation and mid-term outcomes of the sirolimus-eluting stent.

BACKGROUND: The sirolimus-eluting stent (SES) is currently the sole drug-coated stent approved for use in Japan, but there are few reports on its safety and outcomes in Japan. METHODS AND RESULTS: From May 2004 to February 2005, a total of 297 patients with 402 lesions were treated with SES at 6 hospitals in the Kansai district. Follow-up angiography was performed in 82% of the patients and 80% of the lesions at 182+/-35 days after stenting. Coronary stenosis was evaluated using quantitative coronary angiography. Clinical and angiographic data were analyzed. Minimum lesion diameter was 0.75+/-0.52 mm and the reference diameter was 2.81+/-0.47 mm before stenting. The SES successfully dilated 99.5% of the lesions with few major adverse cardiac events. Restenosis occurred in 4.0% and the target lesion revascularization rate was 3.7%. Restenosis correlated with chronic hemodialysis, calcification, occlusion, ostial lesions, lesions kinked>45 degrees, right coronary artery (RCA) lesions and lesions at the ostium of the RCA. CONCLUSION: SES demonstrated a high rate of successful implantation with few complications, and mid-term outcomes were excellent. Patients with lesions at the ostium of the RCA or under chronic hemodialysis developed restenosis.