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 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.

Use of ischemia-modified albumin in diagnosis of coronary artery disease.

OBJECTIVE: The diagnosis of coronary artery disease (CAD) is an important clinical problem. Ischemia-modified albumin (IMA) has been demonstrated to be a helpful marker in detecting myocardial ischemia. In this study, we have investigated the diagnostic importance of IMA in CAD. METHOD AND RESULTS: Fifty patients with chest pain were enrolled in the study. IMA levels were measured on admission and within 30-60 min after exercise by albumin cobalt-binding test. Coronary angiography was performed in all patients after the exercise test. The mean preexercise IMA level was 83+/-27 U/ml in the patient group. IMA levels before the exercise test were similar in both patient and control groups (P>0.05). The mean IMA level in the patient group was, however, higher than in the control group after the exercise test (P=0.001). The sensitivity, specificity and positive and negative predictive values of the postexercise IMA levels >85 in diagnosis of CAD were 78, 73, 0.81 and 0.73%; respectively. Postexercise IMA levels were higher in patients with chest pain, ST depression and downsloping and horizontal ST depression of 2 mm or more. CONCLUSION: IMA levels after the exercise test increased in patients with CAD. Our study results indicate that postexercise IMA levels can be helpful markers in the diagnosis of stable CAD in clinical practice.

[Anxiety disorder as a potential for sudden death]. / Anksiyete bozuklugunun ani ölüm yapma potansiyeli.

A close association between anxiety disorder and sudden death is known. If any underlying heart disease exists, it is easy to discuss this association. If it does not, it is difficult to explain anxiety disorder as a cause of sudden death. In case of acute anxiety, many complicated physiologic events, which have capacity of contributing to sudden death, occur. On the other hand, accelerated atherosclerosis ensues in the case of chronic anxiety, and the latter increases vulnerability to sudden death through development of coronary events.

[Impact of psychological factors on development and course of coronary artery disease [corrected]: should negative psychological factors be altered?]. / Psikolojik faktörlerin koroner kalp hastaligina etkisi: Olumsuz psikolojik faktörlere müdahale edilmeli mi?

Psychological factors effect the development and course of coronary heart disease (CHD). Hypothalamic-pituitary-adrenal dysregulation, reduced heart rate variability, diminished baroreflex sensitivity, impaired immune function and altered platelet function are proposed as significant psychophysiologic mechanisms to explain this association. Because psychological factors may influence several different stages of long atherosclerosis period, interventional studies aiming to alter negative psychological factors by behavioral and medical ways, expecting to prevent or improve CHD, have been discussed. Complementary to the traditional treatment, this new treatment strategy could be a different perspective and a nice promise for CHD patients.

[Is intermittent dobutamine treatment beneficial in patients with dilated cardiomyopathy?]. / Dilate kardiyomiyopatili hastalarda aralikli dobutamin tedavisi faydali midir?

OBJECTIVE: Dobutamine is a sympathomimetic drug, which can be used in patients with dilated cardiomyopathy (DCM). We investigated the effects of intermittent dobutamine use on cardiac parameters and quality of life in patients with DCM. METHODS: Twelve patients with ischemic and idiopathic DCM, refractory to conventional therapy, have been included in the study. In addition to traditional treatment, dobutamine (1-2 micro g/kg/min infusion increasing up to 10 micro g/kg/min for 3 days) was administered, and repeated at the 1st, 2nd and 3rd months. The patients were evaluated 3 times, before and immediately after the first treatment and after the treatment on the third month, using echocardiography, exercise stress testing, ambulatory ECG, right ventricular catheterization, cardiac enzymes (creatine kinase MB isoenzyme - CK-MB, troponin-T) and the Minnesota Living with Heart Failure Questionnaire for quality of life. RESULTS: After the first treatment, left ventricular ejection fraction (LVEF), cardiac output, cardiac index (CI), pulmonary wedge pressure and life quality improved significantly (p<0.05); but, after the treatment on the third month, these parameters except PCWP returned to nearly baseline values. Additionally, a significant increase in the number of patients with ventricular premature beats and with troponin-T positivity was detected after the third month of treatment. CONCLUSION: The use of dobutamine in addition to conventional therapy in patients with DCM provided improvements in some systolic parameters and quality of life particularly after the first treatment. In the late period of the treatment, however, it was determined that these beneficial effects tended to disappear and harmful effects became more evident.

Should troponin-T be assessed during exercise stress testing in patients with stable angina pectoris?

OBJECTIVE: This study was planned to investigate whether or not troponin-T positivity has occurred during exercise stress testing in patients with stable angina pectoris and if yes, its relationship with the severity of the disease. METHODS: One hundred patients with stable angina pectoris who presented with typical chest pain were included in this study. They were subjected to the exercise stress testing according to Bruce protocol. Troponin-T was studied 3 times: immediately before, 6 and 24 hours after the exercise testing. Coronary angiography was performed two hours after the last blood sampling. RESULTS: Exercise stress test was found positive in 67 (67%) and negative in 33 (33%) patients. Coronary artery disease was present in 47 (70.1%) of those with positive and in 17 (51.5%) with negative test results. Troponin-T was negative in all the patients before the stress test. Troponin-T was found positive in readings taken 6 and 24 hours after the test in 4 patients (6.2%) with coronary artery disease. Of these patients, 2 had positive and the remaining 2 had negative stress test results. Troponin-T was found negative in readings after the stress test in all the patients without coronary artery disease. The duration of the exercise stress test was found to be significantly shorter in patients with troponin positivity than their counterparts with negativity (277.5 +/- 81 sec vs. 428.8 +/- 195 sec, p = 0.024). Troponin-T positivity after the stress test was found considerably higher in patients with three-vessel disease (p = 0.021). CONCLUSIONS: Heavy exercises like stress test may severely lead to myocardial damage. The study of post-stress test tropinin T readings, in patients with stable angina pectoris and with negative stress test result, may be of great help in detecting especially the patients with multiple vessel disease.

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.

Spontaneous coronary artery dissection and pulmonary thromboembolism: a case report.

Spontaneous coronary artery dissection (SCAD) still is a rare cause of acute coronary syndrome. SCAD has been observed in three groups of patients: those with coronary atherosclerosis, peripartal women and idiopathic group. SCAD may be associated with some conditions. We report an unusual association: SCAD and pulmonary thromboembolism.

Left ventricular pseudoaneurysm causing coronary angiography images resembling myocardial bridging.

Acquired pseudoaneurysm of the left ventricle is a rare disorder that usually occurs after transmural myocardial infarction or after cardiac surgery. Pseudoaneurysms are usually detected because of symptoms; less often incidentally. Here we present a case of pseudoaneurysm as a result of unknown etiology causing myocardial bridging like image at angiography.

Protective effects of carvedilol against anthracycline-induced cardiomyopathy.

OBJECTIVES: The aim of this study was to determine the protective effect of carvedilol in anthracycline (ANT)-induced cardiomyopathy (CMP). BACKGROUND: Despite its broad effectiveness, ANT therapy is associated with ANT-induced CMP. Recent animal studies and experimental observations showed that carvedilol prevented development of CMP due to chemotherapeutics. However, there is no placebo-controlled clinical trial concerning prophylactic carvedilol use in preventing ANT-induced CMP. METHODS: Patients in whom ANT therapy was planned were randomized to administration of carvedilol or placebo. We enrolled 25 patients in carvedilol and control groups. In the carvedilol group, 12.5 mg once-daily oral carvedilol was given during 6 months. The patients were evaluated with echocardiography before and after chemotherapy. Left ventricular ejection fraction (EF) and systolic and diastolic diameters were calculated. RESULTS: At the end of 6 months of follow-up, 1 patient in the carvedilol group and 4 in the control group had died. Control EF was below 50% in 1 patient in the carvedilol group and in 5 in the control group. The mean EF of the carvedilol group was similar at baseline and control echocardiography (70.5 vs. 69.7, respectively; p = 0.3), but in the control group the mean EF at control echocardiography was significantly lower (68.9 vs. 52.3; p < 0.001). Both systolic and diastolic diameters were significantly increased compared with basal measures in the control group. In Doppler study, whereas E velocities in the carvedilol group decreased, E velocities and E/A ratios were significantly reduced in the control group. CONCLUSIONS: Prophylactic use of carvedilol in patients receiving ANT may protect both systolic and diastolic functions of the left ventricle.

Are the high levels of cytomegalovirus antibodies a determinant in the development of coronary artery disease?

In several epidemiological studies, it was suggested that a high titer of cytomegalo-virus (CMV) antibody meant CMV reactivation, and that this condition was a determinant of coronary artery disease (CAD). The purpose of this study was to investigate both the prevalence of the CMV infections in our study population and whether high CMV sero-positivity is a determinant of CAD. Blood samples from 179 (58 female, 121 male) individuals being evaluated for CAD suspicion by coronary angiography were tested for CMV seropositivity and CRP levels. Fifty-six patients had normal coronary arteries and 123 patients had CAD. Six patients did not have anti-CMV antibodies and 87 of the 173 seropositive patients had high levels of anti-CMV antibodies (> or = 8 U/mL). High CMV seropositivity (> or = 8 U/mL) was a significant CAD determinant even after adjustment for traditional CAD risk factors (odds ratio [OR] = 2.1 P = 0.04, respectively). The results indicate that the prevalence of high CMV seropositivity is an independent predictor of CAD in our study population and that our study population with CAD had a high rate of CMV infection.

Preload dependence of Doppler tissue imaging derived indexes of left ventricular diastolic function.

Doppler tissue imaging (DTI) has been proposed as a tool for the evaluation of diastolic function. Controversy exists regarding whether DTI measurements are influenced by preload. Changes in the circulating volume associated with hemodialysis result in preload reduction. To determine the influence of preload reduction on DTI and standard pulsed-Doppler transmitral diastolic velocities, 30 patients (mean age 41 +/- 14) with chronic renal insufficiency without overt heart disease were studied by DTI and standard pulsed Doppler before and after hemodialysis. From the apical window, DTI sample volume was placed at the lateral and septal mitral annulus and at the midsegment of lateral and septal myocardial wall of the left ventricle. Peak early diastolic annular and myocardial, and peak late diastolic annular and myocardial velocities were measured. Transmitral peak early and late diastolic velocities were also recorded by standard pulsed Doppler. The peak velocity of early diastolic mitral flow decreased from 100 +/- 30 to 85 +/- 34 cm/s (P < 0.001) after hemodialysis. Hemodialysis elicited marked reduction in early diastolic lateral mitral annular and midlateral myocardial velocities (6.9 +/- 3.2 to 6.3 +/- 2.9 cm/s, P < 0.04 and 6.7 +/- 0.3 to 5.5 +/- 2 cm/s, P < 0.001, respectively). Early diastolic, septal mitral annular, and midseptal myocardial velocities were also significantly decreased (5.8 +/- 2.8 to 4.6 +/- 2 cm/s, P < 0.006 and 6.2 +/- 2 to 5.1 +/- 1 cm/s, P < 0.008, respectively). Late diastolic mitral annular and myocardial velocities did not change. It is concluded that early diastolic mitral annular and myocardial velocities are affected by acute preload reduction. It is necessary to consider preload when diastolic function is assessed by DTI.

Application of the vena contracta method for the calculation of the mitral valve area in mitral stenosis.

OBJECTIVES: The vena contracta is the narrowest region of the regurgitant or stenotic jet just downstream the orifice and reflects the size of that orifice. This study was performed to assess the accuracy of the vena contracta width (VCW) in evaluating the severity of mitral stenosis (MS) and to compare the mitral valve area (MVA) determined by VCW with MVAs obtained by other more traditional echocardiographic methods. METHODS: We studied 59 patients (43 females, 42 +/- 14 years) with MS. VCW was measured in the apical four chamber view by Doppler color flow mapping. The largest diameter of the VCW during diastole was measured for at least three cardiac cycles and averaged. MVA was calculated from the following equation: pir(2), where r = VCW/2. MVA was also determined by planimetry, the pressure half-time method, and by the Gorlin formula. RESULTS: In this study, the width of the vena contracta ranged from 0.89 to 1.73 cm (mean 1.30 +/- 0.21). MVA, calculated based on the VCW, ranged from 0.63 to 2.35 cm(2) (mean 1.36 +/- 0.41). MVA by VCW (1.36 +/- 0.41 cm(2)) showed good correlations with three comparative techniques: (1) the cross-sectional area by planimetry (1.35 +/- 0.36 cm(2), mean difference = 0.21 +/- 0.16 cm(2), y = 0.91x + 0.14, r = 0.79, SEE = 0.26 cm(2), p < 0.001); (2) the area derived from the Doppler pressure half-time (1.27 +/- 0.32 cm(2), mean difference = 0.22 +/- 0.19 cm(2), y = 0.97x + 0.13, r = 0.76, SEE = 0.27 cm(2), p < 0.001), and (3) the area derived from the Gorlin equation in the 18 patients who underwent catheterization (1.27 +/- 0.35 cm(2), mean difference = 0.19 +/- 0.16, y = 0.98x + 0.05, r = 0.81, SEE = 0.26 cm(2), p < 0.001). CONCLUSIONS: These findings suggest that Doppler color flow imaging of the MS jet in the vena contracta can provide an accurate estimation of MVA and appears to be potentially applicable in the assessment of the severity of MS.

Intracoronary electrocardiogram and angina pectoris during percutaneous coronary interventions as an assessment of myocardial viability: comparison with low-dose dobutamine echocardiography.

The aims of this study were to evaluate the diagnostic value of intracoronary electrocardiogram (ECG) and presence of angina pectoris during percutaneous coronary interventions in the prediction of myocardial viability assessed by low-dose dobutamine echocardiography (LDDE). Seventy-one patients (60 men; mean age, 54 +/- 11 years) with recent Q-wave MI and angiographically documented regional wall motion abnormality in the presence of a significant (>/= 70%) nonocclusive stenosis of the infarct-related vessel who were referred for angioplasty were prospectively included in the study. The intracoronary ECG was recorded using coronary angioplasty guidewire. Significant ST segment elevation was defined as a new or worsening ST segment elevation of >/= 0.1 mV at 80 msec after the J-point. Angina pectoris was noted as present or absent during balloon inflation. All patients underwent LDDE for viability assessment. Significant ST segment elevation in the intracoronary ECG and chest pain were observed in 56 (78.9%) and 49 (69%) of the 71 patients. Viability was present on LDDE in 52 (92.9%) of 56 patients with and 3 (20%) of 15 without ST segment elevation. Viability was detected in 45 (91.8%) of 49 patients with and 10 (45.4%) of 22 without angina pectoris during balloon occlusion. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of ST segment elevation for viability were 94.5%, 75%, 92.9%, 80%, and 90.1%, respectively. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of angina pectoris for viability were 81.8%, 75%, 91.8%, 54.5%, and 80.3%, respectively. The present study demonstrated that a simple assessment of ST segment elevation in the intracoronary ECG or angina pectoris during coronary angioplasty can be used to assess myocardial viability identified by LDDE in patients with previous MI.

Color Doppler tissue imaging in assessing the elastic properties of the aorta and in predicting coronary artery disease.

We hypothesized that the change in aortic elastic properties could directly be shown with color Doppler tissue imaging (CDTI), that these findings could be related to aortic stiffness and distensibility and that, through these, coronary artery disease (CAD) could be predicted. One hundred and twenty six patients (group I: 83 with CAD, mean age 54+/-10 years, 18 female, 65 male; group II: 43 without CAD, mean age 53+/-10 years, 27 female, 16 male) having been evaluated for coronary artery disease by angiography were examined by echocardiography. Arterial pressure was measured immediately before echocardiographic evaluation. Internal aortic systolic and diastolic diameters by M-mode echocardiography and aortic upper wall tissue velocities (Aortic S, E, A, m/sec) by CDTI were measured 3 cm above the aortic valve. Lateral mitral annulus tissue velocities (Annulus S, E, A, m/sec) were also recorded. Aortic distensibility (cm2 x dynes(-1)) and aortic stiffness index were calculated using formulas. In the statistical analyses, CAD risk factors and left ventricular ejection fraction were used for adjustment. Aortic stiffness (2.79+/-3.49 vs 1.62+/-1.31, P=0.03), distensibility (1.55+/-1.46 vs 2.37+/-3.08, P=0.04), and aortic S velocity (0.057+/-0.016 vs 0.064+/-0.015, P=0.02) differed significantly between groups I and II. After adjustment, while aortic stiffness and S velocity were still statistically different (P=0.04; P=0.03 respectively), the significance of the difference in aortic distensibility disappeared (P=0.051). Aortic stiffness and aortic S velocity (0.06 m/sec<) were important CAD determinants (Odds ratio=1.4 P=0.03; Odds ratio=3.6 P=0.01, respectively), but aortic distensibility was not. Aortic stiffness was correlated only with aortic S velocity (r=-0.28, P=0.01), and aortic distensibility had a significantly positive correlation with aortic S velocity (r=0.20, P=0.02). The interobserver and intraobserver correlation coefficients for aortic S velocities were 0.65 and 0.71, respectively (P<0.05). Elastic properties of the aorta can directly be assessed by reproducibly measuring the movements in the upper wall of the aorta by CDTI. Reduced aortic S velocity is associated with increased aortic stiffness. Increased aortic stiffness and reduced aortic S velocity are important predictors of CAD.

Is the change of late potential over time related to enzyme levels? Ischemic burden in acute myocardial infarction.

BACKGROUND: The ventricular late potential (VLP) detected using the technique of signal average electrocardiography (SAECG) interacts with several factors, primarily time. METHOD: In this study, we examined the interaction, over time, of VLP with the initial ischemic burden and enzyme levels in acute myocardial infarction. Patients diagnosed as having acute myocardial infarction were included in the study. On the first day, the patients underwent enzyme analysis and electrocardiography (ECG) follow-up every 6 hours. A 24-hour ambulatory ECG was performed on the seventh day in order to determine the ischemic burden. SAECG findings (TQRS, RMS, LAS) were obtained on the seventh day, in the first and third months. The study was continued with the patients who did not require angioplasty as decided with angiographic evaluation in the first month. RESULTS: The study included 30 patients with acute myocardial infarction (mean age 51 +/- 12, 28 males and 2 females). The initial mean CK-MB levels and the mean ischemic burden were 98 +/- 31 U/L and 44 +/- 96 minutes. The TQRS (ms), LAS (ms), and RMS (microV) values (mean +/- SD ) obtained at day 7, month 1, and month 3 are 97 +/- 12, 96 +/- 9, 103 +/- 11, P = 0.01; 31 +/- 10, 31 +/- 11, 32 +/- 10, P = 0.46; 43 +/- 28, 41 +/- 26, 33 +/- 25, P = 0.01, respectively. We observed that the TQRS and RMS values changed significantly with time, but these levels of significance disappeared when adjusted for the initial ischemic burden and CK-MB levels (P = 0.06; P = 0.53). The VLP frequency was 33% at day 7 and 23% at month 3. Unlike the CK-MB level, the initial ischemic burden was significantly different between the patients with and without VLP at month 3 (150.85 +/- 149.28, 12.34 +/- 26.48, P = 0.001 ). When tested together with age and gender, it was found that the high initial ischemic burden increased the possibility of VLP (OR: 24, CI: 2.09-279.52, P = 0.01 ) at month 3. CONCLUSION: SAECG findings in patients with myocardial infarction changed with time; however, this change occurred depending on the initial ischemic burden and CK-MB levels. Of these, only the initial ischemic burden, especially in high levels, was a determinant for the presence of VLP in the late period of myocardial infarction.

Color Doppler tissue imaging to evaluate left atrial appendage function in mitral stenosis.

Two-dimensional color Doppler tissue imaging (CDTI) has so far been used, in general, to evaluate ventricular function. This study examined if the left atrial appendage tissue velocity could reproducibly be measured with CDTI and if they have any predictive value for left atrial appendage (LAA) function and former thromboembolism. Thirty-six patients (24 women, 12 men; mean age 45 +/- 12 years; 18 AF; 11 former thromboembolic stroke) with mitral stenosis undergoing transesophageal echocardiography were examined with CDTI. Peak systolic tissue velocity (m/sec, peak systolic velocity [PSV]) was measured at the tip of the LAA in the basal short-axis view. LAA flow emptying (LAAEV) and filling (LAAFV) velocities (m/sec) were also recorded 1 cm immediately below the orifice of the appendage. Interobserver and intraobserver variabilities were determined for the PSV. LAA ejection fraction was measured by Simpson's method. Mitral regurgitation, AF, transmitral mean gradient, left ventricular ejection fraction, mitral valve area, and left atrial diameter were used as a covariant for adjustment. The intraobserver and interobserver correlation coefficients for the PSV using CDTI was 0.64 and 0.60, respectively (bothP = 0.01). LAAEV(0.29 +/- 0.09 vs 0.19 +/- 0.04, P = 0.001)and LAA ejection fraction(44 +/- 12 vs 29 +/- 14, P = 0.004)were found to be significantly decreased in the patients with decreased PSV (<0.05 m/sec), even after adjustment. The decreased PSV was positively correlated with the low LAAEV (<0.25 m/sec) and history of thromboembolism (r = 0.59, r = 0.38, respectively), and remained a significant determinant of the low LAAEV (OR 50.03, CI 1.46-1738.11,P = 0.02), but not of history of thromboembolism (OR 4.29, CI 0.52-35.01,P = 0.08) after adjustment. In conclusion, these results suggest that CDTI provides a reproducible method for quantification of contraction at the tip of the LAA. Decreased PSV may be predictive of poor LAA function.

Evaluation of left atrial appendage functions in patients with thrombus and spontaneous echo contrast in left atrial appendage by using color Doppler tissue imaging.

OBJECTIVE: Thrombus and spontaneous echo contrast (SEC) develops in the left atrial appendage (LAA) when LAA function is disturbed. Decrease of left atrial appendage emptying velocity shows LAA dysfunction. The purpose of this study is to examine the incidence of SEC and/or thrombus in LAA in patients with acute myocardial infarction and to assess the LAA function using color Doppler tissue imaging (CDTI) of the patients with detected SEC and/or thrombus. METHOD AND RESULTS: Eighty-four patients with acute myocardial infarction were included in the study. Spontaneous echo contrast and/or thrombus were observed in 24 (29%) of the 84 patients who were categorized as group 1 (mean age 59 +/- 12 years). Sixty patients (71%) without thrombus and/or SEC in LAA were categorized as group 2 (mean age 58 +/- 8 years). Left atrial diameters and left ventricular ejection fraction were measured by using transthoracic echocardiography. Left atrial appendage emptying and LAA filling velocity were measured by transesophageal Doppler echocardiography. Systolic appendage tissue velocities (SaV cm/s) were measured at the basal, mid, and tip of medial wall of LAA by transesophageal CDTI. Group 1 had significantly decreased LAA emptying velocities, mid SaVs, and left ventricular ejection fractions compared to group 2 (37 +/- 9 cm/s vs 55 +/- 22 cm/s, 3.1 +/- 1.6 cm/s vs 3.7 +/- 1.2 cm/s, and 47 +/- 13% vs 58 +/- 10%, respectively, P = 0.002, P = 0.04, P = 0.03). Group 1 had significantly increased left atrial diameters compared to group 2 (40 +/- 5 mm vs 36 +/- 6 mm P = 0.001). Left atrial appendage-filling velocities, basal SaVs and tip SaVs in group 1 were lower than those in group 2 but not significantly. CONCLUSIONS: Mid-SaV of LAA medial wall and LAA emptying velocity decrease in patients with thrombus and/or SEC were an indication of functional disorder of LAA. Color Doppler tissue imaging appears to be a clinically applicable and reliable imaging technique that allows quantitative assessment of regional LAA systolic function.