The aim of the present study was to investigate the prognostic value of plasma interleukin-8 (IL-8) for early complications after percutaneous coronary intervention (PCI).
The pre- and postprocedural plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, and the expression of CD11b/CD18 on neutrophils was assessed by flow cytometry. Early complications (abrupt occlusion, threatened abrupt occlusion, early recurrence of ischemia, myocardial infarction, cardiac sudden death, and target vessel revascularization) occurred intra-procedure and 30 days after PCI and were observed in 121 consecutive patients with coronary heart disease.
Sixteen patients with early complications had high preprocedural levels and high postprocedural differentials of IL-8, CRP, and CD11b/CD18 compared to those without complications (all P < 0.05). The occurrence of complications showed a significant increase in the patients according to the tertiles of IL-8, CRP, and CD11b / CD18. Preprocedural levels of IL-8 (RR = 5.864, CI = 1.658 - 20.734, P = 0.006) and diabetes (RR = 1.587, CI = 1.246 − 2.132, P = 0.038) were independent predictors of early complications. There were significant correlations in the postprocedural differential between IL-8 and CD11b/CD18 (r = 0.776, P = 0.002) in patients with complications.
The results reveal that the early complications after PCI contribute to preprocedural inflammatory responses. Normal levels of IL-8 may be powerful negative predictors of early complications in patients with CHD following PCI.

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Coronary artery ectasia (CAE) is a rare form of coronary artery disease. It has previously been shown that nitrate derivatives induce exertional angina in patients with CAE. Furthermore, there is limited data about the effects of other anti-ischemic agents in CAE. The aim of this study was to investigate the effect of trimetazidine on exercise performance in patients with CAE.
The study population consisted of 56 patients with isolated CAE (32 males, mean age: 58 ± 9 years). The presence of myocardial ischemia was evaluated by treadmill exercise test. The exercise test was positive in 49 patients at baseline and in 27 patients during trimetazidine therapy (P < 0.01). The exercise test induced angina in all of the patients who have had a positive test result. Significant ST depressions were observed in 42 and 23 patients before and after the treatment, respectively (P < 0.01). The extent of ST depression at peak exercise was significantly lower on trimetazidine (0.9 ± 0.5 vs 1.5 ± 0.6 mm, P < 0.01). With trimetazidine, the exercise duration increased from 7.8 ± 2.1 to 8.7 ± 2.4 min (P = 0.04 ) and cardiac work-load also increased from 8.9 ± 2.3 to 10.4 ± 2.1 mets (P < 0.01).
The results suggest that trimetazidine can relieve exercise-induced angina and improve exercise performance in patients with CAE.

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The aim of the present study was to assess the long-term clinical course of patients with syndrome X, focusing on different courses between exercise-induced ST depression and chest pain. Forty-three patitheents with syndrome X were followed up for 6.4 ± 3.8 years. They were divided into the 3 groups according to chest pain: disappeared (n = 24), improved (n = 14), or unchanged (n = 5). No patients had cardiac events and all had a favorable long-term prognosis. In patients showing disappearance of chest pain, exercise-induced ST depression and rate-pressure product (RPP) at peak exercise did not change during follow-up. However, ST depression and RPP decreased significantly in those with improved chest pain. These observations suggest that abnormal pain perception plays an important role in the development of chest pain.

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The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C and increased venous thrombosis. However, the role of factor V Leiden in the formation of left atrial thrombus with nonrheumatic atrial fibrillation has not been studied. We investigated whether factor V Leiden is a risk factor for left atrial thrombus in patients with nonrheumatic atrial fibrillation. We analyzed clinical, echocardiographic, and biochemical data in 105 consecutive patients with nonrheumatic atrial fibrillation. These patients were divided into two groups; group A (n = 37) with left atrial thrombus and group B (n = 68) without left atrial thrombus. The study also included 42 control subjects. Left atrial thrombus was investigated by using both transthoracic echocardiography and transesophageal echocardiography. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. There was no significant difference in the prevalence of factor V Leiden between the patients and control subjects. The prevalence of factor V Leiden mutation was 8.1% (3/37) in patients with left atrial thrombus, and 8.8% (6/68) in patients without left atrial thrombus. The prevalence of factor V Leiden was 7.1% (3/42) in control subjects. The prevalance of factor V Leiden was 10% (2/20) in patients with spontaneous echo contrast and 8% (7/85) in patients without spontaneous echo contrast. Multivariate analyses showed that left ventricular ejection fraction was an independent predictor of left atrial thrombus. Factor V Leiden mutation is not a risk factor for left atrial thrombus formation and spontaneous echo contrast in patients with nonrheumatic atrial fibrillation.

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Endogenous opioids and catecholamines are involved in autonomic activity. Nitroglycerin provocation tilt is a useful modality for evaluating neurally mediated syncope. Endogenous opioids and epinephrine might play an important role in nitroglycerin provocation tilt. To investigate whether or not opioids and catecholamines are involved in the pathogenesis of nitroglycerin provocation tilt, we measured the temporal changes of the plasma levels of β endorphin, norepinephrine, and epinephrine in 64 patients with syncope of unknown etiology, and compared the findings with those of 16 patients who underwent isoproterenol provocation tilt (1-3 µg/min) test with a positive response. We performed a 20 minute control tilt (80°)followed by a nitroglycerin provocation tilt of 20 minutes with the intravenous infusion of nitroglycerin. Nitroglycerin infusion was started at 250 µg/h, and was increased by 250 µg/h every 3 minutes up to 1500 µg/h during the tilt test. β-endorphin, norepinephrine, and epinephrine were measured in peripheral venous blood in the supine position 2, 10, and 20 minutes after the start of the tilt test, and also at the onset of syncope. Twenty-six patients had a positive response to the control tilt (group 1), and 22 patients had a positive response to nitroglycerin provocation tilt (group 2). The remaining 16 patients had a negative response to both control tilt and nitroglycerin provocation tilt (group 3), compared with isoproterenol provocation tilt patients (group 4). >β-endorphin and epinephrine only significantly increased in groups 1 and 2 (β-endorphin; from 7.3 ± 3.3 pg/mL to 19.9 ± 17.7 pg/mL, in group 1, P < 0.05; from 7.3 ± 2.9 to 16.5 ± 10.7 pg/mL, in group 2, P < 0.05: epinephrine; from 42 ± 58 pg/mL to 157 ± 161 pg/mL, in group 1, P < 0.05; from 33 ± 25 to 202 ± 252 pg/mL, in group 2, P < 0.05), but not in groups 3 and 4. β-endorphin and epinephrine might participate in the pathophysiology in conventional tilt-induced as well as nitroglycerin provocation tilt-induced syncope in patients with neurally mediated syncope.

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Apical hypertrophic cardiomyopathy has been divided into two entities: apical asymmetric septal hypertrophy (apical ASH) and apical symmetric hypertrophy (AH). The latter differs clinically from hypertrophic cardiomyopathy (HCM) with ASH, and it is unclear whether AH represents a distinct subtype of HCM. In the present study, the presence or absence and the extent of cardiac muscle cell disorganization, a histologic characteristic of HCM, were compared in patients with AH (n = 10) and ASH (n = 29) in whom cardiac biopsy specimens were obtained from the left ventricular apex and interventricular septum. Disorganization was graded as (1+) in only 1 patient in the AH group and (−) in the remaining 9. In contrast, in the ASH group disorganization was graded as (1+) in 15 patients, (2+) in 7, (3+) in 3, and (−) in only 4 (P < 0.0001). Thus, it was observed that in AH disorganization is virtually absent or at most limited to a very narrow area. It is concluded from a histological stand point as well that the type of apical hypertrophic cardiomyopathy showing apical symmetric hypertrophy differs from usual HCM.

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The present study was undertaken to investigate the relationship between the extent of impaired chronotropic response and cardiac output during exercise, and exercise tolerance in patients with chronic heart failure. The subjects consisted of 24 patients (mean 60.1 ± 14.0 years) who had mild chronotropic incompetence. Cardiopulmonary exercise testing was performed in all patients, and heart rate (HR), anaerobic threshold (AT), maximum oxygen uptake (peak VO₂), slope of the regression line relating the ventilatory equivalent to carbon dioxide output (VE/VCO₂ slope), and exercise time were measured. Cardiac output (CO) was measured by a thoracic bioimpedance method and cardiac index (CI) was calculated. Plasma norepinephrine (NE) was measured at rest and immediately after the exercise test. The changes in HR, NE, and CI from the resting state to immediately after exercise were calculated as ΔHR, ΔNE, and ΔCI, respectively. The ΔNE was converted to a logarithmic scale and ΔHR/log ΔNE was used as a parameter of HR response to sympathetic nerve stimulation. The results were as follows: HR and NE in the resting state had no correlation with AT and with peak VO₂. ΔHR/logΔNE correlated positively with both AT and peak VO₂, and negatively with the VE/VCO₂ slope. ΔHR/logΔNE correlated positively with peak CI, %ΔCI, and ΔCI/exercise time. The data suggest that one of the mechanisms of low exercise tolerance in chronic heart failure patients was due to an inadequate increase in CO response against exercise caused by an impaired HR response to increased NE.

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