Rod Passman

Part 8: Adult Advanced Cardiovascular Life Support 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.

Cryptogenic stroke and underlying atrial fibrillation

BACKGROUND Current guidelines recommend at least 24 hours of electrocardiographic (ECG) monitoring after an ischemic stroke to rule out atrial fibrillation. However, the most effective duration and type of monitoring have not been established, and the cause of ischemic stroke remains uncertain despite a complete diagnostic evaluation in 20 to 40% of cases (cryptogenic stroke). Detection of atrial fibrillation after cryptogenic stroke has therapeutic implications. METHODS We conducted a randomized, controlled study of 441 patients to assess whether long-term monitoring with an insertable cardiac monitor (ICM) is more effective than conventional follow-up (control) for detecting atrial fibrillation in patients with cryptogenic stroke. Patients 40 years of age or older with no evidence of atrial fibrillation during at least 24 hours of ECG monitoring underwent randomization within 90 days after the index event. The primary end point was the time to first detection of atrial fibrillation (lasting >30 seconds) within 6 months. Among the secondary end points was the time to first detection of atrial fibrillation within 12 months. Data were analyzed according to the intention-to-treat principle. RESULTS By 6 months, atrial fibrillation had been detected in 8.9% of patients in the ICM group (19 patients) versus 1.4% of patients in the control group (3 patients) (hazard ratio, 6.4; 95% confidence interval [CI], 1.9 to 21.7; P<0.001). By 12 months, atrial fibrillation had been detected in 12.4% of patients in the ICM group (29 patients) versus 2.0% of patients in the control group (4 patients) (hazard ratio, 7.3; 95% CI, 2.6 to 20.8; P<0.001). CONCLUSIONS ECG monitoring with an ICM was superior to conventional follow-up for detecting atrial fibrillation after cryptogenic stroke. (Funded by Medtronic; CRYSTAL AF ClinicalTrials.gov number, NCT00924638.).

Cardiovascular disease in chronic kidney disease. A clinical update from Kidney Disease: Improving Global Outcomes (KDIGO)

Cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD) is high, and the presence of CKD worsens outcomes of cardiovascular disease (CVD). CKD is associated with specific risk factors. Emerging evidence indicates that the pathology and manifestation of CVD differ in the presence of CKD. During a clinical update conference convened by the Kidney Disease: Improving Global Outcomes (KDIGO), an international group of experts defined the current state of knowledge and the implications for patient care in important topic areas, including coronary artery disease and myocardial infarction, congestive heart failure, cerebrovascular disease, atrial fibrillation, peripheral arterial disease, and sudden cardiac death. Although optimal strategies for prevention, diagnosis, and management of these complications likely should be modified in the presence of CKD, the evidence base for decision making is limited. Trials targeting CVD in patients with CKD have a large potential to improve outcomes.

American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific Statement on Noninvasive Risk Stratification Techniques for Identifying Patients at Risk for Sudden Cardiac Death A Scientific Statement From the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention

The International Classification of Diseases, Tenth Revision, defines sudden cardiac death (SCD) as death due to any cardiac disease that occurs out of hospital, in an emergency department, or in an individual reported dead on arrival at a hospital. In addition, death must have occurred within 1

Part 6: Electrical therapies: Automated external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

The recommendations for electrical therapies described in this section are designed to improve survival from SCA and life-threatening arrhythmias. Whenever defibrillation is attempted, rescuers must coordinate high-quality CPR with defibrillation to minimize interruptions in chest compressions and to ensure immediate resumption of chest compressions after shock delivery. The high first-shock efficacy of newer biphasic defibrillators led to the recommendation of single shocks plus immediate CPR instead of 3-shock sequences that were recommended prior to 2005 to treat VF. Further data are needed to refine recommendations for energy levels for defibrillation and cardioversion using biphasic waveforms.

Sudden cardiac death and dialysis patients

Dialysis patients have extraordinarily high mortality rates. The death rate for all US dialysis patients in 2004 was 230 per 1000 patient‐years. Cardiac disease is the major cause of death in dialysis patients and accounts for 43% of all‐cause mortality. In the United States Renal Data System database 62% of cardiac deaths (or 27% of all deaths) are attributable to arrhythmic mechanisms. The estimated rate of sudden cardiac death in US dialysis patients in 2002 was 7% per year. There are several plausible explanations for the special vulnerability of dialysis patients to sustaining sudden cardiac death. Obstructive coronary artery disease, coupled with diminished tolerance to myocardial ischemia (in the setting of myocardial fibrosis and left ventricular hypertrophy), rapid electrolyte shifts in hemodialysis patients, and derangements in autonomic function may all contribute to this heightened risk of sudden cardiac death. This review focuses on the epidemiology of sudden cardiac death in dialysis patients, underlying mechanisms of sudden death, and potential interventions to reduce the risk of sudden cardiac death in dialysis patients (including medical therapy and defibrillators). It is unlikely that one single therapeutic intervention will prevent sudden cardiac death in dialysis patients; but a more modest (and attainable) goal is the implementation of multiple strategies to reduce the risk of sudden cardiac death in this special high‐risk population.

NON‐CORONARY HEART DISEASE IN DIALYSIS PATIENTS: Sudden Cardiac Death and Dialysis Patients

Dialysis patients have extraordinarily high mortality rates. The death rate for all US dialysis patients in 2004 was 230 per 1000 patient‐years. Cardiac disease is the major cause of death in dialysis patients and accounts for 43% of all‐cause mortality. In the United States Renal Data System database 62% of cardiac deaths (or 27% of all deaths) are attributable to arrhythmic mechanisms. The estimated rate of sudden cardiac death in US dialysis patients in 2002 was 7% per year. There are several plausible explanations for the special vulnerability of dialysis patients to sustaining sudden cardiac death. Obstructive coronary artery disease, coupled with diminished tolerance to myocardial ischemia (in the setting of myocardial fibrosis and left ventricular hypertrophy), rapid electrolyte shifts in hemodialysis patients, and derangements in autonomic function may all contribute to this heightened risk of sudden cardiac death. This review focuses on the epidemiology of sudden cardiac death in dialysis patients, underlying mechanisms of sudden death, and potential interventions to reduce the risk of sudden cardiac death in dialysis patients (including medical therapy and defibrillators). It is unlikely that one single therapeutic intervention will prevent sudden cardiac death in dialysis patients; but a more modest (and attainable) goal is the implementation of multiple strategies to reduce the risk of sudden cardiac death in this special high‐risk population.

Cryptogenic Stroke and underlying Atrial Fibrillation (CRYSTAL AF): design and rationale.

BACKGROUND Patients with atrial fibrillation (AF) are at increased risk for ischemic stroke. In patients who have suffered a stroke, screening for AF is routinely performed only for a short period after the stroke as part of the evaluation for possible causes. If AF is detected after an ischemic stroke, oral anticoagulation therapy is recommended for secondary stroke prevention. In 25% to 30% of stroke patients, the stroke mechanism cannot be determined (cryptogenic stroke). The incidence of paroxysmal AF undetected by short-term monitoring in patients with cryptogenic stroke is unknown, but has important therapeutic implications on patient care. The optimum monitoring duration and method of AF detection after stroke are unknown. The purpose of this study is to evaluate the incidence of AF and time to AF detection in patients with cryptogenic stroke using an insertable cardiac monitor. STUDY DESIGN The CRYSTAL AF trial is a randomized prospective study to evaluate a novel approach to long-term monitoring for AF detection in patients with cryptogenic stroke. Four hundred fifty cryptogenic stroke patients (by definition, without a history of AF) will be enrolled at approximately 50 sites in Europe, Canada, and the United States. Patients will be randomized in a 1:1 fashion to standard arrhythmia monitoring (control arm) or implantation of the subcutaneous cardiac monitor (Reveal XT; Medtronic, Inc, Minneapolis, MN) (continuous monitoring arm). OUTCOMES The primary end point is time to detection of AF within 6 months after stroke. The clinical follow-up period will be at least 12 months. Study completion is expected at the end of 2012.

Risk Stratification for Arrhythmic Sudden Cardiac Death Identifying the Roadblocks

Athough it is difficult to determine the precise number, the range for the number of sudden cardiac deaths (SCDs) per year in the United States alone has been reported from 184 000 to 462 000,1 with estimates that 50% to 70% are due to tachyarrhythmic mechanisms. Regardless of where within this range the true number lies, this represents a large epidemiological problem that warrants serious attention and attempts to identify solutions. There are many obstacles to achieving this laudable goal. First and foremost, although the vast majority of SCD victims have underlying structural heart disease (in particular, coronary artery disease), a significant percentage of SCD victims have previously unrecognized cardiac disease2; on autopsy, advanced coronary artery disease with or without evidence of unstable plaques and acute or healed myocardial infarctions (often clinically silent) are commonly detected.2,3 The American Heart Association estimates that 195 000 first silent myocardial infarctions occur per year.4 Strategies to reduce SCD among individuals without known cardiac disease must therefore focus on better screening and identification of risk factors for coronary disease, with either known risk factors or heretofore unknown or unidentified risk factors. In patients with known cardiac disease, there may be diverse pathogeneses for sudden death, including primary ventricular tachyarrhythmias and acute myocardial ischemia/infarction, among others. Although therapies exist for treatment of life-threatening ventricular tachyarrhythmias and prevention of myocardial infarction/coronary artery plaque rupture, significant challenges exist in identifying the individual patient within population subgroups who is at substantial personal risk of these events, and in whom the most intensive therapies could and should be applied. Although the incidence of out-of-hospital cardiac arrest due to ventricular tachycardia/fibrillation appears to be declining over time,4 this pathogenesis for SCD still occurs commonly. This article will therefore focus on the challenges and roadblocks …

Regulated expression of foreign genes in vivo after germline transfer.

Tight transcriptional control of foreign genes introduced into the germline of transgenic mice would be of great experimental value in studies of gene function. To develop a system in which the spatial and temporal expression of candidate genes implicated in cardiac development or function could be tightly controlled in vivo, we have generated transgenic mice expressing a tetracycline-controlled transactivator (tTA) under the control of a rat alpha myosin heavy chain promoter (MHC alpha-tTA mice), as well as mice harboring a candidate target gene implicated in the control of differentiation, Id1 (tet-Id1 mice). No expression of the target transgene was detected in any tissues of hemizygous tet-Id1 mice. Genetic crosses with MHC alpha-tTA mice resulted in transactivation of the Id1 transgene, but expression was restricted to heart, where tTA was expressed. Furthermore, transactivation of the target gene was tightly and reversibly controlled by systemic therapy with tetracycline, both in utero and postnatally. These studies demonstrate the feasibility of such a binary approach for tightly controlling the timing and extent of expression of transgenes in vivo. This approach should be generally useful for the ectopic expression of candidate genes in selected tissues during delineated developmental stages.