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R M Kass

Publications and source records attributed to R M Kass.

At least 37 records · Page 2Linked to original sources

"Refractoriness" of airflow obstruction associated with isolated lymphocytic bronchiolitis/bronchitis in pulmonary allografts.

The clinical significance of an isolated "lymphocytic bronchiolitis/bronchitis" (grade B) as detected in transbronchoscopic biopsy specimens (TBB) is unclear. We therefore have reviewed the spirometric responses associated with isolated grade B diagnoses and contrasted them with episodes of "acute cellular rejection" (grade A); the latter are manifested by "perivascular lymphocytic infiltration." Because lymphocytic bronchiolitis/ bronchitis is considered a nonspecific histologic pattern that may be observed with either allograft rejection or respiratory infections, episodes were analyzed with respect to the presence (grade B [+] CMV) or absence (grade B [-] CMV) of cytomegalovirus infection. The maximum forced expiratory volume in 1 second (FEV1) during the preceding 3 months was used as a baseline for computing percent change in FEV1 coincident with transbronchoscopic biopsies (delta %FEV1 PRE) and maximum values obtained during the 3 months subsequent to specific therapies (delta %FEV1 POST). All episodes of acute cellular rejection (grades A1 to 4) and symptomatic lymphocytic bronchiolitis/bronchitis (grade B) were treated with "pulsed-dose" methylprednisolone, whereas intravenous ganciclovir was administered to patients at risk for recrudescence of cytomegalovirus. Between March 1, 1989, and September 1, 1995, 366 TBB procedures were performed for clinical indications in 57 lung transplant recipients. Histologic diagnoses with acceptable serial spirometric values included grade A1 (n = 9), grade A2 (n = 27), grade A3 (n = 2), grade B(-)CMV (n = 25) and grade B(+)CMV (n = 9). The delta %FEV1 PRE coincident with TBB were not statistically different for the different histologic groups. For grade A1, delta %FEV1 PRE was -14.6% +/- 5.2% (X +/- SEM); A2, -7.6% +/- 1.8%; B(-)CMV, -14.8% +/- 3.9%; and B(+)CMV, -14.8% +/- 2.3%. After treatment, the delta %FEV1 POST, relative to baseline values, were for grade A1, -8.8% +/- 7.1%, A2, +0.26% +/- 2.6%; B(-)CMV, -12.0% +/- 3.8%; and B(+)CMV, -6.2% +/- 2.8%. The delta %FEV1 POST values after pulsed methylprednisolone were significantly greater for histologic grade A2 than grade B(-)CMV (unpaired Student's t test, P < 0.01; 95% confidence interval for the difference of means: 3.34% to 21.2%). Grade A2 rejection was associated with spirometric improvement to within 10% of baseline values in 52% of episodes; whereas with grade B(-)CMV, this salutary response was observed in only 32% of episodes. Bronchiolitis obliterans syndrome stage 1b developed in 13 of 20 (65%) recipients, approximately 7.9 +/- 3.4 months after detection of histologic grade B and 21.2 +/- 9.5 months after transplantation. We conclude that the relative "refractoriness" of histologic grade B most likely reflects a continuum of bronchiolitis obliterans after lung transplantation and, hence, may warrant different immunosuppressive strategies. Furthermore, spirometric decrement associated with acute cellular rejection (grade A) may be ameliorated, but often not completely reversed, after pulsed methylprednisolone. We speculate that surveillance TBB may prove rewarding by enabling an earlier detection of these histologic diagnoses before the development of physiologic impairment.

Airway Obstruction↗

Upper limit of vulnerability is a good estimator of shock strength associated with 90% probability of successful defibrillation in humans with transvenous implantable cardioverter-defibrillators.

OBJECTIVES: The goals of this study were to determine the probability of successful defibrillation at the upper limit of vulnerability and to evaluate a minimal safety margin for implantable cardioverter-defibrillator first shocks based solely on the upper limit of vulnerability. BACKGROUND: The upper limit of vulnerability is the strength at or above which ventricular fibrillation is not induced when a stimulus is delivered during the vulnerable phase of the cardiac cycle. It has been proposed as an estimate of defibrillation efficacy because it correlates with the defibrillation threshold and can be determined with a single episode of fibrillation. METHODS: We studied 40 patients prospectively at implantation of transvenous cardioverter-defibrillators. Defibrillation threshold was defined as the weakest biphasic shock that defibrillated after 10 s of ventricular fibrillation. The upper limit of vulnerability was defined as the weakest biphasic shock that did not induce ventricular fibrillation when given at 0, 20 and 40 ms before the peak of the T wave in ventricular paced rhythm at cycle length 500 ms. After determination of the upper limit of vulnerability and defibrillation threshold, patients underwent six additional fibrillation-defibrillation episodes. The strength of five of the defibrillation shocks was equal to the upper limit of vulnerability; the strength of one of the six shocks was randomly selected to be equal to the upper limit of vulnerability plus 3 J. The implantable cardioverter-defibrillator was tested at the upper limit of vulnerability plus 3 J in 28 patients. RESULTS: The defibrillation threshold was 8.8 +/- 5.0 J (mean +/- SD), and upper limit of vulnerability was 11.3 +/- 4.6 J; the defibrillation threshold and upper limit of vulnerability were highly correlated (r = 0.89, p < 0.001). The success rate for the 200 defibrillation shocks with strength equal to the upper limit of vulnerability was 90% (95% confidence intervals based on proportion of successes in 40 patients: 86% to 94%). All five defibrillation test shocks at the upper limit of vulnerability were successful in 24 patients (60%); four of five were successful in 12 patients (30%); and three of five were successful in 4 patients (10%). All 40 test shocks and 28 implantable cardioverter-defibrillator shocks with a strength equal to the upper limit of vulnerability plus 3 J were successful. CONCLUSIONS: The upper limit of vulnerability is a good estimator of the shock strength associated with 90% probability of successful defibrillation (DFT90). A strength of 3 J above the upper limit of vulnerability is a good estimate of the minimal acute safety margin for implantable cardioverter-defibrillator first shocks.

Adult↗

Short biphasic pulses from 90 microfarad capacitors lower defibrillation threshold.

For defibrillation between right ventricular and retropectoral patch electrodes using truncated exponential pulses, the stored energy defibrillation threshold (DFT) is lower for short pulses from small 60-microF capacitors than for conventional pulses from 120-microF capacitors, but 60-microF pulses frequently require higher voltages than are currently used. The goal of this study was to determine if DFT could be reduced by intermediate size 90-microF capacitors. This study compared biphasic waveform DFTs for 120 microF-65% tilt pulses, 90 microF-65% tilt pulses, and 90 microF-50% tilt pulses in 20 patients at defibrillator implantation. The 90 microF-50% tilt pulses were selected because their duration is half that of 120 microF-65% tilt pulses. The stored energy DFT for 90 microF-50% tilt pulses (9.1 +/- 4.3 J) was less than both the DFT for 120 microF-65% tilt pulses (12.0 +/- 5.5 J, P < 0.005) and the DFT for 90 microF-65% tilt pulses (11.6 +/- 5.8 J, P < 0.005). There was no significant difference between the latter two values. The voltage DFTs for 90 microF-50% pulses (436 +/- 113 V) and 120 microF-65% tilt pulses (436 +/- 104 V) were not statistically different; the voltage DFT for 90 microF-65% tilt pulses was higher than for either of the other two pulses (490 +/- 131, P < 0.005). The DFT was 20 J or greater in three patients for both 120 microF-65% tilt pulses and 90 microF-65% tilt pulses, but it was 16 J or less in all patients for 90 microF-50% tilt pulses. When pathways were dichotomized by the median resistance of 71 omega, 90 microF-50% tilt pulses significantly reduced DFTs compared to 120 microF-65% tilt pulses for higher resistance pathways (9.2 +/- 4.0 J vs 13.0 +/- 6.2 J, P = 0.002), but not lower resistance pathways (9.0 +/- 4.8 J vs 10.9 +/- 4.6 J, P = NS). For the electrode configuration tested, biphasic 90 microF-50% tilt pulses reduce stored energy DFT in comparison with 120 microF-65% tilt pulses without increasing voltage DFT. However, 90 microF-65% tilt pulses provide no benefit.

Defibrillators, Implantable↗

Delayed development of obliterative bronchiolitis syndrome with OKT3 after unilateral lung transplantation. A plea for multicenter immunosuppressive trials.

There is no consensus regarding the optimal induction immunosuppression regimen after lung transplantation (LT). In addition to the potential benefit of a reduced incidence of early acute allograft rejection, cytolytic induction immunosuppression may impact on long-term allograft function. We retrospectively assessed our incidence of obliterative bronchiolitis syndrome (OBS) stages Ia and IIa in LT survivors given two different cytolytic induction immunosuppression regimens: (between March 1989 and October 1990) OKT3 (5 mg/d)x10 to 14 days (n=11) vs (between November 1990 and April 1993) Minnesota antilymphocyte globulin (MALG) (10 to 15 mg/kgdx5 to 7 days. Cyclosporine (CSA) (whole blood polyclonal assay=600 to 800 ng/mL), azathioprine (1 to 2 mg/kg/d), and maintenance prednisone (0.2 mg/kg/d) were similar. Surveillance spirometry was performed monthly, in accordance with accepted American Thoracic Society criteria. Fiberoptic bronchoscopy with transbronchial biopsies (TBBs) were performed for clinical indications. Surveillance TBBs were not performed during the era of this study. As defined by the ISHLT "Working Formulation for the Standardization of Nomenclature and for Clinical Staging of Chronic Dysfunction in Lung Allografts," latencies to development of OBS stages Ia and IIa were determined by Kaplan-Meir analysis. Stepwise regression (Cox proportional hazards model) was performed for the variables: cytolytic induction regimen, episodes cytomegalovirus (CMV) pneumonitis, episodes CMV infection, serologic CMV donor (+): recipient (-) mismatch, prior pregnancy, HLA (A,B,DR +/- DQ) mismatches, episodes greater than grade A1 acute cellular rejection (ACR). We found that the OKT3 cohort experienced longer latencies for OBS stages Ia and IIa. Latencies to OBS stages Ia for OKT3 ve MALG were 962 +/- 65 vs 354 +/- 85 days (X +/- SEM) respectively. Brookmeyer-Crowley 95% confidence intervals for median latencies were 744 to 1,180 vs 266 to 510 days for OKT3 vs MALG, respectively. The Cox model was significant only for the variable of the induction cytolytic immunosuppression regimen (p=0.0015). By physiologic criteria, a longer course of OKT3 appeared superior to the short-course MALG protocol in delaying chronic lung allograft dysfunction. These effects may be related either to inherent differences in the antilymphocyte preparations or, alternatively, the difference in duration of treatment between groups. Surveillance TBB and treatment of detected occult ACR may serve to negate the observed differences in latencies for OBS.

Acute Disease↗

Optimal electrode configuration for pectoral transvenous implantable defibrillator without an active can.

A new 83 cm3 implantable cardioverter-defibrillator (ICD) designed for pectoral implantation has been implanted most frequently using right ventricular and superior vena cava (RV-->SVC) electrodes; a patch electrode (RV-->patch + SVC) has been added when necessary to decrease the defibrillation threshold (DFT). The goal of this prospective study was to compare biphasic waveform DFTs for 3 electrode configurations: RV-->patch, RV-->SVC, and RV-->patch + SVC in 25 consecutive patients. The patch was positioned in a left retro-pectoral pocket, and the SVC electrode was positioned with the tip at the junction of the SVC and innominate vein. In the first 15 patients, all 3 electrode configurations were tested in random order; in the last 10 patients, only the RV-->patch and RV-->patch + SVC configurations were tested. In the first 15 patients, the stored-energy DFT for the RV-->SVC configuration (15.2 +/- 7.7 J) was higher (p < 0.001) than the DFT for the RV-->patch configuration (11.3 +/- 6.2 J) and the RV-->patch + SVC configuration (10.0 +/- 5.8 J). For all 25 patients, the DFT was lower for the RV-->patch + SVC configuration (9.7 +/- 5.1 J) than for the RV-->patch configuration (12.4 +/- 6.6 J, p = 0.005). The pathway resistance was highest for the RV-->patch configuration (72 +/- 9 omega), lower for the RV-->SVC configuration (63 +/- 6 omega, p < 0.01), and lowest for the RV-->patch + SVC configuration (46 +/- 3 omega, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Assessment of pathological changes associated with chronic allograft rejection and tolerance in two experimental models of rat lung transplantation.

Lung transplantation is now routinely performed for a wide range of end-stage cardiopulmonary disorders. Despite overcoming the problems associated with early acute rejection, chronic rejection (CR) in the form of obliterative bronchiolitis has emerged as the primary cause of late graft loss. The mechanisms involved in the development of CR of lung allografts are poorly understood, and no effective therapy is currently available. To better understand the pathological events associated with CR and tolerance, we examined two models of lung allograft rejection established in our laboratory. First, we exchanged left lung allografts between moderately histoincompatible inbred rat strains (WKY-->F344: n = 42 and F344-->WKY: n = 40). The WKY-->F344 model was previously shown to develop spontaneous tolerance, while the converse model (F344-->WKY) showed persistent acute rejection. The purpose of this investigation was to assess histopathological changes associated with long-term grafts left in place up to 140 days after transplant. To confirm that tolerance had developed, skin-grafting experiments were performed. Five skin grafts from each strain were placed on lung allograft recipients on day 35 after transplant and skin allograft survival was assessed and compared with controls. Acute rejection (AR) was graded histologically (stage O-IV) and the pathologic intensity of inflammation and CR were graded (0-4: 0 = 0%, 1 = 1-25%, 2 = 26-50%, 3 = 51-75%, and 4 = 76-100%) on percentage of involvement with the following categories being examined: (a) lymphocytic infiltration (perivascular, peribronchial, and peribronchiolar) and (b) vasculitis, edema, hemorrhage, and necrosis. Finally, chronic rejection was diagnosed by the presence of intimal hyperplasia, interstitial fibrosis, peribronchiolar fibrosis, bronchiolitis obliterans, and bronchiectasis. The WKY-->F344 animals showed progressive AR (stage III, day 21). Thereafter, the AR subsided spontaneously and was stage 0 on day 140. There were no signs of CR in these animals. In the F344-->WKY model, the AR progressed up to stage III-IV (day 21) and maintained for several weeks at stage III. Thereafter, pictures of the lungs showed CR on days 49, 70, and 98. There were significant differences between the two models during the chronic phase, such as interstitial fibrosis (0 +/- 0 vs. 1.8 +/- 1.3, P < 0.005), peribronchiolar fibrosis (0 +/- 0 vs. 3.6 +/- 0.55, P < 0.01), vasculitis (0.2 +/- 0.45 vs. 2.0 +/- 0, P < 0.008), and intimal hyperplasia (0.2 +/- 0.45 vs. 2.6 +/- 0.9, P < 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Soluble CTLA4Ig modifies parameters of acute inflammation in rat lung allograft rejection without altering lymphocytic infiltration or transcription of key cytokines.

The efficacy of CTLA4Ig in blocking immune activation and allograft rejection (AR) was tested in an aggressive and rapid model of rat lung AR (Brown Norway [BN]-->Lewis [LEW]). CTLA4Ig is a recombinant soluble protein that binds with high affinity to rat B7/BB1 and other surface molecules on APCs, subsequently blocking the binding of B7/BB1 to CD28/CTLA4 on T cells. This interrupts the costimulatory pathway critical for complete T cell activation and completion of the AR process. Left single-lung transplants were performed between BN-->Lew. Five allograft recipients were examined in each group. At transplantation, animals received 250 micrograms of CTLA4Ig or 250 micrograms of control Ig intraperitoneally daily until sacrifice. Animals were sacrificed on days 2, 4, and 7 after transplant. Control (BN-->Lew) grafts show irreversible rejection by day 7. Syngeneic (Lew-->Lew) grafts show no AR on day 7. AR episodes were graded histologically (stages 0-IV) and pathologic intensity of inflammation was graded on percentage of involvement. Cytokine transcript levels were measured in control and CTLA4Ig-treated animals (n = 5 in each group) on day 7 using reverse transcriptase polymerase chain reaction techniques. The most profound differences were found on day 7 after transplant. The degree of lymphocytic infiltration was greater in the CTLA4Ig group (perivascular: 4 +/- 0 vs. 2.6 +/- 0.6, peribronchial: 4 +/- 0 vs. 2.2 +/- 0.4, and peribronchiolar: 3.6 +/- 0.5 vs. 2 +/- 0.3, P < 0.01). However, in striking contrast, the stage of AR (3 +/- 0 vs. 4 +/- 0, P < 0.01), vasculitis (1 +/- 0.7 vs. 2.6 +/- 0.6, P < 0.05), hemorrhage (0.4 +/- 0.6 vs. 3.2 +/- 0.4, P < 0.01), and necrosis (0 +/- 0 vs. 2.4 +/- 0.5, P < 0.005) were significantly reduced in animals treated with CTLA4Ig. Since CTLA4Ig blocks Th1 cell activation in vitro, we compared the levels of Th1 inflammatory cytokines IL-2, gamma-IFN, and TNF-alpha in the two models. The intragraft ratios (CTLA4Ig/control) were IL-2:0.77, gamma-IFN: 1.29, and TNF-alpha:1.33. Thus, CTLA4Ig did not significantly block intragraft production of Th1 cytokines on day 7.(ABSTRACT TRUNCATED AT 400 WORDS)

Abatacept↗

Arrhythmias after cardioverter-defibrillator implantation: comparison of epicardial and transvenous systems.

Surgery for implantable cardioverter-defibrillators can cause postoperative exacerbation of ventricular and atrial arrhythmias. It is not known whether the techniques of electrode implantation (epicardial vs transvenous) influence the incidence of arrhythmia exacerbation. We reviewed the postoperative course of 229 consecutive patients who received either epicardial (n = 119) or transvenous (n = 110) implantations from 1984 to 1994. Exacerbation of ventricular tachycardia (VT) was defined as an increase in the number of sustained VTs during the postoperative versus the preoperative 2 weeks. Of the entire cohort, 18 patients (8%) developed exacerbation of VT after operation, which was more frequent in patients with epicardial than with transvenous implantations (12% vs 4%, p < 0.03, odds ratio 3.5, 95% confidence interval 1.0 to 13.2). New-onset atrial fibrillation occurred in 15% of patients with epicardial versus 1% of those with transvenous implantations (p = 0.00005, odds ratio 19.4, 95% confidence interval 2.7 to 86.7). These differences persisted after excluding patients with concurrent cardiac surgery. Preoperative occurrence of arrhythmias was the strongest independent predictor for postoperative occurrence (p < 0.01 for VT, p < 0.0001 for atrial fibrillation). Epicardial implantation (p = 0.03) and a history of myocardial infarction (p = 0.04) were independent predictors for postoperative VT exacerbation, whereas epicardial implantation (p < 0.05) and concurrent coronary bypass surgery (p = 0.0001) were independent predictors for postoperative new atrial fibrillation. Perioperative discontinuation of antiarrhythmic drugs did not influence postoperative VT exacerbation. Epicardial implantation was associated with longer length of hospital stay than transvenous implantation (p = 0.0005), independent of age, left ventricular ejection fraction, and concurrent cardiac surgery.

Aged↗

Wolff-Parkinson-White syndrome in a cardiac allograft.

A 61-year-old man underwent orthotopic heart transplantation for end-stage ischemic cardiomyopathy. The donor presented with Wolff-Parkinson-White syndrome and the allograft was successfully transplanted. The accessory pathway was interrupted postoperatively by radiofrequency current catheter ablation, and the patient is clinically well and free of preexcitation 24 months later.

Cardiomyopathies↗

Bronchiolitis obliterans in single-lung transplant recipients.

The presentation and clinical course of bronchiolitis obliterans (BO) in single-lung transplant (SLT) recipients has thus far not been well described. We retrospectively analyzed the serial spirometry of 15 SLT patients with BO. All the patients fulfilled the criteria for BO syndrome, and 11 of the 15 had histologically documented BO. Based on serial FEV1 analysis, we identified three patterns of presentation and progression of BO. The first pattern (n = 6) was characterized by a rapid onset and a relentless progressive course; the second pattern (n = 5) was characterized by a similar rapid onset and initial rapid decline, but was followed by stabilization in lung function; the third pattern (n = 4) was characterized by an insidious onset and course. In all patients, a permanent reduction in the mean forced expiratory flow during the middle half of the forced vital capacity appeared to be an early sensitive index for the development of BO. An appreciation of these different modes of presentation and progression of BO is potentially important in the assessment of prognosis and management of the SLT recipient.

Adult↗

Effects of voltage and respiration on impedance in nonthoracotomy defibrillation pathways.

The effects of applied voltage and phase of respiration on impedance of pathways used by implantable cardioverter-defibrillators were investigated. Patients were studied at implantation of cardioverter-defibrillators using epicardial (n = 12) or transvenous and subcutaneous (SQ) (n = 30) electrodes. Transvenous-SQ pathways were right ventricular cathode to SQ anode and coronary sinus cathode to SQ anode. Transvenous-transvenous pathways were right ventricle to coronary sinus and right ventricle to superior vena cava. Patients with nonthoracotomy electrode systems were studied at end-expiration and end-inspiration. Five shocks of 65 to 745 V (0.2 to 34 J) were given in random order in sinus rhythm. Over this range, end-expiratory impedance decreased monotonically for all pathways. This effect was greatest for transvenous-SQ pathways (13 +/- 3% to 17 +/- 4%, p < 0.001), intermediate for transvenous-transvenous pathways (5 +/- 4% to 8 +/- 5%, p < 0.001), and least for epicardial pathways (3 +/- 3%, p = 0.006). Paired data in inspiration and expiration showed that inspiration increased impedance in transvenous-SQ pathways (p < 0.001) but not in transvenous-transvenous pathways. Further, the effects of respiration and voltage on impedance in transvenous-SQ pathways were interactive (p < 0.001): Inspiration increased voltage-dependence of impedance. The magnitude of the inverse relationship between voltage and impedance depends on type of defibrillation pathway. The effect of respiration on impedance suggests that voltage-dependence of impedance is greatest in the lungs. These findings have potential relevance for intraoperative testing of cardioverter-defibrillators and selection of pathways for low-energy cardioversion.

Aged↗

Ten-year experience of cardiac surgery in patients aged 80 years and over.

Five hundred twenty-eight consecutive patients aged 80 years and over (mean age, 83.1 +/- 2.7 years) underwent cardiac operations with hypothermia (mean, 21.9 degrees +/- 2.2 degrees C), hyperkalemic cardioplegia, and cardiopulmonary bypass in a 10-year period. Fifty-six percent of the patients were male. Preoperatively, 68% of the patients were in New York Heart Association functional class IV, and 31% were in class III. Among them, 303 patients had isolated coronary artery bypass grafting (CABG) (group I), 132 had aortic valve replacement only or combined with CABG (group II), 42 had mitral valve replacement only or combined with CABG (group III), 31 had mitral valve repair and CABG (group IV), and 20 had double-valve procedure only or combined with CABG (group V). The 30-day or in-hospital mortality was 8.3% in group I, 4.5% in group II, 29% in group III, 23% in group IV, and 30% in group V. Total 30-day or in-hospital mortality was 10.6%. One-year and 5-year actuarial survival rates were as follows: group I, 82% and 62%; group II, 85% and 58%; group III, 61% and 37%; group IV, 56% and 19%; and group V, 63% and 15%. Total 1-year and 5-year actuarial survival were 79% and 54%. At follow-up (mean, 2 years), 70% of overall survivors reported that their general health had improved. Our experience demonstrates that for select patients aged 80 years and over with unmanageable cardiac symptoms, CABG and aortic valve replacement groups had better results in improving quality of life as compared with patients having mitral or combined procedures.

Actuarial Analysis↗

Underdetection of ventricular tachycardia by algorithms to enhance specificity in a tiered-therapy cardioverter-defibrillator.

OBJECTIVES: The goal of this study was to determine the incidence and clinical significance of underdetection in 125 patients treated with a tiered-therapy cardioverter-defibrillator, the Medtronic PCD. BACKGROUND: Underdetection, distinct from undersensing, is a unique, potential complication of new algorithms that enhance specificity in tiered-therapy cardioverter-defibrillators. These algorithms may delay or prevent recognition of ventricular tachycardia even though electrograms are sensed accurately and RR intervals meet the programmed interval criterion. METHODS: Underdetection was defined as delay in detection > 5 s at electrophysiologic study or symptomatic delay or detection failure at follow-up of 15 +/- 8 months. RESULTS: We identified six specific mechanisms of underdetection caused by algorithms to discriminate sustained ventricular tachycardia from sinus tachycardia, atrial fibrillation, ventricular fibrillation and nonsustained ventricular tachycardia. Underdetection caused detection delays in 13 (1.9%) of 677 induced ventricular tachyarrhythmia episodes in 12 patients (9.6%). During follow-up, underdetection occurred in 7 (9.9%) of 71 patients in whom ventricular tachycardia therapies were programmed. Failure to detect ventricular tachycardia occurred in 6 (0.6%) of 988 spontaneous ventricular tachycardia episodes in four patients (5.6%); 2 episodes required external cardioversion. After defibrillator reprogramming, underdetection did not occur. CONCLUSIONS: Algorithms to enhance specificity cause underdetection of ventricular tachycardia in a significant minority of patients with tiered-therapy cardioverter-defibrillators. Optimal programming can minimize underdetection.

Algorithms↗

Discrimination of ventricular tachycardia from sinus tachycardia and atrial fibrillation in a tiered-therapy cardioverter-defibrillator.

OBJECTIVES: This study was conducted to evaluate criteria for discrimination of ventricular tachycardia from atrial fibrillation and sinus tachycardia in a tiered-therapy cardioverter-defibrillator (Medtronic PCD). BACKGROUND: Interval stability algorithms discriminate ventricular tachycardia from atrial fibrillation. Onset algorithms discriminate ventricular tachycardia from sinus tachycardia. Neither has been validated clinically. METHODS: The stability criterion requires that a ventricular tachycardia interval not vary from any of the three previous intervals by more than the programmable stability value. The onset criterion detects initiation of ventricular tachycardia only if the ratio of an interval to the mean of four previous intervals is less than a programmed onset ratio and either the second or third preceding interval exceeds the ventricular tachycardia detection interval. We evaluated these criteria in 100 patients at electrophysiologic study and exercise testing (65 patients) and during a mean (+/- SD) follow-up of 16.2 +/- 7.9 months. The PCDs were programmed to tiered therapy in 54 patients. In the remaining 46 patients, the PCD's memory for detected ventricular tachycardia was used to study the specificity of the chosen onset criterion for rejecting sinus tachycardia. We used stored intervals preceding appropriate (n = 99) and inappropriate (n = 54) detections to test a new onset criterion that was less sensitive to a single index interval. RESULTS: Programmed stability of 40 ms decreased detection of induced atrial fibrillation by 95% (20 patients), paroxysmal atrial fibrillation by 95% (6 patients) and chronic atrial fibrillation by 99% (9 patients); all episodes of spontaneous (n = 877) and induced (n = 339) ventricular tachycardia were detected. A programmed onset ratio of 87% rejected sinus acceleration (98%) but caused underdetection of 0.5% of ventricular tachycardias. The onset criterion permitted inappropriate detection of premature ventricular complexes during sinus tachycardia, but the new criterion reduced these inappropriate detections by 98%. CONCLUSIONS: The PCD's onset and stability criteria reduced inappropriate detection of atrial fibrillation and sinus acceleration while detecting 99.5% of ventricular tachycardias.

Aged↗

Effect of capacitor size and pathway resistance on defibrillation threshold for implantable defibrillators.

BACKGROUND: The time constant of truncated exponential pulses used with implantable defibrillators is determined by the output capacitor size and defibrillation pathway resistance. The optimal capacitor size is unknown. METHODS AND RESULTS: This study compared defibrillation threshold (DFT) for standard 120-microF capacitors (DFT120) and smaller 60-microF capacitors (DFT60) at implantation of cardioverter-defibrillators in 67 patients using epicardial electrodes (15 patients) or one of four transvenous electrode configurations (52 patients). Paired comparisons of DFT60 and DFT120 were made for 44 defibrillation pathways using monophasic pulses and for 53 pathways using biphasic pulses. Truncated exponential pulses with 65% tilt were used. Pooled data from all electrode configurations showed a significant inverse correlation between pathway resistance and the ratio of stored energy DFT60 to DFT120 (monophasic pulses: r = .75, P = .0001; biphasic pulses: r = .68, P = .0001). Data from all electrode configurations formed a continuum with 120-microF capacitors superior for low-resistance pathways and 60-microF capacitors superior for high-resistance pathways. For pathways with resistance < or = 40 omega, the modest advantage of 120-microF capacitors applied primarily to pathways with low DFTs: 8.2 +/- 6.1 versus 9.6 +/- 5.4 J (P = .001) for monophasic pulses and 4.1 +/- 2.8 versus 5.1 +/- 3.1 J (P < .02) for biphasic pulses. The greater advantage of 60-microF capacitors for pathways with resistance > or = 61 omega applied to pathways with higher DFTs: 12.4 +/- 4.3 versus 23.1 +/- 6.4 J (P = .0001) for monophasic pulses and 8.5 +/- 4.9 versus 12.5 +/- 6.4 J (P = .0001) for biphasic pulses. For pathways using monophasic 120-microF pulses versus 95% for 60-microF pulses. Similarly, the DFT was < or = 10 J for 48% of pathways using biphasic 120-microF capacitors versus 83% for 60-microF pulses. CONCLUSIONS: In comparison with conventional 120-microF capacitors, 60-microF capacitors had clinically insignificant higher DFTs for low-resistance pathways and clinically important lower DFTs for high-resistance pathways. Optimal capacitance is inversely related to pathway resistance for clinical defibrillation pathways and waveforms.

Aged↗

Upper limit of vulnerability reliably predicts the defibrillation threshold in humans.

BACKGROUND: The upper limit of vulnerability is the stimulus strength above which electrical stimulation cannot induce ventricular fibrillation even when the stimulus occurs during the vulnerable period of the cardiac cycle. The purpose of this study was to test the hypothesis that the upper limit of vulnerability can accurately predict the defibrillation threshold in patients undergoing implantable cardioverter-defibrillator (ICD) implantation using nonthoracotomy lead systems. METHODS AND RESULTS: We studied 77 patients at the time of ICD implantation. Multiple endocardial-endocardial and endocardial-subcutaneous shock pathways were used. Two different protocols were used to test the upper limit of vulnerability. In protocol 1 (n = 17), the upper limit of vulnerability was tested with two shocks on the peak or the up-slope of the T wave of paced rhythm. The shocks were given randomly either at the peak and 20 milliseconds before the peak of T wave (n = 7) or at 20 and 40 milliseconds before the peak of T wave (n = 10). In protocol 2 (n = 60), the upper limit of vulnerability was tested with three shocks delivered at 0, 20, and 40 milliseconds before the peak of the T wave. The weakest shock that failed to induce ventricular fibrillation by a 5-J step-down or step-up method was defined as the upper limit of vulnerability. The defibrillation threshold was also determined by a 5-J step-down or step-up method. In protocol 1, the upper limit of vulnerability (9 +/- 6 J) was significantly lower than the defibrillation threshold (13 +/- 7 J) with a correlation coefficient of .87 and P < .001. In protocol 2, the upper limit of vulnerability (13 +/- 6 J) was not significantly different from the defibrillation threshold (13 +/- 6 J) with a correlation coefficient of .85 and P < .001. In 45 of the 60 patients, the upper limit of vulnerability was < or = 15 J; all had a defibrillation threshold of < or = 20 J. In 51 of the 60 patients, the upper limit of vulnerability was within 5 J of the defibrillation threshold. The upper limit of vulnerability overestimated the defibrillation threshold by > 10 J in 8 patients and underestimated the defibrillation threshold by > 10 J in only 1 patient. The overestimation and underestimation occurred only in patients with the upper limit of vulnerability > 15 J. CONCLUSIONS: When tested with three shocks on and before the peak of the T wave, the upper limit of vulnerability accurately predicted the defibrillation threshold in patients undergoing ICD implantation using nonthoracotomy lead systems. This method required either one or no episodes of ventricular fibrillation in most patients.

Aged↗