Serum-Ascitic Fluid Albumin Gradient, Portal Hypertension, and Ascites

Letters Serum-Ascitic Fluid Albumin Gradient, Portal Hypertension, and Ascites To the Editor: I read with interest the article entitled "Ascites and Hepatorenal Syndrome: Pathophysiology and Management" by Roberts and Kamath, which was published in the September 1996 issue of the Mayo Clinic Proceedings (pages 874 to 881), and I want to point out some potentially misleading information in their Table 1. On the basis of the Starling hypothesis, an increased serum-ascitic fluid albumin gradient (SAAG) indicates the existence of portal hypertension as one component in the etiology of ascites-for example, patients with an increased SAAG may have carcinomatosis in addition to portal hypertension. As published, Table 1 could erroneously be interpreted as indicating that patients with an increased SAAG have only portal hypertension. In fact, such patients may also have any of the other causes that are listed under the column "Low SAAG." Elyiahu Rubin, M.D. Department of Veterans Affairs Medical Center Long Beach, California

In response: We thank Dr. Rubin for raising an important point that we should have clarified in our article. A high serum-ascitic fluid albumin gradient (SAAG) indicates that the cause of the ascites is portal hypertension. In patients with ascites and portal hypertension who also have peritoneal carcinomatosis, the SAAG will be high if the major etiologic component is portal hypertension. If the major cause of the ascites is related to carcinomatosis, however, patients with cirrhosis of the liver may have a low SAAG. Mixed types of ascites constitute 4% or less of all causes of ascites, and a combination of cirrhosis of the liver and peritoneal carcinomatosis constitutes less than 1%. Thus, most often, a high SAAG indicates portal hypertension. Lewis R. Roberts, M.D. Patrick S. Kamath, M.D. Mayo Clinic Rochester Rochester, Minnesota

A subset of five patients (four men) from our original study who had high scores for hostile coronary-prone behavior on the type A structured interview and persistent same-site restenosis (occurring within 6 to 26 weeks after PTCA) were enrolled in a restenosis-prone behavior modification program. When our 41 original volunteers were enrolled in our study, we offered this program at no cost (with informed consent) to any who we thought might ultimately experience persistent same-site restenosis. Because hostile, coronary-prone behavior, as assessed, measured, and scored with use of the audiotaped type A structured interview, correlates well with systolic and diastolic blood pressure hyperreactivity and fluctuations, a prevention program using direct hemodynamic and signal-cued biofeedback was chosen. Patient education and behavioral risk factor counseling were additional important components of the program, which included five office visits after angiographic documentation of at least two same-site restenoses. Inexpensive ($15) portable biofeedback units were prescribed for the patients to use at home and at work to assist in generalization and retraining of the sympathetic nervous system hyperreactivity response to hostility-provoking stimuli. The objective was to use biofeedback to aid in circumventing the pathophysiologic consequences of hostile responses. Although our original study failed to find that caffeine was a significant postangioplasty restenosis risk factor (perhaps because of the limited sample size), at the time of intervention, the data analysis was incomplete, and thus, we recommended abstinence from caffeine. At this writing, four of the five patients (three men) who were included in this pilot intervention study are free of restenosis and other clinical cardiac events at 21 months after their final PTCA. Posttreatment hostility scores were not obtained because the patients were no longer blinded to our hypothesis after the debriefing and counseling procedures. These findings are encouraging for preventive cardiology and cardiac rehabilitation programs," inasmuch as restenosis is most likely to occur within the first 6 months after PTCA and is the major factor that limits long-term success of the procedure. My colleagues and I hope that the results of our pilot intervention study will inspire other investigators and clinicians to pursue similar and larger intervention trials examining this postangioplasty restenosis risk factor in order to improve PTCA outcomes and postpone or decrease the need for coronary artery bypass grafting. Mark Goodman, Ph.D., M.A. Behavioral Medicine Center West Orange, New Jersey

Pilot Findings of a Percutaneous Transluminal Coronary Angioplasty-Restenosis-Prone Prevention Program

REFERENCES 1. Hines EA Jr. Range of normal blood pressure and subsequent development of hypertension: a follow-up study of 1,522 patients. JAMA 1940; 115:271-274 2. Menkes MS, Matthews KA, Krantz DS, Lundberg U, Mead LA, Qaqish B, et al. Cardiovascular reactivity to the cold pressor test as a predictor of hypertension. Hypertension 1989; 14:524-530 3. Keys A, Taylor HL, Blackburn H, Brozek J, Anderson JT, Simonson E. Mortality and coronary heart disease among men studied for 23 years. Arch Intern Med 1971; 128:201-214 4. Friedman M, Thoresen CE, Gill JJ, Ulmer D, Powell LH, Price VA, et al. Alteration of type A behavior and its effect on cardiac recurrences in post myocardial infarction patients: summary results of the Recurrent Coronary Prevention Project. Am Heart J 1986; 112:653-665

To the Editor: In a study published in the August 1996 issue of the Mayo Clinic Proceedings (pages 729 to 734), my colleagues and I were the first to report identification of type A hostile, coronaryprone, antagonistic, disagreeable behavior as a risk factor that could predict restenosis after percutaneous transluminal coronary angioplasty (PTCA). Coronary-prone behavior has as its antecedent the sympathetic hyperreactivity phenomenon, 1 which has prospectively predicted hypertension in individual subjects 20 years before its clinical manifestation? as well as mortality.' Mayo CUn Proc 1997; 72:487

487

© /997 Mayo Foundation for Medical Education and Research

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.