Biomedical subjects
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The question is addressed whether patients with thoracotomy defibrillators and failing epicardial electrodes can be effectively treated with the implantation of prepectoral unipolar ("active can") defibrillators. Results indicate that abandoned epicardial patches in the pathway of unipolar defibrillation currents do not affect defibrillation thresholds and active can efficacy.
The database of the registry for an implantable cardioverter defibrillator was analyzed to determine the efficacy and safety of antitachycardia pacing for the termination of ventricular tachycardia. In 22,339 episodes treated, termination occurred in 94% and acceleration in only 1.4%.
BACKGROUND: Implantable cardioverter-defibrillators (ICDs) with intravenous electrode systems and downsized generators can be implanted by use of operative techniques similar to those employed for the insertion of permanent pacemakers. However, the safety, efficacy, and long-term follow-up of simplified implantation procedures remain to be evaluated. This report is a prospective long-term evaluation of nonselected patients receiving ICDs in the prepectoral subfascial position under conscious sedation. METHODS AND RESULTS: Clinical characteristics of the 231 consecutive patients included a mean age of 63 years, a male-to-female ratio of 6.4, a left ventricular ejection fraction of 0.34, a mild-to-moderate heart failure in 91%, coronary artery disease in 84%, and a history of aborted sudden cardiac death or refractory ventricular tachyarrhythmias. Insertion of transvenous leads and prepectoral subfascial ICD implantation were performed in electrophysiology laboratories under local anesthesia and conscious sedation with intravenous midazolam and propofol. Successful implantation in all patients (operation time, 80 +/- 32 minutes, mean +/- SD) irrespective of body size and skin thickness was free of major complications, including need for emergency intubation. After surgery, 1 pocket hematoma, 1 seroma, and 1 pneumothorax required treatment. There was no operative or first-month mortality. During long-term follow-up averaging 453 +/- 296 days, six leads required repositioning, but pocket erosions or infections did not occur. First-year total survival was 97%. CONCLUSIONS: Implantation under conscious sedation of ICDs in the prepectoral subfascial position is a safe and effective procedure with low operative and postoperative morbidity and favorable long-term outcome.
The aim of the study was to compare the accuracy of multiplane transesophageal echocardiography (TEE) with the more conventional biplane technique in the direct assessment of aortic valve area in patients with aortic stenosis. Short-axis images of the aortic valve adequate for measuring aortic valve area were obtained in all 81 patients studied by multiplane TEE but in only 56 of 64 patients (88%) using the biplane approach. The correlation coefficient for aortic valve area determined by multiplane TEE (r = 0.89; SEE = 0.04 cm2) was higher (p < 0.01) than biplane TEE (r = 0.74; SEE = 0.06 cm2). Correlations were higher for bicuspid valves (multiplane, r = 0.93; biplane, r = 0.75) than tricuspid valves (multiplane, r = 0.87; biplane, r = 0.75). Our study has demonstrated the superiority of multiplane TEE to both biplane TEE and transthoracic echocardiography (TTE) in the direct evaluation of aortic valve area in patients with aortic stenosis.
To study the long-term evolution, determinants, and clinical relevance of the conduction abnormalities after orthotopic heart transplantation, 87 patients, followed for a mean of 105 +/- 72 weeks, were divided into 3 groups according to the characteristics of their electrocardiograms compared with their initial electrocardiogram recorded at study entry. The first group consisted of 24 patients whose initial electrocardiogram was normal, and subsequent electrocardiograms remained normal throughout the study. The second group included 27 patients who developed electrocardiographic evidence of progressive conduction system damage. The third group comprised 36 patients whose initial electrocardiogram was abnormal and subsequent electrocardiograms remained unchanged during follow-up. Although the hemodynamic and echocardiographic evaluation of right and left ventricular function were initially similar among the 3 groups, groups 2 and 3 demonstrated a significant deterioration of left ventricular ejection fraction (62 +/- 12% to 55 +/- 16% and 62 +/- 8% to 57 +/- 14%, respectively; p < 0.05) and cardiac index (2.7 +/- 0.6 to 2.3 +/- 0.5 and 3.0 +/- 0.9 to 2.5 +/- 0.9 L/min/m2, respectively; p < 0.05) while patients in group 1 maintained their normal baseline indices. Incidence and progression of coronary artery disease, as well as frequency of rejection episodes, were comparable among the groups. Mortality was higher in the 2 groups with evidence of conduction defects. Sudden death associated with complete heart block (2 patients) or ventricular arrhythmias (3 patients) was exclusively confined to patients with evidence of progressive electrocardiogram abnormalities. We conclude that, following orthotopic heart transplantation, stable or progressive conduction system damage on the electrocardiogram is associated with left ventricular dysfunction and increased mortality. Sudden death is not uncommon among patients demonstrating worsening cardiac conduction and, in some cases, is related to the development of potentially preventable complete heart block.
BACKGROUND: The purpose of this study was to prospectively analyze redetection problems after unsuccessful shock with different lead systems and devices. METHODS AND RESULTS: We prospectively analyzed detection and redetection characteristics among transvenous implantable cardioverter-defibrillators (ICDs) using standard bipolar and integrated bipolar sensing. Monophasic and biphasic ICDs were included. Subthreshold shocks were intentionally delivered, and redetection of ventricular fibrillation (VF) was assessed before discharge and at 1, 3, 6, and 12 months later. Sensing of VF resulting from antitachycardia pacing and low-energy cardioversion ( < or = 2 J) also was analyzed. Before inclusion in the study, each patient underwent subthreshold shock testing at three different time intervals. Among the 160 ICDs with standard bipolar sensing, 530 VF inductions were analyzed. After the failed shocks, undersensing was more frequent (3% versus 20%, P<.01) but did not remarkably prolong redetection (3.1 +/- 0.8 versus 3.3 +/- 1.1 seconds). Among the 201 ICDs with integrated bipolar sensing, 80 were connected to a CPI device (60 Ventak 1600-Endotak 60 series and 20 PRx II 1715-Endotak 70 series) and 121 to the Ventritex defibrillator (91 Endotak 60 series, 14 TVL systems, and 16 Endotak 70 series). After 252 failed shocks, redetection was prolonged with the CPI system (3.1 +/- 1.4 versus 4.6 +/- 3.6 seconds, P<.05) but did not change after 396 failed shocks with the Ventritex ICD (5.4 +/- 1.9 versus 4.9 +/- 2.2 seconds). This may reflect different nominal settings for detection and redetection. In 9 of 121 patients with Ventritex and 1 of 80 with the CPI ICDs, the devices failed to redetect VF. However, redetection malfunction was never observed in patients with integrated bipolar systems with >6-mm electrode separation. After antitachycardia pacing in 1 patient and a 2-J shock in 1 patient, ventricular tachycardia turned into VF, which was undetected. Both patients used the Endotak 60 series-Cadence combination. None of the patients showing VF undersensing had sudden death at follow-up. Only 3 of the 12 patients with sensing malfunction were on antiarrhythmia drugs at the time of testing. Analysis of endocardial electrograms showed that failure to redetect VF is not associated with a uniform reduction but with a rapid and repetitive change of electrogram amplitude. CONCLUSIONS: Standard bipolar sensing redetects VF more effectively than integrated bipolar sensing. Endocardial electrogram analysis provides insights into the understanding of the mechanism of undersensing, and certain lead-device combinations result in a higher occurrence of VF undersensing. The clinical relevance of this phenomenon remains unknown.
This retrospective study characterized the recurring ventricular arrhythmias with an electrogram-storing defibrillator in survivors of sudden cardiac death who had no inducible sustained ventricular arrhythmias at baseline electrophysiologic testing (EPS). The study group was composed of 24 selected patients with documented ventricular fibrillation (VF) without need of revascularization or chronic antiarrhythmic therapy. The EPS protocol usually consisted of three extrastimuli at two drive cycles at two right ventricular sites. Nonischemic cardiomyopathy was the most frequent structural abnormality (n = 11) followed by coronary artery disease (n = 7). The mean ejection fraction was 0.37 +/- 0.13. Cardiac status did not appear to change during a mean follow-up period of 16.4 +/- 12.5 months, and eight (33%) patients received appropriate shocks in that time period. On the basis of intracardiac electrograms, 7 (88%) patients experienced VF and 1 (12%) patient had ventricular tachycardia as the first recurring arrhythmia. Four patients had additional recurrences and all were VF episodes. VF was usually present from the onset of the arrhythmia. In addition, 9 (38%) patients had nonsustained ventricular arrhythmias that were solely VF in 6 (67%). In conclusion, VF of sudden onset was the most frequent recurring sustained ventricular arrhythmia in this group.
This article describes a patient who underwent right ventricular disconnection for medically refractory ventricular tachycardia associated with arrhythmogenic right ventricular dysplasia. After the operation there was no ventricular tachycardia recurrence. Two years after the operation, he received a permanent VVI pacemaker for the symptomatic second-degree AV block. Sensing function of the pacemaker was normal for the normal QRS complexes, but the tiny QRS complexes that appeared after the arrhythmia surgery were not sensed by the pacemaker and therefore caused no problem.
BACKGROUND: After several days of loading, oral amiodarone, a class III antiarrhythmic, is highly effective in controlling ventricular tachyarrhythmias; however, the delay in onset of activity is not acceptable in patients with immediately life-threatening arrhythmias. Therefore, an intravenous form of therapy is advantageous. This study was designed to compare the safety and efficacy of a high and a low dose of intravenous amiodarone with bretylium, the only approved class III antiarrhythmic agent. METHODS AND RESULTS: A total of 302 patients with refractory, hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation were enrolled in this double-blind trial at 82 medical centers in the United States. They were randomly assigned to therapy with intravenous bretylium (4.7 g) or intravenous amiodarone administered in a high dose (1.8 g) or a low dose (0.2 g). The primary analysis, arrhythmia event rate during the first 48 hours of therapy, showed comparable efficacy between the bretylium group and the high-dose (1000 mg/24 h) amiodarone group that was greater than that of the low-dose (125 mg/24 h) amiodarone group. Similar results were obtained in the secondary analyses of time to first event and the proportion of patients requiring supplemental infusions. Overall mortality in the 48-hour double-blind period was 13.6% and was not significantly different among the three treatment groups. Significantly more patients treated with bretylium had hypotension compared with the two amiodarone groups. More patients remained on the 1000-mg amiodarone regimen than on the other regimens. CONCLUSIONS: Bretylium and amiodarone appear to have comparable efficacies for the treatment of highly malignant ventricular arrhythmias. Bretylium use, however, may be limited by a high incidence of hypotension.
OBJECTIVE: To evaluate and quantitate cardiac involvement in myotonic dystrophy and assess whether the size of the trinucleotide (cytosine-thymine-guanine [CTG]) repeat expansion is a significant predictor of cardiac abnormalities. DESIGN: Case-control study of a large kindred with myotonic dystrophy. PATIENTS: Ninety-one bloodline members of the kindred underwent clinical and cardiac evaluation with electrocardiograms, echocardiography (with Doppler in the majority of cases), and genetic and neurologic evaluations. Affected individuals were age-matched to normal family members. MAIN OUTCOME MEASURES: Electrocardiographic conduction abnormalities, wall motion abnormalities, mitral valve prolapse, and global parameters of systolic and diastolic function were determined by an observer blinded to all clinical data and genetic analysis. RESULTS: Compared with age-matched normals, patients with myotonic dystrophy (n = 25) were more likely to have conduction abnormality (52% vs 9%), mitral valve prolapse (32% vs 9%), and wall motion abnormality (28% vs 0%) (all P < .05). Left ventricular ejection fraction and stroke volume were reduced compared with normals matched for age and heart rate (P < .05), whereas Doppler indexes of diastolic function were only marginally altered. Using multivariate analysis, the number of CTG repeats (range, 69 to 1367; normal, < or = 37) was the strongest predictor of abnormalities in wall motion and electrocardiographic conduction (odds ratio of 16.5 and 5.07 per 500 repeats, respectively). The relation of mitral valve prolapse to the size of the CTG repeat was of borderline significance. Patients with more extensive neurologic findings (n = 12) had a higher incidence of wall motion and/or electrocardiographic conduction abnormalities (83% vs 43%; P = .04). CONCLUSIONS: Cardiac involvement in myotonic dystrophy affects predominantly the conduction system and myocardial function. Alterations in myocardial relaxation and diastolic properties, in contrast to skeletal muscle myotonia, are minor. In this kindred, the number of CTG repeats was a significant predictor of cardiac dysfunction in myotonic dystrophy.
The time of the minimum slope (i.e., the fastest negative deflection) in monopolar (MP) electrograms from normal hearts compares closely with time of phase 0 of the action potential in cells underlying the electrode, but poor rejection of far-field activity may limit the utility of MP electrode technology in dense arrays used for the study of ventricular tachycardia and fibrillation. The purpose of this study is to evaluate more myopic discrete bipolar (BP) and nondirectional, two-dimensional current source density (CSD) based arrays for rejection of far-field potentials and precision of activation time determination. Simultaneous recordings of the CSD, MP, and multiple BP electrograms were performed on normal dog epicardium. The time of the minimum slope in MP electrograms was compared to activation times in CSD and BP derivations using: (1) peak; (2) steepest slope; (3) zero crossing of the steepest sloping segment in either direction; and (4) waveform morphology. In vivo, CSD amplitude was reduced significantly more than MP and BP amplitudes by insertion of inert media between the heart and the electrodes. The time of the steepest slope in CSD electrograms designated activation times closest to the time of the minimum slope in MP electrograms (0.9 +/- 1.3 msec). We conclude that CSD provides a nondirectional electrode system that accurately defines the time of local activation and possesses better spatial specificity than MP electrode systems and BP electrode systems having the same interelectrode distances.
Prospective evaluations of intravenous lidocaine as therapy for sustained monomorphic ventricular tachycardia (VT) in the absence of acute myocardial infarction are lacking. Lidocaine has been promulgated as first-line therapy in patients with VT, but studies evaluating its efficacy in the electrophysiology laboratory suggest that it has poor effects in terminating or preventing induction of VT. Thus, this study sought to evaluate the clinical effectiveness of lidocaine in 3 cohorts with induced or spontaneous VT. One hundred twenty-eight patients with stable VT, occurring either spontaneously or induced at the time of electrophysiologic study either in the baseline state or at the time of pharmacologic testing, were evaluated. The response rate to lidocaine therapy as manifested by termination of VT was the primary goal of the study. Of these patients, 10 (8%) had termination of VT after lidocaine therapy. There were no significant differences in age, ejection fraction, VT cycle length, and mean dose of lidocaine between responders and 118 nonresponders. There were no serious side effects or adverse events (death, myocardial infarction, angina, or congestive heart failure). Lidocaine, although safe, is ineffective in terminating stable VT not associated with acute myocardial infarction.
The ability of Holter monitoring to predict clinical events during amiodarone therapy was evaluated in 83 patients with coronary artery disease and inducible monomorphic ventricular tachycardia. Sixty-four patients (77%) had significant ventricular ectopy activity (> or = 10 ventricular premature complexes [VPCs]/hour) at baseline, and 19 (23%) did not; patients were similar in age (63 and 65 years, respectively; p = 0.24) and ejection fraction (31 and 32%, respectively; p = 0.75). Over a mean of 23 +/- 17 months, there was no difference in arrhythmia recurrence (33 and 26%; p = 0.89) or sudden death (16 and 20%; p = 0.94) in patients with and without significant ectopy, respectively. In patients with significant ectopy, amiodarone decreased VPC frequency from baseline to 2 weeks, but not from 2 to 6 weeks. Forty-two patients had > 85% reduction in ectopy at 2 weeks; 20 patients did not. However, this reduction of simple VPCs did not predict a decrease in arrhythmic recurrence (29 vs 40%; p = 0.59) nor sudden death (25 vs 11%; p = 0.56) in patients with and without VPC suppression, respectively. Forty-five patients had Holter monitoring at 6 weeks. Twenty-one patients (47%) had > 95% suppression of ectopy, and 24 did not. Neither the recurrence (38 vs 38%; p = 0.54) nor sudden death (33 vs 13%; p = 0.45) rate was predicted by the degree of VPC suppression. Amiodarone is a powerful suppressant of VPCs, but Holter suppression of this ectopic activity is not predictive of clinical outcome.
To define the clinical significance of conduction defects after orthotopic heart transplantation sequential electrocardiograms (ECG) of 124 patients were analyzed during their postoperative hospital stay. The first ECG was abnormal in 90 patients (73%), with a predominance of right bundle branch block, and normal in 34 (27%). Sex, age, mean donor ischemic time, duration of aortic cross clamping and use of previous antiarrhythmic therapy were not significantly different in the 2 groups. During hospital follow-up, patients were grouped according to evolution of the initial electrocardiographic abnormalities. In group 1, 25 patients continued to have an initially normal ECG. In groups 2 and 3, 30 and 48 patients, respectively, had evidence of transient and permanent conduction defects. The 21 patients in group 4 showed progressive deterioration of conduction with either a new (9 patients) or worsening preexisting conduction defect (12 patients). The evolution of the initial ECG was strongly dependent on the duration of the donor heart ischemic time and the severity of the in-hospital cardiac rejection. Patients with persistent conduction abnormalities had a statistically longer ischemic time than either patients with normal or transient conduction defects (182 +/- 84 vs 144 +/- 68 and 130 +/- 66 minutes, p = 0.04). Although the overall percentage of patients with histologic evidence of moderate to severe rejection was similar across the groups, 66.6 and 46.1% of patients in groups 3 and 4, respectively, had multiple episodes of rejection compared with 16.6 and 0% in the remaining 2 groups (p = 0.044).(ABSTRACT TRUNCATED AT 250 WORDS)
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Adequate spatial resolution of local activation is fundamental for the correct depiction of myocardial activation during ablative treatment of ventricular tachycardia. The widest allowable distances between recording sites that provide an accurate description of the field potential distribution is dictated by the Nyquist sampling theorem. Activation times are derived from the field potentials. However, because of noise intrinsic in activation detection algorithms, closer recording sites may be required than those theoretically computed. The purpose of this study is to examine the spatial frequency spectrum of epicardial activation time sequences computed by common activation detection algorithms, determine which algorithm is least noisy, and derive the recording site density necessary to avoid distortion of the epicardial activation map. Using 40 to 80 electrode linear arrays, monopolar and bipolar electrograms from the epicardium were recorded vertically (base to apex) and horizontally in 11 dogs. Activation times for bipolar electrograms were estimated using Peak, Fastest Zero Crossing, and Morphological algorithms. Activation times for monopolar electrograms were set equal to the time of the fastest negative deflection. Activation time sequences were analyzed using conventional Fourier techniques. Anomalous activation times from serially adjacent bipolar electrograms, which constitute algorithm noise, were studied. Horizontal and vertical interelectrode distances are 3.2 mm and 2.4 mm, respectively. Of the bipolar algorithms, the Morphological algorithm produced the fewest anomalous activation times. Mapping systems having more than 256 channels are required for accurate representation of epicardial activation in a typical 20-kg dog. The endocardial electrode spacing is unknown, but is expected to be at least as dense. Large global mapping systems or regionally dense arrays may offer advantages during catheter ablations for ventricular tachycardia and for studies into the mechanisms of ventricular tachycardia by accurately defining the cardiac activation pattern.
Progressive capillary occlusion often leads to severe retinopathy within 15-20 years of the onset of Type 1 (insulin-dependent) diabetes mellitus. Lipoprotein(a), a complex formed by apolipoprotein(a), apo B-100 and lipids, is considered an independent, genetically determined, predictor of cardiovascular disease. It may have antifibrinolytic properties in view of its similarity to plasminogen. To test the hypothesis that circulating lipoprotein(a) is associated with the process that leads to clinically active diabetic retinopathy, we measured the circulating levels of apolipoprotein(a) (which are strictly correlated with those of lipoprotein(a)) in two groups of patients with Type 1 diabetes of at least 15 years duration: 25 with active retinopathy and 27 without clinically detectable retinal lesions. Thirty-eight healthy subjects of the same age and sex served as controls. Serum apolipoprotein(a) was higher in the patients with active retinopathy (36(2-193) U/dl, geometric mean and range) than in those without clinically detectable retinal lesion (17(1-160)) and the control subjects (14(0-115)), p < 0.01 in both cases. The distribution of apolipoprotein(a) levels was skewed to the left, as expected, in the patients without clinically evident retinal lesions and the control groups, but there was a bimodal trend of distribution among those with active retinopathy. The levels of glycated haemoglobin were similar in the two groups of diabetic patients, and no significant differences were found for total and HDL cholesterol, triglycerides or apolipoproteins A1 and B between them and the control subjects. These preliminary results suggest that serum apolipoprotein(a) is elevated in patients with active retinopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Designation of the time of local activation is fundamental to electrophysiological mapping. In normal myocardium, the minimum slope in extracellular monopolar (MP) electrograms has been linked through simultaneous intracellular and extracellular recordings to phase 0 of the action potential. However, no similar correlation has been demonstrated for a parameter from bipolar (BP) electrograms, now commonly used during electrophysiological studies and intraoperative mapping. The purpose of this work is to compare the activation time, determined according to several common algorithms applied to BP electrograms, with the time of the minimum slope in MP electrograms. Simultaneous normal epicardial MP and BP electrograms were acquired from subjects undergoing surgery for Wolf-Parkinson-White Syndrome and from dogs. The activation time in BP electrograms was defined by four algorithms: (1) peak (P); (2) greatest absolute slope (S); (3) zero crossing of the segment containing the greatest slope (FZC); and (4) morphological (M). Each was compared to the time of the minimum slope in the simultaneously recorded MP response. The incidence of outliers was tabulated. The distribution of activation times computed using each BP algorithm was statistically different from the distribution of activation times derived from MP electrograms. M performed best (absolute difference: 2.6 +/- 2.9 msec; cor coef: 0.9925 in man). The M, P, FZC, and S algorithms produced 3.2%, 3.5%, 4.7% and 4.7% outliers, respectively. The overall performance of a morphologically based algorithm is superior to simplistic BP algorithms based only on slope or peak.(ABSTRACT TRUNCATED AT 250 WORDS)