Same-day discharge transradial percutaneous coronary intervention (TRI) has been reported to be safe and feasible in Western countries. However, Asia has not produced any reports related to this matter. The present study explored the safety and feasibility of patients with indications for TR coronary angiography and ad hoc PCI with a same-day discharge protocol. Between October 1995 and December 2002, 660 adult patients were admitted to our hospital for ad hoc PCIs. Of these, 214 patients were discharged on the day of their PCI (group A), while the remaining 446 patients were referred for out-patient department (OPD) PCI with subsequent admission (group B). Periprocedural complications were not significantly different between the groups. There were no differences in 1-month major adverse cardiac events including death, myocardial infarction, and target vessel revascularization (1.4% versus 0.2% for groups A and B, respectively; P = 0.068). Three group A cases (1.4%) experienced peri- and post-PCI myocardial infarction and one group B case (0.2%) experienced a post-PCI myocardial infarction. No patient died or required emergency bypass surgery. In group A, 8 cases (3.7%) required cutting balloon angioplasty and 2 cases (0.9%) needed rotational atherectomy. TRI is safe and feasible on an outpatient basis. For select patients, even though PCI can carry the potential risk of subsequent cutting balloon angioplasty or rotational atherectomy, the procedure should still be considered.

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The long-term safety and efficiency of sirolimus-eluting stent (SES) treatment in unprotected left main coronary artery (ULMCA) have not yet been ascertained.
From 2003 to 2006, 126 consecutive patients with de novo lesions in ULMCA who underwent SES were retrospectively analyzed in a single center in China. During 4-year follow-up, major adverse cardiovascular event (MACE)-free survival was 74.6%. Cardiac death occurred in 5 (4.0%), and target lesion revascularization (TLR) and target vessel revascularization (TVR) occurred in 15 (11.9%) and 24 (19.0%) patients, respectively. One (0.8%) experienced probable stent thrombosis while 1 (0.8%) presented possible stent thrombosis. Impaired LVEF (< 40%) and high surgical risk (Euro score > 6) were the independent predictors of MACEs.
PCI with SES for de novo lesions in ULMCA is feasible with a low procedural risk. However, SES was associated with a relatively higher rate of TLR and TVR. Impaired LVEF and high surgical risk were important predictors of MACEs.

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Plaque disruption, which may be associated with some coronary risk factors, plays a key role in the development of acute coronary syndromes and progression of atherosclerosis. However, the clinical profile of asymptomatic plaque disruption in stable ischemic heart disease has not been well evaluated. The aim of the present study was to investigate the frequency and determinants of silent plaque disruption (SPD) in patients with stable ischemic heart disease using coronary angioscopy. Forty-one patients with stable angina or old myocardial infarction (OMI) without any complaints within 3 months were included in the present study. Angioscopy was successfully performed through 49 nonischemic related coronary arteries. The presence of SPD and coronary risk factors were recorded. Silent plaque disruption was found in 12 patients with stable ischemic heart disease (12/41, 29.3%), and the frequency of SPD in nonischemic related coronary arteries was 26.5% (13/49). A significantly higher frequency of SPD was noted in yellow plaques than in white plaques (35.3% versus 6.7%, P = 0.043). Overall, the independent clinical risk factors of SPD in nonischemic related coronary arteries were diabetes mellitus (P = 0.018; OR, 18.8209; 95% CI, 1.6525 to 214.3523) and hypertension (P = 0.0313; OR, 6.6485; 95% CI, 1.1850 to 37.3019). These results suggest silent plaque disruption was commonly observed in nonischemic related coronary arteries in patients with stable ischemic heart disease and its determinants were diabetes mellitus and hypertension.

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Frequent premature ventricular complexes (PVCs) from the right ventricular outflow tract (RVOT) have recently been reported to be a cause of dilated cardiomyopathy. We studied the clinical impact of the elimination of PVCs from RVOT and non-RVOT.
Thirty-six patients with symptomatic PVCs that were treated with radiofrequency catheter ablation (RFCA) were studied. The patients were assigned to one of two groups according to the origin of the PVCs (group I, RVOT-origin, n = 24; group II, non-RVOT-origin, n = 12) and observed for 10.5 ± 7.1 months.
The burden of PVCs at baseline was 19.7 ± 10.6% and 18.7 ± 8.7% in group I and group II, respectively (P = 0.779). In group II, hypertension was more common (16.7% versus 58.3%, P = 0.020) and LV diastolic function was worse (Em, 8.7 ± 3.0 versus 6.4 ± 1.8 cm/second, P = 0.018). The LV end diastolic volume index (LVEDVI) decreased in both groups (59.7 ± 14.6 to 50.9 ± 9.6 mL/m², P = 0.004 in group I; 60.0 ± 19.9 to 51.6 ± 12.4 mL/m², P = 0.044 in group II), while the left atrial volume index (LAVI) decreased only in group I (36.7 ± 11.7 to 31.7 ± 10.0 mL/m², P = 0.002 in group I; 35.6 ± 11.9 to 33.8 ± 10.3 mL/m², P = 0.317 in group II). The left ventricular ejection fraction (LVEF) significantly improved in both groups (51.1 ± 6.6 to 59.8 ± 7.2 %, P < 0.01 in group I; 49.9 ± 6.9 to 59.0 ± 5.9 %, P < 0.01 in group II).
RFCA of PVCs leads to a reduction of LV volume and improvement of LV systolic function regardless of the origin of the PVCs. Conversely, a non-RVOT-origin as well as an RVOT-origin of the PVCs can cause DCM-like changes in the left ventricle.

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To examine the electrophysiologic characteristics of the subvalvular mitral region, we retrospectively searched for the presence of subvalvular diastolic potentials (DP) in 91 patients (mean age, 46.9 ± 16.6 years) who underwent catheter ablation of left-sided accessory pathways (AP).
We detected low-amplitude (0.19 ± 0.09 mV) DP in 14 patients (15.4%), including 8 with overt preexcitation and 6 patients with concealed AP. The mean interval between ventricular electrogram and DP was 383 ± 46 ms (range, 306-475). DP were detected in 4 of 20 patients with antero-lateral, 3 of 38 with lateral, 4 of 12 with postero-lateral, 2 of 14 with posterior, and 3 of 10 patients with postero-septal AP. In 6 of 14 patients, DP were detected before ablation. In 4 of 8 patients with overt preexcitation, DP were consistently recorded after elimination of the delta wave, suggesting that they were not associated with AP conduction. In 6 of 11 patients, DP were observed during both sinus rhythm and ventricular pacing, suggesting that they were not artifacts.
The electrophysiologic characteristics of clinically relevant DP around the mitral annulus suggest that, in normal human hearts, an anatomical substrate may be present around the mitral annulus.

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Although bucolome has been used empirically to enhance and stabilize warfarin action in some institutes, the clinical risks and benefits of this combination are unclear. In the present study, warfarin monotherapy (WM) and bucolome combination (BC) therapy were compared in anticoagulation therapy.
One hundred and ninety-five patients indicated for anticoagulation therapy were randomly assigned to WM (n = 98) or BC (bucolome 300 mg/day, n = 97). The dosage of warfarin was optimized in each patient to maintain the international normalized ratio (INR) level in the appropriate zone, ie, 1.6-2.6 for lower risk and 2.0-3.0 for higher risk patients. The clinical characteristics, clinical events, and time in therapeutic range (TTR) were evaluated and compared between the two groups. TTR was calculated using Rosendaal’s linear interpolation method.
The optimal dosage of warfarin was 3.3 ± 1.0 mg/day in WM and 1.4 ± 0.5 mg/day in BC (P < 0.001). During the observation period of 18 ± 6 months, no serious complication was observed and INR was measured 11 ± 3 times in each case. TTR was 0.61 ± 0.13 in WM and 0.62 ± 0.14 in BC (NS), but TTR in the WM subgroup with warfarin > 3 mg (0.58 ± 0.13) was lower than in the WM subgroup with warfarin ≤ 3 mg (0.64 ± 0.13, P = 0.026) and BC (P = 0.042).
BC reduced the optimal dosage of warfarin without increasing clinical events. There was no significant difference in TTR between WM and BC, but BC may have benefits in selected cases, such as warfarin resistance.

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The serum levels of matrix metalloproteinases (MMPs) increase during chronic heart failure (HF) and the MMP-2 are related to a poor prognosis. However, the roles of MMP-2 in acute HF (AHF) remain unclear. We investigated the change and clinical significance of MMP-2 in these conditions. The serum levels of MMP-2 were measured in 83 AHF patients before starting treatment (day 1), 3 (day 3) and 7 (day 7) days after admission, and before discharge (predischarge). MMP-2 decreased rapidly and significantly from day 3 to day 1 (902.9 ± 304.2 versus 1220.4 ± 330.5 ng/mL; P < 0.0001), whereas that of MMP-2 was not significantly different on day 7 and at predischarge (894.7 ± 278.9 and 920.0 ± 269.6 ng/mL, respectively) compared to day 3. We evaluated the relationships between ΔMMPs, defined as the changes in MMPs from day 1 to day 3 and HF events including cardiac death, readmission to hospital for HF, and uncontrollable HF. The MMP-2 value was significantly (P = 0.004) more decreased in the event-free group (381.4 ± 256.5 ng/mL) than in the event group (211.9 ± 225.5 ng/mL) between day 1 and day 3. The results of the multivariate logistic regression model for predicting HF events found that the specific factor for HF events was ΔMMP-2. Cutoff values of ΔMMP-2 were determined and event-free curves were constructed. Kaplan-Meier curves showed that the prognosis was significantly better among the patients with reductions in ΔMMP-2 values of more than 342 ng/mL. The serum levels of MMP-2 decreased with improvements in AHF. Rapid decreases in MMP-2 may be important for a better clinical outcome in patients with AHF.

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The phosphodiesterase III inhibitor milrinone (MIL) is considered to be effective for “wet and cold” heart failure. In some cases, however, the inotropic effects of milrinone are insufficient. A previous study suggested that baroreflex sensitivity (BRS) predicts the cases in which MIL increases left ventricular dp/dt. The aim of this study was to determine whether BRS measured using the spontaneous sequence method predicts the MIL responders. Twenty-four patients with “wet and cold” heart failure whose systolic blood pressure > 100 mmHg were enrolled. At 2 hours MIL improved dys-pnea, general fatigue, urine volume, and tricuspid regurgitant pressure gradient in 13 patients (responders; R group), whereas it failed to improve in 11 patients (nonresponders; NR group). BRS in the R group was significantly higher than that in the NR group prior to the MIL infusion. At 2 hours after the MIL infusion, BRS was further increased in the R group, but did not increase in the NR group. The sensitivity and specificity of BRS at a cut-off level of 5 ms/mmHg for the prediction of R group were 0.94 and 0.93, respectively. BRS might be useful for identifying potential responders to milrinone in patients with blood pressure-preserved “wet and cold” heart failure.

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Biomarkers are needed for early risk stratification and improved inpatient management to obtain better outcomes in acute pulmonary embolism (PE) patients. The aim of the present study was to evaluate biomarkers of right ventricular dysfunction (RVD) in order to predict a complicated clinical course and long-term respiratory complications in acute PE.
We retrospectively enrolled 50 consecutive patients hospitalized for acute PE. Plasma brain natriuretic peptide (BNP), troponin-I, fibrin degradation products, D-dimer, C-reactive protein, and arterial pH were measured to assess their prognostic significance. RVD was evaluated by echocardiography at admission, the clinical course during hospitalization was monitored for the development of complications (death, cardiopulmonary resuscitation, mechanical ventilation or circulatory shock), and the need for home oxygen therapy (HOT) was assessed at/after discharge.
Thirty-two patients (64%) had RVD at admission, 6 (12%) developed a complicated clinical course, and 7 (14%) required HOT. Plasma BNP was significantly higher in patients with RVD (median value, 319.3 versus 50.5 pg/mL, P = 0.001). Plasma BNP was also significantly higher (median value, 1307.9 versus 102.6 pg/mL, P = 0.02) and arterial pH significantly lower (acidic) (median value, 7.371 versus 7.438, P = 0.008) in patients who developed a complicated clinical course. In addition, plasma BNP was also significantly higher in patients who required HOT (median value, 505.1 versus 91.1 pg/mL, P = 0.02).
Plasma BNP at admission is not only a reliable marker of RVD and predictor of short-term prognosis, but also a predictor of long-term respiratory prognosis in acute PE patients.

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The objective of the present study was to evaluate whether left ventricular (LV) pressure changes influence left atrial (LA) function during acute LV ischemia by strain rate imaging.
In 11 healthy dogs, the left anterior descending coronary artery was occluded to cause regional acute ischemia. The peak strain rate (PSR) values of the LA walls during the reservoir, conduit, and contractile phases of the LA cycle, as well as the LV pressures, were measured before and after ischemia. All PSR values increased significantly after ischemia (P < 0.001). Left ventricular end-diastolic pressure (LVEDP) increased after ischemia (P < 0.0001) and its percent change was positively correlated with the LA contractile phase and conduit phase percent changes of PSR for the anterior and lateral walls of the atrium (r = 0.72, 0.72, 0.83, and 0.73; P = 0.05, 0.05, 0.002, and 0.01, respectively).
LA function is influenced by the change of LVEDP during regional LV ischemia. There is a compensatory increase in wall motion after regional acute LV ischemia.

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Statins improve left ventricular (LV) remodeling in spontaneously hypertensive rats (SHRs). This study was designed to investigate the effects of atorvastatin administered in the early stage on LV remodeling in SHRs, and to explore the underlying mechanisms.
Sixteen male 8-week-old SHRs were randomized to receive distilled water (SHR-DW) or atorvastatin (SHR-ATV) for 12 weeks. Age-matched male Wistar-Kyoto (WKY) rats gavaged with distilled water served as controls. LV remodeling was evaluated, myocardial CTGF expression levels were detected using Western blotting, and cardiomyocyte apoptosis was detected with the TUNEL method.
Compared with WKY and SHR-DW, atorvastatin treatment significantly decreased systolic blood pressure in SHRs; atorvastatin significantly inhibited LV remodeling, as indicated by the reduced LV weight/body weight ratio (SHR-ATV: 4.0 ± 0.4 versus SHR-DW: 4.7 ± 0.4 mg/g, P < 0.05), cardiomyocyte diameter (SHR-ATV: 16.2 ± 2.8 versus SHR-DW: 19.0 ± 1.0 μm, P < 0.05), and interstitial fibrosis (SHR-ATV: 3.3 ± 2.1 versus SHR-DW: 4.5 ± 1.8%, P < 0.05). Compared with WKY, myocardial CTGF expression was significantly increased and cardiomyocyte apoptosis decreased in SHRs. Compared with the SHR-DW group, atorvastatin treatment significantly inhibited myocardial CTGF expression (SHR-ATV: 0.69 ± 0.21 versus SHR-DW: 1.12 ± 0.27, P < 0.05) and induced cardiomyocyte apoptosis in SHRs (SHR-ATV: 5.2 ± 0.6 versus SHR-DW: 1.9 ± 0.3%, P < 0.05).
The results indicate that early-stage administration of atorvastatin effectively prevented LV remodeling in SHRs, and that inhibition of myocardial CTGF expression and induction of cardiomyocyte apoptosis may be the underlying mechanisms.

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We report the case of a 65-year-old woman with a solitary kidney who developed hypertension due to renal artery stenosis caused by fibromuscular dysplasia. In addition, an echocardiogram revealed severe left ventricular systolic and diastolic dysfunction. Despite antihypertensive drug treatment that included diuretics, her serum concentration of brain natriuretic peptide was persistently elevated and associated with progressive worsening of renal function. She underwent iliac artery to renal artery bypass grafting. After the surgery, blood pressure control was good, the serum concentration of brain natriuretic peptide decreased, and left ventricular diastolic function improved. This case exemplifies the efficacy of renal revascularization in patients with fibromuscular renal artery stenosis and heart failure.

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