A slightly elevated level of N-terminal pro-brain natriuretic peptide can predict coronary artery disease in a population with normal left ventricular function.

The prognostic and diagnostic values of N-terminal pro-brain natriuretic peptide (NT-pro-BNP) in ischemic heart disease have already been investigated in many previous studies. Although NT-pro-BNP is affected by many factors, these previous studies did not strictly exclude them. This study included 110 patients who received coronary arteriography between November 2007 and September 2009. Excluded from the study were those patients who had clinical symptoms of heart failure, asynergy by echocardiography or left ventriculography (LVG), atrial fibrillation, prior myocardial infarction, valvular disease, lung disease, anemia or renal dysfunction. We compared the laboratory data, LVG and early transmitral-to-early diastolic annular velocity ratio (E/E (a)) in echocardiography between the group with coronary stenosis and the group without it. NT-pro-BNP and the low-density lipoprotein/high-density lipoprotein ratio (LDL/HDL) independently associated with the presence of coronary artery stenosis (odds ratio of NT-pro-BNP, each 50 pg/ml 2.367, 95% confidence interval 1.302-4.303, p = 0.005). The area under the curve of the receiver-operating characteristic (ROC) curve of NT-pro-BNP, used to predict coronary artery stenosis, was 0.801 (0.719-0.883, p < 0.001). According to the ROC curve, the optimal cut-off level for predicting coronary stenosis was 64.3 pg/ml (sensitivity 82.5%, false-positive 34%). NT-pro-BNP is an attractive supplemental marker to predict the presence of coronary artery stenosis in a population that strictly excluded any affecting factors. In the population without factors affecting NT-pro-BNP, a slight increase suggests the presence of ischemic heart disease. The normal criteria for NT-pro-BNP in the patients undergoing coronary angiography may be much lower than the one currently used.

Aggressive statin therapy in multicenter and effectiveness for the reduction of intra-myocardial damage caused by non-ST elevation acute coronary syndrome: AMERICA study.

BACKGROUND: While preprocedural statin treatment for acute coronary syndrome (ACS) is widely regarded as beneficial, there has been no prospective randomized multicenter trial of patients with non-ST elevation ACS in the Japanese population to examine the efficacy of preprocedural aggressive statin use. The aim of this study was to confirm this effect by prospective randomized multicenter design. METHODS: Fifty patients who presented with non-ST elevation ACS were enrolled, and randomly assigned to aggressive statin administration before percutaneous coronary intervention (PCI). Troponin-T (TnT), creatine phosphokinase (CK), CK-myocardial band (CK-MB), high-sense C-reactive protein (hs-CRP), and brain natriuretic peptide (BNP) were measured at baseline and/ or after procedure. RESULTS: Three days after PCI, the statin group had significantly less CK elevation compared with the nonstatin group (84+/-17 IU/l versus 180+/-68 IU/l, respectively, p = 0.02). CK-MB elevation also tended to be lower in the statin group than in the nonstatin group (3.2+/-1.9 versus. 7.0+/-3.0, respectively, p = 0.07), as was BNP level (3.2+/-1.9 versus 7.0+/-3.0 pg/ml, respectively, p = 0.07). The change of serum LDL cholesterol was significantly correlated with CK (p = 0.01) and TnT (p = 0.02) at 1 day after PCI. CONCLUSIONS: Aggressive statin usage before PCI to Japanese patients with non-ST elevation ACS appears to reduce myocardial damage after procedure. The degree of serum lipid level reduction may reflect the vulnerability of atheromatous plaques that could cause cardiac damage after PCI.

Intervention for jailed diagonal branch is not necessary while stenting the left anterior descending artery.

OBJECTIVES: To evaluate whether or not to treat diagonal branches interventionally while implanting sirolimus-eluting stents (SES) in left anterior descending artery (LAD). BACKGROUND: Percutaneous coronary intervention (PCI) procedures are complicated, especially in the case of a bifurcation lesion. The complicated strategy of PCI may increase the quantity of contrast medium, fluoroscopy time, and the number of devices. METHODS: We retrospectively included 35 patients with stable angina who were treated with SES between July 2005 and December 2006. They had 40 LAD/diagonal branch bifurcation lesions. The diagonal branches had a diameter greater than 1.5 mm. We finished the procedure without inflating diagonal branches when their flow showed thrombolysis in myocardial infarction (TIMI) flow grade 3, even if the ostium of the branches had severe stenosis. Follow-up angiographies were performed 6 months later. The LAD and ostium of diagonal branches were evaluated according to the quantitative coronary angiography (QCA) measurements. RESULTS: The percent diameter stenosis (%DS) of the ostium of diagonal branches was worse post-PCI than at baseline (P = 0.0101). When comparing the follow-up values with the baseline values, there were no significant differences. Additionally, follow-up values were significantly better than the post-PCI values (P = 0.0016). There was no hospitalization for heart failure, angina, or cardiac death. There was only one restenosis in LAD at follow-up, and no diagonal branch became totally occluded or delayed. CONCLUSIONS: In the diagonal branches, the minimal lumen diameter decreased and diameter stenosis progressed temporarily; however, both parameters recovered at the time of follow-up.

Hemostatic and fibrinolytic activation is less following cutting balloon angioplasty of the coronary arteries.

Recent studies have shown that percutaneous coronary intervention (PCI) activates systemic hemostatic activity, reflecting platelet activation and thrombin formation in the coronary arteries. The present study compared systemic levels of hemostatic markers induced by plain old balloon angioplasty (POBA), coronary stenting (STENT), and cutting balloon (CB) angioplasty. Sixty-one patients with stable angina pectoris, who underwent elective PCI or diagnostic coronary angiography (CAG) alone, were investigated. Patients who underwent PCI were divided into the POBA group (n = 11), the STENT group (n = 27), and the CB group (n = 11). Patients who underwent CAG alone were assigned to the CAG group (n = 12). Blood samples were collected before, 24 hours after, and 3 days after PCI or CAG. Plasma concentrations of prothrombin fragment 1+2 (F1+2), fibrinopeptide A (FPA), thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor-1 (PAI-1) were measured. In the CB group, the F1+2 (1.23 +/- 0.4 nmol/L) level 3 days after PCI was significantly smaller than that of the POBA group (2.37 +/- 0.5 nmol/L) (P < 0.05). The FPA (1.81 +/- 0.9 ng/mL), TAT (3.36 +/- 1.2 ng/mL) and PAI-1 (23.0 +/- 4.1 ng/mL) levels in the CB group 3 days after PCI were significantly smaller than those of the POBA group (P < 0.05, respectively) and STENT group (P < 0.05, respectively), but similar to the CAG group. Systemic hemostasis is activated to a greater extent after POBA and stenting than it is after CB angioplasty of the coronary arteries. This may contribute to the favorable long-term outcome of CB angioplasty.

Intravascular ultrasonic comparisons of mechanisms of vasodilatation of cutting balloon angioplasty versus conventional balloon angioplasty.

Intimal hyperplasia after balloon dilatation may be related to the severity of vascular injury, and cutting balloon angioplasty (CBA) may reduce vascular injury. The present study investigated the mechanism of vasodilation by CBA. Intravascular ultrasound examination was performed before and after intervention in 40 lesions treated with CBA and in 25 lesions treated with conventional balloon angioplasty. Intravascular ultrasound measurements included the vessel area, luminal area, and plaque area. Vessel expansion was evaluated as the ratio of the postprocedural vessel area to that before intervention. The vessel area was 13.9 +/- 3.2 and 14.8 +/- 3.2 mm(2) after CBA versus conventional angioplasty, respectively, whereas the luminal area was 5.5 +/- 1.2 versus 5.7 +/- 1.2 mm(2) and the plaque area was 8.5 +/- 2.7 versus 9.1 +/- 2.2 mm(2), respectively. The vessel area was smaller and the plaque area significantly smaller after CBA. Vessel expansion accounted for 45% of luminal enlargement, and plaque compression or shift accounted for 55% after CBA. After conventional angioplasty, vessel expansion accounted for 67%, and plaque compression or shift for 33% of luminal enlargement. The vessel expansion ratio was significantly smaller after CBA than after conventional angioplasty (1.05 vs 1.22, p <0.05). These findings suggest that the predominant mechanism of dilatation after CBA is plaque compression or shift rather than vessel expansion, unlike conventional angioplasty.