Favourable outcome in sclerotherapy for bleeding oesophageal varices in schistosomiasis: Results in 30 patients

Abstract Thirty consecutive patients with bleeding oesophageal varices secondary to schistosomal liver disease received injection sclerotherapy. These formed a part of a prospective study, to evaluate the role of sclerotherapy in the treatment of bleeding oesophageal varices due to different aetiological factors in patients seen at the Gastroenterology Unit, Riyadh Armed Forces Hospital, Saudi Arabia, between December 1980 and July 1984.
Schistosomiasis is endemic in parts of Saudi Arabia. Sclerotherapy has a special place in schistosomal liver disease as liver function is well preserved in this disease. The new antischistosomal drugs are effective and may halt the progress of the disease. However, in many patients portal hypertension with bleeding oesophageal varices is found at diagnosis. Of the patients with schistosomiasis, 63.3% were Group A Child's Classification. Oesophageal varices have been eradicated in 11 cases during the mean follow-up period of 28 months (range 3-44 months). Four patients were referred for surgery because of bleeding gastric varices, two of whom died following operation. One patient, who was also hepatitis B surface antigen positive, died due to re-bleeding from gastric varices. The remaining 25 patients had no recurrence of bleeding and their liver function remained satisfactory.
Surgical procedures for oesophageal varices in schistosomiasis carry the risk of peri-operative and postoperative morbidity and mortality. In contrast, complications following sclerotherapy are minor compared to surgical procedures and none of our patients had any serious sclerotherapy complications.     

Management of recurrent ventricular tachyarrhythmias associated with Q-T prolongation

Eleven patients with acquired prolongation of the Q-Tc interval and recurrent ventricular tachyarrhythmias were studied. Five patients required 5 to 44 direct current shocks to correct prolonged ventricular tachyarrhythmias, and five were given at least two antiarrhythmic agents in an attempt to control the arrhythmias. In 4 of the 11 patients, when thioridazine, diuretic drugs and antiarrhythmic agents were withdrawn and hypokalemia or hypocalcemia corrected, ventricular tachyarrhythmias did not recur. The Q-Tc interval normalized in 2 to 3 days. Ventricular tachyarrhythmias were recurrent in the remaining seven patients, despite withdrawal of the drugs that caused the Q-Tc prolongation, attempted correction of hypokalemia when present and the administration of antiarrhythmic agents to four of the seven. All antiarrhythmic agents were then withdrawn in this group.

Immediately on the establishment of overdrive ventricular or atrioventricular sequential pacing in these patients, ventricular tachyarrhythmias were abolished. No breakthrough ventricular tachyarrhythmias occurred during temporary pacing. Temporary pacing was required for an average of 10 days and the Q-Tc interval normalized an average of 5 days from the onset of pacing. Three patients required a permanent pacemaker, one because of chronic complete heart block, one because of the sick sinus syndrome, and one because of frequent ventricular ectopic complexes complicating ischemic heart disease. All 11 patients survived their period of hospitalization.     

Increased mitochondrial uncoupling proteins, respiratory uncoupling and decreased efficiency in the chronically infarcted rat heart

Heart failure patients have abnormal cardiac high energy phosphate metabolism, the explanation for which is unknown. Patients with heart failure also have elevated plasma free fatty acid (FFA) concentrations. Elevated FFA levels are associated with increased cardiac mitochondrial uncoupling proteins (UCPs), which, in turn, are associated with decreased mitochondrial respiratory coupling and low cardiac efficiency. Here, we determined whether increased mitochondrial UCP levels contribute to decreased energetics in the failing heart by measuring UCPs and respiration in mitochondria isolated from the viable myocardium of chronically infarcted rat hearts and measuring efficiency (hydraulic work/O₂ consumption) in the isolated, working rat heart. Ten weeks after infarction, cardiac levels of UCP3 were increased by 53% in infarcted, failing hearts that had ejection fractions less than 45%. Cardiac UCP3 levels correlated positively with non-fasting plasma FFAs (r = 0.81; p < 0.01). Mitochondria from failing hearts were less coupled than those from control hearts, as demonstrated by the lower ADP/O ratio of 1.9 ± 0.1 compared with 2.5 ± 0.2 in controls (p < 0.05). The decreased ADP/O ratio was reflected in an efficiency of 14 ± 2% in the failing hearts when perfused with 1 mM palmitate, compared with 20 ± 1% in controls (p < 0.05). We conclude that failing hearts have increased UCP3 levels that are associated with high circulating FFA concentrations, mitochondrial uncoupling, and decreased cardiac efficiency. Thus, respiratory uncoupling may underlie the abnormal energetics and low efficiency in the failing heart, although whether this is maladaptive or adaptive would require direct investigation.     

Low acid output in Pima Indians

Duodenal ulcer has not been observed in full-heritage Pima Indians, while gastric cancer is relatively frequent. To investigate possible underlying factors for this phenomenon, we determined gastric acid output, gastric emptying rate, and plasma levels of gastrin, pepsinogen I, and pepsinogen II in apparently healthy Pima Indian and in Caucasian controls. The Pimas had significantly lower basal and stimulated outputs of gastric acid and higher fasting and postprandial plasma gastrin concentrations than the caucasians. Plasma pepsinogen I levels were similar in the two groups, but plasma pepsinogen II was significantly higher and the ratio of pepsinogen I to pepsinogen II was significantly lower in the Pima Indians. In addition, gastric emptying of an acaloric liqid meal was significantly delayed in the Pimas. The results suggest that the absence of duodenal ulcer in Pima Indians may be related to low gastric acid production and aslow rate of gastric emptying in this population. The associated findings of hypergastrinemia, hyperpepsinogenemia II, and a low ratio of pepsinogen I to pepsinogen II suggest that the hypochlorhydria may reflect an increased pervalence of chronic gastritis in full-heritage Pima Indians. This, in turn, could represent a risk factor for the development of gastric cancer in this population.Supported in part by research Contract 1-Am-6-2219 and grant AM 13233 from the National Institutes of Health, Bethesda, Maryland     

Plasma beta-thromboglobulin as a measure of platelet activity: Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction

The plasma concentration of beta-thromboglobulin (BTG), a platelet-specific protein released during platelet aggregation, is considered a sensitive marker of in vivo platelet activity. The mean plasma level in 133 asymptomatic individuals was 32.3 ± 1.1 ng/ml, and there was no difference between those with no risk factors (32.2 ± 1.2 ng/ml, n = 56), those who smoked (31.8 ± 1.8 ng/ml, n = 45), those with hyperlipidemia (32.8 ± 1.7 ng/ml, n = 15), and those exposed to both of these risk factors (34.1 ± 2.7 ng/ml, n = 17). The mean plasma BTG level in 104 patients with symptomatic ischemic heart disease was significantly elevated (40.9 ± 1.4 ng/ml, p < 0.01), but there was considerable overlap with normal levels. Although no difference was found between patients with no risk factors (38.1 ± 4.0 ng/ml, n = 13) and those with only 1 risk factor (37.0 ± 1.8 ng/ml, n = 44), patients with 2 or more risk factors had a significantly elevated plasma BTG level (45.2 ± 2.2 ng/ml, n = 47, p < 0.01). It is concluded that risk factors themselves do not increase platelet activity, but that patients with vascular disease have activated platelets that may contribute to the progression of the disease. Plasma BTG was also measured serially for 10 days in 29 patients after hospitalization with acute ischemic cardiac pain. Although the median plasma level was elevated above normal there were no acute changes in plasma BTG after either acute infarction (n = 22) or acute ischemia (n = 7), except in 2 patients in whom pericardial friction rubs developed. Thus, measurement of systemic plasma BTG did not detect platelet involvement in acute coronary occlusion or acute ischemia.     

Prognostic significance of preoperative left ventricular ejection fraction and valve lesion in patients with aortic valve replacement

After aortic valve replacement, depressed left ventricular function, as assessed from the preoperative left ventricular ejection fraction, has been reported to improve significantly in patients with aortic stenosis, but to improve little or to a lesser degree In patients with aortic regurgitation. Accordingly, the effect of preoperative left ventricular ejection fraction and other variables on postoperative survival was examined in 229 patients after aortic valve replacement. The preoperative left ventricular ejection fraction, cardiac index and left ventricular end-diastolic pressure were found not to affect the 3 year postoperative survival rate in patients with aortic stenosis and mixed aortic valve disease. However, patients with aortic regurgitation and a left ventricular ejection fraction of less than 0.50 had a significantly poorer 3 year survival rate (64 ± 10 percent) than patients with aortic regurgitation and an ejection fraction of 0.50 or more (91 ± 8 percent) (p <0.02). The 3 year postoperative survival rate in patients with a reduced cardiac index (less than 2.5 liters/min per m²) and aortic regurgitation was also significantly lower (63 ± 10 percent) than the rate in patients with aortic regurgitation and a normal cardiac index (p <0.02). There was less significance in the difference between the 3 year postoperative survival rate of patients with aortic regurgitation whose left ventricular end-diastolic pressure was 15 mm Hg or less and those whose pressure was greater than 15 mm Hg (p <0.05). Thus, it may be advisable to monitor left ventricular ejection fraction noninvasively in patients with aortic regurgitation and to advise aortic valve replacement before the ejection fraction becomes severely depressed.