1997 JCO Orthodontic Practice Study. Part 2. Practice success.
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Biomedical subjects
Publications and source records attributed to A H Nelson.
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The effects of carvedilol, a novel vasodilating beta-blocker and antioxidant, and propranolol on survival, neurobehavioral deficits, cardiovascular parameters, plasma renin, plasma aldosterone levels and renal pathology were determined in stroke-prone spontaneously hypertensive rats. Stroke-prone spontaneously hypertensive rats were allowed access to 1% NaCl as the drinking solution and a high fat diet supplemented with carvedilol (1200 or 2400 ppm) or propranolol (2400 ppm). The control group consisted of stroke-prone spontaneously hypertensive rats placed on the same diet with no drug supplement. Animals fed propranolol had a blood level of 864 +/- 68 ng/ml, whereas carvedilol-fed animals had blood levels of 24 +/- 4 ng/ml at 1200 ppm and 471 +/- 145 ng/ml at 2400 ppm. Carvedilol and propranolol treatment resulted in significant beta adrenoceptor blockade. Both compounds reduced heart rate, but had no significant effects on systolic arterial blood pressure. Carvedilol- and propranolol-treated animals also exhibited significant, prolonged protection from neurobehavioral deficits and mortality (P < .01). Elevated plasma renin activity and aldosterone levels seen in untreated controls were significantly decreased by propranolol (P < .05), and to a considerably greater extent by the same dose of carvedilol (P < .01). Carvedilol decreased renal histopathological damage and cardiac hypertrophy to a greater extent (P < .01) than propranolol (at equal doses). Both carvedilol (P < .01)- and propranolol (P < .01)-treated animals had considerably reduced renal damage at 18 weeks of treatment. Carvedilol reduced renal damage more than propranolol (P < .05). In addition, the lower (1200 ppm) dose of carvedilol, which decreased neurobehavioral deficits and mortality, had no significant effects on organ mass or renal function, but significantly (P < .01) reduced renal damage. These data indicate that both beta adrenoceptor blockers, especially carvedilol to a considerably greater degree, convey significant protection in a genetic model of severe hypertension that results in renal and cardiovascular organ pathology, neurobehavioral deficits and premature death.
STUDY OBJECTIVE: To determine the relationship between postoperative ST segment changes and clinically apparent cardiac morbidity in noncardiac surgery patients. DESIGN: Prospective, cohort study. SETTING: General inpatient and intensive care units at a tertiary care hospital. PATIENTS: 145 high-risk noncardiac surgery patients. MEASUREMENTS AND MAIN RESULTS: Patients were monitored for ST segment changes using ambulatory electrocardiographic (ECG) recorders from the end of the surgical period for up to the third postoperative day. Patients were evaluated for a clinically apparent cardiac event (cardiac death or myocardial infarction) by daily 12-lead ECGs, and CK-MB isoenzymes, as clinically indicated. Nine patients sustained a clinically apparent cardiac event, 7 of whom had a cardiac event during the period in which they were monitored by ambulatory ECG. All 7 patients who sustained a cardiac event during the monitoring period had at least one episode of myocardial ischemia, which persisted for a minimum of 30 minutes either prior to or at the same time of the event, with no morbidity occurring in the group of patients who had only short durations of myocardial ischemia. Three of the patients with events had continuous ST segment changes, while the other patients had transient ST segment changes. CONCLUSIONS: These observations suggest that clinically apparent cardiac events are associated with prolonged ST segment changes detected on ambulatory ECG recorders. The cardiac ischemia leading to prolonged postoperative ST segment changes may itself result in cardiac morbidity, or it may be a reflection of underlying pathophysiology.
BACKGROUND: Dipyridamole thallium imaging (DTI) and ambulatory electrocardiography (AEGC) have been advocated as means to stratify risk before vascular surgery. The purpose of this study was to compare the predictive value of both tests in noncardiac surgery patients for perioperative cardiac morbidity and long-term mortality. METHODS: One hundred eighty patients were referred to the nuclear cardiology laboratory for DTI before noncardiac surgery. In patients with normal electrocardiograms and who consented, an ambulatory electrocardiogram was recorded for 24 h. DTI results were classified as negative, positive, or strongly positive (included in positive). Patients were assessed for a minimum of 12 months, and Kaplan-Meier cardiovascular survival curves were constructed with a log-rank statistic of equality with P < 0.05 significant. RESULTS: One hundred nine patients had both tests and then underwent surgery, sustaining 10 perioperative cardiac events (cardiac death, myocardial infarction, or symptomatic ischemia). The positive predictive values for DTI (18%) and AECG (25%) were similar, as were the likelihood ratios for positive tests (DTI = 2.1, AECG = 3.3). The likelihood ratios of a negative test were also similar (DTI = 0.45, AECG = 0.48). A strongly positive thallium defect had a somewhat greater likelihood ratio (3.5) for in-hospital events and was the only test result associated with a significantly worse long-term cardiac survival. CONCLUSIONS: AECG and DTI demonstrated a similar, although lower than initially reported, ability to stratify risk and predict short-term outcome. Only quantitative dipyridamole thallium also had predictive value for long-term prognosis.
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The consequences of cerebral ischemia were studied in three different strains (BDF, CFW, and BALB/C) of mice. The different strains exhibited significant differences in susceptibility to 24-h focal ischemia. Following middle cerebral artery occlusion (MCAO), infarct volumes (mm3) were 5 +/- 3 in BDF, 15 +/- 5 in CFW, and 23 +/- 3 in BALB/C mice (p < 0.05). MCAO plus ipsilateral common carotid artery occlusion (CCAO) resulted in infarct volumes of 15 +/- 9 in BDF, 38 +/- 10 in CFW, and 72 +/- 12 in BALB/C mice (p < 0.05). In addition, MCAO plus CCAO produced death by 24 h in 42% of CFW and 67% of BALB/C mice, but not in any BDF mice (p < 0.05). CCAO alone produced multifocal hemispheric infarctions in 36% of BALB/C mice but not in the other two strains. Brains of all mouse strains subjected to sham surgery were free of any ischemic injury. Arterial blood pressures, blood gases, and blood cell profiles were relatively similar for the three mouse strains. However, carbon black studies of the cerebrovascular anatomy revealed an incomplete circle of Willis (i.e., a significant decrease in the frequency of patent posterior communicating arteries) for BALB/C compared with BDF mice (p < 0.05), with CFW mice being intermediary. Based on these anatomical data, BALB/C mice also were evaluated following transient global brain ischemia produced by bilateral CCAO. BALB/C mice exhibited a > 85% reduction in cortical microvascular perfusion and EEG power within 1 min of bilateral CCAO. Also, hippocampal neuronal CA1 damage and mortality over 7 days were related to the duration of global brain ischemia (p < 0.05). These data demonstrate a significant difference between mouse strains in their sensitivity to cerebral ischemia that appears to be related, at least in part, to the functional vascular anatomy at the level of the posterior communicating arteries. In particular, we point out the potential usefulness of BALB/C mice as a sensitive and reproducible model of focal and global ischemia.
OBJECTIVE: To determine if postoperative anemia is associated with postoperative myocardial ischemia and morbid cardiac events DESIGN: Case control study. SETTING: Postanesthesia care unit and surgical intensive care unit. PATIENTS: A total of 27 high-risk patients undergoing infra-inguinal arterial bypass procedures. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: After informed consent, patients were continuously monitored by ambulatory electrocardiographic recorders from the evening before surgery up to 80 hrs during the postoperative period. Myocardial ischemia was defined as > or = 1 mm of horizontal or downsloping ST depression or > or = 2 mm ST segment elevation persisting for at least 60 secs on the ambulatory electrocardiogram. Morbid cardiac events were defined as: cardiac death, myocardial infarction, unstable angina, and ischemic pulmonary edema. Using a receiver operating characteristic curve, a hematocrit of 28% was determined to be the best threshold hematocrit value below which morbid cardiac events were most likely to occur. Statistical significance between hematocrit and cardiac outcome was determined by Fisher's exact test where appropriate. Thirteen of 27 patients had a hematocrit < 28%. Of these 13 patients, ten demonstrated postoperative myocardial ischemia and six sustained a morbid cardiac event. Of 14 patients with a hematocrit > or = 28%, two displayed myocardial ischemia and none sustained a morbid cardiac event. A hematocrit of < 28% was significantly associated with myocardial ischemia (p = .001) and morbid cardiac events (p = .0058). No significant differences in baseline heart rate and heart rate at the onset of myocardial ischemia were noted between the anemic and nonanemic patients. CONCLUSIONS: This study suggests that postoperative anemia may play a role in postoperative myocardial ischemia and cardiac morbidity.
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Three cases of postoperative myocardial infarction are reported in patients with normal or fixed defects on preoperative dipyridamole thallium scans (interpreted as "negative" for active cardiac ischaemic risk). All patients were monitored with an ambulatory electrocardiographic recorder from the evening before surgery through the first two postoperative days. Two of the patients demonstrated preoperative or early postoperative ischaemia, suggesting that the test was a false negative. The third patient did not demonstrate ischaemia during the period of monitoring, but developed a myocardial infarction during the third postoperative day, suggesting progression of the underlying coronary artery disease. Preoperative dipyridamole thallium imaging may result in false negative scans in selected high-risk populations.
ECG changes suggestive of myocardial ischemia are common during cesarean delivery under regional anesthesia. To determine the time course, duration, and significance of these ECG changes, we monitored 111 parturients with continuous ambulatory ECG (Holter) during and after cesarean delivery. Twenty-two parturients undergoing vaginal delivery were similarly monitored. ST segment depression was present in 25% of patients undergoing cesarean delivery but was not found in those patients delivering vaginally. ST segment elevation was not detected in either group. The incidence of ST segment depression during cesarean delivery was similar with epidural (29%), spinal (17%), and general (18%) anesthesia, occurring most commonly in the 30 min following delivery (P less than 0.001). Transthoracic echocardiographic imaging was performed in 23 patients undergoing cesarean section. Five of the 23 patients had seven episodes of intraoperative ST segment depression. Regional wall motion abnormalities were not present in any patient. A decrease in ejection fraction area greater than 15% from baseline or from previous interval ejection fraction area was present during four episodes of ST change. Three episodes of ST depression were not associated with significant decreases in ejection fraction area. Precordial Doppler monitoring for detection of venous air embolism in 25 patients revealed no association between the occurrence of venous air embolism and ST segment depression. We conclude that although significant myocardial impairment during cesarean delivery does not occur, episodes of ST depression may not all be merely an artifact of parturition.