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Biomedical subjects

C Hwang

Publications and source records attributed to C Hwang.

At least 55 records · Page 3Linked to original sources
PubMed1996

Reentrant wave fronts in Wiggers' stage II ventricular fibrillation. Characteristics and mechanisms of termination and spontaneous regeneration.

The mechanisms of Wiggers' stage II ventricular fibrillation (VF) are poorly understood. Using computerized mapping techniques, we studied the patterns of activation during Wiggers' stage II VF in 13 open-chest dogs. In 7 of the 13 dogs, the right ventricular Purkinje fibers and adjacent subendocardial myocytes were ablated with Lugol solution. VF was induced electrically, and 3 to 5 seconds of data were obtained beginning approximately 2.5 seconds after the onset of VF. Dynamic displays of the activation patterns and isochronal maps revealed the presence of reentrant wave fronts in 17 of 33 runs of VF in ablated ventricles and in 12 of 45 runs of VF in intact ventricles. The incidence of reentry was not different between the subendocardium-ablated group versus the nonablated group (1.7 +/- 1.6 versus 1.2 +/- 1.6 rotations per episode of VF, P = .19). There were no differences in the core size (25 +/- 19 versus 29 +/- 18 mm2), life span (3.4 +/- 1.1 versus 3.2 +/- 1.2 rotations), or cycle length (111 +/- 12 versus 107 +/- 8 ms) in ablated ventricles versus intact ventricles, respectively. The core was unstable as it meandered within the mapped area displacing the entire reentrant wave front. In all episodes, the reentrant wave fronts were spontaneously initiated by an interaction between two propagating wave fronts roughly perpendicular to each other. The second wave front met the tail of the first wave front 69 +/- 11 ms (range, 40 to 90 ms) after its latest activation, indicating that the interaction occurred during a vulnerable period. The reentrant wave fronts terminated spontaneously (n = 7), as the result of interference by an invading wave front (n = 19 or meandered off the mapped region (n = 3). We conclude the following: (1) Reentrant activities with short life spans and meandering cores are present during Wiggers' stage II VF in dogs. (2) New reentrant wave fronts are generated when one wave front interacts with another wave front during its vulnerable period. (3) The reentrant wave fronts terminate spontaneously or as the result of interference. (4) Chemical subendocardial ablation does not affect the incidence, life span, cycle length, or core size of the reentrant wave fronts.

Animals↗
PubMed1995

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↗
PubMed1995

Life-threatening alterations in heart rate after the use of adenosine in atrial flutter.

Adenosine has become the preferred treatment for common types of supraventricular tachycardia because it is extremely effective and rarely associated with with serious side effects. It has also been advocated as an intervention for diagnostic use to assess uncommon types of tachycardia. Evidence is shown in this report that adenosine was associated with dangerous worsening of arrhythmia in patients with atrial flutter. In two patients, adenosine precipitated acceleration of ventricular response, in one case necessitating emergent cardioversion. Both patients had atrial flutter with 2 to 1 atrioventricular block that evolved into 1 to 1 atrioventricular conduction. In three other patients, adenosine was associated with prolonged bradyasystole and hypotension. In each of the five patients, adenosine was given in a standard fashion (6 or 12 mg). In summary, adenosine should be recognized as a potentially dangerous intervention in patients with atrial flutter. If it is used for diagnostic purposes, resuscitative equipment should be readily available.

Adenosine↗
PubMed1995

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↗
PubMed1995

hilA is a novel ompR/toxR family member that activates the expression of Salmonella typhimurium invasion genes.

During infection of its hosts, Salmonella enters intestinal epithelial cells. Many Salmonella typhimurium genes required for bacterial entry into host cells are encoded on a 40 kb 'pathogenicity island'. We report here the identification of hilA, a gene within the 'island' that appears to encode an activator of invasion gene expression. By using a set of lacZY transcriptional fusions to S. typhimurium invasion genes, we found that hilA activates the expression of invasion genes located on the 'pathogenicity island'. hilA is required for efficient entry into HEp-2 cells in vitro. The predicted amino acid sequence of hilA shares significant homology with the DNA-binding domains of the OmpR-ToxR family of transcriptional activators. However, unlike OmpR and ToxR, HilA contains neither a phosphoryl acceptor nor a membrane-spanning domain, and, therefore, its activity may be modulated by a novel mechanism. Many environmental conditions modulate the ability of Salmonella to enter non-phagocytic mammalian cells. It has been proposed that induction of Salmonella invasion proteins in response to a combination of environmental cues ensures that bacterial entry is limited to specific sites and times during infection. Our results are consistent with the hypothesis that hilA plays a key role in the regulation of Salmonella invasion during infection.

Amino Acid Sequence↗
PubMed1995

Interaction between strong electrical stimulation and reentrant wavefronts in canine ventricular fibrillation.

This study was designed to test the hypothesis that the effects of a strong electrical stimulus on reentrant wavefronts in ventricular fibrillation (VF) are dependent on the timing of the stimulus. We studied six open-chest dogs by computerized mapping techniques. A plaque electrode array with up to 509 bipolar electrodes was placed on the right ventricular epicardium. The interelectrode distance was 1.6 mm, and the interpolar distance was 0.5 mm. After eight baseline pacing stimuli (S1) with cycle lengths of 300 ms, a strong premature stimulus (S2) (73 +/- 10 mA) was given to induce VF. In subsequent episodes, a second strong premature stimulus (S3) was given at progressively longer S2-S3 intervals in 20-ms increments. The results showed that, at baseline, the S2 consistently induced figure-eight reentry and VF. The VF cycle length immediately after the S2 averaged 108 +/- 17 ms. The S3 resulted in one of the following responses: (1) termination of reentry and VF; (2) induction of different reentrant wavefronts or a focal pattern of repetitive activation; or (3) persistence of the same figure-eight reentry. The intervals between the S3 and the immediately preceding activation at the site of the S3 (the recovery intervals) were 39 +/- 12 ms (range, 20 to 60 ms) and 61 +/- 20 ms (range, 30 to 90 ms) for response patterns 1 and 2, respectively. The recovery intervals associated with response pattern 3 were either < or = 30 ms (22 +/- 8 ms) or > or = 80 ms (94 +/- 15 ms). The differences among these four intervals were significant (P < .001). We conclude that the effects of strong electrical stimulation on the reentrant wavefronts in VF are dependent on the recovery interval since the previous local activation. A protective zone occurred between 20 and 60 ms, during which time a strong electrical stimulus could terminate reentry and abort VF. This zone was followed by a vulnerable period during which new activation wavefronts could be induced. If a strong electrical stimulus was given shortly after or sufficiently long after the previous local activation, the same figure-eight reentrant pattern continued.

Animals↗
PubMed1994

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↗
PubMed1994

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↗
PubMed1994

Controlled evaluation of copper-silver ionization in eradicating Legionella pneumophila from a hospital water distribution system.

A controlled evaluation was made of the efficacy of copper-silver ionization in eradicating Legionella pneumophila from a hospital water supply. Copper-silver ionization units were installed on the hot water recirculation line of one building with water fixtures positive for Legionella species. Another building with the same water supply served as a control. Legionella species persisted within the system when copper and silver concentrations were < 0.3 and < 0.03 ppm, respectively. When copper and silver concentrations were > 0.4 and > 0.04 ppm, respectively, there was a significant decrease in Legionella species colonization, but the percentage of water fixtures positive for organisms was unchanged in the control building. When the ionization unit was inactivated, water fixtures continued to be free of Legionella species for 2 additional months. Copper-silver ionization can eradicate L. pneumophila in a water distribution system. The advantages of copper-silver ionization include relatively low cost, straightforward installation, easy maintenance, nontoxic by-products and the presence of a disinfecting residual.

Copper↗
PubMed1994

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↗
PubMed1994

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↗
PubMed1993

Mechanism of release of soluble forms of tumor necrosis factor/lymphotoxin receptors by phorbol myristate acetate-stimulated human THP-1 cells in vitro.

The mechanism involved in the release of the soluble forms of 55 and 75 kDa TNF and lymphotoxin (LT) membrane receptors was studied in a continuous human monocytic cell line, THP-1, in vitro. THP-1 cells were found to spontaneously release soluble forms of both 55 and 75 kDa TNF/LT receptors. Release was up-regulated by PMA, and optimal release was achieved at 10(-8) M PMA. Serine protease inhibitors such as PMSF,3,4 dichloroisocoumarin, N alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK), and N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) were found to inhibit the production of both soluble TNF/LT receptors. PMSF (2 mM) also blocked receptors shedding from paraformaldehyde-fixed THP-1 cells coincubated with conditioned media from PMA-stimulated THP-1 cells. Colchicine at 1 and 10 microM stimulated the production of both soluble TNF/LT receptors, but the PMA-induced release of both soluble TNF/LT receptors was inhibited. It appears that the PMA-induced release of soluble TNF/LT receptors involves serine proteases in the extracellular space where the soluble parts of the TNF/LT receptors are cleaved directly off the cell membrane.

Cell Line↗
PubMed1993

Measurement of the soluble membrane receptors for tumor necrosis factor and lymphotoxin in the sera of patients with gynecologic malignancy.

The shed portion of the 55 and 75 kDa membrane receptors for tumor necrosis factor (TNF) and lymphotoxin (LT) have been described in the serum of patients with cancer. This study was designed to determine whether serum levels of the 55 and 75 kDa soluble TNF/LT receptors (sTNFr) had clinical significance in patients with gynecologic malignancies. Serum samples from 79 patients with ovarian, endometrial, or cervical cancer were assayed for CA 125 levels by RIA and the 55 and 75 kDa sTNFr levels by ELISA. Receptor and CA 125 levels were also analyzed with respect to disease status and response to treatment in banked serum samples from 14 patients with epithelial ovarian cancer who had been followed clinically for 1-3 years. Patients resulted were compared to serum samples tested from normal donors. We found that serum levels of both sTNFr's were elevated in the 79 patients with various gynecologic malignancies [55 kDa of 3.07 +/- 3.79 ng/ml (P < 0.02) and 75 kDa of 2.93 +/- 1.27 ng/ml (P < 0.001)] compared to 16 normal controls (55 kDa of 0.65 +/- 0.22 ng/ml and 75 kDa of 1.62 +/- 0.37 ng/ml). Serum levels of 55 and 75 kDa TNF/LT receptors were a more sensitive indicator of active cancer and had greater predictive value for detecting tumor in patients with ovarian cancer than CA 125. The sTNFr's were also more sensitive than CA 125 in detecting persistent or recurrent tumor and measuring response to therapy. These preliminary results suggest that measurement of serum levels of 55 and 75 kDa sTNFr's, even though not tumor specific, may be a uniquely new method for identifying and monitoring patients with gynecologic malignancy.

Adult↗