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Biomedical subjects

A Pacifico

Publications and source records attributed to A Pacifico.

At least 19 recordsLinked to original sources
PubMed1998

Altering molecular mechanisms to prevent sudden arrhythmic death.

Trials of drug treatment for prevention of sudden arrhythmic death have been disappointing, perhaps because suppressive therapy with arrhythmic agents fails to address the mechanisms leading to electrophysiological failure. We propose that preventive treatment should pay more attention to molecular mechanisms responsible for the progression of cardiac disease to electrophysiological failure. Most sudden cardiac deaths occur in people with atherogenic dyslipidaemias. Our hypothesis is that the pathogenic molecular mechanisms of dyslipidaemias contribute directly to arrhythmogenesis. Proinflammatory-prothrombotic lipid-derived mediators that may play a part in arrhythmogenesis include phospholipids and leucotrienes acting through the platelet-activating-factor and peroxisome proliferator-activated-receptor pathways. There are drugs available to test the hypothesis of dyslipidaemias-specific prevention of electrophysiological failure.

Arrhythmias, Cardiac↗
PubMed1998

Microwave catheter design.

A microwave antenna system for transcatheter ablation of cardiac tissue is investigated. A numerical model based on the finite-difference time-domain method incorporating a Gaussian pulse excitation has been constructed and frequency domain electric and magnetic fields are obtained through Fourier transformation. Results are presented for a coaxial line fed monopole catheter which is modified by the successive inclusion of a Teflon sheath outer coating, a terminating disk at the tip of the antenna, a sleeve choke, and a high dielectric constant cylinder surrounding the monopole antenna. The effects of these design features are characterized in terms of specific absorption rate (SAR) and return loss (RL). Numerical calculations are confirmed by comparing with the RL measurement of a Teflon-coated monopole containing a disk and choke.

Animals↗
PubMed1997

Effect of preexisting epicardial patch electrodes on defibrillation thresholds of unipolar defibrillators.

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.

Aged↗
PubMed1997

Long-term follow-up of cardioverter-defibrillator implanted under conscious sedation in prepectoral subfascial position.

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.

Adolescent↗
PubMed1997

Comparison of multiplane and biplane transesophageal echocardiography in the assessment of aortic stenosis.

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.

Adult↗
PubMed1997

Conscious sedation with combined hypnotic agents for implantation of implantable cardioverter-defibrillators.

OBJECTIVES: The objective of this study was to evaluate the feasibility, safety and efficacy of placing implantable cardioverter-defibrillators (ICDs) in the electrophysiology laboratory using conscious sedation with combined hypnotic agents and deep sedation with etomidate. BACKGROUND: Implantable cardioverter-defibrillators with transvenous leads permit the use of simplified implantation techniques similar to those used for the insertion of permanent pacemakers. However, implantation of ICDs without general anesthesia has thus far gained limited acceptance. METHODS: In 162 patients, conscious sedation during ICD placement was achieved with combined intravenous midazolam, morphine and promethazine (Phenergan). Intravenous etomidate was administered to induce deep sedation for defibrillation threshold testing. First-time implantations were in the prepectoral position (n = 142), but some patients with preexisting devices received abdominal implants (n = 20). The results were compared with those of concurrent patients (n = 56) who received prepectoral implants under propofol anesthesia administered by an attending anesthesiologist. RESULTS: The anesthetic protocol was implemented without major intraoperative complications. During deep sedation with etomidate, episodes of apnea, hypoxia or arterial hypotension requiring therapeutic intervention did not occur. During a mean (+/-SD) follow-up period of 257 +/- 140 days (median 227, range 14 to 482), there were, among the 162 patients, a total of two nonsudden cardiac deaths-one 71 days and the other 157 days after the operation. There were two nonsudden deaths in the concurrent control subjects (n = 56)-one 13 days and the other 110 days after the operation. CONCLUSIONS: Implantation of ICDs under conscious sedation with combined hypnotic agents and deep sedation with etomidate is a safe and effective procedure with low perioperative morbidity and low long-term complication rates.

Aged↗
PubMed1997

Right side implant of the unipolar single lead defibrillation system.

The active can defibrillator has been designed for implantation in the left prepectoral region. Whether this system can be successfully implanted on the right side is unknown. We describe six cases in which placement of the unipolar single lead defibrillation system was successfully attempted in the right prepectoral region due to impediments on the left side. The mean age of the patients was 62 +/- 12 years. Five patients had ischemic heart disease and one idiopathic dilated cardiomyopathy. The endocardial defibrillation electrode was placed in the right ventricle through the right subclavian vein and positioned at the apex in two patients and in the septal position in four patients. Defibrillation threshold testing was performed using a step-up/step-down protocol beginning at 12 J with 3-J increments or decrements. Defibrillation threshold was defined as the lowest energy of the first shock able to terminate ventricular fibrillation. The generator models used were the Medtronic 7218C in 1 patient, the Medtronic 7219C in 3 patients, and the Ventritex Cadet 115 AC in 2 patients. The mean defibrillation threshold was 15 +/- 3 J. The defibrillation thresholds were retested at 1, 3, and 6 months, and showed no significant change in five patients but decreased from 15 J to 12 J in one patient. The presence of impediments on the left side should not preclude attempts to place the unipolar active can system in the right prepectoral region.

Aged↗
PubMed1997

Sudden cardiac death: still more questions than answers.

Sudden cardiac death is the leading cause of death in industrialized countries. It is most frequently due to ventricular tachyarrhythmias occurring in the presence of coronary heart disease, but mechanisms linking sudden death to coronary atherosclerosis are still unclear. In autopsy studies of sudden death patients, the incidence of acute thrombotic coronary occlusions has varied between 4 and 74%. In over 600 consecutive patients with implantable cardioverter-defibrillators, we observed that appropriate shocks for electrogram-verified ventricular tachyarrhythmias was only very rarely followed by signs of acute myocardial infarction (< 3% of cases), not supporting the coronary occlusion theory of fatal arrhythmias. Cellular hypertrophy compensating for cell loss due to ischemia, intraventricular hypertension, cardiomyopathy, and myocarditis might play a role in arrhythmogenesis as evidenced by the fact that experimental induction and regression of hypertrophy are paralleled by changes in the inducibility of ventricular tachyarrhythmias. Atherogenic hyperlipidemias are associated with a systemic inflammatory response manifested by leukocytosis (lymphocytosis) and complex upregulations of proinflammatory-prothrombotic mediators, such as platelet-activating factor, cytokines, and hemostasis factors. The diurnal regulation of these mediators parallels circadian rhythms of coronary morbidity and mortality. Some upregulated mediators have been shown to exert direct arrhythmogenic effects. The potential contribution of hyperlipidemia-associated inflammatory factors to arrhythmogenesis is important, because it opens new molecular targets for antiarrhythmic drug design.

Cardiomegaly↗
PubMed1996

Natural history, determinants, and clinical relevance of conduction abnormalities following orthotopic heart transplantation.

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.

Adult↗
PubMed1996

Undetected ventricular fibrillation in transvenous implantable cardioverter-defibrillators. Prospective comparison of different lead system-device combinations.

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.

Adult↗
PubMed1996

Characterization of spontaneous recurrent ventricular arrhythmias detected by electrogram-storing defibrillators in sudden cardiac death survivors with no inducible ventricular arrhythmias at baseline electrophysiologic testing.

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.

Aged↗
PubMed1996

Undersensing of the tiny QRS complexes that emerged after the isolation of the right ventricle in a patient with ventricular tachycardia.

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.

Adult↗
PubMed1995

Randomized, double-blind comparison of intravenous amiodarone and bretylium in the treatment of patients with recurrent, hemodynamically destabilizing ventricular tachycardia or fibrillation. The Intravenous Amiodarone Multicenter Investigators Group.

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.

Aged↗
PubMed1995

Cardiac involvement in a large kindred with myotonic dystrophy. Quantitative assessment and relation to size of CTG repeat expansion.

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.

Adolescent↗
PubMed1995

Improved spatial resolution for cardiac mapping using current source density-based electrode arrays.

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.

Animals↗
PubMed1994

Evaluation of intravenous lidocaine for the termination of sustained monomorphic ventricular tachycardia in patients with coronary artery disease with or without healed myocardial infarction.

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.

Adult↗
PubMed1994

Usefulness of Holter monitoring in predicting efficacy of amiodarone therapy for sustained ventricular tachycardia associated with coronary artery disease.

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.

Actuarial Analysis↗