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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.

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

Background: Pulmonary vein isolation (PVI) is the cornerstone of atrial fibrillation (AF) ablation in both paroxysmal and persistent AF. However, this procedure is still challenging and time consuming. Objective: The aim of this study was to present our approach for PVI using a novel circular irrigated multielectrode mapping and ablation catheter (nMARQTM) and to present acute and mid-term results. Methods: The study included 31 consecutive patients with symptomatic AF (4 had persistent and 27 had paroxysmal AF) who underwent PVI using the nMARQTM catheter. Circular ablation was guided by CT image integrated into fast anatomical map and by intra cardiac echo. Isolation of pulmonary veins was identified using the nMARQTM catheter if it was possible to advance it into the veins, otherwise Lasso catheter was used. Patients were followed up to 20 months. Results: PVI was achieved in 119 (98%) out of 121 pulmonary veins identified, and final PVI was obtained in 30 (97%) out of 31 patients. Lasso catheter was needed for PVI confirmation in 16 (52%) patients. Touch up ablation using standard catheter guided by Lasso catheter was needed in 4 (13%) patients. Pericardial tamponade occurred in 1 patient who was treated with pericardiocentesis. No other major complications were detected. During follow-up (mean 15.9 ± 3.6 months, range 9 - 20 months), 4 (13%) patients had recurrence of atrial tachyarrhythmia. Conclusion: PVI using the novel nMARQTM catheter is safe with good acute and mid-term efficacy. Long term follow up trials are needed.

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.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.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.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 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.

To investigate the impact of using computed tomography (CT) and contact force (CF) technology on recurrence of atrial tachyarrhythmia after atrial fibrillation (AF) ablation.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.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.These preliminary results suggest that CT image integration and CF technology may reduce the recurrence of atrial tachyarrhythmia after catheter ablation for AF.

Background: Twenty to thirty percent of patients with left heart failure in randomized trials do not respond clinically to cardiac resynchronization therapy (CRT). The objectives of our work were to estimate the effec-tiveness of CRT in our routine practice, and to find predictors of favorable response to CRT. Methods: Retrospective analysis of consecutive patients who underwent CRT from 2003-2007. Results: Fifty six consecutive patients (73.2% men, age 66.3 ± 10.2 years) with left heart failure (LHF) (ischemic cardiomyopathy 60.7%) received CRT and were followed for a mean of 27 months. After the implantation: Mean NYHA improved by one class (p < 0.001), LHF admissions were reduced by 79% (p < 0.0001) and mean ejection fruction improved by 31% (19.5% vs 25.6%, p < 0.002). Significant improvement in severity of mitral regurgitation (MR) was an important predictor of high responsiveness (p = 0.004). Improvement of MR was associated with complete left bundle branch block (CLBBB) (p = 0.04) and lower total mortality (p = 0.005). Improvement in synchronization between the mid lateral and mid septal segments, as was calculated with longitudinal strain using echocardiography (105 ± 38 vs 20 ± 23 msec, p = 0.008) was predictor of super responsiveness and reduction in MR among patients with moderate to severe MR prior to implantation. Worsening the delay between the mid posterior and mid anterior septal segments (21 ± 27 vs 120 ± 0 msec, p = 0.006) was associated with absence of response and lack of improvement in MR. Conclusions: Patients who improve mid segments dyssynchrony in four chamber view, have more chance to improve MR and to become super responders.

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 8 g/dL (adjusted HR 2.2, 95% CI 1.5 to 3.3; p

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.

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.

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.To evaluate whether electrocardiographic characteristics of VPCs during ST distinguish patients with CPVT from healthy subjects.Electrocardiographic characteristics of VPCs during ST in 16 calsequestrin-2 (CASQ2) mutation carriers CPVT patients were compared with that in 36 healthy subjects.CPVT patients had more VPCs (31 ± 14 vs 3 ± 4, P0.0001), longer QRS duration (139 ± 18 ms vs 121 ± 21, P = 0.004), and coupling interval (CI; 476 ± 58 ms vs 355 ± 61 ms, P0.0001). The most sensitive characteristics for CPVT were10 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 duration120 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.Several electrocardiographic criteria can help distinguish VPCs originating from CPVT compared with healthy subjects.

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. Cardiol Res. 2012;3(2):67-72 doi: https://doi.org/10.4021/cr146w

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.

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.To evaluate the incidence, predictors and clinical outcomes of STH and premature discontinuation of thienopyridines after implantation of DES in real-world practice.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.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).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.

Aims To study the prevalence and long-term prognostic significance of changes in haemoglobin levels during hospital course in survivors of acute myocardial infarction (AMI). Methods and results A prospective study involving 1390 patients who were admitted with AMI. Median follow-up was 24 months. Multivariable Cox models were used to evaluate the relationship between nadir and discharge haemoglobin and mortality after hospital discharge. Anaemia was present in 248 patients on admission (17.8%) and in 502 patients at discharge (36.1%). Nadir haemoglobin during hospital course was 1.3 g/dL lower (IQR 0.6–2.2) when compared with baseline haemoglobin ( P < 0.0001). Low nadir haemoglobin and discharge haemoglobin were strongly associated with increased mortality. After adjusting for clinical variables and ejection fraction, the hazard ratios for a 1 g/dL decrease in nadir haemoglobin and discharge haemoglobin were 1.36 (95% CI 1.19–1.55; P < 0.0001) and 1.27 (95% CI 1.16−1.40; P < 0.0001), respectively. Conclusion The development of anaemia during hospitalization for AMI is frequent and is associated with an increased long-term mortality.

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).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 index30) and hypertensive patients (blood pressure140/90 mm Hg), ECV was less successful in restoring sinus rhythm (p0.05, p0.021, 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 (p0.013, p0.034, 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.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.

To define the incidence, contemporary utilization patterns, efficacy, and complications of thromboembolic prophylactic treatment in patients with chronic (CAF) and paroxysmal atrial fibrillation (PAF).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.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.(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 (p0.001), patients with limited activity of daily living (ADL) (p0.012) or instrumental activity of daily living (IADL) (p0.001), and patients with PAF (p0.0001) were less likely to be treated with warfarin. (5) Three new risk factors found for thromboembolic event were limited ADL (p0.001), limited IADL (p0.002), and extended duration of AF (p0.006).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.