[Guidelines for the implantation of defibrillators].
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Defibrillators, Implantable↗
Biomedical subjects
D Andresen
Publications and source records attributed to D Andresen.
[Position paper on "automated external defibrillation" ].
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Advanced Cardiac Life Support↗
[Position paper to the taking of quality controls for resting, exercise, and long-term-ECG].
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Electrocardiography↗
[Position paper on "Automatic external defibrillation"].
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Critical Care↗
[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↗
[Sudden cardiac death (SCD) and guidelines for SCD].
Sudden cardiac death is mainly caused by arrhythmic events, triggered by ischemia. About half of the affected persons had no previous diagnosis of coronary heart disease, thus rendering them practically unreachable for specific preventive measures. This fact makes it necessary to optimize reanimation conditions. The establishment of international reanimation standards (ILCOR) has stimulated an intensified scientific evaluation of therapeutic options. While the use of vasopressin, adrenaline and reanimation by bystanders is being evaluated at the moment, amiodarone has not fulfilled the expectation of reducing mortality. Secondary prevention of sudden cardiac death after cardiac events is based on betablockers, ACE inhibitors and antilipemic therapy. Guidelines on prevention of sudden cardiac death also recommend aldosterone blockade and n-3-fatty acids. Persons at highest risk gain most from the use of ICDs, yet it has not been shown that their use immediately after myocardial infarction reduces mortality.
Arrhythmias, Cardiac↗
[Drug therapy of cardiac arrhythmias].
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Anti-Arrhythmia Agents↗
Combination reperfusion therapy with abciximab and reduced dose reteplase: results from TIMI 14. The Thrombolysis in Myocardial Infarction (TIMI) 14 Investigators.
Aims Abciximab has previously been shown to enhance thrombolysis and improve myocardial perfusion when combined with reduced doses of alteplase. The purpose of the reteplase phase of TIMI 14 was to evaluate the effects of abciximab when used in combination with a reduced dose of reteplase for ST-elevation myocardial infarction. Methods and Results Patients (n=299) with ST-elevation myocardial infarction were treated with aspirin and randomized to a control arm with standard dose reteplase (10+10 U given 30 min apart) or abciximab (bolus of 0.25 mg. kg(-1)and 12-h infusion of 0.125 microg. kg(-1). min(-1)) in combination with reduced doses of reteplase (5+5 U or 10+5 U). Control patients received standard weight-adjusted heparin (bolus of 70 U. kg(-1); infusion of 15 U. kg(-1). h(-1)), while each of the combination arms with abciximab and reduced dose reteplase received either low dose heparin (bolus of 60 U. kg(-1); infusion of 7 U. kg(-1). h(-1)) or very low dose heparin (bolus of 30 U. kg(-1); infusion of 4 U. kg(-1). h(-1)). The rate of TIMI 3 flow at 90 min was 70% for patients treated with 10+10 U of reteplase alone (n=87), 73% for those treated with 5+5 U of reteplase with abciximab (n=88), and 77% for those treated with 10+5 U of reteplase with abciximab (n=75). Complete (>/=70%) ST resolution at 90 min was seen in 56% of patients receiving a reduced dose of reteplase in combination with abciximab compared with 48% of patients receiving reteplase alone. Conclusions Reduced doses of reteplase when administered in combination with abciximab were associated with higher TIMI 3 flow rates than reported previously for reduced doses of reteplase without abciximab and were at least as high as for full dose reteplase alone
Abciximab↗
Diagnostic assessment of recurrent unexplained syncope with a new subcutaneously implantable loop recorder. Reveal-Investigators.
AIM: Patients with recurrent syncope undiagnosed after extensive non-invasive and invasive testing pose a diagnostic and therapeutic dilemma. Holter monitoring is nondiagnostic in 90% of cases. Recent developments in loop recorder technology permit long-term ECG monitoring in patients with recurrent unexplained syncope. The aim of this study was to report the worldwide experience with a new subcutaneously implantable loop recorder, implanted in 133 patients with unexplained syncope and negative laboratory investigations. METHODS AND RESULTS: The implantable loop recorder monitors continuously a single lead electrogram using two sensing electrodes on the device shell. The device was implanted in 133 patients, 67 male and 66 female with recurrent syncope. During a mean follow-up of 10.8 +/- 4.3 months after device implantation, 83 patients (62%) experienced syncope or pre-syncope. In the remaining 50 patients no diagnosis could be made because either no events occurred, the patients were lost to follow-up, had adverse events, or died prior to diagnosis. In 72 of the 83 patients with syncope during follow-up (87%), loop recording definitively determined whether an arrhythmia was the cause of symptoms or not. Diagnosis included bradycardia in 21 patients, pacemaker dysfunction in one patient, and tachycardia in 10 patients. One patient experienced multiple rhythm disturbances. Syncope was non-arrhythmic in 40 patients. The remaining 11 patients failed to press the activator. Therapy was instituted in all patients, in whom an arrhythmic cause was found. Severe anticipated device related complications occurred in three patients. CONCLUSION: An implantable loop recorder is useful for establishing a diagnosis when symptoms are recurrent but too infrequent for conventional monitoring techniques.
Equipment Design↗
Beta blockers: evidence versus wishful thinking.
Catecholamines and ischemia play an important role in the induction of ventricular tachyarrhythmias. Beta blockers antagonize the effect of catecholamines and have anti-ischemic properties. Several controlled studies performed in the early 1980s in patients after myocardial infarction have shown that beta-blocker therapy clearly decreases sudden and nonsudden cardiac death. Despite the lack of recent randomized trials, data from uncontrolled studies suggest that the beneficial effect of beta blockers is still present in the thrombolytic era. Thus, it is incomprehensible that today in the United States and in most parts of Europe, < 40% of post-myocardial infarction patients are treated with beta blockers. Even in patients with documented sustained ventricular tachycardias (VTs) or ventricular fibrillation (VF), clinical studies indicate that beta blockers improve survival. Thus, even in the thrombolytic era, beta blockers should be used as a basic therapy in patients who are at risk of sudden cardiac death.
Adrenergic beta-Antagonists↗
Risk stratification following myocardial infarction in the thrombolytic era: a two-step strategy using noninvasive and invasive methods.
OBJECTIVES: We prospectively performed a two-step risk assessment in patients in the early phase after acute myocardial infarction (MI). BACKGROUND: Noninvasive methods like Holter electrocardiographic monitoring (HM) and determination of the left ventricular ejection fraction (EF) as well as the invasive technique of programmed ventricular stimulation (PVS) have been used to identify patients in the late phase after MI as candidates for prophylactic implantation of a cardioverter/defibrillator. However, it is unclear whether these results can be transferred to patients following acute MI. METHODS: A series of 657 patients with acute MI (< or = 75 years) underwent HM and EF. If one of the two methods yielded abnormal findings (HM > or = 20 ventricular ectopic beats/h/> or =10 ventricular pairs/day/ventricular tachycardia; EF < or = 40%), PVS was done (abnormal PVS: induction of monomorphic ventricular tachycardia, duration >10 s, cycle length > or = 230 ms). RESULTS: Of 657 patients, 304 (46%) had either an abnormal HM or EF. The PVS performed in 146 of 304 patients was abnormal in 22. During a mean follow-up of 37 months, there were 106 (16%) deaths, being sudden in 24 (3.6%), nonsudden cardiac in 45 (6.8%). The incidence of arrhythmic events (sudden cardiac death, symptomatic ventricular tachycardia, cardiac arrest) was 18% (4/22) with an abnormal PVS and only 4% (5/124) with a normal PVS (odds ratio 4.0, p=0.032). CONCLUSIONS: The rate of arrhythmic events is low in post-MI patients in the 1990s. Nevertheless, a two-step risk stratification is helpful in selecting candidates for a defibrillator trial aiming at primary prevention of sudden cardiac death after MI.
Combined Modality Therapy↗
Heart rate variability preceding onset of atrial fibrillation.
The purpose of this article is to discuss the relationship between sympathovagal dysfunction and the occurrence of paroxysmal atrial fibrillation. Onset of atrial fibrillation is subject to circadian variation; shorter episodes occur more frequently during the day, whereas longer episodes occur less frequently at night. Vagally mediated atrial fibrillation typically is preceded by bradycardia, is not triggered by stress, occurs more often at night, is more common in men, and occurs at a younger age. Sympathetically mediated atrial fibrillation is less frequent, typically occurs during the day, can be triggered by stress, and often is accompanied by increasing sinus rate and frequent supraventricular extrasystoles. Determination of heart rate variability can be used to evaluate the effects of the autonomic nervous system on sinus rate. The onset of atrial fibrillation at night may be preceded by an increase in high-frequency components of heart rate variability. This is not the case for episodes that occur during the day. The heart rate in sympathetically mediated atrial fibrillation is higher before and during the episode in comparison with the vagal type. Heart rate variability is a promising method for evaluation of the interplay of sympathetic and vagal activity before the onset of atrial fibrillation. However, the role of heart rate variability for diagnostic assessment and therapeutic decision-making in patients with paroxysmal atrial fibrillation remains to be clarified by controlled studies.
Atrial Fibrillation↗
Modification of the circadian pattern of ventricular tachyarrhythmias by beta-blocker therapy.
BACKGROUND: Sudden cardiac death exhibits a circadian variation and predominantly occurs during morning hours, Beta-adrenergic antagonists have shown to blunt this morning peak. However, previous reports studying the effects of beta blockers on the circadian variation did not analyze the underlying cause of sudden cardiac death. It thus remains unclear whether ventricular tachyarrhythmias are influenced by beta-blocker therapy. HYPOTHESIS: This study tested the hypothesis that beta-blocking agents blunt the morning peak of life-threatening ventricular tachyarrhythmias. METHODS: In 87 patients who were treated and monitored with an implantable cardioverter defibrillator, the circadian distribution of ventricular tachyarrhythmias terminated by appropriate shocks was analyzed and compared in those receiving beta blockers versus those not receiving beta-blocker therapy. RESULTS: Tachyarrhythmic episodes in the absence of beta-blocker therapy (n = 344) exhibited a circadian variation with a distinct morning peak (16, 38, 28, and 18% of episodes at 0-6, 6-12, 12-18, and 18-24 h, respectively, p < 0.001). In contrast, tachyarrhythmic episodes during beta-blocker therapy (n = 104) were equally distributed over time (22, 27, 24, and 27% of episodes at 0-6, 6-12, 12-18, and 18-24 h, respectively, p = 0.95). The circadian distribution of episodes was significantly different in patients with and those without beta blockade (p < 0.05). CONCLUSION: Beta-adrenergic antagonists influence the circadian distribution of malignant ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator. The blunted morning peak of tachyarrhythmic events during beta blockade supports the hypothesis that a sympathetic surge is involved in the circadian pattern of malignant arrhythmias.
Adrenergic beta-Antagonists↗
Risk of ventricular arrhythmias in survivors of myocardial infarction.
The most recent studies have made it clear that the prognosis of asymptomatic post-MI patients has significantly improved in the last two decades. Holter monitoring as well as a low LVEF still is an important method for the risk stratification in the thrombolytic era of patients with post-MI. Patients with normal noninvasive tests do have a good prognosis. The electrophysiological stimulation seems to be the clinically most valuable single method to predict arrhythmic events. However, as an invasive procedure it is not suitable as a screening test for a large cohort. The stepwise risk stratification technique using first noninvasive followed by invasive procedures seem to be most suitable and effective for identifying asymptomatic infarct survivors which incidence of arrhythmic events is as high as the recurrence rate of patients who had been resuscitated from ventricular fibrillation. Consequently, prophylactic implantation of a defibrillator in asymptomatic MI patients, whose positive predictive value is around 30% becomes more and more interesting.
Arrhythmias, Cardiac↗
[Implantable defibrillators--current status of guidelines. Recognized and possible indications--prerequisites].
Ten to twenty percent of the patients, who were resuscitated as a result of a persistent ventricular tachycardia or ventricular fibrillation outside of an acute myocardial infarction, die of sudden cardiac death already in the first year after this event. Anti-arrhythmic agents also do not decisively improve this unfavorable prognosis. There is no doubt that the implantable cardioverter/defibrillator (ICD) safely and reliably terminates ventricular tachycardias and ventricular fibrillation and has thus led to an improvement in the care of these high risk patients. Studies have shown that the ICD reduces the risk of sudden cardiac death to 1-2% per year. However, whether the reduction of sudden cardiac death is also accompanied by a reduction in overall mortality has not yet been substantiated. It was, however, been assumed that especially patients with good left ventricular function, whose mortality risk is mainly sudden cardiac death, also profit from the overall prognosis of an ICD. The following presentation and discussion of the indication catalogue for the implantation of defibrillators is based on a guideline paper published by the study group "Interventional Electrophysiology" in the German Society for Cardiology. The statements clearly show how difficult it is to make long-term binding and valid recommendations due to insufficient scientific data and rapid technical development. Identifying patients who should be treated with an ICD requires complete noninvasive and invasive cardiological diagnostics and should ultimately be limited to cardiological centers which possess a large arsenal of diagnostic and therapeutic procedures.
Death, Sudden, Cardiac↗
Circadian variation of sustained ventricular tachyarrhythmias terminated by appropriate shocks in patients with an implantable cardioverter defibrillator.
To determine the circadian variation of sustained ventricular tachyarrhythmias, 78 consecutive patients with an implanted cardioverter defibrillator were analyzed with regard to the occurrence of spontaneous shock episodes during a mean follow-up period of 18 +/- 12 months. In 39 patients 207 shock episodes that terminated potentially life-threatening ventricular tachyarrhythmias could be related to an exact time of onset. A circadian variation (p < 0.001) of these events was demonstrated, with a primary morning peak between 7 hours and 11 hours and a secondary, much smaller peak between 16 hours and 20 hours. This finding indicates the relevance of endogeneous or exogeneous triggers in the cause of malignant arrhythmias that potentially lead to sudden cardiac death. Subgroup analyses revealed an association of the circadian pattern to the New York Heart Association functional classification, indicating perhaps a different role of triggers in different patient populations.
Aged↗
Management and prophylaxis of life-threatening arrhythmias--recent achievements.
Patients resuscitated from ventricular fibrillation or haemodynamically compromising ventricular tachycardias have an unfavourable clinical outcome. Moreover, there is no evidence that the prognosis can be improved by empirical use of antiarrhythmic therapy. Therapy guided by electrophysiological stimulation or long-term ECG identifies a subgroup of patients with a better outcome (in whom arrhythmias are suppressed) and a subgroup with a bad prognosis (in whom arrhythmias are not suppressed). However, this does not say that antiarrhythmic drugs actually improve the outcome. It may simply identify patients with an intrinsically good prognosis, regardless of whether they receive drug treatment. Because retrospective trials have reported that empiric administration of amiodarone provides long-term control in two-thirds or more of patients with refractory ventricular tachyarrhythmias, a direct comparison with other drugs guided by electrophysiological testing or long-term ECG was performed (CASCADE-study). Six-years survival was 41% under amiodarone versus 20% with other drugs. Even those conventionally treated patients, whose inducible arrhythmias were suppressed, had a trend toward a worse prognosis compared to those who were inducible and treated empirically with amiodarone. However, the high recurrence rate of arrhythmic events demonstrates the limitation of any antiarrhythmic drug, irrespective of the drug used and irrespective of whether it is given empirically or in a study.
Anti-Arrhythmia Agents↗