Preventing left ventricular (LV) remodeling after coronary artery bypass graft surgery (CABG) is important to avoid long-term congestive heart failure. The present study evaluated the effects of angiotensin converting enzyme inhibitors (ACEIs) and β-blockers on LV remodeling. Twenty-three patients with angina pectoris and 36 with old myocardial infarction underwent CABG. We assessed end diastolic volume index (EDVI), end systolic volume index (ESVI), and ejection fraction (EF) using left ventriculography before and after CABG. Changes in EDVI, ESVI, and EF were studied in the ACEI, β-blocker, and control groups. Although EDVI was reduced in the ACEI group, ESVI and EF improved only slightly, whereas in the group given β-blockers, ESVI was reduced, EF improved, and EDVI was minimally reduced. These results indicate that ACEIs and β-blockers both protect against LV remodeling, although through different mechanisms.

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An increased serum interleukin-6 (IL-6) level is associated with an increased risk of cardiovascular events in healthy subjects. However, it is unknown whether the level of serum IL-6 or genetic IL-6 polymorphism is correlated with the complexity of coronary plaque in patients with stable coronary artery disease (CAD).
Patients with stable CAD (n = 135) were divided into 3 groups: insignificant coronary plaque (n = 77), simple coronary plaque (n = 15), and complex coronary plaque (n = 43). IL-6-174G > C polymorphism and serum levels of IL-6 and C-reactive protein (CRP) were investigated.
No significant difference in the distribution of IL-6 genotypes was found among the groups. The presence of complex coronary plaque was associated with higher serum concentrations of IL-6 (P = 0.026) and CRP (P < 0.0001). To predict the presence of complex lesions, IL-6 > 5.8 ng/L and CRP > 2.6 mg/L had sensitivities of 86% and 74%, and specificities of 61% and 62%, respectively. By multivariate analysis, IL-6 > 5.8 ng/L and CRP > 2.6 mg/L were independently related to the presence of complex coronary plaque (P = 0.0002 and 0.004, respectively). IL-6 > 5.8 ng/L and CRP > 2.6 mg/L were associated with a 4.5-fold increase in the odds of having complex coronary plaque (P < 0.005).
A simple measurement of the serum IL-6 level in patients with CAD can potentially identify subjects with complex coronary lesions and provide the option of aggressive medical strategies in a clinical setting.

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The aim of this study was to determine how body mass index (BMI) influences the N-terminal pro-B-type natriuretic peptide (NT-proBNP) level in patients with significant coronary artery disease (CAD).
A total of 348 patients (61.5 ± 9.2 years, male 67.5%) who had normal left ventricular systolic function were enrolled. All patients underwent percutaneous coronary intervention. We excluded patients with acute myocardial infarction, chronic heart failure, or renal dysfunction. Baseline NT-proBNP level was measured on admission. All underwent follow-up (F-U) coronary angiography (CAG) and the F-U NT-proBNP level was measured before F-U CAG. The patients were divided into two groups: an NT-proBNP < 100 pg/mL group (group I, n = 228) and an NT-proBNP > 200 pg/mL group (group II, n = 120). BMI was significantly higher in group I than that in group II (26.5 ± 2.2 versus 22.9 ± 2.5 kg/m ², P < 0.001). The level of NT-proBNP was negatively correlated with BMI and the levels of hemoglobin and apolipoprotein A1, and positively correlated with age, lipoprotein (a), and the Gensini score. In multivariate analysis, BMI was significantly related to a low NT-proBNP level in patients with CAD (odds ratio, 6.83; 95% confidence interval, 2.67-17.47; P < 0.001).
The NT-proBNP level was not elevated in patients with a high BMI despite having significant CAD, and BMI was significantly related to a low NT-proBNP level in patients with significant CAD.

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Aspirin resistance as defined by failure to effectively inhibit thromboxane synthesis is associated with a higher risk of recurrent myocardial ischemia and cardiovascular death. Heart rate variability (HRV) analysis has been extensively used to identify patients at risk for increased cardiac mortality. The aim of this study was to evaluate the association between HRV and aspirin resistance in patients with stable coronary artery disease (CAD).
Sixty-nine (69) consecutive patients with stable CAD were included in this study. Of the 69 patients, 18 (26%) were aspirin nonresponders. When the aspirin responders were compared with the nonresponders, there was no significant difference between the groups with respect to most clinical parameters, major cardiovascular risk factors, medical treatments, and aspirin dosages. However, the patients with aspirin resistance had a higher previous myocardial infarction history and lower left ventricular ejection fraction. Moreover, mean platelet volume, CT/EPI, CT/ADP values, LF and LF/HF ratio were higher while HF, SDNN, SDANN, and RMSSD were lower in the nonresponder group than the responders. Regarding HRV parameters, CT/ADP time was negatively correlated with SDNN (r = -0.5, P = 0.02) and HF (r = -0.4, P = 0.03), and positively correlated with LF (r = 0.6, P = 0.01) and LF/HF (r = 0.7, P = 0.001). Similarly, CT/EPI time was negatively correlated with SDNN (r = -0.4, P = 0.03), and positively correlated with LF (r = 0.5, P = 0.02) and the LF/HF ratio (r = 0.5, P = 0.02). Regression analysis revealed that the only parameters affecting SDNN and LF/HF ratio were left ventricle ejection fraction and aspirin resistance.
The heart rate variability decreased and sympathetic activity increased in the patients with aspirin resistance and stable CAD. This may contribute to a higher risk of recurrent myocardial ischemia and cardiovascular death in patients with aspirin resistance.

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The beneficial effects of statins in patients with coronary artery disease (CAD) may be balanced by concerns that statins can depress production of ubiquinone (CoQ10), which serves as a component of mitochondrial energy production and an antioxidant. Accordingly, the effects of atorvastatin (ATO)-induced changes in plasma CoQ10 on BNP and oxidative stress were investigated. In 29 patients with CAD, the plasma levels of CoQ10 and BNP and urinary excretion of 8-iso-prostaglandin F2α (8-iso-PGF) were determined before and after 3-month treatment with ATO. Ten patients had received pravastatin and 10 patients fluvastatin, while 9 patients had not received any statin before ATO. There was a linear correlation between ATO-induced changes in total cholesterol and CoQ10 (r = 0.632, P < 0.01), and an inverse correlation between ATO-induced changes in CoQ10 and BNP (r = -0.497, P < 0.01). There was no significant correlation between ATO-induced changes in CoQ10 and 8-iso-PGF. Multivariate analysis revealed that ATO-induced decreases in plasma CoQ10 were significantly associated with increasing BNP levels. In conclusion, long-term treatment with ATO might increase plasma levels of BNP in patients with CAD when it is accompanied by a greater reduction in plasma CoQ10. However, ATO-induced decreases in CoQ10 might not increase oxidative stress.

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The purpose of this study was to examine the relationship between long-term efficacy of amiodarone therapy (100-200 mg/day) combined with angiotensin converting enzyme inhibitor (ACEI; enalapril 5 mg/day) administration, and the development of structural atrial remodeling in patients with paroxysmal atrial fibrillation (AF). Fifty-eight patients (40 men, 18 women, mean age, 68 ± 8 years, mean follow-up period, 43 ± 18 months) with AF refractory to ≥ two class I antiarrhythmic drugs were divided into two groups; those treated with enalapril on amiodarone (group A, n = 25) and those treated with amiodarone alone (group B, n = 33), to evaluate the efficacy of combination therapy.
1) At 12 and 24 months, the survival rates for patients free from AF recurrence were 80% and 64% in group A, and 45% and 30% in group B, respectively (P < 0.05, group A versus group B). The percentage of patients with conversion to permanent AF despite amiodarone therapy was 20% in group A and 48.5% in group B (P < 0.05, group A versus group B). 2) In group B, left atrial dimension (LAD) was significantly greater after amiodarone therapy (40.2 ± 6.3 mm) than at baseline (35.2 ± 6.6 mm) (P < 0.01), whereas there was no significant difference in LAD between baseline and after amiodarone therapy in group A (39.1 ± 5.0 mm versus 41.0 ± 5.0 mm, respectively).
In patients with paroxysmal AF, ACE-I appears to enhance the efficacy of amiodarone therapy in maintaining sinus rhythm and preventing the development of structural remodeling in atria.

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Although white coat hypertension (WCH) is believed to have an effect on health, there is no term defining WCH in metabolic syndrome.
Consecutive patients 20 years old or older who underwent a check-up were included. The study included 1068 cases. The prevalences of hyperbetalipoproteinemia, hypertriglyceridemia, dyslipidemia, impaired glucose tolerance (IGT), and WCH were similar to excess weight in that they increased significantly until the seventh decade of life and decreased thereafter significantly (P < 0.05 in most steps). On the other hand, the prevalences of hypertension (HT), diabetes mellitus (DM), and coronary heart disease (CHD) always increased significantly with age without any decrease (P < 0.05 in most steps), indicating their irreversibility in contrast to the reversibility of excess weight, hyperbetalipoproteinemia, hypertriglyceridemia, dyslipidemia, IGT, and WCH.
Metabolic syndrome is a reversible progression step between health and irreversible final diseases terminating with increased mortality and disabilities. Thus, the definition of metabolic syndrome should include reversible metabolic risk factors such as excess weight (overweight and obesity), hyperbetalipoproteinemia, hypertriglyceridemia, dyslipidemia, IGT, and WCH, instead of irrevesible diseases such as DM, HT, CHD, and stroke that have already developed and require drug therapy. After development of one of the final metabolic diseases, the term metabolic syndrome probably loses most of its significance, since from that point on, nonpharmaceutical approaches such as lifestyle changes, diet, and exercise will provide little benefit to prevent development of the others, most likely due to the cumulative effects of the risk factors on body systems over a long period of time.

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Determining the type of cardiac dysfunction is important for implementing therapeutic strategies and for prognostic insights. We characterized systolic dysfunction (SD) and isolated diastolic dysfunction (IDD) in adults referred for echocardiographic evaluation, and compared their clinical and other characteristics. In the present work, we studied 218 patients (137 males) with cardiac dysfunction (mean age, 66.3 ± 8.3 years). SD was defined as a left ventricular ejection fraction (LVEF) of < 45%, whereas IDD was defined as a LVEF ≥ 45% in addition to the standard Doppler-echocardiography diagnostic criteria for IDD. Approximately 68% of subjects had SD (70% males). The proportions of hypertension, diabetes, and dyslipidemia were 44%, 26%, and 22%, respectively, without significant association with the type of dysfunction. Myocardial infarction (MI) was found in 31% of patients, and was significantly (P < 0.001) more prevalent among SD compared with IDD cases. Cerebral stroke (18%) and malignancy (16%) were significantly associated with IDD (29% versus 13% for SD in the case of stroke, and 26% versus 11% for SD in the case of malignancy; P = 0.008 for each). In multivariately-adjusted logistic regression analysis, the following variables were found to be significantly (P < 0.05) and independently associated with IDD: female gender (odds ratio [OR] = 2.207 [95% CI = 1.302-4.608]), stroke (OR = 2.009 [1.119-3.980]), and malignancy (OR = 2.016 [1.230-4.010]). On the other hand, previous MI (OR = 2.075 [1.769-4.808]) was independently associated with SD. In conclusion, some factors/comorbidities were more likely to associate with IDD (female gender, stroke, and malignancy) or SD (previous MI) when IDD and SD were compared with each other.

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Sleep-disordered breathing (SDB) is frequently observed in patients with congestive heart failure. Recent studies have shown that SDB negatively affects the onset of congestive heart failure; however, no studies have addressed the relationship between the level of SDB and the onset time of acute dyspnea. We hypothesized that SDB affects the acute onset time of dyspnea (AOT) and investigated the relationship between SDB and AOT.
We examined 80 patients (mean age, 61.6 years) with congestive heart failure in a clinically stable condition. AOT was divided into 5 time periods (0:00 - 6:00, 6:00 - 12:00, 12:00 - 18:00, 18:00 - 24:00, and unknown). The apnea-hypopnea index (AHI) was obtained based on the results of polysomnography (PSG) to evaluate the severity of SDB.
Acute dyspnea occurred in 59 (73.7%) of the 80 patients. When we divided the patients into an AHI < 5 group and an AHI ≥ 5 group, there was no significant difference in the AOT; however, a significant difference was observed in those divided into AHI < 20 and AHI ≥ 20 groups (P < 0.001). The patients with AHI ≥ 20 had more acute dys-pnea between 18:00 - 24:00 and between 0:00 - 6:00 than those with AHI < 20 (32% and 19%, and 4.1% and 4.1%, respectively).
Severe SDB patients tended to have acute dyspnea between midnight and dawn. The results suggest SDB might be one of the risk factors of heart failure.

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Left ventricular (LV) remodeling after acute myocardial infarction (MI) causes heart failure, and thus it is important to evaluate cardiac repair as the early stage of LV remodeling. Tenascin-C (TNC), an extracellular matrix glycoprotein, is transiently and abundantly expressed in the heart during the early stage of tissue remodeling after MI. However, it is not expressed in healthy adult heart. This study was undertaken to develop a new noninvasive diagnostic technique to detect cardiac repair after acute MI using ¹¹¹In Fab fragment of a monoclonal antibody specific for TNC.
¹¹¹In-anti-TNC-Fab was injected intravenously in 13 rats at 1 (D1, n = 3), 3 (D3, n = 5), and 5 (D5, n = 5) days after producing MI and in 5 sham-operated rats (S). We performed autoradiography and dual-isotope single-photon emission computed tomography imaging (SPECT) of ¹¹¹In-anti-TNC-Fab and ^99mTc methoxyisobutyl isonitrile (MIBI).
The radioactivity in the heart was significantly higher in D (D1, 0.45 ± 0.06% injected-dose/g; D3, 0.64 ± 0.12; D5, 0.38 ± 0.07) than S (0.27 ± 0.06, P < 0.01 versus D1 and D3, P < 0.05 versus D5). By autoradiography, higher radioactivities were observed in the infarcted area than in the noninfarcted area of MI hearts. Dual-isotope SPECT demonstrated the regional myocardial uptake of ¹¹¹In-anti-TNC-Fab, which was complementary to the perfusion image.
The results of the present study indicated that we can localize the infarcted region in the heart by ex vivo and in vivo imaging methods using ¹¹¹In-anti-TNC-Fab, and suggested the potential usefulness of noninvasive detection of cardiac repair.

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Radiofrequency catheter ablation (RFCA) for supraventricular arrhythmias results in parasympathetic nervous damage. Recently, RFCA around the pulmonary veins (PVs) has become a standardized curative therapy for atrial fibrillation (AF). The aim of the present study was to elucidate the relationship between the degree of vagal denervation and RFCA sites, including the PV areas. In 21 dogs, RFCA was performed at the ostium of the right PV (n = 7), ostium of the left PV (n = 7), and posteroseptal site of the right atrium (n = 7). Electrical stimulation of the cervical vagal trunk (ESCV) was performed and the resultant increase in the P-P interval (PPI) observed on the ECG was measured. The PPI was compared between the different RFCA sites. In another 7 animals, the vagal ganglia located in the fat pads that innervate the sinoatrial (SA) node were also stimulated (ESFP), testing the degree of postganglionic damage. The PPI after RFCA was decreased with right PV RFCA whereas there was no change with left PV RFCA. The ESFP yielded a significantly greater decrease in the PPI than the ESCV. The PPI during ESFP was completely blocked by hexamethonium, injected into the fat pad. The ESCV after the hexa-methonium injection did not result in complete disappearance of the PPI. Thus, right PV RFCA markedly damaged the vagal innervation of the SA node, whereas left PV RFCA produced little damage. The major type of damage was partial postganglionic fiber damage. An alternate vagal pathway external to the fat pads is proposed.

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Stent thrombosis is an infrequent event but a potentially fatal complication of coronary stenting. Adherence to long-term antiplatelet therapy plays an important role in the prevention of late stent thrombosis after drug-eluting stent (DES) implantation. Poor glycemic control due to nonadherence to diabetic treatments is likely to result in severely diffuse coronary atherosclerosis and diabetic microvascular complications. This case report describes fatal very late stent thrombosis in a young diabetic patient, which teaches us about the potential risk of DES in patients with acute myocardial infarction and the importance of patient education about long-term dual antiplatelet therapy after DES implantation. Furthermore, it demonstrates severely diffuse atherosclerosis in a young diabetic patient with nonadherence to diabetic treatments.

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