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4,300 | Specificity of the stress electrocardiogram during adenosine myocardial perfusion imaging in patients taking digoxin. | In patients taking digoxin, the exercise electrocardiogram has a lower specificity for detecting coronary artery disease. However, the effect of digoxin on adenosine-induced ST-segment depression is unknown. The purpose of this study was to evaluate the specificity of the electrocardiogram during adenosine myocardial perfusion imaging in patients taking digoxin.</AbstractText>Between May 1991 and September 1997, patients (n = 99) taking digoxin who underwent adenosine stress imaging with thallium-201 or technetium-99m sestamibi and coronary angiography within 3 months were retrospectively identified. Exclusion criteria included prior myocardial infarction, coronary artery angioplasty or bypass surgery, left bundle branch block, paced ventricular rhythm, or significant valvular disease. Twelve-lead electrocardiograms were visually interpreted at baseline, during adenosine infusion, and during the recovery period. The stress electrocardiogram was considered positive if there was > or =1 mm additional horizontal or downsloping ST-segment depression or elevation 0.08 seconds after the J-point compared with the baseline tracing.</AbstractText>ST-segment depression and/or elevation occurred in 24 of 99 patients. There were only 2 false-positive stress electrocardiograms, yielding a specificity of 87% and positive predictive value of 92%. All 8 patients with > or =2 mm ST segment depression had multivessel disease by coronary angiography.</AbstractText>ST-segment depression or elevation during adenosine myocardial perfusion imaging in patients taking digoxin is highly specific for coronary artery disease. Marked (> or =2 mm) ST-segment depression and/or ST-segment elevation is associated with a high likelihood of multivessel disease.</AbstractText> |
4,301 | A randomized study of intravenous magnesium in acute myocardial infarction treated with direct coronary angioplasty. | Notwithstanding the negative result of the International Study of Infarct Survival-4 (ISIS-4), the controversy about the role of magnesium in acute myocardial infarction is still open because, according to experimental data, magnesium could decrease myocardial damage and mortality only if infusion is started before reperfusion. This randomized placebo-controlled trial was designed to evaluate the effect of intravenous magnesium, delivered before, during, and after direct coronary angioplasty, in patients with acute myocardial infarction.</AbstractText>One-hundred fifty patients were randomized to intravenous magnesium sulfate or placebo. The primary end point was an infarct zone wall motion score index at 30 days, as a measure of infarct size. The secondary end points included creatine kinase peak, ventricular fibrillation/tachycardia within the first 24 hours, death and congestive heart failure within the 30-day follow-up, and 30-day left ventricular ejection fraction. Analysis was by intention to treat.</AbstractText>There were no significant differences between the magnesium and placebo groups in the 30-day infarct zone wall motion score index (1.93 +/- 0.61 vs 1.85 +/- 0.51, P =.39), ventricular arrhythmias (24% vs 15%, P =.15), death (0 vs 1%, P =.32), heart failure (8% vs 7%, P =.75), and 30-day left ventricular ejection fraction (49% +/- 11% vs 50% +/- 9%, P = 0.55). There was a trend toward a higher creatine kinase peak in the magnesium group (3059 +/- 2359 vs 2404 +/- 1673,P =.052).</AbstractText>Intravenous magnesium delivered before, during, and after reperfusion did not decrease myocardial damage and did not improve the short-term clinical outcome in patients with acute myocardial infarction treated with direct angioplasty.</AbstractText> |
4,302 | New atrial fibrillation after acute myocardial infarction independently predicts death: the GUSTO-III experience. | Atrial fibrillation (AF) or flutter occurring after myocardial infarction may occur alone or in association with other complications. Whether the arrhythmia portends a poor prognosis independent of other complications with contemporary therapy is unknown.</AbstractText>As part of the Global Use of Strategies To Open occluded coronary arteries (GUSTO-III) trial, we evaluated whether postinfarction complications were associated with the subsequent development of AF and whether AF independently predicted death over periods of 30 days and 1 year. Information including exact timing was collected on deaths and major in-hospital postinfarction complications up to 30 days. Of the 13,858 patients with sinus rhythm at enrollment, 906 later had AF or flutter and 12, 952 did not. We compared outcomes between these 2 groups, adjusting for differences in baseline characteristics and prefibrillation complications. Worsening heart failure, hypotension, third-degree heart block, and ventricular fibrillation were independent predictors of new-onset AF. The unadjusted odds ratio (OR) for death among patients with versus those without AF was 2.74 (95% confidence interval [95% CI], 2.56-3.34). After adjusting for baseline differences, the OR was reduced to 1.63 (95% CI, 1.31-2.02). Adjustment for other in-hospital complications before the onset of AF further reduced the OR to 1.49 (95% CI, 1.17-1.89).</AbstractText>Atrial fibrillation or flutter occurs secondary to other postinfarction complications but independently portends a worse prognosis. Prevention and management may improve outcome.</AbstractText> |
4,303 | Rate-control versus conversion strategy in postoperative atrial fibrillation: a prospective, randomized pilot study. | Atrial fibrillation remains a frequent complication after heart surgery. The optimal strategy to treat the condition has not been established. Several retrospective studies have suggested that a primary rate-control strategy may be equivalent to a strategy that restores sinus rhythm.</AbstractText>Fifty patients with atrial fibrillation after heart surgery were randomly assigned to a strategy of antiarrhythmic therapy with or without electrical cardioversion or ventricular rate control. Both arms received anticoagulation with heparin overlapped with warfarin. The primary end point was time to conversion to sinus rhythm analyzed by the Kaplan-Meier method. Atrial fibrillation relapse after the initial conversion was monitored in the hospital over a 2-month period.</AbstractText>There was no significant difference between an antiarrhythmic conversion strategy (n = 27) and a rate-control strategy (n = 23) in time to conversion to sinus rhythm (11.2 +/- 3. 2 vs 11.8 +/- 3.9 hours; P =.8). With the use of Cox multivariate analysis to control for the effects of age, sex, beta-blocker usage, and type of surgery, the antiarrhythmic strategy showed a trend toward reducing the time from treatment to restoration of sinus rhythm (P =.08). The length of hospital stay was reduced in the antiarrhythmic arm compared with the rate-control strategy (9.0 +/- 0.7 vs 13.2 +/- 2.0 days; P =.05). In-hospital relapse rates in the antiarrhythmic arm were 30% compared with 57% in the rate-control strategy (P =.24). There were no significant difference in relapse rates at 1 week (24% vs 28%), 4 weeks (6% vs 12%), and 6 to 8 weeks (4% vs 9%). At the end of the study, 91% of the patients in the rate-control arm were in sinus rhythm compared with 96% in the antiarrhythmic arm (P =.6).</AbstractText>This pilot study shows little difference between a rate-control strategy and a strategy to restore sinus rhythm. Regardless of strategy, most patients will be in sinus rhythm after 2 months. A larger randomized, controlled study is needed to assess the impact of restoration of sinus rhythm on length of stay.</AbstractText> |
4,304 | [Time series analysis of abnormal heart beat signals]. | The variability of electric and magnetic signals from the heart during the depolarization phase is investigated. A signal processing method is developed which provides estimates for the beat-to-beat variability of the QRS-complex. The method is based on the decomposition of the depolarization signal into bandpass signals by means of the Morlet wavelet transform. The beat variability of the depolarization signal is estimated by normalized variances of the envelope and instantaneous frequency of bandpass signals. Time intervals of the bandpass filtered depolarization signals having a high signal-to-noise ratio are selected by applying an analysis based on phase statistics. The method was tested by experimental data taken from ECG and MCG measurements of healthy persons and patients prone to malignant ventricular tachycardia (VT) or ventricular fibrillation (VF). Results suggest that the calculated variance parameters permit the characterization of beat variable depolarization signals and distinguish VT/VF patients from healthy persons. The method developed can be used to obtain additional information concerning abnormal heart signals which is attenuated when applying signal averaging. |
4,305 | Ventricular fibrillation threshold and local dispersion of refractoriness in isolated rabbit hearts with left ventricular dysfunction. | Patients with congestive heart failure or left ventricular dysfunction (LVD) have a high incidence of ventricular tachyarrhythmias and sudden cardiac death. In addition to structural, metabolic and neuroendocrine changes, mechanoelectrical feedback may play a role in arrhythmogenesis in heart failure. Three groups of rabbits (n = 10 for each) were studied: chronic coronary ligation with ejection fraction (EF) > or = 0.45 or < 0.45, and sham-operated controls. Ventricular fibrillation (VF) thresholds were measured at LV pressures of 0 and 40 mm Hg during modified Langendorff perfusion. Intervals between local activations during VF (VFI) were used as an index of refractoriness. Global dispersion was expressed as coefficient of variation of VFI; local dispersion by maximum difference in VFI between adjacent sites. Median VF threshold was lower at 0 mm Hg in the lower EF group compared to controls (30 vs. 67.5 mA, P<0.05). VF threshold in control hearts was lower at 40 mm Hg than at 0 mm Hg (P<0.01), but there was no further reduction in threshold in LVD hearts at 40 mm Hg. Global dispersion of VFI did not differ significantly between groups. Local dispersion of VFI in the lower EF group was greater than in controls at 0 mm Hg in the infarct border zone (P<0.05). At 40 mm Hg, local dispersion of VFI in zones bordering and remote from the infarct were greater in both LVD groups than in controls (P<0.05). Local inhomogeneity of refractoriness is more marked in the infarct border zone, but latent abnormalities are evident in normal myocardium of rabbits with left ventricular dysfunction and are revealed by left ventricular distension. |
4,306 | Inhibition of nitric oxide synthase enhances the myocardial toxicity of phenylpropanolamine. | To investigate the direct and indirect effects of the anorexic agent phenylpropanolamine (PPA) on the heart and to determine whether nitric oxide deficiency exacerbates the myocardial toxicity of PPA.</AbstractText>Dose response effects using sequential drug administration.</AbstractText>Animal research laboratory of a large tertiary academic medical center.</AbstractText>Isolated hearts (n = 8) from male Sprague-Dawley rats weighing 300-400 g.</AbstractText>Measurement of heart rate, maximal change in pressure over time (dP/dtmax), -dP/dtmax, and coronary blood flow in isolated hearts perfused on a Langendorff apparatus. PPA was infused through the aortic cannula at 0.05, 0.125, 0.25, 0.5, and 1.25 mmol/L before and after inhibition of nitric oxide synthesis with N-nitro-L-arginine methyl ester (L-NAME).</AbstractText>PPA had little effect on myocardial contractility of normal hearts until the highest dose of PPA (1.25 mmol/L). However, after L-NAME, PPA significantly depressed contractility at a dose of 0.25 mmol/L. PPA had no significant effects on coronary blood flow. PPA failed to induce arrhythmias in normal hearts. However, after L-NAME, PPA induced ventricular fibrillation in 50% of the hearts.</AbstractText>PPA causes myocardial contractile depression without altering global coronary artery blood flow. Inhibition of nitric oxide synthesis sensitizes the heart to the myocardial depressant effects of PPA and increases the risk for ventricular fibrillation.</AbstractText> |
4,307 | Echo-Doppler observations during cardiac arrest and cardiopulmonary resuscitation. | We describe a series of investigations that used transesophageal echo-Doppler observations during cardiac arrest and cardiopulmonary resuscitation. Regular contractions of the left atrium persisted during the initial 7 mins of untreated ventricular fibrillation. Ventricular chamber deformation and mitral valve closing and opening followed precordial compression and relaxation. Stroke volumes computed from differences between diastolic and systolic areas of the left ventricle were predictive of the success of the resuscitation. Progressive decreases in left ventricular compliance were associated with decreases in left ventricular diastolic and stroke volumes and progressed to a stone heart. |
4,308 | Effects of repetitive electrical shocks on postresuscitation myocardial function. | Whereas myocardial cell injury can occur during electrical defibrillation proportional to the energy level of individual shocks, only minimal (or no) injury seems to develop when the energy is limited to the levels typically required to terminate ventricular fibrillation. During cardiac arrest, however, multiple shocks are often required to terminate ventricular fibrillation or to treat episodes that appear subsequently during the resuscitation effort or the postresuscitation interval. Concern exists because an inverse relationship has been reported between the number of electrical shocks delivered during cardiac resuscitation and both resuscitability and survival. Repetitive electrical shocks can alter diastolic function and prompt leftward shifts of the end-diastolic pressure-volume curves. Repetitive shocks may, therefore, contribute to the recently recognized phenomenon of postresuscitation myocardial dysfunction and hamper efforts to reestablish competent myocardial function after resuscitation. Thus, strategies aimed at limiting the number of electrical shocks during cardiopulmonary resuscitation are highly desirable. These may include real-time ventricular fibrillation waveform analysis to improve targeting of individual shocks and efforts (using mechanical and pharmacologic means) to render the myocardium more responsive to individual shocks and to promote greater electrical stability after successful defibrillation. |
4,309 | Experimental studies on precordial compression or defibrillation as initial interventions for ventricular fibrillation. | Countershock of prolonged ventricular fibrillation is usually followed by asystole or a nonperfusing rhythm. Data from three laboratory investigations indicate that administration of epinephrine and cardiopulmonary resuscitation (CPR) preceding countershock of prolonged ventricular fibrillation significantly improves cardiac resuscitation outcome compared with immediate countershock (relative risk reduction of failed resuscitation, 0.61). Preliminary investigations indicate that a similar improvement is not observed when the ventricular fibrillation period is of shorter duration, e.g., 5 mins. This time interval is probably at the lower limit at which CPR preceding shock of ventricular fibrillation provides benefit in terms of cardiac resuscitation. A single clinical trial of "CPR first" supports the use of a brief period of CPR before countershock of prolonged ventricular fibrillation. Additional trials with and without epinephrine are anticipated. |
4,310 | Low-energy biphasic waveform defibrillation reduces the severity of postresuscitation myocardial dysfunction. | Both clinical and experimental studies have demonstrated substantial impairment of ventricular function after resuscitation from cardiac arrest. Indeed, postresuscitation myocardial dysfunction has been implicated as a potentially important mechanism, accounting for fatal outcomes after successful resuscitation in 70% of victims within the first 72 hrs. Recent experimental studies implicated the total electrical energy delivered during defibrillation as an important correlate with the severity of postresuscitation myocardial dysfunction and postresuscitation survival. This prompted us to investigate the option of using lower electrical energy biphasic waveform defibrillation. We compared the effects of low-energy biphasic waveform defibrillation with conventional monophasic waveform defibrillation after a short (4 mins), intermediate (7 mins), or prolonged (10 mins) interval of untreated ventricular fibrillation. Biphasic waveform defibrillation with a fixed energy of 150 joules proved to be as effective as conventional monophasic damped sine waveform defibrillation for restoration of spontaneous circulation, with significantly lower delivered energy. This was associated with significantly less severity of postresuscitation myocardial dysfunction. The low-energy biphasic waveform defibrillation is, therefore, likely to be the future direction of transthoracic defibrillation in settings of cardiopulmonary resuscitation. |
4,311 | Electrophysiology of ventricular fibrillation and defibrillation. | The survival rate from ventricular fibrillation is very high for short-duration fibrillation (<30 secs) but decreases to approximately 3% to 30% in out-of-hospital conditions. During short-duration fibrillation, action potentials occur rapidly with no intervening period of electrical diastole; a shock defibrillates by interacting with the fibrillation action potential to produce a uniformly long postshock extension of refractoriness. In contrast, during long-duration fibrillation, ischemia-induced degradation of cellular electrophysiology occurs, which causes intervening periods of electrical diastole between fibrillation action potentials and, thus, slowing of fibrillation frequency. A successful defibrillation shock must now not only prolong refractoriness when delivered during the action potential but must also excite cells during the periods of depolarized diastole. Biphasic waveforms enhance both effects by causing premature membrane repolarization with the first pulse, thereby allowing sodium channel recovery from inactivation so that the second pulse produces better-formed responses both during the cellular action potential and during the depolarized diastole. Therefore, biphasic waveforms remain superior to monophasic waveforms for treatment of long-duration fibrillation. Improved understanding of the ischemia-induced changes in cellular electrophysiology will suggest further improvements in both defibrillator waveforms and resuscitation techniques. |
4,312 | Suspended animation for delayed resuscitation from prolonged cardiac arrest that is unresuscitable by standard cardiopulmonary-cerebral resuscitation. | Standard cardiopulmonary-cerebral resuscitation fails to achieve restoration of spontaneous circulation in approximately 50% of normovolemic sudden cardiac arrests outside hospitals and in essentially all victims of penetrating truncal trauma who exsanguinate rapidly to cardiac arrest. Among cardiopulmonary-cerebral resuscitation innovations since the 1960s, automatic external defibrillation, mild hypothermia, emergency (portable) cardiopulmonary bypass, and suspended animation have potentials for clinical breakthrough effects. Suspended animation has been suggested for presently unresuscitable conditions and consists of the rapid induction of preservation (using hypothermia with or without drugs) of viability of the brain, heart, and organism (within 5 mins of normothermic cardiac arrest no-flow), which increases the time available for transport and resuscitative surgery, followed by delayed resuscitation. Since 1988, we have developed and used novel dog models of exsanguination cardiac arrest to explore suspended animation potentials with hypothermic and pharmacologic strategies using aortic cold flush and emergency portable cardiopulmonary bypass. Outcome evaluation was at 72 or 96 hrs after cardiac arrest. Cardiopulmonary bypass cannot be initiated rapidly. A single aortic flush of cold saline (4 degrees C) at the start of cardiac arrest rapidly induced (depending on flush volume) mild-to-deep cerebral hypothermia (35 degrees to 10 degrees C), without cardiopulmonary bypass, and preserved viability during a cardiac arrest no-flow period of up to 120 mins. In contrast, except for one antioxidant (Tempol), explorations of 14 different drugs added to the aortic flush at room temperature (24 degrees C) have thus far had disappointing outcome results. Profound hypothermia (10 degrees C) during 60-min cardiac arrest induced and reversed with cardiopulmonary bypass achieved survival without functional or histologic brain damage. Further plans for the systematic development of suspended animation include the following: a) aortic flush, combining hypothermia with mechanism-specific drugs and novel fluids; b) extension of suspended animation by ultraprofound hypothermic preservation (0 degrees to 5 degrees C) with cardiopulmonary bypass; c) development of the most effective suspended animation protocol for clinical trials in trauma patients with cardiac arrest; and d) modification of suspended animation protocols for possible use in normovolemic ventricular fibrillation cardiac arrest, in which attempts to achieve restoration of spontaneous circulation by standard external cardiopulmonary resuscitation-advanced life support have failed. |
4,313 | Electrocardiographic waveform analysis for predicting the success of defibrillation. | A new electrocardiographic predictor of the likelihood that an electrical shock would restore a perfusing rhythm is described. The intent was to develop a prognosticator that would be displayed during precordial compression. We anticipated that such a predictor would allow more selective timing of electrical shocks and reduce electrical injury to the myocardium caused by repetitive shocks. In a porcine model of cardiac arrest because of ventricular fibrillation, electrocardiographic recordings of ventricular fibrillation wavelets were analyzed and transformed into an amplitude spectrum area (AMSA). An AMSA value of 21 mV x Hz predicted restoration of perfusing rhythm with a positive predictive value equivalent to that of coronary perfusion pressure. More important, the negative predictive value that a shock would fail to reestablish spontaneous circulation was 96%. AMSA, therefore, has the potential for guiding optimal timing of defibrillation. |
4,314 | Improving the efficiency of cardiopulmonary resuscitation with an inspiratory impedance threshold valve. | In an effort to improve the efficiency of cardiopulmonary resuscitation (CPR), a new inspiratory impedance threshold valve has been developed to enhance the return of blood to the thorax during the chest decompression phase. This new device enhances negative intrathoracic pressure during chest wall recoil or the decompression phase, leading to improved vital organ perfusion during both standard CPR and active compression-decompression CPR. With active compression-decompression CPR, addition of the impedance threshold valve results in sustained diastolic pressures of >55 mm Hg in patients in cardiac arrest. The new valve shows promise for patients in asystole or shock refractory ventricular fibrillation, when enhanced return of blood flow to the chest is needed to "prime the pump." The potential long-term benefits of this new valve remain under study. |
4,315 | Cardiopulmonary resuscitation with a hydraulic-pneumatic band. | Improved blood flow during cardiopulmonary resuscitation (CPR) has been shown to enhance survival from cardiac arrest. Chest compression with a circumferential pneumatic vest enhances blood flow, but the size, weight, and energy consumption of the inflation system limit its portability and, thereby, have made clinical studies difficult. The purpose of this investigation was to study an improved circumferential chest compression device that uses a constricting band that is pneumatically actuated. The constricting band applies its force to a hydraulic cushion that contacts the anterior and lateral aspects of the chest. The hydraulic cushion transfers the circumferential constriction to inward force. CPR was performed on subjects 5 mins after induction of ventricular fibrillation, with the hydraulic-pneumatic band system (HB-CPR), with a pneumatic vest system (PV-CPR), and with standard manual CPR (S-CPR), each done for 2 mins in randomized order. Aortic and right atrial pressures were measured with micromanometers. Coronary perfusion pressure was calculated as the mean difference between the aortic and right atrial pressures during the release phase of chest compression. Aortic pressure and coronary perfusion pressure with HB-CPR and PV-CPR were improved over S-CPR, and HB-CPR produced comparable pressures to those of PV-CPR. The system for performing HB-CPR, however, was substantially lighter (10 vs. 50 kg) and consumed less energy (300 vs. 1000 watts) than that for PV-CPR. Thus, HB-CPR appears to produce a similar improvement in hemodynamics over S-CPR as PV-CPR but may be more portable than PV-CPR. Therefore, HB-CPR may allow larger scale testing of circumferential chest compression approaches. |
4,316 | Role of mouth-to-mouth rescue breathing in bystander cardiopulmonary resuscitation for asphyxial cardiac arrest. | There is increasing evidence that mouth-to-mouth rescue breathing may not be necessary during brief periods of bystander cardiopulmonary resuscitation (CPR) for ventricular fibrillation. In contrast to ventricular fibrillation cardiac arrests, it has been assumed that rescue breathing is essential for treatment of asphyxial cardiac arrests because the cardiac arrests result from inadequate ventilation. This review explores the role of mouth-to-mouth rescue breathing during bystander CPR for asphyxial cardiac arrests. Clinical data suggest that survival from apparent asphyxial cardiac arrest can occur after CPR consisting of chest compressions alone, without rescue breathing. Two randomized, controlled swine investigations using models of bystander CPR for asphyxial cardiac arrest establish the following: a) that prompt initiation of bystander CPR is a crucially important intervention; and b) that chest compressions plus mouth-to-mouth rescue breathing is markedly superior to either technique alone. One of these studies further demonstrates that early in the asphyxial pulseless arrest process doing something (mouth-to-mouth rescue breathing or chest compressions) is better than doing nothing. |
4,317 | Cardiopulmonary resuscitation without ventilation. | Current resuscitation methods, although occasionally effective, rarely perform as well as initially anticipated. Some of the disappointment can be attributed to the difficulty of the task for many, including both professional and lay first responders. Significant attention has been paid recently to the need to simplify both the technique and the teaching of resuscitation. In considering simplification of the current resuscitation scheme, a logical start is an honest reappraisal of the importance and priorities of each of the once sacrosanct ABCs, specifically, establishment of an Airway, artificial Breathing (mouth-to-mouth breathing), and chest compressions for temporary Circulation. Experimental data continue to accumulate indicating that most important within this triad is circulation. Adequate oxygen exists within the blood during at least the first 10 mins of cardiac arrest. If circulation is provided to distribute such oxygen, no survival disadvantage results with chest compression-only basic life support (BLS) efforts. Even a totally occluded airway during the first 6 mins of cardiac arrest does not compromise survival if reasonable circulation is provided with chest compressions. Clinical studies support the same conclusion that what most influences survival in any BLS effort is circulation, not ventilation. Belgium investigators have shown equal survival rates among those treated with chest compressions plus ventilation and those who received chest compressions alone. Telephone dispatcher-guided BLS cardiopulmonary resuscitation (CPR) has likewise shown no survival disadvantage to chest compression-only CPR when compared with telephone-guided standard BLS CPR. Based on this reasoning, a new simplified BLS method has been proposed. "Staged" CPR consists of a strategy to initially teach laypersons a simplified approach to BLS, which requires only chest compressions and not mouth-to-mouth breathing. "Bronze" CPR, in which chest compression-only BLS is taught, was compared with the standard European Resuscitation Council BLS course for laypersons. Manikin "exit testing" at course completion has revealed significant advantages of the simplified approach compared with standard CPR courses for the lay public. |
4,318 | Immediate countershock versus cardiopulmonary resuscitation before countershock in a 5-minute swine model of ventricular fibrillation arrest. | Prior laboratory and clinical studies demonstrate that cardiopulmonary resuscitation (CPR) preceding countershock of prolonged ventricular fibrillation (VF) increases the likelihood of successful cardiac resuscitation. The lower limit of VF duration at which time preshock CPR provides no benefit has not been specifically studied. The purpose of this study was to compare countershock and cardiac resuscitation outcome between immediate countershock of VF of 5-minute duration and CPR without drug therapy before countershock in a swine model.</AbstractText>VF was induced in anesthetized and instrumented swine. After 5 minutes of VF, animals received 1 of 2 treatments. Animals in group 1, a "historical" control group (n=20), received immediate countershock followed by CPR and repeated shocks if needed. Group 2 animals (n=11) received CPR for 90 seconds preceding countershock, then continued CPR and repeated countershock if necessary. Drugs were not administered to either group, and resuscitation efforts were discontinued if a perfusing rhythm was not restored within 10 minutes of the first countershock. First shock success rate (defined as termination of VF), the number of shocks required to terminate VF, and the cardiac resuscitation rate were compared between groups.</AbstractText>The first shock terminated VF in 13 of 20 group 1 animals and 2 of 11 group 2 animals (P =.023). All but 1 animal in group 1 developed pulseless electrical activity after countershock. All but 1 animal in group 1 were eventually successfully resuscitated with CPR and repeated shocks if necessary. Four group 2 animals could not be resuscitated (P =.042).</AbstractText>Although effective in improving outcome of prolonged VF, CPR preceding countershock of VF of 5-minute duration does not improve the response to the first shock, decrease the incidence of postshock pulseless electrical activity, or the rate of return of circulation. In this study, CPR preceding countershock resulted in a significantly lower cardiac resuscitation rate.</AbstractText> |
4,319 | Arrhythmias in Heart Failure. | Cardiac arrhythmias are very common in the setting of heart failure, with atrial and ventricular arrhythmias often present in the same patient. The risk and the benefit of antiarrhythmic therapies are still a matter of debate. Class I antiarrhythmic drugs should be avoided in patients with heart failure, cardiac ischemia, or previous myocardial infarction. Beta-blocker agents reduce morbidity and decrease mortality in patients suffering from moderate to severe heart failure. Amiodarone may be beneficial in patients with advanced heart failure and increased resting heart rates. This class III drug may be effective to suppress episodes of atrial fibrillation but can also be beneficial in reducing ventricular response by slowing atrioventricular conduction during chronic atrial fibrillation. Implantable cardioverter-defibrillators (ICDs) markedly reduce sudden cardiac death in patients with ventricular tachycardia or ventricular fibrillation. In patients with advanced heart failure, however, the ICD may not markedly extend survival. Recently analyzed data from the Canadian Implantable Defibrillator Study (CIDS), Antiarrhythmics Versus Implantable Defibrillators (AVID) registry, Multicenter Unsustained Tachycardia Trial (MUSTT), and Multicenter Automatic Defibrillator Implantation Trial (MADIT) have consistently shown that it is the sickest patient who benefits the most from ICD therapy. Patients with markedly depressed ejection fraction (<30%), poor New York Heart Association functional class, and advanced age have been identified as those who really need ICD therapy. Studies of implantable cardioverter-defibrillators in patients with moderate to severe heart failure have been launched and will provide necessary answers to the question of whether a reduction in sudden death will translate into a reduction of all-cause mortality. For patients resuscitated from sustained ventricular tachycardia or ventricular fibrillation, an ICD or, in some cases, amiodarone should be considered. Catheter or surgical ablation can be considered for selected patients with ventricular tachycardia. |
4,320 | A new dual activation simulator of the left heart that reproduces physiological and pathological conditions. | Heart valve replacements are often associated with cardiac pathologies, but valvular prostheses are still tested in vitro under the same physiological conditions as for a healthy young man. Therefore a new mock circulatory system of the left heart, the dual activation simulator (DAS), has been built. The DAS allows atrial and ventricular dynamics to be controlled with pumps that activate anatomically shaped silicon models of the cavities. The mitral flow is a two-peak waveform. The E/A ratio can be changed, and the A-wave can be suppressed to simulate, for instance, atrial fibrillation. The cardiac rhythm and the mean flow-rate can be changed at will. The ability of the DAS to reproduce physiological flow is assessed by computation of the aortic input impedance and by harmonic analysis of left ventricular and atrial pressures. It allows the behaviour of valve prostheses to be studied in various conditions of concern to clinicians and can be a useful tool for engineers to improve valve prostheses or validate diagnostic tools such as 3D colour Doppler. The DAS and its capacities are described. |
4,321 | Complexity measure and complexity rate information based detection of ventricular tachycardia and fibrillation. | On the basis of non-linear dynamics, the paper uses a Lempel-Ziv complexity measure and presents a new definition of the information complexity rate: cc(n). Using such a definition, relative properties are obtained to help identify chaotic process accurately. Applying complexity analysis to abnormal ECGs recorded from patients with an implantable cardioverter defibrillator, the reasonableness of this information complexity and complexity rate approach are confirmed by means of biological experiments and computer simulations. Finally, objective analysis and explanations of the mechanisms of VT and VF are reported. The results indicate that, with the help of the complexity measure and complexity rate, recognition of ventricular tachycardia (VT) and ventricular fibrillation (VF) signals can be achieved with accuracy up to 100% (VT: 100%; VF: 98.7%). |
4,322 | Perioperative management of a patient requiring surgery for pituitary apoplexy and severe angina pectoris. | We describe the management of a 71-yr-old man with pituitary apoplexy and severe angina pectoris who underwent treatment of an intra-cranial haemorrhage and open-heart surgery requiring anticoagulant therapy within a very short period. Subtotal removal of the pituitary tumour was undertaken under stable cardiovascular conditions. But ventricular fibrillation occurred after the neurosurgery in the intensive care unit. After the patient was defibrillated, intra-aortic balloon pumping was necessary to assist coronary artery blood flow. Twenty hours after neurosurgery, oozing from the surgical wound stopped and coronary artery bypass grafting with full heparinization was performed uneventfully. |
4,323 | [Dofetilide to patients with heart failure and left ventricular dysfunction]. | Dofetilide, a new class III antiarrhythmic drug, was tested for its ability to reduce mortality and morbidity in patients with congestive heart failure and left ventricular dysfunction.</AbstractText>In 34 Danish centers, 1518 patients with NYHA class III or IV heart failure and wall motion index of the left ventricle < or = 1.2 (ejection fraction < or = 35%) were randomized to receive dofetilide or placebo in a double blind study. The dose of dofetilide was adjusted to renal function and the QT interval. Patients were monitored continuously with ekg during the first three days in the study. Minimum follow up was one year.</AbstractText>Dofetilide did not affect mortality. Hospitalizations for worsening of heart failure were reduced significantly, hazard ratio 0.75 (0.63-0.89) Dofetilide effectively converted atrial fibrillation to sinus rhythm. After one year, 61% of patients with atrial fibrillation had converted on dofetilide and 33% on placebo (p < 0.001).</AbstractText>Dofetilide can be used to convert atrial fibrillation to sinus rhythm and to maintain sinus rhythm in patients with congestive heart failure and left ventricular dysfunction. Dofetilide does not affect mortality.</AbstractText> |
4,324 | Atrial fibrillation: the most common arrhythmia. | Atrial fibrillation is the most common sustained arrhythmia, increases with age, and presents with a wide spectrum of symptoms and severity Paroxysmal, persistent, and permanent forms require very individualized approaches to management. New information about electrical and anatomic remodeling emphasizes the importance of time-related thrombogenicity and progressive interference with mechanical function of the atria and ventricles. The most important aspect of diagnosis is risk stratification with respect to risk of thromboembolism. The general goals in treatment are, in order of importance: prevention of thromboemboli, control of ventricular response, restoration of sinus rhythm, and maintenance of sinus rhythm by preventing recurrences. This review focuses on the above issues. The therapeutic choices are discussed under each category Antiarrhythmic drugs, radiofrequency ablation techniques, and device therapy are reviewed with respect to prevention of recurrent atrial fibrillation. |
4,325 | Outcome of pregnancy in women with mechanical valves. | In women who have prosthetic heart valves, pregnancy is risky for mother and fetus. Heparin has been considered safer for the fetus than warfarin, but may not provide adequate anticoagulation for the mother. We examined prospectively gathered data from 100 pregnancies in 67 women with mechanical valves (age range, 19 to 45 years). A subgroup of 20 patients was compared with a control group of relatives and neighbors who conceived at similar ages. Fetal loss occurred in 44 of the 100 pregnancies, due to the following causes: spontaneous abortion (28), intrauterine fetal death (4), stillbirth (3), neonatal death (1), premature birth (2), Rh incompatibility (2), and maternal death (4). Age, parity, atrial fibrillation, and left ventricular enlargement did not affect the outcome. Tricuspid valve disease that required diuretics was associated with a higher rate of fetal loss (17 out of 23 pregnancies, versus 27 out of 77; p = 0.001), but did not affect the mother Of 66 pregnancies in which the mother was on heparin, 38 (576%) resulted in a healthy baby, compared with 18 out of 34 (52.9%) pregnancies in which the mother was on warfarin (p = NS). All thromboembolic complications occurred with heparin therapy (9 cases; p = 0.02). In the control group, fetal loss was 24 %, due exclusively to spontaneous abortion. Women with mechanical valves have higher rates of fetal loss and maternal complications. In our study, tricuspid valve disease adversely affected fetal outcome, which is a new finding that warrants further study. Warfarin was more effective than heparin in preventing thromboembolism in the mothers, and it did not show a significant impact on the babies. |
4,326 | Cardioprotective effects of MET-88, a gamma-butyrobetaine hydroxylase inhibitor, on cardiac dysfunction induced by ischemia/reperfusion in isolated rat hearts. | Inhibition of fatty acid metabolite accumulation may be beneficial for treatment of cardiac dysfunction induced by ischemia. MET-88, 3-(2,2,2-trimethylhydrazinium)propionate dihydrate, inhibits gamma-butyrobetaine hydroxylase which catalyzes conversion of gamma-butyrobetaine to carnitine. In this study, we investigated whether MET-88 has cardioprotective effects against cardiac dysfunction induced by ischemia/reperfusion. Rats were divided into four groups: (1) control; (2) MET-88 at 50 mg/kg; (3) MET-88 at 100 mg/kg; (4) nifedipine at 30 mg/kg. MET-88 was administered orally once a day for 10 days, and nifedipine was administered orally 30 min before the experiments. Cardiac functions (heart rate, left ventricular systolic pressure and coronary flow) were measured in rat working heart preparations for 30 min under ischemia followed by 20 min under reperfusion. Myocardial carnitine levels were measured at the end of the experiments. Before ischemia, MET-88 did not affect cardiac functions, but nifedipine significantly increased only coronary flow. Under the ischemic condition, cardiac functions were markedly decreased in all groups. During reperfusion, MET-88 and nifedipine promoted recovery of cardiac functions and decreased the incidence of ventricular fibrillation. MET-88 also prevented the accumulation of long-chain acylcarnitine induced by ischemia. These results indicated that MET-88 protected against cardiac dysfunction in ischemia/reperfusion, and preventing the accumulation of long-chain acylcarnitine may be responsible for the cardioprotective effects. |
4,327 | Obstacle-induced transition from ventricular fibrillation to tachycardia in isolated swine right ventricles: insights into the transition dynamics and implications for the critical mass. | The study was done to test the hypothesis that an artificial anatomical obstacle prevents the maintenance of ventricular fibrillation (VF) by stabilizing reentrant wavefronts (RWF) and increases the critical mass (CM) of myocardium required to sustain VF.</AbstractText>Artificial obstacles can anchor RWF in simulated models of VF. Whether an artificial obstacle affects multiple-wavelet VF in real tissue is unclear.</AbstractText>The endocardial surfaces of seven isolated, perfused swine right ventricles were mapped using a plaque of 477 bipolar electrodes with 1.6-mm resolution. An 8-mm hole was punched in the tissue. The CM was reached by tissue mass reductions, at which VF converted to periodic activity (ventricular tachycardia, VT).</AbstractText>After the creation of the obstacle, the VF cycle length increased from 71.6+/-18.4 ms to 87.5+/-13.0 ms (p<0.05). The obstacle, together with the papillary muscle, facilitated the transition from VF to VT by serving as attachment sites for the RWF. When one RWF attaches to the obstacle and another attaches to the papillary muscle, it may result in stable VT with figure-eight patterns. The CM for VF in the presence of an 8-mm hole (28.7+/-3.8 g) was higher than in the control group (swine right ventricles without holes, 24.0+/-3.4 g, p<0.05).</AbstractText>An artificial anatomical obstacle induces slowing and regularization of VF, impairs the persistence of VF as judged by an increase of the CM, and can convert VF to VT by serving as an attachment site to reentrant excitation.</AbstractText> |
4,328 | Anticoagulants. | Anticoagulation is a treatment with significant and life threatening complications requiring that the balance of risk and benefit be individually assessed in each patient. The risks are greater in the elderly and those with hypertension, falls and gastrointestinal disease. The use of anticoagulants is now established in patients with symptomatic non-rheumatic atrial fibrillation, especially older patients with hypertension, cardiac failure or a large left atrium or left ventricular dysfunction. There is, however, no place for the routine use of anticoagulants in acute stroke or as part of secondary prevention in patients in sinus rhythm. There may be a place, though as yet the evidence would not support this, for the limited use of anticoagulants in special situations such as cortical venous thrombosis or carotid dissection. |
4,329 | Factors associated with preventable out-of-hospital nontraumatic cardiac arrest. | To identify ways to decrease the risk of out-of-hospital cardiac arrest (CA) caused by an acute coronary syndrome, we examined factors associated with the development of CA > or = 1 hour after symptom onset. Multivariate analysis revealed that a low level of physical activity, a history of diabetes mellitus, and a history of unstable angina are associated with out-of-hospital CA occurring > or = hour after symptom onset. |
4,330 | Prophylactic implantable cardioverter defibrillator trials: MUSTT, MADIT, and beyond. Multicenter Unsustained Tachycardia Trial. Multicenter Automatic Defibrillator Implantation Trial. | MUSTT and MADIT have clearly shown the survival benefit of an implantable cardioverter defibrillator (ICD) in patients with previous myocardial infarction, left ventricular ejection fraction < or = 0.40, and nonsustained ventricular tachycardia (VT), and who have had sustained VT induced at electrophysiology study. Progress in primary prevention of sudden cardiac death (SCD) depends on a concerted effort by clinicians to identify and appropriately treat MUSTT/MADIT-type patients; further research to more precisely define patient subgroups at risk for SCD and the willingness of industry to develop a lower priced ICD for prophylactic use are needed. |
4,331 | The Brugada syndrome: a recently recognised genetic disease causing sudden cardiac death. | Australian doctors need to be aware of this little-known syndrome, which is a cause of sudden cardiac death. It is more common among Southeast Asian people, who make up a considerable proportion of our population. We report two cases which represent very different clinical presentations of this condition. |
4,332 | Alternans and the onset of ventricular fibrillation. | Ventricular fibrillation (VF) remains a major cause of death in the industrialized world. Alternans (a period-doubling bifurcation of cardiac electrical activity) have recently been causally linked to the progression from ventricular tachycardia (VT) to VF, a more spatiotemporally disorganized electrical activity. In this paper, we show how alternans and thus VT degenerate to chaos via multiple, specific dynamical routes, largely associated with spatial components of VF dynamics, explaining failures of many recently proposed antiarrhythmic drugs. Identification of dynamical mechanisms for the onset of VF should lead to the design of future experiments and consequently to more effective antiarrhythmic drugs. |
4,333 | Comparing cardiac action potentials recorded with metal and glass microelectrodes. | Machine-pulled high-impedance glass capillary microelectrode is standard for transmembrane potential (TMP) recordings. However, it is fragile and difficult to impale, especially in beating myocardial tissues. We hypothesize that a high-impedance pure iridium metal electrode can be used as an alternative to the glass microelectrode for TMP recording. The TMPs were simultaneously recorded from isolated perfused swine right ventricles with a metal microelectrode and a standard glass microelectrode during pacing and during ventricular fibrillation. The basic morphology of TMP recorded with these electrodes was comparable. The action potential duration (APD) at 90% repolarization was 241 +/- 29 ms for the metal microelectrode and 236 +/- 31 ms for the glass microelectrode with a good correlation (r = 0.99, P < 0.0001). The maximum slope value of the APD restitution curves during pacing was also significantly correlated. One metal microelectrode and >20 glass microelectrodes were needed per study. We conclude that, in isolated perfused swine right ventricles, the TMP recorded by the metal microelectrode is comparable with that recorded by the glass microelectrode. Because the metal microelectrode is more durable than the glass microelectrode, it can serve as an alternative for APD recording and for restitution analyses. |
4,334 | Effects of [K(+)](o) on electrical restitution and activation dynamics during ventricular fibrillation. | To test whether hyperkalemia suppresses ventricular fibrillation (VF) by reducing the slope of the action potential duration (APD) restitution relation, we determined the effects of the extracellular K(+) concentration ([K(+)](o)) ([KCl] = 2.7-12 mM) on the restitution of APD and maximum upstroke velocity (V(max)) the magnitude of APD alternans and spatiotemporal organization during VF in isolated canine ventricle. As [KCl] was increased incrementally from 2.7 to 12 mM, V(max) was reduced progressively. Increasing [KCl] from 2.7 to 10 mM decreased the slope of the APD restitution relation at long, but not short, diastolic intervals (DI), decreased the range of DI over which the slope was >/=1, and reduced the maximum amplitude of APD alternans. At [KCl] = 12 mM, the range of DI over which the APD restitution slope was >/=1 increased, and the maximum amplitude of APD alternans increased. For [KCl] = 4-8 mM, the persistence of APD alternans at short DI was associated with maintenance of VF. For [KCl] = 10-12 mM, the spontaneous frequency during VF was reduced, and activation occurred predominantly at longer DI. The lack of APD alternans at longer DI was associated with conversion of VF to a periodic rhythm. These results provide additional evidence for the importance of APD restitution kinetics in the development of VF. |
4,335 | Cardiac arrhythmias in surgically repaired total anomalous pulmonary venous connection: a follow-up study. | Twenty-five patients with diagnosis of total anomalous pulmonary venous connection, who had undergone corrective surgery, were studied at variable time period after surgery with 24-hour ambulatory electrocardiographic monitoring (Holter) and echocardiography. The aim of this study was to record arrhythmias, if any, and to correlate occurrence of arrhythmia with adequacy of repair and other related variables. All the patients were clinically asymptomatic. Twenty-four hours ambulatory electrocardiographic monitoring of these patients showed the presence of significant arrhythmias in 21 of the 25 patients. These included supraventricular ectopics in 19 patients, ventricular ectopics in 8, atrioventricular block in 2, right bundle branch block and atrial fibrillation 1 each and atrial tachycardia in 2 patients. There was no correlation between development of arrhythmia and age at repair, type of connection, operative approach and adequacy of repair. The study indicates that cardiac arrhythmias can occur in otherwise asymptomatic patients after correction for total anomalous pulmonary venous connection. Thus, these patients require long-term follow-up, even if they are asymptomatic. |
4,336 | Profiling risk from arrhythmic or hemodynamic death. | Congestive heart failure is increasing in prevalence and, despite recent advances in therapy, mortality remains high. Sudden cardiac death (SCD) represents a significant percentage of overall mortality, accounting for almost 1 in 2 deaths in patients with congestive heart failure. In patients with asymptomatic left ventricular dysfunction or mild degrees of functional impairement, overall annual mortality is low, although a significant portion of the deaths are sudden; on the other hand, in advanced heart failure annual mortality increases, but SCD contributes to it to a lesser degree. The mechanisms of SCD in heart failure are multiple, including ventricular tachycardia/ventricular fibrillation, bradyarrhythmias, electromechanical dissociation, acute coronary events, and thromboembolic events. Only a minority of patients with advanced heart failure or on the waiting list for heart transplant experience SCD as a consequence of ventricular tachycardia (VT) or ventricular fibrillation (VF). The availability of effective therapies to prevent sudden arrhythmic death, such as that provided by automatic implantable cardioverter defibrillators, may help to reduce the burden of SCD in congestive heart failure, but major efforts will be needed to identify the candidates who may benefit from this approach. |
4,337 | Prospective randomized trials on pacing mode: what have we learned? | Retrospective studies and observational clinical data on pacemaker mode selection indicate that physiologic pacing is associated with better clinical outcomes and reduced mortality when compared with single-chamber ventricular pacing. Methodologic flaws in such studies, especially in respect of selection bias, have cast doubt upon the validity of the results and have mandated the performance of randomized, prospective studies of pacemaker-mode prescription. Evidence available to date suggests that atrial-based pacing may confer improved quality of life and a reduction in the incidence of chronic atrial fibrillation and thromboembolic events in sinus node disease. Physiologic pacing modes have, to date, not demonstrated benefit with congestive heart failure or patient longevity. The results of ongoing, large prospective trials of mode prescription in patients with AV block and sinus node disease are needed before any change from current guidelines can be recommended. |
4,338 | Effect of stored electrograms on management in the paced patient. | Advances in modern pacemaker technology offer possibilities to diagnose asymptomatic arrhythmias and to document the causal relation between symptoms and infrequently occurring arrhythmias. Diagnostic and memory functions of pacemakers allow both the automatic detection of arrhythmias and retrieval of stored electrograms of the arrhythmia episodes. Asymptomatic episodes of atrial fibrillation (AF), sustained ventricular tachycardia (VT), and nonsustained VT of the patients with impaired left ventricular function may have real clinical importance in pacemaker patients. Recognition of these arrhythmias may result in changes in the treatment of the patients, such as anticoagulation of patients with episodes of paroxysmal AF, and therapy guided by electrophysiologic testing of patients with nonsustained or sustained VT. Stored electrograms may also help in defining whether the symptoms experienced by pacemaker patients are due to arrhythmias. Improvements in the arrhythmia detection algorithms and memory functions will still be needed in the future to reliably detect the occurrence of various arrhythmias in pacemaker patients. After these improvements, the diagnostic features of pacemakers should offer a unique opportunity to further improve the clinical management of pacemaker patients. |
4,339 | Transvenous biventricular defibrillation. | The recent success of biventricular pacing with transvenously implantable left ventricular leads suggests that left ventricular leads may be useful for other modes of therapy. Animal studies showed small leads inserted into a left ventricular vein dramatically reduced defibrillation strength requirements. This article describes a human investigation of the feasibility of biventricular defibrillation. Fifty-one patients undergoing implantable cardioverter defibrillator (ICD) implantation were enrolled. After insertion of a standard ICD lead, a prototype over-the-wire left ventricular defibrillation lead was inserted through the coronary sinus and into a vein on the left ventricle. Lead insertion was guided by retrograde venography. The left ventricular lead's location was randomized to the anterior or posterior vein. Randomized, paired defibrillation threshold (DFT) testing was performed to compare a standard ICD shock configuration (Control: right ventricle- --> superior vena cava+ + CAN+) to 1 of 3 biventricular shock configurations. In the anterior vein, the left ventricular lead was tested with either a single biphasic shock from right ventricle + left ventricle- --> superior vena cava+ + CAN+ or a dual biphasic shock. In the posterior vein, the left ventricular lead was tested with a dual biphasic shock. Dual shocks consisted of a 40% tilt biphasic shock from right ventricle- --> superior vena cava+ + CAN+ followed by another 40% tilt biphasic shock from left ventricle- --> superior vena cava+ + CAN+, delivered from a single 225 microF capacitance. Left ventricular lead positioning was successful in 41 of 46 patients (89%). Mean left ventricular lead insertion time was 17 +/- 17 minutes and 13 +/- 15 minutes for anterior and posterior locations, respectively. Mean DFTs were not statistically lower for the left ventricular shock configurations, but retrospective analysis showed a well-defined region of the posterolateral left ventricle where consistent DFT reduction was achieved with dual shocks (14.0 +/- 2.7 J vs 7.8 +/- 0.9 J; n = 5; p = 0.04). There were no adverse events requiring intervention due to the use of the left ventricular lead. Biventricular defibrillation is feasible and safe under the conditions used in this study. Additional studies are needed to verify whether dual shocks with posterolateral left ventricular lead positions consistently reduce DFTs. |
4,340 | Optimal method to achieve consistently low defibrillation energy requirements. | Reduction of the defibrillation energy requirement offers the opportunity to decrease implantable cardioverter defibrillator (ICD) size and to increase device longevity. Therefore, the purpose of this prospective study was to obtain confirmed defibrillation thresholds (DFTs) of < or = 15 J in each patient with an endocardial dual-coil lead system incorporating an active pectoral pulse generator (TRIAD lead system: RV- --> SVC+ + CAN+). According to our previous clinical and experimental studies, we tried to lower DFTs that were > 15 J by repositioning the distal coil of the endocardial lead system in the right ventricle. A total of 190 consecutive patients requiring ICDs for ventricular fibrillation and/or recurrent ventricular tachycardia were investigated at the time of ICD implantation (42 women, 148 men; mean age 61.9 +/- 12.0 years; mean left ventricular ejection fraction 42.7 +/- 16.6%). Coronary artery disease was present in 139 patients; nonischemic dilated cardiomyopathy in 34 patients; and other etiologies in 17 patients; 47 patients had undergone previous cardiac surgery. Regardless of optimal pacing and sensing parameters, for patients having DFTs > 15, we repositioned the distal coil of the endocardial lead system toward the intraventricular septum to include this part of both ventricles within the electrical defibrillating field. In 177 of 190 patients, induced ventricular fibrillation was successfully terminated with < or = 15 J (group I) using the initial lead position. Repositioning of the endocardial lead was necessary in 13 patients whose DFT(plus) (DFT(plus) = second additional success at lowest energy level) were > 15 J (group II). In all patients, repositioning was successful within a 15 J energy level (100% success). The mean DFT(plus) was 7.3 +/- 3.5 J (group I) and 11.0 +/- 4.5 J (group II; p<0.005). The mean DFT(plus) of all patients enrolled in the study was 7.6 +/- 3.7 J (range: 2 to 15 J). In 87% of all patients, DFT(plus) of < or = 10 J was achieved. Repositioning of the endocardial lead in the right ventricle is a simple and effective method to reduce intraoperative high DFTs. As a result of this procedure, ICDs with a 20 J output should be sufficient for the vast majority (87%) of our patients. Furthermore, we were able to avoid additional subcutaneous or epicardial electrodes in all patients. |
4,341 | Matching cardiac rhythm management technology to patient needs: pacing/ablation/implantable cardioverter defibrillators. | Data from 2 decades of clinical electrophysiologic studies have allowed great progress in the evaluation and treatment of patients with sustained ventricular arrhythmias and the appropriate identification of those patients at high risk for subsequent sudden death. The goals of treatment of the patient with ventricular arrhythmias are to suppress symptoms and prevent a fatal event. The steps in providing such therapy include (1) defining the cardiac anatomy; (2) assessing arrhythmia risk through noninvasive or invasive testing; and (3) prescribing treatment based on these results. Patients may be separated into high- and low-risk groups to help identify appropriate treatment. Although low-risk groups may benefit from reassurance or medications such as beta-blockers or verapamil, high-risk groups have been more difficult to treat. Recent randomized trials of implantable cardioverter defibrillators (ICDs) for ventricular arrhythmias suggest that they may provide better protection for high-risk patients than do antiarrhythmic medications. |
4,342 | Evidence rather than costs must guide use of the implantable cardioverter defibrillator. | Randomized controlled trials have shown superior survival rates with implantable cardioverter defibrillators (ICDs) compared with antiarrhythmic drugs in survivors of cardiac arrest and life-threatening ventricular tachyarrhythmias, as well as in high-risk patients with ischemic heart disease and inducible ventricular tachycardia (VT). Current defibrillators are small and implanted with techniques similar to standard pacemakers. They provide high-energy shocks for ventricular fibrillation (VF) and rapid VT, antitachycardia pacing for monomorphic VT, and antibradycardia pacing. Limited evidence suggests that ICD therapy is cost-effective when compared with other widely accepted treatments. The use of ICDs is likely to continue to expand in the future. Ongoing clinical trials will define further prophylactic indications of the ICD and clarify its cost-effectiveness ratio in different clinical settings. |
4,343 | Therapeutic decision tree for patients with sustained ventricular tachyarrhythmias or aborted cardiac arrest: a critical review of the Antiarrhythmics Versus Implantable Defibrillator trial and the Canadian Implantable Defibrillator Study. | Antiarrhythmic drugs, mainly amiodarone and sotalol, radiofrequency catheter ablation, and the implantable cardioverter defibrillator (ICD) are the 3 therapeutic options in patients with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Idiopathic VT, incessant VT, frequently recurring, hemodynamically stable VT, and VT based on bundle branch reentry, are candidates for radiofrequency catheter ablation. Patients with high-risk ventricular tachyarrhythmias should receive ICDs as initial therapy. Two studies, the Antiarrhythmics Versus Implantable Defibrillator trial (AVID) and the Canadian Implantable Defibrillator Study (CIDS) have tried to approach the problem of these high-risk ventricular tachyarrhythmias. Although at 3 years, the ICD in AVID demonstrated a significant relative risk reduction over amiodarone of 31.5%, CIDS could not duplicate this finding. At 3 years, the relative risk reduction conferred by the ICD over amiodarone in CIDS was only 13.7%. A careful analysis of both studies suggests that CIDS was insufficiently powered to demonstrate statistically significant benefits similar to those shown by AVID, and furthermore, seemed to include an undetermined number of low-risk VT patients. The problem in the CIDS trial in this regard was the recruitment of patients in whom the inclusion criteria were met by the arrhythmias induced during the electrophysiology stimulation study, but which did not exist in real life. In addition CIDS included 14% of patients with (1) undocumented syncope and inducible monomorphic sustained VT; or (2) long runs of spontaneous nonsustained VT. Under these circumstances, the therapeutic implications of AVID remain unchallenged. |
4,344 | Multisite atrial pacing: an option for atrial fibrillation prevention? Preliminary results of the Dutch Dual-site Right Atrial Pacing for Prevention of Atrial Fibrillation study. | Multisite pacing is a novel concept for the prevention of recurrent drug-refractory atrial fibrillation (AF). Two different pacing methods have been described, biatrial pacing and dual-site right atrial stimulation. The use of multisite pacing as preventive therapy for recurrences of atrial fibrillation is still under investigation. We conducted a prospective, randomized, crossover study in patients with recurrent drug-refractory AF without or with minimal structural heart disease. After implantation of a DDD pacemaker, patients were randomized to either dual-site pacing first (Group I) or single-site (high right atrium) pacing first (Group II) and, after 6 months of treatment, the device was reprogrammed to the other pacing mode. Preliminary results of 13 patients in each group are presented. Clinical characteristics of patients in both groups with respect to age, sex, left atrial dimension, left ventricular function, and New York Heart Association (NYHA) functional class were comparable. Pacing therapy was combined with antiarrhythmic drug treatment. After completion of the study protocol, the arrhythmia-free interval was not remarkably different in either group. However, the endpoint free interval (i.e., the need for electrical cardioversion because of recurrent AF lasting >24 hours, was less during dual-site pacing in Group II. Within 6 months, 43 patients enrolled in this study will have completed the protocol. |
4,345 | Prevalences of ECG findings in large population based samples of men and women. | To obtain accurate estimates of the prevalence of ECG abnormalities in the general population and to describe them in relation to age, sex, and some lifestyle related factors.</AbstractText>The results were obtained from the records of 47 358 men and women participating in four large Belgian epidemiological studies during the past 30 years. All tracings were read and coded by two trained cardiologists on the basis of Minnesota code criteria.</AbstractText>Prevalences of coronary heart disease and abnormal ECG findings rose exponentially with age in both sexes, with the exception of atrioventricular block and the Wolff-Parkinson-White (WPW) syndrome. Major ECG findings were observed in 6.0% of all men and 4.3% of women, resulting in a significant adjusted sex ratio of 1.66 (95% confidence interval 1.46 to 1.88). The prevalence of minor ECG changes was slightly higher among men (10.4% v 9.5% in women). The occurrence of ischaemia-like findings on the ECG was comparable between men and women (9.0% v 9.8%). Independent of age, smoking, obesity, diabetes, employment status, positive history of angina or infarction, and region, there were significantly higher prevalences of Q/QS patterns, left ventricular hypertrophy, left axis deviation, arrhythmias, and atrial fibrillation or flutter in men than in women. Right bundle branch block and WPW syndrome both occurred 3.5 times more often in men, while the prevalence of left bundle branch block was comparable between the sexes.</AbstractText>The large sample size allowed a precise description of the most important ECG abnormalities. These are not rare in the adult population and most are strongly age related. Sex differences occur with some, but not all, abnormalities. The less common ECG abnormalities were more often observed among men.</AbstractText> |
4,346 | Intradevice interaction in a dual chamber implantable cardioverter defibrillator preventing ventricular tachyarrhythmia detection. | Failure to detect ventricular tachycardia and/or ventricular fibrillation by implantable cardioverter defibrillators (ICDs) is a rare but serious problem. We report a case of failure to detect an episode of induced ventricular tachycardia by a dual chamber ICD, due to abbreviation of ventricular detection window secondary to programmed pacing parameters and a rate-smoothing algorithm. In this patient, the intradevice interaction was corrected by programming rate-smoothing off. This report highlights the potentially lethal consequences of critical timing relationships among the pacing function, arrhythmia detection, and the characteristics of the arrhythmia when using a modern dual chamber ICD. Physicians responsible for patients with ICDs must be aware of such interactions. |
4,347 | Infant case with a malignant form of Brugada syndrome. | We report a 6-month-old Japanese infant with a malignant form of Brugada syndrome, who had frequent episodes of ventricular fibrillation (VF) and nonsustained polymorphic ventricular tachycardia (VT). To the best of our knowledge, this infant is the youngest patient reported to have Brugada syndrome. Continuous infusion of a beta-adrenergic agonist and intravenous injection of a parasympathetic antagonist suppressed the electrical storm of polymorphic VT and VF. Combined oral administration of a beta1-adrenergic agonist, a parasympathetic antagonist, and quinidine has successfully suppressed recurrences of VT or VF for 6 months, and the combination may have the potential to decrease the incidence of VT or VF as an adjunctive therapy with prophylactic placement of an implantable cardioverter defibrillator. |
4,348 | Association between atrial fibrillation and appropriate implantable cardioverter defibrillator therapy: results from a prospective study. | Atrial fibrillation (AF) is associated with significant morbidity and mortality that may be related to hemodynamic impairment, thromboembolic events, or enhanced electrical instability of the ventricular myocardium. There is, however, a lack of data concerning the association of AF and ventricular tachyarrhythmias.</AbstractText>Consecutive patients with indication for an implantable cardioverter defibrillator (ICD) were classified for the presence or absence of persistent AF at the time of device implantation. Incidence of device therapy, stored electrograms, and clinical events during follow-up were evaluated prospectively. Two hundred fifty patients were included. During follow-up (20+/-14 months), patients in AF experienced appropriate device therapy for recurrent ventricular arrhythmias more frequently compared with patients in sinus rhythm (SR) (63% vs 38%, P = 0.01). On multivariate analysis, AF was an independent predictor of appropriate ICD therapy (relative risk 1.8; 95% confidence interval [CI] 1.2 to 2.9) and inappropriate device therapy (relative risk 2.3; 95% CI 1.2 to 4.5). Predefined clinical events (cluster endpoint: death, syncope, and hospitalizations) were observed more frequently in AF than in SR patients (55% vs 31%, P = 0.01). Analysis of device-stored electrograms revealed a higher incidence of short-long-short cycles preceding ventricular arrhythmias in AF compared with SR patients (50% vs 16%, P = 0.002). Baseline heart rate preceding ventricular arrhythmias did not differ between the two groups.</AbstractText>AF is an independent predictor of recurrent ventricular arrhythmias in ICD recipients. The underlying electrophysiologic mechanism seems to be irregular rather than rapid ventricular activation, with a high incidence of short-long-short sequences preceding ventricular tachyarrhythmias in AF patients.</AbstractText> |
4,349 | Diagnosis and therapy of atrial tachyarrhythmias in the dual chamber implantable cardioverter defibrillator. | Devices capable of monitoring and treating atrial tachyarrhythmias provide information about the natural history of the arrhythmias and potentially can influence their natural course by electrical therapy early after onset.</AbstractText>Types of atrial arrhythmias and efficacy of device therapies were evaluated in 30 patients implanted with the Medtronic model 7250 Jewel AF implantable cardioverter defibrillator (ICD). All patients had structural heart disease and documented sustained ventricular and atrial arrhythmias (27 with atrial fibrillation [AF]) before implant. Twenty patients were taking amiodarone, and three were taking sotalol. During 20+/-10 months of follow-up, 600 atrial arrhythmia recurrences were documented in 50% of patients. AF was diagnosed in 19%, fast polymorphic atrial tachycardia (AT) in 20%, fast monomorphic AT in 57%, and slow AT in 4% of episodes. The two adaptive pacing therapies, burst and ramp, together with the 50-Hz burst, were successful in 57% of detected atrial arrhythmias. Burst and ramp were responsible for 49% and 50-Hz burst for 51% of successfully treated arrhythmias; 33% of the episodes terminated spontaneously. No ventricular proarrhythmia was observed due to atrial pacing therapies. In 30% of episodes, dual chamber pacing was required due to post termination bradycardia. Atrial arrhythmia recurrences in patients with dilated cardiomyopathy were not amenable to pacing therapies. Several aspects of atrial arrhythmia diagnosis, therapy, and documentation that are specific for functioning of the Jewel AF are discussed.</AbstractText>Atrial arrhythmias in ICD patients with diseased hearts who are taking Class III antiarrhythmics frequently had longer cycle lengths than AF. Half of these arrhythmias could be terminated with pacing therapies; one third terminated spontaneously.</AbstractText> |
4,350 | Pharmacological profile of SL 59.1227, a novel inhibitor of the sodium/hydrogen exchanger. | 1. The NHE1 isoform of the Na(+)/H(+) exchanger plays an important role in the regulation of intracellular pH and in cardiac cell injury caused by ischaemia and reperfusion. SL 59.1227 is a novel imidazolypiperidine Na(+)/H(+) antiport inhibitor which is structurally unrelated to previously described acylguanidine inhibitors such as cariporide. 2. Recovery of pH(i) following an intracellular acid load was measured in CCL39-derived PS120 variant cells, selectively expressing either NHE1 or NHE2 isoforms of the Na(+)/H(+) exchanger. pH(i) recovery was potently and selectively slowed by SL 59.1227 in NHE1-expressing cells (IC(50) 3.3+/-1.3 nM) versus NHE2-expressing cells (2.3+/-1.0 microM). The respective IC(50) values for cariporide were 103+/-28 nM (NHE1) and 73+/-46 microM (NHE2). 3. In anaesthetized rats following left coronary artery occlusion (7 min) and reperfusion (10 min) SL 59.1227 (10 - 100 microg kg(-1) min(-1) i.v.) inhibited ischaemia-mediated ventricular tachycardia (71 - 100%) and reperfusion-induced ventricular fibrillation (75 - 87%) and prevented mortality. Bolus i.v. administration of SL 59.1227 (1 mg kg(-1)) produced anti-arrhythmic effects when administered either before or during ischaemia. 4. Cardiac infarct size was determined in anaesthetized rabbits following left coronary artery occlusion (30 min) and reperfusion (120 min). Infarct size measured as a percentage of the area at risk was 36.2+/-3.4% (control group) versus 15.3+/-3.9% (SL 59.1227 0.6 mg kg(-1) i.v.). 5. SL 59.1227 is the first example of a potent and NHE1-selective non-acylguanidine Na(+)/H(+) exchanger inhibitor. It possesses marked cardioprotective properties. |
4,351 | [Clinical evaluation of a dual chamber implantable cardioverter-defibrillator]. | Single-chamber ventricular cardioverter-defibrillator (ICD) has been shown to significantly reduce the incidence of sudden cardiac death due to malignant ventricular arrhythmias. However, inappropriate therapy due to supraventricular tachyarrhythmias (mainly atrial fibrillation) affects up to 34% of patients. Moreover, it has been estimated that up to 20% of ICD patients are in the need of physiological antibradycardia pacing. Use of dual-chamber ICD offers an atrial signal for better ability to discriminate atrial from ventricular tachyarrhythmias as well as a maintenance of AV synchrony, what may be of critical importance for patients with a compromised left ventricular function. In the present study we describe our preliminary clinical experience with a dual-chamber ICD's implanted in 20 patients. During the implantation and in-hospital testing, 95 induced VT/VF episodes were correctly diagnosed by ICD, as well as 28 induced FA episodes. Over a mean follow-up period of 10 +/- 6 months, 98 tachycardia episodes were recorded. All 76 VT/VF episodes were correctly diagnosed, as were 18 of 22 FA. Four FA episodes were diagnosed as VT/VF and treated by antitachycardia pacing in 2 cases and by shock in 2. Thus, sensitivity and specificity of VT/VF detection are 100% and 82% respectively. A dual-chamber ICD appears to improve discrimination of atrial from ventricular tachyarrhythmias without loss of sensitivity and to decrease occurrence of inappropriate therapy. AV synchrony, by improving the hemodynamic status of the patient (mainly in those with impaired left ventricular function), may demonstrate better survival and comfort of life. |
4,352 | [Treatment of cardiac arrhythmia in pregnant women]. | The management of arrhythmias during pregnancy is, in principle, similar to that in nonpregnant patients, however, special consideration must be given, to avoid adverse fetal effects. In pregnant women without organic heart disease, no drug therapy is usually needed for the management of supraventricular or ventricular premature beats, but potential stimulants, such as smoking, caffeine, and alcohol should be eliminated. In patients with mitral valve prolapse beta blocker may be preferred drug. In pregnant patients with organic heart disease, paroxysmal atrial or ventricular tachycardia may induce hemodynamic changes with consequences to the fetus. In paroxysmal atrial tachycardia vagal stimulation maneuvers should tried and, if this is not effective, adenosine or beta-adrenergic blocking agents should be used. Alternatively, verapamil may be given. In pregnant with atrial fibrillation, the goal of treatment is conversion to sinus rhythm or control of the ventricular rate by digoxin. Synchronized electrical cardioversion may become necessary when signs of cardiac decompensation or hypotension were developed. Ventricular arrhythmias may occur in the pregnant women with cardiomyopathy, valvular heart disease, mitral valve prolapse and congenital Q-T prolongation. Termination of ventricular arrhythmias can usually be achieved by intravenous lignocaine or procainamide or by electrical cardioversion. To prevent recurrences, quinidine can be used if the arrhythmia was not induced by QT prolongation or procainamide. |
4,353 | High defibrillation threshold at cardioverter defibrillator implantation under amiodarone treatment: favorable effects of D, L-sotalol. | A 57-year-old man with primary dilated cardiomyopathy and obesity received an implantable cardioverter defibrillator because of recurrent, poorly tolerated ventricular tachycardia despite continuous treatment with amiodarone. When the device was implanted, assessment of the ability to defibrillate induced ventricular fibrillation showed high energy requirements, with a lack of conventional safety margin between energies effective at defibrillation testing and maximal device output. Treatment with oral amiodarone was withdrawn and substituted with oral sotalol. A repeat defibrillation test, performed 54 days after amiodarone withdrawal and during D,L -sotalol treatment, showed a reduction in defibrillation energy requirements. In view of this experience, replacement of amiodarone treatment with an alternate class III agent (D,L -sotalol or other agents, if available) can be considered as a possible option in case of high defibrillation threshold at the time of the implantation in a patient receiving continuous amiodarone treatment. |
4,354 | Simultaneous maps of optical action potentials and calcium transients in guinea-pig hearts: mechanisms underlying concordant alternans. | 1. The mechanisms underlying electro-mechanical alternans caused by faster heart rates were investigated in perfused guinea-pig hearts stained with RH237 and Rhod-2 AM to simultaneously map optical action potentials (APs) and intracellular free Ca2+ (Ca2+i). 2. Fluorescence images of the heart were focused on two 16 x 16 photodiode arrays to map Ca2+i (emission wavelength (lamdda;em) = 585 +/- 20 nm) and APs (lamdda;em > 715 nm) from 252 sites. Spatial resolution was 0.8 mm x 0.8 mm per diode and temporal resolution 4000 frames s-1. 3. The mean time-to-peak for APs and [Ca2+]i was spatially homogeneous (8.8 +/- 0.5 and 25.6 +/- 5.0 ms, respectively; n = 6). The durations of APs (APDs) and Ca2+i transients were shorter at the apex and progressively longer towards the base, indicating a gradient of ventricular relaxation. 4. Restitution kinetics revealed increasingly longer delays between AP and Ca2+i upstrokes (9.5 +/- 0.4 to 11.3 +/- 0.4 ms) with increasingly shorter S1-S2 intervals, particularly at the base, despite nearly normal peak [Ca2+]i. 5. Alternans of APs and Ca2+i transients were induced by a decrease++ in cycle length (CL), if the shorter CL captured at the pacing site and was shorter than refractory periods (RPs) near the base, creating heterogeneities of conduction velocity. 6. Rate-induced alternans in normoxic hearts were concordant (long APD with large [Ca2+]i) across the epicardium, with a magnitude (difference between odd-even signals) that varied with the local RP. Alternans were initiated by gradients of RP, producing alternans of conduction that terminated spontaneously without progressing to fibrillation. |
4,355 | Mode of onset of ventricular fibrillation in patients with Brugada syndrome detected by implantable cardioverter defibrillator therapy. | We sought to demonstrate the mode of spontaneous onset of ventricular fibrillation (VF) in patients with Brugada syndrome.</AbstractText>The electrophysiologic mechanisms of VF in Brugada syndrome have not been fully investigated.</AbstractText>Nineteen patients (all male, mean age 47 +/- 12 years) with Brugada syndrome were treated with an implantable cardioverter defibrillator (ICD). The implanted devices were capable of storing electrograms during an arrhythmic event. We investigated the mode of spontaneous onset of VF according to the electrocardiographic features during the episode of VF, which were obtained from stored electrograms of ICDs and/or electrocardiographic (ECG) monitoring.</AbstractText>During a follow-up of 34.7 +/- 19.4 months (range 14 to 81 months), 46 episodes of spontaneous VF attacks were documented in 7/19 (37%) patients. The event-free period between ICD implantation and the first spontaneous occurrence of VF was 14.6 +/- 12.1 months (range 3.7 to 27.4 months). We investigated 33/46 episodes of VF, for which electrocardiographic features (10 to 20 s before and during VF) were obtained from ICDs and/or ECG monitoring in five patients. A total of 22/33 episodes of VF were preceded by premature ventricular contractions (PVCs), which were almost identical to the initiating PVCs of VF. Furthermore, in three patients who had multiple VF episodes, VF attacks were always initiated by the same respective PVC. The coupling interval of the initiating PVCs of VF was 388 +/- 28 ms.</AbstractText>Spontaneous episodes of VF in patients with Brugada syndrome were triggered by specific PVCs. These findings may provide important insights into the pathophysiological mechanisms causing VF in Brugada syndrome.</AbstractText> |
4,356 | Bosentan the mixed endothelin-A- and -B-receptor antagonist suppresses intrapericardial endothelin-1-induced ventricular arrhythmias. | In earlier studies severe ventricular arrhythmias developed during intrapericardial (i.p.) endothelin-1 (ET-1) infusion. Monophasic action potential duration (MAPD90) increase and significant ST segment elevation preceded the onset of arrhythmias. The aim of this study was to test the antiarrhythmic and anti-ischemic efficacy of the mixed endothelin-A- and -B- (ETA/B) receptor antagonist bosentan (BOS) on ET-1-induced arrhythmias on six mongrel dogs. Ten minutes after an intravenous bolus dose of BOS (10 mg/kg), ET-1 (33 pmol/kg/min) was given into the pericardial space for 30min (BOS group). Six control dogs received only ET-1 infusion (control group). Mean arterial blood pressure (MAP), cardiac output, electrocardiograph (ECG), right and left ventricular endo- and epicardial (RVEND, RVEP, LVEND, LVEP) MAPD90s were recorded. MAP and cardiac output did not change significantly in the BOS group. Significant MAPD90 prolongation was found in all investigated regions of the control group (ET start vs ET 20 min: LVEP, 174 +/- 3 vs 208 +/- 10*; RVEND, 206 +/- 9 vs 241 +/- 12* ms, *p < 0.05), while significant MAPD90 alterations were not observed in the BOS group (basic vs ET 20 min: RVEP, 189 +/- 5 vs 196 +/- 5; LVEP, 199 +/- 5 vs 199 +/- 4; RVEND, 194 +/- 5 vs 195 +/- 6; LVEND, 209 +/- 3 vs 213 +/- 5 ms). Early after depolarizations (EADs) were observed in three control dogs. Severe ventricular arrhythmias [incessant nonsustained ventricular tachycardias (nsVTs) in all cases, sustained VTs (sVTs) in four, ventricular fibrillation (VF) in two instances] were present in the control group, whereas nsVTs were observed only in two dogs in the BOS group. ST segment elevation was more pronounced in the control group than in the BOS group (1.01 +/- 0.2 vs 0.41 +/- 0.07 mV, p < 0.05). In summary, bosentan effectively inhibits intrapericardial ET- 1-induced ventricular arrhythmias, moreover it may have a protective effect against epimyocardial ischemia. |
4,357 | Endothelin-A-receptor antagonist LU 135.252 inhibits the formation of ventricular arrhythmias caused by intrapericardial infusion of endothelin-1. | Intrapericardial endothelin-1 (ET-1) infusion causes dose-dependent severe ventricular arrhythmias. We examined the effects of the endothelin-A- (ETA) receptor antagonist LU 135.252 (LU) on ET-1-induced arrhythmias on six open-chest mongrel dogs. Ten minutes after an intravenous bolus of LU (5 mg/kg), ET- 1 (33 pmol/kg/min) was given into the pericardial space for 30 min (LU group). Six dogs received ET-1 infusion without LU treatment (control group). Mean arterial blood pressure (MAP), cardiac output, electrocardiograph (ECG), right ventricular endocardial and epicardial (RVEND, RVEP), and left ventricular endocardial and epicardial (LVEND, LVEP) monophasic action potential durations (MAPDs) were recorded. No significant changes were observed in MAP and cardiac output. MAPD90s did not change significantly in the LU group (basic vs ET 20min: RVEP, 186 +/-7 vs 190 +/- 7; LVEP, 189 +/- 8 vs 201 +/- 11; RVEND, 191 +/- 10 vs 192 +/- 9; LVEND, 199 +/- 11 vs 203 +/- 11 ms), while significant MAPD90 prolongation was found in all investigated regions of the control group (ET start vs ET 20 min: LVEP, 174 +/- 3 vs 208 +/- 10*; RVEND, 206 +/- 9 vs 241 +/- 12* ms, *p < 0.05). No early after depolarization (EAD) was observed in the LU group, while EADs occurred in three controls. In the LU group, we have not found any significant arrhythmias except nonsustained ventricular tachycardias (nsVTs) in one animal. In the control group incessant nsVTs were observed in six, sustained VTs (sVTs) in four and ventricular fibrillation (VF) in two instances. Significant ST-elevation was observed in all animals in the LU and control groups (LU: 6.7 +/- 2.1 mV; control: 10.1 +/- 2.0 mV, p = NS). In conclusion, the arrhythmogenic action and the main electrophysiological effects of pericardial ET-1 infusion, MAPD prolongation and EAD formation, are inhibited by LU. However, LU could not prevent the ischemic changes resulting from ET-1 infusion. |
4,358 | The selective endothelin-A-receptor antagonist LU 135.252 inhibits the direct arrhythmogenic action of endothelin-1. | Besides being a strong vasoconstrictor, endothelin-1 (ET-1) also causes severe ventricular arrhythmias. The aim of our study was to differentiate between the vasoconstrictor and arrhythmogenic actions of ET-1 by using the selective endothelin-A-(ETA) receptor antagonist LU 135.252 (LU). A bolus injection of 5 mg/kg LU was administered to 10 anesthetized mongrel dogs in group A. The 30 min intracoronary ET-1 infusion was started 20 min after the LU bolus at a rate of 60 pmol/min. In the control group (group B, n = 8) only ET-1 was administered (60 pmol/min). The left anterior descending coronary artery blood flow (CBF), cardiac output, electrocardiograph (ECG) and arterial blood pressure were monitored. Two monophasic action potential duration (MAPD) catheters were placed onto the left ventricular epicardium (LVEP) and into the right ventricular endocardium (RVEND) to follow electrophysiologic changes. No significant changes were observed in blood pressure (0 min vs 30 min: group A, 99.0 +/- 4.5 vs 90.0 +/- 5.2 mmHg, p = NS; group B, 103 +/- 6 vs 104 +/- 3 mmHg, p = NS), cardiac output (0 min vs 30 min: group A, 3.5 +/- 0.7 vs 3.2 +/- 0.8 l/min, p = NS; group B, 3.6 +/- 0.4 vs 3.3 +/- 0.3 l/min, p = NS), and MAPD90 (0 min vs 30 min: group A, LVEP, 241 +/- 11 vs 260 +/- 14 ms; RVEND, 233 +/- 5 vs 239 +/- 8 ms, p = NS), whereas a significant decrease was observed in CBF (deltaCBF 30 min: group A, -28 +/- 2%, p < 0.05; group B, -32 +/- 3%, p < 0.05). In group A ventricular fibrillation (VF) occurred once. Ventricular premature contractions (VPCs) and short, nonsustained ventricular tachycardias (nsVTs) were observed in seven cases. Early after depolarizations and a MAPD90 increase were observed in the control group B (0 min vs 30 min: LVEP, 244 +/- 10 vs 292 +/- 12 ms; RVEND, 255 +/- 9 vs 290 +/- 8 ms) accompanied by VPCs, incessant nsVTs. Sustained VT and VF were evident in seven cases. Our results indicate, that the applied single bolus injection of LU effectively prevents ET-1-induced major ventricular arrhythmias, whereas it has no effect on coronary vasoconstriction. These data support the notion that ET-1 possesses a direct arrhythmogenic action. |
4,359 | Sarafotoxin 6c protects against ischaemia-induced cardiac arrhythmias in vivo and in vitro in the rat. | The aim of this study was to investigate whether the endothelin-B- (ETB) receptor agonist sarafotoxin 6c (S6c) can protect against ischaemia-induced cardiac arrhythmias. Arrhythmias were induced by a 30 min period of coronary artery occlusion in pentobarbitone-anaesthetized male rats, or in Langendorff-perfused rat hearts. Rats or rat hearts were administered a bolus dose of vehicle or S6c (0.8 nmol/kg i.v. or 10(-8) M into the coronary circulation, respectively) 5 min before the onset of ischaemia. In vivo administration of S6c significantly reduced the incidence of ventricular fibrillation (VF) from 59% to 13% and the number of premature ventricular beats. This effect was associated with a transient fall in mean arterial blood pressure. In isolated hearts, S6c reduced significantly both the incidences of ventricular tachycardia (VT) and VF while having no statistically significant effect on coronary perfusion pressure. This is the first report to show that stimulation of ETB-receptors, with a bolus dose of S6c, has an antiarrhythmic effect on rat hearts both in vivo and in vitro, suggestive of a direct effect on the myocardium. |
4,360 | Significance of R-on-T phenomenon in early ventricular tachyarrhythmia susceptibility after acute myocardial infarction in the thrombolytic era. | We investigated the clinical significance and mechanism of the R-on-T phenomenon in the current thrombolytic era as potential precipitant of R-on-T-induced early ventricular tachyarrhythmias in patients with a thrombolysed acute myocardial infarction. We also examined the role of QT dispersion on ventricular vulnerability and its association with R-on-T-initiated ventricular tachyarrhythmias. A total of 93 patients underwent 24-hour Holter monitoring starting at hospital admission before thrombolysis. Patients were classified into 2 groups: those with (n = 76) and those without (n = 17) reperfusion according to electrocardiographic criteria. All R-on-T ventricular premature complexes (VPCs) and R-on-T-initiated arrhythmic events (ventricular tachycardia [VT], ventricular fibrillation) were counted to estimate arrhythmia density and severity in 2 time periods during and after completion of thrombolysis. Measurements of QT and QTc intervals and dispersion parameters were obtained on the 12-lead electrocardiogram before thrombolysis and at 24 hours in patients with and without R-on-T VTs. Overall, R-on-T VPCs were rarely observed (1.8% of total VPCs over 24 hours), occurring more frequently during than after thrombolysis (at a rate of 8 vs 0.6 VPCs/hour, p = NS) and at a higher rate during thrombolysis in nonreperfused than in perfused patients (15 vs 8/hour, p = NS). Three VF episodes were observed in 1 reperfused patient, and all were R-on-T initiated. Episodes of nonsustained R-on-T VTs (3.3% of total VTs over 24 hours) appeared more frequent during than after thrombolysis (at a rate of 0.8 vs 0.05 VPCs/ hour, p = NS), and compared with non-R-on-T VTs they were significantly faster (374 +/- 56 ms vs 411 +/- 69 ms; p < 0.05), with a trend toward longer duration. Our findings indicate that R-on-T VPCs and R-on-T VTs are early rare features in acute myocardial infarction, and do not serve as triggers of severe ventricular tachyarrhythmia. The study of ventricular repolarization did not elicit an identifiable risk factor of R-on-T VT susceptibility. |
4,361 | Long-term prognostic value of time domain analysis of signal-averaged electrocardiography in idiopathic dilated cardiomyopathy. | The aim of this study was to evaluate the long-term prognostic value of signal-averaged electrocardiography (SAECG) in idiopathic dilated cardiomyopathy (IDC). Time domain analysis of SAECG was assessed in 131 patients with angiographically confirmed IDC (age 52+/-12 years; 108 men; left ventricular ejection fraction 33+/-12%) using specific criteria in 44 patients with bundle branch block. Late potentials (LP) on SAECG were present in 27% of the patients. Patients with LP had a similar left ventricular ejection fraction and a similar left ventricular end-diastolic diameter than patients with a normal SAECG. With a follow-up of 54+/-41 months, 24 patients suffered cardiac death and 19 had major arrhythmic events (sudden death, resuscitated ventricular fibrillation, or sustained ventricular tachycardia). Patients with LP had an increased risk of all-cause cardiac death (RR 3.3, 95% confidence interval 1.5 to 7.5, p = 0.004) and of arrhythmic events (RR 7.2, 95% confidence interval 2.6 to 19.4, p = 0.0001). Using multivariate analysis, only LP on SAECG (p = 0.001), reduced SD of all normal-to-normal intervals (SDNN) (p = 0.002), increased pulmonary capillary wedge pressure (p = 0.005), and history of sustained ventricular tachyarrhythmia (p = 0.02) predicted cardiac death. A history of previous sustained ventricular tachyarrhythmia (p = 0.0001), reduced SDNN (p = 0.003), and LP on SAECG (p = 0.006) were the only independent predictors of major arrhythmic events. Results were not altered when considering separately patients with or without bundle branch block, or after exclusion of patients with a history of sustained ventricular tachyarrhythmia. This study is one of the first to suggest that LP on SAECG is an independent predictor of all-cause cardiac death and is of high interest for arrhythmia risk stratification in IDC. |
4,362 | Effect of ethanol on defibrillation energy requirements in humans. | The purpose of this double-blind study was to determine the effect of intravenous ethanol administration on defibrillation efficacy in 18 patients with an implantable defibrillator. The equivalent of 60 ml of 100 proof ethanol did not impair defibrillation efficacy. |
4,363 | Effect of rhythm regularization on left ventricular contractility in patients with atrial fibrillation. | In 10 patients with atrial fibrillation, echocardiographic measures of left ventricular function-interval relations were used to assess contractility and to test the hypothesis that rhythm regularization produces a higher contractile state than is seen when the rhythm is irregular. Regularization, following direct-current cardioversion, did not augment ventricular contractility above that seen during atrial fibrillation. |
4,364 | CPR artifact removal from human ECG using optimal multichannel filtering. | The purpose of this study was to assess whether the artifacts presented by precordial compressions during cardiopulmonary resuscitation could be removed from the human electrocardiogram (ECG) using a filtering approach. This would allow analysis and defibrillator charging during ongoing precordial compressions yielding a very important clinical improvement to the treatment of cardiac arrest patients. In this investigation we started with noise-free human ECGs with ventricular fibrillation (VF) and ventricular tachycardia (VT) records. To simulate a realistic resuscitation situation, we added a weighted artifact signal to the human ECG, where the weight factor was chosen to provide the desired signal-to-noise ratio (SNR) level. As artifact signals we used ECGs recorded from animals in asystole during precordial compressions at rates 60, 90, and 120 compressions/min. The compression depth and the thorax impedance was also recorded. In a real-life situation such reference signals are available and, using an adaptive multichannel Wiener filter, we construct an estimate of the artifact signal, which subsequently can be subtracted from the noisy human ECG signal. The success of the proposed method is demonstrated through graphic examples, SNR, and rhythm classification evaluations. |
4,365 | [Implantable cardioverter/defibrillator: long-term stability of the defibrillation threshold with a unipolar electrode configuration (active-can")]. | The majority of cardioverter/defibrillator (ICD) implantations are currently performed with a non-thoracotomy approach. From November 1993 to January 1995, 46 patients underwent implantation of a PCD 7219C with an "active-can" lead configuration at our institution. While the chronic stability of the defibrillation threshold (DFT) for an epicardial lead system is well established, the results are still inconsistent for non-thoracotomy lead systems. Accordingly, the aim of the present study was to compare the acute and chronic defibrillation thresholds of the ICDs implanted with an "active-can" lead system in order to assess the chronic stability of these systems. The defibrillation energy requirements were measured at implant, prior to hospital discharge, three, six and twelve months after implantation of the defibrillator. The patient group consisted of 8 females and 38 males with a mean age of 57.2 years. The mean left ventricular ejection fraction was 43.8%. The most frequent underlying heart disease was coronary artery disease in 31 of 46 patients. Eight patients had idiopathic dilated cardiomyopathy. In 39 of 46 patients, the defibrillation threshold could be successfully determined at all 4 time points after implantation. The mean defibrillation energy requirement at the time of implantation was 9.2 +/- 5.9 Joules (J). The subsequent mean energy requirements were 7.6 +/- 4.8 J at pre-hospital discharge, 8.6 +/- 5.7 J at the 3 month, 8.1 +/- 6.0 J at the 6 month and 8.6 +/- 5.8 J at the 12 month follow-up visits. The mean defibrillation threshold was lowest at the time of prehospital discharge, significantly lower than at the time of initial implantation (p = 0.021). However, at all later time points up to one year, there was no significant difference in the DFT as compared with the time of initial implantation. Comparing the DFT at the time of implantation and the DFT at all other time points, there were no significant differences (9.23 vs. 8.56 J, p = 0.291). Although there was an initial decrease in the DFT at seven to ten days, the long-term stability of the DFT up to one year remained stable in the devices with the "active-can" lead system. |
4,366 | [Treatment of tachycardic atrial fibrillation by catheter-assisted electrical stimulation of the cardiac parasympathetic nervous system]. | Treatment of tachycardic atrial fibrillation (AF) is difficult in patients with congestive heart failure because many drugs which exert negative dromotropic effects (beta-blockers, calcium channel antagonists) may depress ventricular contractility and/or decrease arterial blood pressure. We have identified 2 intravascular sites in the superior (SVC) and inferior vena cava (IVC) where parasympathetic nerves, which innervate the atrioventricular node, can be stimulated electrically. In 8 dogs, a 7-F catheter with an expandable electrode basket at its tip was non-fluoroscopically positioned in the SVC and in the proximal IVC (time for positioning: 3-5 minutes). High-frequency electrical parasympathetic stimulation (PS) with 20 Hz at an impulse duration of 0.1 ms was performed during pacing induced AF.</AbstractText>With increasing stimulus strength, a graded ventricular rate slowing was observed during PS in the SVC and IVC (P < 0.01, ANOVA). The negative dromotropic effect started instantaneously after onset of PS and ceased immediately after termination of PS. During ventricular pacing at a constant rate, no decrease of the arterial blood pressure was observed during PS. PS in the IVC yielded significantly lower stimulation thresholds than in the SVC.</AbstractText>Transvenous parasympathetic stimulation for ventricular rate control during AF can easily be achieved in the SVC and IVC in dogs. This procedure may provide a foundation for investigating the usefulness of PS in humans. If the results translate to patients, PS may be very beneficial in the treatment of AF in patients with congestive heart failure.</AbstractText> |
4,367 | Ablate and pace for drug refractory paroxysmal atrial fibrillation. Is ablation necessary? | Atrio-ventricular junctional ablation with pacemaker insertion has been shown to improve quality of life in patients with drug refractory paroxysmal atrial fibrillation. It is unknown whether this improvement is secondary to the ablation procedure or to the pacemaker mode utilised. To investigate this we reviewed our experience of implanting a dual chamber rate responsive pacemaker with mode switching (DDDR/MS) alone on quality of life in this patient group.</AbstractText>Over a 1-year period, 19 patients (mean age 62+/-9 years, 13 female) with drug refractory paroxysmal atrial fibrillation (mean duration of symptoms 8.7+/-7 years, failed 3.1+/-0.9 anti-arrhythmic drugs, amiodarone in 15) were recruited. Quality of life was assessed at baseline and after 1 month using a cardiac specific questionnaire, the modified Karolinska questionnaire. The mean score for all patients significantly improved by 39% at follow up (baseline 59+/-24, 1 month 36+/-24, P=0.001). Individually 15 patients (79%) had an improvement in their score, whilst for 13 patients (68%) their symptoms were sufficiently improved after pacing that ablation was not required. The benefit was maintained to a mean follow up of 12+/-5 months (score 31+/-20, P<0.001). Six patients remained symptomatic after pacing and requested further treatment. Benefit was unrelated to symptoms at baseline or the number and total duration of paroxysmal atrial fibrillation episodes recorded on pacemaker Holter.</AbstractText>Patients with drug refractory paroxysmal atrial fibrillation, DDDR/MS pacing alone can improve quality of life without concurrent atrio-ventricular junctional ablation in a significant proportion of patients.</AbstractText> |
4,368 | Clinical and genetic heterogeneity of right bundle branch block and ST-segment elevation syndrome: A prospective evaluation of 52 families. | The ECG pattern of right bundle branch block and ST-segment elevation in leads V(1) to V(3) (Brugada syndrome) is associated with high risk of sudden death in patients with a normal heart. Current management and prognosis are based on a single study suggesting a high mortality risk within 3 years for symptomatic and asymptomatic patients alike. As a consequence, aggressive management (implantable cardioverter defibrillator) is recommended for both groups.</AbstractText>Sixty patients (45 males aged 40+/-15 years) with the typical ECG pattern were clinically evaluated. Events at follow-up were analyzed for patients with at least one episode of aborted sudden death or syncope of unknown origin before recognition of the syndrome (30 symptomatic patients) and for patients without previous history of events (30 asymptomatic patients). Prevalence of mutations of the cardiac sodium channel was 15%, demonstrating genetic heterogeneity. During a mean follow-up of 33+/-38 months, ventricular fibrillation occurred in 5 (16%) of 30 symptomatic patients and in none of the 30 asymptomatic patients. Programmed electrical stimulation was of limited value in identifying patients at risk (positive predictive value 50%, negative predictive value 46%). Pharmacological challenge with sodium channel blockers was unable to unmask most silent gene carriers (positive predictive value 35%).</AbstractText>At variance with current views, asymptomatic patients are at lower risk for sudden death. Programmed electrical stimulation identifies only a fraction of individuals at risk, and sodium channel blockade fails to unmask most silent gene carriers. This novel evidence mandates a reappraisal of therapeutic management.</AbstractText> |
4,369 | Effects of digoxin on acute, atrial fibrillation-induced changes in atrial refractoriness. | Atrial fibrillation (AF) shortens the atrial effective refractory period (ERP) and predisposes to further episodes of AF. The acute changes in atrial refractoriness may be related to tachycardia-induced intracellular calcium overload. The purpose of this study was to determine whether digoxin, which increases intracellular calcium, potentiates the acute effects of AF on atrial refractoriness in humans.</AbstractText>In 38 healthy adults, atrial ERP was measured at basic drive cycle lengths (BDCLs) of 350 and 500 ms after autonomic blockade. Nineteen patients had been treated with digoxin for 2 weeks. After a several-minute episode of AF, atrial ERP was measured serially at alternating BDCLs. Compared with pre-AF ERPs, the first post-AF ERPs were significantly shorter in both the digoxin and the control groups (P:<0.001). The post-AF ERP at a BDCL of 350 ms shortened to a greater degree in the digoxin group (37+/-16 ms) than in the control group (20+/-13 ms, P:<0.001); similar changes occurred at a BDCL of 500 ms. During post-AF determinations of the atrial ERP, secondary AF episodes occurred significantly more often in the digoxin group (32% versus 16%; P:<0. 04).</AbstractText>After a brief episode of AF, digoxin augments the shortening that occurs in atrial refractoriness and predisposes to the reinduction of AF. These effects occur in the setting of autonomic blockade and therefore are more likely to be due to the effects of digoxin on intracellular calcium than to its vagotonic effects.</AbstractText> |
4,370 | Proarrhythmic effects of fluoroquinolone antibacterial agents: in vivo effects as physiologic substrate for torsades. | Drug-induced prolongation of the QT interval is often associated with the onset of Torsades de Pointes (TdP) resulting in a life-threatening ventricular arrhythmia. The potential of the proarrhythmic effects of the new fluoroquinolone antibacterial agents, levofloxacin and sparfloxacin, was examined in the chronic complete atrioventricular block dogs with stable idioventricular automaticity using Holter ECG monitoring in conscious state (Experiment 1). Next, to better analyze the mechanisms of the proarrhythmic property, the cardiovascular effects of these two drugs were compared in the halothane-anesthetized dogs under the monitoring of ECG, His bundle electrogram, systemic and left ventricular pressure, monophasic action potential, cardiac output, and effective refractory period (Experiment 2). In Experiment 1, oral administration of 6 mg/kg (n = 4) as well as 60 mg/kg (n = 4) of levofloxacin did not induce any ventricular premature depolarization. On the other hand, oral administration of 60 mg/kg of sparfloxacin (n = 4) induced TdP leading to ventricular fibrillation in all animals within 24 h, while 6 mg/kg of sparfloxacin (n = 4) did not induce any ventricular premature depolarization. In Experiment 2, intravenous administration of 0.3 mg/kg as well as 3.0 mg/kg of levofloxacin slightly increased cardiac output, but no significant changes were detected in the other parameters (n = 6). On the other hand, intravenous administration of 0.3 mg/kg of sparfloxacin prolonged the effective refractory period. Additional administration of 3.0 mg/kg of sparfloxacin decreased the heart rate and prolonged the effective refractory period and ventricular repolarization phase in a similar extent, but no significant changes were detected in the other parameters (n = 6). These results suggest that backward shift of the relative repolarization period in a cardiac cycle may be the mechanism responsible for the torsadegenic effect of sparfloxacin. |
4,371 | [Experience in 1,500 patients undergoing radiofrequency ablation in the treatment of tachycardias]. | Several reports have demonstrated that radiofrequency catheter ablation provides effective control of a variety of supraventricular and ventricular tachycardias. This report details the results of radiofrequency catheter ablation in 1500 consecutive patients with a wide variety of supraventricular and ventricular tachycardias treated in the Instituto Nacional de Cardiología "Ignacio Chavez", between April 22, 1992 until December of 1999. Tachycardias were associated with the presence of an accessory pathway in 987 patients (65.8%). Dual accessory pathways were present in 24 patients giving a total of 1,012 accessory pathways. The mechanism of the arrhythmia was atrioventricular nodal reentrant tachycardia in 321 patients (21.4%). Ablation of the reentrant circuit of atrial flutter within the right atrium was attempted in 109 (7.2%) patients and a primary atrial tachycardia in 13 patients (0.8%). Atrioventricular node ablation and permanent pacemaker implantation were performed in 26 patients (1.7%). Finally we performed radiofrequency catheter ablation in 37 (2.4%) patients with ventricular tachycardia. Radiofrequency catheter ablation was successful in 908 of 1012 (89.7%) patients with accessory pathways with a complication rate of 10 (0.98%) and a recurrence rate of 92 (9%). AV nodal reentry was successfully abolished in 319 of 321 patients by selective ablation of the slow pathway in 297/321 (92.5%) patients and the fast pathway in 22/24 (92%) patients. The complication rate of this group was 8/321 (2.4%) with a recurrence rate of 34 patients (10.5%). The reentrant circuit of atrial flutter was ablated successfully in 86 of 109 (76.8%) patients with a recurrence flutter in 14 (12.8%) patients. Five of 13 (38.4%) cases of primary atrial tachycardia were successfully ablated. Complete AV block was achieved in 26 of 26 (100%) patients with atrial fibrillation or flutter treated by AV nodal ablation. The procedure was successful in 28 of 37 (75.6%) patients with fascicular ventricular tachycardia. The results of this series of patients demonstrates the safety and efficacy of radiofrequency ablation for the treatment of a wide variety of taquicardias with high rate of success 1375 of 1500 patients (91.6%), with 142 recurrences (9.4%), 15 complications (1%), and no mortality. |
4,372 | Effect of implantable cardioverter-defibrillator shocks on QT dispersion. | Following transvenous implantable cardioverter defibrillator shocks, a significant increase in QT dispersion was observed. We suggest shock-induced increased dispersion of myocardial repolarization as one of the mechanisms of shock-induced proarrhythmia. |
4,373 | Use of automated external defibrillators by a U.S. airline. | Passengers who have ventricular fibrillation aboard commercial aircraft rarely survive, owing to the delay in obtaining emergency care and defibrillation.</AbstractText>In 1997, a major U.S. airline began equipping its aircraft with automated external defibrillators. Flight attendants were trained in the use of the defibrillator and applied the device when passengers had a lack of consciousness, pulse, or respiration. The automated external defibrillator was also used as a monitor for other medical emergencies, generally at the direction of a passenger who was a physician. The electrocardiogram that was obtained during each use of the device was analyzed by two arrhythmia specialists for appropriateness of use. We analyzed data on all 200 instances in which the defibrillators were used between June 1, 1997, and July 15, 1999.</AbstractText>Automated external defibrillators were used for 200 patients (191 on the aircraft and 9 in the terminal), including 99 with documented loss of consciousness. Electrocardiographic data were available for 185 patients. The administration of shock was advised in all 14 patients who had electrocardiographically documented ventricular fibrillation, and no shock was advised in the remaining patients (sensitivity and specificity of the defibrillator in identifying ventricular fibrillation, 100 percent). The first shock successfully defibrillated the heart in 13 patients (defibrillation was withheld in 1 case at the family's request). The rate of survival to discharge from the hospital after shock with the automated external defibrillator was 40 percent. A total of 36 patients either died or were resuscitated after cardiac arrest. No complications arose from use of the automated external defibrillator as a monitor in conscious passengers.</AbstractText>The use of the automated external defibrillator aboard commercial aircraft is effective, with an excellent rate of survival to discharge from the hospital after conversion of ventricular fibrillation. There are not likely to be complications when the device is used as a monitor in the absence of ventricular fibrillation.</AbstractText> |
4,374 | Outcomes of rapid defibrillation by security officers after cardiac arrest in casinos. | The use of automated external defibrillators by persons other than paramedics and emergency medical technicians is advocated by the American Heart Association and other organizations. However, there are few data on the outcomes when the devices are used by nonmedical personnel for out-of-hospital cardiac arrest.</AbstractText>We studied a prospective series of cases of sudden cardiac arrest in casinos. Casino security officers were instructed in the use of automated external defibrillators. The locations where the defibrillators were stored in the casinos were chosen to make possible a target interval of three minutes or less from collapse to the first defibrillation. Our protocol called for a defibrillation first (if feasible), followed by manual cardiopulmonary resuscitation. The primary outcome was survival to discharge from the hospital.</AbstractText>Automated external defibrillators were used, 105 patients whose initial cardiac rhythm was ventricular fibrillation. Fifty-six of the patients 153 percent) survived to discharge from the hospital. Among the 90 patients whose collapse was witnessed (86 percent), the clinically relevant time intervals were a mean (+/-SD) of 3.5+/-2.9 minutes from collapse to attachment of the defibrillator, 4.4+/-2.9 minutes from collapse to the delivery of the first defibrillation shock, and 9.8+/-4.3 minutes from collapse to The arrival of the paramedics. The survival rate was 74 percent for those who received their first defibrillation no later than three minutes after a witnessed collapse and 49 percent for those who received their first defibrillation after more than three minutes.</AbstractText>Rapid defibrillation by nonmedical personnel using an automated external defibrillator can improve survival after out-of-hospital cardiac arrest due to ventricular fibrillation. Intervals of no more than three minutes from collapse to defibrillation are necessary to achieve the highest survival rates.</AbstractText> |
4,375 | Fatal arrhythmia in a juvenile athlete due to myocardial hypertrophy and infarction. | This report is a case history of a 16-year-old highly trained athlete who suffered from ventricular fibrillation during exhaustive physical activity. After resuscitation and admission into hospital ECG revealed posterior wall infarction. Thrombolytic therapy was advised and ST-segment elevation reversed. Within 48 h cerebral edema evolved due to hypoxic brain damage and the subject deceased after 16 days despite prolonged maximum antiedematous therapy. Autopsy confirmed the diagnosis of concentric myocardial hypertrophy (total heart weight 568 g) without signs of coronary artery disease. Systemic inflammatory diseases and drug abuse were ruled out by lab studies, evidence for viral infection was not found. Thus, relative coronary insufficiency in regard to myocardial hypertrophy during excessive athletic activity must be viewed as cause for the fatal arrhythmia. |
4,376 | [Non-invasive evaluation of the hemodynamic profile in patients with heart failure: estimation of left atrial pressure]. | The management of patients with heart failure requires an accurate and non-invasive estimation of left ventricular filling pressures. This is essential in order to optimize unloading treatment, interpret equivocal symptoms, assess disease severity (and prognosis), and follow up the hemodynamic effect of long-term treatments. Since Doppler technique was implemented, several non-invasive methods to estimate left ventricular filling pressures were developed. Among these, a method based on the calculation of the left ventricular-atrial pressure gradient and its subtraction from systolic arterial blood pressure can be used in patients with significant mitral regurgitation and well-defined continuous wave Doppler signal of the regurgitant flow. Mitral and pulmonary venous flow velocities, as assessed by pulsed Doppler, are closely related to left atrial pressures, and several derived indices can be used to qualitatively estimate left ventricular filling pressures in patients with heart failure due to left ventricular systolic dysfunction who are in sinus rhythm. Furthermore, the combination of these indices in multivariable equations can improve this relationship and allows for a quantitative estimation of filling pressures, even in patients with significant mitral regurgitation and atrial fibrillation. There are, however, several groups of patients with heart failure in whom pulsed Doppler of mitral and pulmonary venous flow provides limited hemodynamic information. These include those with a) sinus tachycardia and/or prolonged P-R interval; b) normal left ventricular systolic function (and "pure" diastolic heart failure); c) primarily abnormal left atrial dysfunction (such as patients who had undergone heart transplantation), and d) technically inadequate Doppler recordings of pulmonary venous flow. To assess left ventricular filling pressures in these patients, two new methods which combine pulsed Doppler mitral flow indices with load-independent indices of left ventricular relaxation (either early diastolic velocity of mitral annulus, as assessed by tissue Doppler, or propagation velocity of mitral inflow, as assessed by color M-mode) can be used. |
4,377 | [Non-invasive evaluation of the hemodynamic profile in patients with heart failure: estimation of right atrial pressure]. | The estimation of right atrial pressure is often needed for the diagnosis, management and monitoring of various pathologic hemodynamic conditions and plays a significant role in patients with chronic heart failure. In the past decade several attempts have been made to non-invasively estimate right atrial pressure, and echocardiography has always been considered the most reliable tool. Morphologic parameters such as respiratory motion of the inferior vena cava, its respiratory diameters and percent collapse (caval index), left hepatic vein diameter or right atrial dimension (areas, volumes) were initially studied. More recently, functional data such as left hepatic or tricuspid flow variables have been considered. Some of these indexes, however, offer only semiquantitative measures of right atrial pressure, and have failed to demonstrate any prognostic value. Others, although highly sensitive and specific, are useful only in selected groups of patients because of technical or clinical limitations. In recent years, attention has focused on Doppler diastolic tricuspid flow as a means of predicting mean right atrial pressure. Analyzing the Doppler tricuspid velocity profile and mean right atrial pressure (Swan-Ganz catheter) simultaneously recorded in patients with severe left ventricular systolic dysfunction and chronic heart failure, acceleration rate of early filling emerged as the strongest independent predictor of right atrial pressure both in patients in sinus rhythm and in those with atrial fibrillation (r = 0.98), irrespective of whether the recordings are at baseline or after acute loading manipulations. |
4,378 | Improved cerebral blood supply and oxygenation by aortic balloon occlusion combined with intra-aortic vasopressin administration during experimental cardiopulmonary resuscitation. | Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to improve myocardial and cerebral blood flow. Aortic balloon occlusion during CPR may also augment myocardial and cerebral blood flow and can be used as a central route for the administration of resuscitative drugs. We hypothesized that, as compared with intravenously administered vasopressin, the administration of this drug above the site of an aortic balloon occlusion would result in a greater increase in cerebral perfusion and oxygenation during CPR and after restoration of spontaneous circulation (ROSC).</AbstractText>Twenty piglets were subjected to 5 min of ventricular fibrillation followed by 8 min of closed-chest CPR and were treated with 0.4 U kg(-1) boluses of vasopressin intravenously (the IV-vasopressin group with sham aortic balloon) or above the site for an aortic balloon occlusion (the balloon-vasopressin group). The aortic balloon catheter was inflated in the latter group 1 min after commencement of CPR and was deflated within 1 min after ROSC. Systemic blood pressures, cerebral cortical blood flow, cerebral tissue pH and PCO2 were monitored continuously and the cerebral oxygen extraction ratio was calculated.</AbstractText>During CPR, arterial blood pressure and cerebral perfusion pressure were greater in the balloon-vasopressin group, as compared with the IV-vasopressin group. These pressures did not differ between the groups after ROSC. Cerebral cortical blood flow was not significantly greater in the balloon-vasopressin group during CPR, whereas significantly higher cortical blood flow levels were recorded after ROSC. Cerebral tissue pH decreased in the IV-vasopressin group during the post-resuscitation hypoperfusion period. In contrast, decreasing pressures during the hypoperfusion period did not result in increasing tissue acidosis in the balloon-vasopressin group.</AbstractText>During CPR, intra-aortic vasopressin combined with aortic balloon occlusion resulted in significantly greater perfusion pressures but not in greater cerebral cortical blood flow. After ROSC, however, a greater increase in cortical blood flow was recorded in the balloon-vasopressin group, even though the aortic balloon was deflated and perfusion pressures did not differ between the groups. This suggests that vasopressin predominantly gives vasoconstrictive effects on cerebral cortical vessels during CPR, but results in cerebral cortical vasodilatation after ROSC.</AbstractText> |
4,379 | Clinical variability and molecular diagnosis in a four-generation family with X-linked Emery-Dreifuss muscular dystrophy. | To describe the clinical variability of X-linked Emery-Dreifuss muscular dystrophy (X-EDMD) with cardiac involvement in a four-generation family with a novel mutation in the STA gene.</AbstractText>Clinical data were provided for 4 affected males and a female carrier. The Western blot analysis of emerin was performed on lymphoblastoid cell lines and followed by sequencing of the emerin gene.</AbstractText>A thymine insertion at nucleotide 417 in exon 2, resulting in a frameshift with a premature stop codon at position 62 and absence of functional protein, was found in one of the three available patients. In ten-year-old proband's dizygotic twin-nephews the intermittent first-degree A-V block, atrial and ventricular ectopy, atrial runs, and exit sinus block were found, although the echocardiographic findings were normal. One of the twins also had short episodes of atrial fibrillation, idioventricular rhythm, and junctional rhythm.</AbstractText>Cardiac abnormalities in the proband's ten-year-old dizygotic twins without evident clinical features suggestive of EDMD were remarkable in contrast to the oldest patient in the family, who lived to the age of 63 without a pacemaker, and to the proband who had a very early onset of muscle wasting and weakness, and a pacemaker implantation at the age of 27. This striking intra-familial variability in cardiac involvement associated with specific null mutation (417 ins T) has practical early diagnostic and possibly preventive implications. It also points at genetic and environmental factors as causes of clinical features in X-EDMD.</AbstractText> |
4,380 | Incidence and risk factors for subtypes of cerebral infarction in a general population: the Hisayama study. | We estimated the incidence of first-ever cerebral infarction in regard to its subtypes and analyzed their risk factors separately in a community-based prospective cohort study in Japan.</AbstractText>Stroke-free subjects (n=1621) aged >/=40 years were followed up for 32 years from 1961. During this period, 298 cerebral infarctions occurred and were divided into 167 lacunar, 62 atherothrombotic, 56 cardioembolic, and 13 undetermined subtypes of infarction on the basis of clinical information including brain imaging and autopsy findings.</AbstractText>The age-adjusted incidence of lacunar infarction (3.8 per 1000 person-years for men and 2.0 for women) was higher than that of atherothrombotic infarction (1.2, 0. 7) and cardioembolic infarction (1.3, 0.5) in both sexes. Time-dependent Cox's proportional hazard analysis revealed systolic blood pressure as well as age to be independent risk factors for all subtypes of cerebral infarction except for cardioembolic infarction in men. Additionally, ST depression on ECG, glucose intolerance, and smoking in men and left ventricular hypertrophy on ECG and body mass index in women remained significant risk factors for lacunar infarction. ST depression was also significantly related to events of atherothrombotic infarction in women. The risk of atrial fibrillation for cardioembolic infarction was outstandingly high in both sexes, and left ventricular hypertrophy and lower total cholesterol were additional risk factors for cardioembolic infarction in women.</AbstractText>In this Japanese population, lacunar infarction was the most common subtype of cerebral infarction and had a greater variety of risk factors, including not only hypertension but also ECG abnormalities, diabetes, obesity, and smoking, than did atherothrombotic infarction or cardioembolic infarction.</AbstractText> |
4,381 | Influence of autothreshold sensing and sinus rate on mode switching algorithm behavior. | Mode switching is beneficial to pacemaker patients with paroxysmal atrial tachyarrhythmias. However, the optimal mode switching algorithm is still in evolution. Mode switching algorithms and atrial sensing circuitry can influence mode switching behavior. This study compared the mode switching behavior of four Medtronic, Inc. implantable devices: Thera DR model 7960 pacemaker, Kappa 700 model KDR701 pacemaker, Gem DR model 7271 dual chamber pacing defibrillator, and Jewel AF model 7250 dual chamber pacemaker atrial and ventricular defibrillator. The Thera and Gem DR use the same mean atrial rate mode switch algorithm. The Kappa and Jewel AF use four of seven short atrial intervals and an atrial fibrillation evidence counter algorithm, respectively. The Thera and Kappa devices use fixed gain sensing and the Gem DR and Jewel AF use autothreshold atrial sensing. Digitally recorded atrial electrograms from 52 episodes of human atrial fibrillation were fed into each device with differing simulated sinus rates before and after the atrial fibrillation. The percent of appropriate mode switching was highest for the Kappa 700 (94%) and lowest for the Thera (85%) (P = 0.046). The time to mode switching was significantly longer for the Thera and Gem DR compared to the Kappa 700 or Jewel AF (all P < 0.05). The time to mode switching was shorter for the Gem DR (9.0 +/- 1.6 s) using autothreshold atrial sensing than for the fixed gain Thera (11.1 +/- 2.1 s, P < 0.05). The mean atrial electrogram amplitude and cycle length were not correlated with the time to mode switching for any device. Faster sinus rates shortened the time to mode switching and prolonged the time to resynchronization in the two devices using the mean atrial interval algorithm. In conclusion, (1) mode switching function among these devices is influenced by algorithms and sensing circuitry, (2) the time to mode switching among these devices is influenced by the algorithm and use of autothreshold atrial sensing, and (3) the sinus rate before and after episodes of atrial fibrillation greatly influences the times to mode switching and resynchronization in devices using the mean atrial interval algorithm. |
4,382 | Effects of a thin-sized lead body of a transvenous single coil defibrillation lead on ICD implantation. Kainox RV Study Group. | In the interest of patients receiving implantable cardioverter defibrillators (ICDs), the clinical benefits of newer and thinner transvenous defibrillation leads have to be determined. The aims of this study were to evaluate the ICD procedure duration and the frequency of lead dislocation at the 3-month follow-up of a new defibrillation lead with a thin-sized lead body and its conventional-sized predecessor. The thin-sized single coil defibrillation lead (Kainox RV, Biotronik; lead body 6.7 Fr) was implanted in 61 patients and the conventional-sized defibrillation lead (SPS, Biotronik; lead body 7.8 Fr) in 60 patients. Both leads were connected to a left-sided, prepectorally implanted Phylax ICD (Biotronik) with active housing. The lead implantation time and total procedure duration were determined. Lead implantation time was defined as the time from lead insertion to the end of the pacing measurements. The total procedure duration spanned skin incision to closure. The incidence of lead repositioning during the lead implantation time and during ventricular fibrillation conversion testing was also assessed. The frequency of lead dislocations was recorded at the 3-month follow-up. Mean lead implantation time and total procedure duration of the thin-sized lead (23 +/- 22 minutes 76 +/- 37 minutes) were not statistically different from the time needed for the conventional-sized lead (22 +/- 20 minutes 81 +/- 34 minutes). The number of lead repositionings during the lead implantation time was similar (thin-sized lead: 1.4 +/- 2.4; conventional-sized lead: 1.1 +/- 1.9). An additional lead repositioning was not necessary during ventricular fibrillation conversion testing in 93.4% of the patients with thin-sized and in 94.4% with conventional-sized leads (not significant). At the 3-month follow-up, there were four (6.6%) lead dislocations in the thin-sized and four (6.7%) in the conventional-sized lead group. In conclusion, the down-sized lead body of the new defibrillation lead influenced neither ICD procedure duration nor the incidence of lead dislocation during follow-up. |
4,383 | Azimilide dihydrochloride: a new class III anti-arrhythmic agent. | Azimilide dihydrochloride (Stedicor) is a new class III anti-arrhythmic agent that is being developed by Proctor & Gamble to treat supraventricular and ventricular arrhythmias. Development of this agent is being undertaken due to the high prevalence of atrial fibrillation and the lack of satisfactory therapy for this arrhythmia, along with the desire to develop therapy to reduce the risk of life-threatening ventricular arrhythmias in patients following myocardial infarction. The mechanism of action of azimilide is to block both the slowly conducting (I(Ks)) and rapidly conducting (I(Kr)) rectifier potassium currents in cardiac cells. This differs from other class III agents that block I(Kr) exclusively or in combination with sodium, calcium, or transient outward (I(to)) potassium current channels. Azimilide is distinguished by a relative lack of reverse use-dependence, excellent oral absorption, no need for dose titration, an option for out-patient initiation, no need for adjustment associated with renal or liver failure and a lack of interaction with warfarin or digoxin. It carries some risk of torsade de pointes and rarely, neutropoenia. Azimilide has shown dose-related efficacy in prolonging the time to recurrence of atrial fibrillation. A large trial examining the impact of azimilide on mortality in high-risk patients following myocardial infarction has completed enrolment and should yield data in the next couple of years and further studies are planned. Even if this trial fails to show a survival benefit, a neutral effect on mortality will make the agent attractive for atrial arrhythmias. |
4,384 | Dofetilide: a class III anti-arrhythmic drug for the treatment of atrial fibrillation. | Dofetilide is a class III anti-arrhythmic drug that has been approved for the treatment of atrial fibrillation. Two clinical studies, which enrolled 996 patients, demonstrated pharmacological conversion to sinus rhythm to occur in 30% of patients. Following pharmacological or electrical conversion, median time to relapse exceeded one year. Two large clinical studies that enrolled 3028 patients have been performed in high-risk patients with severe heart failure and large myocardial infarctions. The outcomes of these studies were neutral with respect to survival and demonstrated the safety of dofetilide. After pharmacological or electrical conversion of atrial fibrillation to sinus rhythm in these studies, the probability of remaining in sinus rhythm during the following year was 75%. Dofetilide has a single significant side effect: risk of developing torsade de pointes ventricular tachycardia. Therefore, dosage must be carefully adjusted to the length of QTc interval, calculated creatinine clearance and the presence of heart failure or recent infarction. In addition, treatment must be initiated in hospital with three days of continuous telemetry. Dofetilide can be co-administered with digoxin and beta-blockers. Other anti-arrhythmic drugs, as well as drugs that interfere with the renal elimination or the metabolism of dofetilide, must be avoided. Dofetilide is an option when persistent atrial fibrillation is a clinical problem. In the setting of severe heart failure and large myocardial infarctions, only amiodarone and dofetilide have proven safety and dofetilide is a strong candidate for first choice treatment when the aim is to achieve sinus rhythm. |
4,385 | D-Sotalol: death by the SWORD or deserving of further consideration for clinical use? | D-Sotalol is the dextro-rotatory isomer of sotalol and a class III anti-arrhythmic. D-Sotalol prolongs cardiac repolarisation by inhibiting the fast component of the delayed outward rectifying potassium channel. In animal studies, D-sotalol has been shown to be more effective in prolonging atrial, rather than ventricular, action potentials, suggesting that D-sotalol may be more effective against supra-ventricular than ventricular arrhythmias. Furthermore, in animal studies, D-sotalol induces after-depolarisations, which are predictors of pro-arrhythmic activity. D-Sotalol shows little or no reverse use dependence in animal and humans and has slow offset kinetics. This suggests that, in addition to being a preventative treatment for arrhythmias, D-sotalol may be effective at the start or during arrhythmia. As D-sotalol does not block the slow component of the delayed outward rectifying potassium channel, which is activated by the sympathetic nervous system, D-sotalol will not protect against sympathetic hyperactivity. D-Sotalol also has no effect on the K(ATP) channel, which is activated in ischaemia to shorten the action potential. Thus D-sotalol is less effective in ischaemia. Anti-arrhythmic activity with D-sotalol has been demonstrated in dog models of ventricular tachycardia and sudden death. Arrhythmias with D-sotalol have been demonstrated in an ischaemic guinea-pig ventricle model in the absence of action potentials. D-Sotalol is a weak beta-adrenoceptor antagonist and may also be a positive inotrope. In humans, D-sotalol has 100% systemic oral bioavailability, a terminal half-life of 7.2 h and is mainly excreted unchanged in the urine. Preliminary, mainly hospital-based, clinical trials showed that D-sotalol was effective in a variety of supraventricular and ventricular arrhythmias. However, a large clinical trial of D-sotalol as a preventative treatment for arrhythmias and sudden death after myocardial infarction, the SWORD trial, was terminated early because of increased mortality with D-sotalol. The group at greatest risk was those with a remote myocardial infarction and relatively good left ventricular function, the group that showed the lowest mortality when untreated. It is assumed that excessive prolongation of the action potential leading to pro-arrhythmia with D-sotalol, underlies the increased risk of death. However, there is little objective evidence in the SWORD trial to support this. Obviously D-sotalol should not be used in humans with a remote myocardial infarction and relatively good left ventricular function. D-Sotalol could still be considered for short-term hospital use in resistant arrhythmias and for longer-term use to prevent atrial fibrillation in those with remote myocardial infarction and poor left ventricular function. |
4,386 | [Epicardial mapping of reentrant activation during ventricular fibrillation. An experimental study]. | High-resolution epicardial mapping was used in an experimental model to analyze reentrant activation during ventricular fibrillation.</AbstractText>In 30 isolated Langendorff-perfused rabbit hearts, recordings were made of ventricular fibrillation activity using an epicardial multiple electrode. In the activation maps with reentrant activation patterns, determinations were made of the number of consecutive rotations, the maximum length of the central core, the area encompassed by the core and two electrodes surrounding it, and the cycle defined by reentrant activation.</AbstractText>Most of the activation maps analyzed showed complex patterns with two or more wave fronts that either collided or remained separated by functional block lines (514 maps, 86%). In 112 maps (19%) activation patterns compatible with epicardial breakthrough of the depolarization process were observed. Reentrant activity was recorded in 42 maps (7%) - the maximum number of consecutive rotations being 3 (mean = 1.3 +/- 0.5). The maximum length of the central core ranged from 3 to 7 mm (mean = 5 +/- 1 mm), while the area encompassed by the central core plus two electrodes surrounding it ranged from 35 to 55 mm2 (mean = 45 +/- 6 mm2). The reentrant cycle length (mean = 47 +/- 8 ms) showed a linear relation to the maximum length of the central core reentry (cycle = 4.52 x length + 24.6; r = 0.7; p < 0.0001).</AbstractText>a) Epicardial mapping allowed the identification of reentrant activation patterns during ventricular fibrillation in the experimental model used; b) the reentrant activity detected is infrequent and unstable, and c) a linear relation exists between the duration of the cycles defined by reentrant activity and the maximum length of central core reentry.</AbstractText> |
4,387 | Laplacian electrograms and the interpretation of complex ventricular activation patterns during ventricular fibrillation. | During ventricular fibrillation (VF), interpretation of a local electrogram and determination of the local activation moment are hampered by remote activity or intervening repolarization waves. Successful defibrillation depends on critical timing of the shock relative to local activation. We tested the applicability of Laplacian electrograms for detection of the moment of local activation during VF.</AbstractText>From isolated perfused porcine intact hearts, 247 local unipolar electrograms were recorded simultaneously (13 x 19 matrix, interelectrode distance 0.3 mm) from the left ventricular wall during sinus rhythm, following pacing or during VF. Activation maps were constructed based on local unipolar electrograms, and Laplacian electrograms were calculated from local electrograms and its eight neighbors. The Laplacian electrogram displayed a sharp R/S complex with local activation indicated by the moment of zero crossing without interference from remote activity or repolarization waves. Its amplitude increased with decreasing interelectrode distance. Following epicardial stimulation, Laplacian amplitude was significantly larger than during a breakthrough pattern. During VF, identical unipolar electrograms corresponded to Laplacian complexes with different morphology. Collision of wavefronts was associated with entirely positive Laplacian waveforms; "focal" appearance of activity was associated with an entirely negative waveform. Activation block in the activation maps was correlated with the appearance of sustained episodes of negativity or positivity in the Laplacian electrogram (depending on the location of the recording site relative to the line of block).</AbstractText>Laplacian electrograms allow detection of the moment of local activation without interference from remote activity or repolarization, especially during complex arrhythmias. The technique applied to automatic sensing devices, such as the internal defibrillator, may optimize defibrillation success.</AbstractText> |
4,388 | Dual chamber arrhythmia detection in the implantable cardioverter defibrillator. | Dual chamber implantable cardioverter defibrillator (ICD) technology extended ICD therapy to more than termination of hemodynamically unstable ventricular tachyarrhythmias. It created the basis for dual chamber arrhythmia management in which dependable detection is important for treatment and prevention of both ventricular and atrial arrhythmias.</AbstractText>Dual chamber detection algorithms were investigated in two Medtronic dual chamber ICDs: the 7250 Jewel AF (33 patients) and the 7271 Gem DR (31 patients). Both ICDs use the same PR Logic algorithm to interpret tachycardia as ventricular tachycardia (VT), supraventricular tachycardia (SVT), or dual (VT+ SVT). The accuracy of dual chamber detection was studied in 310 of 1,367 spontaneously occurring tachycardias in which rate criterion only was not sufficient for arrhythmia diagnosis. In 78 episodes there was a double tachycardia, in 223 episodes SVT was detected in the VT or ventricular fibrillation zone, and in 9 episodes arrhythmia was detected outside the boundaries of the PR Logic functioning. In 100% of double tachycardias the VT was correctly diagnosed and received priority treatment. SVT was seen in 59 (19%) episodes diagnosed as VT. The causes of inappropriate detection were (1) algorithm failure (inability to fulfill the PR<RP condition in atrial tachyarrhythmias with 1:1 AV conduction, and far-field R wave sensing intermittently present during sinus tachycardia); (2) programming settings (atrial fibrillation/atrial flutter with ventricular rate above the SVT limit); and (3) algorithm limitations (atrial tachycardia with ventricular rate around the shortest programmable SVT limit and SVT redetection following VT therapy). Programming measures improved detection ability in 13 of 59 of inappropriately detected arrhythmias.</AbstractText>Dual chamber detection algorithms evaluated in a subset of diagnostically difficult arrhythmias allow safe detection of double tachycardias but require further extension and programmability to improve VT:SVT discrimination rules.</AbstractText> |
4,389 | Effect of a single oral dose of pilsicainide on pacing thresholds in pacemaker patients with and without paroxysmal atrial fibrillation. | A single oral dose of pilsicainide, a class 1c antiarrhythmic drug, is effective in terminating acute-onset atrial fibrillation (AF), but its effect on pacing thresholds in pacemaker patients is unknown. The present study measured atrial and ventricular pacing thresholds after a single oral dose of pilsicainide in patients with and without AF. Twelve patients with dual-chamber pacemakers were evaluated. Pacing thresholds as well as plasma pilsicainide concentration were measured prior to and then at 30, 60, 90, 120 and 180 min and 24h following a single oral dose of pilsicainide (150 mg). Six patients had paroxysmal AF and the remaining 6 did not. Pacing thresholds increased significantly (134+/-8%) in the atrium (p<0.05) and in the ventricle (155+/-11%; p<0.001) following pilsicainide administration in all 12 patients. Plasma concentrations of pilsicainide showed a positive liner correlation with pacing thresholds (R=0.62, p<0.0001 in the atrium; R=0.74, p<0.0001 in the ventricle). Atrial pacing thresholds in the patients with AF showed a significant increase at 90, 120 and 180 min compared with the patients without AF (p<0.05). There was no significant difference in either the ventricular pacing threshold or the plasma pilsicainide concentration in the patients with and without AF. It was concluded that a single oral dose of pilsicainide increases the pacing thresholds in both the atrium and ventricle in a selected group of pacemaker-implanted patients; that is, those who are aged and with AF. Thus, careful attention should be paid to pacemaker-dependent patients, particularly those with paroxysmal AF, when administering pilsicainide. |
4,390 | A two-stage discrimination of cardiac arrhythmias using a total least squares-based prony modeling algorithm. | In this paper, we describe a new approach for the discrimination among ventricular fibrillation (VF), ventricular tachycardia (VT) and superventricular tachycardia (SVT) developed using a total least squares (TLS)-based Prony modeling algorithm. Two features, dubbed energy fractional factor (EFF) and predominant frequency (PF), are both derived from the TLS-based Prony model. In general, EFF is adopted for discriminating SVT from ventricular tachyarrhythmias (i.e., VF and VT) first, and PF is then used for further separation of VF and VT. Overall classification is achieved by performing a two-stage process to the indicators defined by EFF and PF values, respectively. Tests conducted using 91 episodes drawn from the MIT-BIH database produced optimal predictive accuracy of (SVT, VF, VT) = (95.24%, 96.00%, 97.78%). A data decimation process is also introduced in the novel method to enhance the computational efficiency, resulting in a significant reduction in the time required for generating the feature values. |
4,391 | [Circadian rhythm of the ventricular fibrillation threshold in a model of hypoventilation-reoxygenation in female Wistar rats]. | Hypoxia, similarly as myocardial ischemia, decreases the electric stability of the heart and thus produces the conditions for the genesis of ventricular arrhythmias within the 24 h period however a prompt restoration of oxygen supply or blood flow within myocardium causes serious ventricular arrhythmias. Therefore the aim of our study was to evaluate the reoxygenation impact on myocardium after hypoventilation in circadian dependence. The experiments were performed in female Wistar rats (pentobarbital anesthesia 40 mg/1 kg i.p., open chest experiments). The animals were adapted to the light regimen 12:12 hours, with the dark phase from 18.00 h to 06.00 h. Normal ventilation was used in the control group (n = 17) and in the second one (n = 4), 20 min reoxygenation followed 20 min of hypoventilation. The heart rate (HR) had been recorded just before the ventricular arrhythmias rose. Hypoventilation decreased significantly (p < 0.001) the VFT and HR when compared with the control group and changed the 24-hour rhythm of VFT to moderate bi-phase one. Reoxygenation counter changed this rhythm to inverse in the comparison with the control group. The lowest VFT values occurred when the top of VFT circadian rhythm was detected during normal ventilation. No dependence was detected between VFT and HR in both ventilation types. It is concluded that reoxygenation alternates the myocardial vulnerability to ventricular arrhythmias in dependence on alternation of light and dark and without the evident dependence on HR in the course of the whole 24-hour period. (Tab. 2, Fig. 2, Ref. 43.) |
4,392 | Commotio cordis: a deadly consequence of chest trauma. | Commotio cordis is arrhythmia or sudden death from low-impact, blunt trauma to the chest without apparent heart injury. Ventricular fibrillation is the most common associated arrhythmia, and heart block, bundle branch block, and ST-segment elevation are also seen. Commotio cordis occurs most commonly in baseball but has also been reported in hockey, softball, and several other sports. Approximately two to four cases are reported each year, but the true incidence is uncertain. Survival is low, even when resuscitation is performed. Preventive measures include education of participants and coaches, chest protection, and softer baseballs. Other considerations include having external automatic defibrillators and trained personnel at youth sporting events. |
4,393 | The role of electroporation in defibrillation. | Electric shock is the only effective therapy against ventricular fibrillation. However, shocks are also known to cause electroporation of cell membranes. We sought to determine the impact of electroporation on ventricular conduction and defibrillation. We optically mapped electrical activity in coronary-perfused rabbit hearts during electric shocks (50 to 500 V). Electroporation was evident from transient depolarization, reduction of action potential amplitude, and upstroke dV/dt. Electroporation was voltage dependent and significantly more pronounced at the endocardium versus the epicardium, with thresholds of 229+/-81 versus 318+/-84 V, respectively (P=0.01, n=10), both being above the defibrillation threshold of 181.3+/-45.8 V. Epicardial electroporation was localized to a small area near the electrode, whereas endocardial electroporation was observed at the bundles and trabeculas throughout the entire endocardium. Higher-resolution imaging revealed that papillary muscles (n=10) were most affected. Electroporation and conduction block thresholds in papillary muscles were 281+/-64 V and 380+/-79 V, respectively. We observed no arrhythmia in association with electroporation. Further, preconditioning with high-energy shocks prevented reinduction of fibrillation by 50-V shocks, which were otherwise proarrhythmic. Endocardial bundles are the most susceptible to electroporation and the resulting conduction impairment. Electroporation is not associated with proarrhythmic effects and is associated with a reduction of vulnerability. |
4,394 | Emergencies related to implantable cardioverter-defibrillators. | Implantable cardioverter-defibrillators (ICDs) have become the dominant therapeutic modality for patients with life-threatening ventricular arrhythmias. ICDs are implanted using techniques similar to standard pacemaker implantation. They not only provide high-energy shocks for ventricular fibrillation and rapid ventricular tachycardia, but also provide antitachycardia pacing for monomorphic ventricular tachycardia and antibradycardia pacing. Devices incorporating an atrial lead allow dual-chamber pacing and better discrimination between ventricular and supraventricular tachyarrhythmias. Intensivists are increasingly likely to encounter patients with ICDs. Electrosurgery can be safely performed in ICD patients as long as the device is deactivated before the procedure and reactivated and reassessed immediately afterward. Prompt and skilled intervention can prove to be life-saving in patients presenting with ICD-related emergencies, including lack of response to ventricular tachyarrhythmias, pacing failure, and multiple shocks. Recognition and treatment of tachyarrhythmia can be temporarily disabled by placing a magnet on top of an ICD. The presence of an ICD should not deter standard resuscitation techniques. Multiple ICD discharges in a short period of time constitute a serious situation. Causes include ventricular electrical storm, inefficient defibrillation, nonsustained ventricular tachycardia, and inappropriate shocks caused by supraventricular tachyarrhythmias or oversensing of signals. ICD system infection requires hardware removal and intravenous antibiotic therapy. Deactivation of an ICD with the consent of the patient or relatives is reasonable and ethical in terminally ill patients. |
4,395 | Management of malignant ventricular arrhythmias and cardiac arrest. | Sudden cardiac death continues to be a major health problem in the United States, accounting for approximately 400,000 deaths per year. The last 10 yrs have seen major advances in the primary and secondary prevention of this problem. In patients who have survived an episode of cardiac arrest, the AVID study conclusively established the superiority of the implantable cardioverter defibrillator over empiric amiodarone. For patients with recurrent hemodynamically destabilizing ventricular tachycardia and ventricular fibrillation, intravenous amiodarone has emerged as a potent therapeutic agent, especially when other agents such as lidocaine and procainamide have not been effective. Finally, recent work has focused on the risk stratification of patients for sudden cardiac death. Both the MADIT and MUSTT studies suggest that patients with coronary artery disease, reduced ejection fraction, and nonsustained ventricular tachycardia who are inducible to a sustained ventricular arrhythmia at electrophysiology testing have improved survival with an implantable cardioverter defibrillator. |
4,396 | Noncardiac surgery: postoperative arrhythmias. | Postoperative arrhythmias are common and represent a major source of morbidity after both cardiac and noncardiac surgical procedures. Postoperative dysrhythmias are most likely to occur in patients with structural heart disease. The initiating factor for an arrhythmia in a given patient after surgery is usually a transient insult, such as hypoxemia, cardiac ischemia, catecholamine excess, or electrolyte abnormality. Management includes correction of these imbalances and medical therapy directed at the arrhythmia itself. The physiologic impact of arrhythmias depends on arrhythmia duration, ventricular response rate, and underlying cardiac function. Similarly, urgency and type of treatment is determined by the physiologic impact of the arrhythmia, as well as by underlying clinical status. The purpose of this review is to provide current concepts of diagnosis and acute management of arrhythmias after noncardiac surgery. A systematic approach to arrhythmia diagnosis and evaluation of predisposing factors is presented, followed by consideration of specific bradyarrhythmias and tachyarrhythmias in the postoperative setting. |
4,397 | Cardiac surgery: postoperative arrhythmias. | Arrhythmias are common after surgery, particularly after cardiac surgery. Atrial fibrillation is the most common arrhythmia encountered postoperatively, although ventricular arrhythmias and conduction disturbances can also occur. Older age is the most consistent predictor of postoperative atrial arrhythmias. beta-adrenergic blockers, amiodarone, and sotalol are the most effective at preventing postoperative atrial fibrillation. Sustained ventricular arrhythmias in the recovery period after cardiac surgery warrant aggressive therapy, usually with an implantable cardioverter-defibrillator in the absence of reversible causes. Postoperative, nonsustained ventricular tachycardia in the setting of left ventricular dysfunction and ischemic coronary disease also usually warrants risk stratification and possible treatment, often with electrophysiologic testing and implantation of an implantable cardioverter-defibrillator, if sustained ventricular arrhythmias are induced. Transient bradyarrhythmias may be managed with temporary pacing wires placed at surgery, but significant and persistent atrioventricular block or sinus node dysfunction can occur and indicate a need for permanent pacing. |
4,398 | Dofetilide: a new pure class III antiarrhythmic agent. | Although there are a variety of antiarrhythmic agents used for the treatment of atrial fibrillation of flutter, each drug has drawbacks, and room exists for new pharmacologic agents. Dofetilide, a pure class III agent, has recently been approved by the Food and Drug Administration for therapy of these arrhythmias and is reviewed.</AbstractText>Data for dofetilide, published in full or in abstract form, were reviewed, concentrating on the properties related to its efficacy for the therapy of supraventricular arrhythmias.</AbstractText>Results from animal and human studies indicate that dofetilide, a renally excreted drug, has pure class III properties related to blockade of the delayed rectifier potassium current. It is effective for the therapy of atrial arrhythmias, particularly atrial fibrillation and flutter, and has no demonstrable negative inotropic effect. Despite an incidence of torsades de pointes of approximately 2% in patients with impaired ventricular function, dofetilide exhibited no association with an increased mortality rate when studied in a large series of patients with a reduced ejection fraction.</AbstractText>Dofetilide's electrophysiologic and clinical profiles suggest that it will be safe and clinically useful for the termination and prevention of atrial fibrillation or flutter, even in patients with impaired ventricular function.</AbstractText> |
4,399 | Left ventricular diastolic dysfunction in lone atrial fibrillation determined by Doppler tissue imaging of mitral annular motion. | In this study, we sought evidence for an underlying atrial or ventricular myopathy in patients with paroxysmal lone atrial fibrillation using standard echocardiographic parameters in addition to Doppler tissue imaging of mitral annular motion. No impairment in atrial contractile function was found, but there was evidence for impaired diastolic function in these patients. |
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