OBJECTIVETo describe the effectiveness of investigating and treating the cause of refractory chest pain in patients with coronary artery disease who are receiving optimal antianginal therapy.DESIGNCohort study.SETTINGTertiary referral center.PATIENTSBetween January 1988 and December 1989, 34 patients were identified as having angiographically proven coronary artery disease and atypical chest pain symptoms despite their having received aggressive medical or surgical antianginal therapy, or both.INTERVENTIONPatients with confirmed acid-related symptoms were treated with high-dose histamine-2 (H2) blockers or omeprazole for 8 weeks in an open-label study.MEASUREMENTSEsophageal manometry and simultaneous 24-hour pH and Holter studies; global improvement in or disappearance of chest pain.RESULTSOf the 34 patients, 30 (88%) experienced their identical chest pain symptoms during the study. A total of 164 pain episodes was recorded: 38 (23.2%) correlated with acid reflux; 6 (3.7%) were related to cardiac ischemia; and the remaining 120 (73.2%) had no identifiable cause. Of these 30 patients, 20 (67%) had some of their episodes of chest pain (range, 14% to 100%) secondary to acid reflux. After 8 weeks of vigorous acid suppression, 13 of these 20 patients had marked improvement or resolution of chest pain. Four other patients had ischemia-related episodes of chest pain that responded to more aggressive antianginal therapy. No episodes of acid reflux were clearly followed by ischemic chest pain. One patient had both acid- and ischemic-related episodes of chest pain that were indistinguishable. Overall, 24 of 34 (71%) patients had a definite cause of chest pain identified by combined pH and Holter monitoring.CONCLUSIONSGastroesophageal reflux disease is a common, treatable cause of chest pain in patients with coronary artery disease who have atypical symptoms and remain symptomatic despite aggressive antianginal therapy. Combined Holter and 24-hour esophageal pH studies are complementary investigations for elucidating the cause of chest pain in these patients.

The purpose of our study was to assess the prevalence of esophageal test abnormalities in patients with known cardiovascular disease and persistent chest pain. We performed a retrospective review of symptoms, manometry, and provocative test results performed on patients with undiagnosed chest pain. The 220 patients with angiographically determined cardiac disease and persistent chest pain were divided into three groups: coronary artery disease (125 patients), mitral valve prolapse (38 patients), and coronary bypass/angioplasty (57 patients). A comparison group consisted of 159 patients with noncardiac chest pain. All patients underwent esophageal manometry and placebo-controlled provocative testing (acid perfusion test and edrophonium chloride test). The prevalence of esophageal motility disorders in the noncardiac chest pain group (27%) was similar to that in the coronary artery disease (24%), mitral valve prolapse (37%), and coronary bypass/angioplasty (30%) groups. The frequency of nutcracker esophagus (11% to 16%) and diffuse esophageal spasm (2% to 7%) was remarkably constant. The prevalence of any positive provocative result in the noncardiac chest pain group (27%) was similar to that in the coronary artery disease (19%), mitral valve prolapse (32%), and coronary bypass/angioplasty (20%) groups. Furthermore, completely negative results of esophageal investigation occurred in 55%, 62%, 42%, and 59% of the respective patient groups.

In acute aortic regurgitation, left ventricular pressure rises rapidly during diastole, which produces presystolic mitral valve closure. This does not occur in chronic aortic regurgitation. Since normal, nonregurgitant mitral valve closure may depend on properly coordinated atrial and ventricular contractions, we hypothesized that abnormal mitral valve closure occurring before systole in acute aortic regurgitation may produce diastolic mitral regurgitation detectable by Doppler echocardiography. Accordingly, we performed ultrasonic Doppler examination of seven patients with acute aortic regurgitation and 12 patients with chronic aortic regurgitation. Regurgitant aortic flow was severe in all cases. Doppler sampling within the left atrium demonstrated regurgitant mitral flow in late diastole in all patients with acute aortic regurgitation. The onset of diastolic mitral regurgitation coincided with mitral valve preclosure in patients with acute aortic regurgitation and occurred regardiess of the position of the mitral leaflets at the initiation of closure. In contrast, none of the 12 patients with chronic aortic regurgitation had mitral valve preclosure or diastolic mitral regurgitation (p < 0.05 versus acute aortic regurgitation). We conclude that diastolic mitral regurgitation accompanies mitral valve preclosure, which occurs in acute but not chronic aortic regurgitation. Thus diastolic mitral regurgitation may be a Doppler sign of acute aortic regurgitation, in the absence of a markedly prolonged PR interval. Furthermore, this observation suggests that normal, nonregurgitant mitral closure requires more than an increase in left ventricular pressure above left atrial pressure, regardless of the position of the mitral leaflets before closure.

We have reported the case of a 38-year-old white woman with substernal chest pain, hypotension, and ECG changes suggesting acute anterior myocardial infarction. Cardiac catheterization revealed no coronary artery pathology, but severe global hypokinesia was noted on left ventriculogram and endomyocardial biopsy revealed myocytic degeneration and mononuclear cell infiltration consistent with acute viral myocarditis. Viral serologies confirmed a recent Epstein-Barr virus infection.

Questionnaires were sent to 119 patients with noncardiac chest pain, all of whom had previous detailed esophageal evaluations in which 63 were diagnosed as having pain from the esophagus. Mean follow-up period was 21.8 months. Patients diagnosed as having an esophageal etiology of their noncardiac chest pain usually continued to have recurrent pain. Furthermore, a specific diagnosis did not significantly increase the likelihood of pain resolution. However, patients who understood that the esophagus was the source of their pain were significantly less likely to feel disabled by their pain and to require continued physician evaluation. This finding was independent of any treatment program. This study emphasizes the importance of a careful evaluation of the esophagus as a potential source of pain and clearly communicating this information to the patient.