Timing of Coronary Angiography After Successful Fibrinolytic Therapy in ST-Segment Elevated Myocardial Infarction.

BACKGROUND: We aimed to compare outcomes of patients received successful fibrinolytic treatment (FT) for ST-segment elevated myocardial infarction (STEMI) and performed coronary angiography (CAG) within 24 - 72 h or after 72 h. METHODS: Between March 2013 and November 2014, 76 STEMI patients received successful FT and performed CAG > 24 h were included in the study. Patients were divided into two groups according to the time-interval from FT admission to CAG performing (Group-1, 24 - 72 h (n = 29), Group-2, > 72 h (n = 47)). The primary end point was major adverse cardiac events (MACE) defined as cardiovascular death, non-fatal myocardial infarction, and heart failure. RESULTS: The mean age of patients were 56 ± 11.4 years old (27.6% female). CAG was performed within mean 2.17 ± 0.38 days in the Group-1 and 2.9 ± 11.5 days in the Group 2 (P < 0.001). At short-term follow-up (6 months), MACE rate was higher in Group-2 (21.3%) than Group-1(13.8%), but it was not statistically significant (P = 0.661). The rate of MACE was 37.9% in Group-1 and 38.3% in Group-2 (P = 0.974) in the long-term follow-up (median: 57 months). Overall cardiac mortality rate was 7.9%, the re-infarction rate was 19.7% and heart failure was 17.1% in long-term follow-up, and there were no significant difference between groups. CONCLUSIONS: Present study has shown that performance of CAG after 24 h of successful FT, within 24 - 74 h or > 72 h, did not shown any difference in term of MACE both in short and long-term follow-up.

The role of specialized prevention clinics for the short term follow-up of acute coronary syndromes.

OBJECTIVE: This study aimed to investigate the effect of specialized prevention clinics and standard clinics follow-ups on secondary protection after acute coronary syndrome (ACS) on cardiovascular risk factors. METHODS: A total of 118 patients who received thrombolytic therapy after being diagnosed with ST-segment elevation myocardial infarction were followed up for 6 months. After ACS, patients in a specialized prevention clinic (Group 1) (n=67) and those in a standard clinic (Group 2) (n=51) were compared in terms of the change in their lifestyle, management of risk factors, and drug compliance. RESULTS: No significant difference was found between groups in terms of baseline clinical and laboratory findings except for triglyceride level (Group 1: median 174 mg/dL; Group 2: median 136 mg/dL; p=0.039). Six months after indexing, smoking cessation (72.4% vs. 50%, p=0.037), diet compliance (43% vs.19.6%, p=0.012), and exercise rates (31% vs. 13.7%, p=0.044) were significantly higher in Group 1. Although the weight control rate was higher in Group 1, no significant difference was noted between the groups (27% vs. 15.6%, p=0.219). The rate of systolic and diastolic blood pressures >140/90 mmHg was significantly higher in Group 2 (23.5% vs. 9%, p=0.029) at 6 months. The median low-density lipoprotein cholesterol (LDL-C) value was significantly lower in Group 1 patients (Group 1: 91 mg/dL; Group 2: 102 mg/dL; p=0.042). Moreover, the rate of LDL-C ≤70 mg/dL or ≥50% reduction compared with baseline was significantly higher in Group 1 (32.8% vs. 13.7%, p=0.016). Although the recommended treatments were similar in both groups, the statin use rate was significantly higher in Group 1 (95.5% vs. 80.3%, p=0.021) at 6 months. CONCLUSION: The results of the study showed that specialized prevention clinics were more effective during the management of cardiovascular risk factors after ACS.

Brugada syndrome, Brugada phenocopy or none?

Brugada syndrome is a form of inherited arrhythmia syndrome characterized by a distinct ST-segment elevation in the right precordial leads. Brugada phenocopies are clinical entities that present with an electrocardiographic pattern identical to Brugada syndrome and may obey to various clinical conditions. We present a case of a suicidal attempt using a high dose of propafenone causing a Brugada-type electrocardiographic pattern. Is this a Brugada syndrome case, a Brugada phenocopy or something else?

Levosimendan versus dobutamine in heart failure patients treated chronically with carvedilol.

INTRODUCTION: Although beta-blockers are highly effective in the treatment of heart failure (HF), many patients with HF receiving a beta-blocker continue to become decompensated and require hospitalization for worsening HF. Levosimendan and dobutamine are used to manage decompensated HF, but their comparative effects on left ventricular (LV) function in patients prescribed beta-blockers are unknown. AIMS: The aim of this study was to compare the effects of dobutamine and levosimendan on LV systolic and diastolic functions in chronic HF patients treated chronically with carvedilol. Forty patients with chronic HF who had NYHA class III to IV symptoms, a LV ejection fraction (LVEF) <40%, and ongoing treatment with carvedilol were enrolled in this randomized (1:1), dobutamine controlled, open-label study. Before and 24 h after treatment, LVEF, mitral inflow peak E and A wave velocity, E/A ratio, the deceleration time of the E wave (DT), isovolumic relaxation time (IVRT), peak systolic (Sm) and early diastolic (Em) mitral annular velocity, and systolic pulmonary artery pressure (SPAP) were measured by echocardiography. RESULTS: Levosimendan produced a statistically significant increase in LVEF (28+/-5% vs. 33+/-3%), Sm (6.5+/-1.2 cm/s vs. 7.4+/-0.9 cm/s), DT (120+/-10 ms vs. 140+/-15 ms), and Em (7.5+/-0.4 cm/s vs. 8.1+/-0.5 cm/s) and significant decrease in E/A ratio (2.1+/-0.3 vs. 1.7+/-0.4) and SPAP (55+/-5 mmHg vs. 40+/-7 mmHg). No significant change occurred in LV systolic and diastolic function parameters, or SPAP with dobutamine treatment. Levosimendan did not significantly alter the heart rate (72+/-4 bpm vs. 70+/-3 bpm), systolic (105+/-5 mmHg vs. 102+/-4 mmHg), or diastolic blood pressure (85+/-5 mmHg vs. 83+/-5 mmHg) whereas with dobutamine treatment, all these parameters significantly increased. CONCLUSIONS: Dobutamine and levosimendan have different effects on LV functions in patients treated chronically with carvedilol. These differences should be considered when selecting inotropic therapy for decompensated HF receiving long-term carvedilol.

Statin use is associated with decreased CD-40 ligand expression on T lymphocytes of coronary atheroma plaque in patients with stable coronary artery disease.

OBJECTIVE: Atherosclerosis is a chronic inflammatory disease. Statins suppress the inflammation in the plaque. This cross-sectional study was planned to evaluate the effect of statins on plaque T cell activation markers in patients with stable angina pectoris undergoing coronary intervention and atherectomy procedures. METHODS: Twenty-six patients with stable angina with suitable for atherectomy coronary lesions were enrolled in the study. Fourteen of 26 patients who had been taking statin treatment for at least six months were assigned to the Group 1 (Statin group) and 12 patients who had not received any lipid lowering treatment comprised the Group 2 (Control group). Atherectomy specimens were studied with single and double immunohistochemical staining (CD25, CD69, and CD40L). Statistical analysis was performed using Student's t-test and Fisher's exact test. RESULTS: There was no significant difference between the total tissue area of sections (Group 1: 8.4+/-0.9 mm2, Group 2: 7.8+/-0.9 mm2, p>0.05). CD3, CD25, CD69, and CD40L positive cells did not show statistically significant difference between the groups in unit area (mm2). There was no significant difference between the groups for percentage of T lymphocytes expressing CD25 (Group 1: 7.8+/-4.6%, Group 2: 7.8+/-5.9%, p=0.97) and CD 69 (Group 1: 12.9+/-4.6%, Group 2: 15.5+/-5.2%, p=0.203). The expression of CD40L was significantly lower in Group 1 than in Group 2 (Group 1: 4.8+/-3.9%, Group 2: 11.2+/-8.7%, p=0.034). CONCLUSION: We concluded that, statin treatment may decrease the expression of CD40L on plaque T lymphocytes in patients with stable angina pectoris.

Effect of mean platelet volume on postintervention coronary blood flow in patients with chronic stable angina pectoris.

OBJECTIVES: In our study we sought to determine whether mean platelet volume (MPV), measured on admission, could be used in determining decreased coronary blood flow (CBF) in stable coronary artery disease (CAD) patients after percutaneous coronary intervention (PCI). BACKGROUND: Platelets play a crucial role in the pathophysiology of CAD. MPV reflects platelet function and activity. There are no reports regarding the effect of MPV on CBF in patients with stable CAD undergoing PCI. METHODS: A total of 66 consecutive patients (mean age: 58 +/- 5 years, 74% male) with the diagnosis of stable CAD who were hospitalized for PCI were prospectively enrolled in our study. Coronary flow rates of all subjects were documented by corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC) for each major coronary artery before and after PCI. Blood samples for MPV estimation, platelet count and other laboratory data obtained on admission were measured on the day of the scheduled PCI. Patients were divided into two groups according to MPV levels measured on admission: 1) high MPV group and 2) normal MPV group. RESULTS: A final TIMI 3 flow was achieved in all patients with no complications. Procedural characteristics of PCI, except left anterior descending artery intervention, were similar in the two groups. Patients with high MPV had significantly higher CTFC than those with a normal MPV (24 +/- 3 vs. 17 +/- 5; p = 0.001). The MPV correlated strongly with post-PCI CTFC (R = 0.625; p = 0.0001). Multiple logistic regression analysis showed that only MPV was an independent predictor of post-PCI CTFC after adjustment for baseline characteristics (OR 1.9, 95% CI 1.2-2.3; p = 0.001). CONCLUSIONS: MPV may be considered a useful hematological marker, allowing for early and easy identification of patients with stable CAD who are at a higher risk of post-PCI low-reflow.

Angiographic analysis of the anatomic relation of coronary arteries to mitral and tricuspid annulus and implications for radiofrequency ablation.

Coronary artery (CA) narrowings and/or occlusions after radiofrequency ablation (RFA) have been reported. The aim of this study was to describe the in vivo topographic anatomy of CAs and their anatomic relation to the mitral and tricuspid annulus using selective coronary angiography. Fifty consecutive patients undergoing RFA for narrow QRS complex tachycardia were included in the study. Multipolar electrode catheters were inserted into the right atrial appendage, His bundle region, distal coronary sinus (CS), and right ventricle. A mapping catheter was placed across the subeustachian isthmus (SEI). Selective coronary angiography was performed. The maximum and minimum distances between the distal CAs and the mapping catheter located along the mitral and tricuspid annulus were measured during systole and diastole and in right and left anterior oblique projections. The large (> or =1.5 mm) distal right CA was < or =5 mm from the mapping catheter in the SEI in 4 patients (8%). The large posterolateral branch of the right CA was < or =2 mm from the CS Os-middle cardiac vein in 10 patients (20%). The large left circumflex CA was < or =2 mm from the floor or ceiling of the CS in 7 patients (14%) and < or =2 mm from the CS catheter at the lateral and anterolateral mitral annulus in 12 patients (24%). RFA was canceled in 2 patients because of the close proximity (< or =2 mm) of the distal CA to the ablation site. In conclusion, large CAs are frequently located in close proximity to the common ablation sites. Coronary angiography should be considered in children and adults who may develop any signs or symptoms suggestive of acute CA occlusion until larger controlled series are available.

Impaired endothelial function in patients with myocardial bridge.

OBJECTIVE: The relationship between myocardial bridging (MB) and ischemic heart disease is still controversial. In this study, we aimed to evaluate the existing atherosclerosis and noninvasive endothelial function of brachial artery in patients with MB. METHODS: The present study included 50 patients (group I) who had MB in left anterior descending (LAD) on coronary angiography. All of the coronary artery segments were evaluated by intravascular ultrasound (IVUS). Endothelial function was assessed with measurement of flow-mediated dilatation (FMD) and nitrate-dependent dilatation in the brachial artery. The study also included 30 healthy control subjects (group II). Patients in the group I were further subdivided into two subgroups based on the findings on IVUS: group IA included 20 patients without atherosclerotic lesions and group IB included 30 patients with atherosclerotic coronary artery disease in addition to MB. RESULTS: FMD values were found to be significantly lower in the patients with MB (group I) than in the control (6.4 +/- 3% vs 11 +/- 4%, P <0.001). In regard to FMD values in subgroups, FMD was 7 +/- 2% in the group IA and 5.8 +/- 1% in the group IB (P = 0.023). On IVUS, atherosclerotic plaque was found proximal to the bridge in the same coronary artery segment in addition to MB in 75% of the patients in group I (group IB). No atherosclerotic plaque was found in within or distal segments of MB. CONCLUSION: Endothelial function is impaired in patients with MB and there is an increased tendency for atherosclerosis proximal to the bridge in the patients with MB. Endothelial dysfunction is more severe in the patients with atherosclerosis proximal to the bridge.

Homozygous factor V Leiden mutation in two siblings presenting with acute myocardial infarction: a rare cause of myocardial infarction in the young.

Although factor V Leiden mutation, is the most common established genetic risk factor for venous thrombosis, its effect on the development of myocardial infarction remains unclear. We describe a family case of homozygous factor V Leiden mutation in two siblings presenting with acute myocardial infarction as a rare cause of myocardial infarction in the young.

[The relationship between serum C-reactive protein levels and coronary artery disease in patients with stable angina pectoris and positive exercise stress test]. / Kararli Anjina Pektorisi Olan ve Efor Testi Pozitif Bulunan Ayaktan Hastalarda Serum C-Reaktif Protein Düzeyleri ile Koroner Arter Hastaligi ile Iliskisi.

OBJECTIVE: In this study we aimed to investigate whether serum C- reactive protein (CRP) levels are related with the incidence of coronary artery disease (CAD) and selection of management approaches in stable angina pectoris (SAP). METHODS: Overall 134 patients (pts) with SAP and positive exercise stress test were investigated. All pts were divided into two groups according to the baseline levels of CRP. In group 1 (mean age 57.8+/-10.3 years) there were 41 pts with the level of CRP >0.50mg/dl (high levels of CRP) and group 2 consisted of 93 pts (mean age 56.0+/-11.7 years) with the CRP levels <0.50mg/dl (normal levels of CRP). We investigated the relationship between CRP levels with coronary artery disease and treatment strategies. RESULTS: There were no significant differences in age, sex, hypertension and hyperlipidemia between groups. In group 1 (n=41) 36 pts, and in group 2 (n=93) 58 pts had CAD (p= 0.004). We found statistically significant relationship between high levels of CRP and smoking and diabetes mellitus. After adjustment of these risk factors by multivariate regression analyses the CRP association with CAD become attenuated but was still statistically significant (p=0.03). CONCLUSION: In this study we found that high level CRP is an independent strong marker of CAD in middle-aged patients with stable angina and positive treadmill exercise test. There was no correlation between CRP levels and interventional procedures.

The effect of atorvastatin on platelet function in patients with coronary artery disease.

BACKGROUND: Lipid-lowering therapy was shown to have several beneficial effects in patients with coronary artery disease (CAD). AIM: The objective of this study was to investigate the effect of atorvastatin on platelet aggregation in patients with CAD. METHODS: Twenty-five hypercholesterolaemic patients who had angiographically proven CAD and 16 normal subjects were enrolled. All patients received 10 mg/day atorvastatin for two months. Anti-platelet agents were discontinued 15 days prior to blood sampling at the beginning and at the end of the atorvastatin therapy. Aggregometric curves of the platelets in response to ADP, collagen and epinephrine were obtained using the aggregometry (turbidimetric) technique. RESULTS: In patients with CAD, total cholesterol (TC) and LDL cholesterol (LDL-C) basal levels were measured (230 +/- 49 mg/dl, 140 +/- 41 mg/dl, respectively). Following lipid-lowering therapy, TC and LDL-C decreased significantly (p < 0.05). The activation measurements of aggregometric curves decreased significantly compared with basal parameters in response to ADP but not in response to collagen and epinephrine. CONCLUSION: Lipid-lowering therapy with the HMG-CoA reductase inhibitor, atorvastatin, had a marked reduction effect on platelet aggregation.

Treatment of mild-to-moderate hypertension with calcium channel blockers: a multicentre comparison of once-daily nifedipine GITS with once-daily amlodipine.

BACKGROUND: Hypertension is one of the most important causes of cardiovascular disease, and treatment of hypertension leads to a significant reduction in cardiovascular mortality and morbidity. Although calcium channel blockers are regarded as an important part of the therapeutic armamentarium against cardiovascular diseases, and are among the most frequently prescribed antihypertensive medications, concern has been aroused about these drugs, particularly the short-acting dihydropyrldine derivatives. However, the value of nifedipine GITS(Adalat-Crono), the long-acting dihydropyrldine, is in need of being re-established. OBJECTIVE: To compare the effectiveness, safety and tolerability of once-daily nifedipine and amlodipine treatment in patients with mild-to-moderate essential hypertension. DESIGN: Randomised multicentre trial with an open comparison of treatments for 12 weeks, with a preceding placebo run-in period of 2 weeks (patients on beta-blockers at the time of enrollment entered a mandatory 2-week wash-out period before being allowed In the placebo run-in period;this wash-out period was one week for patients using any antihypertensive medication other than beta-blockers). SETTING: Nine centres (all university hospitals) in Turkey. PATIENTS: 155 patients with essential hypertension(diastolic blood pressure 95-109 mmHg). INTERVENTIONS: Initial treatment (step 1) consisted of 30 mg nifedipine GlTS (n = 76; (Adalat-Crono tablets), or 5 mg amlodipine (n = 79; Norvasct5-mg tablets), either administered once daily, as a morning dose, or f the blood pressure was not below 140/90 mmHg, or the reduction In diastolic blood pressure was lower than 10 mmHg after a treatment period of 6 weeks, the dose was increased (Step 2) to 60 mg once daily in the nifedipine group, or 10 mg once daily in the amlodipine group. MAIN EFFICACY PARAMETER: Diastolic blood pressure at trough after 12 weeks of active compound therapy adjusted to baseline. RESULTS: After 12 weeks of treatment, the mean diastolic blood pressure was 83.1 and 81.9 mmHg,in the nifedipine and amlodipine groups, respectively (p = 0.436). The mean decrease in systolic blood pressure (28.5 +/- 11.9 and 28.2 +/- 11.2 mmHg in the nifadipine and amlodipine groups, respectively) and the mean decrease in diastolic blood pressure (16.4A +/- 7.0 and 17.5 +/- 6.9 mmHg in the nifedipine and amlodipine groups, respectively), as well as the responder rates (88.1%and 92.1%, in the nifediplne and amlodipine groups, respectively) were comparable at the end of the study. No significant differences between groups were detected In the efficacy parameters assessed in this study. Both drugs were well tolerated. The overall incidence of adverse events was 7.9% in the nifadipine group and 10.1% In the amlodipine group. However, more patients discontinued treatment prematurely in the amlodipine group (13 patients; 19.7%), than in the nifedipine group (four patients; 5.6%). CONCLUSIONS: The results of this study demonstrated that once-daily nifedipine in GITS formation and amlodipine are comparably safe and effective treatment options in patients with mild-to-moderate essential hypertension.

Serial analyses of ventricular late potentials in patients with reciprocal ST segment changes during acute myocardial infarction.

The aim of this study was to determine whether successful reperfusion may alter substrate that is responsible for late potentials in the presence or absence of reciprocal ST segment changes (RC). The study population consisted of 50 patients (27 with RC and 23 without RC) with anterior acute myocardial infarction (AMI) undergoing successful thrombolytic therapy (TT). The presence of reciprocal changes was defined as ST-segment depression >1 mm, measured 80 ms after the J point in at least 2 leads other than those reflecting the infarct on admission ECG. All patients were evaluated with coronary angiography at predischarge. Signal averaged ECG (SAECG) recordings were obtained before and 10 days after TT. Baseline characteristics, SAECG findings, and angiographic data were similar between the groups. The only different baseline finding was the time from symptom onset to TT (204 +/- 150 minutes for patients with RC vs 312 +/- 174 minutes for patients without RC. P = 0.021). After TT, RMS values improved in patients with RC (from 35 +/- 17 microV to 43 +/- 14 microV, P = 0.038) and LAS and RMS were significantly better in this group. However, patients without RC did not show any changes in SAECG parameters after TT. LV ejection fraction (10th day) was better in patients with RC (45 +/- 11% vs 39 +/- 6%, P = 0.014). The frequency of ventricular arrhythmias during the hospitalization period was also similar between the groups. Reciprocal ST depression that regresses simultaneously with the infarction related ECG changes after TT in anterior AMI seems to be related to the time that has elapsed since the symptom onset. The improvement in SAECG parameters after TT in these patients is probably the result of earlier reperfusion leading to less myocardial damage.

The angiographic correlation between ST segment depression in noninfarcted leads and the extent of coronary artery disease in patients with acute inferior myocardial infarction: a clue for multivessel disease.

BACKGROUND: Although reciprocal ST segment depression (RSTD) in patients with acute inferior myocardial infarction is a common electrocardiogram finding, its significance is not yet established. In this prospective study, the relationship between RSTD and the extent of coronary artery disease (CAD) was investigated. PATIENTS AND METHODS: One hundred eighty-eight patients with acute inferior myocardial infarction who received thrombolytic therapy were enrolled in this study. The magnitude and location of ST segment depression in noninfarcted leads and the maximum ST segment elevation (STEmax) in inferior leads were measured. All patients were divided into two main groups according to the presence of RSTD and five subgroups according to the location of RSTD, the maximum RSTD and the STEmax. The coronary angiography was performed in all patients 28 +/- 4 days after acute myocardial infarction. RESULTS: There were no significant differences in the proportion of coronary disease risk factors in patients with, versus those without, RSTD (P=0.6). Multivessel CAD was present in 63 of the 108 (58%) patients with RSTD and in 32 of the 80 (40%) patients with no RSTD (P=0.02). According to the location of reciprocal changes, multivessel disease was present in significantly more patients with anterior RSTD concomitant with or without lateral ST segment depression (P=0.01 and P=0.03, respectively); the proportion of single vessel disease was greater in patients with only lateral RSTD (P=0.02). In addition, the presence of anterior RSTD to a greater magnitude than the STEmax in inferior myocardial infarction increases the likelihood of multivessel disease (P=0.006). CONCLUSIONS: The presence of RSTD during an acute inferior myocardial infarction correlates with the presence of multivessel CAD and may not be only an electrical phenomenon.

Successful balloon angioplasty of native aortic coarctation in a young adult with refractory hypertension.

Controversy exists with regard to the role of balloon angioplasty in the treatment of native aortic coarctation. Recent data and studies have showed that percutaneous balloon angioplasty is a safe and effective treatment for aortic coarctation. We report a young adult with aortic coarctation who has been treated with successful balloon angioplasty.

Early use of pravastatin in patients with acute myocardial infarction undergoing coronary angioplasty.

AIM: To determine whether statin therapy initiated early in acute myocardial infarction together with thrombolytic therapy in patients with acute myocardial infarction results in clinical benefit through early plaque stabilization. METHODS AND RESULTS: The study population consisted of 77 patients who underwent coronary balloon angioplasty of the infarct-related artery during the first month of acute myocardial infarction. These patients belonged to the cohort of the Pravastatin Turkish Trial (PTT). Forty of them were assigned randomly to have immediate pravastatin (40 mg/day) therapy adjunctive to thrombolytic therapy regardless of serum lipid levels and received statin treatment throughout the study. Lipid levels were determined immediately after admission and before angioplasty and at the end of 6 months. Patients were re-evaluated clinically and angiographically for cardiovascular adverse events and restenosis after a 6-month follow-up period. The baseline angiographic and clinical characteristics of the two groups were similar. The incidence of angina was significantly lower in the pravastatin group (30.0%, 12 patients) compared to the control group (59.5%, 22 patients) (p = 0.018). The cumulative major adverse cardiac events in the pravastatin group were significantly lower when compared to the control group (32.5% vs. 75.6%, p = 0.0001). CONCLUSIONS: Early initiation of pravastatin therapy immediately after an acute myocardial infarction significantly decreased the frequency of major cardiac adverse events. Such early potential clinical benefits further strengthen the rationale for starting statin treatment as soon as possible after acute coronary events particularly in patients in whom invasive intervention is planned.

Cardiovascular involvement in Behçet's disease.

The incidence and nature of cardiac involvement in Behçet's disease are not yet clearly documented. We first used transesophageal echocardiography in combination with resting and signal averaged electrocardiography to define cardiac involvement in Behçet's patients. Transthoracic and multiplane transesophageal echocardiography, and resting and signal averaged electrocardiography were performed in 35 Behçet's disease patients (9 women and 26 men, mean age: 38 +/- 12 years) and 30 normal subjects. Higher incidences of interatrial septum aneurysm (31% to 6%), mitral valve prolapse (25% to 3%), mitral regurgitation (40% to 6%) and aneurysmal dilatations of sinus valsalva and ascendan aorta were observed in the Behçet's disease patients than in the normal subjects. Mean QT dispersion and mean corrected QT dispersion values were significantly greater in the patients with Behçet's disease. Patients with interatrial septum aneurysm (and/or PFO), valvular dysfunction or proximal aorta dilatation had greater QT dispersion values than thase without these pathologies in the Behçet's group (63 +/- 11 vs 44 +/- 19 ms, 58 +/- 23 vs 41 +/- 24 and 60 +/- 27 vs 42 +/- 23 ms respectively, P<0.05). Positive signal averaged electrocardiography parameters were detected in 18 (51%) Behçet's disease patients compared with one (3%) in controls (P<0.001). Dilatation of the proximal aorta, interatrial septal aneurysm, mitral valve prolapse, and mitral regurgitation are the common findings of cardiac involvement in Behçet's disease. Increased dispersion of ventricular repolarisation and positive late potentials are also detected. QT dispersion is significantly higher in patients with these cardiac abnormalities. These findings suggest that cardiac involvement in this disorder is a diffuse process which involves both cardiac structure and vascular elements.

[Effects of metoprolol on the signal averaged electrocardiogram and QT dispersion in acute myocardial infarction]. / Akut miyokard infarktüsünde metoprolol'ün sinyal ortalamali elektrokardiyogram ve QT dispersiyonu uzerine etkisi.

OBJECTIVE: The determination of high risk patients for sudden death and sustained ventricular tachycardia after acute myocardial infarction constitutes the main goal to decrease morbidity and mortality. Every attempt that decreases the frequency of late potentials (LPs) on signal averaged ECG (SAECG) and corrected QT dispersion (QTc-d) may improve prognosis of patients. In this study, the effect of metoprolol on frequency of LPs and QTc-d was investigated. METHODS: Thirty-five patients (mean age 53 +/- 9 years) with acute myocardial infarction who were not given thrombolytic therapy were enrolled. Patients in whom metoprolol was not administered formed group I (n = 20) and patients who were given metoprolol constituted group II (n = 15). Metoprolol was administered as an initial dose of 15 mg intravenously, following 6-8 hours 100 mg/d orally. To determine the frequency of LPs, SAECG records were performed on admission and at the end of the first week. At the same time, resting ECG recordings (12 leads, 50 mm/s) were obtained to calculate QTc-d. Variance analysis was used for statistical analysis. RESULTS: In group I; frequency of LPs were found 30% on admission and at the end of the first week. In group II; frequency of LPs were 6% on admission and at the end of the first week there was no LPs. There was no statistically significant difference between two groups according to TQRS, RMS-40, LAS40 and QTc-d CONCLUSION: Metoprolol decreases the frequency of LPs. It has no effect on cQT-d.

QT dispersion in patients with different etiologies of left ventricular hypertrophy: the significance of QT dispersion in endurance athletes.

Left ventricular hypertrophy (LVH) increases the risk of ventricular arrhythmias and sudden death and has a significant effect on total cardiovascular mortality. QT dispersion (QTd) is a measure of inhomogeneous repolarization and is used as an indicator of arrhythmogenicity. In this study we detected QTd in patients with different etiologies of left ventricular hypertrophy and the effect of LVH in QTd on endurance athletes. The study group consisted of 147 white male subjects with 3 different etiologies of LVH and 30 healthy male individuals. The underlying etiologies of LVH were essential hypertension, valvular aortic stenosis and long-term training (athletic heart). QTd was measured by surface electrocardiogram and Bazett's formula was used to correct QTd for heart rate (QTcd). Left ventricular mass was determined by transthoracic echocardiography and left ventricular mass index was calculated in relation to body surface area. The QTcd was significantly higher in patients with pathological LVH (due to hypertension and aortic stenosis) than in the athletes' group (physiological LVH) and healthy subjects (P<0.05). The magnitude of QTcd was similar between athletes and the control group (P=0.6). The difference of QTcd between the groups with pathological LVH was not statistically significant (P=0.1). In conclusion; the increasing of QT dispersion is associated with only pathological conditions of LVH. The left ventricular hypertrophy has not a negative effect in QT dispersion on endurance athletes. The measurement of QT dispersion may be a non-invasive useful method for screening additional pathological conditions in endurance athletes.

Relationship Between Echocardiographic Determinants of Left Atrial Spontaneous Echo Contrast and Thrombus Formation in Patients with Rheumatic Mitral Valve Disease.

Spontaneous echo contrast (SEC) may be detected by ultrasonography in environments favoring blood stasis. It is most commonly seen through the use of transesophageal echocardiography in the left atrium of patients with rheumatic mitral valve disease especially in the presence of atrial fibrillation. We studied the predictors of SEC, such as cardiac rhythm, left atrium and left atrial appendage functions, and mitral and pulmonary vein flow parameters, in patients with rheumatic mitral valve disease. The relationship between these parameters and the severity of SEC and appearance of thrombus was evaluated.