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BACKGROUND Vascular endothelial dysfunction is an underlying pathophysiological feature of chronic heart failure (CHF). Patients with CHF are characterized by impaired vasodilation and inflammation of the vascular endothelium. They also have low levels of endothelial progenitor cells (EPCs). EPCs are bone marrow derived cells involved in endothelium regeneration, homeostasis, and neovascularization. Exercise has been shown to improve vasodilation and stimulate the mobilization of EPCs in healthy people and patients with cardiovascular comorbidities. However, the effects of exercise on EPCs in different stages of CHF remain under investigation. AIM To evaluate the effect of a symptom-limited maximal cardiopulmonary exercise testing (CPET) on EPCs in CHF patients of different severity. METHODS Forty-nine consecutive patients (41 males) with stable CHF [mean age (years): 56 ± 10, ejection fraction (EF, %): 32 ± 8, peak oxygen uptake (VO2, mL/kg/min): 18.1 ± 4.4] underwent a CPET on a cycle ergometer. Venous blood was sampled before and after CPET. Five circulating endothelial populations were quantified by flow cytometry: Three subgroups of EPCs [CD34+/CD45-/CD133+, CD34+/CD45-/CD133+/VEGFR2 and CD34+/CD133+/vascular endothelial growth factor receptor 2 (VEGFR2)] and two subgroups of circulating endothelial cells (CD34+/CD45-/CD133- and CD34+/CD45-/CD133-/VEGFR2). Patients were divided in two groups of severity according to the median value of peak VO2 (18.0 mL/kg/min), predicted peak VO2 (65.5%), ventilation/carbon dioxide output slope (32.5) and EF (reduced and mid-ranged EF). EPCs values are expressed as median (25th-75th percentiles) in cells/106 enucleated cells. RESULTS Patients with lower peak VO2 increased the mobilization of CD34+/CD45-/CD133+ [pre CPET: 60 (25-76) vs post CPET: 90 (70-103) cells/106 enucleated cells, P < 0.001], CD34+/CD45-/CD133+/VEGFR2 [pre CPET: 1 (1-4) vs post CPET: 5 (3-8) cells/106 enucleated cells, P < 0.001], CD34+/CD45-/CD133- [pre CPET: 186 (141-361) vs post CPET: 488 (247-658) cells/106 enucleated cells, P < 0.001] and CD34+/CD45-/CD133-/VEGFR2 [pre CPET: 2 (1-2) vs post CPET: 3 (2-5) cells/106 enucleated cells, P < 0.001], while patients with higher VO2 increased the mobilization of CD34+/CD45-/CD133+ [pre CPET: 42 (19-73) vs post CPET: 90 (39-118) cells/106 enucleated cells, P < 0.001], CD34+/CD45-/CD133+/VEGFR2 [pre CPET: 2 (1-3) vs post CPET: 6 (3-9) cells/106 enucleated cells, P < 0.001], CD34+/CD133+/VEGFR2 [pre CPET: 10 (7-18) vs post CPET: 14 (10-19) cells/106 enucleated cells, P < 0.01], CD34+/CD45-/CD133- [pre CPET: 218 (158-247) vs post CPET: 311 (254-569) cells/106 enucleated cells, P < 0.001] and CD34+/CD45-/CD133-/VEGFR2 [pre CPET: 1 (1-2) vs post CPET: 4 (2-6) cells/106 enucleated cells, P < 0.001]. A similar increase in the mobilization of at least four out of five cellular populations was observed after maximal exercise within each severity group regarding predicted peak, ventilation/carbon dioxide output slope and EF as well (P < 0.05). However, there were no statistically significant differences in the mobilization of endothelial cellular populations between severity groups in each comparison (P > 0.05). CONCLUSION Our study has shown an increased EPCs and circulating endothelial cells mobilization after maximal exercise in CHF patients, but this increase was not associated with syndrome severity. Further investigation, however, is needed.

The Hellenic Heart Failure Association has undertaken the initiative to develop a national network of heart failure clinics (HFCs) and cardio‐oncology clinics (COCs). We conducted two questionnaire surveys among these clinics within 17 months and another during the coronavirus disease 2019 outbreak to assess adjustments of the developing network to the pandemic. Out of 68 HFCs comprising the network, 52 participated in the first survey and 55 in the second survey. The median number of patients assessed per week is 10. Changes in engaged personnel were encountered between the two surveys, along with increasing use of advanced echocardiographic techniques (23.1% in 2018 vs. 34.5% in 2020). Drawbacks were encountered, concerning magnetic resonance imaging and ergospirometry use (being available in 14.6% and 29% of HFCs, respectively), exercise rehabilitation programmes (applied only in 5.5%), and telemedicine applications (used in 16.4%). There are 13 COCs in the country with nine of them in the capital region; the median number of patients being assessed per week is 10. Platforms for virtual consultations and video calls are used in 38.5%. Coronavirus disease 2019 outbreak affected provision of HFC services dramatically as only 18.5% continued to function regularly, imposing hurdles that need to be addressed, at least temporarily, possibly by alternative methods of follow‐up such as remote consultation. The function of COCs, in contrast, seemed to be much less affected during the pandemic (77% of them continued to follow up their patients). This staged, survey‐based procedure may serve as a blueprint to help building national HFC/COC networks and provides the means to address changes during healthcare crises.

Heart failure (HF) is rapidly growing, conferring considerable mortality, morbidity, and costs. Dedicated HF clinics improve patient outcomes, and the development of a national HF clinics network aims at addressing this need at national level. Such a network should respect the existing health care infrastructures, and according to the capacities of hosting facilities, it can be organized into three levels. Establishing the continuous communication and interaction among the components of the network is crucial, while supportive actions that can enhance its efficiency include involvement of multidisciplinary health care professionals, use of structured HF‐specific documents, such as discharge notes, patient information leaflets, and patient booklets, and implementation of an HF‐specific electronic health care record and database platform.

Aims Risk stratification in Brugada syndrome (BrS) still represents an unsettled issue. In this multicentre study, we aimed to evaluate the clinical characteristics and the long-term clinical course of patients with BrS. Methods and results A total of 111 consecutive patients (86 males; aged 45.3 ± 13.3 years) diagnosed with BrS were included and followed-up in a prospective fashion. Thirty-seven patients (33.3%) were symptomatic at enrolment (arrhythmic syncope). An electrophysiological study (EPS) was performed in 59 patients (53.2%), and ventricular arrhythmias were induced in 32 (54.2%). A cardioverter defibrillator was implanted in 34 cases (30.6%). During a mean follow-up period of 4.6 ± 3.5 years, appropriate device therapies occurred in seven patients. Event-free survival analysis (log-rank test) showed that spontaneous type-1 electrocardiogram pattern (P = 0.008), symptoms at presentation (syncope) (P = 0.012), family history of sudden cardiac death (P 113 ms (P Conclusions Multiparametric models including common risk factors appear to provide better risk stratification of BrS patients than single factors alone.

Background There is a controversy in the literature concerning the origin, course, and distribution of the atrioventricular (AV) node artery. Methods Postmortem coronary angiography, dissection, and microscopic examination were performed in 100 human hearts specimens, providing anatomical, histological, and postmortem angiographic features of the AV node artery. Results Two anatomical types of AV node artery, depending on its length (long–short), were found. “Long-length” (LL) AV node artery supplied with blood almost all the AV conducting tissue in 72 cases. It consisted of a horizontal and descending part ending in two branches. “Short-length” (SL) AV node artery had only a horizontal part, perfusing exclusively the AV node and several times the nonpenetrating main bundle of His. In 67 of 100 cases, the AV arteries were arising from the right coronary artery, distal to the posterior descending (PD) artery. The AV node artery never originated from the PD artery. In 54 of 100 cases, it passed under the coronary sinus (CS) and in the remaining 46 it passed underneath the right atrium endocardium. Conclusions The above-described postmortem coronary angiographic findings are essential for interventional cardiologists and cardiac surgeons. Damage to the LL or SL type of AV node artery may cause severe or limited AV conduction abnormalities, respectively. Furthermore, the course of AV node artery under the CS makes it susceptible to injuries provoked by diagnostic or therapeutic procedures involving the CS area.

A 17-year-old apparently healthy individual with recurrent syncopal episodes during walking was referred to our institution for further evaluation. Baseline ECG showed sinus rhythm with prominent J-waves and ST-segment elevation and a short QT interval of 320 ms (Fig. 1). The corrected QT (QTc) interval was 283, 295 and 288 m using the Bazett’s, the Fredericia’s and the Framingham’s formula, respectively. There was no family history of sudden cardiac death. Transthoracic echocardiography revealed a structurally normal heart. Exercise treadmill test failed to induce any arrhythmic or ischemic events, while the early repolarization features (J-waves and ST-segment elevation) were normalized. A drug-free tilt table test was negative for neurocardiogenic syncope. Holter monitoring revealed several asymptomatic episodes of abrupt advanced AV block during day and night, with a maximum pause of 4.2 s (Fig. 2). No episodes of atrial or ventricular arrhythmic events were recorded. Late potentials (RMS-40, LAS-40) as detected and calculated by signal-averaged ECG were positive. Sodium channel blocking test with procainamide (10 mg/kg) failed to induce the diagnostic type 1 ECG pattern of Brugada syndrome (BS) in the right precordial leads. Quinidine administration (900 mg) normalized the absolute QT and QTc values to 380 and 425 m, respectively. Electrophysiological study (EPS) demonstrated normal AH (110 ms) and HV (49 ms) intervals. Right ventricular programmed stimulation at three basic cycle lengths (600, 500 and 430 m) with up to three extra stimuli failed to induce any ventricular arrhythmias. The atrial and ventricular refractory periods were 190 and 200 ms, respectively. No atrial arrhythmias were induced and no episodes of AV block were documented during EPS. A dual-chamber cardioverter defibrillator (ICD) was implanted. The patient was asymptomatic after a 12-month follow-up period. Genomic DNA was prepared from peripheral blood lymphocytes using standard methods. The entire open reading frame of the KCNQ1, KCNH2 and SCN5A genes was analyzed. The following non-coding genetic variants were identified: KCNQ1 (1638 G [ A S546S), KCNH2 (G3152 ? 22 G [ A) and SCN5A (5457 C [ T D1819D, 3183 G [ A E1061E). The KCNJ2, CACNA1C and CACNB2 genes were not screened for mutations.

The present report highlights on exceptional angiographic and histologic features of coronary artery fibromuscular dysplasia in a young man complaining of chest discomfort during strenuous exercise. The striking features of fibromuscular dysplasia were the relative proximal localization of the lesion in left anterior descending coronary artery, the extensive length of the lesion, and the exclusive involvement of the intima producing a diffuse regular narrowing lesion. An eccentric intimal proliferation of the small left anterior descending coronary artery branches along their epicardial and intramural course was additionally demonstrated. No involvement of other coronary arteries or arteries of any other organs was observed.

AIMS The purpose of the present study was to determine for the first time the prevalence of Brugada-type electrocardiographic (ECG) pattern (Brugada sign) in unselected individuals served by an urban Greek tertiary hospital during a 4-year time period. METHODS AND RESULTS Among 11,488 individuals (6640 males, 4848 females), 25 (23 males, 2 females, aged 36.8 +/- 19.2 years) were found to display the Brugada sign (0.22%). Two cases exhibited the diagnostic type 1 ECG pattern (0.02%) and 23 subjects fulfilled the ECG criteria for type 2 or 3 patterns (0.2%). The incidence of Brugada sign was higher among men (0.34%) than in women (0.04%). Structural heart disease was established in four cases (one of them exhibiting a type 1 ECG pattern). Twenty-one individuals (19 males, 2 females, aged 29.7 +/- 10.7 years) without structural heart disease displaying Brugada-type ECG features (4 cases with spontaneous or procainamide-induced type 1 ECG pattern) were subsequently selected and closely followed up for 24 +/- 12 months. No mortality or life-threatening ventricular arrhythmias were recorded during this period. CONCLUSION The Brugada-type ECG pattern is infrequently seen in a Greek hospital-based population. All subjects with Brugada sign and structurally normal hearts displayed a benign clinical course without arrhythmic events during a relatively long follow-up period.

OBJECTIVE The present study aimed at investigating the incidence of paroxysmal atrial fibrillation in 10 patients with spontaneous or induced type 1 electrocardiographic pattern of Brugada syndrome (three with syncopal episodes and seven asymptomatic). Both clinical entities are closely associated with changes in autonomic modulation and, particularly, with increased vagal tone. METHODS Transthoracic echocardiography, exercise treadmill test and 24-h Holter recordings were performed to all patients. RESULTS Episodes of atrial fibrillation were recorded in 2/10 patients (20%). These patients suffered from syncopal episodes, exhibited a positive electrophysiological study, and finally received an implantable cardioverter-defibrillator. CONCLUSIONS The present case series points out a high incidence of paroxysmal atrial fibrillation predominantly in symptomatic patients with type 1 electrocardiographic pattern of Brugada syndrome, indicating that the presence of atrial tachyarrhythmias may reflect an advanced stage of the disease. The prognostic significance of paroxysmal atrial fibrillation, particularly in asymptomatic patients with an electrocardiographic pattern consistent with Brugada syndrome requires further evaluation. Physicians should always be aware of Brugada syndrome in young patients with lone atrial fibrillation, especially in those with a history of syncope.

Congenital coronary artery malformations occur infrequently in the general population. In this report, we describe a rare case of anomalous origin of all three coronary arteries from separate ostia within the right coronary sinus.

A series of 44 consecutive elderly, admitted to a busy general hospital following deliberate self-poisoning, is reviewed for associated medical and psychosocial factors. In all but 3 cases the act involved an overdose of drugs prescribed for the treatment of a chronic medical and/or psychiatric disorder. Women outnumbered men by 2.7 to 1. There was high proportion of chronic psychiatric (80%, mostly depressive) and medical (60%) conditions. Chronic stress from the physical illness, social isolation, or tacit family conflict were common and seemed instrumental in the self-poisoning act. Most attempts were carried out around the weekend and during winter. One man succumbed to complications of the overdose but the rest of the patients recovered. Psychosocial (especially depressive) and medical vulnerability, plus availability of prescribed drugs, were the most important determinants of suicidal behavior among these elderly attempters.

Emerging evidence suggests a pathophysiological role of micronutrient dyshomeostasis in heart failure, including promotion of adverse remodeling and clinical deterioration. We sought to evaluate serum copper (Cu) and zinc (Zn) levels in acute (AHF) and chronic (CHF) heart failure. We studied 125 patients, 71 % male, aged 69 ± 11 years, 37 % with preserved left ventricular ejection fraction (LVEF ≥40 %) (HFPEF), including 81 with AHF and 44 with CHF; 21 healthy volunteers served as controls. Serum Cu and Zn levels were determined using air–acetylene flame atomic absorption spectrophotometry. Serum Cu levels were significantly higher in AHF (p = 0.006) and CHF (p = 0.002) patients compared to controls after adjusting for age, gender and comorbidities, whereas they did not differ between AHF and CHF (p = 0.840). Additionally, serum Cu in patients with LVEF

The ECG features of Brugada syndrome are dynamic and frequently concealed. Sodium channels blockers are widely used to unmask the Brugada electrocardiographic (ECG) pattern. The sensitivity and specificity of I(Na) channel blocking test varies significantly. A negative I(Na) blocking test does not exclude the presence of a SCN5A mutation, which is responsible for the phenotype of Brugada syndrome. Herein, we describe the case of a 65-years-old asymptomatic male who underwent a I(Na) channel blocking test, seven years ago due to a type 2 ECG pattern (saddleback configuration) which failed to induce the diagnostic type 1 ECG pattern. Diagnostic considerations at a molecular level and their clinical relevance are being discussed.

Myxoma is the most common type of primary tumors of the heart in adults. The majority of patients with myxomas may experience symptoms due to central or peripheral embolism or intracardiac obstruction, while in some cases, they may be completely asymptomatic. Rarely, patients develop unusual symptoms that complicate the diagnostic evaluation. Herein, we describe the case of a 70-year-old patient with a long-lasting low-grade fever due to a large left atrial myxoma revealed during a transthoracic echocardiography.

Early repolarization syndrome is a well-recognized idiopathic electrocardiographic phenomenon characterized by prominent J wave and ST-segment elevation predominantly in left precordial leads. The syndrome shares remarkable cellular, ionic, and electrocardiographic similarities with the Brugada syndrome and idiopathic ventricular fibrillation (a variant of the Brugada sydrome with ST-segment elevation in inferior leads). Although early repolarization syndrome is considered a benign entity, its arrhythmogenic potential still remains unknown. We report the case of a 39-year-old male with a family history of sudden death and an electrocardiogram consistent with early repolarization syndrome. Diagnostic dilemmas are discussed.

We report two cases of transient coronary artery ischemia manifested as chest discomfort with ST-segment elevation in inferior leads during the transseptal procedure for radiofrequency catheter ablation of atrial fibrillation. This unexpected complication was resolved by intravenous administration of nitrates. All patients exhibited normal coronary arteries in angiography. A neurally mediated pathway activated by the mechanical effects of the transseptal puncture on the interatrial vagal network leading to coronary artery spasm may be considered as a possible explanation of this phenomenon. Coronary artery embolism following the transseptal procedure represents a different underlying mechanism.

Persistent intercoronary communications, forming the so-called open ended coronary circulation pattern, are rare findings of coronary angiography. A case of intercoronary connection between the left anterior descending artery (LAD) and the right coronary artery (RCA), with an obstructive lesion, and no evidence of myocardial infarction is presented. This is an exceptional variant, only 20 cases of which were found in the literature. The potential protective role of this anomaly against occlusive coronary artery disease is discussed and similar reports are reviewed.

In this report we describe the case of a 42-year-old woman who experienced an episode of near drowning during recreational swimming. A diagnosis of Andersen-Tawil syndrome was made based on the patient's dysmorphic features, characteristic T-U-wave patterns and ventricular arrhythmias. To our knowledge, this is the first report of a swimming-triggered cardiac event in a patient with Andersen-Tawil syndrome.

The incidence of sinoatrial artery variants and their significance have been repeatedly reported in the literature. Herein we describe a rare post mortem angiographic finding which concerns a unique and previously unreported case where the sinus node artery had an abnormal origin from the proximal conus artery. Although it was asymptomatic, any possible involvement with invasive or surgical procedures and its clinical consequences should be considered.

The Intek-Apollo stent (Switzerland) employs a polysulfone polymer coating which has demonstrated low interaction with blood and high thrombo-resistance. The aim of this study was to assess the clinical and angiographic outcomes after Intek-Apollo stent utilisation in a real-world setting.A total of 130 patients (77.7% males) were enrolled with 174 lesions in native coronary arteries (92.4%), saphenous vein grafts (7.5%) and in-stent restenosis (6.3%). Indications for stenting were stable coronary artery disease (CAD) 52.3%, acute coronary syndrome (ACS) 37.7% and STEMI 10%. Clinical follow-up and coronary angiography (after symptoms occurrence or positive stress test) was performed at 6 and 12 months.The primary end points were target lesion revascularization (TLR) and target vessel revascularization (TVR), while secondary end points were major adverse cardiac events (MACE) during the follow-up period.The mean age of patients included was 61.62±11.13 years. Complex lesions treatment (ostial, bifurcation) reached 13.7%. Mean stenosis diameter was 83.52±10.5%. Reference vessel diameter was 2.85±0.39 mm with a mean lesion length of 14.66±4.5mm. Average stent size was 2.93±0.39mm × 16.6±4.73 mm. At 15±3 months, primary events included TLR (4.6%), TVR (4.6%) and MACE (2.3%). There was 1one myocardial infarction and no cardiac death). No incidence of early or late stent thrombosis was demonstrated.Intek-Apollo stent implantation is safe and efficient in a real world population. The unique properties of polysulfone polymer coating can effectively protect from late stent thrombosis and lead to reduced rates of TLR, TVR and MACE.

Out-of-hospital cardiac arrest remains a major cause of mortality and morbidity despite progress in resuscitative practices. The number of survivors with severe neurological impairment at hospital discharge is similarly dismal. Recently, much attention has been directed toward the use of mild therapeutic hypothermia in the care of comatose survivors with postcardiac arrest syndrome. Recent research suggests mild hypothermia lowers mortality and improves neurological outcome after successful treatment of cardiac arrest. The current 2005 updated guidelines of International Liaison Committee on Resuscitation and European Resuscitation Council recommend the utilization of mild induced hypothermia in postresuscitation treatment. Hypothermia induction in order to avoid the pathophysiological mechanisms of euthermia and hyperthermia and subsequent complications are briefly discussed. Cooling methods, potential side effects and questions regarding implementation of therapeutic hypothermia recommendations in every day clinical practice and future investigation are also addressed.

Uric acid is a cardiovascular risk marker associated with oxidative stress and inflammation. Recently, atrial fibrillation (AF) has been associated with inflammation and oxidative stress. We therefore investigated the association between AF and uric acid levels.Consecutive patients with AF and healthy control subjects were screened. Demographic, clinical, and echocardiographic characteristics were carefully recorded. In each participant, uric acid levels and conventional inflammatory markers were determined. The final study population consisted of 45 patients with paroxysmal AF, 41 patients with permanent AF, and 48 control subjects.A significant variance in uric acid levels was evident between patients with paroxysmal AF (5.7 +/- 1.1 mg/dl), permanent AF (6.7 +/- 1.4 mg/dl), and control subjects (5.1 +/- 1.3 mg/dl) (p0.001). After univariate analysis considering 2 groups (control, AF patients), the following variables were significantly associated with the presence of AF: age, hypertension, -blocker use, low left ventricular ejection fraction (LVEF), increased left atrial diameter, uric acid levels, and C-reactive protein (CRP) levels. After multivariate logistic regression analysis, only CRP was an independent predictor for AF (odds ratio, OR: 2.172). In a subgroup analysis, CRP (OR: 1.434) and LVEF (OR: 0.361) were independent predictors of paroxysmal AF, while CRP (OR: 3.048), uric acid (OR: 2.172), and LVEF (OR: 0.34) were predictors of permanent AF.There is an association between increased levels of uric acid and permanent AF. Also, uric acid elevation may be related to the burden of AF. Undoubtedly, larger studies should further examine this potential association.

OBJECTIVE The present study aimed to compare the effectiveness and safety of the potential- and the anatomic-guided approach for slow pathway ablation in patients with recurrent episodes of symptomatic common type atrioventricular (AV) nodal reentrant tachycardia. METHODS Two hundred and twenty-eight patients were randomly assigned to undergo either a potential- (n=114, 47% men, mean age 52.85 +/- 14.04 years) or an anatomic-guided approach (n=114, 50% men, mean age 52.45 +/- 14.46 years) for radiofrequency ablation of the slow pathway.The mean duration of the follow-up period was 26.7 +/- 7.9 and 24.8 +/- 7.6 months in the potential- and anatomic- guided approach, respectively (P > 0.05). RESULTS The success rate for slow pathway ablation was 100% in both ablative methods.The mean duration of atrial electrograms at the successful ablation sites of the potential- and the anatomic-guided approaches was 69 +/- 14 msec and 57 +/- 10 msec, respectively (P = 0.001).There were no significant differences between the potential- and the anatomic-guided approach regarding the duration of the procedure (121.13 +/- 56.83 vs. 109.93 +/- 57.12 min, P = 0.139), the duration of fluoroscopic exposure (6.12 +/- 3.32 vs. 6.64 +/- 3.33 min, P = 0.239) or the mean number of radiofrequency applications delivered (3.96 +/- 2.77 vs. 4.33 +/- 2.73, P = 0.311). Residual dual AV nodal pathway following successful ablation was observed in 9.6% of patients who underwent the potential-guided approach and in 23.7% of patients who underwent the anatomic method (P = 0.004). During followup, arrhythmia recurrence was observed in four patients (1.8%), two in each group (P > 0.05). CONCLUSIONS The efficacy and safety of the slow pathway ablation is very high using either the potential- or the anatomic-guided approach.

Background Limited data are available on the predictors of atrial fibrillation (AF) recurrence in patients with chronic AF. Objectives To evaluate potential clinical, echocardiographic and electrophysiological predictors of AF recurrence after internal cardioversion for long-lasting AF. Methods A total of 99 consecutive patients (63 men and 36 women, mean age 63.33±9.27 years) with long-standing AF (52.42±72.02 months) underwent internal cardioversion with a catheter that consisted of two defibrillating coils. Shocks were delivered according to a step-up protocol. Clinical follow-up and electrocardiographic recordings were performed on a monthly basis for a 12-month period or whenever patients experienced symptoms suggestive of recurrent AF. Results Ninety-three patients (93.94%) underwent a successful uncomplicated cardioversion, with a mean atrial defibrillation threshold of 10.69±6.76 J. Immediate reinitiation of AF was observed in 15 patients (15.78%) of whom a repeated cardioversion restored sinus rhythm in 13 cases. Early recurrence of AF (within one week) was observed in 12 of 93 patients (12.90%). At the end of the 12-month follow-up period, during which seven patients were lost, 42 of the 86 remaining patients (48.84%) were still in sinus rhythm. Multivariate regression analysis showed that left atrial diameter (OR 1.126, 95% CI 1.015 to 1.249; P=0.025) and mitral A wave velocity (OR 0.972, 95% CI 0.945 to 0.999; P=0.044) were significant and independent predictors of AF recurrence, whereas age, left ventricular ejection fraction and AF cycle length were not predictive of arrhythmia recurrence. Conclusion The present study showed that the left atrial diameter and mitral A wave velocity are the only variables associated with AF recurrence after successful cardioversion.

The authors describe the case of a 66-year-old woman with arrhythmogenic right ventricular dysplasia masqueraded as dilated cardiomyopathy. Her medical history included recurrent episodes of syncope beginning at the age of 28. The natural history of the disease is discussed.

Several agents and conditions have been reported to unmask or accentuate the electrocardiographic pattern of Brugada syndrome including fever. At a molecular level, sodium channels have been showed to be temperature dependent. Herein, we describe a case of Brugada electrocardiographic pattern unmasked during febrile state and marked leukocytosis.

The present study aimed to investigate the causative medications and underlying risk factors that predispose to drug-induced QT interval prolongation. Twenty-one patients with drug-induced long QT (90% females, mean age 64.3 +/- 14.1 years) were included in the study. Transthoracic echocardiography as well as continuous or ambulatory 48-h electrocardiographic monitoring was carried out in all patients during their hospitalization. The mean corrected QT (QTc) interval was 542 +/- 56.8 ms. Known cardiac agents (mainly class III antiarrhythmics) were implicated in 13/21 (62%), antipsychotics in 8/21 (38%), and antibiotics in 5/21 patients (24%). Potential drug-interactions through inhibition of cytochrome P450 isoenzymes were considered responsible in 5/21 cases (24%). The underlying cardiovascular diseases included hypertension (57%) with left ventricular hypertrophy (29%), paroxysmal atrial tachyarrhytmias (48%), heart failure (14%), valvular heart disease (10%), and coronary artery disease (5%). Torsade de pointes (TdP) was recorded in 6/21 of patients, and cardiac arrest necessitating resuscitation occurred in five of them. A significant correlation was observed between administration of cardiac agents and TdP events (P0.05). TdP and cardiac arrest events were both associated with a QTc interval510 ms (P0.05). Advanced age (60 years), female gender, hypertension and paroxysmal atrial tachyarrhytmias were the most common identifiable pre-existing factors for drug-induced long QT in our patient cohort. Marked QTc interval prolongation should be considered of prognostic significance for TdP and cardiac arrest events.

A 20-year-old woman with known Kearns-Sayre syndrome was transferred to the emergency department due to syncopal episodes. The electrocardiogram on admission showed complete atrioventricular block. The diagnosis of mitochondrial encephalomyopathy was made when she was 14 years old. At the time of the initial diagnosis, she displayed a normal electrocardiogram pattern. At the age of 17, electrocardiogram recordings demonstrated right bundle branch block with left anterior fascicular block and a prolonged QTc interval of 485 milliseconds (Figure). She was taking coenzyme Q10, oral nicotinamide adenine dinucleotide (reduced), piribedil, amantadine, and primidone.Transthoracic echocardiography revealed normal wall motion of both ventricles and mitral valve prolapse without regurgitation.A permanent dual-chamber pacemaker was immediately implanted. Figure Figure. Twelve-lead electrocardiogram showing bifascicular block and QTc interval prolongation (485 milliseconds).

A ntiphospholipid syndrome (APS) is an acquired, immune- mediated thrombophilic disorder characterized by arterial and venous thrombosis, recurrent abortus, thrombocytopenia, and the presence of antiphospholipid antibodies (aPL) [anticardiolipin (aCL), anti-s 2 glycoprotein 1 and lupus anticoagulant (LA) antibodies]. Subcategories of APS include primary (PAPS), secondary in the presence of an autoimmune disorder, and catastrophic when thrombotic events occur over a short period of time and at multiple sites. Deep venous thrombosis of the lower limbs is the most common clinical presentation of the APS, seen in 38.9% of patients. Arterial thrombosis is less frequent, and mainly affects the central nervous system. Strokes and transient ischemic attacks occur in 19.8% and 11.1% of patients respectively. Cardiac manifestations of PAPS include mitral and aortic valve disease, vegetation- like lesions (non-bacterial thrombotic . . .

The incidence of calcified debris coronary embolism after aortic valve replacement (AVR) with a bioprosthesis is a rare but potentially life-threatening condition. We sought to describe a case of immediate postoperative left main coronary artery embolism, resulting to severe acute coronary syndrome and cardiogenic shock, after aortic valve surgery due to severe aortic valve stenosis, with the use of bioprosthesis. Complex interventional procedures and possible diagnostic challenges are being described.

A mechanical alteration during manoeuvring of stiff guidewires in tortuous coronary arteries frequently induces vessel wall shortening and coronary psedostenosis, referred as accordion phenomenon. Subtraction of the guidewires normally leads to the entire resolution of the lesions. A case of this transient angiographic finding, during percutaneous coronary intervention in a tortuous right coronary artery, which resulted in a flow limiting effect and myocardial ischemia, is described in the present report. Differential diagnosis from potential procedure complications and interventional methodology issues are discussed, while similar reports are reviewed.