Philosophy of antiarrhythmic approaches to ventricular tachyarrhythmias close to the 21st century

The scientific basis and the reasoning underlying the changes in antiarrhythmic approaches to ventricular arrhythmias during recent decades are discussed. The early enthusiasm in the use of antiarrhythmic drugs in patients after myocardial infarction to prevent sudden cardiac death was severely affected by the results of the Cardiac Arrhythmia Suppression Trial (CAST) which show an increased mortality of patients on sodium-channel antagonist antiarrhythmic drugs. A transient euphoria for drugs that prolong repolarization received criticism after premature termination of the Survival With Oral D-sotalol-trial (SWORD). Recently, attention has focused on the use of the implantable cardioverter defibrillator in both secondary and primary prevention of sudden death. In contrast, catheter ablation, although very useful in supraventricular tachycardia, still plays a limited role in the management of ventricular tachyarrhythmias in the presence of organic heart disease.     

Antiarrhythmic therapies for the prevention of sudden cardiac death

Despite remarkable advances in cardiovascular therapeutics, sudden cardiac death remains a significant problem. In this review, data from clinical trials and other studies on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention of sudden cardiac death in high risk patients. Overall, routine prophylactic use of class I antiarrhythmic agents in high risk patients, mostly survivors of acute myocardial infarction, is associated with increased risk of death [61 trials, 23,486 patients: odds ratio (OR) 1.13; 95% confidence interval (CI) 1.01 to 1.27, p < 0.05]. Conversely, beta-blockers are associated with highly significant reductions in risk of death in postinfarction patients (56 trials, 53,521 patients: OR 0.81; 95% CI 0.75 to 0.87, p < 0.00001). Overall data from the amiodarone trials on high risk patients, including postinfarction patients, patients with congestive heart failure or survivors of cardiac arrest, suggest that this agent is effective in reducing the risk of death (14 trials, 5713 patients: OR 0.83; 95% CI 0.72 to 0.95, p = 0.01) although further studies are needed to better define which types of patients will potentially benefit most from this agent. No benefits were seen with calcium channel blockers (26 trials, 21,644 patients: OR 1.03; 95% CI 0.94 to 1.13, p = NS). The implantable cardioverter-defibrillator is a promising option for high risk patients, but definition of its role awaits the completion of ongoing clinical trials. Since causes of sudden death are heterogeneous, the clinician should pursue a multifactorial approach to its prevention. Primary and secondary prevention of cardiac ischaemia, through the treatment of cardiovascular risk factors and maximising the use of aspirin, beta-blockers, lipid-lowering drugs, and angiotensin converting enzyme inhibitors after acute myocardial infarction, should lead to a future decrease in the incidence of sudden cardiac death.     

Peroxidase activity of liver microsomal vitamin D 25-hydroxylase and cytochrome P450 1A2 catalyzes 25-hydroxylation of vitamin D3 and oxidation of dopamine to aminochrome

OBJECTIVES: This study sought to determine the long-term risk of sudden cardiac death in patients with hemodynamically stable sustained ventricular tachycardia complicating coronary artery disease. BACKGROUND: The prognosis and risk of sudden cardiac death in patients with a history of myocardial infarction and ventricular tachyarrhythmias have not been clearly defined. Prior studies are limited by a short follow-up period and by inclusion of patients with heterogeneous cardiac diseases and presenting arrhythmias. METHODS: A retrospective cohort analysis was performed on data from 124 patients, followed up for a mean of 36 +/- 30 months, who received electrophysiologically guided therapy for hemodynamically stable ventricular tachycardia after remote myocardial infarction. RESULTS: Seventy-eight patients were treated pharmacologically (medical group), and 46 patients underwent map-guided subendocardial resection (surgical group). Nine patients (7.3%) died suddenly, 5 (4.0%) died of noncardiac causes, 9 (7.3%) died of a perioperative complication, and 20 (23.4%) died of other cardiac causes. At 1, 2 and 3 years, sudden death occurred at cumulative rates of 2 +/- 1%, 3 +/- 2% and 7 +/- 3%, whereas total mortality was 20 +/- 4%, 28 +/- 4% and 32 +/- 5% (mean +/- SD). Sudden cardiac death (p = 0.047) and total mortality (p = 0.036) were higher in patients with multivessel disease and were similar for both treatment groups. CONCLUSIONS: Although the overall mortality in postinfarction patients presenting with hemodynamically stable ventricular tachycardia treated with electrophysiologically guided antiarrhythmic therapy is high, the risk of sudden death in these patients appears to be low (average 2.4%/year).     

Renaissance of beta blocker therapy in myocardial infarct

Beta-adrenergic blocking drugs have been evaluated for the treatment of arrhythmias and for the prevention of sudden cardia death, particularly in post-myocardial infarction patients. Betablockers have been demonstrated to reduce mortality, reinfarction, ventricular fibrillation and cardiac rupture in acute infarction. Therefore, in patients with suspected myocardial infarction and without contraindications, treatment with betablockers should be initiated early and continued for at least 2 years. Side-effects are mild and occur in approximately 10% of patients. Patients who have contraindications for betablockers use early in myocardial infarction should be reevaluated before discharge from the hospital and considered for such therapy. Because betablockers prevent some of the adverse arrhythmogenic mechanisms seen in chronic heart failure, it may be reasonable to expect that these drugs could have a role in preventing sudden cardiac death in these patients. Analysis of some of the betablocker post-infarction trials indicate that betablockers reduced the risk of sudden death in patients with heart failure at baseline. Some studies demonstrated also the symptomatic improvement following therapy with betablockers in patients with heart failure. But the currently available data are too limited to provide conclusive information.     

Should survivors of myocardial infarction with low ejection fraction be routinely referred to arrhythmia specialists?

Because survivors of myocardial infarction are at risk for ventricular arrhythmias and sudden death, physicians must decide whether to refer these patients to specialists for arrhythmia assessment and therapy. However, this decision is complex as few randomized data are available concerning either diagnostic or therapeutic options. Therefore, we modeled the potential impact of current arrhythmia detection and management strategies on mortality in survivors of myocardial infarction with reduced left ventricular function who are managed in a contemporary manner. Based on recent data we estimated that the mortality for myocardial infarction survivors with left ventricular ejection fraction less than 0.40 is 20 percent over 3.5 years and that half of the deaths are sudden. The sensitivity and specificity of a Holter electrocardiogram (ECG), a signal-averaged ECG, and an invasive electrophysiology study for predicting sudden death were obtained from a literature review of trials published after 1990 that included more than 300 patients. A series of models were constructed to predict mortality achieved by different arrhythmia management strategies that reduced sudden death by 50 percent and 75 percent--reductions estimated to be within the range for amiodarone and implantable defibrillators. We found that, when routinely applied to all infarct survivors with depressed ventricular function, a therapy that reduces sudden death by 50 percent with 1 percent fatal adverse effects (potentially amiodarone) saves approximately 1 life for every 25 patients treated. Therapy that reduces sudden death by 75 percent with 2 percent fatal adverse effects (potentially implantable defibrillators) saves 1 life for every 14 patients treated. Using Holter ECG recordings, a signal-averaged ECG, or an invasive electrophysiology study to select higher-risk groups, 1 life can be saved for every 4 to 11 patients treated, and the negative impact of adverse effects can be reduced. However, to achieve this benefit, additional and potentially invasive arrhythmia testing must be applied to 28 to 47 patients for each life saved. Thus, with contemporary management of acute myocardial infarction, the risk of sudden death for survivors is sufficiently low that broad application of available antiarrhythmic therapies has limited potential for further improving survival, particularly if therapy also has significant adverse effects. Thus, routine referral to arrhythmia specialists is not warranted for the majority of infarct survivors and should be largely reserved for patients with serious, symptomatic arrhythmias.     

Antiarrhythmic versus antifibrillatory actions: inference from experimental studies

Pathophysiology of the coronary circulation is a major contributor to altering the myocardial substrate, rendering the heart susceptible to the onset of arrhythmias associated with sudden cardiac death. Antiarrhythmic drug therapy for the prevention of sudden cardiac death has been provided primarily on the basis of trial and error and in some instances based on ill-suited preclinical evaluations. The findings of the Cardiac Arrhythmia Suppression Trial (CAST) requires a reexamination of the manner in which antiarrhythmic drugs are developed before entering into clinical testing. The major deficiency in this area of experimental investigation has been the lack of animal models that would permit preclinical studies to identify potentially useful or deleterious therapeutic agents. Further, CAST has emphasized the need to distinguish between pharmacologic interventions that suppresses nonlethal disturbances of cardiac rhythm as opposed to those agents capable of preventing lethal ventricular tachycardia or ventricular fibrillation. Preclinical models for the testing of antifibrillatory agents must consider the fact that the superimposition of transient ischemic events on an underlying pathophysiologic substrate makes the heart susceptible to lethal arrhythmias. Proarrhythmic events, not observed in the normal heart, may become manifest only when the myocardial substrate has been altered. We describe a model of sudden cardiac death that may more closely simulate the clinical state in humans who are at risk. The experimental results show a good correlation with clinical data regarding agents known to reduce the incidence of lethal arrhythmias as well as those showing proarrhythmic actions.     

Corticosteroid therapy in cardiac sarcoidosis

Corticosteroid treatment of cardiac sarcoidosis is not conclusive, although sarcoid granulomas in the heart may be more responsive to steroid therapy than in other organs. Healing of sarcoidosis lesions in the heart results in fibrosis and sinning of the myocardium, which may lead to aneurysm formation causing congestive heart failure or sudden death. Congestive heart failure is the leading cause of death in patients with cardiac sarcoidosis in Japan. It is reasonable to initiate steroid therapy as soon as the diagnosis of cardiac sarcoidosis is established in order to prevent fibrosis. Early initiation of steroid therapy with conventional treatment for specific cardiac manifestations (antiarrhythmic therapy, pacemaker implantation and heart failure medication) should bring improvement in the left ventricular systolic and diastolic function with prevention from malignant arrhythmias. Systemic disorder represents a contraindication to organ transplantation, but heart transplantation is now a feasible treatment for patients with end-stage cardiac sarcoidosis with congestive heart failure.     

Cardiac death prediction and impaired cardiac sympathetic innervation assessed by MIBG in patients with failing and nonfailing hearts

BACKGROUND: Although cardiac sympathetic nerve dysfunction is related to poor clinical outcome, a critical sympathetic dysfunction level for predicting cardiac death is still unclear. The current study was designed to investigate which indices derived from metaiodobenzylguanidine (MIBG) imaging have prognostic value compared with clinical and cardiac function variables, and to determine the threshold of cardiac MIBG activity for identifying patients likely to suffer cardiac death in both failing and nonfailing hearts. METHODS AND RESULTS: Myocardial I-123-MIBG activity was quantified as a heart-to-mediastinum ratio in 414 consecutive patients, 173 (42%) of whom had symptomatic heart failure. After cardiac function measurements, patients were followed up with an end-point of cardiac or noncardiac death. During a mean follow-up period of 22 months, 37 cardiac deaths occurred: 23 resulted from heart failure, 9 were sudden cardiac deaths, and 5 were fatal myocardial infarctions. Multivariate analysis using the Wald chi2 and the Cox proportional hazard model revealed that late heart-to-mediastinum ratio, the use of nitrates, early heart-to-mediastinum ratio, and left ventricular ejection fraction were independent predictors of cardiac death; late heart-to-mediastinum ratio, New York Heart Association (NYHA) class, the presence of previous myocardial infarction, and age were independent predictors of heart failure and sudden cardiac death. Late heart-to-mediastinum ratio was the most powerful predictor of overall cardiac death among the variables. The Kaplan-Meier analysis showed that a late heart-to-mediastinum ratio of 1.74 or less, age greater than 60 years, the presence of myocardial infarction, and NYHA functional class 3 or 4 strongly indicated poor clinical outcomes. Furthermore, the more powerful incremental prognostic values were obtained by using MIBG imaging in combination with conventional clinical variables. CONCLUSIONS: Impaired cardiac sympathetic innervation assessed by MIBG activity has the greatest potential for predicting cardiac death and may be useful for identifying a threshold level for selecting patients at risk for death by heart failure, sudden cardiac death, and fatal myocardial infarction.     

Resuscitation in ventricular fibrillation as the first manifestation of Bland-White-Garland syndrome in adulthood

CASE REPORT: This case presents a 31-year-old male patient with anomalous origin of the left coronary artery from the pulmonary trunc. First symptom of the disease was a survived sudden cardiac death. Subsequent angiographic and echocardiographic studies demonstrated the anomalous origin of the left coronary artery from the pulmonary artery. There were no signs of prior myocardial infarction. After reimplantation of the anomalous originating left coronary artery no myocardial ischemia could be detected in the thallium-201 myocardial imaging, which was present before surgical correction. In this case myocardial ischemia was the only potential triggering mechanism responsible for the sudden cardiac death, which was no longer detectable after surgical correction. Therefore no additional pharmacological and nonpharmacological antiarrhythmic treatment was initiated. CONCLUSION: In rare cases the first manifestation of Bland White Garland syndrome in the adult patient could be sudden cardiac death due to ventricular fibrillation.     

Acute myocardial infarction related to cocaine use. Report of a case

Cocaine use has been associated with ischemic syndromes, especially angor pectoris, myocardial infarction, cardiac arrhythmias and sudden death. A significant number of persons suffering from myocardial infarction associated with cocaine abuse do not have significant coronary atherosclerosis, and the mechanism for infarction in these patients have remained obscure. This report describes a young man with angiographically normal coronary arteries in whom cocaine abuse probably produced coronary artery spasm leading to coronary thrombosis and infarction.     

Prognostic value of ventricular arrhythmia in hypertensive patients

OBJECTIVE: Hypertensive left ventricular hypertrophy (LVH) is associated with increased risk of arrhythmias and mortality. However, no clinical study demonstrated a significant relation between ventricular arrhythmias and mortality in systemic hypertension. DESIGN AND METHODS: To evaluate the prognostic value of arrhythmogenic markers in systemic hypertension, we included between 1987 and 1993. 214 hypertensive patients, 59.1 +/- 12.8 years old, without symptomatic coronary disease, myocardial infarction, systolic dysfunction, electrolyte disturbances or antiarrhythmic therapy. At inclusion, an ECG, a 24 h Holter ECG (204 patients) with Lown classification of ventricular arrhythmias, an echocardiography (reliable in 187 patients) with left ventricular mass index and ejection fraction calculation, a SAECG (125 patients, enrolled after 1988) with ventricular late potentials (LP) were recorded. QT interval dispersion (QTd) was calculated on 12 leads standard ECG and LVH was appreciated. RESULTS: At baseline echocardiographic LVH was recorded in 63 patients (33.7%) with normal ejection fraction (75 +/- 7.4%). Non-sustained ventricular tachycardia (Lown IVb) was found in 33 pts (16.2%) and LP in 27 patients (21.6%). After a mean follow up of 42.4 +/- 26.8 months, all-cause mortality was 11.2% (24 patients); 17 patients died of cardiac causes (7.9%); of these 9 patients (4.2%) died suddenly. In univariate analysis, age, strain pattern of LVH, advanced Lown classes and abnormal QT dispersion (> 80 ms) were significantly related to global, cardiac and sudden death (p < or = 0.01). Left ventricular mass index was closely related to cardiac mortality (p = 0.002). LP failed to predict mortality. In multivariate analysis, only Lown class IVb was an independent predictor of global and cardiac mortality, increasing the risk of global death 2.6 fold [1.2-6.0] (CI 95%) and the risk of cardiac death 3.5 fold [1.2-9.7] (CI 95%). CONCLUSIONS: In hypertensive patients the presence of non-sustained ventricular tachycardia on 24 h Holter has a prognostic value.     

The implantable cardioverter/defibrillator

Despite all advances in the diagnosis and therapy of cardiovascular diseases, the mortality from malignant ventricular tachyarrhythmias is still a major health problem. In addition to established therapeutic strategies in the prevention of sudden cardiac death such as antiarrhythmic drug treatment, catheter ablation or antiarrhythmic drug treatment, cardioverter/defibrillator was introduced to clinical practice in 1980. The number of 50,000 overall implants reflects the current clinical status of the therapy with implantable cardioverter/defibrillators. Significant technical improvements in the defibrillator therapy may contribute to an increase in therapy acceptance. These advances include the introduction of nonthoracotomy lead systems, enhanced defibrillation efficacy, full programmable devices providing tiered electrical therapy, improved diagnostic Holter functions and enhanced arrhythmia detection algorithms. The major present goals of defibrillator therapy are detection and termination of malignant ventricular tachyarrhythmias, prevention of sudden cardiac death, reduction in patient's mortality and improvement in quality of life. The efficacy and safety of defibrillator therapy to prevent sudden arrhythmic death has been proven in several large clinical investigations In patients with this device the annual sudden cardiac death mortality is < 2% even in high-risk patient populations. Compared to sudden cardiac death rate there is a much higher rate of overall cardiac mortality because a defibrillator is not able to prevent nonarrhythmic cardiovascular deaths. There is a clinical impression that cardiovascular mortality is lower in patients treated with an implantable cardioverter/defibrillator compared to patients treated with other therapies. However, there are no results from controlled studies providing scientific evidence that defribillator therapy can decrease overall cardiovascular mortality.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sudden cardiac death in the aged

The problem of sudden cardiac death (SCD) in the aged impends on 14% of the adult population in the Slovak Republic and it often involves people who are still effectively active. It is now generally known that a person ill with his heart is never too old to benefit from the stratification of his/her cardiovascular risk. In clinical practice it is possible to suggest to use the combination of non-invasive methods as the first step in basic stratification of risk in the aged (Holter ECG monitoring, echocardiographically assessed ejection fraction of the left ventricle, ergometric test). Regarding the prevention of SCD it is necessary to teach the patients at risk to distinguish the symptoms of the impending collapse/SCD. After myocardial infarction, also in the aged, the therapy by acetylosalicylic acid, Beta-blockers and ACE inhibitors is indicated. There are fewer contraindications to this therapy than it has been presented until now. Antiarrhythmic drugs class I are not to be used. Also in the aged, regarding the prevention of tachycardiac SCD, the most prospective antiarrhythmic drugs are amiodaron and sotalol. The attention should be paid also to other factors in coincidence with sudden cardiac death that can be influenced by therapy (consequential antiischaemic therapy, homeostasis of the internal environment, early cardiostimulatory therapy of bradycardiac disturbances of rhythm, optimal timing of surgical therapy of valvular defects if indicated, prevention of pulmonary embolism, etc.). In the aged it is necessary to create a wider space in the field of invasive cardiological therapy. In general it is possible to state that the knowledge on etiopathogenetic stratification and specific characteristics of prevention and therapy of SCD in the aged are limited. This fact only emphasizes the inevitability to concentrate on the research in this area.     

The role of intravenous amiodarone in the management of cardiac arrhythmias

PURPOSE: To review the electropharmacology, clinical applications, side effects, and hemodynamic profile of intravenous amiodarone. DATA SOURCES: The MEDLINE database was searched for English-language material, including reports of clinical trials and in vivo studies, review articles, and abstracts presented at national symposia, that was published between 1985 and 1996. Bibliographies of textbooks and articles were also examined. STUDY SELECTION: Studies that reported on the efficacy, toxicity, and hemodynamic profile of intravenous amiodarone and studies that examined the pharmacologic behavior of intravenous amiodarone in laboratory models were reviewed. DATA EXTRACTION: Study design and quality and relevant data on efficacy of suppression and treatment of arrhythmias with oral and intravenous amiodarone therapy, the reported mechanisms of antiarrhythmic effect, and hemodynamic changes seen with therapy were analyzed. DATA SYNTHESIS: Amiodarone is a unique antiarrhythmic agent that is now available in oral and intravenous forms in the United States. The use of intravenous amiodarone in the short-term treatment of life-threatening or hemodynamically unstable rhythm disturbances has generated much interest. Amiodarone has many electropharmacologic actions, some of which differ between the oral and intravenous forms. The wide clinical application of amiodarone includes treatment and prevention of supraventricular and ventricular arrhythmias and arrhythmias related to myocardial infarction. Intravenous amiodarone is effective for supraventricular and ventricular arrhythmias that are resistant to other antiarrhythmic agents. The effectiveness of intravenous amiodarone as short-term treatment also suggests that the drug has an important role in protocols of advanced cardiac life support. Intravenous amiodarone seems to have an overall favorable hemodynamic profile and does not produce many of the unwanted long-term side effects associated with oral therapy. CONCLUSION: Intravenous amiodarone shows much promise for the short-term treatment of unstable arrhythmias. Its favorable hemodynamic effects and minimal short-term side effects make it an attractive option in the management of cardiac arrhythmias.     

Troponin T in patients with low grade or atypical angina. Identification of a high risk group for short- and long-term cardiovascular events

AIMS: Cardiac troponin T is an established marker of cardiovascular risk in patients with severe angina pectoris. Data are scarce on patients admitted to a coronary care unit with low grade or atypical angina pectoris to rule out myocardial infarction. METHODS AND RESULTS: We investigated 106 patients (57.4 SD 11.6 years) with low grade (Braunwald class I) or atypical symptoms out of 702 patients admitted to the coronary care unit with suspected acute myocardial infarction. Serum concentrations of troponin T were measured at admission and 4 h later. In hospital cardiovascular events including acute myocardial infarction, life threatening cardiac arrhythmias, congestive heart failure, and death were recorded. Patients were additionally observed after 3 and 6 months post-discharge regarding acute myocardial infarction, unstable angina, rehospitalization for cardiac causes and death. The patients were divided into a troponin T positive (> or =0.2 microg x 1(-1) at admission or 4 h later; n=11) and a troponin T negative group. The mean value of troponin T 4 h after admission in the positive group was 0.58 microg x 1(-1). Of the troponin T positive patients, 0.82 (0.95 CI: 0.48-0.98) had a cardiovascular event during their stay in hospital vs 0.41 (0.95 CI: 0.31-0.52) of troponin T negative patients (P<0.05). In the troponin T positive group 0.64 (0.95 CI: 0.31-0.89) developed myocardial infarction in hospital vs 0.07 (0.95 CI: 0.03-0.15) in the troponin T negative group (P<0.001). Troponin T predicts outcome after 3 and 6 months significantly (P<0.05). CONCLUSION: Troponin T identifies patients with low grade or atypical angina at risk of severe short- and long-term cardiovascular events. Therefore, troponin T adds substantial information in patients with ruled out acute myocardial infarction. Troponin T positive patients have to be observed carefully regardless of their symptom intensity and may have to receive early cardiac catheterization; troponin T negative patients could be released safely from the coronary care unit early.     

Dispersion of the Q-T interval after myocardial infarct

Non-homogenity of ventricular myocardial repolarization is a substrate for the reentry mechanism of ventricular arrhythmias. It is manifestant by dispersion of Q-T and Q-Tc intervals on the standard ECG curve. The authors studied the possibility of using the dispersity of Q-T and Q-Tc intervals in clinical practice. They evaluated the dispersion of these intervals within the set of 21 patients after myocardial infarction with sustained ventricular tachycardia, and compared it with the dispersion within the control set of 17 patients after myocardial infarction without an arrhythmic episode. By means of comparison, they have discovered that: 1) the dispersion of Q-T and Q-Tc intervals is significantly higher in patients with ventricular tachycardia: Q-T (mean +/- SE) 82.8 +/- 7.8 msec vs 42.2 +/- 4.8 msec, Q-Tc 93.0 +/- 10.2 msec vs 47.1 +/- 4.8 msec, p > 0.001, 2) the dispersion of Q-Tc when higher than 60 msec is an optimum discrimination value for the prognosis of sudden arrhythmic death after myocardial infarction (sensitivity 81%, specificity 76%) and 3) the dispersion of Q-T and Q-Tc intervals has no relation to the function of the left ventricle. Therefore the authors consider the dispersion of Q-T and Q-Tc intervals as being a useful marker of malignant ventricular arrhythmia which could be included into the algorithm of assessment of the risk of sudden arrhythmic death after myocardial infarction.     

Ventricular arrhythmias and sudden cardiac death in acute myocardial infarct in the era of thrombolytics

Sudden cardiac death (SCD) in the setting of acute myocardial infarction (AMI) remains an actual problem. There is a very close relationship between ventricular arrhythmias and SCD in AMI. Malignant ventricular arrhythmias, such as ventricular fibrillation and ventricular tachycardia are the major causes of SCD in coincidence with AMI. Frequent and complex ventricular arrhythmias are also important predictors of the risk of SCD in coincidence with and after AMI. In this article the authors emphasize the importance of the complexity of pathophysiological mechanisms responsible for the genesis of ventricular arrhythmias in coincidence with AMI. The necessity of taking into account the current knowledge about pathophysiology in prevention and therapy of separate forms of ventricular arrhythmias is also emphasized. The incidence and time course of ventricular arrhythmias and SCD in coincidence with AIM in prethrombolytic and thrombolytic periods is described. The importance of separate forms of ventricular arrhythmias in coincidence with AMI with regard to short and long-term prognoses is described. There are discussed also the possible mechanisms of thrombolytic and adjuvant therapies that affect the incidence and frequency of ventricular arrhythmias. The authors recommend the optimal therapy for each form of ventricular arrhythmia and the following management of patients with AMI. In the prevention and therapy of ventricular arrhythmias in the setting of AMI the authors emphasize the importance of early recanalization and prevention of re-occlusion of the infarction-related coronary artery. Great importance is attributed also to other adjuvant measures directed to the restriction of the size of infarction, myocardium protection, prevention and attenuation of remodelling of the left ventricle and thereby to the prevention of heart failure and attenuation of adverse effects of the sympathetic nervous system. An early administration of beta-blockers which favourable effect in and after AMI was documented with conclusive evidence is considered as one of the most important measures in prevention and therapy of malignant ventricular arrhythmias and SCD. The occurrence of malignant ventricular arrhythmias in the setting of heart failure and/or 24-48 hours after AMI should be an indication for aggressive management directed to arrhythmia (programmed ventricular stimulation, electrophysiologically guided pharmacologic or nonpharmacologic therapy) as well as to underlying coronary heart disease (coronary angiography and revascularization).     

Secondary prevention of myocardial infarct

Preventive measures are the most powerful measures to treat manifestations of ischemic cardiopathy. Secondary prevention of myocardial infarction involves the following intervention areas: a) Limitation of adverse physiological and emotional consequences of the acute illness; b) Identification of the patients particularly exposed to the risk of new episodes of ischemic cardiopathy or to their consequences, namely reinfarction and sudden death; c) Institution of therapeutic attitudes, surgical or medical, that can prolong life and can oppose functional deterioration and prevent symptoms; d) Institution of measures that can oppose the progression of the initial disease that is, in almost all cases, atherosclerosis. Measures that can oppose the progression of cardiac disease and its consequences after an episode of myocardial infarction, and measures that can oppose the evolution of atherosclerosis are described in this article. The measures that can influence the risk factors after an episode of myocardial infarction are briefly commented: characteristics related to life style and physical exercise; smoking habits; plasmatic lipid levels; high blood pressure; and therapeutic substitution with estrogens after menopause. Pharmacological interventions in secondary prevention of myocardial infarction are described, namely with the following groups of substances: beta-adrenergic blocking agents; platelet active agents; anticoagulants; and angiotensin-converting enzyme inhibitors.     

Spectral turbulence versus time-domain analysis of signal-averaged ECG used for the prediction of different arrhythmic events in survivors of acute myocardial infarction

INTRODUCTION: Spectral turbulence analysis of the signal-averaged ECG (SAECG) combines spectral analysis with statistical evaluation of spectrograms of individual parts of the QRS complex. It has been suggested that it may be superior to conventional time-domain analysis of the SAECG. METHODS AND RESULTS: This study compared the power of conventional time-domain (40 to 250 Hz) and spectral turbulence analyses of SAECG for the prediction of cardiac death, ventricular tachycardia, sudden arrhythmic death, and arrhythmic events (ventricular tachycardia or fibrillation, and/or sudden arrhythmic death) after acute myocardial infarction in 603 patients. The population excluded patients with bundle branch block and other conduction abnormalities. During the first 2 years of follow-up, there were 40 cardiac deaths, 21 cases of ventricular tachycardia, 1 sudden arrhythmic deaths, and 29 arrhythmic events. The positive predictive accuracy of spectral turbulence analysis was significantly higher than time-domain analysis for cardiac death at most levels of sensitivity (e.g., 26% vs 20% at 40% sensitivity, P < 0.05). The positive predictive accuracies of the two techniques were not statistically different for the prediction of ventricular tachycardia. For the prediction of sudden arrhythmic death and arrhythmic events, the positive predictive accuracy of spectral turbulence was better than that of time-domain analysis only at the higher levels of sensitivity (9% vs 2%, P < 0.001 for sudden arrhythmic death at 60% sensitivity, and 14% vs 11%, P < 0.05 for arrhythmic events at 60% sensitivity). CONCLUSIONS: Spectral turbulence analysis is essentially equivalent to time-domain analysis for the prediction of arrhythmic events after myocardial infarction. However, it performed significantly better than time-domain analysis for the prediction of cardiac death.     

Survival and incidence of myocardial infarction in men with ambulatory ECG-detected frequent and complex ventricular arrhythmias. 10 year follow-up of the 'Men born 1914' study in Malm?, Sweden

AIM: To assess to what extent do frequent or complex ventricular arrhythmias, detected during 24 h ambulatory electrocardiographic recording (ECG), influence prognosis with regard to survival and incidence of ischaemic heart disease. METHODS AND RESULTS: The study subjects were the 456 randomly selected men born in 1914, the population-based cohort study of 1982-83, in Malm?, Sweden. The main outcome measures were total mortality and incidence of cardiac event (myocardial infarction and death from ischaemic heart disease). Frequent or complex ventricular arrhythmias (Lown classes 2-5) were detected in 49% of the men with (n = 77), and in 35% of those without, a history of myocardial infarction or angina pectoris at baseline, P = 0.019. Independent of clinically evident coronary artery disease at baseline, and after adjustment for traditional atherosclerotic risk factors and use of digitalis or beta-blocker therapy, frequent or complex ventricular arrhythmias were associated with an increased mortality from ischaemic heart disease (relative risk (RR), 2.1; 95% confidence interval (CI), 1.2-3.9) and an increased cardiac event rate (RR, 1.6; 95% CI, 1.0-2.5)). Men free from both ischaemic-type ST depression and frequent or complex ventricular arrhythmias (used as the control group) had the lowest ischaemic heart disease death rate, 5.9 per 1000 person-years. The combination of ST depression and frequent or complex ventricular arrhythmias was associated with an ischaemic heart disease death rate of 20.9 per 1000 person-years. The cardiac event rate in these two groups was 15.6 and 76.1 per 1000 person-years, respectively (adjusted RR, 2.3; CI, 1.1-4.6). CONCLUSIONS: In elderly men without a history of myocardial infarction and angina pectoris, frequent or complex ventricular arrhythmias during ambulatory ECG recording is associated with an increased incidence of myocardial infarction and mortality. Men who, during ambulatory ECG recording, also demonstrate ST-segment depression have an even less favourable prognosis.