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Recently, unstable angina pectoris (UAP) and non-ST-segment-elevation myocardial infarction (NSTEMI) have been considered together because they exhibit indistinguishable clinical and electrocardiogram features, and constitute non-ST-segment-elevation acute coronary syndrome (NSTE-ACS). However, no optical coherence tomography (OCT) studies have reported the association between vulnerable plaque morphology and clinical characteristics in NSTE-ACS patients based on assessment of clinical symptoms and myocardial necrosis. The aim of this study was to investigate the differences in clinical characteristics and plaque morphology assessed by OCT between patients with UAP and NSTEMI. Preinterventional OCT images of 84 NSTE-ACS patients were studied, 19 with NSTEMI and 65 with UAP, according to levels of high-sensitivity troponin T. The frequency of plaque rupture and thrombus in patients with NSTEMI was higher than in UAP patients with either class I or II + III (rupture: NSTEMI, 68 %; UAP classes II + III, 30 %; UAP class I, 19 %, thrombus: NSTEMI, 73 %; UAP classes II + III, 22 %; UAP class I, 14 %). In NSTEMI patients, the frequency of occurrence of both thrombus and rupture was the highest. Conversely, patients with UAP class I or those with UAP classes II + III most frequently had no thrombus and rupture, and the frequencies of the presence of thrombus were only 14 and 22 %, respectively. Multivariate analysis revealed that thrombus and plaque rupture were independently associated with NSTEMI. This study demonstrates that the morphological features of culprit lesions could be related to clinical severity in NSTE-ACS patients.

Many investigators have reported that the total amount of coronary calcium correlates with the overall magnitude of atherosclerotic plaque burden in the entire coronary tree and is a powerful predictor of future cardiovascular events. However, the development and spatial distribution of coronary calcifications remain unclear. We investigated the spatial distribution of calcifications throughout the coronary tree during coronary artery evaluation using coronary computed tomography angiography (CTA). A further aim was to assess the progression of existing calcifications and the development of new deposits in a follow-up study. The study population consisted of 287 patients for the cross-sectional study using CTA to evaluate the spatial distribution of calcifications by parent coronary arteries. Next, we analyzed a CTA dataset of 57 patients who had undergone two CTA examinations. In this group, the two CTA images were used for assessing the progression of existing calcifications and the development of new deposits. The coronary calcifications tended to be clustered within the proximal and middle portions. Moreover, in the proximal left anterior descending coronary artery (LAD), small calcifications were located more toward the inner pericardial side. Finally, new calcium deposits developed within the proximal and middle portions of the LAD and left circumflex coronary artery, but those in the right coronary artery were likely to appear evenly from the proximal to the distal portion. This study shows the characteristic patterns of the longitudinal and circumferential distribution of calcifications by parent coronary arteries.

Several intravascular ultrasound studies have reported that culprit lesion-attenuated plaque (AP) is related to slow flow/no reflow after percutaneous coronary intervention (PCI). Long-term prognostic impact of the AP is unknown. The aim of this study was to investigate acute and long-term clinical impact of the AP in patients with acute coronary syndrome (ACS). A total of 110 ACS patients who underwent successful PCI were enrolled. Acute and long-term clinical outcomes were compared between patients with AP (AP group: n = 73) and those without AP (non-AP group: n = 37). Long-term cardiac event was defined as a composite of death and ACS. Baseline characteristics in 2 groups were similar. AP was associated with higher TIMI frame count immediately after the first balloon inflation. After thrombectomy and intracoronary drug administration, final TIMI frame count became similar between AP and non-AP group. Although AP was associated with higher incidence of fatal arrhythmia during hospitalization, in-hospital mortality did not differ between the 2 groups. During follow-up (median 6.2 years), cardiac event-free survival did not differ between the 2 groups. Despite the initial unfavorable effect on coronary reflow, presence of AP did not affect acute as well as long-term clinical outcome in patients with ACS.

Several coronary angiographic studies have reported that enlarged and tortuous epicardial coronary arteries are characteristic of patients with left ventricular concentric hypertrophy (LVCH). Recently, we showed that small volumes opacified by contrast medium can be accurately measured by 64-multislice computed tomography (MSCT) and that there is a direct relationship between the coronary artery volume and left ventricular (LV) mass. However, the relationship of coronary artery volume with LV mass in patients with dilated cardiomyopathy (DCM) is unknown. The present study was designed to investigate this issue. Thirteen patients with DCM and 18 patients with LVCH who underwent MSCT angiography were included in this analysis. The coronary arteries were segmented on a workstation, and the appropriate window settings obtained from the results of the phantom experiments were applied to the volume-rendered images to calculate the total coronary artery volume (right and left coronary arteries). The absolute coronary lengths and volumes in patients with LVCH and DCM were greater than those in controls. The coronary artery volumes adjusted for LV mass in patients with DCM were found to be smaller than those in patients with LVCH or in controls, and these values did not differ between patients with LVCH and controls (DCM 4.1 ± 0.9, LVCH 5.4 ± 1.4, controls 5.5 ± 2.3 ml/100 g of LV mass, P < 0.005; DCM vs LVCH, P < 0.01; and DCM vs control, P < 0.0005). This study showed that the increase in the coronary artery volume in patients with LVCH matched the increase in LV mass, but a decreased coronary volume with regard to LV mass was characteristic of patients with DCM.

It has been suggested that oxidative stress plays a pathogenic role in idiopathic interstitial pneumonias. Macrophage- or neutrophil-derived oxidants seem to be important sources of oxidative stress in this group of inflammatory disorders. Recent experimental studies have revealed that oxidative injury during inflammation or apoptosis can change phosphatidylcholine of cell membrane into its oxidized form, which serves as a ligand for macrophage scavenger receptor CD36. Recently, we developed a monoclonal antibody against oxidized phosphatidylcholine. Using this novel antibody, we performed an immunohistochemical investigation to clarify the localization of oxidized phosphatidylcholine in lung tissues of idiopathic interstitial pneumonias and a relationship between oxidized phosphatidylcholine localization and CD36 expression. Lung specimens obtained from patients with desquamative (n = 8) or usual interstitial pneumonia (n = 15) were studied. Thirteen normal lung tissues were also examined as controls. Antibodies against oxidized phosphatidylcholine, CD36, epithelial cells, macrophages, and neutrophils were used as primary antibodies. The positive cell number was counted by computer-aided morphometry. While there were no oxidized phosphatidylcholine-positive cells in normal lungs, lungs of desquamative or usual interstitial pneumonia contained large numbers of oxidized phosphatidylcholine-positive cells in the alveolar spaces. Double-staining analysis revealed that most oxidized phosphatidylcholine-positive cells were macrophages. The oxidized phosphatidylcholine-positive cells were increased in association with the increase in the densities of macrophages (Rs = 0.87, p < 0.0001) and neutrophils (Rs = 0.89, p < 0.0001). Accumulated macrophages also showed distinct CD36 expression. These findings suggest that oxidative stress and the related product, oxidized phosphatidylcholine, play an important role in the pathophysiology of idiopathic interstitial pneumonias.

Hypertrophic cardiomyopathy (HCM) is defined as inappropriate ventricular hypertrophy without a cardiac or systemic cause. On the other hand, hepatitis C virus (HCV) causes extrahepatic manifestations as well as chronic persistent infection in hepatocytes. We studied the association of HCV infection with HCM, comparing the prevalence of HCV antibodies between HCM patients and age- and gender-matched controls with other cardiovascular diseases at a single institution, for reasons of exclusion of bias. We then described the clinical features and genotype analysis of HCV RNA in HCM. The diagnosis of HCM was established by echocardiographic demonstration of a hypertrophied (> or =15 mm), nondilated left ventricle in the absence of another systemic or cardiovascular disease capable of producing the magnitude of hypertrophy observed. The study population consisted of 80 patients with HCM, in whom HCV antibody was examined (55 men and 25 women; mean age 56.6 +/- 12.4 years; ranging from 19 to 80 years), compared with a total of 80 age- and gender-matched controls without HCM. The prevalence of HCV infection in patients with HCM (18/80) was significantly higher than in control subjects (5/80) (Chi(2) = 7.312, P = 0.007). Of the 12 patients in whom the genotype of HCV was analyzed, 7 had type 1b and 5 had type 2a. The prevalence of HCV infection was higher in patients with HCM than in age- and gender-matched control subjects with other cardiovascular diseases. The result suggests that HCV may play an important role in these HCV-positive HCM patients.

The Multi-Link stent is superior to other stents in terms of low rates of restenosis and target vessel revascularization. However, few data exist regarding short- and long-term outcomes for side branches after stenting. We evaluated short and long clinical outcomes and angiographic predictors of side-branch occlusion after the deployment of 137 Multi-Link stents. Thirty-four (25%) of the 137 side branches occluded immediately after stenting. We attempted reangioplasty for the side branches and our success rate was 85%. The incidence of side branches with intrinsic ostial disease was more than 50% before stenting and origination from the stented midsegment was a powerful angiographic predictor of side-branch occlusion. Side-branch patency is well maintained long-term. The incidence of restenosis within and near the stented segment of the parent vessel was 19%, and the incidence of target vessel revascularization was 15%. We recommend the use of Multi-Link stents regardless of the presence of side branches in the vicinity of the stenosis.

The pathogenesis of alcoholic cardiomyopathy (ACM) is not well understood. However, recent reports have shown that mutations in mitochondrial DNA (mtDNA) were associated with mitochondrial encephalomyopathy and cardiomyopathy. Our objective was to explore point mutations in mtDNA and the pathogenesis of ACM. We obtained heart biopsy specimens from ten male habitual drinkers with congestive heart failure. We amplified the total mtDNA obtained from these specimens using a two-step polymerase chain reaction method and analyzed the products using automated fluorescence-based direct sequencing. The sequences were compared with those of controls. MtDNA from the ACM patients contained multiple point mutations. Specifically, four of the ten patients carried five point mutations that had been detected previously in several other mitochondrial diseases. These point mutations were not observed in controls. These results suggest that mtDNA abnormalities are involved in the pathogenesis of ACM.

This study was designed to determine whether the restrictive filling transmitral flow velocity pattern is associated with increased plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). It was also designed to evaluate the prognostic value of these parameters from patients with chronic congestive heart failure (CHF) admitted for episodes of acute decompensation. We performed Doppler echocardiography, measured plasma levels of ANP and BNP in 33 patients at the time of admission, and assessed the subsequent cardiac mortality for 3 months. Eleven patients (33%) had a restrictive filling pattern of deceleration time (DcT) < 120ms. Plasma ANP and BNP levels were markedly increased in all patients to 189 +/- 145 pg/ml and 865 +/- 559 pg/ml, respectively. Seventeen patients (52%) showed more than 700 pg/ml of plasma levels of BNP. There was a significant correlation of DcT with the plasma ANP level (r = -0.41, P = 0.017), and a better correlation of DcT with the plasma BNP level (r =-0.50, P = 0.003). The combined index of both shorter DcT (< 120 ms) and higher plasma BNP levels (>700 pg/ml) was the best predictor of cardiac mortality by Cox univariate analysis (chi2 = 5.87, P = 0.015). Furthermore, the sensitivity and specificity of this index for the detection of cardiac mortality were 80% and 86%, respectively. In conclusion, the combined analysis of the Doppler transmitral flow velocity pattern and measurement of the plasma BNP level is noteworthy since it is noninvasive and convenient. Moreover, it is extremely useful in predicting the prognosis for patients with chronic CHF admitted for episodes of acute decompensation.

A 43-year-old man with progressive right common carotid, subclavian artery, and brachiocephalic artery stenoses due to aortitis syndrome is presented. The patient's right common carotid artery had been treated by percutaneous transluminal angioplasty (PTA) four times previously, but it was finally occluded. The right subclavian artery was treated by PTA once, which resulted in restenosis. The stenosis extended to the brachiocephalic artery. For this patient, PTA followed by stent placement was performed for the right subclavian and brachiocephalic artery stenosis. Because arterial stenosis is progressive in cases of aortitis syndrome, simple PTA alone does not appear to be sufficient for treatment. We suggest that PTA followed by stent placement may be an alternative treatment for recurrent stenosis in aortitis syndrome.

Purpose: TAS-103 [6-((2-(dimethylamino) ethyl)amino)-3-hydroxy-7H-iindeno(2,1-c)quinolin-7-one dihydrochloride] is a newly synthesized dual inhibitor of topoisomerase I and II. Since anticancer drugs are used in combination with other drugs for effective chemotherapy, we investigated the cytotoxic effect of TAS-103 in combination with other conventional anticancer agents, such as cisplatin, vindesine, doxorubicin, 5-fluorouracil, and the antitopoisomerase inhibitors SN-38 and etoposide in vitro., Methods: Inhibition of the growth of the human small-cell lung cancer cell line SBC-3 was evaluated using the tetrazolium dye (MTT) assay. Drug interactions were evaluated by isobologram analysis and the determination of combination indices supplemented by a three-dimensional model., Results: Simultaneous use of TAS-103 and cisplatin had a supraadditive effect, but combinations of TAS-103 with other drugs had an additive or marginally subadditive effect. Three-dimensional model analysis added more information about the synergistic concentration ranges of two drugs (cisplatin 200-400 nM and TAS-103 7 10 nM). Sequential use of TAS-103 and cisplatin had only an additive effect., Conclusion: These results suggest that the concomitant use of TAS-103 and cisplatin has a greater cytotoxic effect on cancer cells than single drug use, and may provide a beneficial effect in the treatment of small-cell lung cancer.

The purpose of this study was to examine the effects of the long-acting calcium channel antagonist pranidipine on ventricular remodeling, systolic and diastolic cardiac function, circulating humoral factors, and cardiac mRNA expression in myocardial infarcted rats. Myocardial infarction (MI) was produced by ligation of the coronary artery in Wistar rats. Three mg/kg per day of pranidipine was randomly administered to the infarcted rats. Hemodynamic measurements, Doppler echocardiographic examinations, analyses of the plasma levels of humoral factors, and myocardial mRNA expression were performed at 4 weeks after myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 24.2 +/- 1.2mmHg and 5.4 +/- 0.6 mmHg. Pranidipine reduced LVEDP and CVP to 13.6 +/- 1.4mmHg (P < 0.01) and 2.5 +/- 0.4mmHg (P < 0.01). The weight of the left and right ventricles in MI was significantly higher than in the sham-operated rats (sham, 2.02 +/- 0.04 and 0.47 +/- 0.02g/kg; MI, 2.18 +/- 0.05 and 0.79 +/- 0.04g/ kg; P < 0.01). Left ventricular end-diastolic dimension (LVDd) in MI increased to 10.3 +/- 0.3mm (P < 0.01) (sham, 6.4 +/- 0.3mm). Pranidipine prevented an increase in the weight of the left and right ventricles (2.02 +/- 0.04 and 0.6 +/- 0.03g/kg, P < 0.01) and LVDd (7.9 +/-0.2mm, P < 0.01 to MI). Plasma renin activity (PRA), and plasma epinephrine, norepinephrine, and dopamine concentrations in MI were higher than those of the sham-operated rats. Pranidipine decreased the PRA and plasma cathecolamine levels of the myocardial infarcted rats to the level of the sham-operated rats. Moreover, the rats in MI showed systolic dysfunction, shown by decreased fractional shortening (sham, 31 +/- 2% vs MI, 15 +/- 1%; P < 0.01) and diastolic dysfunction shown by the E-wave deceleration rate (sham, 12.8 +/- 1.1 m/s2; MI, 32.6 +/- 2.1 m/s2; P < 0.01). Pranidipine significantly prevented systolic and diastolic dysfunction. The increases in beta-myosin heavy chain (MHC), alpha-skeletal actin, and atrial natriuretic polypeptide mRNAs in the noninfarcted left ventricle and right ventricle at 4 weeks after the myocardial infarction were significantly suppressed by the treatment with pranidipine. On the other hand, depressed alpha-MHC was restored to normal levels by pranidipine in both regions. In conclusion, pranidipine prevents the left ventricular remodeling process accompanied by systolic and diastolic dysfunction, and inhibits abnormal cardiac gene expression after myocardial infarction.

The purpose of this study was to examine the histopathological findings of right ventricular endomyocardial biopsies from ten patients less than 60 years of age (47 +/- 9.8 (mean +/- SD) years) with documented atrioventricular block but without apparent heart disease. They underwent electrophysiological testing, echocardiography, coronary angiography, and right ventricular endomyocardial biopsy. Biopsy specimens were assessed for morphologic changes in myocyte diameter, fibrosis, disarray, and degeneration. Electrophysiological testing demonstrated atrioventricular nodal block in 2, intra-His bundle block in 2, and infra-His bundle block in 6 patients. Histology revealed evidence of myocardial fibrosis with either myocyte hypertrophy or disarray in 7 of the 10 patients. The results of electrophysiological testing did not correlate with the histopathological findings or severity. In one patient, heart failure appeared during the follow-up period. We conclude that patients with atrioventricular block of unknown etiology have histological abnormalities of the ventricular endomyocardium in addition to the conduction system disturbances. We consider such cases as constituting one of the disease groups of cardiomyopathy, and suggest that it is necessary to follow up the clinical course in these patients.

Purpose: To evaluate the effects of bare stents and covered stents on the aortic wall, especially the vasa vasorum., Methods: Eight bare stents and nine covered stents were placed in the infrarenal aorta of nine dogs. The dogs were euthanized at 4-45 weeks after stent placement. The vasa vasorum was evaluated by microstereoscopy with vascular casting, and the histopathology of the aortic wall was examined by light microscopy., Results: In the unstented normal aorta, vasa vasorum nourished the adventitia and the outer media, and the intima and inner media were avascular. In the stented segment, vascular dilatation and proliferation of vasa vasorum, medial atrophy, and intimal hyperplasia were observed, more prominent for covered stents than for bare stents., Conclusion: Intravascular stent placement caused not only medial atrophy and intimal hyperplasia but also proliferation of the vasa vasorum, probably due to hypoxia in the aortic wall.

Purpose: To assess the histologic findings associated with stenosed and occluded transjugular intrahepatic portosystemic shunt (TIPS) tracts., Methods: Four TIPS tracts within three autopsy livers were histologically studied for vascular components by routine staining and immunohistochemical staining. TIPS had been performed for bleeding from esophageal varices in patients with cirrhosis of the liver., Results: Two TIPS, examined on days 4 and 53, showed occlusion by fibrin thrombus. In the former, no endothelial cells were detected, but coagulative necrosis of hepatocytes was found in the surrounding liver. In the latter, bile pigments were seen on the luminal surface. In the two other TIPS without tract occlusion, examined on days 49 and 293, a layer of endothelial cells, proliferation of smooth muscle cells, and deposition of an extracellular matrix such as collagen were confirmed. In the tract examined on day 293, there was protrusion of hepatocytes into the lumen through the stent wires., Conclusion: Short- and midterm TIPS occlusions were caused by thrombus forming after necrosis of hepatocytes and bile leakage, respectively. Long-term TIPS stenosis was associated with a combination of pseudointimal hyperplasia and ingrowth of hepatocytes.

We report a cirrhotic patient with complete occlusion of the portal vein with marked cavernous transformation due to chronic thrombosis in whom a transjugular intrahepatic portosystemic shunt (TIPS) was successfully created after direct minilaparotomy mesenteric vein catheterization, lysis and aspiration of the thrombus, and stenting in the portal vein. The methods used, we believe, provide a new technique for performing TIPS in chronically thrombosed portal veins in which previously no effective surgical therapeutic options were available.

To improve safety and efficacy of the transjugular intrahepatic portosystemic shunt (TIPS) procedure, we introduced a new, thin-needle (21-gauge long PTC needle) puncture technique using biplane fluoroscopy and targeting of a guidewire tip in the right hepatic artery. After puncture of the right portal vein, a 0.016-inch guidewire was inserted into the portal vein, followed by a 4 Fr dilator. The 4 Fr dilator allowed introduction of a 0.035-inch working guidewire. We successfully performed TIPS in seven patients with postnecrotic cirrhosis using this technique and encountered no technical difficulties or complications.

The local therapeutic effects and 5-year survival rates obtained following subsegmental transcatheter arterial embolization (TAE) therapy for small hepatocellular carcinomas (HCCs) were retrospectively analyzed. A total of 124 nodular-type HCC lesions measuring less than 4 cm in diameter in 100 patients with liver cirrhosis were subjected to the analysis. All lesions became opaque on digital subtraction angiography. Complete necrosis was seen in 64% of 11 resected lesions. Among the remaining 113 lesions, the 1- and 5-year local recurrence rates following one performance of TAE were 18% and 33%, respectively. The 1- and 5-year survival rates were 100% and 53%, respectively. No significant side effect was observed after TAE therapy. Subsegmental TAE therapy significantly improved the long-term survival rates of patients with small HCCs associated with liver cirrhosis as compared with those treated by conventional TAE therapy.

The authors report a case of Budd-Chiari syndrome treated by percutaneous transluminal angioplasty (PTA). In this case, the occlusion of three major hepatic veins with a big collateral to the inferior vena cava via the right inferior hepatic vein (RIHV) and stenosis of the ostium of RIHV were seen. We performed successful PTA of this stenosis.