SURVEILLANCE CAN BE THE STANDARD OF CARE FOR STAGE I NONSEMINOMATOUS TESTICULAR TUMORS AND EVEN HIGH RISK PATIENTS

PURPOSE: We investigate the results of a surveillance program for stage I nonseminomatous germ cell tumors to validate a surveillance policy, and furthermore improve it by analyzing diagnostic instruments and identifying prognostic factors for relapse. MATERIALS AND METHODS: From 1982 to 1994, 90 patients with stage I nonseminomatous germ cell tumors entered a surveillance protocol after orchiectomy. Patients with relapse were treated with cisplatin based chemotherapy. A statistical analysis of possible prognostic factors for relapse was performed. RESULTS: Relapse occurred in 23 (26%) patients. Disease specific survival was 98.9%, and 1 patient died of tumor. Most relapses were located in retroperitoneal lymph nodes only (78%). Tumor markers were the most important indicators of relapse. However, in 22% of patients with relapse abdominal x-ray of lymphangiographic contrast showed the first sign of relapse. Computerized tomography located all but 1 relapse. Vascular invasion (p = 0.0001), tumor size (p = 0.0341) and presence of immature teratoma (p = 0.0154) were significantly predictive of relapse with the multivariate analysis, percentage embryonal carcinoma only by univariate analysis (p = 0.032). The relapse rate was highest (52%) when vascular invasion was present. CONCLUSIONS: With surveillance for stage I nonseminomatous germ cell tumors, excellent treatment results can be achieved that are comparable to primary retroperitoneal lymph node dissection. Tumor markers and computerized tomography are highly reliable for detecting relapse. Lymphangiography is still of staging value. Pathological factors may influence the choice of adjuvant treatment. However, relapse risks of 50% to 60% are maximally achieved with presently available prognostic factors, and so sparing morbidity of adjuvant treatment by a surveillance protocol remains a feasible option even in these patients.     

Clinical Profile of Commotio Cordis: An Under Appreciated Cause of Sudden Death in the Young During Sports and Other Activities

Blunt Chest Impact Leading to Cardiac Arrest. Not particularly well recognized are athletic Held catastrophes in which virtually instantaneous cardiac arrest is produced by nonpenetrating chest blows in the absence of heart disease or identifiable morphologic injury to the chest wall or heart (commotio cordis). To better characterize the clinical profile of this syndrome, we have assembled 70 cases, including 34 occurring during organized competitive athletics and 36 others that occurred during informal recreational sports at home, school or the playground, or during nonsporting activities. Ages were 2 to 38 (mean age: 12) with 70% < 16 years old. Most common sports involved were youth baseball (n = 40), softball (n = 7), and ice hockey (n = 7). Seven (10%) of the 70 commotio cordis victims, including six with documented ventricular fibrillation, have survived the consequences of their chest blow. Eleven of the events (16%) occurred despite the presence of chest padding believed to be potentially protective. Four victims experienced modest chest blows while in circumstances completely unrelated to sports activities; three of the four individuals who delivered these blows were ultimately convicted of criminal acts within the justice system. An experimental model of low-energy chest wall impact demonstrates that commotio cordis events are due largely to the exquisite timing of blows during a narrow window within the repolarization phase of the cardiac cycle, 15 to 30 msec prior to the peak of the T wave.     

True Incidence of Pacemaker Syndrome

HELDMAN, D., ET AL.: True Incidence of Pacemaker Syndrome. Although the purported incidence of pacemaker syndrome according to the literature is only 5%–15%, this is based on a series of patients with VVI pacing. Increasing numbers of studies are being reported in which patients prefer the dual chamber mode despite little benefit being demonstrated on objective testing, suggesting that pacemaker syndrome may be more common than is generally reported. This study was designed to evaluate the reported symptoms in a series of patients programmed to both the VVI and one or more dual chamber modes. Forty unselected patients with dual chamber pacemakers were entered into a blind, randomized trial comparing the symptoms associated with VVI pacing to those associated with dual chamber pacing. Patients were randomized to either WI or dual chamber pacing. At the end of 1 week, questionnaires rating 16 different symptoms were completed. Blood pressure, LV function, presence of ventriculoatrial conduction, and ability to override the pacemaker were evaluated. The pacemaker was then programmed to the other mode. Overall, 12 of 16 symptoms were significantly worse in the VVI as compared to dual chamber mode. The most highly significant (p < 0.005) were shortness of breath, dizziness, fatigue, pulsations in the neck or abdomen, cough, and apprehension. Pacemaker syndrome was clinically recognized in 83% of patients paced in the WI mode with 65% of patients experiencing moderate to severe symptoms. There were no readily identified clinical, hemodynamic, or electrophysiological parameters that predicted which patients would develop pacemaker syndrome. Thus, when patients have an opportunity to experience both pacing modes in close proximity to one another, there is a high incidence of pacemaker syndrome in the VVI mode.     

Analysis of the Effectiveness of In-Office and Transtelephonic Follow-Up in Terms of Pacemaker System Complications

A study was undertaken to determine the most effective method of pacemaker follow-up in terms of the total number of complications detected and yield per follow-up in single and dual chamber pacing systems. The analysis involved 9,786 patient records from 635 patients. The records were reviewed with respect to method of follow-up, number of chambers paced, and complications detected. Complications included: oversensing, undersensing, noncapture, pocket and diaphragmatic stimulation, pacemaker mediated tachycardia, crosstalk, pulse generator malfunction, lead malfunction, infection/erosion, premature end of service, exit block, and other miscellaneous problems. Eight thousand two hundred eighty-eight of the 9,786 follow-ups were performed in the office while 1,498 were transtelephonic. Single chamber pacing systems were implanted in 329 patients and 306 were dual chamber systems. A total of 599 complications were detected. Analysis yielded a per patient complication rate of 5.1 % (single chamber) and 8.4% (dual chamber) for in-office follow-up. This compared to a transtelephonic follow-up per patient complication rate of only 0.3% (single chamber) and 1.0% (dual chamber). In-office pacemaker follow-up is significantly more effective (P < 0.001) than transtelephonic follow-up in detecting both single and dual chamber pacemaker system complications.     

Long-term Survival of VDD Pacing

All patients with VDD systems implanted at a tertiary pacing center were identified from a computer database and data collected on pacing indications, follow-up duration, rate response, reasons for programming changes, and implant P wave amplitudes. Results: 366 implants were identified for which complete data were available for 335 leads implanted in 316 patients. The mean follow-up period was 24.1 months, and age at implant was 73.5 ± 11.8 years. During follow-up, 19 patients died (6%) and 62 (19.6%) were followed elsewhere. Indications for pacing were complete heart block, 56.6%; intermittent AV block, 21.8%; postablation complete heart block, 5.4%; 2:1 AV block, 13%; and others, 3.2%. Two groups: no mode change (NMC, n = 280) and mode change (MC, n = 36) were identified. Reasons for reprogramming in the MC group were as follows: atrial sensing, 11; AF/atrial flutter, 18; chronotropic incompetence, 3; and others 4. Significantly more MC patients had rate response programmed ON (44.4% vs 22.1%, P < 0.05). No significant differences between the two groups were found in other variables, including male gender (55.5% vs 54.6%), length of follow-up (27.1 ± 17.8 vs 23.8 ± 20.6 months), age at last follow-up (72 ± 12.3 vs 75.9 ± 11.9years), and P wave amplitude (1.7 ± 0.9 vs 1.8 ± 0.9mV). Conclusion: Reprogramming of VDD systems is infrequent. When necessary, it is usually prompted by atrial arrhythmias or failure of atrial sensing. When adequate atrial chronotropy has been verified, VDD is an acceptable alternative to DDD pacing and survives well over the long term.     

Cardiorespiratory response to spontaneous cortical arousals during stage 2 and rapid eye movement sleep in healthy children

Arousal from sleep is associated with transient and abrupt cardiorespiratory changes, and elevated arousals associated with sleep disorders may trigger adverse cardiovascular sequela. In this paper, we provide the first data in children on cardiorespiratory responses to cortical arousal. Heart rate and ventilatory responses to arousal from stage 2 and rapid eye movement (REM) sleep were investigated in 40 normal, healthy Caucasian children (age: 7.7 ± 2.6 years; body mass index z‐score: 0.30 ± 0.8). All children underwent overnight polysomnography studies. Cortical arousals were scored according to standard criteria. Heart rate changes were assessed over 30 s, starting 15 s prior to cortical arousal onset. Breathing rates were quantified three breaths before and after arousal onset. Arousals from stage 2 as well as REM sleep resulted in an R–R interval shortening of about 15%, independent of age and gender. The R–R interval shortening initiated at least 3 s before the cortical arousal onset. The breathing interval immediately after cortical arousal onset was significantly shortened (P < 0.001). In conclusion, cortical arousals in children are associated with an increase in breathing rate and significant heart rate accelerations, which typically precede the cortical arousal onset.     

Defensive hostility and anger expression: Relationship to additional heart rate reactivity during active coping

The main purpose of the present study was twofold: (a) to assess the relationship between defensive hostility (high hostility/high defensiveness) and additional heart rate reactivity during active coping and (b) to determine if the construct of anger-out might lend additional, sensitivity to the predictive power of the defensive hostility model. Forty individuals were randomly assigned to complete a mental arithmetic task with or without the threat of shock. Participants also completed the Cook-Medley Hostility Inventory (Ho), the Marlowe-Crowne Social Desirability Scale (MC), and the Spielberger Anger Expression Scale. Defensive hostile subjects (high Ho/high MC) were significantly more reactive than any other subgroup. In addition, the combination of low Ho/high anger-out scores yielded a subgroup significantly less reactive than any other subgroup. These findings clarify the complex relationship of hostility and cardiovascular reactivity.     

Systolic Arterial Pressure Recovery After Ventricular Fibrillation/Flutter in Humans

Although the elective induction of cardiac arrest for implantable defibrillator insertion under general anesthesia is widely used, the hemodynamics of recovery of arterial blood pressure after cardiac arrest is not well-defined. Accordingly, the time course of recovery of systolic arterial pressure was studied in seven patients during the repetitive induction of ventricular fibrillation (n = 6) or ventricular flutter (n = 1). The mean number of episodes of cardiac arrest was 7 ± 2, and the mean drop in systolic pressure was 84 ± 16mmHg. The mean recovery time for systolic pressure was 10 ± 6 seconds, the average systolic pressure recovery rate was 13 ± 14 mmHg/sec, and the mean percent systolic pressure recovery was 94%± 9%. A negative logarithmic relation was found to exist between the rate of systolic arterial pressure recovery and the duration of ventricular fibrillation or flutter with a correlation coefficient of 0.68 to 0.97 (P < 0.05) in five of the seven patients. A linear relation between the time for systolic pressure recovery and duration of asystole was also defined. These results are consistent with the view that prolongation of ventricular fibrillation or flutter increases the duration of arterial pressure recovery through a negative effect on left ventricular contractility. Increased understanding of these relations may lead to increased safety of implantable defibrillator insertion.     

Atopic asthma: T lymphocyte subpopulations

Atopy is associated with diminished cell-mediated immunity and increased amounts of IgE, both of which may be caused by imbalances of T lymphocyte subsets. We compared the composition of highly purified peripheral-blood T cells of fifteen atopic asthmatics with ten non-atopic control subjects. Each subject was examined on five separate occasions. Indirect immunofluorescence using monoclonal antibodies was used to define T cell subsets. We examined the proportion of T cells with T3 (most T cells), T4 (helper/inducer), T8 (suppressor/cytotoxic), M1 (natural killer), and Ia (activated T cells) surface antigens. Blood was obtained at the same time of day to eliminate the effects of circadian rhythm. Subjects were taking no medications. We found no difference between the groups of the percentage of T cells with T4, T8, M1, and Ia antigens, nor the ratio of T4+ (helper) to T8+ (suppressor) cells. T3 percent was slightly (94.3 vs 92.5%) higher in the atopic group. We conclude that atopic asthma is not associated with imbalances of peripheral-blood T cell subsets.