Mahmut Acikel

Left atrial mechanical function in patients with essential hypertension

Objective — This study was carried out to assess the left atrial (LA) mechanical function in patients with essential hypertension with two-dimensional echocardiography by means of left atrial volume measurements. Methods — LA volumes were measured echocardiographically in 36 untreated hypertensive patients and 20 age-sex-matched healthy controls according to biplane area-length method. LA volume measurements were done at the time of mitral valve opening (Vmax), at the onset of atrial systole (p wave at the electrocardiography = Vp) and at closure (Vmin). All volumes were indexed for body surface area, and the following left atrial emptying functions were calculated: LA passive emptying volume = Vmax – Vp, LA passive emptying fraction = LA passive emptying volume / Vmax, conduit volume = left ventricular stroke volume-(Vmax- Vmin), LA active emptying volume = Vp- Vmin, LA active emptying fraction = LA active emptying volume / Vp, LA total emptying volume = (Vmax-Vmin), LA total emptying fraction = LA total emptying volume / Vmax. Results — Vmax (p < 0.01), Vmin (p < 0.005) and Vp (p < 0.001) were significantly greater in hypertensives than in controls. Although LA passive emptying volume (p < 0.001), LA passive emptying fraction (p < 0.001), conduit volume (p < 0.005) and LA total emptying fraction (p < 0.05) were found to be significantly lower in hypertensives than in controls, LA active emptying volume (p < 0.001) and LA active emptying fraction (p < 0.01) were found to be significantly greater in hypertensives than in controls. LA total emptying volume (p > 0.05) was similar in both groups. Conclusion — The results of the present study indicate that chronic hypertension is associated with an increased in left atrial volumes, a decrease in left atrial passive emptying function, and an increase systolic pump function. Increased left atrial pump function represents a compensatory mechanism in hypertensive patients with left ventricular hypertrophy.

The relation of serum gamma-glutamyl transferase levels with coronary lesion complexity and long-term outcome in patients with stable coronary artery disease

BACKGROUND Relation of serum gamma-glutamyl transferase (GGT) levels with extent, severity, and complexity of coronary artery disease has not been adequately studied. Therefore, we evaluated the relationship between GGT levels and coronary complexity, severity and extent assessed by SYNTAX score and long-term adverse events. METHODS We enrolled 442 consecutive patients with stable angina pectoris who underwent coronary angiography. Baseline serum GGT levels were measured and SYNTAX score was calculated from the study population. Median follow-up duration was 363 days. Endpoints were all cause mortality and any revascularization. RESULTS GGT levels demonstrated an increase from low SYNTAX tertile to high tertile. In multivariate analysis serum GGT, diabetes mellitus, HDL-cholesterol, eGFR and ejection fraction were found to be independent predictors of high SYNTAX score. The survival analysis showed that long-term revascularization rates were comparable between the GGT groups (for 36 U/l cut point) of the overall population (7.7% vs 8.6% logrank, p = 0.577), whereas long-term all cause mortality rate was higher in the GGT ≥ 36 U/l group (3.6% vs 11.6% logrank, p = 0.001). In Cox proportional hazards regression model, GGT ≥ 36 U/l group was found to be an independent predictor of long-term all cause mortality in the unadjusted (HR 2.54, 95% CI 1.17-5.48, p = 0.018) and age- and gender-adjusted (HR 2.58, 95% CI 1.19-5.58, p = 0.016) models. CONCLUSION Serum GGT level was independently associated with coronary complexity and long-term mortality in patients with stable coronary artery disease.

Pulsed Doppler tissue imaging can help to identify patients with right ventricular infarction.

This study was planned to assess whether tissue Doppler imaging is a useful method for the detection of the right ventricular myocardial infarction. Forty-eight patients with acute inferior myocardial infarction and 24 age- and sex-matched healthy controls were included in this study. Twenty-four patients had electrocardiographic signs of inferior myocardial infarction without right ventricular infarction (group I), and the other 24 patients had electrocardiographic signs of inferior myocardial infarction with right ventricular infarction (group II). From the echocardiographic apical four-chamber view, peak systolic, early diastolic, and late diastolic velocities of the tricuspid annulus at the right ventricular free wall were recorded with the use of pulsed-wave Doppler tissue imaging. The tricuspid annular peak tissue Doppler imaging systolic velocity was significantly lower in group I (14.03 ± 2.57 cm/s, P ≪ 0.005) and in group II (8.50 ± 0.84 cm/s, P ≪ 0.005) than in controls (16.63 ± 2.31 cm/s). The tricuspid annular peak systolic (8.50 ± 0.84 cm/s vs 16.63 ± 2.31 cm/s) and peak early diastolic (10.99 ± 3.28 cm/s vs 19.39 ± 4.3 cm/s) velocities were significantly lower in group II than in group I, as compared with controls (P ≪ 0.001). Peak early diastolic velocity of tricuspid annulus (10.99 ± 3.28 cm/s vs 19.39 ± 4.3 cm/s) was significantly lower in group I than in controls (P ≪ 0.001); however, late diastolic velocity was significantly lower in group II (15.98 ± 5.08 cm/s, P ≪ 0.05) than in group I (18.21 ± 2.63 cm/s, P ≪ 0.05) and in controls (19.02 ± 5.29 cm/s). The results of this study indicate that tricuspid annular peak systolic and early diastolic velocities are reduced in patients with right ventricular infarction. The velocity of the tricuspid annulus by tissue Doppler imaging is simple and can be used to distinguish whether patients with inferior myocardial infarction have right ventricular infarction.

Protective effects of melatonin against myocardial injury induced by isoproterenol in rats.

Abstract: This study was performed to determine whether melatonin could have a protective effect against myocardial injury (MI) induced by isoproterenol (ISO) in rats. Twenty‐four rats were divided into three treatment groups: (1) control (n = 8): saline solution. (2) ISO (n = 8): ISO only. (3) melatonin + ISO (n = 8). Melatonin (10 mg/kg/day, i.p.) was administered 30 min before the initiation of ISO (150 mg/kg/day, s.c.). Drugs and saline were given at 14:00 hr for two consecutive days. At the end of the second day, blood samples were taken from the abdominal aorta shortly after the rats were anesthetized for the purpose of measuring cardiac troponins T (cTnT) and I (cTnI); hearts were removed, preserved and examined microscopically. Additionally, based on the histological changes in myocardial tissue, the rats were divided into three groups: no change, mild changes and moderate and/or marked changes. The mean cTnT and cTnI values were significantly increased in ISO group compared with control group [(1.29 ± 0.22 ng/mL versus 0.46 ± 0.07 ng/mL, P < 0.0001) and (0.56 ± 0.11 ng/mL versus 0.21 ± 0.01 ng/mL, P < 0.001)], respectively, and were significantly reduced in the ISO + melatonin group (0.65 ± 0.06 ng/mL for cTnT and 0.25 ± 0.01 ng/mL for cTnI) compared with the ISO only group (P < 0.01), respectively. cTnT and cTnI values were significantly increased in rats with moderate and/or marked cardiac changes compared with hearts where there were mild changes and no change (P < 0.05). ISO + melatonin group showed less histological changes than the ISO group (P < 0.01). In conclusion, this study revealed a protective effect of melatonin against ISO‐induced MI in rats, and its potential clinical application in the treatment of MI.

The Role of the Nonspecific Inflammatory Markers in Determining the Anatomic Extent of Venous Thromboembolism

We aimed to investigate the relationship between the extent of venous thromboembolism (VTE) and nonspecific inflammatory markers such as neutrophil to lymphocyte ratio (NLR) and high-sensitivity C-reactive protein (hs-CRP). We retrospectively enrolled 77 patients with VTE (distal deep vein thrombosis [DVT], n = 19; proximal DVT, n = 32; and pulmonary thromboembolism [PTE], n = 26) and 34 healthy controls. In the performed analysis of variance, the levels of white blood cell, NLR, and hs-CRP were clearly different among the groups (control, distal and proximal DVT, and PTE) (P < .001). Especially, a significant increase from the control group to the DVT and PTE was observed in the analysis made for NLR. In the performed receiver–operating characteristic curve analysis, area under curve (AUC) = 0.849 and P < .001 were detected for NLR > 1.84. For this value, the sensitivity and specificity were determined as 88.2% and 67.6%, respectively. The NLR is an inexpensive and a readily available marker that may be effective in determining the extent of VTE, and it is useful for risk stratification in patients with VTE.

Tissue Doppler properties of the left atrial appendage in patients with mitral valve disease.

Objective: The purpose of this study was to compare the left atrial appendage (LAA) tissue Doppler imaging (TDI) with the classical LAA function parameters in patients with mitral valve disease. Methods: Twenty patients who had pure mitral regurgitation (group 1), 20 patients who had pure rheumatic mitral stenosis (group 2), and 20 healthy patients (group 3) were included in this study. All the cases were sinus rhythm. In order to determine the LAA functions, LAA late filling (LAALF), and late emptying (LAALE) flow velocities and LAA fractional area change (LAAFAC) were measured. LAA tissue Doppler evaluations were obtained from the PW Doppler, which was placed on the LAA lateral wall in a transverse basal short‐axis approach. LAA late systolic (LAALSW) and late diastolic (LAALDW) wave velocities were obtained from TDI records transesophageal echocardiography (TEE). Results: There were no significant differences among groups 1, 2, and 3 in terms of age, left ventricular (LV) ejection fraction, gender, and heart rate. No differences were observed between group 1 and the control group with respect to LAALE, LAALF, and LAAFAC. LAALE velocity and LAAFAC were significantly decreased in group 2 than group 1. LV diastolic diameter was significantly greater, whereas LAALSW and LAALDW velocities were significantly decreased in group 1 compared with group 3. There were no differences between groups 1 and 2 regarding to LAALSW and LAALDW velocities. LAALE, LAALF, LAALSW, LAALDW velocities, and LAAFAC were significantly decreased in group 2 than group 3. Conclusion: The TDI method may detect the LAA systolic dysfunctions, which cannot be detected using classical methods, on tissue level in patients with mitral regurgitation. In addition, the deterioration of the LAA functions at tissue level in patients with rheumatic mitral stenosis was also detected. (ECHOCARDIOGRAPHY, Volume 21, May 2004)

ST segment elevation in leads V1 to V3 due to isolated right ventricular branch occlusion during primary right coronary angioplasty

It is rare to observe ST elevation in anterior derivations caused by isolated right ventricular branch occlusion. We described the case with acute inferior and right ventricular myocardial infarction (MI) who developed ST segment elevation in precordial leads V1 to V3 due to isolated right ventricular branch occlusion during primary right coronary angioplasty. Catheter Cardiovasc Interv 2003;60:32–35.

Comparison of serum levels of inflammatory markers and allelic variant of interleukin-6 in patients with acute coronary syndrome and stable angina pectoris.

ObjectivesAlthough the relationship between atherosclerosis and inflammatory cells has been recognized in recent years, the effect of interleukin-6 (IL-6) genetic variants associated with atherosclerosis is still controversial. Therefore, we investigated the association between IL-6 polymorphism and levels of IL-6 in patients with coronary artery disease (CAD). MethodsWe conducted a case–control study on 294 unrelated participants who were referred to the cardiology department of the university hospital for coronary angiography because of suspected ischemic heart disease. Group I comprised patients with clinically acute coronary syndrome, and group II comprised patients (individuals matched for age and sex) with clinically stable angina pectoris; both groups were categorized, based on their angiographic findings, as either having angiographically documented less extensive CAD (1 vessel narrowed) or extensive CAD (≥2 vessels narrowed). They were studied to examine effect of the IL-6 gene variants in CAD. Genotyping was determined by polymerase chain reaction. ResultsThe IL-6 G/C-174 polymorphism was found in 19 of 106 (18%) in group I and in four of 188 (2%) in group II (P<0.001). Median IL-6 levels were significantly higher in group I (6.7±13.6 pg/ml) than in group II (4.1±3.8 pg/ml) (P<0.05). In addition, high sensitivity C-reactive protein levels were significantly higher in group I (8.2±6.2 mg/dl) than in group II (4.6±3.4 mg/dl) (P<0.001). ConclusionThese results demonstrated that the presence of the IL-6 G/C-174 polymorphism and increased IL-6 and high sensitivity C-reactive protein levels are strongly associated with the inflammatory system and the course of clinical and hemodynamically significant CAD.

Plasma Homocysteine Level and the Angiographic Extent of Coronary Artery Disease

Recent epidemiologic studies have shown that moderately elevated plasma homocysteine concentrations are associated with an increased risk for the development of atherosclerotic cardiovascular diseases. But, it is not known whether moderate hyperhomocysteinemia is associated with the angiographic extent of atherosclerotic cardiovascular disease in patients with coronary artery disease (CAD). A possible relationship was investigated between admission plasma homocysteine level and the angiographic extent of coronary artery disease in patients with CAD. In this study, 156 consecutive patients presenting with coronary artery disease (group 1) and control group (group 2) of 35 age-matched persons with normal coronary angiography were enrolled. Blood samples for homocysteine were obtained on admission. Plasma homocysteine concentration was measured with high-performance liquid chromatography with fluorescence detection. Radiographs from coronary angiography were viewed and scored using Sullivan’s method to assess the atherosclerotic involvement of coronary artery disease. There were significant elevations in homocysteine level in group 1 compared to group 2 (15.59 ±5.7 µmol/L, 9.24 ±1.50 µmol/L; respectively, p<0.001). All scores (demonstrated angiographic extension of CAD) correlated significantly with plasma homocysteine levels; however, the Sullivan’s extent score correlated more closely (r =0.68, p<0.001) than both the stenosis score (r =0.44, p<0.01) and vessel score (r =0.35, p<0.05). Elevated homocysteine levels in patients with coronary artery disease correlated with the angiographic extent of atherosclerotic disease.

Left Atrial Mechanical Functions in Elite Male Athletes

I athletic conditioning is associated with hemodynamic changes and affects the loading conditions of the heart. It is known that the heart of an athlete has become physiologically adapted by prolonged training. These changes include an increase in left ventricular (LV) chamber size, wall thickness, and mass. It is reported that athletes involved in mainly static or isometric exercise develop concentric hypertrophy, and in contrast to this, athletes involved in endurance training or isotonic exercise develop eccentric hypertrophy. There are a large number of echocardiographic studies on LV wall thickness and dilatation, but there are very few studies concerning left atrial (LA) mechanical function in the athlete’s heart. This study was undertaken to assess the possible adaptive changes in LA mechanical function in elite athletes. • • • Thirty-six top-level male athletes (21 4 years), all members of the national running team, wrestling team, skiing team, or other professional sports teams (14 runners, 10 wrestlers, 4 boxers, 5 basketball players, and 3 skiers) and 21 age-matched healthy male controls (21 4 years) were included. Mean athletic competition time was 7.7 4.1 years and the mean average training time was 11.5 3.9 hours/week in the athletes. All athletes were in the intense training period. Athletes in the off-training period or during prolonged rest ( 10 days) were not included. All subjects enrolled in this study were free from cardiac disease on the basis of a negative medical history and normal physical examination and electrocardiogram. The subjects who had a history of taking any cardioactive medication or anabolic steroids were excluded from this study. The study protocol was approved by the ethics committee of our institute and all subjects gave written consent for the study. A Vingmed System Five Doppler echocardiographic unit (GE Vingmed Ultrasound, Horten, Norway) with 2.5-MHz FPA probe was used. All echocardiograms were recorded by the same investigator. An echocardiographic study was performed in the left lateral decubitus position, with parasternal long and apical 2-, 4-, and 5-chamber views. Diastolic ventricular septal thickness, diastolic posterior wall thickness, and LV end-diastolic and end-systolic dimensions were measured in the parasternal long-axis view, and LV mass was determined by the method of Devereux and Reichek and indexed to body surface area. A sample volume of pulsed-wave Doppler was placed between tips of mitral leaflets on the apical 4-chamber view. Peak early (E) and late (A) mitral inflow velocities, E/A ratio, and deceleration time of E velocity were obtained. Isovolumic relaxation time was obtained with the sample volume of the pulsedwave Doppler positioned between mitral inflow and LV outflow tract as the time interval from the cessation of aortic flow to the onset of mitral valve inflow. LV end-diastolic and end-systolic volumes were determined from the apical 4-chamber view according to the modified Simpson’s method, and LV stroke volume and ejection fraction were calculated. LA volumes were measured echocardiographically at the time of mitral valve opening (maximal, Vmax), at the onset of atrial systole (p wave on electrocardiography Vp), and at mitral valve closure (minimal, Vmin) according to the biplane area-length method in the apical 4and 2-chamber view. All volumes were corrected for body surface area and the following LA emptying functions were calculated: LA passive emptying volume Vmax Vp; LA passive emptying fraction LA passive emptying volume/Vmax; conduit volume LV stroke volume (Vmax Vmin); LA active emptying volume Vp Vmin; LA active emptying fraction LA active emptying volume/Vp; LA total emptying volume (Vmax Vmin); LA total emptying fraction LA total emptying volume/ Vmax. 10 All measurements were averaged over 3 cardiac cycles. Data are expressed as mean SD. The differences between groups were assessed with the Student’s t test. The relation between different variables was assessed with the Pearson correlation. A p value 0.05 was considered statistically significant. Athletes and members of the control group did not differ significantly in mean age and body surface area (21 4 vs 20 4 years and 1.8 0.2 vs 1.8 0.2 m, respectively, p 0.05). Heart rate was significantly lower in athletes than in controls (p 0.001). Systolic and diastolic blood pressures were similar in both groups (p 0.05). LV end-diastolic diameter and volume were significantly higher in athletes than in controls (p 0.05). LV end-systolic diameter and volume and ejection fraction were similar in the 2 groups (p 0.05). Posterior wall thickness (p 0.01), ventricular septal thickness (p 0.001), and LV mass index (p 0.001) were significantly greater in athletes than in controls. E and A transmitral flow velocity, and E/A ratio were similar in both groups (p 0.05). LA dimension was significantly greater in athletes than in controls (p 0.005) (Table 1). LA volume indexes, Vmax (p 0.005), Vmin (p 0.05), and Vp (p 0.005) were greater in athletes From the Department of Cardiology, Medical School Hospital, and Department of Physical Education and Sport, Ataturk University, Erzurum, Turkey. Dr. Erol’s address is: Ataturk University, Department of Cardiology, Medical School Hospital, 25050 Erzurum, Turkey. E-mail: mkerol@superonline.com.tr. Manuscript received April 10, 2001; revised manuscript received and accepted June 7, 2001.