Edward L. Cattau
Georgetown University
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Journal of the American College of Cardiology | 1990
Richard O. Cannon; Arshed A. Quyyumi; William H. Schenke; Lameh Fananapazir; Eben Tucker; Alexandra M. Gaughan; Richard H. Gracely; Edward L. Cattau; Stephen E. Epstein
The causes of chest pain in patients found to have angiographically normal coronary arteries during cardiac catheterization remain controversial. Cardiac sensitivity to catheter manipulation, pacing at various stimulus intensities and intracoronary injection of contrast medium was examined in several groups of patients who underwent cardiac catheterization. Right heart (especially right ventricular) catheter manipulation and pacing and intracoronary contrast medium provoked chest pain typical of that previously experienced in 29 (81%) of 36 patients with chest pain and angiographically normal coronary arteries and 15 (46%) of 33 symptomatic patients with hypertrophic cardiomyopathy. In contrast, only 2 (6%) of 33 symptomatic patients with coronary artery disease experienced their typical chest pain with these sensitivity tests (p less than 0.001). None of 10 patients with valvular heart disease but without a chest pain syndrome experienced any sensation with these tests. Cutaneous pain threshold testing demonstrated that patients with chest pain and normal coronary arteries had a higher pain threshold to thermal stimulation compared with patients who had coronary artery disease or hypertrophic cardiomyopathy. No relation existed between cardiac sensitivity and cutaneous sensitivity testing. Thus, patients who have chest pain despite angiographically normal coronary arteries may have abnormal cardiac sensitivity to a variety of stimuli. This increased sensitivity may be of causal importance to their chest pain syndrome or may contribute to their perception of ischemia-induced pain. The same phenomenon was also commonly seen in symptomatic patients with hypertrophic cardiomyopathy. Whether this phenomenon represents abnormal activation of pain receptors within the heart or abnormal processing of visceral afferent neural impulses in the peripheral or central nervous system is unknown.
The American Journal of Medicine | 1990
Richard O. Cannon; William H. Schenke; Stephen E. Epstein; Edward L. Cattau; Paul N. Yakshe; Kathleen A. Maher; Stanley B. Benjamin
PURPOSE AND METHODS To ascertain the relative prevalence of abnormalities of coronary flow reserve and esophageal function in patients with chest pain despite angiographically normal coronary arteries, 87 patients underwent invasive study of coronary flow reserve and, during the same week, esophageal testing. RESULTS Sixty-three of the 87 patients (72%) demonstrated abnormalities of coronary flow reserve, as evidenced by an increase in coronary resistance during the stress of rapid atrial pacing after administration of ergonovine 0.15 mg intravenously (1.33 +/- 0.36 mm Hg.minute/mL), compared with pacing at the same heart rate before ergonovine administration (1.10 +/- 0.33 mm Hg.minute/mL). This higher coronary vascular resistance occurred in the absence of significant epicardial coronary artery luminal narrowing. Fifty-seven of these 63 patients (90%) with a coronary vasoconstrictor response to ergonovine described their typical chest pain during pacing stress, compared with only six of 24 patients (25%) who demonstrated no coronary flow abnormality (p less than 0.001). After administration of dipyridamole 0.5 to 0.75 mg/kg intravenously to 65 patients, the 48 patients with ergonovine-induced vasoconstriction had a significantly higher minimum coronary resistance, compared with the 17 patients without a coronary vasoconstrictor response to ergonovine (0.65 +/- 0.21 versus 0.47 +/- 0.13 mm Hg.minute/mL, p less than 0.03). Twenty of 87 patients (23%) had abnormal esophageal motility [nutcracker esophagus (11), nonspecific motility disorder (seven), and diffuse esophageal spasm (two)], including 16 of the 63 patients (25%) with abnormal coronary flow reserve. Twenty-four (28%) patients experienced their typical chest pain during motility testing, but only five of these patients met criteria for abnormal esophageal motility. Nine of 75 patients tested (12%) had their typical chest pain during Bernstein testing, and 18 of 38 patients (47%) tested had their typical chest pain provoked by intraesophageal balloon distention. CONCLUSIONS Seventy-one of 87 patients (82%) with anginal-like chest pain and normal epicardial vessels in our series had a disorder of either coronary flow reserve, esophageal motility, and/or reproduction of typical chest pain during acid infusion. Of interest, chest pain was commonly encountered during cardiac and esophageal testing (85% of patients), regardless of the ability to demonstrate an abnormality of coronary flow reserve or abnormal esophageal function. This suggests that pain experienced by these patients may be a consequence of myocardial ischemia, esophageal dysfunction, abnormal visceral nociception, or a combination of any or all of these entities.
Gastrointestinal Endoscopy | 1991
Patricia C. Hsia; Kathleen A. Maher; James H. Lewis; Edward L. Cattau; David E. Fleischer; Stanley B. Benjamin
The diagnostic yield of esophagogastroduodenoscopy, esophageal manometry, and Bernstein testing was assessed in 100 consecutive patients being evaluated for non-cardiac chest pain. Manometric studies revealed the nutcracker esophagus in 21 patients; non-specific esophageal motility disorders in 19 patients; a hypertensive lower esophageal sphincter in 4 patients; diffuse esophageal spasm in 2 patients; and normal motility in 54 patients. Endoscopy was normal in 38 patients; but revealed grades II to IV esophagitis in 24 patients; gastritis and/or duodenitis in 18 patients; a sliding hiatal hernia without evidence of esophagitis in 14 patients; and gastric or duodenal ulcers in 6 patients. Twenty-five individuals were found to have normal manometric studies in combination with a negative Bernstein test. Among these 25 patients, however, 7 patients had esophagitis (grade II or higher); 6 patients had gastritis and/or duodenitis; five patients had a sliding hiatal hernia without esophagitis; 1 patient had peptic ulcer disease; and only 6 patients had a normal endoscopic exam. Our results indicate that endoscopy can identify a significant number of patients with acid-peptic disease who present with non-cardiac chest pain, that would not have been otherwise diagnosed by esophageal manometry or Bernstein testing alone or in combination.
Gastrointestinal Endoscopy | 1991
Irving Waxman; Janice S. Mathews; Jane Gallagher; Ja Kidwell; Martin J. Collen; James H. Lewis; Edward L. Cattau; Firas H. Al-Kawas; David E. Fleischer; Stanley B. Benjamin
A prospective double-blind trial was performed comparing atropine (0.5 mg) by slow intravenous administration to placebo as premedication for colonoscopy, to assess the possible beneficial effects of this vagolytic agent on the performance and safety of the procedure. A total of 77 patients was randomly assigned to receive atropine (38 patients) or placebo (39 patients) before colonoscopy in conjunction with our standard initial medications for conscious sedation (meperidine, 0.4 mg/kg and midazolam, 0.03 mg/kg). Total procedure time was 31 min for the atropine group and 35 min for the placebo group (p greater than 0.05), and there was no overall difference in the total amount of intra-procedural medications required. No statistically significant differences were observed relative to the number or severity of vagal episodes, and neither the endoscopist nor the patients noted any differences in the ease or tolerance of the procedure (p greater than 0.05). Although these results fail to demonstrate a significant benefit of atropine when given routinely as premedication for colonoscopy, this study does not rule out the potential usefulness of atropine in counteracting vagal episodes when they occur.
The American Journal of Gastroenterology | 1989
Ansher Af; James H. Lewis; David E. Fleischer; Edward L. Cattau; Martin J. Collen; O'Kieffe Da; Korman Ly; Stanley B. Benjamin
Gastroenterology | 1989
William Kern Deschner; Kathleen A. Maher; Edward L. Cattau; Stanley B. Benjamin
Radiology | 1988
Robert K. Zeman; L V McVay; P M Silverman; Edward L. Cattau; Stanley B. Benjamin; Df Fleischer; Brian S. Garra; M H Jaffe
The American Journal of Gastroenterology | 1990
Deschner Wk; Maher Ka; Edward L. Cattau; Sb Benjamin
Radiology | 1990
Robert K. Zeman; William J. Davros; J A Goldberg; Brian S. Garra; W S Hayes; Edward L. Cattau; S C Horii; C Cooper; Paul M. Silverman
The American Journal of Gastroenterology | 1989
David E. Fleischer; Stanley B. Benjamin; Edward L. Cattau; Martin J. Collen; James H. Lewis; Jaffee Mh; Robert K. Zeman