The impact of an occluded internal carotid artery on the mortality and morbidity of patients undergoing coronary artery bypass grafting.

PURPOSE: To evaluate whether the presence of stenosis or an occluded internal carotid artery (ICA) influences perioperative stroke and mortality rates in patients subjected to coronary artery bypass grafting (CABG). MATERIAL AND METHODS: Between January 1995 and July 1998, 3,344 patients (59% males; 41% females) had CABG performed at our institution. Preoperative carotid duplex scans performed by registered vascular technologists at an ICAVL accredited laboratory were available for review in all patients. Of these, 3,101 (92.7%) had < 60% ICA stenosis (group A), 182 (5.4%) had 60% to 99% ICA stenosis (group B), and the remaining 61 (1.8%) had a occluded ICA (group C). In the latter group, 53 patients (87%) had < 60% contralateral ICA stenosis, while 8 (13.1%) had significant (60% to 99%) contralateral stenoses. Concomitant carotid endarterectomies (CEAs) were performed in 70 patients in group B (40%) and in 2 patients in group C (3.2%). Age, indications for surgery, prevalence of diabetes, hypertension, and smoking were similar in all groups. The mean pump time for groups A, B and C were 132, 138, and 125 minutes, respectively. The aortic cross-clamp time for group A, B, C were 78, 75, and 75 minutes, respectively. Statistical analyses were performed using the chi-square, Fisher's exact test, and unpaired t test. RESULTS: Perioperative stroke rates (30 days) were 1.6%, 3.8%, and 6.5% for groups A, B, and C, respectively. Group A results varied significantly from groups B (P < 0.03) and C (P < 0.003). No statistically significant difference was noted between groups B and C (P = 0.6). The presence of a contralateral ICA stenosis in group C patients was predictive of a perioperative stroke (25% versus 3.8%; P < 0.0001). Concomitant CEAs for contralateral severe ICA stenosis in group C were associated with higher stroke rate (100%) when compared with those in group B patients (4.2%; P < 0.02). Perioperative (30 days) mortality rates for groups A, B, and C were 3.6%, 6.6%, and 8.6%, respectively. The mortality rate for group A was lower than for groups B (P < 0.05) and C (P < 0.05). CONCLUSION: The presence of an ICA occlusion increases the morbidity and mortality in patients undergoing CABG. To the best of our knowledge, this is the first reported large series of patients that investigates the role of carotid occlusions.

Quantification of swallowed saliva in aspirated gastric juice.

OBJECTIVE: The aim of this study was to test a new mathematical model of the electrolyte concentrations in basal gastric secretion and to demonstrate whether this model was better than the old formula. Previous evidence suggests that primary gastric acid secretion has an electrolyte composition of [H+] 145, [Na+] 7, [K+] 17 and [Cl] 170 mmol/l, and that this can be modified by an extragastric component consisting of duodenogastric reflux and swallowed saliva. The only quantitative measurement available to date ignores the swallowed saliva. METHOD: Under basal conditions, gastric juice was aspirated and simultaneous sampling of saliva was performed in 60 adult subjects (33 men, 27 women), aged 23-85. Na+, K+, Cl-, phenol red (marker for pyloric loss) and titratable acidity or alkalinity were measured in aspirated gastric juice, and epidermal growth factor (EGF) was measured in saliva and gastric juice. Estimates of the primary gastric acid secretion were made by two methods: (1) V(G) formula which corrects for the duodenogastric reflux and assumes that there is no swallowed saliva: and (2) V(acid) formula, a novel procedure intended to correct for swallowed saliva as well and based on the known concentrations of electrolytes in saliva secreted at varying rates. RESULTS: The mean EGF concentrations were 3.42 ng/ml in saliva, 3.40 ng/ml in gastric juice. From the relationship of EGF output versus calculated primary acid secretion, the concentration of EGF in the extragastric component could be calculated. The V(G) formula gave a zero value of EGF whilst with V(acid), the calculated concentration of salivary EGF was 3.73 ng/ml and showed close correspondence with the measured EGF concentration in spat saliva. CONCLUSION: It is concluded that the new formula is more accurate, and gives a reasonable measurement for the volume of saliva in aspirated gastric juice.

Epidermal growth factor in saliva and gastric juice: response to histamine.

Epidermal growth factor (EGF) was measured in saliva and in gastric juice under basal conditions and after histamine stimulation (0.04 mg kg-1h-1). Sixty subjects studied comprised 20 normal volunteers, 20 patients with duodenal ulcer (DU), and 20 patients with non-ulcer dyspepsia (NUD). There was no difference in basal salivary EGF concentrations between control and DU or control and NUD subjects, but the EGF concentration in DU patients exceeded that in NUD patients (p < 0.05). Basal gastric juice concentrations of EGF were similar in all three groups. There was no difference between basal salivary and gastric EGF concentrations (p > > 0.05). After histamine stimulation, salivary and gastric EGF concentrations increased in all three groups: the increase was greater in gastric juice than saliva (p < 0.0001). There were no significant differences in the salivary EGF concentrations of controls and NUD patients, or controls and DU patients, but values were significantly higher when DU and NUD patients were compared (p = < 0.05). In the gastric juice, EGF increased more in DU patients than in controls or NUD patients (p < 0.05). This effect was not linked to the greater acid secretion in DU than in the other groups. There was no influence of gender or smoking on the EGF concentration. This evidence suggests that the stomach itself may be able to secrete large amounts of EGF and that histamine is a potent stimulus. It is more likely that the gastric EGF is responding to the presence of a duodenal ulcer than that lack of EGF is responsible for persistence of the ulcer.

Gastric juice epidermal growth factor concentration and Helicobacter pylori in patients with duodenal ulcer.

The level of epidermal growth factor (EGF) was measured in the basal and maximally stimulated gastric juice of 20 control subjects and 20 patients each with duodenal ulcer and non-ulcer dyspepsia. Basal gastric juice was analysed for ammonia and urea concentrations, and the [ammonia]3/[urea] ratio was used to show Helicobacter pylori status, as was the [13C]urea breath test in nine controls. There was complete concordance in the nine controls between the two methods for determining H. pylori status. Twenty-five subjects were H. pylori positive (seven with duodenal ulcer, nine with non-ulcer dyspepsia, nine controls) and 35 H. pylori negative (13, 11 and 11 respectively). In H. pylori-positive subjects, the median EGF concentrations in the stimulated secretion of patients with duodenal ulcer and without (non-ulcer dyspepsia and controls combined) were 46.7 and 18.0 ng/ml (P < 0.001), and in H. pylori-negative subjects were 40.0 and 26.5 ng/ml respectively (P < 0.01). There was no difference in EGF concentration between controls and subjects with non-ulcer dyspepsia irrespective of H. pylori status. Lack of EGF is unlikely to be a cause of duodenal ulcer. The increased EGF concentration in patients with ulcer bore no relationship to the H. pylori status of the individual. If this bacterium causes duodenal ulcer, it is not via a reduction in EGF concentration.