It is well established that coronary artery disease with healed myocardial infarction is the most common backdrop for ventricular tachycardia (VT). Although the clinical benefits of biventricular pacing (BivP) in the treatment of severe heart failure are well documented, exact relation with ventricular arrhythmias remains still unclear. We describe a case of a patient, whitout a previous history of arrhythmic episodes, in which the onset of several episodes of VT presented immediatly after cardiac resynchronization therapy (CRT) and did not occur after BivP discontinuation.

Cardiac Pacing, Artificial↗

PubMed2005

One conversion of ventricular fibrillation is adequate for implantable cardioverter-defibrillator implant: an analysis from the Low Energy Safety Study (LESS).

OBJECTIVES: The purpose of this study was to analyze defibrillation conversion data from the Low Energy Safety Study (LESS) to determine how implant criteria that use fewer inductions of ventricular fibrillation (VF) correlate with outcome and, in particular, to assess the reliability of using a single VF induction and test shock at 14 J. BACKGROUND: A safety margin of 10 J has become standard for implantation of an implantable cardioverter-defibrillator (ICD), but the specifics and rigor of the implant test sequence are not standardized. METHODS: In LESS, 611 ICD recipients completed a rigorous VF induction test scheme that began at 14 J and continued until the energy that succeeded three times without a failure was determined (DFT++). The data were analyzed to determine how well the outcome of the first 14-J shock and various other combinations of first and/or second shocks predicted a rigorous gold standard of DFT++ < or =21 J (i.e., three successes at < or =21 J). RESULTS: The positive predictive accuracy for the 91% of patients in whom the first 14-J shock succeeded was virtually identical to the positive predictive accuracy for the commonly used criteria of two successes at < or =17 J (99.1% vs 99.0%, P = .69), and slightly higher than the positive predictive accuracy for two successes at < or =21 J (98.8%, P = .51). A single success at 17 J or 21 J had a somewhat lower positive predictive accuracy of 98.2% (P = .17). Eliminating VF induction testing would have resulted in a significantly lower positive predictive accuracy of 97.1% (P = .01). CONCLUSIONS: A single conversion success at 14 J on the first VF induction provides similar positive predictive accuracy as two successes at 17 J or 21 J. Using this criterion, 91% of patients meet implant criteria with a single induction of ventricular fibrillation.

Aged↗

PubMed2005

Implantable cardioverter-defibrillator product reliability: recalling lessons from a tragic case.

Explore the source record for details and available documents.

Death, Sudden, Cardiac↗

PubMed2005

Death in a young athlete due to commotio cordis despite prompt external defibrillation.

Explore the source record for details and available documents.

Adult↗

PubMed2005

Atrioventricular nodal reverse facilitation in connexin40-deficient mice.

BACKGROUND: Facilitation is an important physiologic property of the atrioventricular (AV) node. Previous studies demonstrated abnormal AV conduction in connexin (Cx)40-deficient mice. OBJECTIVES: We hypothesize that Cx40-deficient mice display altered patterns of AV nodal facilitation compared with wild-type mice. METHODS: Sixteen 36-week-old mice (eight Cx40(-/-) mice and eight Cx40(+/+) controls) underwent in vivo closed chest electrophysiologic study. A 2Fr octapolar catheter was advanced into the right ventricle to record a His-bundle electrogram. A special facilitation stimulation protocol was performed in each mouse to evaluate facilitation. Following atrial drive pacing (S1S1) at 150 ms, a facilitating beat S2 was delivered prior to the test beat S3. S3H3 was measured for varying S1S2 values at fixed H2S3 intervals. RESULTS: Progressive shortening of S1S2 (from 150 ms to 130, 110, and 90 ms) resulted in gradual prolongation of S2H2. The prolongation was more pronounced in Cx40(-/-) mice for each S1S2 compared with wild-type mice (P <.001). In each wild-type mouse, for a given H2S3 interval, this gradual increase in S2H2 produced progressive shortening of S3H3, so-called AV nodal facilitation phenomenon. However, in each Cx40(-/-) mouse, facilitation was seen only at S1S2 of 130 ms (P <.001 vs S1S2 of 150 ms). Evidence of reverse facilitation was documented at S1S2 of 110 and 90 ms. CONCLUSION: Facilitation is observed in wild-type mice. With similar S1S2 intervals in Cx40-deficient mice, facilitation is seen only at longer S1S2 intervals, whereas reverse facilitation is seen at shorter S1S2 intervals, suggesting that Cx40 is involved in the generation of AV nodal facilitation.

Animals↗

PubMed2005

Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis).

INTRODUCTION: Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur. METHODS: In a randomized and blinded experiment, 12 swine (mean 17.1 +/- 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 +/- 18 muM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph. RESULTS: There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53%) compared to those control animals receiving only sterile water (10 of 31: 32%) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 +/- 19 mV) versus controls (61 +/- 46 mV) (P = 0.015). CONCLUSION: Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.

Animals↗

PubMed2005

Extraction of buried P waves from printed electrocardiograms.

BACKGROUND: Morphologic identification of ectopic P-waves from surface ECGs can be challenging, particularly when the P-wave is buried in the QRST wave complex. Because ECGs are often available on paper and not digitally, we developed a method of subtracting the T-wave from the buried P-wave complex on paper ECGs. METHODS: To validate our system, an atrial extrastimulus was introduced during and following the T-wave. The ECGs were scanned and then transformed from an image format to a digital format. A computer algorithm digitally subtracted a QRST with no buried P-wave from one with a buried P-wave, thus resulting in an extracted P-wave. The extracted P-waves were compared to the nonburied P-wave by determining correlation coefficients and by visual grading by two independent reviewers. RESULTS: Visual grading comparing the buried P-wave with the exposed paced P-wave was 94%. The median correlation coefficient was 85%. CONCLUSIONS: An ectopic atrial P-wave obscured by a coincident QRST wave complex can be accurately derived from printed ECG using this PC-based system. Addition of this technique to the existing methods may aid in the localization and ablation of ectopic atrial foci.

Algorithms↗

PubMed2005

Cardiovascular toxicities of performance-enhancing substances in sports.

Athletes commonly use drugs and dietary supplements to improve athletic performance or to assist with weight loss. Some of these substances are obtainable by prescription or by illegal means; others are marketed as supplements, vitamins, or minerals. Nutritional supplements are protected from Food and Drug Administration regulation by the 1994 US Dietary Supplement Health and Education Act, and manufacturers are not required to demonstrate proof of efficacy or safety. Furthermore, the Food and Drug Administration lacks a regulatory body to evaluate such products for purity. Existing scientific data, which consist of case reports and clinical observations, describe serious cardiovascular adverse effects from use of performance-enhancing substances, including sudden death. Although mounting evidence led to the recent ban of ephedra (ma huang), other performance-enhancing substances continue to be used frequently at all levels, from elementary school children to professional athletes. Thus, although the potential for cardiovascular injury is great, few appropriately designed studies have been conducted to assess the benefits and risks of using performance-enhancing substances. We performed an exhaustive OVID MEDLINE search to Identify all existing scientific data, review articles, case reports, and clinical observations that address this subject. In this review, we examine the current evidence regarding cardiovascular risk for persons using anabolic-androgenic steroids including 2 synthetic substances, tetrahydrogestrinone and androstenedione (andro), stimulants such as ephedra, and nonsteroidal agents such as recombinant human erythropoietin, human growth hormone, creatine, and beta-hydroxy-beta-methylbutyrate.

Androstenedione↗

PubMed2004

New concepts in pacemaker syndrome.

After implantation of a permanent pacemaker, patients may experience severe symptoms of dyspnea, palpitations, malaise, and syncope resulting from pacemaker syndrome. Although pacemaker syndrome is most often ascribed to the loss of atrioventricular (A-V) synchrony, more recent data may also implicate left ventricular dysynchrony caused by right ventricular pacing. Previous studies have not shown reductions in mortality or stroke with rate-modulated dual-chamber (DDDR) pacing as compared to ventricular-based (VVI) pacing. The benefits in A-V sequential pacing with the DDDR mode are likely mitigated by the interventricular (V-V) dysynchrony imposed by the high percentage of ventricular pacing commonly seen in the DDDR mode. Programming DDDR pacemakers to encourage intrinsic A-V conduction and reduce right ventricular pacing will likely decrease heart failure and pacemaker syndrome. Studies are currently ongoing to address these questions.

Journal Article↗

PubMed2004

Echocardiographic evidence of left atrial abnormality in young patients with lone paroxysmal atrial fibrillation.

Usual assessment of left atrial size by 2-dimensional echocardiography in the anteroposterior dimension often underestimates the true atrial size. We compared 15 young patients (< or =50 years old) with lone paroxysmal atrial fibrillation to age-matched controls, and measured atrial size in the inferosuperior and mediolateral dimensions. These additional measurements and atrial volumes were significantly increased compared with control patients, revealing that patients with apparent "lone" paroxysmal atrial fibrillation may have subtle structural abnormalities of the left atrium.

Adult↗

PubMed2004

Recommendations for physical activity and recreational sports participation for young patients with genetic cardiovascular diseases.

A group of relatively uncommon but important genetic cardiovascular diseases (GCVDs) are associated with increased risk for sudden cardiac death during exercise, including hypertrophic cardiomyopathy, long-QT syndrome, Marfan syndrome, and arrhythmogenic right ventricular cardiomyopathy. These conditions, characterized by diverse phenotypic expression and genetic substrates, account for a substantial proportion of unexpected and usually arrhythmia-based fatal events during adolescence and young adulthood. Guidelines are in place governing eligibility and disqualification criteria for competitive athletes with these GCVDs (eg, Bethesda Conference No. 26 and its update as Bethesda Conference No. 36 in 2005). However, similar systematic recommendations for the much larger population of patients with GCVD who are not trained athletes, but nevertheless wish to participate in any of a variety of recreational physical activities and sports, have not been available. The practicing clinician is frequently confronted with the dilemma of designing noncompetitive exercise programs for athletes with GCVD after disqualification from competition, as well as for those patients with such conditions who do not aspire to organized sports. Indeed, many asymptomatic (or mildly symptomatic) patients with GCVD desire a physically active lifestyle with participation in recreational and leisure-time activities to take advantage of the many documented benefits of exercise. However, to date, no reference document has been available for ascertaining which types of physical activity could be regarded as either prudent or inadvisable in these subgroups of patients. Therefore, given this clear and present need, this American Heart Association consensus document was constituted, based largely on the experience and insights of the expert panel, to offer recommendations governing recreational exercise for patients with known GCVDs.

Adolescent↗

PubMed2004

High incidence of pacemaker syndrome in patients with sinus node dysfunction treated with ventricular-based pacing in the Mode Selection Trial (MOST).

OBJECTIVES: We evaluated the incidence, predictors, and treatment of pacemaker syndrome in patients with sinus node dysfunction treated with ventricular-based (VVIR) pacing in the Mode Selection Trial (MOST). BACKGROUND: Pacemaker syndrome, or intolerance to VVIR pacing, consists of cardiovascular signs and symptoms induced by VVIR pacing. METHODS: The definition of pacemaker syndrome required that a patient with single-chamber VVIR pacing develop either congestive signs and symptoms associated with retrograde conduction during VVIR pacing or a >or=20 mm Hg reduction of systolic blood pressure during VVIR pacing, associated with reproducible symptoms of weakness, lightheadedness, or syncope. RESULTS: Of 996 patients randomized to VVIR pacing, 182 (18.3%) met criteria for pacemaker syndrome in follow-up. Pacemaker syndrome occurred early in most patients (13.8% at 6 months, 16.0% at 1 year, increasing to 19.7% at 4 years). Baseline univariate predictors of pacemaker syndrome included a lower sinus rate and higher programmed pacemaker rate. Previous heart failure, ejection fraction, and drop in systolic blood pressure with VVIR pacing at implantation did not predict the development of pacemaker syndrome. Post-implantation predictors of pacemaker syndrome were a higher percentage of paced beats, higher programmed low rate, and slower underlying spontaneous sinus rate. Quality of life decreased at the time of diagnosis of pacemaker syndrome and improved with reprogramming to atrial-based pacing. CONCLUSIONS: Severe pacemaker syndrome developed in nearly 20% of VVIR-paced patients and improved with reprogramming to the dual-chamber pacing mode. Because prediction of pacemaker syndrome is difficult, the only way to prevent pacemaker syndrome is to implant atrial-based pacemakers in all patients.

Aged↗

PubMed2004

Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy.

BACKGROUND: Patients with nonischemic dilated cardiomyopathy are at substantial risk for sudden death from cardiac causes. However, the value of prophylactic implantation of an implantable cardioverter-defibrillator (ICD) to prevent sudden death in such patients is unknown. METHODS: We enrolled 458 patients with nonischemic dilated cardiomyopathy, a left ventricular ejection fraction of less than 36 percent, and premature ventricular complexes or nonsustained ventricular tachycardia. A total of 229 patients were randomly assigned to receive standard medical therapy, and 229 to receive standard medical therapy plus a single-chamber ICD. RESULTS: Patients were followed for a mean (+/-SD) of 29.0+/-14.4 months. The mean left ventricular ejection fraction was 21 percent. The vast majority of patients were treated with angiotensin-converting-enzyme (ACE) inhibitors (86 percent) and beta-blockers (85 percent). There were 68 deaths: 28 in the ICD group, as compared with 40 in the standard-therapy group (hazard ratio, 0.65; 95 percent confidence interval, 0.40 to 1.06; P=0.08). The mortality rate at two years was 14.1 percent in the standard-therapy group (annual mortality rate, 7 percent) and 7.9 percent in the ICD group. There were 17 sudden deaths from arrhythmia: 3 in the ICD group, as compared with 14 in the standard-therapy group (hazard ratio, 0.20; 95 percent confidence interval, 0.06 to 0.71; P=0.006). CONCLUSIONS: In patients with severe, nonischemic dilated cardiomyopathy who were treated with ACE inhibitors and beta-blockers, the implantation of a cardioverter-defibrillator significantly reduced the risk of sudden death from arrhythmia and was associated with a nonsignificant reduction in the risk of death from any cause.

Adrenergic beta-Antagonists↗