Images in cardiovascular medicine. Left ventricular pseudoaneurysm: a late complication of low-energy DC ablation.
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Biomedical subjects
Publications and source records attributed to Peter G Guerra.
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BACKGROUND: The risk of systemic thromboemboli associated with transvenous leads in the presence of an intracardiac shunt is currently unknown. METHODS AND RESULTS: To define this risk, we conducted a multicenter, retrospective cohort study of 202 patients with intracardiac shunts: Sixty-four had transvenous leads (group 1), 56 had epicardial leads (group 2), and 82 had right-to-left shunts but no pacemaker or implantable cardioverter defibrillator leads (group 3). Patient-years were accrued until the occurrence of systemic thromboemboli or study termination. Censoring occurred in the event of complete shunt closure, death, or loss to follow-up. Mean ages for groups 1, 2, and 3 were 33.9+/-18.0, 22.2+/-12.6, and 22.9+/-15.0 years, respectively. Respective oxygen saturations were 91.2+/-9.1%, 88.1+/-8.1%, and 79.7+/-6.7%. During respective median follow-ups of 7.3, 9.3, and 17.0 years, 24 patients had at least 1 systemic thromboembolus: 10 (15.6%), 5 (8.9%), and 9 (11.0%) in groups 1, 2, and 3, respectively. Univariate risk factors were older age (hazard ratio [HR], 1.05; P=0.0001), ongoing phlebotomy (HR, 3.1; P=0.0415), and an transvenous lead (HR, 2.4; P=0.0421). In multivariate, stepwise regression analyses, transvenous leads remained an independent predictor of systemic thromboemboli (HR, 2.6; P=0.0265). In patients with transvenous leads, independent risk factors were older age (HR, 1.05; P=0.0080), atrial fibrillation or flutter (HR, 6.7; P=0.0214), and ongoing phlebotomy (HR, 14.4; P=0.0349). Having had aspirin or warfarin prescribed was not protective. Epicardial leads were, however, associated with higher atrial (P=0.0407) and ventricular (P=0.0270) thresholds and shorter generator longevity (HR, 1.9; P=0.0176). CONCLUSIONS: Transvenous leads incur a >2-fold increased risk of systemic thromboemboli in patients with intracardiac shunts.
BACKGROUND: The severity of symptoms caused by atrial fibrillation (AF) is extremely variable. Quantifying the effect of AF on patient well-being is important but there is no simple, commonly accepted measure of the effect of AF on quality of life (QoL). Current QoL measures are cumbersome and impractical for clinical use. OBJECTIVE: To create a simple, concise and readily usable AF severity score to facilitate treatment decisions and physician communication. METHODS: The Canadian Cardiovascular Society (CCS) Severity of Atrial Fibrillation (SAF) Scale is analogous to the CCS Angina Functional Class. The CCS-SAF score is determined using three steps: documentation of possible AF-related symptoms (palpitations, dyspnea, dizziness/syncope, chest pain, weakness/fatigue); determination of symptom-rhythm correlation; and assessment of the effect of these symptoms on patient daily function and QoL. CCS-SAF scores range from 0 (asymptomatic) to 4 (severe impact of symptoms on QoL and activities of daily living). Patients are also categorized by type of AF (paroxysmal versus persistent/permanent). The CCS-SAF Scale will be validated using accepted measures of patient-perceived severity of symptoms and impairment of QoL and will require 'field testing' to ensure its applicability and reproducibility in the clinical setting. CONCLUSIONS: This type of symptom severity scale, like the New York Heart Association Functional Class for heart failure symptoms and the CCS Functional Class for angina symptoms, trades precision and comprehensiveness for simplicity and ease of use at the bedside. A common language to quantify AF severity may help to improve patient care.
A 29-year-old man presenting with syncopal ventricular tachycardia was diagnosed with arrhythmogenic right ventricular (RV) cardiomyopathy. Cardiac magnetic resonance imaging (MRI) revealed an unequivocal dyskinetic segment at the basal portion of the RV lateral free wall. Three-dimensional electroanatomic voltage mapping using the EnSite NavX system recorded a low voltage area corresponding to the diseased portion of the right ventricle identified by MRI. This report describes concordance between cardiac MRI and this novel mapping system in arrhythmogenic RV cardiomyopathy.
BACKGROUND: Cardiac resynchronization therapy (CRT) has been shown to improve symptoms of patients with moderate to severe heart failure. Optimal CRT involves biventricular or left ventricular (LV) stimulation alone, atrio-ventricular (AV) delay optimization, and possibly interventricular timing adjustment. Recently, anodal capture of the right ventricle (RV) has been described for patients with CRT-pacemakers. It is unknown whether the same phenomenon exists in CRT systems associated with defibrillators (CRT-ICD). The RV leads used in these systems are different from pacemaker leads: they have a larger diameter and shocking coils, which may affect the occurrence of anodal capture. METHODS: We looked for anodal RV capture during LV stimulation in 11 consecutive patients who received a CRT-ICD system with RV leads with a true bipolar design. Fifteen patients who had RV leads with an integrated design were used as controls. Anodal RV and LV thresholds were determined at pulse width (pw) durations of 0.2, 0.5, and 1.0 ms. RESULTS: RV anodal capture during LV pacing was found in 11/11 patients at some output with true bipolar RV leads versus 0/15 patients with RV leads with an integrated bipolar design. Anodal RV capture threshold was more affected by changes in pw duration than LV capture threshold. In CRT-ICD systems, RV leads with a true bipolar design with the proximal ring also used as the anode for LV pacing are associated with a high incidence of anodal RV capture during LV pacing. This may affect the clinical response to alternative resynchronization methods using single LV stimulation or interventricular delay programming.
We describe a case of abnormal right atrial (RA) conduction in a patient with atrial tachycardia (AT) but no history of structural heart disease or cardiac surgery. Following ablation of AT, the patient experienced typical atrial flutter (AFL) and a postcardioversion ECG suggestive of low atrial rhythm. Repeat EPS and three-dimensional electroanatomic activation mapping showed unusual RA activation during SR. This case illustrates the possibility that abnormal intraatrial conduction may lead to unusual patterns of activation in the RA which can serve as a necessary substrate for the initiation and maintenance of macro-reentry circuits.
Hypertrophic cardiomyopathy is a genetic disease that affects the cardiac sarcomere, resulting in myocardial hypertrophy and disarray. Affected patients have a predisposition for malignant ventricular tachyarrhythmias and, consequently, sudden cardiac death. With the availability of therapeutic measures that prevent sudden death, the identification of high-risk patients is now of greater importance. Clinical risk factors for sudden death (ie, age, syncope, family history of sudden cardiac death, cardiac arrest survivor, nonsustained ventricular tachycardia and abnormal blood pressure response to exercise) have been identified. The clinical electrophysiological study is of limited use for stratifying these patients. More recently, increased attention has been given to the degree of echocardiographically documented left ventricular hypertrophy and prognostically significant genetic mutations. Once a high-risk patient is identified, prophylactic treatment is warranted. For this purpose, amiodarone has been supplanted by the implantable cardioverter-defibrillator. Implantable cardioverter-defibrillator treatment appears to reduce the risk of sudden cardiac death in both primary and secondary prevention settings. Thus, tools are now available to identify and treat high-risk patients with hypertrophic cardiomyopathy.
The present article reviews pertinent contributions from the Montreal Heart Institute, Montreal, Quebec, to the understanding of the mechanisms and treatment of atrial fibrillation. The article discusses the usefulness of anticoagulant therapy, antiarrhythmic drug therapy for sinus rhythm maintenance, the electrophysiological basis of atrial fibrillation and the investigation of new energy sources for catheter ablation. Future directions at the Montreal Heart Institute are also briefly addressed.
Catheter ablation therapy for the treatment of atrial fibrillation (AF) has evolved considerably in the past decade. Although the therapy was initially limited to ablation of the atrioventricular node to ensure adequate rate control for patients with rapid AF, the possibility of catheter-based rhythm control has now been demonstrated in several studies. Atrial extrasystoles originating from the pulmonary veins are now known to be triggers for the initiation of AF. Consequently, attempts at ablation have focused on the ablation of these triggers or on electrical isolation of these veins using radiofrequency ablation. More recently, three-dimensional electroanatomical imaging techniques have allowed for the development of left atrial ablation techniques, whereby long, linear lesions are created around the pulmonary venous ostia. Both of these techniques have shown interesting success rates in the treatment of symptomatic paroxysmal AF. The present article reviews the evolution of these techniques and lists the recommendations for the use of catheter ablation for both rate and rhythm control of AF.
Atrial fibrillation (AF) is the most common arrhythmia managed by emergency physicians and there is increasing evidence that selected patients with acute AF can be safely managed in the emergency department without the need for hospital admission. The principles of management are identification and treatment of precipitating or underlying causes, hemodynamic stabilization/rate control, reduction of thromboembolism risk and the conversion/maintenance of sinus rhythm. A strategy of rate or rhythm control should be chosen based on the patient's clinical status, the duration of AF, the experience of the treating physician and the status of anticoagulation. Before either electric or pharmacological cardioversion, anticoagulation should be considered. Most patients should be given heparin or low molecular weight heparin while preparing for cardioversion. All patients should be considered for long-term anticoagulation based on their thromboembolic risk and bleeding risk from antithrombotic therapy. Following restoration of sinus rhythm, a decision regarding the use of antiarrhyhmic drugs should be made based on the estimated frequency of recurrence and degree of symptoms. In the setting of acute myocardial infarction, beta-blockers should be administered whenever possible. If beta-blockers are contraindicated, the rate can be slowed with digoxin or amiodarone. Cardioversion should be performed if the patient is hemodynamically unstable. Class IC antiarrhythmic drugs should not be administered in this setting.
BACKGROUND: Creating linear lesions is important for the treatment of arrhythmias such as atrial flutter and fibrillation. Making these lesions with standard radiofrequency catheters can be difficult and may result in charring and thrombosis. The purpose of this study was to evaluate beta-radiation as a novel energy source for creating linear myocardial lesions. METHODS AND RESULTS: Eight dogs with intact conduction across the cavotricuspid isthmus were studied. The isthmus was irradiated (25 to 50 Gy) with strontium/yttrium-90 delivered via a deflectable 7F catheter (Novoste Corporation). There were no immediate effects, but bidirectional conduction block developed during follow-up studies in 7 of 8 dogs. The dog without conduction block received 25 Gy. After the animals were euthanized, histology revealed transmural, linear areas of fibrosis without any thrombus. CONCLUSIONS: Beta-radiation can safely and effectively create linear lesions that are contiguous and nonthrombogenic. This energy source may become an interesting adjunct to radiofrequency for the treatment of atrial flutter and fibrillation.
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BACKGROUND: Atrial fibrillation (AF) is frequently encountered in patients with heart failure (HF) and is also a predictor of morbidity and mortality in this population. Recent experimental studies have shown electrical and structural atrial remodeling with increased fibrosis in animals with HF and have suggested a preventive effect of ACE inhibitors (ACEi) on the development of AF. To verify the hypothesis that ACEi prevent the development of AF in patients with HF, we conducted a retrospective analysis of the patients from the Montreal Heart Institute (MHI) included in the Studies Of Left Ventricular Dysfunction (SOLVD). METHODS AND RESULTS: Clinical charts were reviewed and serial ECGs interpreted by a single cardiologist blinded to drug allocation. Patients with AF or flutter on the baseline ECG were excluded. Baseline characteristics were obtained from the SOLVD databases. The mean follow-up was 2.9+/-1.0 years. Of the 391 patients randomly assigned at MHI, 374 were in sinus rhythm at the time of random assignment, with 186 taking enalapril and 188 taking placebo. Baseline characteristics were similar in the two groups except for a higher incidence of previous myocardial infarction in the enalapril group. Fifty-five patients had AF during the follow-up: 10 (5.4%) in the enalapril group and 45 (24%) in the placebo group (P<0.0001). By Cox multivariate analysis, enalapril was the most powerful predictor for risk reduction of AF (hazard ratio, 0.22; 95% CI, 0.11 to 0.44; P<0.0001). CONCLUSIONS: Treatment with the ACEi enalapril markedly reduces the risk of development of atrial fibrillation in patients with left ventricular dysfunction.
BACKGROUND: Atrial fibrillation (AF) is initiated by ectopic beats originating in the sleeve of atrial tissue in pulmonary veins (PVs). Circumferential ablation of PVs can, thus, result in a cure of AF. Identification of this PV arrhythmogenic tissue has been exclusively on the basis of electrophysiologic recordings. The purpose of this study was to visualize this tissue using intravascular ultrasound (IVUS). Methods and results In all, 15 patients undergoing AF ablation had IVUS studies of their PVs. A total of 21 veins had a wall thickness less than 0.1 mm, whereas 31 veins had well-demarcated areas of thickening measuring 0.81 +/- 0.32 mm. Electrophysiologic recordings from these thickened areas showed typical high-frequency potentials associated with arrhythmogenic atrial tissue in the PVs. Ectopic beats initiating AF always originated from these areas. PVs without thickening on IVUS did not have these potentials. CONCLUSIONS: IVUS permits visualization of atrial tissue in the PVs, and arrhythmogenic PVs are qualitatively and quantitatively different from nonarrhythmogenic PVs.
Despite improvements in management strategies, ventricular arrhythmias remain important markers of electrical instability and contribute to the identification of patients at increased risk of sudden cardiac death post-myocardial infarction (MI). Over the past 20 years, understanding of pathophysiological mechanisms and implications of various types of ventricular arrhythmias has evolved remarkably. This systematic review details the prognostic significance of ventricular arrhythmias classified by type and time of onset post-MI. Subacute and late premature ventricular complexes are associated with increased mortality independent of left ventricular function. Although nonsustained ventricular tachycardia (VT) in the acute phase post-MI is of questionable significance, later onset heralds poorer prognosis. Sustained monomorphic VT in the acute post-MI phase is associated with infarct extension, heart failure and increased mortality. Extensive wall motion abnormalities, left ventricular dysfunction and aneurysm formation correlate with later postinfarct sustained VT. Inhospital mortality is higher when ventricular fibrillation presents in the acute phase but long term prognosis is not adversely affected.
This work develops a mathematical model for the atrioventricular (AV) node in the human heart, based on recordings of electrical activity in the atria (the upper chambers of the heart) and the ventricles (the lower chambers of the heart). Intracardiac recordings of the atrial and ventricular activities were recorded from one patient with atrial flutter and one with atrial fibrillation. During these arrhythmias, not all beats in the atria are conducted to the ventricles. Some are blocked (concealed). However, the blocked beats can affect the properties of the AV node. The activation times of the atrial events were regarded as inputs to a mathematical model of conduction in the AV node, including a representation of AV nodal concealment. The model output was compared to the recorded ventricular response to search for and identify the best possible parameter combinations of the model. Good agreement between the distribution of interbeat intervals in the model and data for durations of 5 min was achieved. A model of AV nodal behavior during atrial flutter and atrial fibrillation could potentially help to understand the relative roles of atrial input activity and intrinsic AV nodal properties in determining the ventricular response.
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