Mehmet Tugrul Inanc

High levels of serum uric acid predict severity of coronary artery disease in patients with acute coronary syndrome.

We aimed to elucidate the relation between serum uric acid (SUA) level and severity of coronary artery disease (CAD) in nondiabetic, nonhypertensive patients (n = 246) with acute coronary syndrome (ACS). Severity of CAD was assessed by the Gensini score. One, 2, and 3 or more diseased vessels were identified in 87 (35.4%), 55 (22.4%), and 104 (42.2%) patients, respectively. Patients with hyperuricemia had higher Gensini score, high number of diseased vessels, critical lesions, and total occlusion. Serum uric acid level was significantly associated with number of diseased vessels. Serum uric acid was an independent risk factor for multivessel disease by univariate analysis. High levels of SUA associated with the severity of CAD in nondiabetic, nonhypertensive patients with ACS.

The relationship between Helicobacter pylori IgG titre and coronary atherosclerosis.

Objectives — The role of Helicobacter pylori (HP) in the progression of atherosclerosis is con-troversial.We investigated the relation between HP IgG antibody titres and severity and intensity of coronary atherosclerosis and also clinical presentation of coronary artery disease (CAD). Methods — The patient group consisted of 353 patients with angiographically proven CAD, which contains 3 different subgroups: 163 patients with myocardial infarction (MI), 106 patients with unstable angina (USAP) and 84 patients with stable angina (SAP). Control group included 163 subjects with angiographically proven normal coronary arteries. Helicobacter pylori IgG antibody titres were measured by an enzyme immunoassay method in all patients. Gensini and Extent scores were used to evaluate the angiographic severity and extent of atherosclerosis. C-reactive protein levels were measured by Behring nephelometry system kits. Results — Seropositivity rates for HP were similar between groups (82.7% in the patient group and 86.6% in the control group (P > 0.05)). Also HP-IgG levels were similar among the MI, USAP and SAP groups. No significant correlation was observed between CRP levels and HP-IgG level titres. There was no significant correlation between HP-IgG level (r = 0.086, P = 0.2) and Gensini score but a significant poor correlation was observed between HP-IgG level and Extent score (r = + 0.156, P = 0.03). Conclusions — Helicobacter pylori IgG titres do not play an important role in the presentation of CAD and do not increase systemic inflammatory response. However, Helicobacter pylori IgG antibody titres may be correlated with the extent of CAD.

Effects of Atorvastatin and Lisinopril on Endothelial Dysfunction in Patients with Behçet's Disease

Objective: Behçets disease is a chronic inflammatory vasculitis. Vascular involvement is one of the major complications of Behçets 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 Behçets disease. Patients and methods: We prospectively studied 92 (48 female) Behçets 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 Behçets disease patients. However, large studies are needed to determine the long‐term effects of atorvastatin and lisinopril therapy. (Echocardiography 2010;27:997‐1003)

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.

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.

Acute Effects of Passive Smoking on Left Ventricular Systolic and Diastolic Function in Healthy Volunteers

BACKGROUND The aim of this study was to investigate the acute effects of passive smoking on left ventricular (LV) function in healthy volunteers. METHODS Sixty-one healthy nonsmoking volunteers were enrolled in this study. LV M-mode, two-dimensional, conventional Doppler, and color tissue Doppler echocardiography were performed, and carboxyhemoglobin (COHb) levels were obtained from subjects before and immediately after exposure to passive smoking for 30 min in a smoking room. The differences between baseline and post-smoke exposure measurements of transmitral E and mitral annular Em velocities, heart rate, systolic blood pressure, diastolic blood pressure, and COHb levels were assessed. RESULTS Mean COHb levels were statistically higher after exposure. There were no changes in LV systolic function and volumes. LV diastolic function changed significantly immediately after passive smoking. The transmitral E wave (0.89 ± 0.12 vs 0.70 ± 0.14 m/sec, P = .001), the pulmonary venous D wave (0.52 ± 0.12 vs 0.49 ± 0.13 m/sec, P = .01), and the transmitral E/A ratio 1.79 ± 0.48 vs 1.47 ± 0.32, P = .001) decreased, while the transmitral A wave did not change. The mitral annular Em velocity decreased (12.5 ± 2.1 vs 11.7 ± 1.9 cm/sec, P = .001), the Am velocity increased (6.3 ± 2.1 vs 6.8 ± 1.6 cm/sec, P = .001), and the Em/Am ratio decreased (2.28 ± 0.82 vs 1.78 ± 0.42, P = .001). Color Doppler echocardiography determined diastolic impairment in only women, whereas color tissue Doppler echocardiography demonstrated diastolic dysfunction in both genders. Acute deleterious effects of passive smoking on color Doppler echocardiographic parameters were more prominent in women. Change in E was related to changes in heart rate and systolic blood pressure and with COHb levels, while change in Em was related only to COHb levels. CONCLUSIONS Acute exposure to passive smoking impairs LV diastolic function in healthy volunteers. The mechanism whereby passive smoking affects diastolic function is probably complex; however, carbon monoxide exposure and an increment in COHb level may be among the causes.

Two daytime icodextrin exchanges decrease brain natriuretic peptide levels and improve cardiac functions in continuous ambulatory peritoneal dialysis patients

Aim:  Peritoneal dialysis patients with ultrafiltration failure frequently have fluid overload. It is known that the increase in the ultrafiltration is associated with decrease in the left ventricle (LV) dysfunction. This study was designed to examine the potential effects of serum brain natriuretic peptide (BNP) on cardiac functions and to determine the relationship between BNP and cardiac parameters in continuous ambulatory peritoneal dialysis (CAPD) patients with ultrafiltration failure.

Acute effects of intracoronary nitroglycerin and diltiazem in coronary slow flow phenomenon.

Background The coronary slow flow phenomenon (CSFP) is a coronary microvascular disorder angiographically defined by delayed opacification of the distal vasculature in the absence of obstructive coronary artery disease. We aimed to investigate and compare the effects of intracoronary nitrate and diltiazem on thrombolysis in myocardial infarction frame count (TFC) in patients with CSFP during coronary angiography. Methods Sixty patients with CSFP were randomly divided into 2 groups. The first group is nitroglycerin group with 30 patients (22 men; mean [SD] age, 50 [12] years), and the second is diltiazem group with 30 patients (27 men; mean age, 54 ± 11 years); intracoronary 5-mg diltiazem or 250-μg nitroglycerin was administered. Heart rate, systolic and diastolic blood pressures, and TFCs in all 3 coronaries were recorded before and after administering these medications. Results After nitroglycerin administration, systolic and diastolic blood pressures decreased, heart rates significantly increased, and TFCs decreased in all coronaries (P < 0.001 for 3 coronaries). After the application of intracoronary 5-mg diltiazem, heart rate, systolic and diastolic blood pressures, and TFCs were found significantly lower than predrug values (P < 0.001 for all values). When the percent TFC reductions, after the application of intracoronary diltiazem or nitroglycerin, in left anterior descending coronary artery, circumflex coronary artery, and right coronary artery were evaluated, diltiazem significantly reduced the TFCs of the left anterior descending coronary artery and circumflex coronary artery compared with nitroglycerin (P < 0.01 for both coronaries). Conclusion Both intracoronary diltiazem and nitroglycerin improve the TFCs in CSFP, and intracoronary diltiazem is superior to nitroglycerin in reducing TFCs in CSFP.

The Importance of Cardiac Biomarkers on Remodelling After Myocardial Infarction

Background The purpose of this study is to evaluate the importance of tenascin-C ( TNC), N-terminal pro brain natriuretic peptide (NT-proBNP) and C-reactive protein (CRP) on LV remodelling after myocardial infarction (MI). Methods Fifty-seven stable patients with subacute anterior MI who had total or subtotal occlusion in the infarct-related left anterior desending artery in coronary angiography were enrolled the study. 18 of patients who had total occlusion received only medical theraphy, 19 of patients who had total occlusion received successful PCI+ medical theraphy and 20 of patients who had subtotal occlusion received successful PCI+ medical theraphy. Left ventricular volumes and ejection fractions (EF) were measured with echocardiography. Serum TNC, NT-proBNP and CRP levels were measured at admission and a month after treatment. Results There was significant increase in LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) baseline to follow-up in total-PCI group. Baseline to follow-up; a borderline significant increase was observed in LVEDV in the total-medical group. No significant difference was seen in LV volumes and EF in the subtotal-PCI group. NT-proBNP, TNC and CRP levels were decreased in all groups. The decrease in NT-proBNP and CRP values were significant in the total-medical and subtotal-PCI group but in the total-PCI group they were not significant. The decrease of TNC was significant in all groups but the lowest decrease was seen in the total-PCI group. Conclusion TNC, NT-proBNP and CRP reflect LV remodelling in accordance with echocardiography after MI. Keywords Tenascin-C; NT-pro BNP; CRP; Remodelling; Myocardial infarction

Effect of maintenance hemodialysis on diastolic left ventricular function in end-stage renal disease

PURPOSE To analyze the effect of maintenance hemodialysis on left ventricular diastolic function in patients with end-stage renal disease. METHODS Study population consisted of 42 patients with end-stage renal disease. Before an arteriovenous fistula was surgically created, the patients were evaluated by conventional and Doppler echocardiography and Doppler tissue imaging. Then, the patients undergoing hemodialysis treatment when the arteriovenous fistula was compleated. After the first hemodialysis session (mean 76.14 ± 11.37 days) the second echocardiographic evaluations were performed. RESULTS Mean age was 58 ± 13 years and 21 (%50) of the patients were female. After maintenance hemodialysis treatment; peak early (E) and peak late (A) diastolic mitral inflow velocities and E/A ratio were not significantly change however the deceleration time of E wave and left atrial diameter were significantly increased. Also there was no change in the early (Em) and late (Am) diastolic myocardial velocities and Em/Am ratios of lateral and septal walls of left ventricular. E/Em ratio was decreased insignificantly. Pulmonary vein velocities and right ventricular functions are remained almost unchanged after hemodialysis treatment. DISCUSSION The acute and long-term effect of hemodialysis on left ventricular diastolic function is unclearly. Patients with end-stage renal disease treatment with hemodialysis via arteriovenous fistula experience a variety of hemodynamic and metabolic abnormalities that predispose to alterations in left and right ventricular functions. The present study showed that left ventricular diastolic function except left atrial diameter and right ventricular functions were not significantly change, however left ventricular systolic functions were impaired after maintenance hemodialysis treatment in patients with end-stage renal disease. CONCLUSION It has been suggested that echocardiographic parameters are useful markers for evaluation of left ventricular and right ventricular functions in patients with end-stage renal disease. However, in patients with endstage renal disease treated with hemodialysis, repeated assessment of echocardiographic examinations to observe serial changes in left and right ventricular functions are not yet well established. In this study, we showed that acute changes of volume status and electrolytes and autonomic regulation by hemodialysis session did not affect left ventricular diastolic and right ventricular functions in a relatively long term.