Antiarrhythmic therapy in patients with heart failure

In patients with severe chronic heart failure, many deaths are sudden due to life-threatening ventricular arrhythmias. Supraventricular arrhythmias such as paroxysmal or chronic atrial fibrillation may also cause serious complications in those patients due to acute loss of atrial contraction, pump failure during rapid ventricular response and embolic events. Two therapeutic strategies are currently available for therapy and prevention of malignant ventricular arrhythmias and subsequent sudden arrhythmic death: antiarrhythmic drug therapy and implantable defibrillators. However, selection of the most beneficial strategy for the individual patient to reduce the risk of sudden death remains a major challenge in cardiology. Betablockers exert a favorable antiarrhythmic action without increasing proarrhythmia, thus betablockers may serve as a basic medication in patients at risk for sudden death. However, the general use of antiarrhythmic drug therapy for symptomatic ventricular arrhythmias is not recommended, as these drugs have been shown to increase mortality in patients with severe congestive heart failure due to proarrhythmic or negative inotropic effects (e.g. class Ia antiarrhythmics). Even class III antiarrhythmic drugs such as amiodarone, which has been studied sufficiently in patients with left ventricular dysfunction, is not effective enough for significant reduction of cardiac mortality in patients with symptomatic ventricular arrhythmias and depressed ventricular function (e.g. EMIAT, CAMIAT). But as a positive result of available studies, amiodarone does not increase mortality in those patients. Dofetilide has also not been shown to prolong life significantly by suppressing malignant ventricular arrhythmias (DIAMOND-Study). In patients with symptomatic ventricular arrhythmias or aborted sudden death, ICD therapy has been proven to be superior to antiarrhythmic drug therapy in cardiac mortality reduction as a secondary prevention strategy (e.g. AVID, CASH, CIDS). For primary prevention of sudden arrhythmic death in high risk patients, 2 studies (MADIT, MUSST) have already demonstrated favorable results, decreasing mortality by ICD therapy in selected patient populations with partly-reduced ventricular function and unsustained but inducible ventricular tachycardias. This topic is, however, undergoing further evaluation by ongoing trials (e.g. MADIT II, SCD-HeFT). From available data, antiarrhythmic drug therapy in high risk patients is not justified on a routine basis, whereas ICD therapy as a secondary and perhaps primary prevention strategy will significantly reduce cardiac mortality in patients with severe heart failure. Sotalol, a class III antiarrhythmic agent, has recently been shown to reduce ICD-shock delivery which indicates that concomitant drug therapy in patients with an ICD device already implanted may be beneficial in terms of reducing ICD discharges due to ventricular and supraventricular tachycardias. In patients with paroxysmal atrial fibrillation and congestive heart failure, restitution of sinus rhythm is the primary therapeutic goal which can be safely achieved by amiodarone and dofetilide (DIAMOND). In the latter, continuous monitoring of the patient is mandatory because of increased risk of torsade de pointes arrhythmias during the first days of drug administration. In patients with chronic atrial fibrillation rate control and anticoagulation with warfarin is the primary therapeutic option, which can be achieved with either drug treatment (Digoxin, betablockers, amiodarone) or by His bundle ablation with subsequent pacemaker insertion.     

Management of Nonsustained Ventricular Tachycardia Guided By Electrophysiological Testing

Two hundred eighty patients with spontaneous nonsusfained ventricular tachycardia were treated based on the results of electrophysiological testing. Seventy-nine patients had no evidence of structural heart disease, 134 had coronary artery disease, 43 had idiopathic dilated cardiomyopathy, and 24 patients had miscellaneous types of heart disease. Sustained monomorphic ventricular tachycardia was induced during electrophysiological testing in the drug free state in 52 of 280 patients (19%). Ventricular tachycardia was induced more frequently in patients with coronary artery disease (32%) than in any of the other groups (P < 0.001). The patients with inducible sustained monomorphic ventricular tachycardia underwent a mean of 1.9 ± 1.3 drug trials. Twenty-five patients had the induction of ventricular tachycardia suppressed by pharmacological therapy and were treated with the drug judged to be effective during electropharmacological testing. Twenty-seven patients continued to have inducible sustained monomorphic ventricular tachycardia despite antiarrhythmic therapy and were discharged on the drug that made induced ventricular tachycardia best tolerated. Forty-five of 280 patients (16.1%) died during a mean follow-up period of 19.6 ± 14.4 months, There were 15 sudden cardiac deaths, 21 nonsudden cardiac deaths, 6 noncardiac deaths, and 3 deaths that could not be classified. Sudden cardiac death mortality was lowest in the patients without structural heart disease (0% at 2 years), intermediate in the patients with coronary artery disease and miscellaneous heart disease (4% al 2 years), and highest in the patients with idiopathic dilated cardiomyopathy (13% at 2 years; P < 0.01 for pairwise comparisons). No patient treated with a drug that had suppressed the induction of sustained ventricular tachycardia died suddenly during the follow-up period whereas four of 27 patients who were discharged on “ineffective antiarrhythmic drugs” and 11 of 228 patients without inducible sustained ventricular tachycardia experienced sudden cardiac death during the follow-up period. By multivariate analysis, ejection fraction and inducible ventricular tachycardia during the predischarge eiectrophysiological test were independent predictors of sudden cardiac death. In conclusion, in patients with spontaneous nonsustained ventricular tachycardia: (1) Arrhythmia inducibility varies depending on the underlying heart disease. Ventricular tachycardia is most often inducible in patients with coronary artery disease and least often in patients without structural heart disease; (2) With the exception of patients with idiopathic dilated cardiomyopathy, management of patients with nonsustained ventricular tachycardia guided by electrophysiological testing appears to result in a low incidence of sudden cardiac death although effects on total mortality are less impressive; and (3) Patients with idiopathic dilated cardiomyopathy and patients with other heart diseases who continue to have inducible ventricular tachycardia despite antiarrhythmic drug therapy are at substantial risk of sudden cardiac death.     

A brief history of sudden cardiac death and its therapy

At the end of the 19th century, there was both experimental and clinical evidence that coronary artery obstruction causes ventricular fibrillation and sudden death and that fibrillation could be terminated by electric shocks. The dominant figure at that time was McWilliam, who in 1923 complained that "little attention was given to the new view for many years." This remained so for many decades. It was not until the 1960s that the medical profession became aware of the magnitude of the problem of sudden death and began to install coronary care units where arrhythmias could be monitored and prompt defibrillation could be delivered. This approach was pioneered by Julian in 1961. Milestones that allowed this development were open-chest defibrillation by Beck, closed-chest defibrillation by Zoll, cardiac massage by Kouwenhoven et al., and development of the DC defibrillator by Lown. In 1980, Mirowski et al. implanted the first implantable cardioverter defibrillator (ICD) in a patient. Thereafter, the use of the ICD increased exponentially. Several randomized trials, largely in patients with coronary artery disease and left ventricular dysfunction or in patients with documented lethal arrhythmias, showed beyond doubt that the ICD is superior to antiarrhythmic drug therapy in preventing sudden death, although a number of trials showed no effect. Trials on antiarrhythmic drugs were disappointing. Sodium channel blockers and "pure" potassium channel blockers actually increase mortality, calcium channel blockers have no effect, and, although amiodarone reduces arrhythmic death, it had no effect on total mortality in the 2 largest trials. Only the beta-blockers have been proven to reduce the incidence of sudden death, but their effect appears not to be related to the suppression of arrhythmias but rather to the reduction in sinus rate. Drugs that prevent ischemic events, or lessen their impact, such as anticoagulants, statins, angiotensin-converting enzyme inhibitors, and aldosteron antagonists, all reduce the incidence of sudden death.     

Malignant Ventricular Arrhythmias in Patients with Mitral Valve Prolapse and Mild Mitral Regurgitation

Mitral valve prolapse (MVP) is a common disorder that, in general, has a good prognosis. Rare occasions of sudden death have been reported in patients with MVP and it is presumed that the basis of sudden death is arrhythmic. We report seven patients with moderate to severe MVP and malignant ventricular arrhythmias. All patients had trivial to mild mitral regurgitation and normal left ventricular function. Three patients presented with syncope, two with out-of-hospital cardiac arrest, and three with recurrent palpitations and presyncope. In a mean follow-up period of 2.5 years (range 6 months to 5 years), two patients died suddenly despite successful control of their nonsustained ventricular tachycardia (VT) with sotalol as shown by ambulatory monitoring. Two patients, who had sustained VT despite antiarrhythmic drug therapy, had mitral valve surgery, however, monomorphic VT could be induced in both even after surgery. The arrhythmias in the remaining three patients are controlled on antiarrhythmic drugs. We conclude that a selected subset of patients with MVP, malignant ventricular arrhythmias, and miid mitral regurgitation are at risk of sudden death. Syncope, inferolateral repolarization changes, complex ventricular ectopy, and a markedly myxomatous valve may be pointers to higher risk of sudden death and mitral valve surgery may not provide control of ventricular arrhythmias.     

Survivors of acute myocardial infarction: who is at risk for sudden cardiac death?

Coronary artery disease is the leading cause of death in the United States. Approximately half of the deaths attributable to coronary artery disease are sudden cardiac deaths. A logical approach to prevention of sudden death is to identify those who are at risk and then to initiate effective therapy. Left ventricular dysfunction, frequent ventricular ectopic activity, nonsustained ventricular tachycardia, and late potentials have been identified as markers for increased risk of sudden cardiac death. The sensitivity and specificity of these risk factors vary, and the positive predictive power is less than satisfactory. The value of invasive electrophysiologic testing for risk stratification in the general postinfarction patient population remains unclear. In addition to these diagnostic difficulties, prevention of sudden death also has been limited by imperfect efficacy and potential lethal effects of the currently available antiarrhythmic agents. Automatic implantable defibrillators are effective for aborting sudden death; however, the potential for more general use of automatic defibrillators in asymptomatic but high-risk postinfarction patients has not been evaluated.     

Induced Sustained Ventricular Tachycardia in Nonischemic Dilated Cardiomyopathy: Dependence on Clinical Presentation and Response to Antiarrhythmic Agents

Thirty-one patients with nonischemic dilated cardiomyopathy either idiopathic or due to regurgitant valvular disease were studied in the cardiac electrophysiology lab. The indications for study were sustained ventricular tachycardia (VT) in 26, ventricular fibrillation (VF) in 11, and syncope of unknown etiology in 4. Sustained VT was reproducibly induced in 17 patients, including 12 with a history of sustained VT, 2 with VF and 3 with syncope. Of 15 patients undergoing serial antiarrhythmic drug studies, sustained VT was rendered noninducible or nonsustained in 23. Three had recurrent arrhythmic events while on therapy predicted to be effective. One of 2 patients discharged on a regimen predicted to be ineffective had a recurrence of sustained VT that resulted in cardiac arrest. Of 14 patients in whom sustained VT could not he reproducibly induced, 2 subsequently had spontaneous occurrences of sustained VT, and 2 experienced aborted sudden death. These results suggest the following; (1) the induction of sustained VT in the setting of nonischemic dilated cardiomyopathy is dependent on the clinical presentation; (2) antiarrhythmic drugs frequently render sustained VT noninducible or nonsustained; (3) antiarrhythmic drug suppression of inducible sustained VT predicts long-term prevention of spontaneous recurrences; and (4) noninducibility of sustained VT in the baseline state does not predict freedom from subsequent episodes of VT or sudden death.     

The impact of implantable cardiac defibrillators for primary prophylaxis in the community: baseline risk and clinically meaningful benefits

OBJECTIVE: To estimate the baseline risk of arrhythmic death required for prophylactic implantable cardiac defibrillators (ICDs) to result in clinically meaningful survival benefits in the population. BACKGROUND: While proven efficacious, the absolute survival impact of ICDs for the primary prevention of sudden cardiac death among patients with left ventricular (LV) dysfunction is highly dependent upon patient's baseline risk of arrhythmic death. METHODS: Using echocardiographic data from a random sample of patients identified from community echocardiographic laboratories, patients with moderate or severe LV dysfunction (ejection fraction < 35%) were linked to administrative databases to characterize baseline mortality risk (median follow-up duration of 4.85 years). Relative efficacy was ascertained from meta-analysis and clinical trial data. The baseline annual risk of arrhythmic death required for prophylactic ICDs to result in clinically meaningful survival benefits in the population was estimated at different ranges of relative efficacy and numbers needed to treat (NNTs) thresholds. RESULTS: LV dysfunction was a significant independent predictor of adverse outcomes. In total, 35.4% of the patients with moderate to severe LV dysfunction died during the follow-up period. Assuming a base-case relative efficacy of 66%, we estimated that the baseline risk for arrhythmic death required to exert a clinically meaningful NNT threshold of 50 in order to prevent one death (from any cause) was 3% per year or higher. CONCLUSIONS: The survival impact and cost-effectiveness of prophylactic ICDs in the population will depend upon the ability to risk-stratify and identify patients whose baseline risk for sudden cardiac death exceed 3% per year.     

Out-of-hospital cardiac arrest in patients with cardiac amyloidosis: presenting rhythms, management and outcomes in four patients

Primary systemic amyloidosis (AL) is a well-recognized systemic disease, and cardiac amyloidosis accounts for 10% of all nonischemic cardiomyopathies [J S C Med Assoc 97 (2001) 201-206]. The median survival of patients with symptomatic congestive heart failure secondary to cardiac amyloidosis is 4 months [New Engl J Med 336 (1997) 1202-1207; Am J Med 100 (1996) 290-298]. The cause of death in most patients is refractory congestive heart failure or sudden arrhythmic [Mayo Clin Proc 59 (1984) 589-597]. While there are reports of in-hospital arrhythmic deaths in these patients, there are no detailed reports that describe the presentation and management of patients with cardiac amyloidosis who have experienced an out-of-hospital cardiac arrest (OHCA). We describe here our experience with four patients with AL who had an OHCA, including presenting rhythms, interventions, and outcomes.     

Long-Term Outcome Following Programmed Electrical Stimulation in Patients with High-Grade Ventricular Ectopy

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.     

Sudden Death Mortality in Implantable Cardioverter Defibrillator Patients

Implanfable Cardioverter defibrillator (ICD) prevention of sudden cardiac death (SCD) is not absolute and our experience was reviewed to determine the frequency and nature of SCO in this population. The incidence and cause of mortality in 56 consecutive patients, who underwent ICD implantation beginning May 1982 with follow-up through May 19, 1990 were analyzed. Twenty-one patients died, 33% of the mortality was due to SCD, and 52% of deaths may be considered arrhythmic. The cumulative 1, 3, and 5 year SCD survivals were 93%, 89%, and 75%. All seven patients dying of SCD presented initially with SCD, all received previous shocks prior to SCD, and two of the seven patients had devices that were probably inactive at the time of death. We conclude that ICDs reduce but by no means eliminate arrhythmic death, particularly in those at highest risk for SCD. Arrhythmic death remained the most common cause of death in this population.     

Evidence for the cardioprotective effects of omega-3 Fatty acids

OBJECTIVE: To review available literature regarding the cardiovascular effects of marine-derived Omega-3 fatty acids and evaluate the benefit of these fatty acids in the prevention of coronary heart disease. DATA SOURCES: Biomedical literature accessed through a MEDLINE search (1966-April 2002). Search terms included fish oil, omega-3 fatty acid, sudden death, hypertriglyceridemia, myocardial infarction, and mortality. DATA SYNTHESIS: Following an early 1970's observational investigation that Omega-3 fatty acids may reduce the occurrence of myocardial infarction-related deaths in Greenland Eskimos, additional trials have been conducted that support this finding. Epidemiologic and clinical trial data suggest that Omega-3 fatty acids may reduce the risk of cardiovascular-related death by 29-52%. In addition, the risk of sudden cardiac death was found to be reduced by 45-81%. Possible mechanisms for these beneficial effects include antiarrhythmic properties, improved endothelial function, antiinflammatory action, and reductions in serum triglyceride concentrations. Omega-3 Fatty acids are fairly well tolerated; potential adverse effects include bloating and gastrointestinal distress, "fishy taste" in the mouth, hyperglycemia, increased risk of bleeding, and a slight increase in low-density-lipoprotein cholesterol. CONCLUSIONS: Omega-3 Fatty acids may be beneficial and should be considered in patients with documented coronary heart disease. They may be particularly beneficial for patients with risk factors for sudden cardiac death.     

The Automatic Implantable Defibrillator

New Modality for treatment of life-threatening ventricular arrhythmias. The automatic implantable defibrillator continuously monitors cardiac rhythm, identifies ventricuiar fibrillation and then delivers corrective defibrillatory discharges when indicated: it weighs 250 grams and has a volume of 145 cc. When a suitable arrhythmia is detected, a 25 Joule pulse is delivered through a superior vena cava catheter electrode and another electrode placed over the cardiac apex. As oj March 1981, sixteen survivors of multiple cardiac arrests refractory io antiarrhythmic therapy had undergone implantation of the automatic defibrillator. There was no operative mortality and the morbidity was minimal. Electrophysiologic studies were performed before and after surgery to confirm failure of drug therapy and to ensure the device's ability to terminate malignant arrhythmias. Eight spontaneous and fourteen of the seventeen induced malignant arrhythmias were properly recognized and corrected by the device. The discharges were well tolerated by awake patients. A number of problems including recycling delays and spurious discharges have been identified and corrected. There were three late deaths with pulmonary edema noted in two patients, and asystole in one. The autopsies revealed no myocardial damage attributable to the automatic defibrillator. Although the ultimate role of this approach to prevention of sudden arrhythmic death has yet to be determined, the results obtained to date are encouraging and indicate that a useful modality for treating malignant ventricular arrhythmias has been added to our armamentarium. (PACE, Vol. 5, May-June, 1982)     

QRS duration in high-resolution methods and standard ECG in risk assessment after first and recurrent myocardial infarctions

Background: Prolonged QRS duration (QRSd) is associated with increased mortality after myocardial infarction (MI). Only little data exist about its predictive ability and relationships to clinical variables in the present era of active treatment of myocardial ischemia and cardiac dysfunction. We investigated whether QRSd in high-resolution methods and standard ECG predict arrhythmic events and cardiac death in post-infarction patients with cardiac dysfunction and how it relates to clinical variables, with a special emphasis on history of previous MI.
Methods and Results: Patients (n = 158) with acute MI and cardiac dysfunction had magnetocardiography (MCG), signal-averaged ECG (SAECG), and ECG registered at discharge. Patients with a previous MI had significantly longer QRSd although their left ventricular function was almost similarly impaired. During the mean follow-up of 50 ± 15 (range 1–72) months, 32 patients died and 17 (53%) of the deaths were classified as cardiac. Eighteen patients had an arrhythmic event. QRSd >121 ms in MCG and >114 ms in SAECG were significant predictors of arrhythmic events and cardiac death, whereas QRSd in ECG predicted only cardiac death. In multivariate analysis, QRSd in MCG (hazard ratio (HR) = 3.6, P = 0.007) and SAECG (HR = 4.6, P = 0.016) predicted only arrhythmic events, whereas QRSd in ECG was an independent predictor of cardiac death.
Conclusions: Prolonged QRSd in MCG and SAECG are powerful indicators of the arrhythmia substrate in post-infarction patients with cardiac dysfunction, whereas prolonged QRSd in standard ECG associates with increased risk of cardiac death.     

Advances in Imaging of the Cardiac Neuronal System

Left ventricular ejection fraction (LVEF) is a useful tool for stratifying risk for heart failure progression and life-threatening arrhythmic events. Yet, the clinical course of heart failure patients with severely reduced LVEF is variable, and the majority of patients who die suddenly do not have an LVEF ≤35%. A recently completed large multicenter trial, ADMIRE-HF, confirms that cardiac neuronal imaging with I-123 metaiodobenzylguanidine is an important independent predictor of heart failure progression and sudden cardiac death. Data from that study indicate that heart failure patients with severe impairment of cardiac sympathetic innervation are at highest risk for heart failure progression, heart failure patients with moderate impairment of sympathetic innervation are at highest risk for life-threatening arrhythmic events, and heart failure patients with preserved sympathetic innervation are at low risk for either death due to heart failure progression or sudden cardiac death.     

Drug and drug-device therapy in heart failure patients in the post-COMET and SCD-HeFT era

Reduced left ventricular ejection fraction and heart failure are the most important risk factors for sudden cardiac death. Recent trials have contributed to the knowledge base of critical therapies for the treatment of left ventricular systolic dysfunction and heart failure as it relates to arrhythmic and sudden cardiac death. Both pharmacologic and device therapies can reduce sudden cardiac death. The trials discussed in this paper have identified the pharmacologic and device interventions that are likely to improve the length and quality of life of the patient with left ventricular dysfunction and reduce the risk of sudden cardiac death. The mortality and anti-arrhythmic effects of angiotensin-converting enzyme inhibitors and beta-blockers have been confirmed in large-scale controlled clinical heart failure trials. Recent trials have evaluated which agents are most effective and which patients will derive the most benefit from device therapy in terms of the reduction in the risk of sudden cardiac death and in the amelioration of heart failure. The recent data from the Carvedilol or Metoprolol European Trial (COMET) and the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) are discussed as the latest in the series of landmark studies that have shaped the current approaches to treating patients with heart failure and that have altered the heart failure treatment paradigm.     

Use of Left Ventricular Ejection Fraction or Wall-Motion Score Index in Predicting Arrhythmic Death in Patients Following an Acute Myocardial Infarction

All-cause mortality and morbidity following an acute myocardial infarction (AMI) are correlated to LV systolic dysfunction. The correlation is closest with mortality and morbidity associated with congestive heart failure (CHF). Prediction of arrhythmic death in patients with AMI relies on the correlation between arrhythmic death and "sudden unexpected death" defined as death within 1 hour of onset of new symptoms. Assessment of late potentials, heart rate variability (HRV), T wave alternans, arrhythmias seen on Holter monitoring or during exercise testing, electrophysiological testing, and baroreceptor assessment have all proven to be useful in the prediction of sudden death even when LV systolic function is known. In selected populations HRV is superior to LV systolic function assessment in predicting sudden death and/or arrhythmic events, and may even predict all-cause mortality with the same precision. Comparisons of other methods with LV function assessment should be interpreted with care because most methods have been evaluated in subgroups of infarct patients with a low risk of death. Results from a large series of high risk patients with AMI (the TRAndolapril Cardiac Evaluation study) have shown that even in patients with severe depressed LV systolic function around one-third of the patients will die suddenly. The current situation is that LV function appears to be the best method of predicting death whereas other methods appear very promising for detecting arrhythmic death in more selected populations. The optimal method for selecting patients at high risk of arrhythmic death has not yet been developed, but a combination of LV function and another method, i.e., HRV, appears promising. This may ensure that the enrolled patients have an increased risk of death and that this risk will be due to arrhythmic events. Patients with LVEF of 10% or less can be excluded as they will most likely not die suddenly.     

Arrhythmic risk stratification after myocardial infarction using ambulatory electrocardiography signal averaging

Ambulatory ECG had been proposed to examine the amplified high resolution signal-averaged electrocardiogram (SAECG). Clinical investigations are required to confirm the predictive value of such a high resolution technique in arrhythmic risk stratification. The prognostic value of ambulatory Holter SAECG was evaluated in 108 postinfarction patients for the purpose of predicting the occurrence of serious arrhythmic (SARR) events (sudden cardiac death [SCD], VT, or VF) in comparison with classical real-time SAECG. During the 42+/-8 months of follow-up, the sudden cardiac death mortality was 4.6% (five deaths), six (5.6%) patients had VT, and one (0.9%) VF. QRSd was found to be the most predictive parameter using ROC curves analysis for SAAR + outcome (W = 0.833 and W = 0.803 for 25-250 Hz and 40-250 Hz filters, respectively) followed by RMS (W = 0.766 and W = 0.721) and LAS (W = 0.759, W = 0.709) (all P < 0.01). Abnormal Holter SAECG for 25 and 40-Hz LP filter were significant predictors of SARR+ by log-rank test (P < 0.01, P < 0.05, respectively). This study confirms that valuable prognostic information can be obtained from the ambulatory high resolution ECG technique and that Holter SAECG may predict arrhythmic risk in a postinfarction population.     

Arrhythmias

There are several underlying factors including anatomical substrates (coronary artery disease, cardiomyopathy, valvular disease, congenital heart disease, WPW syndrome) and modulating factors(autonomic nervous system, electrolyte balance, drugs) which may induce sudden cardiac death. Although studies evaluating mechanisms of sudden cardiac death are increasing, evaluation of risk of each patient and effectiveness of preventive treatments are still inadequate. Sudden death due to life threatening arrhythmias in the out-of-hospital situation can be resuscitated by non-medical staff with automated external defibrillator. In these resuscitated high-risk patients implantable cardioverter and defibrillator could be used to prevent sudden death due to unpreventable further arrhythmic episodes. Widespread availability of automated external defibrillator is mandatory.     

Disaster events and the risk of sudden cardiac death: a Washington State investigation

BACKGROUND: Psychological distress following disaster events may increase the risk of sudden cardiac death. In 2001, the Nisqually earthquake and the 11 September terrorist attacks profoundly affected Washington state residents. HYPOTHESIS: This research investigated the theory that the incidence of sudden cardiac death would increase following these disaster events. METHODS: Death certificates were abstracted using a uniform case definition to determine the number of sudden cardiac deaths for the 48-hour and one-week periods following the two disaster events. Sudden cardiac deaths from the corresponding 48-hour and one-week periods in the three weeks before the events, and the analogous periods in 1999 and 2000 were designated as control times. Using t-tests, the number of sudden cardiac deaths for the periods following the disaster events was compared to those of the control periods. RESULTS: In total, 32 sudden cardiac deaths occurred in the four counties affected by the Nisqually earthquake during the 48 hours after the event, compared to an average of 22 +/- 3.5 (standard deviation) in the same counties during the control periods (p = 0.02). No difference was observed for the one-week period (94 compared to 79.2 +/- 12.4, p = 0.28). No difference was observed in the number of sudden cardiac deaths in the 48-hours or one-week following the terrorist attacks compared to control periods. CONCLUSIONS: A local disaster caused by a naturally occurring hazard, but not a geographically remote human disaster, was associated with an increased risk of sudden cardiac death. A better understanding of the underlying mechanisms may have implications for prevention of sudden cardiac death.     

Chemoreflexsensitivity in Patients with Survived Sudden Cardiac Arrest and Prior Myocardial Infarction

For evaluation of patients with an increased risk of sudden cardiac death, the analyses of ventricular late potentials, heart rate variability, and baroreflexsensitivity are helpful. But so far, the prediction of a malignant arrhythmic event is not possible with sufficient accuracy, For a better risk stratification other methods are necessary. In this study the importance of the ChRS for the identification of patients at risk for ventricular tachyarrhythmic events should be investigated. Of 41 patients included in the study, 26 were survivors of sudden cardiac arrest. Fifteen patients were not resuscitated, of whom 6 patients had documented monomorphic ventricular tachycardia and 9 had no ventricular tachyarrhythmias in their prior history. All patients had a history of an old myocardial infarction (> 1 year ago). For determination of the ChRS the ratio between the difference of the RR intervals in the ECG and the venous pO₂ before and after a 5-minute oxygen inhalation via a nose mask was measured (ms/mmHg). The 26 patients with survived sudden cardiac death showed a significantly decreased ChRS compared to those patients without a tachyarrhythmic event (1.74 ± 1.02 vs 6.97 ± 7.14 ms/mmHg, P < 0.0001). The sensitivity concerning a survived sudden cardiac death amounted to 88% for a ChRS below 3.0 ms/mmHg. During a 12-month follow-up period, the ChRS was significantly different between patients with and without an arrhythmic event (1.64 ± 1.06 vs 4.82 ± 5.83 ms/mmHg, P < 0.01). As a further method for evaluation of patients with increased risk of sudden cardiac death after myocardial infarction the analysis of ChRS seems to be suitable and predicts arrhythmias possibly more sensitive than other tests of neurovegetative imbalance. The predictive importance has to be examined by prospective investigations in larger patient populations.