Electrophysiologic effects of adenosine in patients with supraventricular tachycardia.

BACKGROUND: We correlated the electrophysiologic (EP) effects of adenosine with tachycardia mechanisms in patients with supraventricular tachycardias (SVT). METHODS AND RESULTS: Adenosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVRT; n=59), typical atrioventricular node reentry (AVNRT; n=82), atypical AVNRT (n=13), permanent junctional reciprocating tachycardia (PJRT; n=12), atrial tachycardia (AT; n=53), and inappropriate sinus tachycardia (IST; n=10). There was no difference in incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine, but patients with AVRT showed increases in the ventriculoatrial (VA) intervals (13%) compared with typical AVNRT (0%), P<0.005. Changes in atrial, AV, or VA intervals after adenosine did not predict the mode of termination of long R-P tachycardias. For patients with AT, there was no correlation with location of the atrial focus and adenosine response. AV block after adenosine was only observed in AT patients (27%) or IST (30%). Patients with IST showed atrial cycle length increases after adenosine (P<0.05) with little change in activation sequence. The incidence of atrial fibrillation after adenosine was higher for those with AVRT (15%) compared with typical AVNRT (0%) P<0.001, or atypical AVNRT (0%) but similar to those with AT (11%) and PJRT (17%). CONCLUSIONS: The EP response to adenosine proved of limited value to identify the location of AT or SVT mechanisms. Features favoring AT were the presence of AV block or marked shortening of atrial cycle length before tachycardia suppression. Atrial fibrillation was more common after adenosine in patients with AVRT, PJRT, or AT. Patients with IST showed increases in cycle length with little change in atrial activation sequence after adenosine.

Use of electroanatomic mapping to delineate transseptal atrial conduction in humans.

BACKGROUND: Interaction between wave fronts in the right and left atrium may be important for maintenance of atrial fibrillation, but little is known about electrophysiological properties and preferential routes of transseptal conduction. METHODS AND RESULTS: Eighteen patients (age 44+/-12 years) without structural heart disease underwent right atrial electroanatomic mapping during pacing from the distal coronary sinus (CS) or the posterior left atrium. During distal CS pacing, 9 patients demonstrated a single transseptal breakthrough near the CS os, 1 patient in the high right atrium near the presumed insertion of Bachmann's bundle and 1 patient near the fossa ovalis. The mean activation time from stimulus to CS os was 48+/-15 ms compared with 86+/-15 ms to Bachmann's bundle insertion (P<0.01) and 59+/-23 ms to the fossa ovalis (P=NS and P<0.01, respectively). During left atrial pacing, the earliest right atrial activation was near Bachmann's bundle in 5 and near the fossa ovalis in 4 patients. The activation time from stimulus to CS os was 70+/-15 ms compared with 47+/-16 ms to Bachmann's bundle (P<0.01) and 59+/-25 ms to the fossa ovalis (P=NS). Whereas the total septal activation time was not significantly different during CS pacing compared with left atrial pacing (41+/-16 versus 33+/-17 ms), the total right atrial activation time was longer during CS pacing (117+/-49 versus 79+/-15 ms; P<0.05). CONCLUSIONS: Three distinct sites of early right atrial activation may be demonstrated during left atrial pacing. These sites are in accord with anatomic muscle bundles and may have relevance for maintenance of atrial flutter or fibrillation.

Atypical right atrial flutter patterns.

BACKGROUND: The purpose of our study was to define the incidence and mechanisms of atypical right atrial flutter. METHODS AND RESULTS: A total of 28 (8%) of 372 consecutive patients with atrial flutter (AFL) had 36 episodes of sustained atypical right AFL. Among 24 (67%) of 36 episodes of lower loop reentry (LLR), 13 (54%) of 24 episodes had early breakthrough at the lower lateral tricuspid annulus, whereas 11 (46%) of 24 episodes had early breakthrough at the high lateral tricuspid annulus, and 9 (38%) of 24 episodes showed multiple annular breaks. Bidirectional isthmus block resulted in elimination of LLR. A pattern of posterior breakthrough from the eustachian ridge to the septum was observed in 4 (14%) of 28 patients. Upper loop reentry was observed in 8 (22%) of 36 episodes and was defined as showing a clockwise orientation with early annular break and wave-front collision over the isthmus. Two patients had atypical right AFL around low voltage areas ("scars") in the posterolateral right atrium. CONCLUSIONS: Atypical right AFL is most commonly associated with an isthmus-dependent mechanism (ie, LLR or subeustachian isthmus breaks). Non-isthmus-dependent circuits include upper loop reentry or scar-related circuits.

Syncope in advanced heart failure: high risk of sudden death regardless of origin of syncope.

OBJECTIVES: The purpose of this study was to assess the importance of syncope as a warning sign for sudden death in advanced heart failure and to determine the relative importance of cardiac syncope and syncope from other causes. BACKGROUND: Despite remarkable advances in the pharmacologic approach to advanced heart failure, 20% to 40% of patients with advanced heart failure will die each year. In such patients, the relation between sudden death and the etiology of syncope has not been evaluated. METHODS: The relation of syncope to sudden death was evaluated in 491 consecutive patients with advanced heart failure (New York Heart Association functional class III or IV), no history of cardiac arrest and a mean left ventricular ejection fraction of 0.20 +/- 0.07. Patients were evaluated for the presence and origin of syncope. The severity of heart failure was assessed from serum sodium levels, ejection fraction, functional class and echocardiographic and hemodynamic variables. RESULTS: Sixty patients (12%) had a history of syncope; the condition had a cardiac origin in 29 (48%) and was due to other causes in 31 (52%). The origin of heart failure was coronary artery disease in 234 patients (48%) and dilated cardiomyopathy in 253 (51%) and its severity was similar in patients with and without syncope. During a mean follow-up interval of 365 +/- 419 days, 69 patients (14%) died suddenly and 66 patients (13%) died of progressive heart failure. The actuarial incidence of sudden death by 1 year was significantly greater in patients with (45%) than in those without (12%, p < 0.00001) syncope. In the Cox proportional hazards model, syncope predicted sudden death independent of atrial fibrillation, serum sodium, cardiac index, angiotensin-converting enzyme inhibition and patient age. The actuarial risk of sudden death by 1 year was similarly high in patients with either cardiac syncope or syncope from other causes (49% vs. 39%, p = NS). CONCLUSIONS: Patients with advanced heart failure are at especially high risk for sudden death regardless of the etiology of syncope.

Mechanism of initiation of atrial flutter in humans: site of unidirectional block and direction of rotation.

OBJECTIVES: Using a standardized induction protocol, we investigated the mechanism of initiation of atrial flutter, before ablation, to determine the site of initiating unidirectional block and to test the hypothesis that the direction of rotation of atrial flutter depends on the pacing site from which it initiates. BACKGROUND: The high recurrence rate of atrial flutter after presumed successful ablation may be due to difficulty in reinduction after termination. In addition, induction of clockwise flutter is currently of unknown clinical importance. METHODS: Ten patients with documented typical flutter were studied before ablation. A standard protocol consisting of single and double extrastimuli followed by burst pacing was performed from four sites in the right atrium (high and low trabeculated and smooth right atrium) to assess efficacy at inducing atrial flutter. A 20-pole halo catheter placed around the tricuspid annulus and a decapole catheter placed in the coronary sinus were used for mapping during initiation to determine type of flutter induced and the site of unidirectional block during initiation. RESULTS: Atrial flutter was induced in 52 (6.2%) of 838 attempted inductions. Of these, 33 were counterclockwise and 20 were clockwise. Of the 20 inductions resulting in clockwise flutter, 18 were from the trabeculated right atrium, whereas all the counterclockwise inductions were from the smooth right atrium. In all but the two inductions, the site of unidirectional block was identified between the os of the coronary sinus and the low lateral right atrium for both counterclockwise and clockwise flutter, in the same isthmus at which ablation is targeted. CONCLUSIONS: Even in patients with clinical counterclockwise flutter, clockwise flutter is frequently induced before ablation and is dependent on the site of induction: Pacing from the smooth right atrium induces counterclockwise flutter, whereas pacing from the trabeculated right atrium induces clockwise flutter. The site of the unidirectional block during the initiation of either form of flutter is in the low right atrium isthmus.

Relation of pace mapping QRS configuration and conduction delay to ventricular tachycardia reentry circuits in human infarct scars.

OBJECTIVES: This study sought to determine the relation of the paced QRS configuration and conduction delay during pace mapping to reentry circuit sites in patients with ventricular tachycardia late after myocardial infarction. BACKGROUND: The QRS configuration produced by ventricular pacing during sinus rhythm (pace mapping) can locate focal idiopathic ventricular tachycardias during catheter mapping, but postinfarction reentry circuits may be relatively large and contain regions of slow conduction. We hypothesized that for postinfarction ventricular tachycardia, 1) pacing during sinus rhythm at reentry circuit sites distant from the exit from the scar would produce a QRS configuration different from the tachycardia; and 2) a stimulus to QRS delay during pace mapping may be a useful guide to reentry circuit slow conduction zones. METHODS: Catheter mapping and ablation were performed in 18 consecutive patients with ventricular tachycardia after myocardial infarction. At 85 endocardial sites in 13 patients, 12-lead electrocardiograms (ECGs) were recorded during pace mapping, and participation of each site in a reentry circuit was then evaluated by entrainment techniques during induced ventricular tachycardia or by application of radiofrequency current. RESULTS: Pace maps resembled tachycardia at < 30% of likely reentry circuit sites identified by entrainment criteria and at only 1 (9%) of 11 sites where radiofrequency current terminated tachycardia. Analysis of the stimulus to QRS interval during entrainment with concealed fusion showed that the conduction time from the pacing site to the exit from the scar was longer at sites where the pace map did not resemble tachycardia. Evidence of slow conduction during pace mapping, with a stimulus to QRS interval > 40 ms was observed at > or = 70% of reentry circuit sites. CONCLUSIONS: At many sites in postinfarction ventricular reentry circuits, the QRS configuration during pace mapping does not resemble the ventricular tachycardia QRS complex, consistent with relatively large reentry circuits or regions of functional conduction block during ventricular tachycardia. A stimulus to QRS delay during pace mapping is consistent with slow conduction and may aid in targeting endocardial sites for further evaluation during tachycardia.

Ventricular contraction abnormalities in dilated cardiomyopathy: effect of biventricular pacing to correct interventricular dyssynchrony.

OBJECTIVE: To measure ventricular contractile synchrony in patients with dilated cardiomyopathy (DCM) and to evaluate the effects of biventricular pacing on contractile synchrony and ejection fraction. BACKGROUND: Dilated cardiomyopathy is characterized by abnormal ventricular activation and contraction. Biventricular pacing may promote a more coordinated ventricular contraction pattern in these patients. We hypothesized that biventricular pacing would improve synchrony of right ventricular and left ventricular (RV/LV) contraction, resulting in improved ventricular ejection fraction. METHODS: Thirteen patients with DCM and intraventricular conduction delay underwent multiple gated equilibrium blood pool scintigraphy. Phase image analysis was applied to the scintigraphic data and mean phase angles computed for the RV and LV. Phase measures of interventricular (RV/LV) synchrony were computed in sinus rhythm and during atrial sensed biventricular pacing (BiV). RESULTS: The degree of interventricular dyssynchrony present in normal sinus rhythm correlated with LV ejection fraction (r = -0.69, p < 0.01). During BiV, interventricular contractile synchrony improved overall from 27.5 +/- 23.1 degrees to 14.1 +/- 13 degrees (p = 0.01). The degree of interventricular dyssynchrony present in sinus rhythm correlated with the magnitude of improvement in synchrony during BiV (r = 0.83, p < 0.001). Left ventricular ejection fraction increased in all thirteen patients during BiV, from 17.2 +/- 7.9% to 22.5 +/- 8.3% (p < 0.0001) and correlated significantly with improvement in RV/LV synchrony during BiV (r = 0.86, p < 0.001). CONCLUSIONS: Dilated cardiomyopathy with intraventricular conduction delay is associated with significant interventricular dyssynchrony. Improvements in interventricular synchrony during biventricular pacing correlate with acute improvements in LV ejection fraction.

Body surface mapping of counterclockwise and clockwise typical atrial flutter: a comparative analysis with endocardial activation sequence mapping.

OBJECTIVES: This study was directed at developing spatial 62-lead electrocardiogram (ECG) criteria for classification of counterclockwise (CCW) and clockwise (CW) typical atrial flutter (Fl) in patients with and without structural heart disease. BACKGROUND: Electrocardiographic classification of CCW and CW typical atrial Fl is frequently hampered by inaccurate and inconclusive scalar waveform analysis of the 12-lead ECG. METHODS: Electrocardiogram signals from 62 torso sites and multisite endocardial recordings were obtained during CCW typical atrial Fl (12 patients), CW typical Fl (3 patients), both forms of typical Fl (4 patients) and CCW typical and atypical atrial Fl (1 patient). All the Fl wave episodes were divided into two or three successive time periods showing stable potential distributions from which integral maps were computed. RESULTS: The initial, intermediate and terminal CCW Fl wave map patterns coincided with: 1) caudocranial activation of the right atrial septum and proximal-to-distal coronary sinus activation, 2) craniocaudal activation of the right atrial free wall, and 3) activation of the lateral part of the subeustachian isthmus, respectively. The initial, intermediate and terminal CW Fl wave map patterns corresponded with : 1) craniocaudal right atrial septal activation, 2) activation of the subeustachian isthmus and proximal-to-distal coronary sinus activation, and 3) caudocranial right atrial free wall activation, respectively. A reference set of typical CCW and CW mean integral maps of the three successive Fl wave periods was computed after establishing a high degree of quantitative interpatient integral map pattern correspondence irrespective of the presence or absence of organic heart disease. CONCLUSIONS: The 62-lead ECG of CCW and CW typical atrial Fl in man is characterized by a stereotypical spatial voltage distribution that can be directly related to the underlying activation sequence and is highly specific to the direction of Fl wave rotation. The mean CCW and CW Fl wave integral maps present a unique reference set for improved clinical detection and classification of typical atrial Fl.

Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping.

Ventricular tachycardia late after myocardial infarction is usually due to reentry in the infarct region. These reentry circuits can be large, complex and difficult to define, impeding study in the electrophysiology laboratory and making catheter ablation difficult. Pacing through the electrodes of the mapping catheter provides a new approach to mapping. When pacing stimuli capture the effects on the tachycardia depend on the location of the pacing site relative to the reentry circuit. The effects observed allow identification of various portions of the reentry circuit, without the need for locating the entire circuit. Isthmuses where relatively small lesions produced by radiofrequency catheter ablation can interrupt reentry can often be identified. A classification that divides reentry circuits into one or more functional components helps to conceptualize the reentry circuit and predicts the likelihood that heating with radiofrequency current will terminate tachycardia. These methods are helping to define human reentry circuits.

Amiodarone therapy does not compromise subsequent heart transplantation.

OBJECTIVES: The objective of this study was to determine the frequency of pulmonary complications, feasibility of early hospital discharge and requirements for postoperative inotropic and chronotropic support in patients receiving amiodarone therapy before heart transplantation. BACKGROUND: Although many patients waiting for heart transplantation will die of arrhythmias before a donor heart is found, the use of amiodarone has been limited by concern about increased complications in the perioperative period. METHODS: The 29 patients receiving amiodarone at the time of heart transplantation at University of California, Los Angeles Medical Center between October 1986 and September 1990 were compared with 29 control recipients to evaluate postoperative morbidity. Patients were receiving amiodarone for recurrent ventricular tachyarrhythmias (n = 11), atrial fibrillation (n = 2) or complex ventricular ectopic activity (n = 16). The average daily dose was 360 +/- 230 mg/day for an average of 11 +/- 22 months before transplantation. Amiodarone and control groups had a similar ejection fraction (0.18 +/- 0.07 vs. 0.20 +/- 0.08), frequency of coronary disease, age and gender. There were three more status I patients in the control group. OKT3 was given to only two patients receiving amiodarone and 12 control patients at high risk for renal dysfunction. RESULTS: Postoperatively, the duration of assisted ventilation was 21 +/- 19 h after amiodarone therapy versus 26 +/- 2 h in the control group (20 +/- 18 h vs. 15 +/- 9 h after excluding patients receiving OKT3), discharge arterial oxygen saturation was > 95% in both groups. Two patients in the amiodarone group with a smoking history of > 100 pack-years developed bilateral pulmonary infiltrates of brief duration. Although patients receiving amiodarone required atrial pacing more frequently (eight vs. two patients) and had a lower heart rate at discharge (75 +/- 18 vs. 86 +/- 11 beats/min), the duration of inotropic support (2.1 +/- 1.5 vs. 3.5 +/- 2.5 days) and of hospital stay (10 +/- 3 vs. 15 +/- 10 days) was not higher in the amiodarone than in the control group. The mortality rate at 30 days was similar in the two groups (6.8% vs. 3.4%, p = NS). CONCLUSIONS: Amiodarone therapy before heart transplantation may contribute to occasional pulmonary complications but does not significantly increase perioperative morbidity or mortality with the regimens used in this retrospective study.

Improving survival for patients with atrial fibrillation and advanced heart failure.

OBJECTIVES: We attempted to determine whether changes in heart failure therapy since 1989 have altered the prognostic significance of atrial fibrillation. BACKGROUND: Atrial fibrillation occurs in 15% to 30% of patients with heart failure. Despite the recognized potential for adverse effects, the impact of atrial fibrillation on prognosis is controversial. METHODS: Two-year survival for 750 consecutive patients discharged from a single hospital after evaluation for heart transplantation from 1985 to 1989 (Group I, n = 359) and from 1990 to April 1993 (Group II, n = 391) was analyzed in relation to atrial fibrillation. In Group I, class I antiarrhythmic drugs and hydralazine vasodilator therapy were routinely allowed. In Group II, amiodarone and angiotensin-converting enzyme inhibitors were first-line antiarrhythmic and vasodilating drugs. RESULTS: A history of atrial fibrillation was present in 20% of patients in Group I and 24% of those in Group II. Patients with atrial fibrillation in the two groups had similar clinical and hemodynamic profiles. Among patients with atrial fibrillation, those in Group II had a markedly better 2-year survival (0.66 vs. 0.39, p = 0.001) and sudden death-free survival (0.84 vs. 0.70, p = 0.01) than those in Group I. In each time period, survival was worse for patients with than without atrial fibrillation in Group I (0.39 vs. 0.55, p = 0.002) but not in Group II (0.66 vs. 0.75, p = 0.09). CONCLUSIONS: The prognosis of patients with advanced heart failure and atrial fibrillation is improving. These findings support the practice of avoiding class I antiarrhythmic drugs in this group and may reflect recent beneficial changes in heart failure therapy.

Improving survival for patients with advanced heart failure: a study of 737 consecutive patients.

OBJECTIVES: This study sought to determine whether survival and risk of sudden death have improved for patients with advanced heart failure referred for consideration for heart transplantation as advances in medical therapy were systematically implemented over an 8-year period. BACKGROUND: Recent survival trials in patients with mild to moderate heart failure and patients after a myocardial infarction have shown that angiotensin-converting enzyme inhibitors are beneficial, type I antiarrhythmic drugs can be detrimental, and amiodarone may be beneficial in some groups. The impact of advances in therapy may be enhanced or blunted when applied to severe heart failure. METHODS: One-year mortality and sudden death were determined in relation to time, baseline variables and therapeutics for 737 consecutive patients referred for heart transplantation and discharged home on medical therapy from 1986 to 1988, 1989 to 1990 and 1991 to 1993. Medical care was directed by a single team of physicians with policies established by consensus. From 1986 to 1990, the hydralazine/isosorbide dinitrate combination or angiotensin-converting enzyme inhibitors were the initial vasodilators, and class I antiarrhythmic drugs were allowed. After 1990, captopril was the initial vasodilator, given to 86% of patients compared with 46% of patients before 1989. After mid-1989, class I agents were routinely withdrawn, and amiodarone was used for frequent ventricular ectopic beats or atrial fibrillation (53% of patients after 1990 vs. 10% before 1989). RESULTS: The total 1-year mortality rate decreased from 33% before 1989 to 16% after 1990 (p = 0.0001), and sudden death decreased from 20% to 8% (p = 0.0006). Adjusted for clinical and hemodynamic variables in multivariate proportional hazards models, total mortality and sudden death were lower after 1990. CONCLUSIONS: The large reduction in mortality, particularly in sudden death, from advanced heart failure since 1990 may reflect an enhanced impact of therapeutic advances shown in large randomized trials when they are incorporated into a comprehensive approach in this population. This improved survival supports the growing practice of maintaining potential heart transplant candidates on optimal medical therapy until clinical decompensation mandates transplantation.

Amiodarone and torsades de pointes in patients with advanced heart failure.

Amiodarone is considered to be safe in patients with prior QT prolongation and torsades de pointes taking class I antiarrhythmic agents who require continued antiarrhythmic drug therapy. However, the safety of amiodarone in advanced heart failure patients with a history of drug-induced torsades de pointes, who may be more susceptible to proarrhythmia, is unknown. Therefore, the objective of this study was to assess amiodarone safety and efficacy in heart failure patients with prior antiarrhythmic drug-induced torsades de pointes. We determined the history of torsades de pointes in 205 patients with heart failure treated with amiodarone, and compared the risk of sudden death in patients with and without such a history. To evaluate the possibility that all patients with a history of torsades de pointes would be at high risk for sudden death regardless of amiodarone treatment, we compared this risk in patients with a history of torsades de pointes who were and were not subsequently treated with amiodarone. Of 205 patients with advanced heart failure, 8 (4%) treated with amiodarone had prior drug-induced torsades de pointes. Despite similar severity of heart failure, the 1-year actuarial sudden death risk was markedly increased in amiodarone patients with than without prior torsades de pointes (55% vs 15%, p = 0.0001). Similarly, the incidence of 1-year sudden death was markedly increased in patients with prior torsades de pointes taking amiodarone compared with such patients who were not subsequently treated with amiodarone (55% vs 0%, p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Rate smoothing with cardiac pacing for preventing torsade de pointes.

Cardiac pacing remains one of the most effective means for preventing torsade de pointes in patients with long QT syndrome (LQTS). However, fatal arrhythmias may occur despite combined therapy with beta blockers and pacing, and it is possible that failure of cardiac pacing for preventing arrhythmias in the long run is related (at least in part) to suboptimal pacemaker programming. Preventing sudden pauses may be especially important for preventing arrhythmias in the LQTS because such pauses are highly proarrhythmic in this patient population. Unfortunately, properly functioning pacemakers cannot be expected to prevent postextrasystolic pauses. The use of a pause-prevention pacing algorithm-rate smoothing-for preventing pause-dependent torsade de pointes is described in 12 patients with cardiac arrest or syncope due to congenital LQTS who were followed for 21 +/- 11 months.

Risk of thromboembolism in chronic atrial flutter.

Anticoagulant therapy is not conventionally used in the treatment of patients with atrial flutter. This recommendation has been based on sparse clinical experience, and recent preliminary reports suggest a significant risk of thromboembolism for these patients. A retrospective study was undertaken to assess the frequency of thromboembolic events as well as potential risk factors for these events in a cohort of patients with atrial flutter referred for radiofrequency ablation treatment. Eighty-six consecutive patients with a primary diagnosis of atrial flutter were evaluated. A history of embolic events was noted in 12 of 86 patients (14%) with atrial flutter, with an annual risk of approximately 3%. There were no differences in the prevalence of coronary artery disease, cardiomyopathy, valvular disease, or atrial fibrillation between the 2 groups of patients having an embolic event and those of patients without embolic events. Left ventricular function and left atrial size were also similar between the 2 groups. The only significant risk factor was hypertension (p < 0.05). However, in a regression model with other clinical variables (i.e., age, gender, left atrial size, presence or absence of any cardiac disease, length of time in flutter, left ventricular function, type of flutter, flutter cycle length, type of secondary arrhythmias) no significant predictors were found. Patients with transient ischemic attacks or pulmonary emboli were then excluded from the analysis in order to compare the thromboembolic risk in the present study to that reported in major atrial fibrillation trials. The overall risk becomes 7% (6 of 86), which over a mean follow-up period of 4.5 years yields an annual risk of approximately 1.6%. Although this risk is only 1/3 of that for patients with atrial fibrillation, this risk is higher than previously recognized for patients with chronic atrial flutter. Anticoagulant therapy should be seriously considered for these patients.

Results of radiofrequency catheter ablation for atrial flutter.

RF catheter ablation for symptomatic typical atrial flutter is associated with a high procedural success rate, but a second RF procedure may be required in up to one third of subjects, particularly those with right atrial enlargement. In those subjects with both established AF and flutter, RF ablation for atrial flutter may decrease the recurrence rate of AF. However, patients remain at risk for the development of newly documented AF, most likely secondary to the high incidence of underlying structural heart disease.

Predicting death from progressive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Data were retrospectively reviewed on 528 consecutive patients hospitalized for treatment of advanced heart failure (left ventricular ejection fraction 0.2 +/- 0.07) and cardiac transplant evaluation, who were stabilized with medical therapy and discharged home. Predictors of heart failure death or rehospitalization for urgent transplantation were identified using the Cox proportional-hazards model. Within 1 year, 59 patients (11%) died suddenly and 70 (13%) died of heart failure or required urgent transplantation. A serum sodium < or = 134 mEq/liter, pulmonary arterial diastolic pressure > 19 mm Hg, left ventricular diastolic dimension index > 44 mm/m2, peak oxygen consumption during exercise testing < 11 ml/kg/min and the presence of a permanent pacemaker were independent predictors of hemodynamic deterioration. In the absence of these risk factors the risk of hemodynamic deterioration within 1 year from this study was only 2%. This risk increased to > 50% in the presence of hyponatremia and any 2 additional risk factors. Thus, patients with advanced heart failure at highest risk for progressive hemodynamic deterioration can be identified from clinical variables that could aid in triaging such patients to earlier cardiac transplantation.

Transesophageal echocardiography during radiofrequency catheter ablation of ventricular tachycardia.

Radiofrequency lesion formation requires stable catheter tip/endocardial contact. Energy delivery is limited when temperatures are > 100 degrees C due to coagulum formation at the catheter tip. Transesophageal echocardiographic imaging may be useful for monitoring catheter position and detecting boiling. Transesophageal echocardiographic images were recorded during production of 22 radiofrequency lesions in bovine myocardium in a saline bath. Lesion size, tissue temperature and appearance of echo contrast (bubbles) were assessed. In 11 patients, transesophageal echocardiography was used to guide catheter movement and detect boiling during radiofrequency ablation for ventricular tachycardia. In the tissue bath, the appearance of echo bubbles was associated with visual bubbling at the catheter tip, tissue temperatures > 60 degrees C and larger lesions (284 +/- 165 vs 30 +/- 54 mm3; p < 0.001). In humans, transesophageal images easily identified the catheter tip in either ventricle and enabled continuous observation of electrode-tissue contact during radiofrequency application. Transesophageal echocardiographic bubbles appeared in 59 of 217 radiofrequency applications (27%). Continued radiofrequency application after appearance of bubbles was followed by an increase in impedance. Prolonged placement of the probe in heavily sedated patients resulted in a mild sore throat, but no other complications. Transesophageal echocardiographic imaging enables continuous monitoring of catheter position during radiofrequency energy application. The abrupt appearance of echo bubbles indicates boiling and impending coagulum formation at the catheter tip.

Biventricular pacing in patients with congestive heart failure: two prospective randomized trials. The VIGOR CHF and VENTAK CHF Investigators.

Epidemiologic studies suggest that 20-30% of patients diagnosed with symptomatic congestive heart failure (CHF) have intraventricular conduction disorders characterized by a discoordinate contraction pattern and wide QRS. Biventricular pacing is an emerging therapy allowing simultaneous electrical stimulation of the right and left ventricles with the use of an implantable pacing system. The aim of this article is to describe 2 prospective randomized multicenter trials examining the effects of biventricular pacing on functional capacity, quality of life, and hemodynamic status in patients with dilated cardiomyopathy and intraventricular delay. The VIGOR CHF Trial is designed to assess functional and symptomatic improvement in heart failure patients with biventricular pacing and without a concomitant indication for conventional bradycardia pacemaker therapy. To assess for potential placebo effects, patients are randomized to receive either biventricular pacemaker therapy or no pacing therapy for the first 6 weeks, after which both groups receive pacing therapy. The VENTAK CHF trial uses an implantable cardioverter defibrillator system (ICD) designed to provide chronic biventricular pacing therapy in addition to treating ventricular tachyarrhythmias. All patients receive conventional ICD and CHF therapy throughout the study and are randomized in a 2-period crossover design to receive either no pacing or biventricular pacing for 3-month intervals. Patient enrollment in both studies is ongoing, with a closed analysis. The unique designs of these trials provide the opportunity to study this therapy in high-risk patients who have been optimally treated for heart failure.

Depressed central respiratory drive causing weaning failure. Its reversal with doxapram.

A patient failed to wean from mechanical ventilation. Her problem was unique in that she had a depressed central drive to breathe manifested by hypopnea when removed from the ventilator. After excluding the known problems that impair successful weaning, we empirically administered three separate infusions of doxapram, a respiratory stimulant. These infusions produced a dramatic improvement in spontaneous ventilation and led to successful weaning and hospital discharge.