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Aims Multiple re-entry circuits may operate simultaneously in the atria in the form of dual loop re-entry using a common isthmus, or multiple re-entrant loops without a common isthmus. When two or more re-entrant circuits coexist, ablation of an individual isthmus may lead to a seamless transition (without significant changes in surface electrocardiogram, coronary sinus activation or tachycardia cycle length) to a second rhythm, and the isthmus block can go unnoticed. Methods and results We hypothesize and subsequently illustrate in three patient cases, methods to rapidly identify a transition in the rhythm and isthmus block using local electrogram changes at the ablation site. Conclusion Local activation sequence changes, electrogram timing, and the behaviour of pre-existing double potentials can reveal isthmus block promptly when rhythm transitions occur during ablation of multiloop re-entry tachycardias.

His-refractory premature ventricular complexes perturbing a supraventricular tachycardia (SVT) establish the presence of an accessory pathway (AP). Earlier premature ventricular complexes (ErPVCs) may perturb SVTs but are considered nondiagnostic.The purpose of this study was to test the hypothesis that an ErPVC will always show a difference35 ms in its advancement of the next atrial activation during atrioventricular nodal reentrant tachycardia (AVNRT). During atrioventricular reentrant tachycardia (AVRT), a PVC delivered close to the circuit can result in greater advancement of atrial activation due to retrograde conduction via an AP. Thus, an AP response, defined as ErPVC (HSixty-five consecutive patients with SVT were retrospectively evaluated. ErPVCs were defined when the ventricular pacing stimulus was35 ms ahead of the His during tachycardia.Among the 65 cases, 43 were AVNRT and 22 AVRT. Fourteen AVRT cases had an AP response with a mean HAn AP response to PVCs (A

This study sought to determine if atrial fibrillation (AF) ablation can be performed safely without bladder catheterization.Patients undergoing AF ablation often receive bladder catheters. Catheterization is associated with potential complications. The ABCD-AF (Avoiding Bladder Catheters During Atrial Fibrillation) ablation study evaluates the advantages of performing AF ablation without routine catheterization.In this single-center, prospective, randomized controlled trial, 80 patients received bladder catheterization (group A), and 80 patients received only as-needed catheterization (group B). The primary endpoint was a composite of cystitis, urethral injury, hematuria, dysuria, or urinary retention.The mean patient age was 63 ± 13 years, and 33% of patients were female. The primary outcome was reached in 45 patients in group A and 11 patients in group B (p 0.001). Urinary tract infection occurred in 7 patients in group A and 2 patients in group B (p = 0.17). Urinary retention occurred in 12 patients in group A and 5 patients in group B (p = 0.07). Randomization to catheterization carried an odds ratio of 8.1 (95% confidence interval [CI]: 3.7 to 17.5; p 0.001), and male sex carried an odds ratio of 3.8 (95% CI: 1.7 to 8.6; p = 0.001) for the primary endpoint. On subgroup analysis, randomization to undergo catheterization had no association with the primary outcome in female patients but had an odds ratio of 14.6 (95% CI: 5.6 to 38.1; p 0.001) in male patients. In multivariable analysis, sex and catheter status remained independently associated with the primary outcome.Bladder catheterization can be safely avoided in patients undergoing AF ablation and is associated with a significant reduction in adverse outcomes, especially in men.

BACKGROUND Technical advances have improved the safety of cardiac implantable electronic device (CIED) insertion, but periprocedural complications persist. Despite ultrasound (US) guidance for vascular access being feasible and exhibiting shorter fluoroscopy times, it is not widely adopted for insertion of CIEDs. Thus, we studied the use of US for CIED insertion to (1) quantify the success rate of venous cannulation, (2) identify predictors of failed cannulation, and (3) quantify the rate of complications using US guidance. METHODS We studied 166 consecutive patients who underwent US-guided CIED implantation. Anatomic parameters of the axillary vein were measured. The primary outcome was success (group 1) or failure (group 2) to obtain vascular access utilizing US guidance. Secondary outcomes included pneumothorax and hematoma. RESULTS Successful US-guided cannulation occurred in 154 of 166 patients (93%). No patient had a pneumothorax. Hematoma occurred in 1 of 166 patients (0.01%). Group 2 exhibited higher male proportion at 11 of 12 (92%) compared with 94 of 154 (61%) in group 1 (P = .03), increased vein depth at 3.84 versus 2.85 cm (P = .003), more right-sided implants (P = .03), higher weight at 104.6 versus 85.3 kg (P = .017), higher body mass index at 35.6 versus 29.2 kg/m2 (P = .049), and higher body surface area at 2.24 versus 1.99 m2 (P = .013). Other parameters were statistically nonsignificant. In multivariate analysis, vein depth remained significantly associated with failure. CONCLUSION Using US guidance for CIED implantation is successful in the vast majority (93%) of patients. Rare cases of unsuccessful cannulation were associated with right-sided implants and increased venous depth.

Introduction Elevated left atrial pressure (LAP) during catheter ablation of atrial fibrillation (AF) is associated with an increased risk of AF recurrence, but it is unknown if this correlates with heart failure (HF). The objective of the study was to determine if elevated LAP after AF ablation correlates with HF events. Methods Prospective, single-center, cohort study measuring LAP and right atrial pressure (RAP) during AF ablation in 100 patients. The primary endpoint was clinical HF within 30 days of ablation. The secondary outcome was AF-free HF. Results One hundred patients (63% male, mean age 64.5) were enrolled and 20% had clinical HF within 30 days. Bivariate correlates included mitral valve (MV) disease, persistent AF, class III antiarrhythmics, LAP, and recurrent AF. Multivariate analysis revealed class III antiarrhythmics were protective (odds ratio [OR]: 0.24 [0.1-0.5], p = .04), while MV disease (OR: 8.7 [3.3-23], p = .03) and loop diuretics (OR: 4.8 [2.6-9.1], p = .01) were hazardous. AF-free HF occurred in 9% of patients and correlated with higher LAP and RAP, and chronic kidney disease. Conclusion Patients with HF after AF ablation had higher LAP. MV disease, diuretic use, and class III antiarrhythmics also correlated to HF. These present opportunities to target future interventions to reduce a common complication of AF ablation.

Catheter ablation is a safe and effective procedure to reduce symptoms from atrial fibrillation (AF), but one potential complication is early occurrence of heart failure (HF). Elevated intraoperative left atrial pressure is associated with an increased risk of AF recurrence, but it is unknown if

Introduction Focal impulse and rotor modulation (FIRM)-guided ablation has had mixed results of published success, and most studies have had a follow-up for a year or less. We aimed to study a consecutive group of patients followed for at least 1.5 years, subgrouped into those with an initial FIRM ablation and those with a previous, failed ablation who now received a FIRM guided one, to evaluate for success in each group and factors that might affect success. Methods Of 181 patients, 167 were available for analysis. Group 1 (n = 122) had a first or primary ablation (paroxysmal atrial fibrillation [PAF] 51; persistent atrial fibrillation [PeAF] 71) and group 2 (n = 45) had a redo ablation (PAF 18; PeAF 27). All patients were done under general anesthesia. FIRM mapping was done in the right atrium first and then the left, and only rotors consistently seen on multiple epochs were ablated, using 15 to 30 W. Rotor ablation was discontinued when remapping showed elimination of rotational activity at the site. Wide area catheter ablation was done for pulmonary vein isolation (PVI). Routine follow-up was at 3, 6, and 12 months of the first year, with a Holter monitor at 6 months, and then every 6 months thereafter. Event recorders were given to patients with potential arrhythmic symptoms. Results Mean follow-up was 16 months. Nearly 40% of patients had obstructive sleep apnea; mean body mass index was 32; and average left atrial size was 39.7 mm and 46.2 mm for PAF and PeAF patients, respectively. Freedom from atrial arrhythmia recurrence was: in group 1 patients, 82.4% for PAF and 67.6% for PeAF patients; in group 2 patients, 83.3% for PAF, but only 40.7% for PeAF patients. Comparing outcomes for the first 10 patients studied to the next 20 or more done by three operators showed no difference, suggesting no learning curve affecting the ablation results. Furthermore, the univariate analysis did not show any demographic factor to have an independent significance for ablation success or failure. Spontaneous termination during rotor ablation occurred in 76.8% of PAF and 27.6% of PeAF patients but did not affect the long-term outcomes for maintenance of sinus rhythm. Conclusions FIRM-guided atrial ablation plus PVI in our patient population resulted in good success from a recurrence of atrial arrhythmias in patients undergoing an initial ablation procedure. For those with persistent AF undergoing a second procedure now using FIRM guidance plus PVI, the results are lower. Further research is needed to define better the appropriate population for FIRM-guided ablation and the degree of ablation needed for success in these patients.

Sudden death can occur as a consequence of cardiac-conduction abnormalities in the neuromuscular disease myotonic dystrophy type 1. The determinants of the risk of sudden death remain imprecise.We assessed whether the electrocardiogram (ECG) was useful in predicting sudden death in 406 adult patients with genetically confirmed myotonic dystrophy type 1. A patient was characterized as having a severe abnormality if the ECG had at least one of the following features: rhythm other than sinus, PR interval of 240 msec or more, QRS duration of 120 msec or more, or second-degree or third-degree atrioventricular block.Patients with severe abnormalities according to the entry ECG were older than patients without severe abnormalities, had more severe skeletal-muscle impairment, and were more likely to have heart failure, left ventricular systolic dysfunction, or atrial tachyarrhythmia. Such patients were more likely to receive a pacemaker or an implantable cardioverter-defibrillator during the follow-up period. During a mean follow-up period of 5.7 years, 81 patients died; there were 27 sudden deaths, 32 deaths from progressive neuromuscular respiratory failure, 5 nonsudden deaths from cardiac causes, and 17 deaths from other causes. Among the 17 patients who died suddenly in whom postcollapse rhythm was evaluated, a ventricular tachyarrhythmia was observed in 9. A severe ECG abnormality (relative risk, 3.30; 95% confidence interval [CI], 1.24 to 8.78) and a clinical diagnosis of atrial tachyarrhythmia (relative risk, 5.18; 95% CI, 2.28 to 11.77) were independent risk factors for sudden death.Patients with adult myotonic dystrophy type 1 are at high risk for arrhythmias and sudden death. A severe abnormality on the ECG and a diagnosis of an atrial tachyarrhythmia predict sudden death. (ClinicalTrials.gov number, NCT00622453.)

A wealth of useful diagnostic criteria is available to assist the health care worker in arriving at the correct diagnosis in cases of a wide QRS tachycardia (WQRST). Despite the abundance of good criteria for determining the diagnosis in cases of WQRST, they are of no use if they cannot be readily applied in an urgent clinical situation because they cannot be easily recalled or are too complex and cumbersome to use. It may be that refresher courses in the differential diagnosis of WQRST, especially for emergency physicians who are often the "first responders" to patients with WQRST, can improve physicians' diagnostic accuracy in this important disorder.

Background: Myocardial injury and platelet activation play important roles in the pathogenesis of unstable coronary syndromes. We sought to determine whether the combined measurement of platelet and necrosis markers would improve risk stratification, and yield higher diagnostic utility in patients presenting to the emergency department with chest pain. Methods and Results: Platelet and soluble P-selectin together with myoglobin, creatine kinase, CK-MB fraction, and troponin I were measured from the autologous samples in 122 consecutive patients. Statistical analysis revealed strong Spearman correlation coefficients (0.141–0.412; p 0.7) for acute myocardial infarction, while plasma P-selectin exhibited random distribution. Elevated soluble P-selectin and myoglobin were the most valuable in identifying patients with congestive heart failure. None of the markers were useful for triaging chest pain patients with unstable angina. Analysis of incremental gains (Chi-squares) reveals that with respect to platelet P-selectin, myoglobin adds 50%% to AMI diagnostic value, and creatine kinase yields an additional 20%% in triaging these patients. The diagnostic value of soluble P-selectin is substantially (72%%) increased by myoglobin measurements, and enhanced even further (44%%) by adding cardiac troponin I for identifying heart failure patients among the chest pain population. Conclusion: Simultaneous determination of platelet and necrosis markers improve the early diagnosis of acute myocardial infarction and congestive heart failure among patients with chest pain presenting into the Emergency Department. Well controlled clinical trials are needed to prove the advantage of combining platelet and necrosis data over presently used techniques in emergency medicine.

Each year, at least 5 million patients in the United States present to hospital emergency departments with the complaint of chest pain, and more than 10% of them will be diagnosed with acute myocardial infarction. One of the foremost tasks of the emergency department physician is to avoid unnecessary admissions and concomitantly to minimize the number of patients discharged home inappropriately. Currently available diagnostic tools, including the electrocardiogram and myocardial markers, have several shortcomings, including low specificity, and delayed sensitivity for the timely detection of myocardial necrosis. Therefore, the search for better methods of rapidly identifying patients with unstable coronary syndromes is one of the utmost priorities of modern emergency medicine. Available biochemical diagnostic tools are discussed in this review, focusing on the potential benefits of combining myocardial necrosis markers with indicators of platelet activation. It is hypothesized that such a combined approach may be more powerful in myocardial infarction risk stratification than separate marker determination.

(2000). The ERA trial: findings and implications for the future. Climacteric: Vol. 3, No. 4, pp. 227-232.

Despite new therapies, the prevalence of heart failure continues to escalate. The prevalence of diabetes, a risk factor for heart failure, also continues to rise. To further understand the increasing prevalence of heart failure, we compared trends in the prevalence of diabetes among individuals with diagnosed heart failure versus those in the general population.Fourteen randomized trials between 1989 and 1999 including subjects with heart failure (n = 34,633) were reviewed. For each trial, the enrollment date was used to estimate the yearly prevalence of diabetes among study participants with heart failure. The prevalence of diabetes in the general population was estimated based on United State's Center for Disease Control statistics from 1989 to 1999. The prevalence of diabetes between heart failure subjects and the general population was compared using a two-sample t-test for independent samples with unequal variances.The prevalence of diabetes increased from 2.6% to 4.0% from 1989 to 1999 in the general U.S. population. Among patients with heart failure, the prevalence of diabetes increased from 13% to 47%. Diabetes prevalence estimates varied significantly (p0.001) between the general population and individuals with heart failure during the study period.The rising prevalence of diabetes may partially explain the growing epidemic of heart failure. Increased efforts targeting diabetes and other cardiovascular risk factors are warranted in attenuating the rising prevalence of heart failure.

There is substantial clinical evidence that the incidence of depression and mortality after acute coronary events are strongly related. As mediators of coronary thrombosis, platelets may represent a link between these events, and could be possibly targeted by therapy with serotonin reuptake inhibitors.

Pulse pressure (PP) has been shown to predict risk for cardiovascular events in men; however, this association has not been well established in women. Hormone replacement therapy may improve arterial compliance, but findings from cross-sectional and prospective studies report inconsistent results. We sought to examine the relationship between PP and risk for cardiovascular events, and to determine the effect of hormone therapy on PP in postmenopausal women with coronary heart disease (CHD).A total of 2,763 postmenopausal women (mean age, 66 +/- 7 years [+/- SD]) with CHD in the Heart and Estrogen/Progestin Replacement Study, a randomized, placebo-controlled, secondary CHD prevention trial of estrogen plus progestin, were followed up on average for 4.1 years. BP was measured at baseline and annually. Mean baseline PP was 62 +/- 16 mm Hg. There were 361 myocardial infarctions (MIs) or CHD deaths, 265 hospitalizations for congestive heart failure (CHF), and 215 strokes or transient ischemic attacks (TIAs). Women in the highest quartile of PP at baseline had a 47% increase in risk for MI or CHD death and more than a twofold increase in risk for stroke and TIA events or hospitalization for CHF (p0.01 for each outcome). After adjustment for other cardiovascular risk factors and mean arterial pressure, PP remained significantly associated with incident stroke or TIA events (odds ratio, 1.25; p = 0.02) and hospitalizations for CHF (odds ratio, 1.31; p0.01) but not with MI or CHD death. After adjustment for diastolic BP, systolic BP was similarly associated with stroke or TIA (odds ratio, 1.30; p0.01) and hospitalized CHF (odds ratio, 1.30; p0.01) and was also weakly associated with risk for MI and CHD death (odds ratio, 1.18; p = 0.02). Mean PP was 1- to 2-mm Hg higher in women randomized to hormone replacement therapy vs those receiving placebo (p0.01).PP had predictive value for CHF and stroke or TIA, but not MI or CHD death in this cohort of postmenopausal women with CHD. Use of hormone replacement therapy produced a small, statistically significant increase in PP. Further research is necessary to determine the clinical utility of PP as a potential therapeutic target.

Pulse pressure, an index of large artery stiffness, has been associated with coronary events. However, mechanisms for this association remain unclear. In this study, we examined the relationship between pulse pressure and the progression of coronary atherosclerosis and the effects of hormone replacement therapy (HRT) on pulse pressure in postmenopausal women with angiographically confirmed coronary disease followed for 3.2 years in the Estrogen Replacement in Atherosclerosis (ERA) trial. In the ERA trial, 309 postmenopausal women (mean age 66±7 years) with coronary disease were randomized to estrogen, estrogen plus progestin, or placebo, and followed for 3.2 years. Ten standardized epicardial segments were measured for minimal diameter values at baseline and follow-up using quantitative coronary angiography. For this study, mixed-model analysis of covariance was used to: (1) test the association between pulse pressure and change in mean minimum diameter (MMD) adjusted for baseline MMD and (2) the effect of HRT on follow-up pulse pressure. After adjustment for potential confounders, there was a significant graded increase in progression of coronary stenosis with increasing quartiles of baseline pulse pressure ( P test for trend=0.0001). The progression rate in women with the highest quartile of baseline pulse pressure was 5-fold higher than in women in the lowest quartile ( P

Coronary heart disease remains the leading cause of death in postmenopausal women around the world, and interest is high in discovering the best treatments and methods of prevention for this disease. For many years, it appeared that one such treatment could be oestrogen, because of its beneficial effects on the vascular endothelium and on cholesterol concentrations. However, recent clinical trials have shown no beneficial effect of long-term hormone replacement therapy (HRT) on risk for major cardiovascular events among women with established coronary disease. These surprising findings have led to still further analyses to elucidate plausible explanations. This paper will review the results from recent trials and clinical studies of HRT, as well as ongoing trials that continue to examine the role of oestrogen in the treatment and prevention of cardiovascular disease.

Knowledge of the pathogenesis of congestive heart failure (CHF) has improved greatly in recent years. However, this disease continues to cause one of the highest morbidities and mortalities in the Western world. The pathophysiology of heart failure is complex and much of our understanding revolves strictly around the neurohormonal mechanisms involved. Various pharmacologic interventions have significantly improved morbidity and include ACE inhibitors, beta-blockers, diuretics, and inotropic agents. Yet, no consensus has been reached regarding the use of anticoagulants or antiplatelet agents. It has been suggested that CHF is associated with altered hemostasis, but whether this prothrombotic state contributes to the pathogenesis and progression of the disease is unknown. The purpose of this review article is to discuss our current knowledge of platelet activation, thrombin generation, fibrinolysis, and endothelial dysfunction in CHF patients, and the potential role of anticoagulants and/or antiplatelet agents in preventing these hemostatic abnormalities.