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The aim of this study was to characterize the abnormalities in glucose homeostasis in intensive care unit patients following an acute coronary event. The study population included all non-diabetic patients ages 20-80 years that were admitted to a coronary intensive unit. Glucose, insulin and C-peptide levels during an oral glucose tolerance test (OGTT) were measured during the acute admission. From January to September 2003, 277 patients were admitted to the coronary unit. Of these, 127 patients underwent an OGTT. Of these, only 29 patients (23%) exhibited normal glucose metabolism. The remainder had type 2 diabetes (32%), impaired glucose tolerance (37%) or isolated impaired fasting glucose (8%, 100-125 mg/dl). Based on homeostasis model assessment (HOMA) calculations, diabetic patients had impaired beta-cell function and patients with elevated fasting glucose levels were insulin resistant. Beta-cell dysfunction during the acute stress seems to contribute to the glucose abnormalities. Most patients who experience an acute coronary event demonstrate abnormal glucose metabolism. Post glucose-load abnormalities are more common than abnormal fasting glucose level in this situation. It is postulated that the acute stress of a coronary event may contribute to the dysglycemia.

Background and objectives The main limitation of primary PCI in acute MI is lack of tissue reperfusion due to distal embolization. We sought to examine the safety and feasibility of a manual thrombus aspiration device in patients undergoing primary PCI. Methods Seventy-eight consecutive patients with ST-elevation MI eligible for primary PCI were included. The device was used immediately after guidewire crossing only if a total occlusion (thrombolysis in myocardial infarction [TIMI] flow 0) existed or if a large filling defect was observed. End points were TIMI flow immediately after thrombus aspiration and at the end of procedure and ST resolution of more than 70%. Results Mean age was 59±12 years, and 79% of patients were males. Risk factor profile included smoking in 62%, diabetes in 21%, hypertension in 46%, and hyperlipidemia in 45%. The infarct-related artery was LAD in 42%, RCA in 36%, and LCX in 22%. Initial TIMI flow was 0 in 71%, I in 10%, and II/III in 19%. Immediately after aspiration, TIMI flow was II/III in 89% of patients and I in 9%. Direct stenting was performed in 73%. Final TIMI flow was III in 90%, II in 9%, and 0 in 1%. ST-segment resolution of more than 70% was observed in 76% of patients. No major device-related complications occurred. Conclusions Based on this preliminary data, manual thrombus aspiration using the Export device during primary PCI appears to be feasible and safe. The advantages over routine primary PCI should be further evaluated in randomized trials.

Left cardiac sympathetic denervation (LCSD) was reported to be effective in patients with intractable ryanodine receptor mutation-associated catecholaminergic polymorphic ventricular tachycardia (CPVT).To report our experience with LCSD in calsequestrin (CASQ2) mutation-associated CPVT.LCSD was performed in three patients with CASQ2 mutation-associated CPVT with symptoms and exercise-induced ventricular arrhythmia despite high dose beta-blockerNone of them experienced symptoms or exercise-induced ventricular arrhythmia after LCSD. However, all had recurrence of symptoms and/or exercise-induced ventricular arrhythmia after 6 months (6-18 months).LCSD conferred short-term suppression but less than optimal long-term suppression of exercise-induced ventricular arrhythmia among CASQ2-associated CPVT patients.

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.

Aims: To compare the clinical response of patients with right ventricular apical pacing (RVAP) upgraded to cardiac resynchronization therapy (CRT) to that of previously nonpaced heart failure (HF) patients who had de novo CRT implantation. Background: The role of CRT in patients with wide QRS and HF due to RVAP is less well established than in other CRT candidates. Methods: Ninety-eight consecutive patients with CRT were studied (mean age 70, mean ejection fraction 0.23). Group A: patients having RVAP prior to CRT implantation (n = 25), group B: patients without prior RVAP (n = 73). Clinical and echocardiographic parameters were recorded prior to, and 3 months after, CRT implantation. Results: Group A patients had a wider QRS at baseline compared to group B (203 ± 32 ms vs 163 ± 30 ms respectively, P < 0.001), and a shorter 6-minute walking distance (222 ± 118 m vs 362 ± 119 m, respectively, P < 0.005). Otherwise, clinical and echocardiographic parameters were not different. At follow up, group A patients had an average 0.7 ± 0.5 decrease in their NYHA functional class, compared to 0.3 ± 0.7 in group B patients (P < 0.05). Six-minute walking distance increased by 93 ± 113 m in group A, versus 36 ± 120 m in group B (P = 0.22). There was no difference in echocardiographic response to CRT between the groups. Conclusions: HF patients with prior RVAP demonstrate clinical improvement after upgrading to CRT that is comparable, and in some aspects, even better than that observed in HF patients with native conduction delay who undergo de novo CRT implantation.

Autoimmunity encompasses a wide spectrum of diseases from organ-specific diseases like Hashimoto thyroiditis, to systemic diseases such as systemic lupus erythematosus. These diseases are characterized by inflammation and the production of a wide range of autoantibodies directed against multiple autoantigens. Although their etiology is still poorly understood, genetic, immunological, hormonal, and environmental factors are major predisposing and triggering factors. These multiple factors, like pieces in a mosaic, may interplay in different forms, leading to the expression of various autoimmune manifestations and diseases. This phenomenon, which has been referred by us as the "mosaic of autoimmunity", illuminates the diversity of autoimmune manifestations among susceptible individuals. From this theoretical framework we conducted a wide search of the literature, on the prevalence of thyroid autoimmunity, the commonest of the autoimmune conditions, among other autoimmune diseases, and discuss the possible clinical significance of this association.

The anticardiolipin (aCL) antibody test was first established in 1983, using cardiolipin (negatively charged phospholipid) as an antigen in a solid-phase immunoassAy. It was first applied to the study of systemic lupus erythematosus patients, and was found associated with thromboses and recurrent pregnancy losses. The wide use of this test was determinant in the definition of the "aCL or antiphospholipid syndrome" (APS).Later, it was demonstrated that aCL antibodies do not recognize anionic phospholipids but are directed against plasma proteins bound to anionic phospholipids, mainly beta-2-glycoprotein I, which is now considered as the autoantigen in APS. Anti-beta-2-glycoprotein I (anti-beta2GPI) is not yet accepted as a serological criterion for APS, but most investigators would consider a patient with anti-beta2GPI antibodies and clinical features of APS to have the syndrome. aCL and anti-beta2GPI are a heterogeneous group of antibodies with different clinical significances and can be present in different autoimmune diseases as well as in infectious diseases.

Background Antiphospholipid antibodies are a family of autoantibodies that exhibit a broad range of target specificities and affinities, all recognizing various combinations of phospholipids, phospholipid binding proteins or both. Objective To evaluate the frequency of anticardiolipin (aCL) or anti-beta-2 glycoprotein I (anti-beta2GPI) antibodies in a cohort of patients with primary (PAPS) and secondary (SAPS) antiphospholipid syndrome and other rheumatic and infectious conditions. Methods Sera were drawn from 226 patients with PAPS (n= 66), SAPS (n= 60), rheumatoid arthritis (RA) (n= 30), scleroderma (SSc) (n= 30) or syphilis (n= 30). IgG, IgM, IgA aCL and anti-beta2GPI antibodies were determined for all patients. We employed Varelisa diagnostic kits (Pharmacia Diagnostics GmbH & Co.KG, Germany). Results In APS patients: aCL and anti-betaGP1 antibodies were detected in 81.8% and 70% in PAPS and SAPS patients, respectively. In PAPS, aCL were detected in 71.2%, and anti-beta2GP1 in 50% of patients. In SAPS, aCL were detected in 63.3%, and anti-beta2GP1 in 53.3% of patients. In syphilis, aCL and anti-beta2GP1 antibodies were detected in 46.7% of patients in low levels: aCL in 36.7% and anti-beta2GP1 in 20% of patients. aCL antibodies were detected in 10%, 13.3%, and 0% of RA patients, SSc patients, and healthy persons, respectively. Anti-beta2GP1 antibodies were not detected in RA patients, SSc patients, and healthy persons. Conclusions aCL and anti-beta2GP1 antibodies are more frequently found in sera of APS patients, and can be found in low levels in syphilis. Anti-beta2GP1 assay found to be more specific than aCL in antiphospholipid antibodies determination.

Randomized clinical trials have shown conflicting data on the benefit of implantable cardioverter defibrillator (ICD) for primary prevention of sudden cardiac death in patients with more advanced heart failure (HF) symptoms. Using the Israeli ICD Registry data, we sought to examine the effect of HF functional class on the outcome of patients who receive device therapy in a real-world setting.The association between HF functional class (categorized as baseline New York Heart Association [NYHA] functional class I and II in [61%] vs class III and IV in [39%]) and clinical outcomes was assessed among 913 patients who received an ICD (n = 514) or a cardiac resynchronization therapy with a defibrillator (CRT-D; n = 399) device and were prospectively followed in the Israeli ICD Registry between July 2011 and June 2013.The risk associated with advanced HF functional class was significantly different in ICD and CRT-D recipients. In the former group, patients with NYHA classes III and IV experienced3-fold increased risk of HF or death (hazard ratio [HR] = 3.28; P0.001), whereas among CRT-D recipients the risk was similar between patients with NYHA III/IV and those with less advanced HF symptoms (HR = 0.97 [95% confidence interval (CI) 0.54-1.78]; P = 0.42; P value for NYHA functional class by device type interaction = 0.002). The risk for ventricular arrhythmia (VA) was significantly lower among patients with more advanced NYHA functional class, regardless of device type (overall HR = 0.52; 95% CI 0.33-0.91; P = 0.04).Our findings suggest that patients with less advanced HF symptoms experience a greater risk for VA and the development of HF is attenuated in CRT-D recipients with more advanced NYHA functional class.

QTc interval prolongation after dipyridamole administration was reported only in patients who had positive pharmacological stress test results. We report a case of QTc prolongation after dipyridamole administration with no evidence of myocardial ischemia.

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.

In this study, the clinical and implantable cardioverter-defibrillator (ICD)–related follow-up of patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) with homogenous missense mutations in CASQ2 was summarized. Patients were followed in a pediatric cardiology clinic and an ICD clinic. All patients were treated with high-dose β blockers. ICDs were recommended for patients who remained symptomatic despite medical treatment. Twenty-seven patients were followed for 1 to 15 years (median 9). Twenty patients (74%) were symptomatic at diagnosis; 13 (65%) remained symptomatic after treatment with high-dose β blockers and thus were advised to receive ICDs. Eight of these patients refused ICDs, and eventually 6 (75%) died suddenly. Four of the 5 patients who received ICDs had ventricular tachycardia storms treated but not terminated by recurrent ICD shocks. These ventricular tachycardia storms (2 episodes in 2 patients and 1 episode in 2 patient) terminated spontaneously after finishing the programmed ICD shocks, without degeneration to ventricular fibrillation. None of the patients who received ICDs died. In conclusion, patients with CASQ2-associated CPVT should be recommended to receive ICDs to prevent sudden death when medical therapy is not effective. These patients may have recurrent ventricular tachycardia storms treated but not terminated by recurrent ICD shocks, without degeneration to ventricular fibrillation.

Background Endothelial dysfunction is considered an important prognostic factor in atherosclerosis. The aim of this study was to detect the long-term association of peripheral vascular endothelial function and clinical outcome in healthy subjects without apparent coronary artery disease (CAD). Methods We prospectively assessed brachial flow-mediated dilation (FMD) in 435 consecutive healthy subjects: 281 (65%) men, mean age 54±12 years and body mass index 28±4 kg/m 2 . After overnight fasting and discontinuation of all medications for ≥12 h, FMD and endothelium-independent nitroglycerin-mediated vasodilation were assessed using high resolution linear array ultrasound. Results Subjects were divided into 2 groups: below ( n =221) and above ( n =214) the median FMD of 10.7%, and were comparable regarding CAD risk factors, lipoproteins, fasting glucose, C-reactive protein, and concomitant medications, with a mean clinical follow-up of 32±2 months. Composite cardiovascular endpoints (all-cause mortality, non-fatal myocardial infarction, heart failure or angina pectoris hospitalization, stroke, coronary artery bypass grafting and percutaneous coronary interventions) were significantly more common in subjects with below median FMD of 10.7%, than above (11.8% vs 4.7%, p =0.007, respectively). Univariate analysis demonstrated that median FMD significantly predicted cardiovascular events [odds ratio (OR) of 2.78 and 95% CI 1.35 to 5.71 ( p =0.003)]. After multivariate analysis including conventional CAD risk factors, median FMD was the best independent predictor of long-term cardiovascular adverse events [OR of 2.70 and 95% CI 1.16 to 6.32 ( p =0.011)]. Conclusions Brachial artery median FMD independently predicts long-term adverse cardiovascular events in healthy subjects in addition to traditional risk factor assessment.

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.To assess the feasibility, safety and efficacy of our initial experience in ablation of scar-related VT.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.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.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 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.

Endothelial dysfunction is considered an important marker in atherosclerosis, having a prognostic value. Antiphospholipid antibodies are considered prothrombotic and have recently been reported to be associated also with atherosclerosis. This study was conducted to investigate a possible association of endothelial dysfunction with various antiphospholipid autoantibodies in healthy subjects and patients with cardiovascular disease. In a single-center, prospective study, 2 groups were included. The study group included patients with cardiovascular diseases (coronary disease and/or cerebrovascular disease) and healthy subjects without apparent heart disease who were referred to the endothelial function laboratory for the assessment of endothelial function. Flow-mediated dilatation, which indicates endothelial function, and nitroglycerin-mediated vasodilatation, which indicates smooth-muscle function, were measured. The 2 groups were evaluated for autoantibodies, including anticardiolipin (aCL; immunoglobulin G [IgG], immunoglobulin M [IgM], and immunoglobulin A [IgA]), antinuclear antibody, anti-beta2-glycoprotein I (IgG, IgM, and IgA), and oxidized low-density lipoprotein. One hundred seven subjects were included in the study: 45 patients (42%) and 62 healthy controls (58%). Flow-mediated dilatation was significantly lower in patients compared with healthy controls (8.0 +/- 9.5% vs 8.0 +/- 13.5%, p = 0.012). In addition, nitroglycerin-mediated vasodilatation was nonsignificantly lower in patients than in healthy controls (8.0 +/- 13.4% vs 11.0 +/- 16.7%, p = 0.084). The mean levels of anti-beta2-glycoprotein I (IgG, IgM, and IgA), aCL (IgM and IgA), antinuclear antibody, and oxidized low-density lipoprotein were not different between groups. However, the mean level of IgG aCL was significantly higher in patients than in healthy controls. In conclusion, in accordance with previous reports of an association between aCL and atherosclerosis, patients with cardiovascular disease had endothelial dysfunction and elevated levels of aCL.

Intravenous immunoglobulin (IVIG) preparations are increasingly being used in the treatment of autoimmune disorders. This treatment is regarded as generally safe, and most of the adverse effects associated with IVIG administration are mild and transient. This paper reports a 72-year-old patient with known ischemic heart disease admitted for a Guillain-Barre syndrome variant, who developed acute ST elevation myocardial infarction (MI) during the first hours of IVIG infusion. The literature on acute MI during IVIG treatment is reviewed. Evaluation of each patient for cardiovascular risk prior to IVIG treatment is recommended as is the assessment of risk versus benefit. If IVIG is prescribed, we propose close monitoring and slow infusion rate.

Endothelial dysfunction is recognized as a major factor in the development of atherosclerosis and it has a prognostic value.To detect the long-term association of peripheral vascular endothelial function and clinical outcome in healthy subjects and patients with cardiovascular disease.We prospectively assessed brachial artery flow-mediated dilatation in 110 consecutive subjects (46 CVD patients and 64 healthy controls), mean age 57 +/- 11 years; 68 were men. After an overnight fast and discontinuation of all medications foror = 12 hours, percent improvement in FMD and nitroglycerin-mediated vasodilatation were assessed using high resolution ultrasound.%FMD but not %NTG was significantly lower in CVD patients (9.5 +/- 8.0% vs. 13.5 +/- 8.0%, P = 0.012) compared to healthy controls (13.4 +/- 8.0% vs. 16.7 +/- 11.0%, P = 0.084; respectively). In addition, an inverse correlation between %FMD and the number of traditional CVD risk factors was found among all study participants (r = -0.23, P = 0.015) and healthy controls (r = -0.23, P = 0.036). In a mean follow-up of 15 +/- 2 months, the composite CVD endpoints (all-cause mortality, myocardial infarction, hospitalization for heart failure or angina pectoris, stroke, coronary artery bypass grafting and percutaneous coronary interventions) were significantly more common in subjects with FMD6% compared to subjects with FMD6% (33.3% vs. 12.1%, P0.03, respectively).Thus, brachial artery %FMD provides important prognostic information in addition to that derived from traditional risk factor assessment.

Benign prostatic hypertrophy is the most common benign tumor in males, resulting in prostatectomy in 20-30% of men who live to the age of 80. There are no data on the association of prostatectomy with autoimmune phenomena in the English-language medical literature.To report our experience with three patients who developed autoimmune disease following prostatectomy.Three patients presented awith autoimmune phenomenon soon after a prostectomy for BPH or prostatic carcinoma: one had clinically diagnosed temporal arteritis, one had leukocytoclastic vasculitis, and the third patient developed sensory Guillian-Barré syndrome following prostatectomy.In view of the temporal association between the removal of the prostate gland andthe autoimmune process, combined with previously known immunohistologic features of BPH, a cause-effect relationship probably exists.

In autoimmune diseases including systemic lupus erythematosus (SLE), the immune system attacks various autoantigens and causes damage in target organs. Recently, it was found that dead cells serve as a repertoire for autoantigens which can stimulate an autoimmune response in sensitive persons. The mechanisms which lead to induction and progress of apoptosis include extra-cellular stimuli, intra-cellular signals, and cleavage of proteins. During apoptosis, several events occur including migration of intra-cellular components to the cell membrane, removal of apoptotic cells by specific proteins and complement systems, and phagocytosis of apoptotic cells by macrophages. In recent years, evidence has accumulated that the autoimmune response can be initiated as a result of defects in apoptosis and/or removal of apoptotic material. In this article, the association of apoptosis to the pathogenesis of systemic lupus erythematosus is discussed.

Hiccup is a sudden contraction of the inspiratory muscles, followed by an abrupt closure of the glottis, thus producing a characteristic sound. Hiccups serve no known physiologic function. Mostly, it is a benign symptom which terminates without treatment. Persistent and intractable hiccups may indicate an organic disorder, thereby requiring evaluation based on history, physical examination, and selected laboratory tests. The treatment is based on the organic disorder, if it is found. The combination therapy with cisapride, omeprazole and baclofen is the most effective empiric treatment. We describe a number of case reports of patients with hiccups due to digitalis intoxication, ischemia of the inferior wall of the heart, peptic disease and gastroesophageal reflux disease.

Minocycline in another drug that can induce drug-induced lupus. Minocycline is frequently used for acne as a prolonged treatment, so it is important to be aware of the risks in this treatment. The risk ratio for the development of lupus due to minocycline is not known, but it seems to be low. We described a 26 year old female who was treated with minocycline due to acne. The treatment was complicated by rash and serological signs of lupus (antinuclear antibodies and anti-DNA antibodies). The aim of this article is to raise the level of awareness of this complication due to minocycline.

Statins, HMG-CoA reductase inhibitors, are widely used for the treatment of hypercholesterolemia and the prevention of cardiovascular diseases. Recent experimental and clinical studies evaluated the effect of statins on immune and inflammatory cells, and the efficacy of statins in treatment of immune diseases. This review discusses the roles of statins in the treatment of immune and inflammatory diseases.

We report a case of a 55-year-old woman with idiopathic ventricular fibrillation (VF) who suffered from recurrent implantable cardioverter-defibrillator shocks triggered by short coupled ventricular premature beat (VPB). This VPB was mapped and ablated from the myocardium of right ventricle close to the lateral tricuspid annulus. Learning objective: Triggering ventricular premature beat (VPB) in idiopathic ventricular fibrillation was reported to originate from the myocardium of right ventricular outflow tract or from Purkinje system. In this case, the origin of triggering VPB is the myocardium of right ventricle close to the lateral tricuspid annulus.>