Search

Background: Sleep-disordered breathing (SDB) has been associated with various benign cardiac arrhythmias occurring during sleep.Objective: The purpose of this study was to demonstrate that SDB contributes to the development of life-threatening ventricular arrhythmias in patients with an established arrhythmic substrate.Methods: We prospectively studied the association between SDB and timing of life-threatening ventricular arrhythmic events in 45 patients with an implantable cardioverter-defibrillator (ICD). SDB was defined as an apnea-hypopnea index (AHI) >10 events/hour based on an overnight sleep study. The primary outcome measure was appropriate ICD therapy, defined as antitachycardia pacing or shock for ventricular tachycardia or ventricular fibrillation during 1-year follow-up.Results: SDB was present in 26 (57.8%) patients. Appropriate ICD therapies were higher among patients with SDB (73% vs 47%, P = .02). Logistic regression identified SDB as a predictor of any appropriate ICD therapy (odds ratio 4.4, 95% confidence interval 1.4-15.3, P = .01). The risk for ventricular arrhythmias was higher in patients with SDB solely due to an increase in events occurring between midnight and 6 AM (odds ratio 5.6, 95% confidence interval 2.0-15.6, P = .001) with no discernible effect on appropriate ICD therapy during nonsleeping hours (odds ratio 0.7, 95% confidence interval 0.2-2.3, P = .61).Conclusion: Patients with an ICD and SDB have a striking increase in the onset of life-threatening ventricular arrhythmic events during sleeping hours. These findings provide a rationale for SDB screening in patients with appropriate ICD therapy if device interrogation reveals a predominance of nocturnal onset of arrhythmias. [ABSTRACT FROM AUTHOR]

Introduction: Arrhythmogenic cardiomyopathy (AC) is an inherited cardiomyopathy characterized by fibro-fatty replacement of cardiomyocytes, leading to life-threatening ventricular arrhythmia and heart failure. Pathogenic variants of desmoglein2 gene (DSG2) have been reported as genetic etiologies of AC. In contrast, many reported DSG2 variants are benign or variants of uncertain significance. Correct genetic variant classification is crucial for determining the best medical therapy for the patient and family members., Methods: Pathogenicity of the DSG2 Ser194Leu variant that was identified by whole exome sequencing in a patient, who presented with ventricular tachycardia and was diagnosed with AC, was investigated by electron microscopy and immunohistochemical staining of endomyocardial biopsy sample., Results: Electron microscopy demonstrated a widened gap in the adhering junction and a less well-organized intercalated disk region in the mutated cardiomyocytes compared to the control. Immunohistochemical staining in the proband diagnosed with AC showed reduced expression of desmoglein 2 and connexin 43 and intercalated disc distortion. Reduced expression of DSG2 and Connexin 43 were observed in cellular cytoplasm and gap junctions. Additionally, we detected perinuclear accumulation of DSG2 and Connexin 43 in the proband sample., Conclusion: Ser194Leu is a missense pathogenic mutation of DSG2 gene associated with arrhythmogenic left ventricular cardiomyopathy., (© 2024 Wiley Periodicals LLC.)

Background: Dilated cardiomyopathy (DCM) caused by Lamin A/C gene (LMNA) mutation is complicated with atrioventricular conduction disturbances, malignant ventricular arrhythmias and progressive severe heart failure., Objective: We hypothesized that early cardiac resynchronization therapy (CRT) implantation in LMNA mutation carriers with an established indication for pacemaker or implantable cardioverter defibrillator (ICD), may preserve ejection fraction, and delay disease progression to end stage heart failure., Methods: We compared the primary outcomes: time to heart transplantation, death due to end stage heart failure or ventricular tachycardia (VT) ablation and secondary outcomes: change in left ventricular ejection fraction (EF) and ventricular arrhythmia burden between LMNA DCM patients in the early CRT and non-CRT groups., Results: Of ten LMNA DCM patients (age 51±10 years, QRS 96±14 msec, EF 55±7%) with indication for pacemaker or ICD implantation, five underwent early CRT-D implantation. After 7.2±4 years, three patients (60%) in the non-CRT group reached the primary outcome, compared to no patients in the CRT group (P=0.046). Four patients in non-CRT group (80%) experienced sustained ventricular tachycardia or received appropriate ICD shock compared to 1 patient (20%) in the CRT group (P=0.058). LMNA patients without early CRT had a higher burden of VPC/24 h in 12-lead holter (median 2352 vs 185, P=0.09). Echocardiography showed statistically lower LVEF in the non-CRT group compared to CRT group [(32±15)% vs (61±4)%, 95% CI: 32.97-61.03, P=0.016]., Conclusion: Early CRT implantation in LMNA cardiomyopathy patients, with an indication for pacemaker or ICD, may reduce heart failure deterioration and life-threatening heart failure complications., Competing Interests: None., (AJCD Copyright © 2024.)

Background: Determining the pathogenesis of sudden cardiac arrest (SCA) in children is crucial for its management and prognosis. Our aim is to analyze the role of broad genetic testing in the prevention, diagnosis, and prognosis of SCA in Children., Methods: ECG, 12-lead holter, exercise testing, cardiac imaging, familial study, and genetic testing were used to study 29 families, in whom a child experienced SCA., Results: After a thorough clinical and genetic evaluation a positive diagnosis was reached in 24/29 (83%) families. Inherited channelopathies (long QT syndrome and catecholaminergic polymorphic ventricular tachycardia) were the most prevalent 20/29 (69%) diagnosis, followed by cardiomyopathy 3/29 (10%). Broad genetic testing was positive in 17/24 (71%) cases. Using the Mann-Whitney test, we found that genetic testing (effect size = 0.625, p  = 0.003), ECG (effect size = 0.61, p  = 0.009), and exercise test (effect size = 0.63, p  = 0.047) had the highest yield in reaching the final diagnosis. Genetic testing was the only positive test available for five (17%) families. Among 155 family members evaluated through cascade screening, 73 (47%) had a positive clinical evaluation and 64 (41%) carried a pathologic mutation. During 6 ± 4.8 years of follow-up, 58% of the survived children experienced an arrhythmic event. Of nine family members who had an ICD implant for primary prevention, four experienced appropriate ICD shock., Conclusions: The major causes of SCA among children are genetic etiology, and genetic testing has a high yield. Family screening has an additional role in both the diagnosis and preventing of SCA., Competing Interests: Authors declare no conflict of interests for this article., (© 2023 The Authors. Journal of Arrhythmia published by John Wiley & Sons Australia, Ltd on behalf of Japanese Heart Rhythm Society.)

Cardiac involvement in acute Q fever is rare. We report 2 cases of an advanced atrioventricular block in young adult patients in Israel who sought care for acute Q fever without evidence of myocarditis. Q fever should be suspected in unexplained conduction abnormalities, especially in febrile young patients residing in disease-endemic areas.

Objective and Background: To evaluate the diagnostic and prognostic yield of a comprehensive protocol involving clinical and broad genetic testing in consecutive sudden cardiac arrest (SCA) population. Determining the pathogenesis of non-ischemic SCA is crucial for management and SCA prevention in other family members METHODS: Families with unexplained non-ischemic SCA event underwent rigorous clinical and genetic protocol after referral to our inherited arrhythmia clinic, during 2011-2017., Results: One hundred and four index cases, 29 ± 16 years, and 421 family members were studied. After a thorough evaluation, diagnosis was made in 80 (77%) of families. The most prevalent 47/104 (45%) diagnosis was inherited channelopathy. The genetic test was positive, in 37 /69 (54%) of patients. Using the Mann Whitney test, we found that electrocardiography (ECG) (effect size 0.5, p < .001), 12 lead Holter (effect size 0.33, p = .001) and family screening (effect size 0.4, p = .001) had the highest yield in reaching the final diagnosis. Family screening, genetic testing, and cardiac MRI were the exclusive modalities for final diagnosis in 14%, 9%, and 2% of families, respectively. Among 421 family members evaluated through cascade screening, 127 (30%), were diagnosed and medically treated. Nine family members from 25 (40%) patients who underwent implantable cardioverter defibrillator (ICD) implantation have experienced appropriate ICD shock., Conclusions: A rigorous, systematic protocol in a specialized inherited arrhythmia clinic has a high diagnostic and prognostic yield. ECG, 12 lead Holter and family screening significantly increased the diagnostic yield. In nine families, without genetic testing, the diagnosis would have been missed., (© 2021 Wiley Periodicals LLC.)

Congenital long QT syndrome (LQTS) is a cardiac channelopathy that leads to the prolongation of the QT interval. This prolongation can lead to ventricular tachyarrhythmia, syncope, and sudden cardiac death. There are various types of LQTS. Treatment of LQT1 and LQT2 is mainly based on antiadrenergic therapy. LQT3, on the other hand, is a result of a mutation of the SCN5A gene, which encodes the sodium channels. In this type, patients are sensitive to vagal stimuli and episodes tend to occur at rest. Sodium channel blocking compounds, such as ranolazine, mexiletine, and flecainide, have been found to be effective in selective mutations.In this case report, we report the case of a child with congenital LQT3 (V411M) who presented first with sudden cardiac death and three weeks later with an implantable cardioverter defibrillator storm. Knowing the specific mutation and understanding the mechanism at the molecular level through an in vitro study yielded a clinically meaningful result. The patient's arrhythmia burden was totally eliminated following successful treatment with flecainide.

Background: Limited information exists about detailed clinical characteristics and management of the small subset of Brugada syndrome (BrS) patients who had an arrhythmic event (AE)., Objectives: To conduct the first nationwide survey focused on BrS patients with documented AE., Methods: Israeli electrophysiology units participated if they had treated BrS patients who had cardiac arrest (CA) (lethal/aborted; group 1) or experienced appropriate therapy for tachyarrhythmias after prophylactic implantable cardioverter defibrillator (ICD) implantation (group 2)., Results: The cohort comprised 31 patients: 25 in group 1, 6 in group 2. Group 1: 96% male, mean CA age 38 years (range 13-84). Nine patients (36%) presented with arrhythmic storm and three had a lethal outcome; 17 (68%) had spontaneous type 1 Brugada electrocardiography (ECG). An electrophysiology study (EPS) was performed on 11 patients with inducible ventricular fibrillation (VF) in 10, which was prevented by quinidine in 9/10 patients. During follow-up (143 ± 119 months) eight patients experienced appropriate shocks, none while on quinidine. Group 2: all male, age 30-53 years; 4/6 patients had familial history of sudden death age < 50 years. Five patients had spontaneous type 1 Brugada ECG and four were asymptomatic at ICD implantation. EPS was performed in four patients with inducible VF in three. During long-term follow-up, five patients received ≥ 1 appropriate shocks, one had ATP for sustained VT (none taking quinidine). No AE recurred in patients subsequently treated with quinidine., Conclusions: CA from BrS is apparently a rare occurrence on a national scale and no AE occurred in any patient treated with quinidine.

Aim: To investigate the impact of using computed tomography (CT) and contact force (CF) technology on recurrence of atrial tachyarrhythmia after atrial fibrillation (AF) ablation., Methods: This non-randomized study included 2 groups of patients. All patients had symptomatic recurrent paroxysmal or persistent AF and were treated with at least 1 anti arrhythmic medication or intolerant to medication. The first group included 33 patients who underwent circumferential pulmonary veins isolation (PVI) for AF during 2012 and 2013 guided by CT image integration (Cartomerge, Biosense Webster, Diamond Bar, CA, United States) of left atrium and pulmonary veins into an electroanatomic mapping (EAM) system (CT group) using standard irrigated radiofrequency catheter (ThermoCool, Carto, Biosense Webster, Diamond Bar, CA, United States) or irrigated catheter with integrated CF sensor (Smart Touch, Carto, Biosense Webster, Diamond Bar, CA, United States). The second group included immediately preceding 32 patients who had circumferential PVI by standard irrigated catheter (ThermoCool) using only EAM (Carto) system (EAM group). Linear lesions were performed according to the discretion of operator., Results: Sex, age, and persistent AF were not different between groups. PVI was achieved in all patients in both groups. Linear ablations including cavo-tricuspid isthmus and or roof line ablation were not different between groups. Free of atrial tachyarrhythmia during follow-up of 24 mo was significantly higher among CT group compared to EAM group (81% vs 55%; respectively; P = 0.027). When 11 patients from CT group who had ablation using Smart Touch catheter were excluded, the difference between CT group and EAM became non significant (73% vs 55%; respectively; P = 0.16). Sub analysis of CT group showed that patients who had ablation using Smart Touch catheter tend to be more free of atrial tachyarrhythmia compared to patients who had ablation using standard irrigated catheter during follow-up (100% vs 73%; respectively; P = 0.07). Major complications (pericardial effusion, cerebrovascular accident/transient ischemic attack, vascular access injury requiring intervention) did not occurred in both groups., Conclusion: These preliminary results suggest that CT image integration and CF technology may reduce the recurrence of atrial tachyarrhythmia after catheter ablation for AF.

Background: Ablation of outflow flow ventricular arrhythmia (VA) originating from aortic cusps can be challenging. The aim of this study was to describe our approach for this ablation., Methods: All patients with outflow VA suspected to originate from aortic cusps according to ECG or after failed ablation from right ventricular outflow tract (RVOT) underwent cardiac CT and radiofrequency ablation. CT image of aortic cusps and coronary arteries was integrated into electroanatomic mapping system by point (left main ostium)-based registration. Ablation was performed at the earliest activation site., Results: Ten patients were included in this case cohort. The ablation catheter was easily maneuvered above and below the aortic valve after registration. Two patients who had previous failed ablation of RVOT focus had successful ablation at right coronary cusp (RCC) and at left coronary cusp (LCC). A patient who had previous failed ablations of RVOT and LCC focuses had successful ablation at RCC-LCC junction. A patient who had previous failed ablation at LCC had successful ablation at RCC-LCC junction. Three patients had successful ablation at RCC-LCC junction, and one patient at LCC. One patient had successful ablation at anterior interventricular vein-great cardiac vein junction. One patient had successful ablation at non-coronary cusp. During follow-up (12-30 months), one patient had recurrence of VA controlled by flecainide. The remaining patients were free of VA without medications., Conclusions: Catheter ablation of VA originating from aortic cusps is safe and effective. CT image integration into electroanatomic mapping system can be helpful in this challenging ablation.

Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare but highly malignant inherited arrhythmic disorder. Although a standardized exercise stress test (ST) is the most reliable way to diagnose CPVT, in 30% only single ventricular premature beats (VPCs) were recorded., Objective: To evaluate whether electrocardiographic characteristics of VPCs during ST distinguish patients with CPVT from healthy subjects., Methods: Electrocardiographic characteristics of VPCs during ST in 16 calsequestrin-2 (CASQ2) mutation carriers CPVT patients were compared with that in 36 healthy subjects., Results: CPVT patients had more VPCs (31 ± 14 vs 3 ± 4, P < 0.0001), longer QRS duration (139 ± 18 ms vs 121 ± 21, P = 0.004), and coupling interval (CI; 476 ± 58 ms vs 355 ± 61 ms, P < 0.0001). The most sensitive characteristics for CPVT were >10 VPCs/test (100% sensitivity, 100% negative predictive value [NPV]), left bundle branch block (LBBB) pattern with inferior axis (88% sensitivity, 94% NPV), and CI longer than 400 ms (88% sensitivity, 94% NPV). Bigeminy or trigeminy or LBBB pattern with inferior axis was most specific for CPVT at 100% (100% positive predictive value PPV, 92% NPV). First VPC during the recovery period and VPC recording more than 1 minute during the recovery period were most specific for healthy subjects (100% specificity, 100% PPV). In multivariate analysis, QRS duration >120 ms (odds ratio 4.2, 95% confidence interval 1-17.6, P = 0.04) and first VPC at ≥10 mets (odds ratio 9.1, 95% confidence interval 2.01-41.1, P = 0.004) each predicted the presence of CPVT., Conclusions: Several electrocardiographic criteria can help distinguish VPCs originating from CPVT compared with healthy subjects., (©2015 Wiley Periodicals, Inc.)

The D1790G mutation was found in all 24 patients of an extended long QT family but not in 200 chromosomes carried by healthy individuals. We describe a 37-year-old man presenting with a typical spontaneous type 1 Brugada pattern who in electrophysiological testing had easily inducible ventricular fibrillation. At the age of 47 years he had an atrial ventricular type 2 block documented by an exercise test and a Holter monitor. Genetic analysis revealed a known D1790G mutation in the gene encoding of the sodium channel (SCN5A) that until now has been associated only with the long QT phenotype. Although this mutation has not been associated with a reduction of sodium channel expression, we hypothesize that sodium currents are further diminished due to the 20-mV shift of the steady-state inactivation curve, and this could contribute to the Brugada phenotype. This case is important as it allows a better understanding of the underlying molecular mechanisms of Brugada syndrome. Moreover, this observation raises concern about the safety of class IC drug therapy in long QT type 3 patients and quinidine therapy in Brugada patients, and emphasizes the importance of a thorough clinical and genetic evaluation., (© 2015 S. Karger AG, Basel.)

Background: Calsequestrin-associated catecholaminergic polymorphic ventricular tachycardia (CPVT2) can cause sudden death in young individuals in response to stress. Beta-blockers are the mainstay medical treatment for patients with CPVT2. However, they do not prevent syncope and sudden death in all patients. Flecainide was reported to reduce exercise-induced ventricular arrhythmias (EIVA) in patients with ryanodine receptor-associated CPVT. The role of flecainide in CPVT2 is not known., Objective: To summarize our experience in combining flecainide and beta-blockers in high-risk patients with CPVT2., Methods: All patients with CPVT2 (10 patients) who have high-risk features (syncope, EIVA, or appropriate implantable cardioverter-defibrillator [ICD] shocks) despite beta-blockers with or without calcium channel blockers were treated with a combination of flecainide and beta-blockers. Exercise test was done before and after beginning treatment with flecainide., Results: All patients had EIVA and 4 had appropriate ICD shocks before flecainide treatment. EIVA-included frequent ventricular premature beats and or ventricular tachycardia during the exercise test while on high dose of beta-blockers with or without calcium channel blockers before treatment with flecainide. After combination therapy with flecainide and beta-blockers, EIVA were suppressed completely in all patients. During follow-up of 15.5 ± 10.4 months (range 2-29 months), 8 patients were free of symptoms and free of arrhythmias. Two patients had 1 VT storm episode with recurrent ICD shocks despite repeated normal stress test., Conclusions: Flecainide can completely prevent ventricular arrhythmia during exercise and partially prevent recurrent ICD shocks in high-risk patients with CPVT2., (© 2013 Heart Rhythm Society. All rights reserved.)

Heparanase, the sole mammalian endoglycosidase degrading heparan sulfate, is causally involved in cancer metastasis, angiogenesis, inflammation and kidney dysfunction. Despite the wide occurrence and impact of heparan sulfate proteoglycans in vascular biology, the significance of heparanase in vessel wall disorders is underestimated. Blood vessels are highly active structures whose morphology rapidly adapts to maintain vascular function under altered systemic and local conditions. In some pathologies (restenosis, thrombosis, atherosclerosis) this normally beneficial adaptation may be detrimental to overall function. Enzymatic dependent and independent effects of heparanase on arterial structure mechanics and repair closely regulate arterial compliance and neointimal proliferation following endovascular stenting. Additionally, heparanase promotes thrombosis after vascular injury and contributes to a pro-coagulant state in human carotid atherosclerosis. Importantly, heparanase is closely associated with development and progression of atherosclerotic plaques, including stable to unstable plaque transition. Consequently, heparanase levels are markedly increased in the plasma of patients with acute myocardial infarction. Noteworthy, heparanase activates macrophages, resulting in marked induction of cytokine expression associated with plaque progression towards vulnerability. Together, heparanase emerges as a regulator of vulnerable lesion development and potential target for therapeutic intervention in atherosclerosis and related vessel wall complications., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Objective: Factors and mechanisms that activate macrophages in atherosclerotic plaques are incompletely understood. We examined the capacity of heparanase to activate macrophages., Methods and Results: Highly purified heparanase was added to mouse peritoneal macrophages and macrophage-like J774 cells, and the levels of tumor necrosis factor-α, matrix metalloproteinase-9, interlukin-1, and monocyte chemotactic protein-1 were evaluated by ELISA. Gene expression was determined by RT-PCR. Cells collected from Toll-like receptor-2 and Toll-like receptor-4 knockout mice were evaluated similarly. Heparanase levels in the plasma of patients with acute myocardial infarction, stable angina, and healthy subjects were determined by ELISA. Immunohistochemistry was applied to detect the expression of heparanase in control specimens and specimens of patients with stable angina or acute myocardial infarction. Addition or overexpression of heparanase variants resulted in marked increase in tumor necrosis factor-α, matrix metalloproteinase-9, interlukin-1, and monocyte chemotactic protein-1 levels. Mouse peritoneal macrophages harvested from Toll-like receptor-2 or Toll-like receptor-4 knockout mice were not activated by heparanase. Plasma heparanase level was higher in patients with acute myocardial infarction, compared with patients with stable angina and healthy subjects. Pathologic coronary specimens obtained from vulnerable plaques showed increased heparanase staining compared with specimens of stable plaque and controls., Conclusions: Heparanase activates macrophages, resulting in marked induction of cytokine expression associated with plaque progression toward vulnerability.

Background: Incidence and predictors of clopidogrel discontinuation after drug eluting stent (DES) implantation, in real world practice, are poorly known., Methods: Prospective study included all patients who underwent implantation of at least one DES between February 2006 and January 2007. Predictors of clopidogrel discontinuation were assessed by a multivariable analysis., Results: In 269 patients, mean period for clopidogrel therapy was 13.2 ± 7.2 month. Twenty eight patients (10.4%) discontinued clolopidogrel prematurely (< 3 months). Early clopidogrel discontinuation was a predictor of late stent thrombosis (P = 0.005) and urgent target vessel revascularization (P = 0.05). There was a trend for higher cardiac mortality among that group (P = 0.07). By 12 months, 173 patients (64.3%) have discontinued clopidogrel therapy. The most frequent circumstance to stop clopidogrel before 12 months was recommendation of family physician. Patients that were followed by cardiologist were more encouraged to longer clopidogrel therapy. In multivariable analysis being non Jew (OR 19.2, 95% CI 2.4 to 142, P = 0.005), not followed by cardiologist (OR 4.7, 95% CI 1 to 23.1, P = 0.05) and lack of information regarding the importance of clopidogrel maintenance at discharge from hospital (OR 10.8, 95% CI 2.7 to 42.9, P = 0.001) were independent predictors of early clopidogrel discontinuation., Conclusions: Clopidogrel discontinuation, in real world practice is not unusual and related to poor outcome. Education for general physicians, clear instructions about the importance of antiplatelet maintenance at discharge and follow up by an expert cardiologist are opportunities to improve adherence do antiplatelet therapy following DES implantation.

Background: For patients with ventricular tachyarrhythmias, implantable cardioverter defibrillators are a mainstay of therapy to prevent sudden death. However, ICD shocks are painful, can result in clinical depression, and do not offer complete protection against death from arrhythmia. Radiofrequency catheter ablation of ventricular tachycardia in the setting of ischemic cardiomyopathy has emerged recently as a useful adjunctive therapy to ICD., Objectives: To assess the feasibility, safety and efficacy of our initial experience in ablation of scar-related VT., Methods: Eleven patients (all males, mean age 71 +/- 8 years) with drug-refractory ischemic VT were referred to our center for scar mapping and ablation procedures using the CARTO navigation system., Results: Eleven clinical VTs (mean cycle length 436 +/- 93 ms) were induced in all patients. An endocardial circuit, identified by activation, entrainment and/or pace mapping, was found in eight patients with stable VT. These patients were mapped and ablated during VT. Three patients had predominantly unstable VT and linear ablation lesions were performed during sinus rhythm. Acute success, defined as termination of VT and/or non-inducibility during programmed electrical stimulation, was found in 9 patients (82%). During followup, a significant reduction in tachyarrythmia burden was observed in all patients who had successful initial ablation, except for one who had recurrence of VT 2 days after the procedure and died 2 weeks later., Conclusions: Ablation of ischemic VT using electroanatomic scar mapping is feasible, has an acceptable success rate and should be offered for ischemic patients with recurrent uncontrolled VT.

Background: Traditionally, stent thrombosis (STH) has been regarded as a complication of percutaneous coronary interventions during the first 30 post-procedural days. However, delayed endothelialization associated with the implantation of drug-eluting stents (DES) may extend the risk of thrombosis beyond 30 days. Data are limited regarding the risks and the impact of this phenomenon outside clinical trials., Objectives: To evaluate the incidence, predictors and clinical outcomes of STH and premature discontinuation of thienopyridines after implantation of DES in real-world practice., Methods: We prospectively collected data from consecutive unselected patients who underwent at least 1 DES implantation at our center from February 2006 until January 2007. The patients were followed by a phone interview or by collecting data from admission files over the course of 2 years after the implantation. Confirmed and suspected STH was defined as accepted in the medical literature., Results: Three hundred fourteen patients were successfully treated with DES (436 lesions). At 20 ± 6.7 months' follow up (median 22 months), 14 patients (4.4%) had STH (incidence density 2.7 cases/100 patients-years). Five patients had early thrombosis (0-30 days), 5 patients had late STH (31-360 days from the procedure) and 4 patients had very late STH (> 360 days). Five of the 14 patients with STH died (case fatality rate, 36%). In multivariant logistic regression analysis, history of a non-cardiac thrombotic event was a risk factor for STH (p = 0.006, odds ratio [OR] 7.7, confidence interval [CI] 1.8-32.9). Clopidogrel therapy lasting less than 3 months was an independent predictor of late and very late STH (p = 0.001, OR 10.8, CI 2.7-42.9). Independent predictors of early discontinuation of thienopyridines (≤ 3 months) were Arab ethnic origin (p = 0.005, OR 19.2, CI 2.4-142), absence of cardiology follow up (p = 0.05, OR 4.7, CI 1-23.1) and absence of explanation about the clopidogrel importance at the time of hospital discharge (p = 0.001, OR 10.8, CI 2.7-42.9)., Conclusions: The incidence of STH at 22- month follow up in real-world patients was substantially higher than the rate reported in previous clinical trials. Subsidizing the cost of thienopyridines, providing a clear explanation to the patient and encouraging cardiology follow up may prevent premature discontinuation of thienopyridines after implantation of DES and reduce the incidence of STH after DES implantation.

Background: Current guidelines suggest the use of atrial synchronous mode (VDD) pacemakers in patients with atrioventricular (AV) block and normal sinus node function. However VDD mode is being used much less than expected. The objectives of our study were to evaluate the efficacy of VDD pacing in long-term follow-up and to find risk factors for VDD loss., Methods: We retrospectively evaluated all patients with VDD pacemakers who were implanted in our center between 1995 and 2007., Results: During the study period, 123 consecutive patients with AV block (51% men, age 62 +/- 17.8 years) received a VDD pacemaker. Mean follow up duration was 4.5 +/- 3.2 years. At the last follow up visit, 21 patients (21.6%) lost their original VDD mode and were programmed to ventricular-based pacing (VVIR) (undersensing, 11; chronic AF, 7; SND, 3). In 28 patients, VDD mode was restored or maintained by increasing atrial sensitivity. No episodes of atrial oversensing were observed. In multivariate analysis history of paroxysmal AF (p = 0.007, odds ratio 36.6, 95% confidence interval 2.7-493.7) and p wave lower than 1 mv during the follow up (p = 0.021, odds ratio 7, 95% confidence interval 1.3-36.7), were found risk factors to VDD loss., Conclusions: VDD pacing has good long-term performance. Absence of paroxysmal AF history predicts maintenance of VDD pacing mode. Taking into account that no atrial oversensing was observed, our recommendation is to increase atrial sensitivity when P wave amplitude declines to less than 1 mv., (Copyright 2010 Wiley Periodicals, Inc.)

Divergent views remain regarding the safety of treating anemia with red blood cell (RBC) transfusion in patients with acute coronary syndrome (ACS). We used a prospective database to study effect of RBC transfusion in patients with acute myocardial infarction (MI; n = 2,358). Cox regression models were used to determine the association between RBC transfusion and 6-month outcomes, incorporating transfusion as a time-dependent variable. The models adjusted for baseline variables, propensity for transfusion, and nadir hemoglobin previous to the transfusion. One hundred ninety-two patients (8.1%) received RBC transfusion. Six-month mortality rates were higher in patients receiving transfusion (28.1% vs 11.7%, p <0.0001). The adjusted hazard ratio (HR) for mortality was 1.9 in transfused patients (95% confidence interval [CI] 1.3 to 2.9). Interaction between RBC transfusion and nadir hemoglobin with respect to mortality (p = 0.004) was significant. Stratified analyses showed a protective effect of transfusion in patients with nadir hemoglobin < or=8 g/dL (adjusted HR 0.13, 95% CI 0.03 to 0.65, p = 0.013). By contrast, transfusion was associated with increased mortality in patients with nadir hemoglobin >8 g/dL (adjusted HR 2.2, 95% CI 1.5 to 3.3; p <0.0001). Similar results were obtained for the composite end point of death/MI/heart failure (p for interaction = 0.04). In conclusion, RBC transfusion in patients with acute MI and hemoglobin < or =8 g/dL may be appropriate. The increased mortality observed in transfused patients with nadir hemoglobin above 8 g/dL underscores the clinical difficulty of balancing risks and benefits of RBC transfusion in the setting of ACS.

Increase of cardiac troponins occurs in a variety of clinical situations in the absence of an acute coronary syndrome (ACS). Few data exist regarding the incidence, clinical characteristics, and predictive value of various cardiac diagnostic tests and outcome of patients with a non-ACS-related troponin increase. We studied 883 consecutive hospitalized patients with increased cardiac troponin I levels. The discharge diagnosis was reclassified and troponin increase attributed to ACS or another process. Clinical data and results of cardiac diagnostic tests were collected. Patients were followed for a median of 30 months. Three hundred eleven patients were classified as having a non-ACS-related troponin increase (35.2%). An alternative explanation for troponin increase was found in 99% of these patients. Troponin level had poor accuracy in discriminating patients with and without ACS (area under the receiver operating characteristics curve 0.63). Coronary angiography was frequently unhelpful in excluding a non-ACS-related troponin increase because 77% of patients in the non-ACS group had significant flow-limiting coronary artery disease. Patients with non-ACS-related troponin increase had significantly higher in-hospital (hazard ratio 2.8, 95% confidence interval 2.0 to 3.8) and long-term (hazard ratio 2.0, 95% confidence interval 1.6 to 2.5) mortalities compared with patients with ACS. In conclusion, cardiac troponin level is frequently increased in hospitalized patients in the absence of an ACS and portends poor short- and long-term outcomes. Most of these patients have an alternative explanation for cardiac troponin increase. Cardiac diagnostic procedures are frequently unhelpful in excluding a non-ACS-related troponin increase.

Aims: To assess the effectiveness and to identify predictors for successful electrical cardioversion (ECV) and maintenance of sinus rhythm, in long term follow up of patients with persistent (PAF) and chronic atrial fibrillation (CAF)., Methods and Results: Retrospective analysis of medical records of 68 patients with PAF or CAF, who underwent 91 cardioversions. ECV was successful in 86 attempts (94.5%). In obese (body mass index>30) and hypertensive patients (blood pressure >140/90 mm Hg), ECV was less successful in restoring sinus rhythm (p<0.05, p<0.021, respectively). Sinus rhythm was maintained more than half a year in 42 cardioversions (61%). Treatment with beta blockers prior to cardioversion and age younger than 75 were independent factors predicting long term success (p<0.013, p<0.034, respectively). Mild or moderate enlargement of left atrium (<6 cm) did not predict relapse of the arrhythmia. Second ECV was as or more effective than the first in 82.3% of patients that underwent more than one cardioversion., Conclusions: Conversion of atrial fibrillation by DC shock was found to be safe and effective procedure. Patients should be treated with beta blockers prior to cardioversion, if possible. Mild or moderate enlargement of left atrium is not contraindication to cardioversion. Recurrent cardioversions may be recommended.

Sarcoidosis is a systemic granulomatous disease of unknown etiology that involves many organs and has different clinical manifestation. We reviewed the clinical manifestations of sarcoid liver disease. Liver involvement in sarcoidosis can be serious and life-threatening, independent of its lung and other organ involvement.

Objectives: To define the incidence, contemporary utilization patterns, efficacy, and complications of thromboembolic prophylactic treatment in patients with chronic (CAF) and paroxysmal atrial fibrillation (PAF)., Background: Although recent randomized trials with antithrombotic therapy in nonrheumatic atrial fibrillation (AF) patients emphasized the benefits of warfarin in preventing stroke, warfarin treatment is still far from optimal., Methods: A retrospective analysis of the medical records of 506 patients with nonrheumatic PAF or CAF from 23 clinics in the north of Israel, including an interview with the patients' family physician., Results: (1) The most effective treatment for preventing thromboembolic events (a reduction of 75.9%) was warfarin at an international normalized ratio (INR) intensity of 2-3. (2) After diagnosis, 26.9% of the patients were treated with warfarin. (3) During the follow-up period (not following a thromboembolic event), an additional 26.9% of the patients began treatment with warfarin. (4) Elderly patients (p<0.001), patients with limited activity of daily living (ADL) (p<0.012) or instrumental activity of daily living (IADL) (p<0.001), and patients with PAF (p<0.0001) were less likely to be treated with warfarin. (5) Three new risk factors found for thromboembolic event were limited ADL (p<0.001), limited IADL (p<0.002), and extended duration of AF (p<0.006)., Conclusions: Less than optimal utilization patterns of thromboembolic prophylactic treatment with anticoagulants were found, especially regarding elderly patients, patients with limited ADL and IADL, and patients with PAF, despite the fact that their thromboembolic risk is as high or higher than that of other patients with AF.

Because platelets play a major role in most thrombotic events, it is not surprising that all cases of myocardial infarctions in patients with idiopathic thrombocytopenic purpura (ITP) have been reported to occur only when platelets counts begin to rise. We report on a 69-year-old man with ITP who had acute myocardial infarction while he was severely thrombocytopenic (2000/microL). We hypothesize that the pathogenesis of myocardial infarction in thrombocytopenic patients with ITP may result from endothelial damage induced by autoantibodies directed against antigens present on both platelets and coronary endothelial cells.