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Inadequate anticoagulation in patients with mechanical prosthetic heart valves can result in a significant incidence of thromboembolic complications. An even more life-threatening complication is massive thrombosis of the valve itself. Thrombolytic therapy was given to a moribund 22-year-old woman with intractable heart failure caused by a thrombosed St. Jude prosthetic mitral valve (St. Jude Medical, Inc., St. Paul, Minn.). Although this form of therapy has been used before, this is the first report of a case in which transesophageal echocardiography was performed during thrombolytic therapy to continually record successful thrombolysis of the clotted prosthetic valve. Serial imaging during thrombolysis displayed progressive dissolution of the thrombus and progressive improvement in valve function. Transesophageal echocardiography is helpful in the diagnosis of prosthetic valve thrombosis and has the ability to monitor continually the effect of treatment with thrombolysis. Although thrombolytic therapy with recombinant tissue plasminogen activator is effective in treating prosthetic valve thrombosis, it carries a high risk for serious thromboembolic complications and thus should be reserved for critically ill patients who are too sick to undergo immediate surgery.

Pulmonic valve endocarditis is a rare clinical entity. In spite of an increase in the frequency of right-sided endocarditis, primarily it is the tricuspid valve that is involved. Two-dimensional transthoracic echocardiography has improved our ability to diagnose infective endocarditis but has not identified many cases of pulmonic valve endocarditis. With the use of transesophageal echocardiography, three recent cases of pulmonic valve endocarditis were diagnosed by our laboratory. Each of these patients had clinical evidence of right-sided endocarditis, yet routine transthoracic echocardiograms failed to identify any pulmonic valve abnormalities. The true incidence of pulmonic valve endocarditis may be higher than previously reported, and the transesophageal echocardiogram is the preferred method for identifying and evaluating pulmonic valve endocarditis in adults.

Dramatic improvements in our ability to treat coronary artery disease have created the need to develop sensitive and specific noninvasive tests for diagnosing and assessing the severity of ischemic disease. The purpose of this review is to examine stress echocardiography and, in particular, quantitative stress echocardiography in this context. Methodology and technical aspects of performing and interpreting stress echocardiography are discussed, including the type of exercise performed, imaging and recording techniques, and methods for on-line and off-line analysis. Qualitative, semiquantitative, and quantitative approaches are compared and contrasted. In assessing quantitative stress echocardiography, the role of global measurements of left ventricular function including ejection fraction, peak systolic pressure to end-systolic volume index ratio, as well as regional measurements including wall-motion analysis and wall stress, are discussed. Pertinent literature using quantitative approaches is reviewed including those comparing quantitative stress echocardiography with other noninvasive modalities. Future directions for study are also addressed. We concluded that quantitative stress echocardiography has excellent sensitivity and specificity for diagnosing ischemic heart disease. It was useful in localizing lesions, defining multivessel disease, and predicting patients with poor prognosis postmyocardial infarction. Its reproducibility makes it a valuable technique in following patients noninvasively over time.

Mechanisms underlying bilirubin encephalopathy and hearing loss remain poorly understood, including the way bilirubin enters the nervous system and how bilirubin accumulates in circumscribed regions of the brain. The present experiments examined the auditory brainstem in heterozygous (Nj) and homozygous (jj) Gunn rats at an age when serum bilirubin levels were highest, and after brain bilirubin concentration was artificially raised by sulfadimethoxine administration. In four litters of 11-12 days old Gunn rats, Nj and jj littermates received a single intraperitoneal injection of sulfadimethoxine (100 mg/kg) or a comparable volume of saline. At 16-17 days of age, brainstem auditory evoked potentials were recorded to assess the severity of bilirubin toxicity in the Nj and jj animals. Following the recordings, each animal was perfusion-fixed and frozen sections of the brainstem were cut in the transverse plane from medullary through mesencephalic levels. Sections were mounted on slides, stained with thionin and coded to avoid observer bias. Quantitative analysis revealed no differences between saline and sulfa-treated Nj rats for cochlear nucleus volume, or for cell size in the cochlear nucleus or superior olive. In the sulfa-treated jj rats, cochlear nucleus volume, and cross-sectional areas of spherical cells in the anteroventral cochlear nucleus and principal cells in the nucleus of the trapezoid body, were all significantly smaller than in the combined groups of Nj animals. The affected areas in the cochlear nucleus and superior olive are innervated by large axosomatic end-bulbs of Held or calyceal endings, and were associated with bilirubin staining of glia in the most severely jaundiced jj sulfa-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The relationship of brainstem structure and function in bilirubin encephalopathy is incompletely understood. The present experiments compare quantitative measures of brainstem structures with brainstem auditory evoked potentials (BAEPs) in infant jaundiced (jj) and nonjaundiced (Nj) Gunn rats. Ten jj's from 4 litters were injected with sulfadimethoxine at 11-12 days of age to raise their brain bilirubin concentration. Littermate controls were jj's given saline, and Nj's given sulfadimethoxine or saline. At 15-17 days of age BAEPs were recorded, and rats were prepared for histological examination, as was reported in the previous paper (Conlee and Shapiro, 1991). Significant differences between groups were seen for BAEP wave I latency (P = 0.002). I-II interwave interval (P = 0.001), and amplitudes of waves I, II, III, and IV (each P less than 0.0005) due to increased latencies and decreased amplitudes in the jj-sulfa group. Animals with the most severe BAEP abnormalities had the most severe histological abnormalities. Cochlear nucleus volume had a positive linear correlation with the amplitude of BAEP waves I, II, and IV, and an inverse correlation with wave I latency and I-II interwave interval (P less than or equal to 0.001). The highest correlations were BAEP I-II interwave interval and amplitude of waves I and II with cochlear nucleus volume (r = -0.78, 0.71 and 0.70, respectively, P less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

Bilirubin toxicity causes encephalopathy associated with lesions of the central auditory nervous system. Abnormal brainstem auditory evoked potentials (BAEPs) in jaundiced Gunn rats made acutely bilirubin toxic suggest abnormal input into the superior olivary complex, which might result in abnormal binaural interaction. Binaural difference waves (BDWs), obtained by subtracting the sum of two monaural BAEPs from a binaural BAEP, were obtained in 16- to 20-day-old jaundiced Gunn rats before and after injection of sulfadimethoxine, which produces bilirubin neurotoxicity by promoting net transfer of bilirubin out of the circulation into brain tissue. Reliable BDWs were recorded with onset 4.5 ms after the stimulus, followed by a large, often bimodal, positive peak occurring at about 6 ms. Following injection of sulfadimethoxine to produce bilirubin neurotoxicity, there was loss of BDW amplitude (21% +/- 14% of baseline, P less than 0.0001) and increase in latency (0.62 +/- 0.42 ms, P = 0.03) in bilirubin-toxic jaundiced rats compared to baseline, but no significant changes in nonjaundiced controls treated similarly. This documents abnormal BDWs in acute bilirubin encephalopathy suggesting that abnormalities of functions dependent on binaural processing of auditory information may be found as neurologic sequelae to bilirubin toxicity. BAEP BDWs may be a sensitive method for detecting neurophysiological abnormalities due to bilirubin toxicity.

With the advent of small inexpensive peak flowmeters, the at-home monitoring of peak flow rates has become an invaluable aid in the treatment of asthmatic patients. In this study, we evaluated the performance of the MiniWright and Assess peak flowmeters for accuracy and reproducibility. Measurements were made at varying peak flow rates and compared with those obtained simultaneously by a calibrated pneumotachograph. When this segment of the study was completed, the peak flow devices were subjected to 200 uses and were then retested. Four MiniWright peak flowmeters that had been extensively used in our clinic were tested as well. The Assess peak flowmeter was more accurate than the MiniWright at low flow rates (less than 300 L/min), while the MiniWright meter was more accurate at high flow rates (greater than 400 L/min). We also found that the accuracy of the MiniWright meter deteriorated after 200 uses and worsened further after extensive use, while the Assess meter retained its accuracy after 200 uses.

We describe a case of air embolism complicating neodymium-YAG laser resection of an endobronchial carcinoid tumor. A 27-year-old man experienced an acute neurologic syndrome during laser photoresection which responded to acute hyperbaric therapy.

Bilirubin toxicity is a significant clinical problem causing neurologic and audiologic sequelae. To better understand the pathogenesis of bilirubin toxicity in the immature nervous system we studied the development of brainstem auditory evoked potentials (BAEPs) in jaundiced (jj) Gunn rats and their non-jaundiced (Jj) littermates. Littermate pairs of Jj and jj rats were studied serially from early infancy to adulthood. Replicated BAEPs to click stimuli at two different intensities (45 and 75 dB SPL) and rates (33 and 89/s) were obtained from animals anesthetized with ketamine and acepromazine and maintained at a constant rectal temperature. Jaundiced (jj) rats had increased latencies of waves II and III and the I-II and I-III intervals, and decreased amplitudes of waves II and III from 17 days of age through adulthood. For both groups, all latencies and interwave intervals decreased with age (P less than 0.0001 for each wave and interwave interval by repeated measures ANOVA), and the amplitude of II increased with age (P less than 0.0001). No group differences were found in wave I latency or amplitude, or in the latency change of waves I, II or III as a function of intensity (about 11 microseconds/dB at all ages), suggesting that peripheral auditory function is normal in jj rats. Finally, there were no different effects of stimulation rate on BAEP wave latencies between groups. The findings suggest dysfunction of the central (brainstem) auditory pathways at and rostral to the cochlear nuclei, and are consistent with studies showing destruction of the cochlear nuclei in this animal model and in humans with bilirubin toxicity. The central abnormalities previously found in adult, jaundiced rats are now demonstrated in animals as early as 17 days of age, when serum bilirubin concentration is maximum. The BAEP findings are similar to changes found in hyperbilirubinemic human neonates, and support the use of the Gunn rat animal model for the study of bilirubin encephalopathy.

To determine the effect of beta-adrenergic blockade on the submaximal stress test after acute myocardial infarction (AMI), 36 post-AMI patients performed their treadmill test on 2 separate days, with and without metoprolol, in a double-blind, placebo-controlled, crossover design study. Rest and peak submaximal exercise heart rate was diminished by 100 mg of metoprolol administered twice daily (from 84 +/- 3 to 68 +/- 2 beats/min, p less than 0.001, and from 126 +/- 3 to 97 +/- 2 beats/min, p less than 0.001, respectively) compared with placebo. Rest and peak submaximal systolic blood pressure was also decreased (from 121 +/- 3 to 108 +/- 2 mm Hg, p less than 0.001, and from 151 +/- 4 to 124 +/- 3 mm Hg, p less than 0.001). Exercise-induced ST-segment depression of 1 mm or more from baseline occurred in 12 patients taking placebo. However, only 4 of these patients had ST depression when they exercised while taking metoprolol (p less than 0.05). Angina pectoris occurred in 4 patients taking placebo but in only 1 of these taking a beta-blocking drug. It is concluded that beta-blocking therapy renders the post-AMI submaximal stress test less sensitive for markers of exercise-induced ischemia than if the test is performed without the drug. Therefore, when using the prognostic information of published studies, it is important to define the conditions surrounding the exercise test.

Bilirubin toxicity produces significant neurologic and audiologic sequelae. Successful therapeutic intervention requires an understanding of the timing of neural dysfunction after exposure to bilirubin. BAEP were used in an animal model of bilirubin encephalopathy to study the onset of neural dysfunction after acute injection of a sulfonamide used to displace bilirubin out of the bloodstream and into tissue. Fourteen pairs of jaundiced Gunn rats from eight litters were studied at postnatal day 18. Baseline BAEP recordings were performed in anesthetized animals; then either sulfadimethoxine or an equal volume of saline was injected into the peritoneum. Another BAEP was done immediately, and then 2, 4, and 8 h after injection. Human serum albumin was injected into an additional 10 animals after the 2-h BAEP recording to see if induced BAEP abnormalities could be corrected. The sulfonamide-treated jj rats developed increased latencies for waves II and III, and I-II and I-III interwave intervals (p less than 0.0001). The latencies were prolonged by 2 h after injection and became progressively longer at 4 and 8 h. The amplitudes of waves II and III progressively decreased at 2, 4, and 8 h (p less than 0.0001). Latency and amplitude of waves I and IV did not change. The rats injected with albumin at 2 h showed improvement of BAEP abnormalities at 8 h. These studies show that neurophysiologic abnormalities occur as early as 2 h after intraperitoneal injection of sulfadimethoxine, and are reversible with appropriate therapy. These abnormalities are hypothesized to be due to the sulfonamide driven net transfer of free, toxic bilirubin into the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Bilateral hearing loss occurred in 9.7% of infants who survived despite very low birth weight (less than or equal to 1500 gm), 16.7% of infants who survived neonatal seizures, and 28.6% of infants who survived both low birth weight and neonatal seizures. All neonates received treatment in a single neonatal intensive care unit between 1976 and 1980. Twenty-two of 36 hearing-impaired children were normal physically and mentally, with IQ scores of greater than or equal to 85. Significant neonatal predictors of hearing loss in high-risk premature infants (less than or equal to 36 weeks gestation), as determined by multivariable testing, were prolonged respirator care, high serum bilirubin concentration, and hyponatremia. Exchange transfusions were associated with a decreased risk of hearing loss.

Bilirubin encephalopathy causes potentially preventable brain damage and hearing loss. The site of auditory dysfunction is controversial, despite pathologic studies showing damage to brain stem auditory nuclei in humans and experimental animals. We studied the effects of bilirubin toxicity on the auditory system of homozygous jaundiced Gunn rats by use of brain stem auditory evoked potentials. Small but statistically significant abnormalities were found for wave latencies, interwave intervals, and amplitudes.

A digital computing technique was used to extract continuous calculations of average alveolar pressure and airway resistance from body plethysmographic measurements during forced inspiratory and expiratory vital capacity maneuvers and tidal breathing in human subjects. Derived alveolar pressures were similar to those obtained using an interrupter technique (linear regression slope, 0.99 +/- 0.02; r = 0.98) and by comparison with esophageal pressure measurements. Studies in normal subjects revealed a characteristic pattern of increasing airway resistance throughout the expiratory phases of maximal and submaximal respiratory maneuvers, with maximal resistance of 33 to 110 cm H2O/L/s at low lung volumes during forced vital capacities. In contrast, inspiratory resistance remained low and constant throughout maximal and submaximal inspiratory maneuvers. Patients with COPD showed substantially higher inspiratory and expiratory resistances. In three patients with flow-volume loops suggestive of variable extrathoracic upper airway obstruction, measurements of alveolar pressure and airway resistance made it clear that two of the patients had upper airway obstruction, whereas the other was exerting an inadequate effort. We conclude that this noninvasive technique provides valid estimates of alveolar pressure and airway resistance continuously throughout both phases of the respiratory cycle over a wide range of volumes and flow rates. It may prove to be useful in the assessment of effort and airway obstruction in patients with a variety of pulmonary conditions.

Brain-stem auditory evoked potentials (BAEPs) are relatively resistant to alteration by barbiturate drugs, but the effects of the high doses that are used clinically to produce deep barbiturate coma for the treatment of intracranial hypertension and postischemic anoxic encephalopathy on BAEPs are unknown. We gave high-dose pentobarbital infusions to mechanically ventilated rats while recording serial BAEPs from the scalp. Pentobarbital progressively suppressed and then abolished all peaks. First the later waves, then all but the first wave, and finally all waves were abolished at intravenous doses of 120, 220, and 260 mg/kg, respectively, in addition to the initial anesthetic dose of 60 mg/kg i.p. The changes were at least partially reversible; peaks returned in reverse order of their disappearance. Peak latencies increased with dose. The results show a significant effect of pentobarbital on BAEPs in the rat, suggesting that BAEPs may be useful in assessing the depth of and recovery from barbiturate coma.