Assessment of left ventricular systolic asynchrony in patients with clinical hypothyroidism.

BACKGROUND: Hypothyroidism has a large number of adverse effects on the cardiovascular system such as impaired cardiac contractility. Left ventricular (LV) asynchrony is defined as loss of the simultaneous peak contraction of corresponding cardiac segments. OBJECTIVE: To assess systolic asynchrony in patients with overt hypothyroidism. METHODS: Asynchrony was evaluated in 31 patients with overt hypothyroidism and 26 controls. Clinical hypothyroidism was defined as serum thyroid-stimulating hormone (TSH) more than 4.2 microIU/mL with reduced free T4 less than 1.10 ng/dL. All the patients and controls were subjected to an echocardiographic study including tissue synchronization imaging (TSI). The time to regional peak systolic velocity (Ts) in LV via the six-basal-six-mid-segmental model was measured on ejection phase TSI images, and four TSI parameters of systolic asynchrony were computed. LV asynchrony was described by these four TSI parameters. RESULTS: The demographic characteristics and conventional echocardiographic parameters of both groups were similar (except total and LDL cholesterol, TSH, free T3, and free T4). All TSI parameters of LV asynchrony were prolonged in hypothyroid patients compared to controls. The standard deviation (SD) of the 12 LV segments Ts was (53.5 +/- 14.1 vs. 29.3 +/- 15.5, P < 0.0001); the maximal difference in Ts between any 2 of the 12 LV segments was (154.5 +/- 37.3 vs. 91.9 +/- 45.2, P < 0.0001); the SD of Ts of the 6 basal LV segments was (47.9 +/- 15.9 vs. 27.1 +/- 16.4, P < 0.0001); and the maximal difference in Ts between any 2 of the 6 basal LV segments was (118.4 +/- 37.9 vs. 69.3 +/- 39.0, P < 0.0001). The prevalence of LV asynchrony was significantly higher in patients with hypothyroidism compared with controls (83.9% vs. 26.9%, P < 0.0001). CONCLUSION: Patients with overt hypothyroidism show evidence of LV asynchrony by TSI.

The relationship between endothelial damage and aortic augmentation index.

Augmentation index (AIx), a measure of wave reflection, is regulated by a number of factors, including endothelial function and vascular smooth muscle tone. The relationship between local endothelium-derived factors and AIx is well known; however, association between endothelial damage markers and AIx has not been sufficiently studied. This study investigates whether endothelial damage markers-von Willebrand factor (vWF) soluble thrombomodulin (sTM)--are associated with wave reflections. We studied 46 (48.5 +/- 10.6, years) never-treated patients with hypertension (HT) and an age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. von Willebrand factor and sTM levels were determined in all subjects. We evaluated the aortic AIx of the study population using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. Endothelial damage markers and AIx@75 were significantly higher in hypertensive patients than in controls. In the whole population, the vWF level (beta = 0.24, p = 0.01) was an independent determinant of AIx@75 in multivariate analysis. However, the sTM level was not associated with AIx@75. We found that the vWF level was an independent determinant of AIx@75. Our results suggest that increased an vWF level contributes significantly to increased wave reflections.

Effects of prehypertension on arterial stiffness and wave reflections.

The Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure classifies blood pressure (BP) as normal, prehypertension, and hypertension. Although it has been shown that there is a relationship between hypertension and arterial stiffness, there is not sufficient data about arterial stiffness in patients with prehypertension. The present study was designed to evaluate arterial stiffness and wave reflections in subjects with prehypertension. We evaluated arterial stiffness and wave reflections of 45 subjects with prehypertension and an age-matched control group of 40 normotensive individuals, using applanation tonometry (Sphygmocor, AtCor Medical, Sydney, Australia). Aortic pulse wave velocity (PWV) was measured as indices of elastic-type aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Aortic PWV (10 +/- 2.5 vs. 8.6 +/- 1.7, m/s, p = 0.004) and AIx@75 (21 +/- 8.3 vs. 10 +/- 9.1, %, p = 0.0001) were significantly higher in subjects with prehypertension than in the control group. In multiple linear regression analysis, we found that the presence of the prehypertension was a significant predictor of aortic PWV (beta = 0.26, p = 0.009) and AIx@75 (beta = 0.46, p = 0.0001). Our results suggest that arterial functions were impaired even at the prehypertensive stage.

Low total antioxidative capacity levels are associated with augmentation index but not pulse-wave velocity.

It is well known the relationship between oxidative stress and vascular function. However, association between total antioxidative capacity and arterial stiffness was not studied in patients with hypertension (HT). This study investigated whether total antioxidative capacity is associated with arterial stiffness and wave reflections. We studied 46 (age 48.5 +/- 10.6 years) never treated patients with HT and age-matched control group of 40 (age 47 +/- 8.6 years) normotensive individuals. Total antioxidative capacity level was determined in all subjects. We evaluated arterial stiffness and wave reflections of the study population, using applanation tonometry (SphygmoCor). Carotid-femoral pulse-wave velocity (PWV) was measured as index of aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Carotid-femoral PWV (10.5 +/- 2.2 vs 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT compared with age-matched control subjects. Total antioxidative capacity level (274 +/- 70 vs 321 +/- 56 micromol/l, P = 0.001) was significantly lower in hypertensive patients than controls. In the whole population, total antioxidative capacity level negatively correlated with AIx@75 (r = -0.24, P = 0.02) in univariable analysis, but not with carotid-femoral PWV (r = -0.08, P = 0.43). Also, we found that total antioxidative capacity level (beta = -0.21, P = 0.03) was an independent determinant of AIx@75 in multivariable analysis. Our results suggest that the decrease in the ability of antioxidant defenses contributes significantly to increased wave reflections.

Circulating levels of relaxin and its relation to cardiovascular function in patients with hypertension.

BACKGROUND: The role of endogenous relaxin on hypertensive cardiovascular damage remains unknown. We investigated the relaxin level and its relation to cardiovascular function in patients with never treated hypertension (HT). METHODS: We studied 42 (47.8+/-10 years) never treated patients with HT and 40 age-matched (47+/-8.6 years) normotensive individuals. Serum relaxin levels were determined in all subjects using enzyme-linked immunosorbent assay. Left ventricular (LV) diameters were evaluated by transthoracic echocardiography. Ejection fraction and LV mass index were measured. Diastolic functions were evaluated with both conventional and tissue Doppler echocardiography. We evaluated central aortic pressures, heart rate-corrected augmentation index (AIx@75), a marker of wave reflections, and aortic pulse wave velocity (PWV) as indices of elastic-type aortic stiffness of the study population using applanation tonometry (SphygmoCor). RESULTS: Relaxin levels were significantly lower in hypertensive patients as compared with controls (36.5+/-7.3 vs 49.7+/-39.8 pg/ml, p=0.03). The relaxin level was negatively correlated with brachial and central aortic pressure. However, serum relaxin was not significantly associated with LV diameters, ejection fraction, LV mass index, LV diastolic function, AIx@75 or aortic PWV in our study. CONCLUSION: Serum relaxin is decreased in patients with HT. However, low endogenous relaxin is not related to cardiovascular function.

Assessment of left ventricular systolic synchronization in patients with chronic kidney disease and narrow QRS complexes.

OBJECTIVE: The evidence of structural and functional cardiac abnormalities has been demonstrated by echocardiography in patients with chronic kidney disease (CKD). This study investigated whether left ventricular (LV) asynchrony is present in patients with CKD and normal QRS duration. METHODS: Tissue synchronization imaging (TSI) was performed in 25 (56 +/- 14 years) patients with CKD and narrow QRS complexes and 25 (51 +/- 12 years) control subjects. LV asynchrony was identified on TSI images and the time to regional peak systolic velocity (Ts) in LV was measured by the six-basal-six-midsegmental model. Four TSI parameters of systolic asynchrony were computed when Ts was measured in ejection phase. RESULTS: The standard deviation of Ts of 12 LV segments (33.6 +/- 17.8 vs 16.7 +/- 10 ms, P = 0.0001), standard deviation of Ts of the six basal LV segments (30 +/- 20 vs 17.6 +/- 9.6 ms, P = 0.008), maximal difference in Ts between any two of the 12 LV segments (102 +/- 45 vs 54 +/- 32 ms, P = 0.0001), and maximal difference in Ts between any two of the six basal LV segments (78 +/- 50 vs 46 +/- 22 ms, P = 0.007) were prolonged in patients with CKD compared with controls. The prevalence of LV systolic asynchrony was significantly higher in patients with CKD compared with controls (44% vs 12%, P = 0.01). The standard deviation of Ts of 12 LV segments were significantly associated with LV diameters, LV volumes, LV mass, blood pressure levels, and renal functions in univariate analysis. CONCLUSION: The results of this study indicate that LV systolic asynchrony may develop in patients with CKD.

Assessment of left ventricular function and Tei index by tissue Doppler imaging in patients with slow coronary flow.

BACKGROUND: The aim of this study was to assess left ventricular (LV) function and the Tei index by tissue Doppler imaging (TDI), and also to evaluate the relationship of thrombolysis in myocardial infarction (TIMI) frame count (TFC) with the Tei index and LV function in patients with slow coronary flow (SCF). METHODS: We prospectively evaluated 50 patients with SCF and 27 control subjects. Diagnosis of SCF was made by TFC. LV systolic and diastolic function was assessed by conventional echocardiography and TDI. RESULTS: Early diastolic mitral annular velocity (Em), Em/Am, and peak systolic mitral annular velocity (Sm) were lower in patients with SCF than those in controls (13+/-2.8 cm/sec vs 15.2+/-2.8 cm/sec, P = 0.002; 0.88+/-0.22 vs 1+/-0.23, P = 0.03; and 14.1+/-3.51 vs 16.5+/-3.31, P = 0.005, respectively). In patients with SCF, the Tei index was significantly higher than that in controls (0.34+/-9.6 vs 0.29+/-9.5, P = 0.02, respectively). Mean TFC and RCA TFC were positively correlated with the Tei index (r = 0.3, P = 0.02 and r = 0.329, P = 0.02). Left circumflex (LCX) TFC was negatively correlated with Em/Am (r =-0.310, P = 0.03) only in patients with SCF. CONCLUSION: LV systolic and diastolic function is impaired in patients with SCF. TDI analysis of mitral annular velocities such as the Tei index, Em, Em/Am, and Sm is useful to assess LV systolic and diastolic dysfunction in patients with SCF. Mean TFC and RCA TFC were positively correlated with the Tei index and LCX TFC was negatively correlated with Em/Am. TDI may be better than conventional echocardiography in assessing LV function in patients with SCF.

Impairment in flow-mediated vasodilatation of the brachial artery in acromegaly.

OBJECTIVE: The aim of this study was to assess flow-mediated dilatation (FMD) of the brachial artery in patients with acromegaly. SUBJECTS AND METHODS: We prospectively evaluated 25 patients with acromegaly (14 females, 11 males; aged 42 +/- 12 years; growth hormone (GH) levels 34 +/- 14 ng/ml) and 27 control subjects (15 females, 12 males; aged 45 +/- 8 years; GH levels 3 +/- 1.5 ng/ml). The patients and controls were matched for age, gender, body mass index, cigarette smoking, blood pressure, lipid levels, diabetes mellitus, hypertension, and its duration. Endothelial function, measured as FMD of the brachial artery using ultrasound, was calculated in the 2 groups. The endothelial function was evaluated by assessing 1-min postischemic FMD of the brachial artery. RESULTS: The FMD was lower in patients with acromegaly (9.97 +/- 3.5%) than in controls (16.1 +/- 3.4%), and the difference was statistically significant (p = 0.0001). CONCLUSION: Endothelial dysfunction may develop in the preclinical phase of atherosclerosis in patients with acromegaly. Endothelium-dependent FMD may be impaired in acromegalic patients, and measurement of endothelial function may identify high-risk individuals earlier.

[Primary prevention trials performed with statins prior to the JUPITER trial]. / JUPITER çalismasi öncesi statinlerle yapilan primer koruma çalismalari.

The invention of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, namely statins, after the mid-1980s, initiated a new era in the approach to atherosclerotic diseases. Many studies of primary prevention, secondary prevention, and plaque regression have been carried out with statins. This paper will discuss primary prevention studies that were performed with statins prior to the JUPITER trial.

Relationship between arterial stiffness and myocardial damage in patients with newly diagnosed essential hypertension.

BACKGROUND: Arterial stiffness increases in hypertensive individuals. Arterial stiffness is associated with impairment of systolic and diastolic myocardial function in hypertension (HT). However, the relationship between arterial stiffness and serum heart-type fatty acid-binding protein (H-FABP) levels, a sensitive marker of myocardial damage, has not been previously examined in patients with HT. We investigate the relationship between serum H-FABP levels and arterial stiffness in patients with newly diagnosed HT. METHODS: We studied 46 (48.5 +/- 10.6, years) never-treated patients with HT and age-matched control group of 40 (47 +/- 8.6, years) normotensive individuals. H-FABP levels were determined in all subjects. We evaluated arterial stiffness and wave reflections of study population, using applanation tonometry (Sphygmocor). Carotid-femoral pulse wave velocity (PWV) was measured as indices of elastic-type, aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a marker of wave reflections. RESULTS: Carotid-femoral PWV (10.5 +/- 2.2 vs. 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs. 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT than control group. H-FABP levels were increased in hypertensive patients compared with control group (21.1 +/- 14.8 vs. 12.9 +/- 8.5, ng/ml, P = 0.002). In multiple linear regression analysis, we found that the body mass index (beta = 0.42, P = 0.0001) and carotid-femoral PWV (beta = 0.23, P = 0.03) were significant determinants of H-FABP levels. CONCLUSION: Arterial stiffness is associated with serum H-FABP levels, a sensitive marker of myocardial damage, in patients with newly diagnosed HT.

Association between serum C-reactive protein elevation and atrial fibrillation after first anterior myocardial infarction.

BACKGROUND: Elevated inflammatory markers have been found to correlate with higher risk for cardiac events in patients with acute myocardial infarction (AMI). It has been suggested that C-reactive protein (CRP) may be involved in the initiation process of atrial fibrillation (AF). However, the role of CRP levels in the occurence of AF in patients with AMI has not been studied. This study investigated whether CRP is a risk factor for AF in patients with acute anterior MI. METHODS: We prospectively evaluated 92 consecutive patients (25 women and 67 men; aged 58 +/- 11 y) with a first acute anterior wall MI. Blood samples were obtained at the time of admission to the hospital, and serum CRP levels were measured by an ultrasensitive immunonephelometry method. All patients were evaluated by echocardiography to measure the left ventricular (LV) diameter and functions. All patients were monitored continuously for the detection of AF in the coronary care unit. RESULTS: Atrial fibrillation occured in 19 (20%) of 92 patients. Univariate analysis showed that patients with AF had an advanced age (63 +/- 9.9 versus 56.7 +/- 11.7 y, p = 0.034), higher serum CRP level (2.95 +/- 2.5 versus 1.71 +/- 2.12 mg/dL, p = 0.034), larger LV end-systolic volume (74 +/- 15 versus 63 +/- 19, mL p = 0.02), higher LV ejection fraction (31.1 +/- 6.2 versus 38.4 +/- 10%, p = 0.001), and larger left atrial (LA) diameter (37.1 +/- 4.2 versus 34.7 +/- 3.3 mm, p = 0.01). In multivariate analysis, only age (odds ratio [OR]: 1.05, 95% confidence interval [CI]: 1-1.11, p = 0.036) and CRP levels (OR: 1.27, 95% CI: 1-1.59, p = 0.039) were independent predictors of AF. CONCLUSION: These results suggest that CRP may be a risk factor for AF in patients with acute anterior wall MI.

Aortic pulse wave velocity in subjects with aortic valve sclerosis.

BACKGROUND: Aortic stiffness is an independent risk factor for cardiovascular events and mortality. The measurement of pulse-wave velocity (PWV) is the most simple, noninvasive, and robust method to determine aortic stiffness. Whether aortic stiffness contributes to aortic valve sclerosis (AVS) remains unknown. The aim of the present study was to examine the relationship between PWV and AVS in subjects free of clinically evident atherosclerotic disease. METHODS: We enrolled 62 patients (48 men; age 65 +/- 8 years) diagnosed with AVS and an additional 62 age-, hypertension-, diabetes mellitus-, and history of smoking-matched subjects without AVS. Applanation tonometry was applied to assess the augmentation index and aortic PWV. The subjects with symptomatic vascular disease were excluded from the study. AVS was defined by echocardiography as thickening and calcification of the normal trileaflet aortic valve without obstruction to the left ventricular outflow. RESULTS: There was no significant difference between the two groups regarding the aortic PWV and augmentation index (11.7+/-3.3 vs 11.8+/-3.7, P=0.85; 28.0+/-9.4 vs 25.0+/-8.6, P=0. 17, respectively). The presence of AVS was significantly correlated with ejection fraction (r=0.211, P=0.011), male gender (r=0.362, P=0.0001), and age (r=0.200, P=0.026). CONCLUSIONS: The lack of an association between the aortic PWV and AVS suggests that AVS is a complex phenomenon consisting of several distinct processes, related to both atherosclerotic and nonatherosclerotic processes.

Evaluation of left ventricular function using Tei index in patients with preinfarction angina.

OBJECTIVE: The study investigated whether preinfarction angina influences left ventricular functions assessed using Tei index, which is an independent predictor for left ventricular dysfunction in acute myocardial infarction. METHODS: We studied 96 patients with acute myocardial infarction with ST segment elevation (80 men, 16 women; mean age 57.5+/-9.9 years) who were assigned into 2 groups: with and without preinfarction angina. All patients were serially evaluated by 2-dimensional and Doppler echocardiography on the days 1, 6, and 30, and were followed up for 30 days for incidence of complications. RESULTS: We observed that Tei index was lower on the days 1, 6 and 30 (0.49+/-0.20 vs. 0.59+/-0.20, p=0.003, 0.46+/-0.20 vs. 0.56+/-0.20, p=0.001, 0.44+/-0.20 vs. 0.53+/-0.10, p=0.01) in patients with preinfarction angina as compared with those without angina. Tei index significantly decreased during follow-up (0.49+/-0.20, 0.46+/-0.20, 0.44+/-0.20; p=0.02) in patients with preinfarction angina, while it did not change significantly in patients without preinfarction angina (p=0.2). Echocardiographically significant improvements were observed in E deceleration time, isovolumic relaxation time and ejection time in all patients, whereas significant improvements in ejection fraction, wall motion score index and isovolumic contraction time were observed only in patients with preinfarction angina during follow-up. Mortality, Killip class >or=2, pericarditis, atrial fibrillation, and left ventricular thrombus were lower in patients with preinfarction angina. CONCLUSION: These data indicated that the patients with preinfarction angina had better preserved systolic left ventricular function and Tei index values. Also, it was observed that preinfarction angina may cause earlier and more prominent myocardial functional recovery and confer protection against complications on short-term after first acute myocardial infarction.

Assessment of left ventricular function by Doppler tissue imaging in patients with atrial fibrillation following acute myocardial infarction.

AIMS: We studied tissue Doppler parameters in patients with atrial fibrillation following acute myocardial infarction, and their relation to P wave durations and P dispersion. METHODS: Echocardiographic examination was performed in 84 consecutive patients with first anterior acute myocardial infarction. In addition to other conventional echocardiographic parameters, the peak systolic (Sm), early diastolic (Em) and late diastolic (Am) velocities were obtained at the lateral corner of the mitral annulus by pulsed wave tissue Doppler. The Em/Am ratio and the ratio of early diastolic mitral inflow velocity to Em (E/Em), which is a marker of diastolic filling pressure, were calculated. Electrocardiogram was recorded from all patients on admission; P wave measurements were also performed. RESULTS: Atrial fibrillation occurred in 20 (23.8%) of 84 patients. The patients with atrial fibrillation had significant reduction of Em (5.6+/-1.5 vs. 8.7+/-2.7 cm/s, p < 0.001), Em/Am (0.61+/-0.27 vs. 0.84+/-0.23, p = 0.001) and Sm (7.1+/-1.0 vs. 8.3+/-1.9 cm/s, p < 0.001) values compared with those without. The E/Em ratio (14.45+/-4.62 vs. 7.47+/-2.79, p < 0.001), P maximum (102+/-11 vs. 95+/-11 ms, p = 0.02) and P dispersion (35+/-7 vs. 26+/-7 ms, p < 0.001) were significantly higher in patients with atrial fibrillation than in those without. In all patients, P dispersion showed significant correlation with Em (r = -0.33, p = 0.002), Sm (r = -0.40, p < 0.001) and E/Em (r = 0.32, p = 0.003). When E/Em > or = 10 was used as cutpoint, atrial fibrillation could be predicted with a sensitivity of 90%, and a specificity of 84%. CONCLUSIONS: The patients with atrial fibrillation following acute myocardial infarction have reduced systolic and diastolic mitral annular velocities and increased E/Em ratio, P maximum and P dispersion values compared to those without. P dispersion is correlated with systolic and diastolic left ventricular function after acute myocardial infarction. The E/Em ratio appears to be a useful parameter for assessing the risk of atrial fibrillation occurrence after anterior acute myocardial infarction.

Pulsed wave tissue Doppler-derived myocardial performance index for the assessment of left ventricular thrombus formation risk after acute myocardial infarction.

BACKGROUND: Assessment of left ventricular (LV) thrombosis risk after acute myocardial infarction (AMI) is important because of potential embolic sequelae that are reduced by oral anticoagulant agents. The goal of this study was to investigate whether early assessment of LV systolic and diastolic performance with pulsed wave tissue Doppler ultrasound scanning (PWTD) predicts LV thrombosis after AMI. METHODS: Two-dimensional and Doppler ultrasound scanning echocardiographic examinations were performed in 92 consecutive patients (age, 58 +/- 10 years; 11 women) with first anterior AMI within 24 hours after arrival to the coronary care unit. From the apical 4-chamber view, the mitral annular velocities were recorded at the lateral corner of the mitral annulus with PWTD. The myocardial performance index (MPI), which combines parameters of both systolic and diastolic ventricular function, was calculated from the PWTD recordings. To analyze LV thrombus formation, the 2-dimensional echocardiographic examination was repeated on days 3, 7, 15, and 30. The patients were divided in 2 groups according to LV thrombus formation. RESULTS: LV thrombus was found in 32 of 92 patients (35%; group 1) and was not found in 60 patients (65%; group 2). The MPI was significantly higher in group 1 than in group 2 (0.73 +/- 0.20 vs 0.53 +/- 0.14; P <.001). When an MPI >0.6 was used as the cutoff, LV thrombus formation could be predicted with a sensitivity rate of 81%, a specificity rate of 73%, a positive predictive value of 62%, and a negative predictive value of 88%. In multivariate analyses, only MPI and LV wall motion score index were independent predictors of LV thrombus formation (P = .038 and P = .047, respectively). CONCLUSIONS: The MPI derived with PWTD soon after admission appears to be a useful parameter for assessing the risk of LV thrombosis after AMI. Patients with an MPI >0.6 after AMI seem to be at a higher risk for thrombus formation.

Assessment of left ventricular systolic and diastolic function by Doppler tissue imaging in patients with preinfarction angina.

BACKGROUND: The aim of this study was assessment of left ventricular (LV) systolic and diastolic function by pulsed wave Doppler tissue imaging (DTI) in patients with or without preinfarction angina in acute myocardial infarction. METHODS: We prospectively evaluated 31 consecutive patients (4 women, 27 men; age 58 +/- 10 years) with a first acute myocardial infarction. LV systolic and diastolic function was assessed by classic methods and DTI on the third day during acute myocardial infarction. Patients were divided into 2 groups according to the presence (group 1; n = 10) or absence (group 2; n = 21) of preinfarction angina. Mitral inflow velocities and early diastolic mitral annular velocity (Em), late diastolic mitral annular velocity (Am), peak systolic mitral annular velocity, Em/Am, the ratio of early diastolic mitral inflow velocity (E) to Em, and myocardial performance index were calculated by DTI. RESULTS: Group 1 had significantly higher Em and Em/Am than group 2 (11.3 +/- 3.34 cm/s vs 7.4 +/- 2.07 cm/s, P <.0001; 1.01 +/- 0.38 cm/s vs 0.6 +/- 0.2 cm/s, P =.001, respectively). The E/Em ratio and myocardial performance index were significantly lower in group 1 than in group 2 (5.1 +/- 2.92 vs 8.10 +/- 3.15, P=.018; 0.49 +/- 0.15 vs 0.65 +/- 0.24, P =.042, respectively). Wall-motion score index was lower in those with preinfarction angina than in those without (1.6 +/- 0.36 vs 1.9 +/- 0.39; P =.04, respectively). Peak systolic mitral annular velocity and Am were not statistically different between groups (9.4 +/- 1.84 vs 8.3 +/- 2.03, P =.172; 11.7 +/- 3.07 vs 12.1 +/- 3.34, P =.72, respectively). There were no significant differences between the 2 groups regarding transmitral E velocity, atrial contraction mitral inflow velocity (A), E/A ratio, isovolumetric relaxation time, and deceleration time of the mitral E wave (P =.91, P =.08, P =.58, P =.81, and P =.71, respectively). CONCLUSION: LV diastolic function was better in patients with preinfarction angina than in patients without. This condition could not be detected by conventional mitral inflow Doppler velocities, but could be detected by DTI. This preliminary evidence shows that DTI is better than conventional mitral Doppler indices in the assessment of a favorable LV diastolic function in patients with preinfarction angina.

Plasma fibronectin level and its association with coronary artery disease and carotid intima-media thickness.

BACKGROUND: The exact relation of fibronectin with coronary atherosclerosis is unknown. The aim of the present study was to examine the association of fibronectin level with presence and extent of coronary artery disease (CAD) and intima-media thickness (IMT) of common carotid artery (CCA). DESIGN: The IMTs of CCA of 86 patients who underwent coronary angiography were measured; traditional vascular risk factors were also evaluated in these patients. Fibronectin, lipids, C-reactive protein (CRP) and fibrinogen levels were determined. RESULTS: Plasma fibronectin levels of the patients with CAD were found to be significantly elevated compared to patients with normal vessels (0.46+/-0.11 and 0.36+/-0.12 mg/dl respectively, P = 0.001). Fibronectin levels were not associated with extent of CAD. No significant association was observed between fibronectin level and traditional risk factors. IMTs of right and left CCA in patients with CAD were found to be elevated compared to patients with normal vessels (0.89+/-0.1 mm compared with 0.76+/-0.1 mm, P = 0.001 and 0.93+/-0.2 mm compared with 0.71+/-0.1 mm, respectively P < 0.001). Fibronectin levels were positively correlated with CRP (r = 0.45, P < 0.001), low-density lipoprotein-cholesterol (r = 0.23, P = 0.03) and total cholesterol (r = 0.21, P = 0.04) levels and negatively correlated with high-density lipoprotein-cholesterol (HDL-C) levels (r = -0.24, P = 0.02). IMT of left CCA was positively correlated with CRP levels (r = 0.23, P = 0.04) and negatively correlated with HDL-C levels (r = 0.2, P = 0.04). Logistic regression analysis showed that age (P < 0.01) and fibronectin levels (P = 0.01) were independent predictors for the existence of CAD. CONCLUSIONS: The results suggest that fibronectin levels may be a significant predictor of CAD. However, it was shown that fibronectin levels were not associated with extent of CAD and IMT of CCA.

Granulocytic sarcoma presenting as a right atrial mass.

We describe a 48-year-old male who developed acute myelogenous leukaemia (AML) associated with a right atrial mass. The patient was admitted with fatigue, positional dyspnoea and headache. Transthoracic echocardiography (TTE) and transoesophageal echocardiography (TEE) revealed that the right atrium was filled with a mass. Peripheral blood smear revealed 85% blasts, and bone marrow examination showed 74% myeloid blasts and 27% monocytoid cells (monoblast and promonocytes). Immunophenotypic analysis of the bone marrow aspirates showed CD13, CD14 and CD33 positivity, consistent with acute myeloid leukaemia of M4 Fab subtype. The patient achieved remission (but not cure) accompanied by near resolution of the right atrial mass following intensive chemotherapy.

Cannulation of a LIMA graft via the right brachial arterial route using a MANI catheter: an alternative approach.

Some different revascularization methods including coronary artery bypass surgery can be performed in the treatment of coronary artery disease. Saphenous vein grafts and/or arterial grafts including left internal mammary artery (LIMA) can be implanted during coronary bypass surgery. It is necessary to perform cannulation of the LIMA, in order to diagnose and treat these patients. In addition to conventional internal mammary artery catheters, several types of catheters can be used for this purpose. In general, LIMA catheterization via the femoral artery has been preferred over other methods. However, the right brachial arterial approach can be mandatory in some rare conditions. In this report, we describe an alternative method to the conventional techniques of the LIMA graft angiography via the right brachial arterial approach using a MANI catheter. According to our knowledge, no data are available using the MANI catheter for this purpose in the current literature.

The effect of the aspiration of pericardial effusion on intraocular pressure.

OBJECTIVE: To assess the effect of pericardial effusion on intraocular pressure (IOP). PATIENTS AND METHODS: Twenty-two patients with pericardial effusion were enrolled into the study. The average pericardial effusion was 2245 +/- 257 cc, and the mean IOP was 26.1 +/- 2.1 mm Hg in the initial examination. Pericardial effusion was aspirated via canula under topical anaesthesia at two or three-day intervals. IOP was measured after every aspiration of pericardial fluid. We statistically compared the changes in the mean IOP after every aspiration (one-way ANOVA), and calculated the correlation (regression analysis) between the amount of fluid and the changes in IOP. RESULTS: An average of 400 ml of fluid was aspirated at two or three-day intervals. The mean IOP decreased to 23.3, 21.2, 19.1 and 16.3 mm Hg after aspirations, respectively. These decreases in the mean IOP were statistically significant (p < 0.01). In regression analysis, we observed a meaningful relationship between the changes in IOP and the amount of pericardial effusion (p < 0.001). CONCLUSION: We found that pericardial effusion affected IOP due to increased episcleral venous pressure. Therefore, patients with pericardial effusion should be referred for an ophthalmological examination with IOP measurement. IOP-lowering medication can eventually be started or adjusted by the ophthalmologist.