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At least 19 recordsLinked to original sources

PubMed1995

Is ventricular wall stress rather than left ventricular hypertrophy an important contributory factor to sudden cardiac death?

Sudden cardiac death comprises a significant proportion of cardiac mortality in Western society. Left ventricular hypertrophy has been identified by many authors as a possible risk factor for sudden cardiac death, however, left ventricular hypertrophy develops in response to external stimuli on the heart as a means of normalizing wall stress. It is possible that the fundamental abnormalities in wall stress, rather than the left ventricular hypertrophy itself, pose the increased risk of sudden death. Left ventricular hypertrophy, the consequence of raised wall stress, is easy to measure and easy to study and it is understandable why this parameter should have received more attention. Wall stress by contrast is difficult to measure, and worse, is variable throughout the ventricle so that it cannot be measured in a single quantifiable figure. As a consequence, only a limited amount of attention has been paid to wall stress as a possible trigger mechanism for cardiac arrhythmia. However, there is evidence from both basic and clinical research to suggest that raised wall stress may be a risk factor for sudden cardiac death and cardiac arrhythmia. This review discusses the evidence for and against left ventricular hypertrophy and wall stress as risk factors for sudden cardiac death, and also presents recent evidence that left ventricular hypertrophy in isolation can protect the heart against the arrhythmogenic effects of raised wall stress.

Death, Sudden, Cardiac↗

PubMed1999

[Antiarrhythmic agents in the prevention of sudden cardiac death].

Sudden cardiac death due to ventricular arrhythmias remains a significant problem. In most studies about 50% of all death related to coronary artery disease and heart failure are sudden and unexpected and are caused by acute fatal ventricular tachycardia and fibrillation. Most of the patients suffering sudden cardiac death have some kind of structural heart disease but 80% of SCD events are associated with coronary artery disease, 10-15% with dilated and hypertrophic cardiomyopathy, and only small fraction with the less common disorders as valvular heart disease, ventricular dysplasia and cardiac involvement in sarcoidosis or amyloidosis. In some patients the anomaly responsible for sudden cardiac death is not structural but mainly electrical as in patients with the long QT syndrome, WPW syndrome or in patients with a proarrhythmic effect from antiarrhythmic drugs. In this review, data from clinical trials and other studies on on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention sudden cardiac death in high risk patients. Taken together with the mortality data routine prophylactic use of class I antiarrhythmic drugs in the patients survivors of acute myocardial infarction and patients with heart failure is associated with increased risk of death. Conversely beta-blockers are associated with significant reduction in nonfatal cardiac arrest in the short term trials and sudden cardiac death in long term trials. These benefits are likely due to relief ischemia, reduction of heart rate and maintenance favourable autonomic nervous system balance. Overall trial data on amiodarone suggests that this agent is effective in reducing the risk of death in survivors of cardiac arrest, post infarction patients, and patients with heart failure but the routine prophylactic use of amiodarone remains of uncertain efficacy. The physician who considers the use of antiarrhythmic medications in patients with ventricular arrhythmias must be aware of which arrhythmias are malignant or potentially malignant and which are benign and the decision to initiate antiarrhythmic therapy should be based on consideration of the patients absolute mortality risk.

Anti-Arrhythmia Agents↗

PubMed2003

Sudden cardiac death.

Sudden cardiac death is a rare but devastating event. The majority of cases in young athletes are caused by congenital cardiac abnormalities that are routinely clinically silent before causing sudden death. An optimal screening practice to help identify underlying asymptomatic cardiac abnormalities has met with much debate. Beyond the American Heart Association's recommendations for cardiovascular screening guidelines for the preparticipation physical examination [47], there are conflicting views regarding the use of more advanced diagnostic screening tests. Athletes in whom a potentially life-threatening cardiovascular abnormality is found face the probability of being restricted from participating in certain types of athletic activity. Participation guidelines for athletes with cardiovascular disease are detailed in the recommendations of the 26th Bethesda Conference [36]. Future goals should continue to focus on the prevention of SCD. The development of a cost-effective screening process that incorporates the use of echocardiography, although having its own set of inherent limitations, may prove to be the most viable option.

Cardiomegaly↗

PubMed1990

Gender difference in the risk factors for sudden cardiac death.

Sudden cardiac death is most often caused by ventricular dysrhythmias. Although women have an incidence of sudden death lower than that of men, 34% of coronary deaths in women are sudden deaths. The atherogenic risk factors do not predict which women are at the highest risk of sudden cardiac death. Left ventricular hypertrophy is a strong risk factor for sudden cardiac death in women. Asymptomatic ventricular dysrhythmias, a risk factor for death after myocardial infarction in men, do not increase the risk of death in women. This gender difference in the risk of sudden cardiac death deserves further attention, since it affects the evaluation of interventions designed to reduce the rate of sudden cardiac death.

Arrhythmias, Cardiac↗

PubMed2000

The role of the implantable cardioverter-defibrillator for prevention of sudden cardiac death.

Sudden cardiac death, which accounts for approximately 350,000 deaths each year, is a major health care problem. Antiarrhythmic drugs have not been reliable in preventing sudden cardiac death. Although beta-blockers, angiotensin-converting enzyme inhibitors, and revascularization play a role in prevention of sudden cardiac death, the development and subsequent refinement of the implantable cardioverter-defibrillator has made the most important contribution to its management. Several randomized, controlled trials have demonstrated improved survival in patients resuscitated from cardiac arrest. Two recent trials also suggest a role for primary prevention in selected patients with coronary artery disease, ventricular dysfunction, and nonsustained ventricular tachycardia in whom sustained ventricular tachycardia is induced. Further technological refinements and development of new, more sensitive risk stratifiers with a higher positive predictive value for sudden cardiac death will expand the indications for this life-saving therapy.

Anti-Arrhythmia Agents↗

PubMed2004

Calstabin2 - a new target in sudden cardiac death.

Sudden cardiac death is occasionally observed in people with structurally normal hearts. Calstabin2 stabilises the ryanodine receptor (RyR)2, preventing aberrant activation of the sarcoplasmic reticulum calcium channel during the resting phase of the cardiac muscle. Calstabin2-deficient mice have structurally normal hearts, but exhibit exercise-induced cardiac ventricular arrhythmias that cause sudden death. In three models of arrhythmias, the calstabin2 stabiliser JTV519 did not prevent arrhythmias in calstabin2(-/-) mice, but reduced the arrhythmias in calstabin2(+/-) mice, illustrating the antiarrhythmic potential of stabilising calstabin2. Familial polymorphic ventricular tachycardia (FPVT) has been linked to three missense mutants (P2328S, Q4201R and V4653F) in the hRyR2 gene of Finnish families. In HEK293 cells, these RyR2 mutants showed less binding of (35)S-calstabin2 than the wild-type, indicating a reduced binding affinity. JTV519 rescues the gain-of-function defect in the RyR2-P2328S channels via increased binding of calstabin2 to the channel complex. In heart failure (HF), there is excessive disassociation of calstabin2 from the RyR2 receptor, and JTV519 has been shown to be beneficial in an animal model of HF. In conclusion, calstabin2 is an important new target in sudden cardiac death associated with either FPVT or HF.

Comment↗

PubMed2005

Secondary prevention of sudden cardiac death.

Sudden cardiac death is still the largest cause of natural death in western countries, especially in patients with coronary artery disease and in those who have already experienced an episode of resuscitated out-of-hospital cardiac arrest or ventricular tachycardia. Prevention of arrhythmia recurrences (i.e. secondary prevention) in these patients remains a challenge for the cardiologist. To date no studies have demonstrated that drug therapy can be of some value in preventing arrhythmia recurrences or sudden death in these patients, and only cardioverter-defibrillator (ICD) implantation resulted effective in reducing mortality rate. It remains, however, to be defined which patients who survived an out-of-hospital cardiac arrest or who already experienced a sustained ventricular tachycardia could benefit the most from an ICD, but to date no invasive or non-invasive tests have proven to be effective for this stratification. Vaughan-Williams class II and III drugs could be of some value in reducing tachycardia cycle length thus increasing antitachycardia pacing efficacy and reducing ICD shocks.

Anti-Arrhythmia Agents↗

PubMed2000

Therapeutic developments in sudden cardiac death.

Sudden cardiac death is characterised by the unexpected death of a patient who has been clinically stable. It is frequently due to the development of ventricular tachyarrhythmias. With appropriate treatment, patients can be appropriately resuscitated. Clinically, it is essential to develop treatment strategies to prevent such an episode, as most patients do not survive out-of-hospital cardiac arrest. beta-Blockers are an effective pharmacological therapy in patients following myocardial infarction and in those with congestive heart failure. They may also be effective in other types of heart disease. Anti-arrhythmic agents are not useful as prophylactic drug therapy for reducing mortality in patients at risk for sudden cardiac death. Amiodarone is a notable exception, which may have some benefit, particularly in some subgroups. The implantable cardioverter-defibrillator has emerged as the most effective therapy for preventing sudden cardiac death in high-risk patients. Further work is required to enhance the characterisation of high-risk patients. Genetic analyses in patients with cardiovascular disorders may also identify new approaches to the prevention of sudden cardiac death.

Adrenergic beta-Antagonists↗

PubMed1987

An animal model to examine the response to environmental stress as a factor in sudden cardiac death.

Sudden cardiac death is the leading mode of death in adults in the United States. While it appears intimately associated with coronary artery disease, the factors that render some subjects vulnerable to sudden cardiac death, while others with the same coronary disease do not die suddenly, are unknown. An approach is described which considers that sudden cardiac death represents a separate syndrome of coronary artery disease within certain vulnerable subjects. It is suggested that the response to psychosocial stress in vulnerable subjects results in deleterious cerebral cortical influences on the autonomic control of the heart which render it more vulnerable to ischemia-induced ventricular fibrillation. Studies in the pig, an animal known to be susceptible to sudden death resulting from an environmental stress, demonstrate that cerebral cortical influences on autonomic centers play a central role in vulnerability to ventricular fibrillation after coronary artery occlusion. In this model, the incidence of ventricular fibrillation can be reduced by psychologic adaptation of the animal to his environment, cryoblockade of frontal cortical brain stem pathways and by central administration of propranolol. The relative role of adrenergic and cholinergic innervation of the heart is an important consideration.

Animals↗

PubMed2005

[Epidemiology of sudden cardiac death].

Sudden cardiac death remains a major challenge that we are still facing today. The complexity of the trigger mechanisms makes it difficult to achieve a reliable identification of high-risk patients. Three suggestions are made that might help to overcome this epidemiological catastrophe "Sudden Cardiac Death". 1. In patients with known heart disease risk stratification has to be improved by developing new methods to identify specifically those individuals, who are at risk for sudden rather than non-sudden cardiac death. 2. The general population contains an unknown proportion of individuals with advanced coronary disease, which is commonly asymptomatic. In these so called "normal population" classical risk stratification does not work. However, since there is a close relationship between the prevalence of risk factors for coronary disease and sudden death, a consequent treatment of risk factors should have a positive effect on sudden death rate as well. 3. The success rate of resuscitation has to be improved by strengthening each single link of the "chain of survival". Laypersons trained in basic and advanced life support techniques have to play a much major role on this scene.

Cardiomyopathies↗

PubMed2005

[The genetic disorders responsible for sudden cardiac death].

Sudden cardiac death is defined as an unpredictable death within 24 hours. It is estimated to occur with a frequency of more than 50,000 per year in Japan. The inherited arrhythmogenic diseases associated with the transmembranous ionic channels, anchoring proteins or intracellular calcium regulating proteins are thought to be responsible for sudden cardiac death in infants, children, and young adults who have structurally normal hearts. Recent genetic analyses have identified congenital diseases such as the long-QT syndrome (LQTS), the Jervell and Lange-Nielsen syndrome (JLNS), the Brugada syndrome (BrS), the short-QT syndrome (SQTS), the arrhythmogenic right ventricular cardiomyopathy type 2 (ARVC2), and the catecholamine-induced polymorphic ventricular tachycardia (CPVT) /familial polymorphic ventricular tachycardia (FPVT). Loss of function in the slow component of the delayed rectifier potassium current (I(Ks)) channels (KCNQ1, KCNE1), the rapid component of the potassium current (I(Kr)) channels (KCNH2, KCNE2) and the inward rectifier potassium current (I(Kl), Kir2.1) channel (KCNJ2) is linked to the LQTSs (type 1, 2, 5, 6, and 7 (Andersen syndrome)) and the JLNSs (type 1 and 2). Changes of function in the alpha-subunit of cardiac sodium channels (SCN5A) is also linked to the LQTS type 3 and the BrS. A mutation in the ankyrin-B, anchoring proteins, has been identified as cause of the LQTS type 4. The SQTS is caused by gain of function in the KCNH2. Further, the missense mutations in the gene encoding ryanodine receptor 2 (RyR2) or calsequestrin 2 (CASQ2) that regulate intra-cardiac calcium handling is possibly implicated in the ARVC2 and the CPVT/FPVT. Herein, we present a review of the literature regarding the genetic mechanisms of the inherited arrhythmogenic diseases.

Adult↗

PubMed2004

Role of noninvasive studies in risk stratification for sudden cardiac death.

Sudden cardiac death (SCD) is one of the leading causes of mortality in developing countries. To prevent SCD, it is crucial to have effective tools for identifying patients at risk, given that there are now effective devices and medications that can prevent SCD. Two noninvasive electrocardiographic tools have been approved by the Food and Drug Administration and are being used clinically for identifying patients at risk for SCD: the signal-averaged electrocardiogram (SAECG) and T-wave alternans (TWA). This article reviews each of these approaches and includes a discussion of the mechanisms and a summary of the clinical studies published to date.

Arrhythmias, Cardiac↗

PubMed1991

The automatic implantable cardioverter-defibrillator: technology for preventing sudden cardiac death.

Sudden cardiac death is caused by a malignant heart rhythm known as ventricular fibrillation. The automatic implantable cardioverter-defibrillator (AICD) is a device that recognizes this rhythm and converts it to a normal sinus rhythm by delivering an electrical shock directly to the heart. This article reviews the technology and clinical status of AICD technology, and the ongoing research into techniques for detecting malignant arrhythmias.

Arrhythmias, Cardiac↗

PubMed2000

Long-term follow-up after atrioventricular nodal ablation and pacing: low incidence of sudden cardiac death.

Sudden cardiac death (SCD) has been reported in patients with drug refractory AF who underwent AV nodal ablation and pacing. However, whether SCD in these patients is related to the underlying heart disease or to the ablating and pacing procedure remains uncertain. Between May 1987 and January 1997, AV nodal ablation was performed in 585 patients (mean age 66 +/- 11 years) with drug-resistant, paroxysmal (n = 308) or chronic (n = 277) AF in 12 Italian centers. Lone AF was present in 133 patients. After AV junction ablation, patients underwent VVIR (454 patients) or DDDR (131 patients) pacemaker implantation. At a follow-up of 33.6 +/- 24.2 months, 80 (13.7%) deaths were recorded: 40 noncardiac, 23 nonsudden, and 17 sudden cardiac death (3%, 1.04% per year). Among five variables, including age. NYHA functional class, presence of heart disease, paroxysmal or chronic AF, previous embolic events, and LVEF, the presence of heart disease (P = 0.007) and a LVEF < 0.45, (P = 0.003) were associated with a higher risk of SCD. Analysis of SCD-free survival by log-rank test showed a higher incidence of SCD in patients with LVEF < 0.45 (P = 0.0001) and with coronary artery disease (P = 0.005). In this large cohort, a low incidence of long-term SCD after AV nodal ablation and pacing for drug-refractory AF was observed. The presence of underlying heart disease and the extent of baseline LV dysfunction were associated with an increased likelihood of SCD.

Aged↗

PubMed1992

[Sudden cardiac death].

Sudden cardiac death is instant unexpected death that occurs within one hour of an abrupt change in a person's stable clinical state. The mechanism is generally a ventricular tachyarrhythmia. The underlying pathology is usually coronary heart disease. In 1990, 18 patients who survived sudden cardiac death, excluding those with acute myocardial infarction, were evaluated and treated in our institution. 15 patients had coronary heart disease, one had hypertrophic cardiomyopathy, one had dilated cardiomyopathy and one had a replaced aortic valve. Evaluation included heart catheterization and electrophysiological examination. Treatment was specifically tailored to each patient according to etiology, results of all tests and the patient's prognostic factors. Treatment included a permanent pacemaker-cardioverter-defibrillator, antiarrhythmic drug therapy, aortocoronary bypass and betablocker therapy.

Aged↗

PubMed1996

Circadian patterns and triggers of sudden cardiac death.

Sudden cardiac death and other acute cardiovascular events have been demonstrated to occur in certain temporal patterns. The study of these patterns may yield important clues to the pathophysiology of the disease process. Most studies of the timing of onset of sudden cardiac death have revealed a prominent midmorning peak, thought to be related to a surge in catecholamines associated with arising and assuming the upright posture, that is blunted or eliminated by beta blockers. In addition, some studies have also shown a secondary peak in late afternoon or early evening of uncertain cause. The development of third-generation implantable cardioverter defibrillators with memory capabilities offers a unique opportunity to accurately define event chronology.

Adrenergic beta-Antagonists↗

PubMed2003

T-wave alternans: marker, mechanism, and methodology for predicting sudden cardiac death.

Sudden cardiac death (SCD) is a leading cause of cardiovascular mortality. Therefore, identifying patients at highest risk for SCD is crucial. Conventional noninvasive markers of SCD are inadequate because of low positive predictive value. The presence of visible T-wave alternans (TWA) on electrocardiogram often predicts the occurrence of lethal ventricular arrhythmias. Signal processing methods have made it possible to detect microvolt-level and visually inapparent TWA on electrocardiogram. TWA is caused by underlying regional inhomogeneities of ventricular repolarization, which predispose patients to have ventricular arrhythmias. Microvolt TWA provoked either by atrial pacing, pharmacological stress, or exercise is a promising marker of arrhythmia vulnerability. Several large trials have shown TWA to be comparable or superior to other noninvasive markers and electrophysiologic study in the prediction of SCD. The patient populations in these trials include post myocardial infarction, both ischemic and nonischemic heart failure, and suspected arrhythmias. Prospective trials regarding benefits of implantation of cardioverter-defibrillator therapy based on TWA results are ongoing.

Arrhythmias, Cardiac↗

PubMed2000

Cost effectiveness analysis of screening of high school athletes for risk of sudden cardiac death.

Sudden cardiac death of a high school athlete is an alarming tragedy. Three preparticipation screening methods have been recommended to reduce its occurrence: specific cardiovascular history and physical examination, 12-lead ECG, and two-dimensional (2D) echocardiography. This study analyzes the cost effectiveness of each of these methods. The cost to perform each test and to evaluate abnormal screening findings were approximated. The years of life gained through detection of athletes with potential causes of sudden cardiac death were estimated. Overall, the approximate costs per year of life saved for the preparticipation cardiovascular screening examinations are: specific cardiovascular history and physical examination, $84,000; 12-lead ECG, $44,000; and 2D echocardiography, $200,000. The 12-lead ECG is the most cost effective preparticipation cardiovascular modality of the three currently recommended methods. Similar cost effectiveness for history and physical examination or 2D echocardiography would require respectively a 2-fold increase in sensitivity or 4.5-fold decrease in cost.

Adolescent↗