Rotational atherectomy (RA) can facilitate smooth stent delivery and stent expansion through lesion modification for a calcified coronary lesion. Several studies reported that sirolimus-eluting stent (SES) implantation following RA showed a lower rate of revascularization compared with bare-metal stents (BMS). However, there are limited data that compared the clinical outcomes between SES and paclitaxel-eluting stents (PES) after RA. We compared the long-term clinical outcomes of SES and PES following RA. Two hundred and thirty-three consecutive patients (SES n = 179, PES n = 54) who were treated with SES or PES following RA between 10^th September 2004 and 13^th April 2010 were investigated. Follow-up data for clinical outcomes were obtained in 91.4% of all subjects. The median follow-up period was 630 days (interquartile range, 300 to 1170 days) in the SES group, and 625 days (interquartile range, 285 to 900 days) in the PES group. Clinical outcomes including target lesion revascularization (TLR) (SES 4.9% versus PES 9.8%, P = 0.31), target vessel revascularization (TVR) (SES 6.8% versus PES 11.8%, P = 0.25), and major adverse cardiac events (MACE) (SES 14.8% versus PES 13.7%, P = 0.8) were not statistically different between the groups. The unadjusted cumulative event rates estimated by the Kaplan-Meier method and the log-rank test showed no significant differences between the two groups for time to event for TLR, cardiovascular death, all-cause death, or MACE. In conclusion, there was no significant difference in the long-term clinical outcomes between SES and PES following RA.

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Coronary artery calcium score (CACS) measured by multi-detector computed tomography, carotid plaque score (CPS) measured by carotid artery ultrasound, and brachial-ankle pulse wave velocity (baPWV) are noninvasive screening tools for coronary artery disease. The aim of this study was to determine whether the combination of CACS, CPS, and baPWV improves the prognostic value for future cardiac events. CACS, CPS, and baPWV were assessed in 77 patients (mean age, 65 years, 49 males) undergoing invasive coronary angiography. ECG-triggered MSCT was used to assess CACS. CPS was defined as the sum of all plaque heights in bilateral carotid arteries. The highest baPWV was used for analysis. Cardiac events were defined as cardiac death, nonfatal myocardial infarction, or coronary revascularization. Thirty-two cardiac events (41.6%) occurred during follow-up (23.6 ± 20.8 months), consisting of 28 PCIs and 4 CABGs. The best cutoff values of positive CACS, CPS, and baPWV for predicting cardiac events were ≥ 50, ≥ 5, and ≥1.6 m/second, respectively. For the combination of the 3 modalities, the positive test was defined as having at least 1 positive result by each method. The negative predictive value of all 3 modalities combined was better than that of CACS alone. The event-free rate was higher in patients with negative results for all 3 parameters compared with those that were positive (100% versus 44.8%, P < 0.0001). The prognostic value of using combined assessment of CACS, CPS, and baPWV is more effective for predicting cardiac events than CACS alone.

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Some patients with non-ST-elevation myocardial infarction (NSTEMI) have a total occlusive infarct-related artery. However, the long-term prognosis of these patients is uncertain, particularly for those who underwent an early invasive strategy.
The aim of this study was to determine the clinical impact of total occlusion (TO) of an infarct-related artery (IRA) in these patients.
A total of 2,094 patients with NSTEMI who underwent an early invasive strategy with percutaneous coronary intervention (PCI) in the Korea Acute MI Registry (KAMIR) were analyzed (TO group; 665 patients, and non-TO group; 1,429 patients).
In-hospital and one-year clinical outcomes were compared between the two groups. The left circumflex (42.9%) and right coronary artery (31.9%) were the major IRA in the TO group, while the left anterior descending artery was more common as an IRA in the non-TO group (44.1%). In-hospital complications including death and cardiogenic shock occurred frequently in the TO group. Also, the rates of one-month and 12-month adverse cardiac outcomes were higher in the TO group. In the Cox-proportional hazard model, TO in IRA predicted 12-month all-cause death.
In conclusion, NSTEMI patients with TO in IRA showed worse short- and long-term clinical outcomes compared with those of non-TO patients.

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Peri-stent contrast staining (PSS) is an abnormal angiographic finding following drug-eluting stent implantation which suggests the presence of a space outside the stent struts. PSS has been reported to be associated with very late stent thrombosis (VLST). The aims of this study were to compare the occurrence rate of late acquired PSS between sirolimus-eluting stent (SES) and everolimus-eluting stent (EES) implantation, and to identify clinical characteristics associated with PSS. The percutaneous coronary intervention (PCI) database of our hospital was queried to identify patients meeting the following criteria: (i) patients who received SES or EES in de novo coronary artery lesions; and (ii) patients who had angiographic follow-up between 3 and 15 months after stent implantation. There were 221 patients with 249 lesions treated with SES, and 173 patients with 212 lesions treated with EES. The occurrence of PSS was evaluated and compared between SES and EES implantation on a patient and lesion basis. The occurrence rate of late acquired PSS with EES was lower than that with SES. (On a patient basis; 1.2% versus 4.5%, P = 0.045, on a lesion basis; 0.9% versus 4.0%, P = 0.043). Among the clinical characteristics, chronic total occlusion (CTO) lesions were associated with PSS. The occurrence of late acquired PSS in EES was lower than that in SES. In conclusion, the occurrence rate of late acquired PSS with EES was lower than that with SES, however, it remains to be determined whether this difference translates to the difference in the rate of VLST.

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Flow-mediated vasodilatation of the brachial artery (FMD) is a marker which is related to endothelial nitric oxide bioavailability. Commercially available ultrasound machines equipped with online computer-assisted semi-automatic analysis software to measure FMD have recently become available in Japan. These devices enable more convenient examination, enhanced reproducibility of FMD measurement, and a shortened examination time. Using such devices, in the present multicenter prospective study we propose to: 1) establish standardized FMD values and determine the annual rates of FMD change in healthy subjects; 2) confirm the predictive value of FMD for future cardiovascular events in Japanese subjects; 3) evaluate the potential usefulness of a multimarker strategy, including measurements of FMD, pulse-wave velocity (PWV), ankle-brachial pressure index, biochemical markers, and proteomic biomarkers obtained by mass spectroscopic analysis to assess the prognosis of subjects with coronary artery disease; and 4) clarify the usefulness of FMD measurement to predict the rate of progression of carotid atherosclerosis, arterial stiffness and microalbuminuria in subjects with hypertension or diabetes mellitus. In total, we estimate that approximately 4000 Japanese subjects in 3 different study groups will eventually be enrolled in this prospective observational investigation. We anticipate that the present study will provide important evidence for the usefulness of FMD measurement in the risk stratification for cardiovascular disease.

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Diabetes mellitus (DM) is a strong risk factor for cardiovascular (CV) disease. Plasma B-type natriuretic peptide (BNP) levels are elevated in various types of cardiac diseases. Increased plasma BNP levels have been reported to be associated with CV risk in apparently healthy individuals. However, no studies have yet examined the specific value of plasma BNP for predicting CV incidence in unselected DM subjects in a community-based population.
In a community-based DM cohort (n = 1,059, mean = 66 years), baseline BNP levels were determined, and CV events were followed and captured prospectively. The cohort was divided by plasma BNP quintiles. The Cox proportional hazard model was used to determine the relative hazard ratios (HR) among the quintiles. In addition, the effects of adding the plasma BNP or urine albumin-to-creatinine ratio (UACR) to an established CV risk scoring model was examined by calculating the area under the receiver operating characteristic (ROC) curve (AUC).
During the 5.7 year follow-up period, CV events were identified in 65 of the DM cohort. There was a significant association between plasma BNP levels and CV event rate (P < 0.001). HR was significantly increased in the highest quintile compared to the lowest (HR = 4.38; 95%CI 1.69 -11.84). The AUC generated from ROC analysis of the Framingham risk score for predicting general CV events was improved by adding BNP testing (from 0.66 to 0.74; P = 0.05), but not by adding UACR (from 0.66 to 0.67; P = 0.49).
In a community sample of people with DM, plasma BNP levels above the 80 percentile are directly associated with CV risk, and measurement of plasma BNP alone or in conjunction with an established CV risk score is of value in predicting CV events in these subjects.

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The Fas/Fas Ligand system is a major apoptosis signaling pathway that is up-regulated in patients with chronic heart failure (CHF). Serum soluble Fas (sFas) levels increase in proportion to the CHF severity and may have prognostic value, therefore, sFas is a promising biomarker of heart failure. In this study, we attempted to identify the determinants of sFas levels in patients with CHF. Serum levels of tumor necrosis factor (TNF)-α and its soluble receptors (sTNF-R1 & sTNF-R2), interleukin (IL)-6, soluble IL-6 receptor (sIL-6R), glycoprotein (gp)130, and sFas were measured in 106 patients with CHF and 39 controls. All subjects performed a symptom-limited cycle ergometer exercise test with expired gas analysis. CHF patients had higher levels of TNF-α, sTNF-R1, sTNF-R2, IL-6, and gp130. Serum levels of sFas (controls versus CHF; 2.60 ± 0.88 versus 3.38 ± 1.23 ng/mL, P = 0.0004) were higher in CHF. On univariate analysis, age (P = 0.0003), NYHA functional class (P = 0.0012), peak VO₂ (P < 0.0001), plasma norepinephrine (P = 0.0013), log IL-6 (P < 0.0001), log TNF-α (P = 0.0002), log sTNF-R1 (P < 0.0001), and log TNF-R2 (P < 0.0001) were significantly related to log sFas levels. Multivariate analysis showed that age and log IL-6 and log sTNF-R1 levels were independently associated with log sFas levels (overall R = 0.603, P < 0.0001). Serum levels of sFas were increased in patients with CHF, and age and serum IL-6 and sTNF-R1 levels were independent determinants of sFas levels. These data suggest that proinflammatory cytokine activation is linked to the Fas/Fas Ligand system in patients with CHF.

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Adenosine and related compounds have been shown to produce atrioventricular (AV) conduction block during acute myocardial ischemia. We investigated the effects of the antianginal drug trapidil, which has been shown to inhibit phosphodiesterase, on AV conduction disturbances in a canine model of acute myocardial ischemia. In 35 anesthetized dogs, the AV node artery was cannulated and perfused with arterial blood. Adenosine (300 μg, 650 μg, or 1000 μg) was injected into the AV node artery. With administration of adenosine at 300 μg, 650 μg, or 1000 μg, the atrio-His (AH) interval was increased by 14.6 ms, 22.3 ms, and 29.7 ms, respectively. The effects of adenosine were potentiated by pretreatment with intravenous dipyridamole (250 μg/kg), an inhibitor of adenosine uptake, but the effects of adenosine were attenuated with intravenous trapidil (3 mg/kg), an inhibitor of phosphodiesterase. AV node artery occlusion resulted in prolongation of the AH interval in 4 of 12 dogs. The ischemia-induced AH prolongation was potentiated with intravenous dipyridamole and attenuated with intravenous trapidil. AV conduction disturbances associated with inferior myocardial infarction may be related in part to endogenously released adenosine, and trapidil may be useful in treating AV block associated with acute AV node ischemia.

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Reactive oxygen species (ROS) in rostral ventrolateral medulla (RVLM) of brainstem contribute to sympathoexcitation and are critically involved in the pathogenesis of hypertension. Baroreflex sensitivity (BRS) is a valuable prognostic parameter of the autonomic nervous system, and is impaired in hypertension. The aim of the present study was to determine whether or not a chronic reduction of ROS in the RVLM improves impaired BRS in hypertensive rats. We transfected adenovirus vectors encoding either manganese superoxide dismutase (AdMnSOD) or β-galactosidase (AdLacZ) into the RVLM of stroke-prone spontaneously hypertensive rats (SHRSP). We measured BRS using the spontaneous sequence method. BRS was significantly lower in SHRSPs than in Wistar-Kyoto rats. In the AdMnSOD-transfected SHRSP, blood pressure, heart rate, and sympathetic nervous system activation were significantly decreased from day 5 after the gene transfer. BRS in the AdMnSOD-transfected SHRSP was significantly increased from day 4 after the gene transfer with the reduction of ROS in the RVLM. Furthermore, in the AdMnSOD-transfected SHRSP, intravenous infusion of atropine dramatically decreased BRS. In contrast, in the AdLacZ-transfected SHRSP, atropine did not decrease BRS. These results suggest that chronic reduction of ROS in the local RVLM improves the impaired BRS in SHRSP through inhibition of the sympathetic component.

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Cytomegalovirus (CMV) infection remains a major problem in recipients with heart transplantation (HTx), because it may play a significant role in the development of cardiac allograft vasculopathy, which is one of the major causes of death after HTx. Valganciclovir (VGC) is effective for the treatment of CMV infection, but is often associated with neutropenia, especially when used with mycophenolate mophetil (MMF). We experienced an HTx recipient with positive CMV antigenemia who suffered progressive neutropenia after administration of VGC. We switched MMF to everolimus (EVL) and assay for CMV antigenemia was constantly negative even after discontinuation of VGC. In all other 14 HTx recipients who received EVL for any reason, we found that assay for CMV antigenemia remained negative throughout the period of EVL administration. Considering the prophylactic effect on CMV, EVL can not only be an alternative to rescue from comorbidity, but might also be indicated earlier especially in CMV-seronegative HTx recipients.

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A 60-year-old man was admitted to our hospital due to acute ST-segment elevation myocardial infarction. He had a history of self-expanding stent implantation in the proximal left anterior descending artery due to stable angina pectoris 7 years earlier. Emergent coronary angiography on admission showed occlusion in the distal portion of the previously stented segment, in which observation by optical coherence tomography revealed the existence of a remarkable proliferation of lipid-laden neointimal tissues with rupture and thrombus. This suggests that very late stent thrombosis in a self-expanding stent may occur through the process of atheromatous formation.

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Malignancy is not uncommon with immunosuppressive therapy, but pancreatic cancer is infrequently complicated in recipients of heart transplantation. Here we report a transplant case diagnosed with pancreatic cancer 4 years and 8 months after the heart transplantation. We changed the immunosuppressive regimen after the malignancy was detected, and administered everolimus along with chemotherapy using S-1, an oral fluoropyrimidine prodrug. The patient lived for 8 months after the diagnosis, and received metallic stenting for the biliary and duodenal obstruction. Also, to the best of our knowledge, this is the first report about chemotherapy and endoscopic intervention for pancreatic cancer in a heart transplantation patient.

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Announcement of Retraction
The editorial office of International Heart Journal has recently determined that the clinical study written by En Ze Jin, Long Hao Yu, and Xue Qi Li, published in the January 2012 issue of International Heart Journal (Int Heart J 2012; 53: 1-4), was subsequently found to have not met the publication criteria of IHJ. Therefore, we hereby notify our readers that the paper has been officially retracted.

Ryozo Nagai, MD
Editor-in-Chief
International Heart Journal

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