Further information: The Implantable Cardioverter-Defibrillator (see p2119) from Cardiovascular Medicine, 3rd Edn*

The implantable cardioverter-defibrillator (ICD) is a widely used and trusted therapy for the prevention of sudden death from ventricular arrhythmia (VA). The design of the ICD requires the use of transvenous leads. Complication of lead insertion that result in difficulty obtaining venous access, as well as lead failure, led the investigators [1] to conduct two short-term trials to evaluate a subcutaneous ICD system that eliminated the need for placement of sensing and therapy electrodes within or on the heart. The first trial enrolled 78 patients from September 2001 to February 2004, and was conducted to identify the best electrode configuration out of four options for the subcutaneous ICD. Each patient was temporally implanted subcutaneously with an ICD to test the defibrillation threshold. After testing, the device was explanted, and a conventional ICD was implanted in each patient. The second short-term trial enrolled 49 patients from April 2004 to June 2005 in order to test the best of the previously tested subcutaneous ICD devices. In this trial, both a subcutaneous and a transvenous device were implanted in the same procedure. The defibrillation thresholds were compared, and after data were compiled, the subcutaneous device was explanted. Subsequently, two trials involving permanent implantation of a subcutaneous ICD were conducted. In a pilot trial in Australia, six patients were permanently implanted, and in a second trial conducted in New Zealand and Europe, 55 patients were permanently implanted. Investigators concluded that in these small, nonrandomized trials, the subcutaneous ICD was consistent and successful in detecting VA. There were 12 episodes of ventricular tachyarrhythmia that were also detected and treated.

[1] Bardy GH, Smith WM, Hood MA, et al. An entirely subcutaneous implantable cardioverter-defibrillator. N Engl J Med 2010;363:36-44

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Further information: Coronary Artery Disease: Pathologic Anatomy and Pathogenesis (see p593), Arterial Compliance (see p1811), Atrial Fibrillation and Flutter (see p1955), and Sudden Cardiac Death (see p2039) from Cardiovascular Medicine, 3rd Edn*

In 1985 and 1986 respectively, two articles were published in Circulation [1,2] that reported that myocardial platelet thrombi were embolic and that the emboli were a cause of acute coronary syndromes (ACS). Although prior histopathological studies had shown intramyocardial microemboli and microvascular obstruction (MVO) were present in patients with ischemic cardiac death, the association between culprit coronary morphology and intramyocardial emboli had not been reported. Therefore, the investigators in this study [3] determined to evaluate the frequency of intramyocardial microemboli and MVO in sudden cardiac death from acute coronary thrombosis. Differentiating between plaque rupture and plaque erosion were important elements of the study. Plaque rupture was defined as “disruption of a fibrocellular cap overlying a pool of lipid with pultaceous debris,” and plaque erosion was defined as “surface ulceration of the upper plaque layers without rupture into a lipid core.”

Through analysis at autopsy of coronary arteries of 44 hearts, 26 plaque ruptures and 21 erosions were found, and there was a mean of 4.5 microemboli per heart. Microemboli and MVO occurred in eroded plaques more often, and although all vessels contained fibrin and platelets, microemboli and occluded intramyocardial vessels were more common in the LAD of the coronary artery. The mean stenosis of the culprit lesion was 74% in the arteries with microemboli and 75% in those without (P=NS). Intramyocardial microemboli were more common in plaque erosion than in plaque rupture.

The investigators concluded that plaque erosion was dominant in the histopathology of clot embolization causing sudden cardiac death, was more likely to occur in vessels of less than 120 µm, and was associated with focal necrosis.

[1] Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion. Circulation 1985;71:699-708

[2] Davies MJ, Thomas AC, Knapman PA, Hangartner JR. Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. Circulation 1986;73:418-27

[3] Schwartz RS, Burke A, Farb A, et al. Microemboli and microvascular obstruction in acute coronary thrombosis and sudden coronary death. J Am Coll Cardiol 2009;54:2167-73

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Further information: Atrial Fibrillation and Flutter (see p1955) and Antiarrhythmic Drugs (see p2085) from Cardiovascular Medicine, 3rd Edn*

In order to compare two heart rate control strategies in patients with permanent atrial fibrillation, a randomized, multicenter, open-label, prospective, noninferiority trial was conducted at 33 centers in the Netherlands. Recruitment for the Rate Control Efficacy in Permanent Atrial Fibrillation: A Comparison Between Lenient versus Strict Rate Control II (RACE II) trial began in January of 2005 and ended in June of 2007 [1]. Eligible patients were 80 years of age or younger, had permanent atrial fibrillation for up to 12 months, had a mean resting heart rate above 80 beats per minute, and had a medical regimen that included the use of oral anticoagulation therapy. A total of 614 patients were recruited. The patients were randomized to undergo either a lenient rate-control strategy with a resting heart rate <110 beats per minute, or a strict rate-control strategy with a resting heart rate <80 beats per minute, to determine which strategy reduced the incidence of heart failure and stroke. Because prior studies had shown that strict rate control reduced symptoms, improved quality of life and exercise capacity, reduced heart failure, and improved survival, it has been the preferred strategy. However, strict control could also cause drug-related adverse effects, such as bradycardia, syncope, and the need for a pacemaker, and the study was conducted to test the hypothesis that lenient rate control is not inferior to strict rate control.

Primary outcome was a composite of death from cardiovascular causes, heart failure-induced hospitalization, stroke, systemic embolism, major bleeding, and arrhythmic events. Secondary outcomes included all of the primary outcomes plus death from any cause, symptoms, and functional status. The follow-up period was a maximum of 3 years, and at the end of that time, the estimated cumulative incidence of the primary outcome was 12.9% in the lenient rate-control group and 14.9% in the strict rate-control group. There was an absolute difference in the lenient rate-control of 2.0 percentage points (90% CI, -7.6 to 3.5; P<0.001 for the prespecified noninferiority margin). The frequencies of symptoms and adverse events were similar in the two groups, and the investigators concluded that lenient rate-control is as effective as strict rate-control, which should prove helpful to patients being treated for permanent atrial fibrillation.

[1] Van Gelder IC, Groenveld HF, Crijins HJGM, et al. Lenient versus strict rate control in patients with atrial fibrillation (RACE II). N Engl J Med 2010;362:1439-41

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Further information: Atrial Fibrillation and Flutter (see p1955) from Cardiovascular Medicine, 3rd Edn*

This study [1] was a prospective, multicenter, randomized trial designed to compare catheter ablation with antiarrhythmic drug therapy (ADT) in an effort to find the best control of recurrent atrial fibrillation (AF). Patients who have AF have increased risk of stroke, heart failure (HF), and impaired quality of life. ADT has long been the common treatment, but an ineffective one that subjected patients to adverse effects, with recurrence likely within 6 to 12 months. In this study, catheter ablation was evaluated as the alternate treatment to ADT.

Enrollment to the study was conducted from October 25, 2004 to October 11, 2007 in 19 hospitals, and 167 patients were enrolled who were refractory to at least one antiarrhythmic drug and had had at least three reoccurrences of AF within 6 months. Patients were randomized at a 2:1 ratio to either catheter ablation (n=106) or ADT (n=61), with the primary outcome being the time to protocol-defined treatment failure. The evaluation period lasted 9 months, and data showed that only 16% of patients in the ADT arm were free of recurrence of AF, while 63% in the catheter ablation group remained free. Hazard ratio of catheter ablation to ADT was 0.30 (95% confidence interval [CI], 0.19–0.47; P<0.001). Major 30-day treatment-related adverse events occurred in five of 57 patients (or 8.8%) in the ADT arm, contrasting with five of 103 patients (4.9%) in the catheter ablation arm. Because the study showed that patients treated with catheter ablation had an early and sustained reduction in symptom frequency and in the severity of symptoms, this result corresponded with an improvement in quality of life.

[1] Wilber DJ, Pappone C, Neuzil P, et al. Comparison of antiarrhythmic drug therapy and radiofrequency catheter ablation in patients with paroxysmal atrial fibrillation (ThermoCool AF Trial). JAMA 2010;803:333-40

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Further information: Treatment of Acute ST-Elevation Myocardial Infarction (see p963) and Sudden Cardiac Death (see p2039) from Cardiovascular Medicine, 3rd Edn*

Investigators for the Immediate Risk Stratification Improves Survival (IRIS) trial sought to prove that when compared to optimal medical therapy after myocardial infarction (MI), early implantation of an implantable cardioverter-defibrillator (ICD) would improve survival of patients at risk of sudden death [1]. The trial was a multicenter, randomized, prospective trial that was investigator-initiated and open-label. From a total of 62,944 patients registered with MI between June 1999 and October 2007, 898 patients met the criteria for enrollment 5–31 days after the event. Of those, 453 were randomized to medical therapy alone and 445 to treatment with an ICD. Overall mortality was not reduced in the ICD group, although there were fewer sudden cardiac deaths ( 27 vs. 60; hazard ratio [HR], 0.55; 95% confidence interval [CI], 0.31–1.00; P=0.049). The number of cardiac deaths that were not sudden death was higher (68 vs. 39; HR, 1.92; 95% CI, 1.29–2.84; P=0.001). Investigators concluded that no evidence was found to substantiate that early implantation of an ICD improved survival in patients with acute MI who had clinical features that put them at increased risk of sudden death.

[1] Steinbeck G, Andresen D, Seidl K, et al. Defibrillator implantation early after myocardial infarction. N Engl J Med 2009;361:1427-1436

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Further information: Atrial Fibrillation and Flutter (see p1955) from Cardiovascular Medicine, 3rd Edn*

Investigators conducted the Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) trial to compare two fixed doses of dabigratran with the open-label use of warfarin in patients who had atrial fibrillation (AF) and were at risk for stroke [1]. In the randomized, noninferiority trial, the blinded, fixed doses of dabigatran administered were 110 mg twice daily or 150 mg twice daily and were compared with unblinded, adjusted-dose warfarin. Primary outcome of the trail was stroke or systemic embolism, and secondary outcomes were stroke, systemic embolism, and death. Between December 2005 and December 15, 2007, 18,113 patients from 951 clinical centers in 44 countries were enrolled into the three treatment groups. A patient’s eligibility included documented AF within 6 months prior to recruitment, and at least one additional characteristic, such as previous stroke or transient ischemic attack, left ventricular ejection fraction (LVEF) less than 40%, NYHA class II or higher heart failure symptoms 6 months prior, and at least 75 years of age. Patients who had diabetes, hypertension, or CAD could be age 65–74. Median follow-up was 2.0 years.

Warfarin is a vitamin K antagonist used in patients with AF to reduce their risk of stroke and death, but it has a primary complication of intracranial hemorrhage. Therefore, results showing that the dose of 150 mg of dabigatran was associated with lower rates of stroke and systemic embolism (primary outcome) were of interest (1.69% per year in warfarin group; 1.53% per year in group who received 110 mg of dabigatran; 1.11% per year in group who received 150 mg of dabigatran). Major bleeding rate was 3.36% per year in warfarin group, 2.71% in the 110 mg dabigatran group, and 3.11% per year in the 150 mg of dabigatran group. Hemorrhagic stroke rate was 0.38% per year for warfarin, 0.12% per year for 110 mg of dabigatran 10% per year for 150 mg of dabigatran.

The investigators concluded that from the data that in comparison with warfarin, dabigatran dosed at 150 mg revealed lower stroke and systemic embolism, but had similar rates of major hemorrhage.

In an accompanying editorial [2], Brian Gage emphasized that while warfarin has been a recommended treatment for AF patients at risk for stroke for some time, the complications in administration of the medication have precluded its use for some patients, and he believes it is necessary to develop new oral anticoagulants. He concludes that in regard to the current study of dabigatran, patients who are currently on a well-controlled INR regimen should stay with warfarin, but patients with AF and an additional risk factor for stroke would benefit from the use of dabigatran. He stated that the 110 mg dose appears safer, the 150 mg dose appears more efficacious, and that while additional studies are needed, patients with AF plus additional risk factors could benefit from its use.

[1] Connolly SJ, Ezekowitz MD, Yusuf S, et al. Dabigatran versus warfarin in patients with atrial fibrillation (RE-LY). N Engl J Med 2009;361:1139-1151

[2] Gage BF. Can we rely on RE-LY? N Engl J Med 2009;361:1200-1202

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Further information: Sudden Cardiac Death (see p2039) from Cardiovascular Medicine, 3rd Edn*

This study [1] is a large, retrospective cohort study intended to compare the two classes of antipsychotic drugs, typical and atypical, and the associated risk of sudden cardiac death in patients using each class of medication. Typical antipsychotic drugs are known to block repolarizing potassium currents in vitro and prolong the QT interval, a mechanism causing ventricular tachyarrhythmias that lead to sudden death. These drugs also cause serious movement disorders, another limiting factor in their use. Atypical antipsychotic drugs are less likely to cause movement disorders, thus are considered safer, and they have largely replaced the older, typical drugs in clinical practice. Although a link had been established between the use of atypical drugs and both torsades de pointes and sudden cardiac death, the atypical drugs were thought to have a lower risk.

Study data were obtained from computerized files of Tennessee Medicaid of individuals who had enrolled from January 1, 1990 through December 31, 2005. Only people of 30–74 years of age were included in this study. The primary analysis included 44,218 and 46,089 baseline users of single typical and atypical drugs, respectively, and 186,600 matched nonusers of antipsychotic drugs. A secondary analysis of users of antipsychotic drugs who had no baseline diagnosis of schizophrenia or related psychoses and with whom users were matched according to propensity score was conducted to assess residual confounding related to factors associated with the use of antipsychotic drugs.

Current users of typical and atypical antipsychotic drugs had higher rates of sudden cardiac death than did nonusers of antipsychotic drugs, with adjusted incidence-rate ratios of 1.99 (95% confidence interval [CI], and 1.68–2.34) and 2.26 (95% CI, 1.88–2.72), respectively. The incidence-rate ratio for users of atypical antipsychotic drugs as compared with users of typical antipsychotic drugs was 1.14 (95% CI, 0.93–1.39). Former users of antipsychotic drugs had no significantly increased risk (incidence-rate ratio, 1.13; 95% CI, 0.98–1.30). For both classes of drugs, the risk for current users increased significantly with an increasing dose. Among users of typical antipsychotic drugs, the incidence-rate ratios increased from 1.31 (95% CI, 0.97–1.77) for those taking low doses to 2.42 (95% CI, 1.91–3.06) for those taking high doses (P<0.001). Among users of atypical drugs, the incidence-rate ratios increased from 1.59 (95% CI, 2.25–3.65) for those taking high doses (P=0.01). The findings were similar in the cohort that was matched for propensity score.

The study concluded that a similar dose-related increased risk of sudden cardiac death was present in both typical and atypical antipsychotic drugs.

[1] Ray WA, Chung CP, Murray KT et al. Atypical antipsychotic drugs and the risk of sudden cardiac death. N Engl J Med 2009;360:225-35

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Further information: Sudden Cardiac Death (see p2039) from Cardiovascular Medicine, 3rd Edn*

The authors [1] evaluated whether the incidence and outcome of out-of-hospital cardiac arrest (OHCA) differ according to the geographic residence of patients. A prospective observational study, the Resuscitation Outcomes Consortium (ROC), was designed to evaluate all OHCAs in 10 North American sites (eight in the US and two Canadian) from May 1, 2006 to April 30, 2007. These patients were followed to hospital discharge, thus data were included as of June 28, 2008.

Patients (aged 0–108 years) were assessed by organized emergency medical services (EMS) personnel, did not have traumatic injury, and either received attempts at external defibrillation of chest compressions, or resuscitation was not attempted. Rates were adjusted for age and gender. Among the 10 sites, the population studied totaled 21.4 million. Of the total, 20,520 cardiac arrests were documented. Resuscitation was attempted in 11,898 cases, and of those, 2729 had initial rhythms of ventricular fibrillation, ventricular tachycardia, or rhythms shockable by an automatic external defibrillator (AED). Nine hundred fifty-four patients (4.6%) were discharged alive.
The median incidence of EMS-treated cardiac arrest across sites was 52.1 (interquartile range [IQR], 48.0–70.1) per 100,000 population; survival ranged from 3.0% to 16.3%, with a median of 8.4% (IQR, 5.4%–10.4%). Median ventricular fibrillation incidence was 12.6 (IQR, 10.6–5.2) per 100,000 population; survival ranged from 7.7% to 39.9%, with a median of 22.0% (IQR, 15.0%–24.4%). According to data documented in the five tables in this study, there were significant and important regional differences in incidence and outcome of OHCA. This report helps to provide an accurate estimation of the burden of OHCA and may assist local regions in improving public health by improving the ability to assess and treat cardiovascular disease in centers throughout North America.

[1] Nichol G, Thomas E, Callaway CW, et al. Regional variation in out-of hospital cardiac arrest incidence and outcome. JAMA 2008;300(12):1423-1431

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Sudden Cardiac Arrest Associated with Early Repolarization

Further information: Electrocardiography from Cardiovascular Medicine, 3rd Edn*

The authors of this study [1] examined the possibility that the electrocardiographical pattern called “early repolarization” is a marker of malignant cardiac arrhythmias. Although early repolarization is commonly considered benign, experimental studies have suggested that it has a potential relationship to sudden cardiac arrest.

In order to find substantiating clinical data to support this, data from 22 centers of 206 subjects who had been resuscitated after cardiac arrest due to idiopathic ventricular fibrillation were reviewed, and the prevalence of electrocardiographic repolarization was assessed. Early repolarization is defined by a slurring or notching that creates a positive hump, a J wave, that is found at the end of the QRS complex and the beginning of the ST segment. Idiopathic ventricular fibrillation is defined as a class of patients having no identifiable structural heart disease demonstrated by normal echocardiographic biventricular dimensions and function, no detectable coronary artery disease, and no repolarization abnormalities. The prevalence and amplitude of early repolarization was also assessed in a control group of 412 subjects from a population of health care professionals with normal echocardiographic biventricular dimensions, function, and no history of syncope.

The investigators found higher-than-expected prevalence of early repolarization in patients who had idiopathic ventricular fibrillation that caused syncope and sudden cardiac arrest (31% vs. 5%, P<0.001). Subjects with early repolarization were more likely to be male and to have a history of syncope or sudden cardiac arrest during sleep than those without early repolarization. In eight subjects, the origin of initiation of the ventricular arrhythmia was traced to a site that coordinated with the localization of repolarization abnormalities. In mean (±SD) follow-up of 61±50 months, defibrillator monitoring showed a higher incidence of recurrent ventricular fibrillation in subjects with early repolarization than in those without (hazard ratio, 2.1; 95% confidence interval, 1.2–3.5; P=0.008). These findings are of potential relevance to patients with syncope or a family history of sudden death, as early repolarization may be responsible for a portion of undiagnosed syncope or unexplained premature death.

[1] Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358:2016-23

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Findings from the International LQTS Registry on congenital LQTS in children and adults

Further information: Sudden Cardiac Death from Cardiovascular Medicine, 3rd Edn*

The authors of the first paper [1] studied congenital long-QT syndrome (LQTS), a genetic disorder caused by mutations that encode regulatory channels for sodium, potassium, and calcium currents, as well as by a mutation in the cytoskeletal gene (ankyrin B) that affects sodium and calcium kinetics and leads to prolonged ventricular tachyarrhythmias that result in sudden cardiac death (SCD) in children. There is usually no structural heart disease associated with LQTS. Using the International Long QT Syndrome Registry, the authors evaluated data from the contributing centers on >3000 children (1–12 years old) and focused on aborted cardiac arrest (ACA) or SCD.

Significant predictors of both conditions were identified as clinical risk factors during childhood and included corrected QT interval (QTc) duration > 500ms (hazard ratio [HR], 2.72; 95% confidence interval [CI], 1.50–4.92; P=0.001) and prior syncope (recent syncope, <2 years: HR, 6.16; 95% CI 3.41–11.15; P<0.001; remote syncope, ≥2 years: HR, 2.67; 95% CI, 1.22–5.85; P=0.01, in boys. In girls, prior syncope was the only significant risk factor (recent syncope: HR, 27.82; 95% CI, 9.72–79.60; P<0.001; remote syncope: HR, 12.04; 95% CI, 3.79–38.26; P<0.001).

Although LQTSs were identified 50 years ago, and in recent years, advances have been made to identify the genotype-phenotype relationships and risk factors for cardiac events, these studies addressed the data using syncope as the primary part of the composite event end points. The authors of this study evaluated the genetic and clinical factors in the LQTS children that contributed toward the development of fatal (SCD) or near-fatal (ACA) events, and they identified clinical risk factors of marked QTc prolongation that were >500 ms in boys and syncope in both boys and girls to be significant predictors of ACA or SCD during childhood, but in girls, prior syncope was the only significant risk factor. The use of β-blocker therapy to prevent ACA or SCD was also assessed, and authors found that it is associated with a significant reduction in the risk of life-threatening events.

Using the same International LQTS Registry, the authors of the second paper (several of whom were also collaborators to the first paper) studied adults more than 40 years old with congenital LQTS [2]. Other studies by these authors assessed the syndrome in the decades of life leading up to 40 years, but until the present, the syndrome had not been studied in the aforementioned population. The belief had been prevalent that subjects affected with the congenital genetic disorder who had lived to the age of 40 or more years had a lower risk of ACA or SCD events. The authors evaluated 2759 subjects from the registry who were ages 41–75 years and categorized them into three subgroups. The groups included electrocardiographically affected (corrected QT interval [QTc] ≥470 ms), borderline (QTc 440–469 ms), and unaffected (QTc <440 ms). The patient population used in this study was made up of LQTS patients enrolled in the registry and their unaffected family members. Genetic testing was performed on 871 unaffected patients who had not been tested previously. A total of 539 genotyped subjects were identified as LQTS carriers and were categorized as genotype positive, and 332 subjects in the registry were not carriers and were categorized as genotype negative.

Affected versus unaffected individuals adjusted HR for ACA or SCD was 2.65 (P<0.001) in ages 41–60 years and 1.23 (P=0.31) in ages 61–75 years. Risk factors for ACA or SCD after age 40 in affected LQTS patients include female gender and time-dependent syncope, but in the unaffected subjects, men in this age group are shown to have a higher risk of life-threatening cardiac events. Additionally, presence of the LQT3 genotype was associated with a five-fold increase in the risk of ACA or SCD.

The authors concluded that for LQTS genotypes in the 40 years or older age group, affected subjects are influenced by age-specific factors related to gender and clinical history, and congenital LQTS continues as a risk factor for life-threatening cardiac events.

[1] Goldberg I, Moss AJ, Peterson R, et al. Risk factors for aborted cardiac arrest and sudden cardiac death in children with the congenital Long-QT syndrome. Circulation 2008;117:2184-2191

[2] Goldenberg I, Moss AJ, Bradley J, et al. Long-QT syndrome after age 40. Circulation 2008;117:2192-2201

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