The objective of the present study was to investigate the effects of percutaneous coronary intervention (PCI) on the development of major cardiac events in patients with chronic total coronary occlusion (CTO). Patients determined to have CTO in at least one coronary artery with stable coronary artery disease were retrospectively enrolled in this study. Among 262 patients (197 males, 65 females), PCI was attempted in 172 while 90 were followed-up conservatively because they had unsuitable angiographic lesions for PCI. PCI was successful in 117 (68.0%) patients. Thirty of the remaining 55 patients, who had multivessel coronary artery disease, underwent coronary artery bypass surgery. The remaining 25 patients were added to the conservative group. Mean follow-up time was 32 ± 12 months. Although a slight degree of development of non-ST elevation acute coronary syndrome was observed in the PCI group (34 [29.1%] versus 21 [18.3%] patients, P = 0.053) mostly because of restenosis (14 of 34 patients, [41.2%]), a significant mortality benefit was observed in patients who underwent successful PCI (17 [14.5%] versus 32 [27.8%] patients, P = 0.013). This benefit was mainly due to the lower number of deaths from heart failure (7 [6.0%] versus 17 [14.8%] patients, P = 0.028) and sudden death (6 [5.1%] versus 12 [10.4%] patients, P = 0.131). In conclusion, despite the low success rate and high restenosis rate of PCI for CTO, it is worthwhile to deal with the revascularization of a CTO for its mortality benefit.

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The purpose of this study was to determine the clinical outcomes of abciximab combined with the low molecular weight heparin (LMWH), dalteparin, in high-risk percutaneous coronary intervention (PCI) patients with acute myocardial infarction (AMI). A total of 140 high-risk PCI patients with AMI were divided into 2 groups: unfractionated heparin (UFH) with abciximab (group I: 70 patients, 58.7 ± 10.5 years), and dalteparin with abciximab (group II: 70 patients, 59.6 ± 9.8 years). Major adverse cardiac events (MACE) during hospitalization and at 4 years after PCI were examined. Baseline clinical characteristics, laboratory findings, echocardiography parameters, and baseline angiographic characteristics were not different between the 2 groups. The incidence of thrombotic total occlusion lesions was 62.9% in both groups. Procedural success was achieved in 91.4% in group I and 90.0% in group II. Bleeding and hemorrhagic events were not different between the 2 groups. No significant intracranial bleeding was observed in either group. The incidence of in-hospital MACE was 7 (10.0%) in group I and 4 (5.7%) in group II. Four-year clinical follow-up was performed in 97% of the patients. Four years after PCI, death occurred in 6 (8.6%) patients in group I and in 7 (10.0%) in group II. MI occurred in 4 (5.7%) and 4 (5.7%), target vessel revascularization (TVR) in 23 (32.9%) and 16 (22.9%), and bypass surgery in 3 (4.3%) and 1 (1.4%), respectively. Overall, a MACE occurred in 33 (47.1%) patients in group I and in 26 (35.1%) patients in group II (P = 0.23). The long-term clinical outcome with dalteparin combined with abciximab may be comparable to that of UFH plus abciximab in high risk PCI patients with AMI.

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Systemic markers of inflammation are considered reliable predictors of future coronary events in patients with acute myocardial infarction (AMI). The aim of this study was to evaluate the prognostic relevance of serial C-reactive protein (CRP) measurements in patients with ST-elevation AMI (STEMI) on one-year outcome. In 31 patients with STEMI, serial measurements of CRP were obtained, and for each patient, the following values were determined: (i) values at admission, up to 12 hours after symptom onset, (ii) maximal values obtained 24-72 hours after symptom onset (early acute values), and (iii) late acute values (96-120 hours after symptom onset). The combined endpoint was any new cardiovascular event, including death.
Early and late acute CRP levels were the only parameters found to be significantly higher in patients with an adverse outcome than in patients with a good outcome. A significantly higher rate of endpoint events was found in patients with elevated early (Hazard ratio [HR] 5.54, 95%CI 2.05-25.40; P = 0.007) and late acute CRP (HR 9.01, 95% CI 1.66-19.56; P = 0.005). Multiple logistic regression analysis identified only early acute CRP as an independent predictor of an unfavorable outcome (Odds ratio 8.00, 95%CI 1.15-55.60; P = 0.04), after adjustment for established risk factors.
CRP level measured 24-72 hours after symptom onset is an independent predictor of one-year outcome in patients with STEMI. Values obtained later in the setting of STEMI do not add further prognostic information. CRP at admission is not related to long-term prognosis.

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Background: Elevated B-type natriuretic peptide levels in patients with acute myocardial infarction are useful in the prediction of poor outcome. It is still not established how often and when assessment of neurohormonal activation provides the best prognostic information.
Aim: To evaluate whether repeated measurements of B-type natriuretic peptide provide additional clinical information in patients with first ST-elevation myocardial infarction.
Methods: In 96 consecutive patients with first ST-elevation myocardial infarction, treated with primary percutaneous coronary intervention, B-type natriuretic peptide concentrations were measured twice: on admission and 24 hours later. A clinical composite endpoint was assessed during hospital stay.
Results: The median B-type natriuretic peptide concentration obtained on admission was 62.9 pg/mL and 24 hours later was 223.6 pg/mL. Thirty-five patients (36.4%) reached composite endpoint, including 3 deaths (3.1%). Both B-type natriuretic peptide levels were related to the clinical and echocardiographic variables, which refer to the large in-farct expansion and acute left ventricular dysfunction. The first measurement was better correlated with current patient status (ie, TIMI Risk Score, admission Killip class). B-type natriuretic peptide 24 hours after admission was significantly higher in patients who had an adverse cardiovascular event during hospitalization (P = 0.02). ROC analysis also identified the second B-type natriuretic peptide measurement as significant to estimate adverse outcome (c = 0.64 CI 0.527 - 0.756 P = 0.007).
Conclusions: Despite there being a time interval of only 24 hours between the two sets of B-type natriuretic peptide sampling, both measurements provide important and different information. Only B-type natriuretic peptide measurement 24 hours after admission identifies patients with a high in-hospital event rate risk.

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The purpose of this study was to examine the relation between adiponectin levels and subclinical carotid atherosclerosis in patients undergoing coronary artery bypass grafting (CABG). Serum concentrations of adiponectin and carotid intima/media thickness (IMT) were measured in 84 consecutive patients who underwent CABG. Carotid IMT both at the common carotid artery and carotid bulb level was correlated negatively and significantly (r = -0.581 and r = -0.415, respectively, P < 0.01) with the serum concentrations of adiponectin. Linear regression modeling identified adiponectin as the strongest predictive variable for carotid IMT both at the common carotid artery and carotid bulb level (P < 0.001). Stepwise regression analyses also showed that adiponectin was the strongest independent determinant of the carotid IMT both at the common carotid artery and the carotid bulb level (F = 20.215 and F = 19.565, respectively, P < 0.001). The mean number of diseased coronary arteries, mean number of distal anastomoses, cardiopulmonary bypass time, and aortic cross-clamping time did not significantly correlate with the serum concentrations of adiponectin. The findings indicate the presence of an inverse relationship between serum concentrations of adiponectin and subclinical carotid atherosclerosis in patients undergoing CABG. In these patients, the absence of a significant correlation between severity of coronary atherosclerosis and adiponectin might suggest that adiponectin levels may predict the early stages rather than further progression of atherosclerosis.

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Several studies have suggested that an increased high sensitivity C-reactive protein (hsCRP) level is a strong independent predictor of increased risk for atherosclerotic cardiovascular mortality and morbidity. Reduced heart rate variability (HRV) has also been reported to predict cardiovascular events such as sudden death and myocardial infarction in apparently healthy subjects. The aim of this cross-sectional study was to test the possible correlation between variation of the R-R interval as one of the markers of HRV and serum hsCRP levels in a general population in Japan.
Resting, supine, 2-minute, beat-to-beat heart rate data were collected in 823 randomly selected participants enrolled in our cohort study. The coefficient of variation of the R-R interval (CVrr) was obtained as a parameter of HRV. To determine which factors predict the presence of low CVrr (below the 5 percentile) in this group, we performed a multivariate logistic regression analysis using cardiovascular risk factors and an elevated hsCRP level as independent variables.
The lowest CVrr group showed significantly higher hsCRP levels compared to those of other quartiles (P < 0.01). After adjustment for confounding factors such as age, heart rate, obesity, hypercholesterolemia, and hypertension by multivariate logistic analysis, an elevated hsCRP level (OR = 3.11, 95%CI; 1.27-7.60: P < 0.02) was a significant independent predictor of low CVrr.
The results of the present study indicate that an increased serum hsCRP level is significantly associated with reduced CVrr in this general population. It is conceivable that the parasympathetic nerve withdrawal and inflammation could interact with each other, resulting in the progression of atherosclerotic cardiovascular disease.

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It has recently been reported that insulin resistance is prevalent in patients with dilated cardiomyopathy (DCM); however, it remains unclear whether insulin resistance is directly induced by DCM or if it is caused by congestive heart failure associated with DCM. We evaluated homeostasis model assessment insulin resistance (HOMA-R) in 14 patients with DCM in comparison with 9 patients with valvular heart diseases (VHD). We also measured the level of serum tumor necrosis factor (TNF)-α as a possible causative factor for inducing insulin resistance. Even after the adjustment for age, body mass index, and cardiac function, HOMA-R was significantly higher in patients with DCM than in those with VHD (P = 0.012) (mean ± SEM: 3.51 ± 0.59, and 0.80 ± 0.64, respectively). The serum TNF-α level tended to be higher in patients with DCM than in those with VHD; however, the difference was not significant. In conclusion, patients with DCM possess insulin resistance independently of the severity of cardiac dysfunction or serum TNF-α, suggesting that insulin resistance in patients with DCM may be closely associated with the pathogenic condition of DCM itself.

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Central sleep apnea (CSA) is thought to arise as a consequence of chronic heart failure. We have attempted to determine the relationship between the severity of CSA and the respiratory gas indexes during cardiopulmonary exercise testing (CPX), indexes well-known to reflect the severity of heart failure. Twenty consecutive cardiac patients (59.0 ± 15.3 years) with CSA underwent CPX. End-tidal PCO₂(PETCO₂) was measured at rest and at peak exercise as a substitute for PaCO₂, along with the peak oxygen uptake (VO₂) and the ratio of the increase in ventilation to the increase in CO₂output (VE/VCO₂ slope). Peak VO₂, % peak VO₂, and the VE/VCO₂ slope of the subjects were 15.5 ± 5.8 mL/min/kg, 52.8 ± 16.7%, and 37.9 ± 12.5, respectively, showing moderate to severely decreased exercise capacity. While PETCO₂ at both rest and peak exercise significantly correlated with peak VO₂ (r = 0.63 and r = 0.51, respectively) and the VE/VCO₂ slope (r = -0.77 and r = -0.91, respectively), none of these 3 parameters correlated with the apnea-hypopnea index. The apnea-hypopnea index in the subjects with lower resting PETCO₂ was not notably different from that in the subjects with relatively high PETCO₂.
Although the severity of CSA is assumed to correlate with the severity of heart failure, and a lowering of PaCO₂ during wakefulness is considered to be one of the mechanisms behind CSA, the severity of CSA does not correlate with the respiratory gas indexes of CPX or the level of PETCO₂ in cardiac patients with moderate to severely decreased exercise capacity.

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Diabetes mellitus (DM), which induces alterations in energy metabolism, is the leading cause of cardiovascular disease. We postulated that peroxisome proliferator activated receptor-γ coactivator 1α (PGC-α), a transcriptional coactivator that is the primary regulator of oxidative metabolism and mitochondrial biogenesis, and cardiac function are depressive in DM and simvastatin and losartan therapy can improve the affects of DM on mRNA expression of PGC-1α and cardiac function. An experimental model of DM (induced by streptozocin 60 mg/kg) in adult male rats (n = 24) was used to investigate the mRNA expression of PGC-1α in the left ventricular myocardium. These rats were divided into group I (insulin therapy only, n = 8), group II (insulin plus simvastatin 20 mg/kg/day orally, n = 8), and group III (insulin plus losartan 20 mg/kg/day orally, n = 8). Diabetic rats and 8 healthy rats (group IV) were sacrificed at 3 weeks following DM induction. The mRNA expression of PGC-1α was measured using real-time polymerase chain reaction (RT-PCR). Additionally, transthoracic echocardiography was performed on days 0 and 21. The experimental results indicated that the mRNA expression of PGC-1α and the left ventricular ejection fraction (LVEF %) were significantly lower in groups I, II and III than in group IV (all P < 0.001). However, the mRNA expression of PGC-1α and the LVEF were significantly higher in group III than in groups I and II (both P < 0.01). Conversely, mRNA expression of PGC-1α and LVEF did not differ between groups I and II (P > 0.5). In conclusion, DM induces suppression of mRNA expression of PGC-1α and LV function in diabetic rats. Losartan and not simvastatin therapy improved the LV function and the expression of this mitochondrial-biogenesis regulator.

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Pulmonary arterial hypertension (PAH), caused by collagen diseases, Eisenmenger syndrome or of idiopathic etiology, generally has a poor prognosis. Recently, bosentan, a dual endothelin receptor antagonist, has become available for treating PAH. This report describes a bosentan-effective case of combined PAH, hemodialysis and mild aortic stenosis. A 71-year-old woman on hemodialysis was referred to our hospital because of repetitive syncope. Although neurological examinations revealed no etiological diseases, echocardiography and cardiac catheterization showed PAH and mild aortic valve stenosis. Bosentan abolished syncope with improvement of hemodynamic parameters. This report suggests bosentan was clinically useful in a hemodialysis patient with pulmonary hypertension and mild aortic valve stenosis.

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The following error appeared in the article titled “Prospective Randomized Trial of Transthoracic Versus Low-Energy Internal Cardioversion in Persistent Atrial Fibrillation: Long-Term Follow-Up” by Murat Ozdemir, Sedat Turkoglu, Mehmet Gungor Kaya, and Atiye Cengel (Vol. 47, No. 5, 753-762, 2006). The line indicating Internal CV in the Figure (p. 757) was not printed due to a printing error. The line for External CV was correct and has not changed. Wrong:See PDF attached
Right:See PDF attached

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