Evaluation of left atrial mechanical function and atrial conduction abnormalities in Maras powder (smokeless tobacco) users and smokers.

OBJECTIVE: In Turkey, a type of smokeless tobacco called Maras powder (MP) is widely used in the south-eastern region. Smokeless tobacco is found in preparations for chewing and for absorption by the nasal and oral mucosae. The purpose of this study was to investigate whether MP damages intra- and inter-atrial conduction delay and left atrial (LA) mechanical function as much as cigarette smoking. METHOD: A total of 150 chronic MP users (50 males, 32.5 ± 5.4 years), smokers (50 males, 32.1 ± 6.0 years) and controls (50 males, 30.1 ± 5.8 years) were included in the study. LA volumes were measured echocardiographically according to the biplane area-length method. Atrial electromechanical coupling was measured with tissue Doppler imaging and LA mechanical function parameters were calculated. RESULTS: The LA passive emptying fraction was significantly decreased and LA active emptying volume (LAAEV) was significantly increased in the MP group (p = 0.012 and p = 0.024, respectively), and the LA active emptying fraction (LAAEF) was significantly increased in the smokers (p = 0.003). There was a positive correlation between the amount of MP used and smoking (pack years) with LAAEV and LAAEF (r = 0.26, p = 0.009 and r = 0.25, p = 0.013, respectively). Lateral atrial electromechanical intervals (PA) were significantly higher in MP users, and the septal mitral PA was statistically higher in the smokers (p = 0.05 and p = 0.04, respectively). CONCLUSION: We suggest that atrial electromechanical coupling intervals were prolonged and LA mechanical function was impaired in MP users and smokers, but there was no significant difference between the MP users and smokers. These findings may be markers of subclinical cardiac involvement and tendency for atrial fibrillation.

Cardiac effects of chronic graft-versus-host disease after stem cell transplantation.

Chronic graft-versus-host disease (GVHD) develops as a result of the immunologic response that donor T-lymphocytes generate against host tissue after allogeneic stem cell transplantation. We tried to elucidate the contribution of cardiac dysfunction to the high morbidity and mortality rates observed after GVHD. Forty patients who had undergone bone marrow transplantation were enrolled in this prospective study: 14 patients who had been diagnosed with chronic GVHD (manifestations beyond day 100 after hemopoietic cell transplantation) and 26 patients who had not. All patients had undergone baseline echocardiography before bone marrow transplantation and were monitored. After the expected period of time had elapsed for GVHD after transplantation, these patients were divided into 2 groups in accordance with whether or not they developed chronic GVHD. No significant differences were observed before bone marrow transplantation in the 2 groups' broad attributes or in their laboratory and echocardiographic findings (P >0.05). After transplantation, high-sensitivity C-reactive protein levels and erythrocyte sedimentation rates were significantly higher in the chronic GVHD group (P < 0.001 and P=0.01, respectively). Mean left ventricular mass was 227 ± 32.3 g in the GVHD group and 149.3 ± 27.4 g in the non-GVHD group (P < 0.001). The E/A flow rate was significantly higher in the non-GVHD group. This study shows that chronic GVHD increases left ventricular mass and impairs left ventricular diastolic function in patients who have developed chronic GVHD. In addition, it shows that inflammatory markers increase to higher levels in these patients. Comprehensive studies with larger samples are needed to more fully elucidate the cardiac effects of this disease.

Protective effects of nebivolol against anthracycline-induced cardiomyopathy: a randomized control study.

BACKGROUND: We aimed to evaluate the effect of prophylactic nebivolol use on prevention of antracycline-induced cardiotoxicity in breast cancer patients. METHODS: In this small, prospective, double-blind study, we randomly assigned 45 consecutive patients with breast cancer and planned chemotheraphy to receive nebivolol 5mg daily (n=27) or placebo (n=18). Echocardiographic measurements and N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels were obtained at baseline and at 6-month of chemotherapy. RESULTS: Both studied groups had comparable echocardiographic variables and NT-pro-BNP levels at baseline. At 6-month, the left ventricular (LV) end-systolic and end-diastolic diameters increased in the placebo group (LVESD: 29.7 ± 3.4 to 33.4 ± 4.5mm; LVEDD: 47.2 ± 3.8 to 52.0 ± 4.6mm, p=0.01 for both) but remained unchanged in the nebivolol group (LVESD: 30.4 ± 3.5 to 31.0 ± 3.6mm, p=0.20; LVEDD: 47.0 ± 4.4 to 47.1 ± 4.0mm, p=0.93). The placebo group also had lower LVEF than the nebivolol group (57.5 ± 5.6% vs. 63.8 ± 3.9%, p=0.01) at 6-month. NT-pro-BNP level remained static in the nebivolol group (147 ± 57 to 152 ± 69 pmol/l, p=0.77) while it increased in the placebo group (144 ± 66 to 204 ± 73 pmol/l, p=0.01). CONCLUSIONS: Prophylactic use of nebivolol treatment may protect the myocardium against antracycline-induced cardiotoxicity in breast cancer patients.

Assessment of aortic elastic properties in patients with sarcoidosis.

BACKGROUND: Sarcoidosis is an inflammatory granulomatous disease of unknown etiology that involves multiple organ systems. Many studies have shown a strong relationship between inflammation and atherosclerosis. The aim of this study is to investigate the relationship between elastic properties of the aorta and the duration of the disease in patients with sarcoidosis. METHOD: The study population included 52 patients with sarcoidosis (22 men, mean age = 42.7 ± 10.7 years, and mean disease duration = 38.8 ± 10.8 months) and 50 healthy control subjects (18 men, and mean age = 42.0 ± 8.0 years). Aortic stiffness (ß) index, aortic strain (AoS) and aortic distensibility (AoD) were calculated from the aortic diameters measured by transthoracic echocardiography and blood pressure obtained by sphygmomanometer. Cardiac functions were determined by using routine echocardiographic evaluation consist of standard two-dimensional and conventional Doppler and tissue Doppler imaging. RESULTS: The conventional echocardiographic parameters were similar between patients and controls. There were significant differences between the control and the patient groups in ß index (1.63 ± 0.55 vs 2.44 ± 1.54, p = 0.001), AoS (15.61 ± 5.69 vs 10.93 ± 4.11%, p < 0.001) and AoD (6.35 ± 2.64 vs 4.66 ± 1.98, 10 (-6) cm(2)/dyn, p = 0.001). There were statistically significant negative correlations between the disease duration and AoD (r = -0.46, p = 0.01) and AoS (r= -0.44, p = 0.002), whereas there was a positive correlation between the disease duration and ß index (r = 0.37, p = 0.01). In multivariate analysis, disease duration was significantly related with AoD, AoS and ß index (respectively, RR = 3.28, p = 0.002; RR = 3.03, p = 0.004; RR = 2.39, p = 0.02). CONCLUSION: We observed that elastic properties of the aorta alter in patients with sarcoidosis. We also have demonstrated a statistically significant correlation between aortic elastic properties and the disease duration.

Dose-dependent acute effects of passive smoking on left ventricular cardiac functions in healthy volunteers.

OBJECTIVE: We have previously shown that acute passive smoking impaired left ventricular diastolic function in healthy volunteers. The aim of this study was to determine whether length of exposure and/or ambient smoke concentration is the key determinant of this outcome. METHODS: We measured blood carboxyhemoglobin (COHb)and lactate level to investigate the acute effects of passive smoking on tissue oxygenation. A total of 90 healthy nonsmoker volunteers were prospectively enrolled into the study. Each of 30 subjects were exposed to carbon monoxide (CO) less than 5.0 ppm smoke in group A for 30 minutes, to CO 5 to 10 ppm smoke in group B for 30 minutes, and to CO less than 5.0 ppm smoke in group C for 60 minutes. Hemodynamic parameters were obtained, blood samples for measuring COHb and lactate levels were taken and echocardiographic examinations were performed at baseline and after exposure to passive smoking. RESULTS: Mean ± SD CO levels in groups A, B, and C were 4.2 ± 0.5 ppm, 9.2 ± 0.3 ppm, and 4.1 ± 0.8 ppm, respectively. There was no change in left ventricular systolic functions in all groups. Left ventricular diastolic functions were impaired in groups B and C, whereas no change was observed in group A. Carboxyhemoglobin and lactate levels increased after passive smoking in groups B and C. However, group B had significantly higher COHb and lactate levels compared to group C (P < 0.001). CONCLUSIONS: Our results suggested that passive smoking at a certain dose in relation with length of exposure and ambient smoke concentration seems to cause relative left ventricular diastolic dysfunction.

The acute effects of passive smoking on mean platelet volume in healthy volunteers.

Mean platelet volume (MPV) is an indicator of platelet activation. We investigated the acute effect of passive smoking on MPV in healthy volunteers. Healthy nonsmoker volunteers (n = 90) spent 120 minutes in a smoke-free room. Then they were exposed to passive smoking in 3 groups consisting of 30 volunteers each in group A (carbon monoxide [CO] < 7.5 ppm), group B (CO = 7.5-15 ppm), and group C (CO > 15 ppm) for 120 minutes in a smoking room. Mean platelet volume did not change in group A and in the smoke-free room. Mean platelet volume increased significantly at the 60th minute and continued to increase at the 90th and 120th minute in group B. Mean platelet volume increased significantly at the 30th minute and continued to increase at the 60th, 90th, and 120th minute in group C. In conclusion, acute exposure to passive smoking affected MPV according to the duration and intensity of smoke.

Long term clinical outcomes of brachytherapy, bare-metal stenting, and drug-eluting stenting for de novo and in-stent restenosis lesions: five year follow-up.

BACKGROUND: We aimed to investigate the effects of brachytherapy, drug-eluting stent (DES) and bare metal stent (BMS) applications in the treatment of coronary artery disease, on five-year clinical outcomes and mortality. METHODS: Two hundred and seventeen patients who were treated in our clinics between January 2000 and December 2003 with brachytherapy, DES, or BMS for both de novo and in-stent restenosis lesions were included in this cohort study. Of these 217 patients, 69 received brachytherapy, 80 were given BMS and 68 were given DES. The clinical outcomes of the patients during hospitalization and over a long-term follow-up were evaluated. Cardiovascular events, revascularizations and mortality rates were compared among the three groups over a five-year follow-up. RESULTS: The mean age was 60.1 ± 9.5 years in the brachytherapy group, 55.7 ± 9.2 years in the BMS group, and 58.9 ± 9.8 years in the DES group (p = 0.44). All-cause mortality rates were 20 (29%) brachytherapy patients, 22 (27.5%) BMS patients, and four (5.9%) DES patients (p = 0.01). Cardiovascular event was the cause of death for 14 (20.3%) brachytherapy patients, 16 (20%) BMS patients and four (5.9%) DES patients (p = 0.001). All-cause mortality rates were 20 (29%) brachytherapy patients, 22 (27.5%) BMS patients and four (5.9%) DES patients. All-cause and cardiovascular mortality rates were significantly lower in the DES group compared to both the BMS and the brachytherapy groups (p = 0.01 and p = 0.001, respectively). CONCLUSIONS: DES application for in-stent restenosis and de novo lesions was superior to brachytherapy and BMS application with respect to all-cause and cardiovascular mortalities.

Impaired aortic elastic properties in patients with chronic graft-versus-host disease.

OBJECTIVES: Graft-versus-host disease (GVHD), which develops as a result of the immunologic response that donor T-lymphocytes generate against host tissue following hematopoietic stem cell transplantation (HSCT), is the leading cause of morbidity and mortality in these patients. The aim of this study is the investigate relation between aortic wall stiffness and duration of the disease in patients with chronic GVHD. METHODS: The study population included 32 patients (18 men; mean age, 36.9±12.5 years, and mean disease duration=14.7±2.9 months) who received HSCT and was diagnosed with GVHD and 44 patients (23 men; mean age, 35.2±9.6 years, and mean disease duration=13.5±2.4 months) who did not develop GVHD following HSCT. All patients underwent baseline echocardiography before HSCT and were followed. After approximately 10-14 months following HSCT, these patients were divided into two groups based on whether they had developed chronic GVHD, and were compared to aortic stiffness parameters and cardiac functions. RESULTS: There was no change in basal characteristics, laboratory and echocardiographic findings, and aortic stiffness parameters in both groups before HSCT (P>0.05). After HSCT, the mean aortic strain and distensibility values of the chronic GVHD patients were significantly lower, compared with the non-GVHD patients (9.8±3.2% vs. 12.9±5.0%, P=0.002 and 4.1±1.5×10(-6) cm2/dyn vs. 5.3±2.1×10(-6) cm2/dyn; P=0.005, respectively). In addition, aortic stiffness index was increased in the chronic GVHD group compared with non-GVHD group (2.7±1.7 vs. 2.0±0.8, P=0.03). CONCLUSION: Aortic stiffness measurements were significantly different in chronic GVHD group compared to non-GVHD group and these findings suggested useful explanation for the potential mechanism about the development of disease.

Assessment of atrial conduction time in patients with sarcoidosis.

OBJECTIVES: Sarcoidosis is an inflammatory granulomatous disease of unknown cause that involves multiple organ systems. Myocardial involvement is usually associated with poor prognosis, but diagnosis of cardiac sarcoidosis is frequently difficult. The aim of this study was to investigate the atrial conduction time in patients with sarcoidosis by using high-usefulness tissue Doppler echocardiography. METHODS: The study population included 49 patients with sarcoidosis (19 men; mean age, 40.5 ± 9.8 years; mean disease duration, 35.7 ± 15.3 months) and 45 healthy control subjects (17 men; mean age, 40.7 ± 7.2 years). From the 12-lead electrocardiogram, P wave dispersion (PWD) was calculated. The timing of atrial contractions (PA) was measured as the intervals between the onset of P wave on electrocardiogram and the beginning of A-wave on TDI, and atrial electromechanical delay (EMD) was calculated from the lateral (PA lateral) and septal (PA septal) mitral annulus and lateral tricuspid annulus (PA tricuspid). RESULTS: Both PA lateral and PA septal were significantly longer in patients with sarcoidosis than control subjects (67.9 ± 16.1 vs 56.3 ± 13.1, P < 0.001; and 54.8 ± 15.2 vs 45.1 ± 14.2 ms, P = 0.002, respectively). Intra-atrial (PA septal-PA tricuspid) and interatrial (PA lateral-PA tricuspid) EMD were significantly higher in sarcoidosis groups (12.6 ± 7.5 vs 8.0 ± 7.1, P = 0.003; and 25.7 ± 9.8 vs 19.3 ± 7.7 ms, P = 0.001, respectively). Similarly, maximum P-wave duration and PWD were significantly longer in patients with sarcoidosis than control subjects (105.2 ± 11.8 vs 96.7 ± 15.4, P = 0.004 and 24.7 ± 5.6 vs 19.7 ± 7.1 ms, P = 0.001, respectively). There were significant positive correlations between the disease duration and interatrial EMD (r = 0.56, P < 0.001) and intra-atrial EMD (r = 0.66, P < 0.001). Positive correlation also was present between the disease duration and PWD (r = .62, P < 0.001). CONCLUSIONS: Atrial EMD was found prolonged in patients with sarcoidosis. We also have demonstrated that PWD, interatrial and intra-atrial EMD were significantly correlated with disease duration. This study calls attention to measurement of atrial conduction time that may be clinically helpful in the recognition of cardiac involvement.

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.

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.

Impaired heart rate recovery index in patients with sarcoidosis.

BACKGROUND: Sarcoidosis, an inflammatory granulomatous disease, is associated with various cardiac disorders, including threatening ventricular arrhythmias and sudden cardiac death. Heart rate recovery (HRR) after exercise is a function of vagal reactivation, and its impairment is an independent prognostic indicator for cardiovascular and all-cause mortality. The aim of our study was to evaluate HRR in patients with sarcoidosis. METHODS: The study population included 56 patients with sarcoidosis (23 men, mean age = 47.3 ± 13.0 years, and mean disease duration = 38.4 ± 9.7 months) and 54 healthy control subjects (20 men, mean age = 46.5 ± 12.9 years). Basal ECG, echocardiography, and treadmill exercise testing were performed on all patients and control participants. The HRR index was defined as the reduction in the heart rate at peak exercise to the first-minute rate (HRR(1)), second-minute (HRR(2)), third-minute (HRR(3)), and fifth-minute (HRR(5)) after the cessation of exercise stress testing. RESULTS: There are significant differences in HRR(1) and HRR(2) indices between patients with sarcoidosis and the control group (25 ± 6 vs 34 ± 11; P < .001 and 45 ± 10 vs 53 ± 12; P < .001, respectively). Similarly, HRR(3) and HRR(5) indices of the recovery period were lower in patients with sarcoidosis when compared with indices in the control group (53 ± 12 vs 61 ± 13; P < .001 and 60 ± 13 vs 68 ± 13; P < .001, respectively). Exercise capacity was notably lower (9.2 ± 2.1 vs 11.6 ± 2.8 METs; P = .001, respectively) and systolic pulmonary arterial pressure at rest was significantly higher in patients with sarcoidosis compared with the control group (29.7 ± 5.5 mm Hg vs 25.6 ± 5.7 mm Hg, P = .001, respectively). Furthermore, HRR indices were found to be different among radiographic stage groups. CONCLUSIONS: The HRR index was impaired in patients with sarcoidosis as compared with control subjects. When the prognostic significance of the HRR index is considered, these results may partially explain the increased occurrence of arrhythmias and sudden cardiac death in patients with sarcoidosis. Our findings suggest that the HRR index may be clinically helpful in identifying high-risk patients with sarcoidosis.

Acute effects of passive smoking on blood pressure and heart rate in healthy females.

OBJECTS: Carbon monoxide (CO) is suspected of playing a major role in cigarette smoke-induced cardiovascular diseases. Hypertension is one of the common chronic cardiovascular diseases that lead to heart attacks, strokes, chronic heart failure, and chronic renal failure. We aimed to investigate the immediate effects of passive smoking on blood pressure and heart rate during and after exposure in healthy females. In addition, we examined that whether carboxyhemoglobin (COHb) levels were correlated with heart rate and blood pressure measurements. METHODS: Thirty healthy nonsmoker female volunteers (mean age: 26±5 years) were prospectively enrolled in the study. Systolic and diastolic blood pressure and heart rate were obtained at baseline, 5th, 10th, 15th, 30th minute of exposure and at 5th, 15th, and 30th minute after exposure. Blood samples for measuring COHb were taken at baseline and after spending 30 min in the smoking room from all volunteers. Difference between baseline and second measurements of COHb were described as ΔCOHb. RESULTS: Mean COHb level was significantly higher at the end of exposure when compared with baseline values (COHb 0.5±0.1 vs. 1.8±0.4%, P<0.05). Heart rate and systolic blood pressure measurements at 15th and 30th minute of exposure were higher than at baseline and 5th minute of exposure (88±3.2 and 90±3.7 vs. 76±3.9 and 78±4.5 beats/min, P<0.05; 135±1.1 and 136±4.0 vs. 113±5.7 and 115±3.5 mmHg, P<0.05). They elevated significantly at the same time interval. Diastolic blood pressure was significantly increased at 30th minute of exposure when compared with earlier measurements (90±5.1 vs. 74±2.2, 72±3.2 vs. 71±4.5 mmHg, P<0.05). Heart rate and systolic blood pressure decreased notably at 15th minute and returned to baseline values at 30th minute after exposure (80±1.2 and 76±3.2 vs. 88±4.5 beats/min, P<0.05; 120±4.4 and 115±1.9 vs. 135±2.2 mmHg, P<0.05). Diastolic blood pressure decreased significantly at 30th minute and returned to baseline values at 60th minute after exposure (75±3.6 and 70±2.5 vs. 89±4.3 mmHg, P<0.05). Heart rate and diastolic blood pressure measurements were moderately correlated and systolic blood pressure measurements were closely correlated with ΔCOHb values at the end of the exposure. CONCLUSION: Our results suggested that passive smoking has remarkable acute effect on heart rate and blood pressure in young healthy females. Beside this, we found that ΔCOHb level is closely correlated with systolic blood pressure and moderately correlated with heart rate and diastolic blood pressure measurements.