Non-ischemic sudden cardiac arrest: Role of 12 lead Holter, family screening and genetic testing.

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.

Modelling the long QT syndrome with induced pluripotent stem cells.

The ability to generate patient-specific human induced pluripotent stem cells (iPSCs) offers a new paradigm for modelling human disease and for individualizing drug testing. Congenital long QT syndrome (LQTS) is a familial arrhythmogenic syndrome characterized by abnormal ion channel function and sudden cardiac death. Here we report the development of a patient/disease-specific human iPSC line from a patient with type-2 LQTS (which is due to the A614V missense mutation in the KCNH2 gene). The generated iPSCs were coaxed to differentiate into the cardiac lineage. Detailed whole-cell patch-clamp and extracellular multielectrode recordings revealed significant prolongation of the action-potential duration in LQTS human iPSC-derived cardiomyocytes (the characteristic LQTS phenotype) when compared to healthy control cells. Voltage-clamp studies confirmed that this action-potential-duration prolongation stems from a significant reduction of the cardiac potassium current I(Kr). Importantly, LQTS-derived cells also showed marked arrhythmogenicity, characterized by early-after depolarizations and triggered arrhythmias. We then used the LQTS human iPSC-derived cardiac-tissue model to evaluate the potency of existing and novel pharmacological agents that may either aggravate (potassium-channel blockers) or ameliorate (calcium-channel blockers, K(ATP)-channel openers and late sodium-channel blockers) the disease phenotype. Our study illustrates the ability of human iPSC technology to model the abnormal functional phenotype of an inherited cardiac disorder and to identify potential new therapeutic agents. As such, it represents a promising paradigm to study disease mechanisms, optimize patient care (personalized medicine), and aid in the development of new therapies.

Left Cardiac Sympathetic Denervation in Patients with CASQ2-Associated Catecholaminergic Polymorphic Ventricular Tachycardia.

BACKGROUND: Left cardiac sympathetic denervation (LCSD) was reported to be effective in patients with intractable ryanodine receptor mutation-associated catecholaminergic polymorphic ventricular tachycardia (CPVT). OBJECTIVES: To report our experience with LCSD in calsequestrin (CASQ2) mutation-associated CPVT. METHODS: LCSD was performed in three patients with CASQ2 mutation-associated CPVT with symptoms and exercise-induced ventricular arrhythmia despite high dose beta-blocker RESULTS: None 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). CONCLUSIONS: LCSD conferred short-term suppression but less than optimal long-term suppression of exercise-induced ventricular arrhythmia among CASQ2-associated CPVT patients.

The role of genetic testing in the prevention, diagnosis, and prognosis of sudden cardiac arrest in children.

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.

Elevated thrombin generation levels in the left atrial appendage in patients with atrial fibrillation.

Background: Atrial Fibrillation (AF) is the most common sustained tachi-arrhythmia. Thrombus formation in the left atrial appendage (LAA) increases the risk of stroke and systemic embolism in patients with AF. Objectives: The aim of this study was to compare thrombin generation in the LAA to the LA among patients with AF. Methods: A cross-sectional study of consecutive patients with AF undergoing pulmonary veins catheter ablation. Blood samples from the femoral vein (FV), right atrium (RA), left atrium (LA), and LAA were collected during the catheter ablation procedures. Thrombin generation was assessed by a Calibrated Automated Thrombogram. The LAA-calibrated automated thrombogram parameters were compared with the RA, LA, and FV. Results: A total of 47 consecutive patients were enrolled in the study. The endogenous thrombin potential and peak height were significantly higher in the LAA compared with the LA, the mean differences and 95% CI between the LA and LAA were -378.9 (-680.5, -77.2) (nM∗min) and -66.7 (-119.6, -13.8) (nM) in the endogenous thrombin potential and peak height respectively. Conclusion: In patients with AF undergoing catheter ablation, the LAA demonstrated increased thrombin generation compared with the LA. This finding might contribute to the understanding of why the LAA is more predisposed to thrombus formation than the LA. Clinical Trials Registration: NCT03795883.

Clinical and electrophysiologic outcomes of patients undergoing percutaneous endocardial ablation of scar-related ventricular tachycardia: a single-center experience.

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.

Arrhythmic burden among asymptomatic patients with ischemic cardiomyopathy and an implantable cardioverter-defibrillator.

BACKGROUND: The clinical benefit of primary prevention implantable cardioverter-defibrillator (ICD) therapy in asymptomatic patients (New York Heart Association [NYHA] functional class I) with ischemic cardiomyopathy and left ventricular dysfunction is continually disputed. OBJECTIVE: The purpose of this study was to evaluate the incidence of ventricular arrhythmias, mortality rates, and appropriate device therapies by NYHA class in a prospective national ICD registry. METHODS: The study comprised 1670 consecutive patients with ischemic cardiomyopathy who were implanted with a primary prevention ICD and enrolled in the prospective national Israeli ICD Registry from 2010. The risk for clinical and arrhythmic events was assessed by NYHA class. RESULTS: Asymptomatic patients (NYHA I) composed 19% of the study cohort. Comparison according to NYHA class showed that the highest mortality rate was in the NYHA III-IV group vs NYHA I and NYHA II (10.5% vs 5.4% and 5.8%, respectively; log rank P = .003). Conversely, cumulative incidence of appropriate ICD therapies, corrected for death as a competing risk, were higher among patients with NYHA I (11% vs 7%; P = .021). In a multivariate model, NYHA I vs ≥II remained independently associated with a significant 2-fold risk for appropriate ICD therapy (hazard ratio 2.03; 95% confidence interval 1.28-3.24). CONCLUSION: Our findings indicate that patients with ischemic cardiomyopathy without heart failure symptoms have a higher risk of appropriate ICD therapy compared with symptomatic patients after adjustment for the competing risk of death, suggesting possible incremental benefit of primary ICD implantation in this population.

Identification of the gene causing long QT syndrome in an Israeli family.

BACKGROUND: Long QT syndrome is an inherited cardiac disease, associated with malignant arrhythmias and sudden cardiac death. OBJECTIVES: To map and identify the gene responsible for LQTS in an Israeli family. METHODS: A large family was screened for LQTS after one of them was successfully resuscitated from ventricular fibrillation. The DNA was examined for suspicious loci by whole genome screening and the coding region of the LQT2 gene was sequenced. RESULTS: Nine family members, 6 males and 3 females, age (median and interquartile range) 26 years (13, 46), who were characterized by a unique T wave pattern were diagnosed as carrying the mutant gene. The LQTS-causing gene was mapped to chromosome 7 with the A614V mutation. All of the affected members in the family were correctly identified by electrocardiogram. Corrected QT duration was inversely associated with age in the affected family members and decreased with age. CONCLUSIONS: Careful inspection of the ECG can correctly identify LQTS in some families. Genetic analysis is needed to confirm the diagnosis and enable the correct therapy in this disease.

Relation of C-reactive protein and new-onset atrial fibrillation in patients with acute myocardial infarction.

Recent studies have implicated systemic inflammation in the genesis and maintenance of atrial fibrillation (AF). A robust inflammatory response is an integral component of the response to tissue injury during acute myocardial infarction (AMI). However, there is no information concerning the association between inflammation and AF in patients with AMI. We studied 1,209 patients admitted for AMI. C-reactive protein (CRP) was measured by a high-sensitivity assay within 12 to 24 hours after symptom onset. The relation between CRP and new-onset AF occurring during the hospital course and at 1 year was analyzed using multivariable logistic regression and Cox models, respectively. New-onset AF during hospitalization occurred in 6.5%, 10.4%, and 17.1% of patients in the first, second and third CRP tertiles, respectively (p trend <0.0001). In a multivariable logistic regression, adjusting for clinical variables and ejection fraction, compared with patients in the first CRP tertile, the odds ratios for AF were 1.5 (95% confidence interval 0.9 to 2.5, p = 0.15) and 2.0 (95% confidence interval 1.2 to 3.3, p = 0.008) in patients in the second and third CRP tertiles, respectively (p for trend = 0.007). In a Cox multivariate analysis, CRP remained an independent predictor of new-onset AF at 1 year. In conclusion, in a large cohort of patients with AMI, there was a graded positive association between increased CRP and new-onset AF. Inflammation may contribute to the development of AF in the setting of AMI.

Catheter ablation of cardiac arrhythmias guided by electroanatomic imaging (CARTO): a single-center experience.

BACKGROUND: Catheter ablation is assuming a larger role in the management of patients with cardiac arrhythmias. Conventional fluoroscopic catheter mapping has limited spatial resolution and involves prolonged fluoroscopy. The non-fluoroscopic electroanatomic mapping technique (CARTO) has been developed to overcome these drawbacks. OBJECTIVES: To report the early and late outcome in patients with different arrhythmias treated with radiofrequency ablation combined with the CARTO mapping and navigation system. METHODS: The study cohort comprised 125 consecutive patients with different cardiac arrhythmias referred to our center from January 1999 to July 2005 for mapping and/or ablation procedures using the CARTO system. Forty patients (32%) had previous failed conventional ablation or mapping procedures and were referred by other centers. The arrhythmia included atrial fibrillation (n = 13), atrial flutter (n = 38), atrial tachycardia (n = 25), ventricular tachycardia (n = 24), arrhythmogenic right ventricular dysplasia (n = 9), and supraventricular tachycardia (n = 16). RESULTS: During the study period, a total of 125 patients (mean age 49 +/- 19 years, 59% males) underwent electrophysiological study and electroanatomic mapping of the heart chambers. Supraventricular arrhythmias were identified in 92 patients (73%) and ventricular arrhythmias in 33 (27%). Acute and late success rates, defined as termination of the arrhythmia without anti-arrhythmic drugs, were 87% and 76% respectively. One patient (0.8%) developed a clinically significant complication. CONCLUSIONS: The CARTO system advances our understanding of arrhythmias, and increases the safety, efficacy and efficiency of radiofrequency ablation.

Acute Kidney Injury After Primary Angioplasty: Is Contrast-Induced Nephropathy the Culprit?

BACKGROUND: Acute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast-induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score-matched patients with ST-segment-elevation myocardial infarction who were not exposed to contrast material. METHODS AND RESULTS: We studied 2025 patients with ST-segment-elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score-matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin-treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra-aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26). CONCLUSIONS: The development of AKI in patients with ST-segment-elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST-segment-elevation myocardial infarction patients with and without contrast material exposure.

Fasting glucose is an important independent risk factor for 30-day mortality in patients with acute myocardial infarction: a prospective study.

BACKGROUND: Stress hyperglycemia in patients with acute myocardial infarction has been associated with increased mortality. Most studies looked at the relationship between admission glucose (AG) and outcome; limited information is available about the clinical significance of fasting glucose (FG). METHODS AND RESULTS: We prospectively studied the relationship between FG and 30-day mortality in 735 nondiabetic patients with acute myocardial infarction. FG (> or =8-hour fast within 24 hours of admission) and AG were measured in each patient. At 30 days, 9 deaths (2%) occurred in patients with normal FG, and 11 (10%), 14 (13%), and 31 (29%) deaths occurred in the first, second, and third tertiles of elevated FG, respectively. Compared with normal FG (<110 mg/dL), the adjusted OR for 30-day mortality progressively increased with higher tertiles of elevated FG (first tertile, 4.6; 95% CI, 1.7 to 12.7; P=0.003; second tertile, 6.4; 95% CI, 2.5 to 16.6; P<0.0001; third tertile, 11.5; 95% CI, 4.7 to 20.0; P<0.0001). Compared with patients categorized as having normal AG (<140 mg/d), the adjusted ORs for tertiles of elevated AG were as follows: first tertile, 1.4 (95% CI, 0.5 to 3.8; P=0.54); second tertile, 3.0 (95% CI, 1.3 to 7.0; P=0.01); and third tertile, 4.4 (95% CI, 2.0 to 9.7; P<0.0001). Compared with patients with normal FG and AG, the adjusted ORs for 30-day mortality were 0.71 (95% CI, 0.15 to 3.4; P=0.67) in patients with elevated AG and normal FG, 3.4 (95% CI, 1.1 to 10.4; P=0.03) for patients with normal AG glucose and elevated FG, and 9.6 (95% CI, 3.5 to 26.0; P<0.0001) for patients with both elevated FG and AG. Comparing nested models showed that including AG failed to improve the prediction of the model based on FG (chi2=5.4, 3 df, P=0.15). In contrast, the addition of FG classes to the model based on AG improved model prediction (chi2=22.4, 3 df, P<0.0001). CONCLUSIONS: There is a graded relation between elevated FG and AG and 30-day mortality in patients with acute myocardial infarction. FG is superior to AG in the assessment of short-term risk.

Magnetic resonance imaging for patients with permanent pacemakers: initial clinical experience.

BACKGROUND: Magnetic resonance imaging is a diagnostic tool of growing importance. Since its introduction, certain medical implants, e.g., pacemakers, were considered an absolute contraindication, mainly due to the presence of ferromagnetic components and the potential for electromagnetic interference. Patients with such implants were therefore prevented from entering MRI systems and not studied by this modality. These devices are now smaller and have improved electromechanical interference protection. Recently in vitro and in vivo data showed that these devices may be scanned safely by MRI. OBJECTIVES: To report our initial experience with three patients with pacemakers who underwent cerebral MRI studies. METHODS: The study included patients with clear clinical indications for MRI examination and who had implanted devices shown to be safe by in vitro and in vivo animal testing. In each patient the pacemaker was programmed to pacing-off. During the scan, continuous electrocardiographic telemetry, breathing rate, pulse oximetry and symptoms were monitored. Specific absorption rate was limited to 4.0 W/kg for all sequences. Device parameters were assessed before, immediately after MRI, and 1 week later. RESULTS: None of the patients was pacemaker dependent. During the MRI study, no device movement was felt by the patients and no episodes of inappropriate inhibition or rapid activation of pacing were observed. At device interrogation there were no significant differences in device parameters pre-, post-, and 1 week after MRI. Image quality was unremarkable in all imaging sequences used and was not influenced by the presence of the pacemaker. CONCLUSION: Given appropriate precautions, MRI can be safely performed in patients with a selected permanent pacemaker. This may have significant implications for current MRI contraindications.

Outflow tract ventricular arrhythmia originating from the aortic cusps: our approach for challenging ablation.

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.

Impact of computed tomography image and contact force technology on catheter ablation for atrial fibrillation.

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.

Heart failure in patients with diabetes undergoing primary percutaneous coronary intervention.

INTRODUCTION: Diabetes mellitus is associated with increased risk after acute coronary syndromes. Primary percutaneous coronary intervention is the most effective method of reperfusion for acute ST-elevation myocardial infarction and can limit the ischaemic damage to the left ventricle. However, there are few data on the impact of diabetes mellitus on the risk of heart failure following primary percutaneous coronary intervention. METHODS: We studied 958 ST-elevation myocardial infarction patients treated with primary percutaneous coronary intervention, of whom 263 (27.5%) had diabetes mellitus, with 67 (7.0%) treated with insulin. The primary end points of the study were re-admission for heart failure. Secondary end points were all-cause mortality and recurrent infarctions. The follow-up period was 5 years after hospital discharge. RESULTS: The cumulative incidence of re-admission for heart failure was 8.4%, 15.2% and 26.7% in patients without diabetes mellitus, non-insulin-treated and insulin-treated diabetes mellitus, respectively. Compared with patients without diabetes mellitus, the adjusted hazard ratio for heart failure was 1.95 (95% confidence intervals 1.30-2.93) and 3.09 (95% confidence intervals 1.71-5.60) in non-insulin-treated and insulin-treated diabetes mellitus, respectively. The corresponding hazard ratios for mortality were 1.03 (95% confidence intervals 0.68-1.55) and 2.04 (95% confidence intervals 1.22-3.42), respectively. There was a J-shaped association between fasting glucose levels in the acute phase and risk of mortality (P=0.0001) and a direct association with heart failure (P=0.03). CONCLUSION: Despite modern treatment of ST-elevation myocardial infarction and high levels of guideline-based medical care, diabetes mellitus had an independent adverse effect on the risk of re-admissions for heart failure, which was particularly high among insulin-treated patients.

Usefulness of electroanatomical mapping to differentiate between right ventricular outflow tract tachycardia and arrhythmogenic right ventricular dysplasia.

Differentiation between the different right ventricular rhythm disorders and specifically between arrhythmogenic right ventricular dysplasia (ARVD) and right ventricular outflow tract (RVOT) tachycardias has important clinical implications but remains a clinical challenge. We tested the hypothesis that the spatial association of local electrographic parameters may be used to discriminate between these 2 entities. Electroanatomic mapping of the right ventricle was performed in 3 groups: patients who had typical RVOT tachycardia, a control group of patients who had no ventricular arrhythmias, and patients who had a diagnosis of ARVD based on clinical, electrocardiographic, and structural findings. Electroanatomic mapping in the RVOT tachycardia group showed normal electrographic parameters throughout the right ventricle (unipolar electrographic amplitude 9.9 +/- 0.9 mV, duration 55 +/- 1 ms, amplitude/duration 0.193 +/- 0.022) that were no different from those in the control group. In contrast, dysplastic regions in the ARVD group were characterized by significantly lower amplitude (unipolar 3.6 +/- 0.4 mV), prolonged electrographic duration (unipolar 73 +/- 4 ms), and a decreased amplitude/duration ratio (unipolar 0.054 +/- 0.008) compared with the unaffected zones in the same hearts and with all regions in the RVOT and control groups. Thus, endocardial electrographic parameters do not differ between patients who have RVOT and control patients. RVOT tachycardia can be differentiated from ARVD by the absence of abnormal right ventricular electrographic findings. This ability may have important clinical implications and supports the concept of different underlying mechanisms for these 2 entities.

The impact of GP IIb/IIIa inhibitors during primary percutaneous coronary intervention in acute myocardial infarction patients.

The use of glycoprotein (GP) IIb/IIIa inhibitors during percutaneous coronary interventions (PCI) in the acute phase of myocardial infarction (AMI) is still a matter of debate. The aim of the present study was to compare the outcomes of patients with acute ST-segment elevation myocardial infarction who underwent primary PCI and were concomitantly treated with GP IIb/IIIa inhibitors with those who were not treated with these drugs. Between January 1996 and November 2003, a total of 418 consecutive patients underwent PCI in the setting of ST-segment elevation AMI. At the operator's discretion, 287 patients were concomitantly treated with GP IIb/IIIa inhibitors and 115 patients were not. Angiographic success and final TIMI 3 flow in the infarct-related artery was achieved more frequently in patients treated with GP IIb/IIIa inhibitors (90% vs. 77%; p=0.001). The in-hospital composite endpoint of death, reinfarction and bleeding complications was significantly better in patients treated with GP IIb/IIIa inhibitors (4% vs. 12%; p=0.005). Furthermore, the adjusted 12-month survival rate was significantly better in these patients (RR: 2.99, CI: 1.29-6.9; p=0.01). Therefore, adjunctive therapy with GP IIbIIIa inhibitors during primary PCI is associated with improved short-term outcomes and one-year survival without an increased risk of bleeding.

Staged versus one-step approach for multivessel percutaneous coronary interventions.

BACKGROUND: Percutaneous coronary interventions (PCIs) in patients with multivessel coronary artery disease (CAD) may be staged or performed in a single session. No data exist about the relative safety and efficacy of these 2 strategies. Our aim was to compare short-term and long-term outcomes of patients with multivessel CAD who underwent PCI in 1 versus 2 sessions. METHODS AND RESULTS: The study included 264 consecutive patients who underwent treatment in our center during 1997 and 1998. PCI was conducted in a single session in 129 patients and was staged in 135 patients. The mean interval between the sessions in the staged group was 45.6 +/- 22.3 days. The rates of major adverse cardiac events (MACEs) during in-hospital stay did not differ significantly between the staged (combined for both stages) and nonstaged groups (2.2% vs 4.6%; P =.28). A trend for lower event rates at 30-day (2.9% vs 6.9%; P =.13) and 1-year follow-up (26.1 vs 35.9; P =.08) favored the staged arm. Diameter stenosis > or =50% was found in 17% of patients in the staged group in the second session and was successfully retreated in most of them. No MACE occurred between the sessions. Multivariate analysis identified staging of the procedure as a single independent predictor of MACE at 1-year follow-up (P =.05). CONCLUSION: Our results suggest that a practical staging strategy within 4 to 8 weeks is safe and allows for identification and treatment of potential excessive proliferative response in the previously intervened lesions during the second procedure.