Predictive power of diastolic parameters on medical cardioversion success in acute atrial fibrillation.

BACKGROUND: Diastolic function assessment has been reported to provide valuable data in patients with atrial fibrillation (AF). The purpose of this study was to evaluate the effects of diastolic parameters on predicting the effectiveness of medical cardioversion in restoring sinus rhythm among patients with acute AF. METHODS: 40 non-valvular, new onset AF patients were included. All participants received an intravenous infusion of amiodarone. In patients whom sinus rhythm could not be restored with amiodarone, an electrical cardioversion was performed. Two groups, patients who achieved sinus rhythm with amiodarone (Group-1) and who failed to achieve sinus rhythm with amiodarone (Group-2) were compared with respect to initial echocardiographic measurements. RESULTS: Group-1 patients were younger comparing with Group-2 (mean age; 54.4 ± 13.9 years vs 63.3 ± 10.3 years, p = 0.028). Comparing with Group-1, Group-2 patients had; a higher left atrium volume index (17.1 ± 4.8 cm3 / m2 vs 22.6 ± 6.6 cm3 / m2 , p = 0.03); a shorter pulmonary vein S (49.6 ± 3.8 cm/sec vs 41.1 ± 3.0 cm/sec, p < 0.001); and a shorter pulmonary vein D peak velocity (55.9 ± 2.4 cm/sec vs 52.3 ± 1.8 cm/sec, p < 0.001). Moreover, both IVRT and DT were significantly shorter in Group-2, comparing with Group-1 (45.1 ± 2.1 msec vs 51.1 ± 2.5 msec, p < 0.001 and 51.3 ± 2.4 msec vs 56.5± 3.2 msec, p < 0.001, respectively). CONCLUSION: The present study revealed that admission pulmonary vein S and D wave peak velocities, IVRT, DT, and Pro-BNP levels could be predictors of failure of medical cardioversion among AF patients.

The effect of prophylactic migraine treatment on arterial stiffness.

BACKGROUND: Migraine is a common type of primary headache predominantly seen in women. This study aimed to evaluate endothelial function in patients with migraine using pulse wave velocity (PWV). METHODS: The study included 73 patients with newly diagnosed migraine and 80 healthy subjects. All patients and controls underwent baseline transthoracic echocardiography and PWV measurements. Patients were randomized to three groups to receive propranolol, flunarizine or topiramate, and the measurements were repeated at the end of 1 month. RESULTS: The newly diagnosed migraine patients and the control group exhibited no differences in baseline clinical characteristics, and the measurements showed that PWV was 7.4 ± 1.0 m/s in the patient group and 6.0 ± 1.0 m/s in the control group (p < 0.001). The same measurements were repeated during a control visit at the end of 1 month. Following treatment, a significant decrease was observed in PWV in all patient groups compared to baseline (p < 0.001). Subgroup analysis showed significantly decreased PWV in all drug groups, with the most prominent decrease in the topiramate group. CONCLUSIONS: The increased PWV demonstrated in migraine patients in this study stands out as an additional parameter elucidating endothelial dysfunction in these patients. Decreasing the number of migraine attacks with prophylactic treatment may reduce PWV and decrease cardiovascular risk in long-term follow-up.

Does estimated glomerular filtration rate have an effect on left ventricular function after ST-elevation myocardial infarction?

OBJECTIVES: Little is known about whether estimated glomerular filtration rates (eGFR) affect left ventricular (LV) function and gain benefit with antiremodeling treatment in patients with ST-elevation myocardial infarction (STEMI). We investigated the effect of eGFR on LV function using tissue Doppler imaging (TDI) parameters. In addition, we sought to evaluate the antiremodeling effect of standard treatment at follow-up in patients with renal insufficiency (RI) after STEMI. METHODS AND RESULTS: A retrospective analysis of 579 patients with STEMI was performed. Patients were divided into 3 groups according to eGFR (Group 1: eGFR > 90 mL/min per 1.73 m(2); Group 2: eGFR = 60-89 mL/min per 1.73 m(2); Group 3: eGFR < 60 mL/min per 1.73 m(2)). Conventional echocardiography and TDI were performed within 48-72 hours after STEMI and at 6-month follow-up. The mean left ventricular ejection fraction (LVEF) was significantly lower in Group 3 than in Group 1 (P = 0.021). The mean peak systolic velocity (Sm) was significantly lower in Group 3 than in Group 1 and Group 2 (P = 0.002 and 0.006, respectively). The estimated GFR had a linear association with Sm and LVEF (P = 0.001, r = 0.161; P = 0.005, r = 0.132, respectively). Multivariate analysis showed that an eGFR < 60 mL/min per 1.73 m(2) was an independent predictor of lower Sm and in-hospital mortality. In addition, an antiremodeling effect of standard treatment was seen in all groups at 6-month follow-up. CONCLUSIONS: Estimated glomerular filtration rate of <60 mL/min per 1.73 m(2) was associated with lower LV function after STEMI, and may gain an antiremodeling effect with standard treatment at follow-up.

Aortic distensibility and aortic intima-media thickness in patients without clinical manifestation of atherosclerotic cardiovascular disease.

BACKGROUND: There is growing evidence that aortic distensibility (AD) is a subclinical marker of early atherosclerosis. Aortic intima-media thickness (IMT) was an earlier marker than carotid IMT of preclinical atherosclerosis. In this study, we aimed to assess the relationship between thoracic aortic IMT and AD. METHODS: We studied 192 patients (mean age: 45.5 ± 8.4 years) who underwent transesophageal echocardiography (TEE) for various indications. Four different grades were determined according to IMT of thoracic aorta (Grade 1 < 1 mm; 1 mm ≤ Grade 2 < 3 mm; 3 mm ≤ Grade 3 < 5 mm; 5 mm ≤ Grade 4). AD was calculated from the echocardiographically derived ascending aorta diameters and hemodynamic pressure measurements in all patients. High sensitive C-reactive protein (hsCRP) and other biochemical markers were measured using an automated chemistry analyzer. RESULTS: TEE evaluation characterized thoracic aortic intimal morphology as grade 1 in 71 patients (37%), grade 2 in 57 patients (29.7%), grade 3 in 34 patients (17.7%), and grade 4 in 30 (15.6%) patients. The lowest AD level was observed in grade 4 group compared with grade 1 and grade 2 groups (P < 0.001, P = 0.009, respectively). AD level of grade 3 group was lower than grade 1 and grade 2 group (P < 0.001, P = 0.021, respectively). In multiple linear regression analysis, AD was independently associated with age (ß = -0.138, P = 0.029), hsCRP (ß = -0.209, P = 0.001), and aortic IMT (ß = -0.432, P < 0.001). CONCLUSION: AD is independently associated with age, thoracic aortic IMT, and hsCRP. Impaired elasticity index of the aorta might be an independent predictor for the severity of thoracic atherosclerosis.

An investigation of tenascin-C levels in rheumatic mitral stenosis and their response to percutaneous mitral balloon valvuloplasty.

OBJECTIVE: The purpose of this study was to evaluate the tenascin-C levels in severe rheumatic mitral stenosis before and after percutaneous mitral balloon valvuloplasty (PMBV). SUBJECTS AND METHODS: Forty patients with severe mitral stenosis requiring PMBV and 20 age-matched healthy subjects were included in the study. The mitral valve areas, mitral gradients and systolic pulmonary artery pressure (sPAP) were measured by echocardiography. The sPAP values and mitral gradients were also measured by catheterization before and after PMBV. The blood tenascin-C levels were measured before PMBV and 1 month after the procedure. RESULTS: The echocardiographic mean mitral gradients had a significant decrease after PMBV (11.7 ± 2.8 vs. 5.6 ± 1.7 mm Hg; p < 0.001) and also those of catheterization (13.9 ± 4.4 vs. 4.0 ± 2.4 mm Hg; p < 0.001). Mitral valve areas increased significantly after PMBV (from 1.1 ± 0.1 to 1.8 ± 0.2 cm(2), p < 0.001). Tenascin-C levels decreased significantly in patients after PMBV (from 15.0 ± 3.8 to 10.9 ± 3.1 ng/ml; p < 0.001). Tenascin-C levels were higher in patients with mitral stenosis before PMBV than in healthy subjects (15.0 ± 3.8 and 9.4 ± 2.9 ng/ml; p < 0.001, respectively). There were no significant differences between patients with mitral stenosis after PMBV and healthy subjects (10.9 ± 3.1 and 9.4 ± 2.9 ng/ml; p = 0.09, respectively). There was a significant positive correlation between tenascin-C levels and sPAP (r = 0.508, p < 0.001). In multivariant analysis, tenascin-C predicted mitral stenosis (p = 0.004, OR: 2.31). CONCLUSIONS: Tenascin-C was an independent predictor for rheumatic mitral stenosis.

Effect of overweight and obesity on the left ventricular systolic and diastolic functions in patients with acute myocardial infarction.

PURPOSE: The purpose of this study was to evaluate whether a association exits among overweight and obesity and left ventricular systolic and diastolic functions in patients admitted with first ST-elevation myocardial infarction (STEMI). METHODS: The present study was performed on 451 consecutive patients diagnosed with first STEMI (376 men, 75 women; mean age 56.1 ± 10.8 years). The patients were classified into three groups based on their body mass index (BMI) as normal weight (BMI < 25 kg/m2), overweight (BMI: 25-29.9 kg/m2) and obese (BMI > 30 kg/m2). Echocardiographic features were evaluated and compared among the three groups. RESULTS: Mitral annulus E velocities were higher in obese individuals than normal weight group (p < 0.01). In contrast, mitral A velocities were lower (p =0.03); consequently, E\A and E'\A' ratios were lower (both p = 0.01) in the obese group with respect to normal weight group. When the correction of entire variations existing among the groups were performed using multivariate linear regressions analyses, it turned out that BMI was independently associated with E/A (ß = -0.19, p = 0.044) and with E'/A' (ß = -0.016, p = 0.021). Ejection fraction, wall motion score index and myocardial S velocities were comparable among the study groups (p > 0.05). CONCLUSION: These results suggest that while obesity has no adverse effect on the left ventricular systolic function, it has unfavorable consequences on the left ventricular diastolic function in the patients with first STEMI. In contrast, no unfavorable effects of overweight on the left ventricular systolic and diastolic function were detected.

Relationship between platelet indices and spontaneous echo contrast in patients with mitral stenosis.

AIMS: To determine the association of platelet indices with spontaneous echo contrast (SEC) in patients with mitral stenosis. METHODS AND RESULTS: A total of 232 consecutive patients with mitral stenosis who undergoing mitral balloon valvuloplasty were enrolled to the study. Patients were divided into two groups according to the formation of SEC in the left atrium. Group 1: mitral stenosis complicated with SEC; Group 2: mitral stenosis without SEC. Transthoracic echocardiography and transoesophageal echocardiography were performed for each patient. Complete blood counting parameters were measured and all routine biochemical tests were performed. There were 133 patients (mean age 42 ± 11 and 74% female) in the SEC(-) group and 99 patients (mean age 45 ± 10 and 64% female) in the SEC(+) group. Plateletcrit (0.25 ± 0.06 vs. 0.27 ± 0.07, P = 0.043) and mean platelet volume (MPV) levels (9.4 ± 1.1 vs. 10.4 ± 1.2, P < 0.001) were significantly higher in the SEC(+) group. When we divided the SEC(+) patients into four subgroups according to previously reported criteria, MPV levels increased to correlate with the degree of SEC (P < 0.001). At multivariate analysis, MPV levels [odds ratio (OR) 2.365, 95% confidence interval (CI) 1.720-3.251; P < 0.001] and PCT levels (OR 2.699, 95% CI 1.584-4.598; P= 0.033) are independent risk factors of SEC in patients with mitral stenosis. CONCLUSION: In patients with mitral stenosis, cheaply and easily measurable platelet indices including MPV and PCT levels are associated with the presence of SEC and are independent risk factors of SEC.

Relationship between mean platelet volume levels and subclinical target organ damage in newly diagnosed hypertensive patients.

BACKGROUND: Significant numbers of asymptomatic hypertensive patients are attacked by subclinical target organ damage (TOD) such as proteinuria, left ventricular hypertrophy and carotid atherosclerosis. Platelets become activated in uncontrolled hypertension and play a crucial role in increased thrombotic tendency. Mean platelet volume (MPV) is one of the markers that correlate closely with platelet activity. We aimed to investigate the relationship between MPV levels and subclinical TOD in newly diagnosed hypertensive patients. METHODS: 80 newly diagnosed hypertensive patients were enrolled to this cross-sectional study. Ambulatory blood pressure monitoring was performed for all patients. Left ventricular mass index (LVMI), carotid intima-media thickness (IMT) and urine albumin/creatinine ratio (UACR) were measured as indices of cardiac, vascular and renal damage, respectively. MPV was measured from blood samples collected in EDTA tubes and high-sensitivity C reactive protein (hs-CRP) was measured by using nephlometer. RESULTS: MPV was significantly correlated with 24-h systolic-diastolic blood pressure (r = 0.52 and r = 0.55, respectively). Correlation analysis indicated that MPV was moderately related with UACR, LVMI, carotid IMT and hs-CRP (r = 0.50, r = 0.55, r = 0.60 and r = 0.69, respectively, p = 0.0001). Multivariable analysis identified that MPV levels were independently associated with severity of proteinuria, carotid IMT and LVMI (p = 0.001). CONCLUSION: Our findings suggested that MPV levels were associated with severity of subclinical TOD including; carotid atherosclerosis, left ventricular hypertrophy and renal damage, in hypertensive patients. In addition to this, MPV levels were significantly correlated with hs-CRP levels and 24-h ambulatory blood pressure measurements.

Effect of long-term and high-dose allopurinol therapy on endothelial function in normotensive diabetic patients.

OBJECTIVES: Endothelial dysfunction is a well known risk factor for atherosclerosis. Uric acid levels are associated with endothelial dysfunction and atherosclerosis even if in physiological range. Xanthine oxidase inhibition with allopurinol decreases uric acid levels and oxidative stress and improves endothelial function. We have investigated the effect of high-dose and long-term allopurinol therapy on endothelial function in diabetic normotensive patients. METHODS: This study is a randomized, single-blind, placebo-controlled trial. Both treatment and placebo groups consisted of 50 patients. In the treatment group, daily oral 900 mg allopurinol was started after randomization and maintained for 12 weeks. Brachial artery flow-mediated dilatation (FMD) and nitrate-induced dilatation (NID) were measured at baseline and after the allopurinol therapy to evaluate endothelial function. RESULTS: HbA1c and uric acid levels decreased after allopurinol therapy (6.1 ± 2.1 vs 5.5 ± 1.0%, 5.0 ± 0.8 vs 3.3 ± 0.5 mg/dl, respectively, p = 0.01) but no change was observed in the placebo group (7.7 ± 1.9% vs 7.6 ± 2.0%, 5.3±2.1 vs 5.6 ± 0.8 mg/dl, respectively, p > 0.05). FMD and NID increased significantly in the treatment group (5.6 ± 2.1% vs 8.5 ± 1.2%, 10 ± 7.4% vs 14 ± 4.0%, 10 ± 7.4% vs 14 ± 4.0%, respectively, p = 0.01), whereas no change was observed in the placebo group (5.8 ± 1.8% vs 6.1 ± 0.8%, 12 ± 9.5 vs 10 ± 3.8%, respectively, p > 0.05). CONCLUSION: Long-term and high-dose allopurinol therapy significantly improved endothelial function in diabetic normotensive patients. In addition, allopurinol therapy contributes to the lower HbA1c levels.

Left ventricular strain and strain rate echocardiography analysis in patients with total and subtotal occlusion in the infarct-related left anterior descending artery.

BACKGROUND: Numerous studies show that percutaneous coronary intervention has no clinical benefit in patients with total occlusion. Both regional and global left ventricle (LV) functions may be evaluated in detail by strain (S) and strain rate (SR) echocardiography. The purpose of this study is to evaluate whether S and SR echocardiography may be used to determine the total occlusion. METHOD: Sixty stable patients who have total or subtotal occlusion in the infarct-related left anterior descending artery were enrolled (Total occlusion group: 35 and subtotal occlusion group: 25 patients). In all patients, LV longitudinal S and SR data were obtained from total 14 segments. RESULTS: S values of middle and apical segments of LV were significantly lower in the total occlusion groups. In SR analysis, middle and apical values of all walls were significantly different between the groups. The total SR of the middle and apical segments was significantly lower in the total occlusion group (respectively, total SR in middle segments: -3.4 ± 0.8% vs. -4.6 ± 1.0%, P < 0.00001 and total SR in apical segments: -1.7 ± 0.5% vs. -2.8 ± 0.6%, P = 0.001). The total SR values of four walls were also significantly lower in the total occlusion group (-10.3 ± 2.0% vs. -13 ± 3.1%, P < 0.0001). For predicting total occlusion, the highest sensitivity levels (84%) were obtained in SR of middle-anterior segment. SR of middle-septum and middle-lateral segments has the highest specificity levels (86%). CONCLUSION: Total occlusion in stable patients with acute coronary syndrome has an unfavorable effect on the LV regional and global functions. Patients with total occlusion may be identified by S and SR echocardiography.

Acute postinfectious glomerulonephritis with native aorta valve endocarditis and myopericarditis due to brucellosis.

Human brucellosis is a systemic disease that involves multiple organs and tissues concomitantly. In this case, we describe a patient with pancarditis and nephrotic syndrome requiring hemodialyses, which is an unusually fatal condition resulting from brucellosis. He was successfully treated with early aortic valve replacement and intensive medical therapy.

Effects of nebivolol therapy on endothelial functions in cardiac syndrome X.

Endothelial dysfunction is major pathophysiologic mechanism in cardiac syndrome X (CSX), which causes a decrease in plasma nitrite oxide (NO) levels. It was demonstrated that nebivolol improves endothelial function and increases NO release. Despite this pathophysiologic relation, the effect of nebivolol therapy on endothelial function in patients with CSX is unknown. The aim of this study is to evaluate the effect of nebivolol on patients in CSX. Thirty-eight patients who were diagnosed with CSX were prospectively enrolled in the study. The treatment group consisted of 20 patients and the control group consisted of 18 patients. An oral 5-mg dose of nebivolol was given daily and maintained for 4 weeks in the treatment group. Ultrasonographic parameters (brachial artery flow-mediated dilatation [FMD], brachial artery lumen diameters) and inflammatory markers (high-sensitivity C-reactive protein [hsCRP], von Willebrand factor [vWf], and fibrinogen) were measured at baseline and end of the 4 weeks. Brachial baseline lumen diameter, brachial lumen diameter after reactive hyperemia, and FMD were 4.61 +/- 0.49 mm, 4.87 +/- 0.53 mm, and 5.6% +/- 2.3% at baseline. After the nebivolol therapy, there was a significant increase in both brachial artery baseline lumen diameter and lumen diameter after reactive hyperemia (P < 0.001 and P = 0.002). However, there was no significant change in FMD (5.6% +/- 2.2% vs 5.3% +/- 2.1%, P not significant). Levels of hsCRP, vWf, and fibrinogen were significantly decreased (hsCRP: 3.4 +/- 0.49 mg/dl vs 2.97 +/- 0.74 mg/dl, P = 0.001; vWf: 107 +/- 62 vs 86 +/- 58, P = 0.004; fibrinogen: 341 +/- 89 mg/dl vs 299 +/- 87 mg/ dl, P = 0.01) in the treatment group. Nebivolol therapy may have a favorable effect on endothelial function in CSX. Further studies are needed to confirm the clinical significance of nebivolol therapy in CSX.

The mean platelet volume in patients with non-dipper hypertension compared to dippers and normotensives.

OBJECTIVES: Increased platelet activation plays an important role in the development of atherosclerosis. Mean platelet volume (MPV) is a determinant of platelet activation. In our study, we aimed to determine whether MPV levels are elevated in non-dipper patients compared with dippers and healthy controls. In addition, we tried to find out if MPV levels are correlated with blood pressure measurements in hypertensive patients. METHODS: This cross-sectional study included 56 hypertensive patients; 27 age- and sex-matched healthy volunteers were enrolled to study as a control subjects. Ambulatory blood pressure monitoring was performed for all patients. Hypertensive patients were divided into two groups: 28 dipper patients (10 male, mean age 51 +/-8 years) and 28 non-dipper patients (11 male, mean age 53+/-10 years). MPV was measured in a blood sample collected in EDTA tubes and was also used for whole blood counts in all patients. RESULTS: In non-dipper patients, 24-h systolic blood pressure (141.5+/-10.21 vs 132.3+/-7.7 mmHg, p<0.001), 24-h diastolic blood pressure (88.2+/-8.5 vs 81.0+/-8.2 mmHg, p<0.01) and 24-h average blood pressure (105.7+/-8.5 vs 97.7+/-7.4 mmHg, p<0.001) are significantly higher than dippers. Whereas daytime measurements were similar between dippers and non-dippers, there was a significant difference between each group during night-time measurements (night-time systolic 137.1 +/-11.0 vs 120.2+/-8.0 mmHg, p<0.001; night-time diastolic 85.3+/-8.0 vs 72.8+/-7.9 mmHg, p<0.001). Non-dipper patients (9.61 +/-0.42 fl) demonstrated higher levels of MPV compared with dippers (9.24+/-0.35 fl) and normotensives (8.87+/-0.33 fl) (p<0.001 and p<0.001, respectively). There was significant correlation between MPV and ambulatory diastolic and systolic blood pressure in non-dipper hypertensives. CONCLUSION: Our results suggest that MPV, a determinant of platelet activation, has a positively correlation with blood pressure and elevated in non-dipper compared with dippers and controls. Increased platelet activation could contribute to increase the atherosclerotic risk in non-dipper patients compared with dippers.

Effects of atorvastatin and lisinopril on endothelial dysfunction in patients with Behçet's disease.

OBJECTIVE: Behçet's disease is a chronic inflammatory vasculitis. Vascular involvement is one of the major complications of Behçet's disease, during the course of the disease. Previous studies showed that ACE inhibitors and statins may improve endothelial functions in endothelial dysfunction. The aim of our study is to compare the effects of atorvastatin and lisinopril to placebo on endothelial dysfunction in patients with Behçet's disease. PATIENTS AND METHODS: We prospectively studied 92 (48 female) Behçet's patients who were diagnosed according to the International Study Group criteria. Endothelial dysfunction was evaluated by brachial artery flow-mediated dilatation (FMD) method using high-resolution vascular ultrasound device at baseline and after for 3-month therapy. Patients were consecutively randomized into three groups as (atorvastatin (n = 31), lisinopril (n = 31), and placebo groups (n = 30). Patients in atorvastatin group received 20 mg atorvastatin, lisinopril group received 10 mg lisinopril per day, and placebo group received placebo per day for 3 months. RESULTS: The baseline characteristics of patients were similar among three groups; however, high-sensitive C-reactive protein (hs-CRP) levels were lower in atorvastatin group than placebo group. A significant improvement in FMD was observed in both atorvastatin (5.0 ± 1.4 vs. 12.8 ± 3.6%, P < 0.001) and lisinopril groups (5.0 ± 1.2 vs. 11.4 ± 5.0%, P < 0.001). Partial significant enhancement was observed in placebo group (4.9 ± 1.1% vs. 5.7 ± 1.0, P = 0.002). However, it was lower than the cutoff value for endothelial dysfunction. CONCLUSION: These findings suggest that atorvastatin and lisinopril improve endothelial functions in Behçet's disease patients. However, large studies are needed to determine the long-term effects of atorvastatin and lisinopril therapy.

The relationship between admission hemoglobin level and left ventricular systolic functions in patients with first ST-segment elevated myocardial infarction.

OBJECTIVES: The goal of this study was to evaluate the relationship between admission hemoglobin levels and left ventricular systolic functions in patients admitted with first ST-segment elevated myocardial infarction (STEMI). STUDY DESIGN: The study was conducted prospectively in three centers in 483 consecutive patients (402 men, 81 women; mean age 56.5 ± 11.2 years; range 24 to 74 years) with first STEMI. All patients were evaluated by echocardiography after a mean of 2.4 days of admission. Evaluation of left ventricular systolic functions included measurements of ejection fraction (EF), wall motion score index (WMSI), and tissue Doppler S wave velocities at four different localizations (anterior, inferior, lateral, posterior septum). Hemoglobin levels were measured within one hour of admission. Anemia was defined according to the World Health Organization criteria (hemoglobin < 13.0 g/dl in men and < 12.0 g/dl in women). Echocardiographic characteristics of the patients with and without anemia were compared. RESULTS: Anemia was detected in 67 patients (13.9%). There were no significant differences between patients with and without anemia with respect to left ventricular end-systolic and end-diastolic diameters, wall thickness, WMSI, and EF. The mean EF in the anemic group (47.5%) was lower than that of the patients without anemia (48.5%), but this difference was not significant. All Sm velocities were lower in the anemic group, but only septal mitral annular Sm velocity reached statistical significance (p = 0.048). There was no correlation between hemoglobin levels and EF (r = 0.027, p = 0.55). CONCLUSION: Our findings suggest that mild to moderate anemia has no deleterious effect on systolic function in patients with first STEMI.

Effects of chronic obstructive pulmonary disease on coronary atherosclerosis.

The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 +/- 0.6 in the COPD group and 2.1 +/- 0.7 in the control group (P = 0.004). The mean Extent score was 37 +/- 16 in the COPD group and 23 +/- 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 +/- 6.3 vs 6.6 +/- 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682-9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023-13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.

The deletion polymorphism of the angiotensin-converting enzyme gene is associated with acute aortic dissection.

Aortic dissection (AD) is a disease characterized by tear of the aortic intimal layer and separation of the arterial wall. Some risk factor such as hypertension and Marfan syndrome is well known in AD. However, the role of genetic factors in AD is largely unknown. Insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene is associated with cardiovascular diseases; patients with D allele have higher serum and tissue ACE levels. We investigated the relationship between the I/D polymorphism of the ACE gene and non-syndromic acute AD. Sixteen patients diagnosed with AD were included in the study (mean age: 60.1 +/- 6.2 years). The diagnosis was established by clinical evaluation and imaging techniques. The control group consisted of 22 age-matched patients without AD (60.9 +/- 7.3 years), who suffered from chest pain. Incidence of hypertension was similar in dissection and control groups (62% vs. 59%). The I/D polymorphism was investigated in both groups by PCR analysis. Dissection types according to the DeBakey classification were identified as type 1 (proximal + distal) in 7 patients (43%), type 2 (proximal) in 5 patients (31%), and type 3 (distal) in 4 patients (25%). The D/D and D/I polymorphisms are present in 13 and 3 AD patients, respectively. None of patients with AD have the II polymorphism. The frequencies of the D allele (DD + ID) are significantly higher in dissection group than control (100% vs. 68%, P < 0001). These results indicate that the D allele of ACE gene is a risk factor for AD.

The relationship between slow coronary flow and angiotensin converting enzyme and ATIIR1 gene polymorphisms.

OBJECTIVES: Endothelial dysfunction in coronary arteries is the main pathogenetic mechanism in patients with slow coronary flow (SCF). Angiotensin converting enzyme (ACE) gene polymorphism has important effects on endothelial function. However, angiographic studies investigating the relation between the ACE and angiotensin II type 1 receptor (ATIIR1) insertion (I)/deletion (D) polymorphism and SCF is limited. METHODS: Fifty-four patients with normal coronary arteries documented by coronary angiography with SCF in any coronary vessel, and 22 subjects with normal coronary arteries without SCF were included in this study. The ID (I/D), II, and DD genotypes were examined. RESULTS: Frequency of DD genotype was found higher in SCF group (50% vs. 27%, respectively; p = .055). Frequency of D allele was significantly higher in the SCF group (p < .05). Presence of DD genotypes increased the possibility of SCF 5.25 times compared to absence of DD genotype (OR, 5.25; 95% CI, 1.30-21.38, p < .05). There was no significant correlation of ATIIR1 gene polymorphism between the 2 groups. CONCLUSIONS: We demonstrated that DD genotype is a risk factor for SCF. Determination of ACE gene polymorphism in patients with SCF may be helpful in medical management and risk stratification.

[A case of aortic coarctation mimicking interrupted aorta]. / Kesintili aort izlenimi veren aort koarktasyonu.

An asymptomatic, healthy, 19-year-old male patient was examined for aortic coarctation upon detection of a heart murmur and hypertension on routine physical examination. Transthoracic echocardiography (TTE) showed rupture of the sinus of Valsalva and bicuspid aortic valve. Findings of aortography and computed tomography (CT) angiography were compatible with an interrupted aorta. For further delineation, transesophageal echocardiography (TEE) was performed and color Doppler imaging showed passage at the site of the descending aorta, which was suggestive of interruption by other imaging methods. The patient underwent surgery for aortic coarctation. At surgery, severe aortic coarctation was noted and corrected. Although TTE is usually adequate for the diagnosis of aortic coarctation, even aortography and CT angiography were misleading in this particular case, and differentiation from interrupted aorta was only possible by TEE.