Pentraxin 3, ischemia-modified albumin, and myeloperoxidase in predicting a cardiac damage in acute carbon monoxide poisoning.

BACKGROUND: Carbon monoxide (CO) poisoning is associated with cardiac injuries or manifestations, frequently attributing to direct hypoxic damage at cellular level. For this, the aims were to evaluate the role of serum pentraxin 3 (PTX 3), ischemia-modified albumin (IMA), and myeloperoxidase (MPO) as an early biomarker for cardiac damage when compared to cardiac troponin I (cTnI) and creatine kinase-MB fraction (CK-MB) in adult patients with acute CO poisoning. METHODS: Forty patients with acute CO poisoning admitted to the emergency department. The patients were divided into 2 main groups as follows: cardiac injury (group I, n=19) and nonsuspected cardiac injury (group II, n=21). Pentraxin 3, IMA, MPO, cTnI, CK-MB, and the other assays in the circulation were measured on admission. RESULTS: Upon measuring the serum PTX 3, IMA, MPO, cTnI, and CK-MB levels as well as large electrocardiography and echocardiography abnormalities of patients with cardiac injury on admission, no statistical difference for PTX 3, IMA, and MPO was found between the groups (P>.05). However, cTnI, CK-MB, and leukocyte count (white blood cell) were higher determined in patients of group I compared to group II (P<.05). Receiver operating characteristic curve was also performed to evaluate the diagnostic performance of these tests in patients with cardiac injury. CONCLUSIONS: Our results suggest that PTX, IMA, and MPO assays are not superior to cTnI and CK-MB in predicting a cardiac damage in patients with acute CO intoxication.

Recurrent left ventricular apical ballooning syndrome in a patient with pheochromocytoma.

Transient left ventricular apical ballooning syndrome is characterized by reversible left ventricular wall motion abnormalities, chest pain or dyspnea, ST-segment elevation, and mild elevation of cardiac enzyme levels in the absence of obstructive coronary artery disease. The pathophysiology of the syndrome is still unknown. The probable mechanism is supposed to be a catecholamine discharge. We report the case of a 66-year-old woman with recently diagnosed pheochromocytoma who presented with chest pain and ST-segment elevation. Coronary angiography revealed normal coronaries and apical dyskinesia at ventriculography. A similar episode of chest pain occurred 4 years ago with same angiographic findings and reversible inferobasal akinesia. In-hospital course was uneventful and the patient was discharged from the hospital 4 days later with treatment of aspirin 1 × 100 mg, metoprolol 1 × 50 mg, lisinopril 1 × 10 mg, and atorvastatin 1 × 20 mg. At 2 years follow-up after the event, the patient remained asymptomatic.

The effects of perindopril on aortic elasticity and inflammatory markers in hypertensive patients.

BACKGROUND: Inflammation plays an important role in hypertension and in atherosclerosis. Inflammatory changes induced even in prehypertensive subjects can lead to increased arterial stiffness. The effects of perindopril on both inflammatory and aortic elasticity markers were tested in hypertensive patients. MATERIAL/METHODS: One hundred nine hypertensive patients not taking any antihypertensive therapy were included in the study. Aortic strain, aortic distensibility, aortic stiffness index, and inflammatory markers, including CRP, IL-1alpha IL-1beta, and TNF-alpha, were measured in all patients before and after twenty weeks of perindopril therapy. RESULTS: While aortic strain and distensibility showed statistically significant increases with perindopril therapy, the aortic stiffness index and inflammatory markers were found to decrease. CONCLUSIONS: Perindopril therapy resulted in an improvement in aortic elastic properties. There was also an attenuation of inflammatory status of the patients as reflected by lower inflammatory marker levels compared with pretreatment values.

The relation between coronary lesion distribution and risk factors in young adults.

OBJECTIVE: In this cross-sectional, case-controlled study, we aimed to evaluate classical and novel risk factors in young patients with coronary artery disease (CAD), and the relation between coronary risk factors and coronary lesion distribution. METHODS: Fifty-three patients under age of 45 years with severe coronary artery stenosis on angiography (group A) and age matched sixty patients having normal or non-critical stenosis on coronary angiography (group B) comprised the study groups. Conventional (smoking, family history, diabetes, hypertension) and novel risk factors (lipoprotein (a), homocysteine) were compared between the groups. Moreover, the relation between risk factors, and coronary lesions distribution, including left main artery (LMA) or proximal or mid left anterior descending (LAD) artery and remaining coronary lesions was investigated. Logistic regression analysis was used to define confounding factors predicting severe CAD and coronary lesion distribution and ROC curve analysis was performed to determine the cut-off value of independent factors, which were assessed by logistic regression analysis. RESULTS: Smoking was more prevalent in group A compared to group B. Lipoprotein (a) and homocysteine levels were also higher in group A than group B. For group A and B median (max-min) values of lipoprotein (a) were 34 (2-174) mg/dl and 38 (2-203) mg/dl (p=0.038), respectively and homocysteine levels were 12.3 (5-56.6) micromol/L and 9 (1.4-19) micromol/L (p=0.012), respectively. Smoking and homocysteine were independent predictors of severe CAD in young patients according to logistic regression analysis with an Odds ratio of 3.7 (95% CI=1.572-8.763; p=0.002) and 1.2 (95% CI=1.045-1.341; p=0.008), respectively. For predicting significant CAD the cut-off value of homocysteine was 11.6 micromol/L with a sensitivity and specificity of 53% and 77%, respectively (AUC=0.637; 95% CI=0.542-0.725; p=0.008). Within group analysis in group A patients revealed that only homocysteine was an independent predictor of LMA or proximal or mid-LAD lesion presence with an odds ratio of 1.2 (95% CI=1.011-1.465; p=0.016). ROC curve analysis revealed a cut-off value of 12 micromol/L in predicting LMA or proximal or mid-LAD lesions with a sensitivity and specificity of 65% and 91%, respectively (AUC=0.735; 95% CI=0.594-0.850; p=0.002). CONCLUSION: In our study, we found that young patients with severe CAD had different risk profile with higher frequency of smoking and increased levels of lipoprotein (a) and homocysteine. While smoking status and homocysteine may be used for prediction of severe CAD in young individuals, only homocysteine predicted coronary lesion distribution in LMA and proximal or mid-LAD.

Common variants in the ATP-binding cassette transporter 1 gene with decreased HDL-cholesterol levels and coronary artery disease.

BACKGROUND: Our aim was to determine whether the common variants within the coding sequence of ABCA1 gene affects low plasma high-density lipoprotein cholesterol (HDL-C) levels in Turkish patients with coronary artery disease (CAD). The study group was composed of 552 CAD patients, of which 251 had HDL-C levels < or =40 mg/dL, and 301 had HDL-C levels >40 mg/dL. METHODS: PCR-RFLP was used to determine the A2589G and G3456C DNA polymorphisms of the ABCA1 gene. The study group was analyzed for potential clinical predictors of low HDL-C. RESULTS: The GG variant of the ABCA1 gene A2589G polymorphism was found in 3.6% patients within the HDL-C < or =40 mg/dL group and in 4% of HDL-C levels >40 mg/dL group. Frequency distributions of the A2589G genotypes were not found to differ significantly among groups. The CC genotype of the G3456C polymorphism was found in 6.8% of HDL-C < or =40 mg/dL group and in 11.6% individuals of the HDL-C levels >40 mg/dL group. Frequency distributions of the G3456G genotypes were not significantly different among groups. The A2589G genotypes were not found to be effective over the analyzed lipid parameters. Among G3456C genotypes, in CAD patients with HDL-C < or =40 mg/dL the low-density lipoprotein (LDL-C) levels were elevated, whereas HDL-C levels decreased in CC genotype carriers compared to GG and GC. CONCLUSIONS: No significant association was found between cardiovascular endpoints and ABCA1 gene A2589G and G3456C genotypes in this study population.

The relation between coronary flow rate, plasma endothelin-1 concentrations, and clinical characteristics in patients with normal coronary arteries.

BACKGROUND: Coronary slow flow (CSF) is characterized by delayed opacification of epicardial arteries in the absence of occlusive disease. In the present study, we aimed to investigate the relation between coronary flow rate, plasma endothelin-1 (ET-1) concentrations, and clinical characteristics in patients with normal coronary arteries. METHODS: The study population included 77 patients with angiographically normal coronary arteries who underwent coronary angiography on suspicion of ischemic heart disease due to typical chest pain or ischemic findings on treadmill exercise test or myocardial scintigraphy. Based on the Thrombolysis In Myocardial Infarction frame count (TFC), patients were grouped into those with normal coronary flow and those with slow coronary flow. RESULTS: Forty-eight (61.5%) patients were found to have CSF. Plasma ET-1 concentrations were significantly higher with the presence of CSF (P=.03). There were significant differences between plasma ET-1 concentrations, and mean TFC, TFC for left anterior descending coronary artery (LAD), TFC for left circumflex coronary artery (CX), and TFC for right coronary artery separately in patients with and without CSF (P=.033, P<.001, P<.001, P<.001, and P<.001, respectively). Mean TFC, TFC for LAD, and TFC for CX, and ET-1 concentrations were significantly higher in smokers than in nonsmokers (P<.001, P<.001, P=.004, and P=.033, respectively). However, logistic regression analysis suggested that ET-1 concentration was not an independent determinant of CSF. CONCLUSIONS: Although there is a significant relation between ET-1 concentrations and coronary flow rate, ET-1 concentrations are not sufficient to determine the presence of CSF. Smoking is strongly associated with CSF, TFC, and increased ET-1 concentrations.

Impact of anemia on nonfatal coronary events after percutaneous coronary interventions.

Anemia is associated with higher rates of cardiovascular events in patients with heart failure, acute myocardial infarction, and in patients undergoing coronary artery bypass graft surgery. Although studies have focused on fatal coronary events in anemic patients following percutaneous coronary intervention (PCI), data is lacking regarding nonfatal coronary events. The aim of our study was to analyze the incidence of anemia in patients who developed nonfatal events after successful PCI, and to make a comparison with event-free patients. Forty-nine consecutive patients with and 51 without nonfatal coronary events (nonfatal myocardial infarction, coronary artery bypass grafting, or repeat PCI) during the 1-year follow-up after the index PCI procedure were included in the study. Anemia was defined using World Health Organization (WHO) criteria as a hematocrit value at initial presentation <39% for men and <36% for women. Baseline hematocrit levels were measured before the procedure. Baseline clinical, lesion, and procedural characteristics were comparable in both groups. Anemia was present in 33.8% of men and 30.4% of women. The incidence of anemia in patients with nonfatal coronary events was 46.9% and 15.7% in the event-free group, which was significantly different (P = 0.001). Anemia was found to be an independent risk factor for nonfatal coronary events in PCI patients (odds ratio: 2.24, 95% confidence interval: 1.05-4.79; P = 0.036). In conclusion, anemia is an important risk factor for predicting nonfatal coronary events after PCI. Although previous studies have shown its impact on fatal events, this study has demonstrated that anemia also has a role in nonfatal thrombotic coronary events and restenosis.