Search

Acquired pseudoaneurysm of the left ventricle is a rare disorder that usually ofvccurs 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.

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.

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.

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 (μV) 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, Cl: 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. A.N.E. 2002;7(3):242–246

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

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.

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. ( Cardiol J 2011; 18, 6: 654–661 )

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.

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.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.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.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.

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.

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.

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.

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.

Two-dimensional color Doppler tissue imaging (CDTI) has so far been used, in general, to evaluate ventricular function. In this study, the left atrial appendage (LAA) tissue velocity was measured by CDTI. LAA function in 38 patients with mitral stenosis in sinus rhythm (SR) and 19 healthy subjects undergoing transesophageal echocardiography were examined by CDTI. Systolic tissue appendage velocity (SaV, m/s) was measured at the tip of the LAA in the basal short-axis view. LAA emptying (LAAEV) and filling (LAAFV) velocities (m/s) were also recorded 1 cm below the orifice of the appendage. LAA ejection fraction was also measured. In addition, two-dimensional imaging was used to determine the presence of thrombus and/or spontaneous echo contrast (SEC). Patients with mitral stenosis in SR had significantly decreased LAAEV, LAAFV, SaV, and LAA ejection fraction compared to controls (0.34 +/- 0.15 vs 0.72 +/- 0.17, 0.37 +/- 0.13 vs 0.63 +/- 0.19, 0.050 +/- 0.015 vs 0.071 +/- 0.093, and 39 +/- 14% vs 69 +/- 13%, respectively, P < 0.001, P < 0.001, P < 0.001, and P < 0.001). Among the patients with mitral stenosis in SR, 10 patients had SEC and one had LAA thrombus. Compared with patients without SEC, patients with SEC had decreased LAAEV, LAAFV, SaV, and LAA ejection fraction (0.24 +/- 0.05 vs 0.37 +/- 0.16, 0.29 +/- 0.05 vs 0.39 +/- 0.14, 0.039 +/- 0.087 vs 0.055 +/- 0.015, and 28 +/- 14% vs 43 +/- 12%, respectively, P = 0.01, P = 0.02, P = 0.01, and P = 0.006). In conclusion, these results suggest that the LAA dysfunction may occur in patients with mitral stenosis in SR and CDTI can successfully be used for the quantification of contraction at the tip of the LAA.

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.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.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).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.

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.