The purpose of this study was to test the hypothesis that plasma levels of adiponectin can predict angiographic in-stent restenosis after coronary stenting. We prospectively examined adiponectin levels in 127 consecutive patients undergoing elective coronary stenting. Restenosis was defined as more than 50% stenosis at follow-up study by quantitative coronary angiography. There were no significant differences in the clinical characteristics or angiographical findings between the groups with restenosis and no restenosis. The levels of adiponectin did not differ between the restenosis group and the no restenosis group (5.7±2.8 vs 5.9±3.6 μg/mL, p=0.72). The plasma levels of adiponectin were not related with the late loss index after coronary stenting (r=0.01, p=0.89). The levels of adiponectin were significantly lower in men than in women (5.5±3.2 vs 8.8±3.7 μg/mL, p<0.001), and negatively correlated with body mass index (r=-0.21, p=0.01). We analyzed adiponectin levels in male, female, obese, non-obese, diabetes, and non-diabetes patients, however, there were no significant differences between the restenosis group and no restenosis group. This study has demonstrated that the measurement of adiponectin could not predict angiographic restenosis after elective coronary stenting, whereas the plasma levels of adiponectin were associated with some coronary risk factors in patients with coronary artery disease.

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The recruitment of circulating leukocytes to atherosclerotic sites is mediated by a family of adhesion molecules.
The objective of the present study was to evaluate the relationship between circulating adhesion molecule levels in the coronary circulation and the severity of coronary atherosclerosis in patients with stable coronary artery disease.
The subjects were 79 patients undergoing coronary angiography. According to the severity of coronary atherosclerosis as assessed by the Gensini Score (GS) of the left coronary artery, they were classified into three groups: group C (no organic stenosis, score 0, n=14), group M (mild organic stenosis, score 1-13, n=39) and group S (severe organic stenosis, score ≥14, n=26). Blood samples were taken from the aorta (Ao) and coronary sinus (CS), and plasma levels of soluble E-selectin (sE-selectin) and soluble intercellular adhesion molecule-1 (sICAM-1) were measured by enzyme-linked immunosorbent assay. These levels were then compared between groups.
There were no significant differences in plasma sICAM-1 levels in the Ao or CS between the three groups. The difference in sICAM-1 levels between the CS and Ao (CS-Ao) also showed no significant difference. Plasma sE-selectin levels in both the Ao and CS were significantly higher in group S than in groups C and M (p<0.05), but there were no significant differences in CS-Ao. There was a weak but significant correlation between the plasma levels of these adhesion molecules and the number of coronary risk factors present. Multivariate analysis showed that the number of coronary risk factors was the only positive predictor (p=0.0048) of the GS; there was no association between the plasma level of either adhesion molecule and the GS.
In patients with stable coronary artery disease, sICAM-1 plasma levels do not indicate the severity of coronary atherosclerosis, while sE-selectin plasma levels appear to reflect the severity of systemic rather than coronary atherosclerosis.

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The aim of the present study was to investigate inflammatory cytokine release and the interaction with platelets in patients with unstable angina (UA) after coronary angioplasty.
In 50 patients with stable angina (SA) and 58 patients with UA, serial venous blood samples were obtained immediately before, and 30 minutes, 4, 12, 24, 48 and 72 hours, and 7 days after coronary angioplasty. Plasma concentrations of IL-8 and vWF were determined by immunoassay, while the expression of CD11b/CD18 on monocytes and the expression of CD41 on platelets were assessed by flow cytometry.
Differences in the baseline plasma concentrations of IL-8, vWF and CD11b/CD18, CD41 were found in the UA and SA groups before angioplasty (101.1 ±31.28 pg/mL to 55.8±17.24 pg/mL, 137.67±38.14% to 107.40±28.67% and 318.67±36.85 MFI to 240.72±28.43 MFI, 147.5±23.18 MFI to 104.43±26.68 MFI all p<0.05). The peak plasma levels of IL-8 (172.24±37.82 pg/mL at 12 hours) and vWF (256±42.32% at 4 hours) significantly increased after coronary angioplasty (both p<0.01), and were associated with significant time course increases in surface expression of CD11b/CD18 (p<0.01) and CD41 (p<0.01). The levels of plasma IL-8 and vWF were significantly higher pre- and post-procedure in UA patients with lesion type C compared to types A or B (p<0.05), but there were no differences for pre-procedure in the SA group patients with different lesion types (p>0.05). There were significant correlations between plasma IL-8 and monocyte CD11b/CD18, vWF and CD41 in the UA group (r=0.5248, r=0.6240 both p<0.01, respectively).
The findings demonstrate increases in plasma IL-8 and CD11b/CD18 as inflammatory mediators, vWF and CD41 as the abnormal coagulation activity may therefore yield a rationale for pharmacological anticytokines in patients with UA after coronary angioplasty.

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The correlation of peripheral endothelial dysfunction and intima-media thickness (IMT) in patients with suspected coronary artery disease (CAD) has been unclear. Inflammation and thrombosis may play a role at early stages of atherosclerosis. Thus, early atherosclerosis was noninvasively examined morphologically by IMT of carotid arteries, and functionally by flow mediated dilation (FMD) of brachial arteries in patients who were suspected of CAD and had undergone coronary angiography. Plasma antigen levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6, representative atherogenic cytokines, tissue factor (TF) and tissue factor pathway inhibitor (TFPI), markers of coagulation, and plasma activity level of plasminogen activator inhibitor type-1 (PAI-1), a marker of defective fibrinolysis, were measured. Patients with coronary atherosclerosis in one or more vessels with lesion ≥50% had significantly reduced FMD compared with those with angiographically normal coronary arteries. Carotid artery IMT increased significantly only in patients with advanced coronary atherosclerosis in one or more vessels with lesion ≥90%. Plasma antigen levels of IL-6 were significantly increased in patients with reduced FMD (<5%) compared to those in patients with FMD between 10 and 15%. Plasma antigen levels of TF, total and free TFPI, and PAI-1 activity tended to increase with a reduction in FMD. Thus, (1) FMD was reduced at early stages of CAD while IMT was increased in advanced CAD, and (2) inflammation and thrombosis may play a role in the early stages of the atherosclerotic process.

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A power spectral analysis of heart rate variability has been applied in order to assess diabetic autonomic neuropathy and high frequency spectra are thus considered to possibly reflect vagal nerve integrity in patients with diabetes mellitus. The purpose of this study was to investigate the relationship between the findings of high frequency spectra analysis and the results of the Ewing battery.
We performed 24-hour power spectral analysis using an ambulatory ECG monitoring system and standard tests in order to assess diabetic autonomic neuropathy (Ewing battery) in 18 diabetic patients to compare their diagnostic values for diabetic autonomic neuropathy. We used the high frequency amplitude (high frequency spectra; 0.15-0.40 Hz) as a direct measure of vagal nerve integrity from each hourly spectral plot. All hourly high frequency spectra decreased along with the impaired assessment of the battery, especially during the night when the high frequency spectra showed a manifest increase in patients classified as normal according to the battery. High frequency spectra during the night while asleep (22:00-05:00) and during a 24-hour period significantly correlated with the results of the battery. These values markedly decreased even in patients classified as having early vagal damage when compared with those classified as normal. High frequency spectra during night closely reflected the intrinsic vagal nerve integrity in patients with diabetes mellitus.
High frequency spectra during night or a 24-hour period is a simple and sensitive measure of diabetic autonomic neuropathy and is considered to be a useful modality for detecting even early changes in autonomic dysfunction.

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Silent brain infarction (SBI) is defined as asymptomatic infarction areas detected in computerized tomography (CT) scans in patients without a history of stroke. The incidence of SBI is increased in CT or magnetic resonance imaging in patients with carotid stenosis and with atrial fibrillation (AF), but its relation with rheumatic mitral stenosis (MS), another major source of emboli, is uncertain. The aim of this study was to investigate the incidence of SBI in patients with MS.
Fifty-three patients with MS (44 females and 9 males; range 25-52 years; mean age 38±7 years) diagnosed by transthoracic echocardiography (TTE) were enrolled in the study. Mitral valve calcification, left atrium (LA) dimension, and the presence of associating mitral regurgitation on TTE were recorded. Electrocardiographic evaluation was done for rhythm analysis and neurologic examination was performed prior to cerebral CT. Carotid artery Doppler examination was carried out in patients with SBI to exclude carotid artery lesions. Patients with a history of hypertension, diabetes mellitus, anticoagulant drug usage, presence of thrombus in LA, left ventricular segmental or systolic dysfunction, or other valve diseases were excluded from the study.
The incidence of SBI was found to be 24.5% in patients with MS (47% cortical, 53% lacunar). SBI was observed to be significantly high in patients with LA dimension >4 cm or in patients with AF (p<0.05). The SBI incidence was markedly higher if AF was found with enlarged LA when compared with patients having sinus rhythm and small LA (p<0.01). When moderate to severe mitral regurgitation was associated with MS, the SBI incidence was found to be lower (p<0.05). Although SBI was higher in patients with MVA<1.5 cm², it was not statistically significant (p>0.05). No significant correlation was found between calcific and noncalcific valves for SBI (p>0.05).
Our data suggest that SBI may be expected in about 1/4 of patients with MS. The presence of LA enlargement and AF increase the incidence of SBI in patients with MS, whereas the presence of moderate to severe mitral regurgitation decreases the incidence of SBI.

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Seven patients with ischemic cardiomyopathy who underwent elective endoventricular circular patch plasty (EVCPP) were included in this study. The mean age of the patients at the time of surgery was 63 years old. All seven patients had anterior left ventricular aneurysms following old myocardial infarction. Two patients were graded NYHA class II, 4 patients class III, and one patient class IV. EVCPP was performed under cardiac arrest with moderate hypothermia in five patients. The two most recent patients underwent EVCPP under on-pump beating and normothermia. Coronary artery bypass grafting was conducted in all cases and the mean number of grafts was 1.8, ranging from one to three. The mitral valve was replaced in one patient. One patient died of myonephrotic metabolic syndrome caused by ischemia of the lower limb. In the follow-up of six patients, the left ventricular end-diastolic volume index (LVEDI) decreased significantly from 128±31 mL/m² to 108±37 mL/m². Left ventricular end-systolic volume index (LVESI) decreased in five patients. Left ventricular end-diastolic and end-systolic diameter remained unchanged after surgery. The left ventricular ejection fraction (LVEF) increased from 0.28±0.08 to 0.32±0.1. LVESI and LVEF did not improve in one patient with a large residual dyskinetic area at the distal LV septum. A residual dyskinetic area at the distal LV septum was observed in two of four patients who underwent EVCPP under cardiac arrest. This condition, however, was not detected in two patients who underwent EVCPP under on-pump beating conditions. In the follow-up study, the grade of NYHA functional classification improved in all six patients. In conclusion, EVCPP under on-pump beating is a realistic and effective procedure with which to complete ideal LV geometry and promote good results in patients with ischemic cardiomyopathy.

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The objective of the present study was to determine the risk factors for operative and short-term mortality, and morbidity after a Bentall operation. Between July 1994 and February 2001, 86 consecutive patients (70 males) underwent a modified Bentall operation at our hospital. The aortic pathology was acute aortic dissection in 12 (14%), chronic dissection in 9 (10.5%) and degenerative aneurysm in 65 (75.6%). Mean age was 48±15 years. Eleven preoperative, 8 intraoperative and 6 postoperative variables of these patients were retrospectively analyzed using univariate and multivariate logistic regression analysis. Six patients died in the hospital (6.9%) and 2 died within four months after being discharged from the hospital. Mean follow-up time was 33±23 months (2 months to 8 years). The survival rate among hospital survivors was 88% at 3 years and 77% at 6 years. Univariate predictors of in-hospital and short-term mortality were the presence of aortic valve calcification, stenotic aortic valves, renal failure, and cardiac failure after the operation. Multivariate analysis revealed no independent risk factors. Risk factors for morbidity were etiology of acute dissection, use of circulatory arrest, transfusion of blood and fresh frozen plasma more than 2 units each, cross clamp and cardiopulmonary bypass times (exceeding 90 and 140 minutes, respectively), and performing concomitant procedures.
Modified Bentall procedures are safe in general. Meticulous dissection, careful handling and positioning of the coronary buttons are of paramount importance in patients with stiff aortic root since technical errors are more likely to occur.

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Invasive cardiology laboratory workers are occupationally exposed to chronic ionizing radiation. It is known that ionizing radiation has a damaging effect on chromosomes. In present study, we investigated the frequency of sister chromatid exchange (SCE) and chromosomal aberrations in 11 invasive cardiology laboratory workers and 11 healthy controls. After a vacation period, we took blood samples for chromosome analysis in months 0, 4, 8 and 12 (last two month period was the nonradiation time).
The SCE frequencies did not change significantly after exposure to ionizing radiation in any worker. Our study has revealed that non-specific structural chromosome aberrations such as gaps, isogaps, acentric chromosomes, chromatids and chromosome breakage could be in the 4^th and 8^th months after ionizing radiation exposure in the metaphase plaques. All abnormal chromosomal effects had disappeared by the end of the two month non-exposure period in each worker.
In conclusion, the results suggest that SCE frequencies are not significantly affected in invasive cardiology laboratory workers who are exposed occupationally to ionizing radiation, although some degree of reversible chromosomal aberrations did appear.

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Prolonged rapid atrial excitation gives rise to atrial electrical remodeling, which perpetuates atrial fibrillation (AF). However, there has been controversy regarding the nature of temporal changes in conduction characteristics during the development and recovery of electrical remodeling. This study was designed to clarify the nature of the development and recovery of electrical remodeling in relation to AF inducibility in dogs subjected to rapid atrial pacing. Eleven dogs underwent rapid atrial pacing (400/min) for 28 days. The electrophysiological study was performed on the day just prior to the commencement of pacing, on days 2, 7, 14, and 28 of rapid pacing, as well as 1 and 7 days after the cessation of pacing. In response to rapid atrial pacing, atrial effective refractory period (ERP), conduction velocity and wavelength decreased significantly (p<0.05). ERP had shortened significantly and rapidly within 2 days of pacing, while conduction velocity decreased more gradually. During the recovery, ERP returned to almost baseline levels within a day, whereas conduction velocity returned to baseline by day 7. Sustained AF became inducible in 37% of the dogs from 7 days of pacing until 1 day after the cessation, when wavelength fell below 8.7 cm. In conclusion, rapid atrial excitation causes a progressive but discordant temporal pattern of a decrease in ERP and conduction velocity. The resultant shortening of the wavelength determines the inducibility and maintenance of AF. The electrophysiological changes produced by one month of rapid atrial pacing can be fully reversed within a week, although in a discordant temporal pattern.

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A 22-year-old Japanese man with Brugada syndrome was resuscitated from cardiopulmonary arrest. In addition to the electrocardiographic evidence of the syndrome and the absence of apparent structural heart disease, no accumulation of iodine-123-metaiodobenzylguanidine (MIBG) was found anywhere throughout the heart. Thallium-201 (Tl) single photon emission computed tomography (SPECT) distribution showed no significant decrease in its uptake. To our knowledge, this is the first report that has demonstrated a homogeneous absence of cardiac accumulation of MIBG in Brugada syndrome.

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We describe a 66-year-old Japanese man in whom central retinal artery occlusion followed cardiac catheterization. After the procedure, blurred vision was noted in the right eye, and ophthalmological examination revealed an occlusion. Central retinal artery occlusion is a very rare but serious complication of cardiac catheterization. We should anticipate this potential risk to ensure prompt detection and treatment.

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A case of right branch retinal artery occlusion (BRAO) due to cholesterol-containing embolus following transfemoral cardiac catheterization is reported. It is extremely rare, however, cardiologists should be alert to any thromboembolic complications during and following cardiac catheterization and choose the suitable approach (either upper extremity or transfemoral).

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A 36 year old Turkish female patient complaining of widespread redness of the skin, shortness of breath, palpitations, nausea, hum and reverberation in the head was examined. The patient was diagnosed with catecholamine induced hypertension, which was caused by paraganglionoma. In addition, left ventricular concentric hypertrophy accompanied by systolic gradient in mid-ventricle, which is rarely observed, was determined by echocardiography. Hypertensive attacks and mid-ventricular systolic gradient disappeared after surgery. This case shows that one of the causes of the heart failure due to catecholamine releasing tumors can be left ventricular obstruction.

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