Lumen enlargement during coronary stenting results from vessel expansion and axial redistribution of atheromatous plaque along the stented segment and proximal and distal reference segments. Plaque burden predicts stenosis at the stent edge. The aim of this study was to investigate the fate of shifted plaque with special reference to whether or not plaque shift (PSh) correlates with late lumen reduction. This is a prospective study conducted on 54 consecutive patients who underwent bare metal stenting. In all stent edges (108 edges), PSh volume was measured as postintervention plaque-media volume (PMV) minus preintervention PMV. Changes in lumen volume (ΔLV), vessel volume (ΔVV), and PMV (ΔPMV) were measured by serial intravascular ultrasound (IVUS) examination. After stenting, PSh was detected in 81.5% of proximal edges versus 72.2% of distal edges (P = 0.36). It correlated significantly with ΔVV (r = 0.34, P = 0.002), and inversely with ΔLV (r = 0.32, P = 0.003). However, at 6-month follow-up, it did not correlate with ΔLV (r = −0.03, P = 0.8), ΔVV (r = 0.1, P = 0.6), or ΔPMV (r = 0.1, P = 0.4). Furthermore, ΔLV correlated more strongly with ΔVV (r = 0.62, P < 0.00001) than with ΔPMV (r = −0.39, P = 0.001). By multivariate analysis, PSh area was an independent predictor of the postintervention change in lumen area (partial eta squared 0.21, P = 0.01), but not the follow-up change. Two patients (3.7%) developed proximal edge stenosis with no evident PSh after stenting. Thus, axial redistribution of atheromatous plaque into the reference segments was frequently encountered after stenting. Although PSh correlated with the immediate reduction in stent edge lumen volume, it did not correlate with the late lumen reduction.

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It remains to be determined whether adding an angiotensin-converting enzyme inhibitor (ACEI) or an angiotensin II receptor blocker (ARB) to antiplatelet therapy has a therapeutic benefit on in-stent restenosis.
After successful coronary stenting, 165 patients (167 lesions) were randomly assigned to a basal (aspirin 162 mg + cilostazol 200 mg/day), ACEI (basal treatment + quinapril 10 mg or perindopril 4 mg/day), or ARB (basal treatment + losartan 50 mg/day) treatment group. Quantitative coronary angiography was performed before, immediately following, and 6 months after stenting. Follow-up coronary angiography was completed in 126 patients (128 lesions). Restenosis rates tended to be higher (12, 26, and 12% for the basal, ACEI, and ARB groups, respectively), and target lesion revascularization rates were higher in the ACEI group than in the other groups (9, 23,* and 5%, respectively, *P < 0.05 versus basal group). Moreover, late lumen loss was higher in the ACEI group than in the basal group (0.60 ± 0.55, 0.98 ± 0.61* and 0.73 ± 0.64 mm in the basal, ACEI, and ARB groups, respectively).
The combinations of an ACEI or ARB with aspirin and cilostazol are ineffective for the prevention of in-stent restenosis, and an ACEI may even promote intimal proliferation after stent implantation.

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The purpose of the present study was to investigate retrospectively which aortic clamping technique, the single clamp technique (SCT) or double clamping technique (DCT), is safer in terms of cerebral functions in patients who have undergone coronary bypass surgery. We evaluated 1100 patients who underwent coronary artery bypass graft surgery at our institute from 1998 to 2004. The two groups, SCT (n = 550, 50%) and DCT (n = 550, 50%), were comparable with respect to smoking, hypertension, hypercholesterolemia, diabetes mellitus, chronic obstructive pulmonary disease, peripheral arterial disease, history of neurological events, creatinine levels, and existence of a carotid lesion. No significant differences between the SCT and DCT groups were observed in terms of cardiac and cerebral complications perioperatively and postoperatively. Both single and double clamping techniques have advantages and disadvantages in patients undergoing coronary bypass surgery.

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The purpose of this study was to elucidate the relationship between the mismatch of thallium-201(Tl) and iodine-123-beta-methyl-iodophenyl-pentadecanoic acid (BMIPP) myocardial single-photon emission computed tomography (SPECT) and autonomic nervous system activity in myocardial infarction (MI) patients. The subjects were 40 patients (34 males, 6 females) who underwent examinations by ¹²³ I-BMIPP and ²⁰¹ Tl myocardial SPECT imaging and 24-hour Holter monitoring within a 3-day period 3 weeks after the onset of their first MI. R-R intervals were analyzed every hour over a period of 24 hours by fast Fourier transformation (FFT). High frequency (HF) and low frequency (LF) were defined as markers of cardiac vagal activity in the former and the LF/HF ratio as sympathetic activity. Greater or more extensive decreases in the BMIPP image than that in the Tl image were defined as a positive mismatch. Patients were divided into positive and negative mismatch groups of 20 patients each.
There were no significant differences between the 2 groups in age, sex, site of infarction, max CK (creatine kinase), max CK-MB, or left ventricular ejection fraction. The incidences of clinical signs suggesting residual myocardial ischemia were significantly greater in the positive than in the negative mismatch group (P < 0.05). The mean values for HF over the entire 24-hour period and over the 5-hour nocturnal period (0-5 AM) in the positive mismatch group were both significantly lower than those in the negative mismatch group (P < 0.001 in both groups). The 24-hour mean HF and mean nighttime HF in patients with signs of residual ischemia were both significantly lower than in those without signs of residual ischemia in the positive mismatch group (P < 0.05 in both groups).The mean LF/HF ratio for both the entire 24-hour and the nocturnal period in the positive mismatch group were significantly higher than those in the negative mismatch group (P < 0.001, P < 0.05, respectively). The daily profile of hourly HF measurements was significantly lower in the positive mismatch group than in the negative mismatch group (P < 0.02). The mean values of HF for 24-hour and 5-hour periods were significantly lower in patients with signs of residual ischemia in the positive mismatch group than in those with signs of residual ischemia in the negative mismatch group (P < 0.01, P < 0.02, respectively). There were no significant differences between the patients with signs of residual ischemia in the negative mismatch group and those without signs of residual ischemia in the positive and negative mismatch group with regard to the mean values of HF and the LF/HF ratio measured every hour for 24 hours and 5 hours.
It is concluded from the present study that the findings of a mismatch on ¹²³I-BMIPP and ²⁰¹ Tl myocardial SPECT 3 weeks after a first acute myocardial infarction with uncomplicated moderate or severe heart failure and decreased heart rate variability are related to residual myocardial ischemia. A combined assessment of heart rate variability in 24-hour Holter ECG monitoring and perfusion-metabolism mismatch in ¹²³ I-BMIPP and ²⁰¹Tl myocardial SPECT is useful for determining residual myocardial ischemia in the follow-up of those with acute myocardial infarction.

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It is of concern that women are more likely to undergo fewer diagnostic tests and receive less treatment for acute myocardial infarction (AMI) than men. Our retrospective Tokai Acute Myocardial Infarction Study (TAMIS) indicated that there were gender differences according to age groups; however, the exact nature of these gender differences remains unclear. Therefore, using data from TAMIS-II, we studied the influence of gender on the delivery of cardiac management according to 2 age groups (< 65, ≥ 65). TAMIS-II is a prospective study of all consecutive patients admitted to the 15 acute care hospitals in the Tokai region with the diagnosis of AMI from 2001 to 2003. A total of 169 younger women, 1246 younger men, 616 older women, and 1240 older men were included. Data on patient demographics, in-hospital course, comorbid conditions, electrocardiography (ECG), ultrasound-echocardiogram (UCG), treadmill test (TMT), coronary angiography (CAG), percutaneous coronary intervention (PCI), coronary artery bypass grafts (CABG), intra-aortic balloon pump (IABP), mechanical ventilation, and in-hospital or discharge medications (thrombolytics, vasopressors, aspirin, β-blockers, angiotensin-converting enzyme (ACE) inhibitors, calcium antagonists, nitrates) were collected. After controlling for these baseline variables, only lipid-lowering therapy tended to be more frequent in women than in men among the elderly (OR 1.55, 95%CI 1.00-2.38). The results from this Japanese chart review study, derived from detailed clinical data, indicated that the delivery pattern of cardiac management for female and male AMI patients during hospitalization and at discharge was very similar among the younger and older populations.

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The aim of this study was to investigate whether segmental ostial catheter ablation (SOCA) designed to prevent the electrical connections (ECs) between the left atrium and pulmonary veins (PVs) might help increase the efficacy of SOCA in paroxysmal atrial fibrillation (PAF).
PV mapping and successful SOCA were performed with a basket catheter in 108 consecutive patients with PAF. Radiofrequency energy was delivered using a maximum output of 30 W with a 4 mm tip catheter (group I; 47) or 40 W with an 8 mm tip catheter (group II; 61). Only in the group II patients were additional radiofrequency deliveries to the specific sites where the ECs tended to recover performed after successful SOCA. After the first procedure, PAF recurred in 47% of the group I patients and 32% of the group II patients. In all 27 patients who underwent repeat procedures, EC recoveries were observed more frequently in group I than in group II (69% versus 49%; P < 0.05). After multiple procedures, there was more freedom from PAF in group II (84%) than in group I (66%) (P < 0.05).
SOCA with a higher RF power, larger tip catheter, and additional RF deliveries could achieve a more effective SOCA.

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The natural history of asymptomatic individuals with a Brugada-type electrocardiogram (ECG) is still controversial. In this study, we evaluated ventricular fibrillation (VF) inducibility in Brugada-type ECG patients and compared it with other risk factors to clarify the significance of these data on their prognosis.
The study population consisted of 38 patients who presented with a typical ST-segment elevation in the precordial leads and underwent an electrophysiological study (EPS). The patients were divided into 3 groups; group A: patients with spontaneous ventricular fibrillation (VF) (n = 5), group B: patients without clinical VF but with inducible VF in EPS (n = 16), and group C: patients with neither clinical nor inducible VF (n = 17). The clinical features, diagnostic results, and prognosis were compared among these groups.
During the follow-up period of 26 ± 19 months, 2/5 (group A), 1/16 (group B), and 0/17 (group C) patients suffered fatal arrhythmic events. None of the clinical features showed any significant difference, although the incidence of positive results in a drug challenge test was higher in groups A and B than in group C (P < 0.05). On the other hand, VF inducibility was higher in patients with positive results in the drug challenge test than in patients with negative results (59% versus 13%; P < 0.05).
No VF episodes were observed in patients without VF induction, although one was observed in 1 of 16 patients with VF induction in asymptomatic Brugada syndrome. The drug challenge test appears to be useful for predicting VF inducibility even though it is a noninvasive test.

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The objective of the present study was to investigate the risk factors for early hospital mortality in reoperations performed for obstructive prosthetic valve dysfunction. Between January 1994 and April 2005, 63 patients underwent reoperation for obstructive prosthetic valve dysfunction. The mean age of the patients was 40.3 ± 12.8 years. The mitral valve was replaced in 47 (74.6%) patients, the aortic valve in 6 (9.5%) patients, and both valves in 10 (15.9%) patients. Forty-three (68.2%) patients underwent emergency reoperations.
Early hospital mortality occurred in 13 (20.6%) patients. The ethiology of the valve dysfunction was pannus formation in 45 (71.4%) patients and thrombus formation in 18 (28.6%). Pannus and thrombus were localized at the atrial side of the prosthetic valve in 15 (23.9%) patients, at the ventricular side in 13 (20.6%), and at both sides in 35 (55.5%). Inadequate anticoagulation was diagnosed in 28 of 63 (44.4%) patients. The mean INR level in these 28 patients was 1.43 ± 0.24. In multivariate analysis, the only risk factor for early hospital mortality was left ventricular ejection fraction (P = 0.015; Odds: 0.000, 95% CI: 0.000-0.043).
It is concluded reoperations for prosthetic valve dysfunction have a high mortality rate. This study revealed that left ventricular dysfunction is the major determinant of surgical mortality in patients requiring reoperation for valve dysfunction due to pannus or thrombus.

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In hypertrophic cardiomyopathy (HCM) a hyperkinetic state is sometimes observed in spite of impaired systolic function in the hypertrophied myocardium. The aim of the present study was to determine the mechanism of this paradox.
Seventeen patients with HCM and 10 normal subjects underwent cine magnetic resonance (MR) imaging to measure percent systolic wall thickening and percent fractional shortening. The ratio of systolic radial wall stress of the LV at the hypertrophied myocardium over that at the nonhypertrophied myocardium was evaluated to describe the focal advantageous condition for wall thickening.
The ratio was 0.66 ± 0.36 at the start of contraction and 0.78 ± 0.31 at early-systole, indicating consistently smaller radial wall stress at the hypertrophied myocardium. Although the condition for contraction was favorable (a ratio less than 1.00), percent systolic wall thickening at the hypertrophied myocardium (23.0 ± 11.8%) was smaller than that at the nonhypertrophied myocardium (70.5 ± 32.3%). Smaller end-diastolic dimension (HCM group; 45.2 ± 4.2 mm, reference group; 48.9 ± 4.1 mm, P = 0.04) with a statistically identical value of systolic decrease in intraventricular dimension (HCM group; 19.7 ± 3.9 mm, reference group; 18.9 ± 3.2 mm, P = 0.60) yielded high percent fractional shortening in patients with HCM (43.5 ± 7.6%).
Although contractile impairment was proven at the hypertrophied region with low radial wall stress in the HCM group, the smaller end-diastolic dimension in this group resulted in high percent fractional shortening.

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The objective of the present study was to develop a simple clinical model for predicting pulmonary embolism (PE) in patients with acute dyspnea in the emergency room.
Patients and measurements: We enrolled 56 patients diagnosed with PE, and 92 consecutive patients without PE, all of whom presented with acute dyspnea in the emergency room. Primary emergency-room physicians assessed the initial evaluation and interpretation of various laboratory findings. Some significantly independent predictors of PE were identified and integrated into a clinical model of pretest probability: low (< 30%), intermediate (≥ 30%, ≤ 70%), and high (> 70%). After setting up the model, another 40 patients (16 with PE, 24 without PE) were tested using the pretest model.
Clinical variables associated with an increased likelihood of PE were being female and having unilateral low-leg edema, a high alveolar-arterial oxygen gradient, a clear chest x-ray, and electrocardiographic findings of right ventricular strain. Variables associated with a decreased likelihood of PE were cough, chest tightness, and unclear breath sounds. Our clinical model predicted that 95% of patients with PE had a high or low probability of PE. The positive predictive value for high probability was 94.1% and the negative predictive value for low probability was 94.4%. In the tested group, the positive predictive value for high probability was 92.9%. The negative predictive value for low probability was 91.3%.
This simple and easily available prediction model was useful for estimating the pretest probability of PE in patients with acute dyspnea.

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Recently, application of the contingent valuation method (CVM) to health care is increasing to measure the willingness to pay (WTP) for specific medical services. In this study, we measured WTP for the outpatient treatment of hypertension and inpatient treatment of myocardial infarction (MI) in Japan's healthcare system, using CVM via an Internet questionnaire survey in 547 citizens aged 40 to 49 years. WTP was measured with the payment cards method from an ex post consumer based perspective. The payment vehicle was out-of-pocket copayment under public medical insurance. The participants were asked their preferences with respect to medical institutions, and 3 comprehensive characteristics were extracted from the requested information by principal component analysis. Categorical regression was performed to analyze the factors affecting WTP. The mean WTP for hypertension treatment was $75.03/month, and that for the treatment of MI was $8,928.70 ($1 = 105 Japanese yen). WTP for hypertension treatment was significantly high in married males and the group without symptoms, but was not associated with income. WTP for the treatment of MI was significantly high in the high-income group, married males, and the group with symptoms. Among the 3 principle components, "objective evaluation" was significantly associated with WTP for the treatment of MI. As for serious diseases such as MI, the income-associated differences in WTP suggest the necessity for reinforcement of the safety net for the low-income group. Although asymptomatic, hypertension requires continuous treatment. For such diseases, uniformly low copayment should be established irrespective of annual income.

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Hemodynamic deterioration due to left ventricular outflow tract (LVOT) obstruction can occur during catecholamine infusion in patients with acute coronary syndrome (ACS). The purpose of the present study was to compare the utility of propranolol, phenylephrine infusion, and rapid saline loading for reversal of dobutamine-induced LVOT obstruction in a canine model of ACS. ACS was induced via left anterior descending artery ligation in 21 open-chest anesthetized dogs, and LVOT obstruction, defined as an LVOT gradient > 30 mmHg, was induced by dobutamine infusion (20 to 40 μg/kg/min). Subsequently, the effects of propranolol infusion (0.7 to 1.0 μg/kg/min, n = 8), phenylephrine infusion (10 to 200 μg/kg/min, n = 7), and saline loading (200 to 400 mL/hr, n = 6) were assessed by serial hemodynamic measurements. All interventions produced significant and comparable improvements in the LVOT pressure gradient (propranolol: 60 ± 16 to 15 ± 12; phenylephrine: 68 ± 15 to 12 ± 10; saline loading: 58 ± 18 to 22 ± 10 mmHg; P < 0.001 for baseline versus postintervention; P = NS for comparison between interventions). Phenylephrine produced the greatest elevation in aortic pressure (propranolol: +15 ± 13; phenylephrine: +51 ± 36; saline loading: +15 ± 15 mmHg; P < 0.05), while saline loading produced the greatest increase in cardiac output (propranolol: +0.05 ± 0.12; phenylephrine: +0.28 ± 0.37; saline loading: +0.73 ± 0.48 L/min; P < 0.05). Propranolol was the only intervention that produced a significant decrease in diastolic pulmonary artery pressure (16 ± 5 to 11 ± 3 mmHg, P < 0.05). Propranolol, phenylephrine infusion, and saline volume loading were similarly effective in reversing dobutamine-induced LVOT obstruction in this canine model of ACS. However, each intervention produced different hemodynamic effects with potentially different clinical indications.

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We investigated the difference in vascular responses and remodeling between coronary and iliac arteries after repeated endothelial denudation. Endothelial denudation of the left anterior descending coronary artery (LAD) and the right common iliac artery (RIA) was repeated 4 times twice a month using a Fogarty catheter in 21 pigs. Vascular responses to vasoactive drugs were evaluated as % luminal diameter changes on contrast angiography 2 weeks after the last denudation. Corresponding nondenuded sites, ie, the left circumflex coronary artery (LCX) and the left common iliac artery (LIA), were used as references. Acetylcholine (1 μg/kg) did not constrict the LCX (0 ± 1%) and the LAD (1 ± 1%, P < 0.05), whereas it constricted the RIA (20 ± 6%) but not the LIA (−3 ± 3%, P < 0.01). Alternatively, serotonin (10 μg/kg) constricted the LAD strikingly (88 ± 5%, P < 0.01 versus LCX and RIA), as well as the RIA (35 ± 10%, P < 0.05 versus LIA). Vasodilator responses to substance P and isosorbide dinitrate were not different after injury in both arteries. The intima-to-media ratio and adventitia-to-media ratio of the relevant site in cross section of tissue sample from LAD were greater than those from LCX, and were more prominent than those from RIA. The results show that vascular tone regulation after the endothelial injury and vascular remodeling might be altered in a vessel-specific manner.

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A 36-year-old woman was admitted for recurring chest pain and hemoptysis. Blood pressure in the right and left arms was equal, and no murmurs or bruits were heard. Body temperature was normal on admission and remained within the normal range during the hospital stay. C-reactive protein was slightly elevated (2.3 mg/dL) and lupus anticoagulant was positive. Angiography showed no abnormality of the aorta or its branches, but the left pulmonary artery showed occlusion at the proximal portion. Computed tomography (CT) revealed segmental wall thickening of the thoracic aorta. Fluorine-18-fluorodeoxyglucose positron emission tomography (¹⁸FDG PET) showed high uptake in the proximal portion of the left pulmonary artery and in the thoracic aorta with wall thickening on CT. Based on these findings, a diagnosis of Takayasu's arteritis associated with antiphospholipid syndrome was made and high-dose steroid therapy (prednisolone 30 mg/day) was started. Two months later, the C-reactive protein level had decreased from 2.3 mg/dL to 1.1 mg/dL, and both the focal wall thickening and ¹⁸FDG uptake of the thoracic aorta were decreased. ¹⁸FDG PET was useful for evaluating the efficacy of the steroid therapy in addition to making a diagnosis of Takayasu's arteritis associated with antiphospholipid syndrome.

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Two episodes of hypotension caused by oral beraprost sodium administration following cardiac surgery are described. The first case was a 67-year-old female who underwent concomitant surgery for mitral valve replacement, tricuspid annuloplasty, and a radiofrequency maze procedure for atrial fibrillation. The second case was a 45-year-old female who underwent 4-vessel coronary artery bypass grafting associated with endarterectomy in the right coronary artery. Beraprost sodium was administered for the treatment of residual pulmonary hypertension in the first case, and was initiated as an antiplatelet agent following coronary endarterectomy in the second case. Hypotension occurred at approximately one hour after beraprost sodium administration in both cases. Careful observation to prevent this adverse effect is critical after the administration of beraprost sodium, especially in patients who have undergone cardiac surgery.

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