Circulating Levels of MicroRNAs in Hypertrophic Cardiomyopathy: The Relationship With Left Ventricular Hypertrophy, Left Atrial Dilatation and Ventricular Depolarisation-Repolarisation Parameters.

BACKGROUND: MicroRNAs are small, endogenous, non-coding RNAs that regulate the expression of many genes. It has recently been shown that circulating microRNAs may be biomarkers of hypertrophy and fibrosis in patients with hypertrophic cardiomyopathy (HCM). OBJECTIVE: To determine whether circulating levels of microRNAs involved in HCM are associated with electrocardiographic and echocardiographic parameters. METHODS: This study enrolled 20 patients with familial HCM and 20 blood donors. Peripheral serum levels of miR-29a-3p, miR-199a-5p and miR-451a were assessed by quantitative real-time polymerase chain reaction and compared with levels in the control group. Whether circulating levels of miRNAs in HCM patients correlated with electrocardiographic and echocardiographic parameters was also assessed. RESULTS: Median circulating levels of miR-29a and miR-451a were significantly higher in HCM than the control group. Median miR-199a levels did not differ between groups. However, circulating levels of miR-199a negatively correlated with corrected QT duration (Bazett formula). Median miR-29a levels positively correlated with QRS duration. In addition, circulating levels of miR-29a correlated with maximal wall thickness, left ventricular mass index and left atrial volume index. CONCLUSIONS: The data suggested that serum levels of miR-29a and miR-451a were significantly increased in HCM patients. As the circulating level of miR-29a correlated with QRS duration, left ventricular hypertrophy and left atrial dilatation, the serum miR-199a level negatively correlated with corrected QT duration. These miRNAs may be seen as potential biomarkers for further research in HCM pathophysiology.

Association between integrated backscatter and arrhythmia in patients with ischemic dilated cardiomyopathy.

BACKGROUND: Ventricular scars due to myocardial infarction provide a substrate for ventricular arrhythmias, and cardiac magnetic resonance (CMR) is the golden standard for the quantification of scar tissue magnitude. CMR has still limitations with patients with ICD despite ICD's becoming MR-compatible. We investigated the association between calibrated integrated backscatter (cIBS) and arrhythmia frequency in patients with ICD. METHODS: Thirty-two ischemic dilated cardiomyopathy (ICM) patients with VVI-ICD (mean age 66.56 ± 9.05, 28 male, and four female) were divided into three groups according to their arrhythmia frequency (ventricular arrhythmia-[VA -], VA + [VA +], and arrhythmia storm [AS]). Then with transthoracic echocardiography (TTE), all patients' cIBS values were calculated and these values were compared with the patients' arrhythmia frequency. RESULTS: cIBS values of patients with VA + and AS were significantly higher in the apical-septal (0.66 ± 0.11 vs. 0.50 ± 0.16, p = .008) and apical-lateral (0.62 ± 0.19 vs. 0.46 ± 0.18, p = .041) segments compared to those of patients with VA -. The cIBS values of apical-septal (0.50 ± 0.16 vs. 0.65 ± 0.08 vs. 0.66 ± 0.13 respectively, p = .032) and apical-anterior (0.53 ± 0.22 vs. 0.48 ± 0.17 vs. 0.79 ± 0.23 respectively, p = .03) segments were significantly different between the groups. Furthermore, in the post hoc analysis, the difference was significantly higher in VA + than VA - in the apical-septal segment and higher in AS than VA + in apical-anterior segments. CONCLUSION: Our findings suggest an association between the cIBS values and arrhythmia frequency in the study group.

The relationship between T-wave peak-to-end interval and hemodynamic parameters in patients with pulmonary arterial hypertension.

BACKGROUND: T-wave peak-to-end interval (TPEI) is a measure of repolarization dispersion on surface electrocardiogram (ECG). TPEI has been reported as a prognostic parameter with heart disorders. In this study, we aimed to evaluate the relationship between echocardiogram-derived right heart parameters, right heart catheterization (RHC) measurements, and TPEI in patients with precapillary pulmonary arterial hypertension (PAH). METHODS: Thirty-eight patients (29 females and 9 males, mean age of 54.9 ± 10.9 years) who had undergone RHC for a preliminary diagnosis of pulmonary hypertension (PH) were included in the study. We performed transthoracic echocardiography (TTE), and resting 12-lead ECG was recorded before RHC. TPEI was measured from leads of V1-V6, DII, DIII, and aVF, and these values are averaged to obtain the global TPEI. RESULTS: Duration of TPEI was significantly correlated with mean PAP, pulmonary vascular resistance (PVR), and cardiac index (CI). Longer TPEI was associated with higher N terminal probrain natriuretic peptide (NT pro-BNP) level, lower 6-min walk distance (6MWD), and lower tricuspid annular plane systolic excursion (TAPSE). CONCLUSION: Prolongation of TPEI could be a new predictor of adverse outcome in PAH and may provide additional prognostic information for patients with PAH.

The role of Beta-1 receptor gene polymorphism in Beta-Blocker therapy for vasovagal syncope.

BACKGROUND: Vasovagal syncope (VVS) is a common clinical condition involving genetic background. The role of beta-blockers in the treatment is controversial. OBJECTIVE: The aim of this study was to investigate the effect of beta-1 gene polymorphism on beta-blocker therapy in patients with VVS. METHODS: We included 123 patients who were diagnosed with VVS after the tilttable test. We searched for the polymorphism Arg389Gly (rs1801253) in the beta-1 adrenoceptor gene. RESULTS: Overall, 64 patients (52%) had Arg389Arg with Arg389Arg genotype were more frequent compared with patients having Arg389Gly genotype (total syncopal episodes [TSE], 7.9 ± 3.7 vs. 6.4 ± 3.0; p = 0.012). TSE in patients with Arg389Arg genotype decreased significantly after 18 months of beta-blocker treatment (7.9 ± 3.7 vs. 3.0 ± 1.4, p < 0.001). After 18 months of beta-blocker treatment, patients with Arg389Arg genotype had significantly fewer syncopal episodes than patients with Arg389Gly genotype (3.0 ± 1.4 vs. 6.8 ± 3.2, p < 0.001). CONCLUSIONS: Results of beta-blocker therapy in patients with Arg389Arg genotype suggest that VVS pathophysiology is a multifactorial condition, with genetic, psychological, and environmental components, and therefore, treatment selection can be based on gene polymorphism.

Serum Asymmetric Dimethylarginine Levels in Patients with Vasovagal Syncope.

Background and Objectives: Vasovagal syncope (VVS) is the most common cause of syncope and has multiple pathophysiological mechanisms. Asymmetric dimethylarginine (ADMA) is the major inhibitor of nitric oxide (NO). In this study, we aimed to investigate the relationship between plasma ADMA levels and syncope during the head-up tilt (HUT) test. Materials and Methods: Overall, 97 patients were included in this study. They were above 18 years of age and were admitted to our clinic with the complaint of at least one episode of syncope consistent with VVS. The HUT test was performed in all patients. Patients were divided into the following two groups based on the HUT test results: group 1 included 57 patients with a positive HUT test and group 2 included 35 patients with a negative HUT test. Blood samples were taken before and immediately after the HUT test to measure ADMA levels. Results: No significant intergroup differences were observed concerning gender and age (female gender 68% vs 60%; mean age 24.85 ± 4.01 vs 25.62 ± 3.54 years, respectively, for groups 1 and 2). ADMA values were similar between groups 1 and 2 before the HUT test [ADMA of 958 (544-1418) vs 951 (519-1269); p = 0.794]. In the negative HUT group, no significant differences were observed in ADMA levels before and after the HUT test [ADMA of 951 (519-1269) vs 951 (519-1566); p = 0.764]. However, in the positive HUT group, ADMA levels were significantly decreased following the HUT test [pretest ADMA of 958 (544-1418) vs post-test ADMA of 115 (67-198); p < 0.001]. Conclusion: ADMA levels significantly decreased after the HUT test in patients with VVS.

Analysis of heart rate variability and risk factors for SUDEP in patients with drug-resistant epilepsy.

BACKGROUND: Cardiac problems have been suggested as causes of sudden unexpected death in epilepsy (SUDEP). Our aim was to investigate possible associations of cardiac autonomic functions based on heart rate variability (HRV) parameters with risk factors of SUDEP in patients with drug-resistant epilepsy. METHODS: Forty-seven patients with drug-resistant seizures and 45 healthy control subjects were enrolled in the study. Interictal time domain parameters of HRV were evaluated with 24-hour Holter recordings. Potential SUDEP risk in patients with epilepsy was estimated using an inventory of seven validated SUDEP risk factors (The SUDEP-7 inventory). RESULTS: When compared with the healthy controls, all time domain measures (SDNN-24, SDNN-index, SDANN-index, RMSSD and pNN50) were significantly suppressed in the patient group. Scores of the SUDEP-7 inventory ranged from 1 to 9 with a median 4 out of a maximum possible risk score of 10. Maximum heart rate value in 24-hour Holter recordings and epilepsy duration were correlated with the SUDEP-7 scores (r=0.3, p=0.03). We found no significant association with HRV measures and SUDEP-7 risk factors. One patient diagnosed with Dravet syndrome died of SUDEP, which was autopsy confirmed; his SUDEP-7 inventory score was 7, HRV measures were significantly diminished, and his maximum heart rate (HR) was 208beats/min (maximum HR is between 104 and 188beats/min in normal subjects). CONCLUSION: Patients with drug-resistant epilepsy present with significantly lower HRV measures, which may increase the risk for sudden cardiac death. Increased heart rate and diminished HRV measures may constitute one of the possible mechanisms underlying SUDEP and should be diagnosed in patients with epilepsy.

Endocan: a novel biomarker associated with well-developed coronary collateral circulation in patients with stable angina and chronic total occlusion.

Angiogenesis and arteriogenesis have a crucial role in the formation of coronary collateral vessels. It has been shown that endocan and vascular cell adhesion molecule-1 (VCAM-1) are potential angiogenetic factors. We investigated the relationship between serum endocan levels and grade of coronary collaterals, and also the correlation of endocan levels with serum VCAM-1 levels. Patients with stable angina and at least one total coronary occlusion at invasive coronary angiography were included in our study. Collateral degree was graded according to Rentrop and Cohen's classification. Patients who had grade 0 or 1 collateral vessels were included in the poorly-developed collateral group, and those with grade 2 or 3 coronary collateral vessels were included in the well-developed collateral group. Serum endocan and VCAM-1 levels were significantly higher in the well-developed collateral group (436.6 ± 213.3 ng/mL vs. 216.1 ± 78.5 ng/mL, p < .001; 11.02 ± 6.58 ng/mL vs. 6.78 ± 1.14 ng/mL, p < .001, respectively). In a logistic regression analysis, only serum endocan level remained as an independent predictor for good collateral development. In the ROC curve analysis, 282 ng/mL endocan level had an a 82 % sensitivity and 86 % specificity for prediction of the well-developed collateral group. Higher endocan level was related to better coronary collateral development. In the event that these results are confirmed in further studies, endocan may be considered as an anti-ischemic treatment strategy in order to improve collateral development.

Galectin-3 correlates with arrhythmogenic right ventricular cardiomyopathy and predicts the risk of ventricular -arrhythmias in patients with implantable defibrillators.

Background Arrhythmogenic right ventricular dysplasia (ARVD) is a heritable disorder characterized by fibro-fatty replacement of right ventricular myocytes, increased risk of ventricular arrhythmias, and sudden cardiac death. Galectin-3 (GAL3) is known to play an important role in a number of fibrotic conditions, including cardiac fibrosis. Many studies have focused on the association between GAL3 levels and cardiac fibrosis in heart failure. However, the role of GAL3 in the pathogenesis of ARVD and ventricular arrhythmias has not yet been evaluated thoroughly. The aim of this study was to explore GAL3 levels in patients with ARVD and its association with ventricular arrhythmias. Methods Twenty-nine patients with ARVD and 24 controls were included. All patients with ARVD had an implantable cardiac defibrillator (ICD) for primary or secondary prevention. Ventricular arrhythmia history was obtained from a chart review and ICD data interrogation. Galectin-3 levels were measured using an enzyme-linked immunosorbent assay. Results Patients with ARVD had higher plasma GAL3 levels (16.9 ± 2.6 ng/mL vs 11.3 ± 1.8 ng/mL, P < 0.001) than the control group. Ten patients had sustained or non-sustained ventricular arrhythmias during follow-up. In the multivariable analysis, left ventricular disease involvement (HR: 1.05; 95% CI: [1.01-1.12]; P = 0.03); functional capacity >2 (HR: 1.21; 95% CI: [1.13-1.31]; P < 0.005); and GAL3 levels (HR: 1.05; 95% CI: [1.00-1.11]; P = 0.01) independently predicted VT/VF. Conclusion We demonstrated that serum GAL3 was significantly elevated in patients with ARVD. Also, serum GAL 3 levels could be regarded as a candidate biomarker in the diagnosis of ARVD which needs to be tested in larger prospective studies. In addition, GAL3 levels were higher in patients with VT/VF as compared with those without VT/VF.

Comorbidities and their impact on chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a complex disease that is associated with devastating outcomes resulting from lung involvement and several comorbidities. Comorbidities could impact on symptomology, quality of life, the complications, the management, economic burden and the mortality of the disease. The importance of comorbidities originates from their impact on the outcome of COPD. The most frequent comorbidities in COPD are cardiovascular, endocrinological, musculoskeletal, phycological disorders and lung cancer. Almost 50% of the COPD patients have 3 or more comorbidities. The recent Global Initiative of Obstructive Lung Disease (GOLD) Guideline suggested proactive search and the treatment of the comorbidities. However, there is no certain evidence demonstrating that active treatment of comorbidities improve the outcomes of COPD. However, it is well known that several comorbidities such as cardiovascular disease and lung cancer have greater impact on mortality caused by COPD. Several studies have shown that Charlson Comorbidity index or more recenty COPD Specific Comorbidity Index (COTE) has been found to be related with mortality of COPD. This concise review intended to summarize the most frequent comorbidities in association with their impact on COPD.

Combined analysis of unipolar and bipolar voltage mapping identifies recurrences after unmappable scar-related ventricular tachycardia ablation.

AIMS: Scars causing ventricular tachycardia can extend deep to and beyond bipolar low-voltage areas (LVAs) and they may be a reason for endocardial ablation failure. Analysis of endocardial unipolar voltage maps has been used to detect scar transmurality and epicardial scar. We hypothesized that endocardial unipolar LVA around the overlying bipolar LVA may predict endocardial ablation recurrence in patients with structural heart disease undergoing substrate modification. METHODS AND RESULTS: Twenty consecutive patients with structural heart disease (11 ischaemic and 9 non-ischaemic cardiomyopathy) and undergoing substrate modification due to unmappable ventricular tachycardia (VT) (18 males, 51 ± 11 age, LVEF: 36 ± 7%) were retrospectively reviewed. Bipolar LVA defined as <1.5 mV and unipolar LVA defined as <8.3 mV, respectively, on electro-anatomic mapping system. Peripheral unipolar LVA (pUni-LVA) surrounding bipolar LVA was measured and compared patients with and without VT recurrence at 6-month follow-up period. : Mean unipolar voltage and mean bipolar voltage was 6.26 ± 4.99 and 1.90 ± 2.30 mV, respectively. Bipolar voltage and unipolar voltage in corresponding points were correlated (r = 0.652, P = 0.0001). In all patients, unipolar LVAs were larger than the bipolar LVAs. Bipolar LVA (91.1 ± 93.5 vs. 87.5 ± 47.5 cm(2), P = 0.91) and unipolar LVA (148.1 ± 96.3 vs. 104.7 ± 44.2 cm(2), P = 0.21) were similar in patients with and without VT recurrence, respectively. Peripheral unipolar LVA was significantly larger in patients with VT recurrence than without (57.0 ± 40.4 vs. 17.2 ± 12.9 cm(2), P = 0.01). CONCLUSION: In patients with structural heart disease and unmappable VT, pUni-LVA surrounding bipolar scar predicts recurrence of VT ablation. The results of this pilot study highlight the importance of intramural/epicardial substrate on endocardial VT ablation outcome.

Infarct characteristics by CMR identifies substrate for monomorphic VT in post-MI patients with relatively preserved systolic function and ns-VT.

BACKGROUND: The extent of peri-infarct zone (PIZ) by contrast-enhanced cardiac magnetic resonance (ce-CMR) has been related to inducibility of ventricular arrhythmia in patients with ischemic cardiomyopathy. However, this relationship has not been established in postmyocardial infarction (post-MI) patients with relatively reserved left ventricular (LV) systolic function yet. In this study, we investigated myocardial scar size and characteristics and its relationship with ventricular arrhythmia inducibility in patients with relatively preserved LV systolic function. METHODS: This study enrolled 28 post-MI patients with a left ventricular ejection fraction between 40% and 50% and nonsustained ventricular tachycardia who underwent programmed ventricular stimulation (PVS) for risk stratification. Cine and gadolinium-enhanced cardiac magnetic resonance imaging was performed before PVS. A computer-assisted algorithm quantified the total scar (TS) size and divided it into the dense scar (DS) and the PIZ based on signal intensity thresholds (>6 standard deviations [SDs] and 2 to 6 SDs above remote normal myocardium, respectively). Scar measurements were determined and compared among noninducible (n = 19) and inducible patients (n = 9). RESULTS: The groups had similar baseline clinical characteristics. The LV masses, volumes, and ejection fractions did not differ significantly between the groups. For the inducible versus noninducible patients, DS percent was similar (3.11 ± 1.02% vs 3.44 ± 0.79%, P = NS). PIZ percent (28.02 ± 7.49% vs 19.86 ± 7.82%, P = 0.01) and TS percent (31.14 ± 7.96% vs 23.31 ± 8.21%, P = 0.02) were associated with inducibility of monomorphic VT. Multivariate analysis demonstrated that PIZ percent (P = 0.021, OR [odds ratio] 1.18, 95% CI [confidence interval] 1.03-1.35), and TS percent (P = 0.03, OR 1.15, 95% CI 1.01-1.30) were independent predictors of inducibility. CONCLUSIONS: Higher PIZ percent and TS percent were correlated with increased ventricular inducibility. These data support the hypothesis that ce-CMR may be used to identify the substrate for ventricular arrhythmia in this cohort.

Usefulness of T(peak) -T(end) interval to distinguish arrhythmogenic right ventricular cardiomyopathy from idiopathic right ventricular outflow tract tachycardia.

BACKGROUND: The two predominant etiologies of right ventricular tachycardia (VT) are arrhythmogenic right ventricular cardiomyopathy (ARVC) and idiopathic VT arising from the right ventricular outflow tract (RVOT). Discrimination between these two entities is critical, as their prognoses and therapeutic options differ. The Tpeak -Tend (Tpe) interval reflects the transmural repolarization dispersion and its prolongation is associated with high mortality. METHODS: We compared the sinus rhythm electrocardiogram (ECG) of 43 patients (24 male, 43 ± 16 years) with VT originating from right ventricle. Five patients under antiarrhythmic drug therapy were excluded. Tpe interval was measured in each precordial leads and compared among patients with ARVC and RVOT-VT. RESULTS: Twenty-five patients (16 male, 42 ± 16 years) met the Task Force criteria for the diagnosis of ARVC, and 13 patients (seven male, 45 ± 14 years) had idiopathic RVOT tachycardia. Patients with ARVC had significantly prolonged Tpe intervals in all precordial leads compared to patients with idiopathic RVOT VT (137.1 ± 32.6 ms vs 93.8 ± 16.9 ms; P < 0.001 in V1, 133.2 ± 35.5 ms vs 104.7 ± 16.9 ms; P = 0.01 in V2, 125.7 ± 31.5 ms vs 99.1 ± 19.6 ms; P = 0.09 in V3, 121.9 ± 26.5 ms vs 92.3 ± 19.7 ms; P = 0.001 in V4, 123.1 ± 26.5 ms vs 99.5 ± 20:1 ms; P = 0.04 in V5 and 126.9 ± 32.2 ms vs 89 ± 11.3 ms; P < 0.001 in V6, respectively). For the diagnosis of ARVC, Tpe cut-off value of 97 ms in V1 had 84% sensitivity and 62% specificity (area under curve = 0.880). CONCLUSION: In patients with VT of RV origin, the prolonged Tpe interval in sinus rhythm electrocardiogram supports the diagnosis of ARVC.

Evaluation of human immunodeficiency virus infection-related left ventricular systolic dysfunction by tissue Doppler strain echocardiography.

OBJECTIVE: Cardiovascular involvement causes significant morbidity and mortality among patients with human immunodeficiency virus (HIV) infection. Since the introduction of highly active antiretroviral treatment (HAART), subtle changes in left ventricular (LV) function, which may be clinically silent, have become more pronounced in HIV patients. Echocardiographic strain imaging (SI) may detect subclinical myocardial dysfunction at an earlier stage compared with conventional echocardiography. The aim of this study was to evaluate tissue Doppler-derived LV strain and strain rate (SR) along with conventional measures of LV function in asymptomatic, stable adult HIV patients on HAART. METHODS: Twenty-one patients with HIV infection (mean age: 37.8 ± 11.9 years, 11 males) who had no cardiovascular complaints and 27 healthy volunteers (mean age: 40.9 ± 5.8 years, 14 males) were enrolled. Traditional parameters including LV ejection fraction (EF) were measured along with tissue velocity imaging (TVI) and tissue Doppler SI parameters using transthoracic echocardiography. RESULTS: The mean duration of HIV infection was 30.8 ± 25.1 (3-120) months. The mean LVEF in HIV group was within normal limits but lower than controls (64.5% ± 10.2% vs. 72.2% ± 6.4%, P = 0.003). There were no differences in other major traditional measures, as well as TVI parameters between groups. LV systolic strain and SR parameters were impaired indicating subtle LV systolic dysfunction in HIV group. No difference in diastolic function was observed between groups. CONCLUSION: Left ventricular systolic strain parameters may be utilized to demonstrate subtle LV systolic dysfunction in asymptomatic HIV patients.

(18)F-fluorodeoxyglucose uptake by positron emission tomography in patients with IPAH and CTEPH.

Pulmonary arterial hypertension (PAH) is driven by pathologies associated with increased metabolism such as pulmonary revascularization, vasoconstriction and smooth muscle cell proliferation in pulmonary artery wall. 18-fluorodeoxyglucose positron emission tomography (18FDG-PET) is an imaging technique sensitive to glucose metabolism and might be considered as a non-invasive method for diagnosis due to significant role of inflammation in idiopathic pulmonary artery hypertension (IPAH) and chronic thromboembolic pulmonary hypertension (CTEPH). The present study aimed to investigate the role of PET/CT imaging of patients with IPAH and CTEPH as an alternative diagnosis method. Demographic characteristics, FDG uptake in lungs, pulmonary artery and right ventricle (RV) of 17 patients (10 IPAH, 7 CTEPH), and 30 controls were evaluated. PET scanning, 6-min walk test, pro-BNP level, right heart catheterization of patients were performed both at the onsert and after 6-month PAH specific treatment. IPAH and CTEPH patients had significantly higher left lung FDG (p = 0.006), right lung FDG (p = 0.004), right atrial (RA) FDG (p < 0.001) and RV FDG (p < 0.001) uptakes than controls. Positive correlation was detected between the RV FDG uptake and the mean pulmonary artery pressure (mPAP) (r = 0.7, p = 0.012) and between the RA FDG uptake and the right atrial pressure (RAP) (r = 0.5, p = 0.02). Increased RV FDG and RA FDG uptakes predicts the presence of pulmonary hypertension and correlates with mPAP and RAP, respectively, which are important indicators in the prognosis of PAH. Further studies are required whether FDG PET imaging can be used to diagnose or predict the prognosis of pulmonary hypertension.

Effects of edaravone on testicular torsion-detorsion injury in rats.

BACKGROUND AND OBJECTIVE: This study aimed to assess the protective ability of edaravone on testicular torsion-detorsion injury in rats. METHODS: Eighteen adult male Sprague-Dawley rats were randomly divided into three groups: Sham group (control, n = 6); testicular torsion/detorsion (T/D group, n = 6) and T/D+edaravone (T/D+E group, n = 6). The spermatic cords of rats of the T/D group and the T/D+E group were rotated 720° in a clockwise direction and maintained for 120 min in this torsion position. Around 90 min after the torsion, edaravone at a dose of 10 mg/kg dissolved in saline was administered IP to the T/D+E group. The testicle was counter-rotated to its normal position to allow reperfusion for 4 h. Left testes of each animal were excised 240 min after beginning of reperfusion. Oxidative stress markers (TAS, TOS, SOD, and MDA) and apoptotic pathways (Caspase 3, Caspase 8, Caspase 9, Bcl-2, and Bax,) were assessed by ELISA methods. Also, testicles were subjected to the histopathologic and ultrasound examinations. RESULTS: Ultrasound imaging showed that edaravone reduced the surface area and increased vascularization in testicles with T/D (p < 0.0001, p < 0.05, respectively). Edaravone pretreatment markedly decreased the levels of MDA, TOS, Bcl-2, Bax, Caspase 3, Caspase 8, and Caspase 9 (p < 0.0001). Also, it increased significantly TAS levels (p < 0.0001) and reduced insignificantly SOD activity. Histopathologic examinations demonstrated that edaravone significantly attenuated the histological damage caused by T/D in testicles. CONCLUSION: Taken together, the findings indicate that pretreatment of edaravone has protective effect against testicular T/D injury.

Aborted sudden cardiac death in a child with left ventricular non-compaction.

Left ventricular non-compaction is a rare form of cardiomyopathy believed to be the result of intrauterine arrest of compaction of the endomyocardial morphogenesis, leading to persistence of the embryonic myocardium. Clinical manifestations are highly variable, ranging from no symptoms to a progressive deterioration in cardiac function that results in congestive heart failure, systemic thromboemboli, arrhythmias, and sudden cardiac death. Presented here is the case of a 4-year-old child with a history of aborted sudden cardiac death. Following resuscitation, he was admitted to the intensive care unit with neurologic sequelae that regressed later on. Transthoracic echocardiography and magnetic resonance imaging showed numerous prominent trabeculations and deep intertrabecular recesses at the apical and anterolateral region of the left ventricle. Electrophysiologic study showed polymorphic ventricular tachycardia. An implantable cardioverter-defibrillator (ICD) was implanted following clinical recovery. Five months after implantation, appropriate ICD shock due to ventricular fibrillation was documented.

Atrioventricular complete block occurring 12 years after successful ablation of slow-slow atrioventricular nodal reentrant tachycardia.

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most frequent form of paroxysmal supraventricular tachycardia. Selective radiofrequency (RF) catheter ablation of the slow pathway is an ideal method for treatment of patients with AVNRT. Complete atrioventricular block is a rare but serious complication of RF ablation, and primarily occurs during or immediately after the procedure. We report on a 45-year-old woman who underwent successful ablation for symptomatic AVNRT at the age of 33. She presented with paroxysmal complete AV block, which developed twelve years after RF ablation of the slow pathway and a permanent DDD pacemaker was implanted. As seen in the case we report, complete AV block complicating RF ablation can occur years after the procedure.

Intracardiac electrogram characteristics of intramural outflow tract ventricular arrhythmias.

BACKGROUND: Annotation of earliest depolarization which depends on maximum dV/dt of unipolar-electrograms and unipolar QS morphology identify site of origin for ventricular premature contractions (VPC). However, identification of unipolar QS morphology has limitations due to low spatial resolution. This study aims to compare electrogram characteristics at successful ablation site in patients with outflow tract (OT) VPC. METHODS: Local activation time (LAT), duration, and voltage data of each bipolar- and unipolar-electrogram at the successful ablation sites from the right ventricle OT (RVOT) and the left ventricle OT (LVOT) cases were analyzed. RESULTS: Forty-four of 60 (73%) of patients were ablated from RVOT and in 16/60 (27%) required ablation from both sides. All patients had acute VPC suppression. Bipolar-electrogram-QRS onset was earlier (36.4 ± 14.5 ms vs 26.3 ± 7.4 ms, p = 0.01), duration of bipolar-electrogram was shorter (56.9 ± 18.9 ms vs 78.9 ± 21.8 ms, p = 0.002), and bi-voltage amplitude was higher (3.2 ± 2.3 mV vs 1.4 ± 1.1 mV, p = 0.07) for patients with RVOT-only ablation. Mean bipolar-unipolar-electrogram difference was 4.4 ± 4.5 ms in the RVOT group vs 12.8 ± 4.9 ms in RVOT + LVOT group (p < 0.001). Unipolar QS morphology was recorded in 3.0 ± 3.9 vs 3.6 ± 1.8 cm2 in RVOT and RVOT + LVOT group, respectively (p = 0.41). Unipolar-electrogram revealed W pattern in 3/44 of RVOT vs 5/16 of RVOT + LVOT group, respectively (p = 0.01). In 18/60 (30%) of patients, unipolar QS was not identified at successful ablation site. CONCLUSION: QS in unipolar-electrogram was not a perfect predictor for successful ablation sites. Analysis of bipolar voltage amplitude and duration with bipolar-unipolar-electrogram time difference may identify presence of a deeper source.

Successful stenting of a left main coronary artery occlusion as a complication of RF ablation for Wolff-Parkinson-White syndrome.

Wolff-Parkinson-White (WPW) syndrome is a disorder characterized by presence of an accessory pathway that predisposes patients to tachyarrhythmias and sudden death. Radiofrequency ablation (RFA) is both effective and safe for patients with symptomatic tachyarrhythmias mediated by accessory atrioventricular pathways. During the procedure, fatal complications may occur but it is considered low in relation to the morbidity associated with the WPW syndrome. Coronary artery occlusion, as a complication of an RF catheter ablation, is quite rare. In this report, we present a 56-year-old male patient with a left main coronary artery (LMCA) occlusion during the ablation of left anterolateral wall accessory pathway. It should be kept in mind if the patient complains of new onset of severe chest pain, an immediate angiography should be performed.