One year psychosocial outcome in head injury.

Psychosocial outcome at one year post-injury was examined prospectively in 466 hospitalized head-injured subjects, 124 trauma controls, and 88 friend controls. The results indicate that head injury is associated with persistent psychosocial limitations. However, the presence and extent of limitations are related to the demographics of the population injured, to other system injuries sustained in the same accident, and particularly to the severity of the head injury. More severe head injuries are associated with limitations implying greater dependence on others including poorer Glasgow Outcome Scale (GOS) ratings, dependent living, unemployment, low income, and reliance on family and social subsidy systems. Head injury severity is more closely related to more objective indices of psychosocial outcome (e.g., employment) than to self-perceived psychosocial limitations, such as measured by the Sickness Impact Profile (SIP).

Neuropsychological outcome in relation to head injury severity. Contributions of coma length and focal abnormalities.

Neuropsychological test performances of 102 consecutive head-injured patients were evaluated at 1 mo and 1 yr after injury. The results of the study indicated that both coma length and the presence of focal abnormalities on computed tomography (CT) scans contribute independently to neuropsychological outcome. The effects of coma length are stronger than the effects of focal abnormalities evident on CT scans and continue to exert a stronger influence on neuropsychological outcome over the year postinjury. These results suggest that the extent of diffuse pathology may be a more important determinant of long-term behavioral outcome than the presence of focal lesions.

Serial follow-up of adults with repaired tetralogy of Fallot.

OBJECTIVES AND BACKGROUND: Sudden death has long been considered a major contributor to mortality in pediatric patients with corrected tetralogy of Fallot. However, this may not apply to the patient with repaired tetralogy of Fallot who has survived into adulthood. Consequently we followed up a cohort of such adults to establish the clinical outcome and risk factors affecting their survival. METHODS: A baseline group of 151 adult patients with repaired tetralogy of Fallot were followed up for a mean of 3.2 years. The overall mortality rate was low (0.009 death/patient-year). Four patients died during follow-up, but only two deaths can be attributed to tetralogy of Fallot repair, and there were no sudden cardiac deaths. Clinically 94% of patients have remained in New York Heart Association functional class I. A subset of 36 patients were followed up for a mean of 6.7 years. This group had three sets of serial testing at 3-year intervals consisting of right heart catheterization at the initial study only, 24-h Holter ambulatory electrocardiographic (ECG) monitoring, exercise ECG and rest and exercise radionuclide angiography. RESULTS: Exercise capacity assessed by serial exercise stress testing remained stable over the follow-up period, whereas the presence of exercise-induced arrhythmias steadily decreased. Most patients had no significant arrhythmias and had no significant change in severity of arrhythmia with time. Radionuclide angiography showed significant improvement in exercise right ventricular ejection fraction over time but a progressive decrease in left ventricular ejection fraction at both rest and exercise. However, the left ventricular ejection fraction is still within the normal limits for our laboratory. CONCLUSIONS: Adults with repaired tetralogy of Fallot have a very good prognosis and a low risk of sudden death. However, ventricular function may change over time and should be carefully monitored.

Cardiac output response to continuous positive airway pressure in congestive heart failure.

The effects of nasal continuous positive airway pressure (CPAP) were examined during cardiac catheterization in 22 patients with congestive heart failure (CHF). CPAP was applied at a level of 5 cm H2O pressure. Hemodynamic measurements were made at baseline and while on CPAP. We hypothesized that patients with high left ventricular (LV) diastolic pressures would experience an increase in cardiac index (CI). To test this hypothesis, patients were divided into two groups based on their baseline pulmonary capillary wedge pressure (PCWP): one group of 11 whose PCWP was greater than or equal to 12 mm Hg (high-PCWP group) and a second group of 11 whose PCWP was less than 12 mm Hg (low-PCWP group). Among the high-PCWP group (mean PCWP +/- SEM = 19.0 +/- 2.7 mm Hg), CI rose significantly while on CPAP (from 2.48 +/- 0.26 to 2.82 +/- 0.26 L/min/m2, p less than 0.01). Stroke volume index (SVI) also rose significantly (from 52.6 +/- 7.0 to 64.1 +/- 8.0 ml/m2, p less than 0.001). In contrast, among the low-PCWP group (PCWP = 8.3 +/- 0.6 mm Hg), CI decreased significantly while on CPAP (from 3.14 +/- 0.44 to 2.89 +/- 0.62 ml/m2, p less than 0.025). SVI fell but not significantly while on CPAP (from 75.5 +/- 8.4 to 74.2 +/- 8.5 ml/m2). Multiple stepwise linear regression analysis revealed that the only significant correlate of the magnitude of change in CI in response to CPAP was baseline PCWP (r = 0.50, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of intracoronary nifedipine on coronary bloodflow and myocardial metabolism during pacing-induced ischemia.

The effects of intracoronary nifedipine on coronary bloodflow, its regional distribution, myocardial oxygen consumption and lactate metabolism during pacing-induced angina were evaluated in 15 subjects. These responses were directly compared to 10 subjects who received an alcohol-based control solvent. Myocardial bloodflow was measured by thermodilution, with changes in regional coronary flow assessed using a dual radiolabelled (technetium-99m and indium-111) intracoronary microsphere technique and single photon emission tomography. Neither intracoronary nifedipine (100 micrograms) or the control solvent produced changes in systemic arterial pressure (nifedipine -2 mmHg and control +2 mmHg, both not significant). Intracoronary nifedipine markedly increased left ventricular end diastolic pressure (pre-nifedipine 13.0 mmHg versus post nifedipine 20.1, P less than 0.05), while increasing total coronary sinus bloodflow (pre-nifedipine 134 mL/min versus post nifedipine 189, P less than 0.05): Regional coronary bloodflow increased in all myocardial segments, regardless of the severity of coronary stenosis (64 to 132% baseline, all P less than 0.05). In addition, intracoronary nifedipine increased myocardial oxygen consumption (pre-nifedipine 12.3 mL/min versus post nifedipine 15.7, P less than 0.05), with a trend towards improved lactate extraction (pre-nifedipine 0.24 mg/mL versus post nifedipine 0.12, not significant). Although decreased ventricular afterload (left ventricular systolic wall stress) may contribute to nifedipine's antianginal properties, a primary increase in regional coronary bloodflow also appears to be an important factor in the alleviation of myocardial ischemia.