Coronary artery spasm (CAS) has been postulated to be a pathophysiologic mechanism in the production of ischemic-like chest pain and ECG changes in patients with idiopathic mitral valve prolapse syndrome. To evaluate the possible role of symptomatic CAS evoked by ergonovine maleate, this agent was administered (0.05 to 0.4 mg IV) to 24 patients with chest pain and mitral valve prolapse who had no significant (less than 50%) coronary artery obstruction. Symptoms, ECG and blood pressure changes were monitored in all patients following ergonovine administration. No significant changes were observed in heart rate, systolic blood pressure, or double product. Six patients developed their typical chest pain. In two of these six with chest pain, ST segment shift greater than 1 mm were seen. Post-ergonovine left ventricular end-diastolic pressure (LVEDP) and coronary angiographic changes were also studied in subgroup of 12 of these patients, including five of the six chest pain responders. In the five chest pain responders, pain was associated with a significant rise in LVEDP, whereas no significant change occurred in those patients not experiencing chest pain (p less than 0.01). Chest pain was also associated with significant CAS (greater than 50% lumen reduction) in two patients, each with ST segment shifts greater than 1 mm. In summary, ergonovine stimulation failed to evoke symptoms, ECG or blood pressure changes in three quarters of mitral valve prolapse patients studied. Six patients developed chest pain. Chest pain was assoicated with ECG changes characteristic of CAS in two of these patients, each with angiographic CAS. Thus, symptomatic CAS induced by ergonovine was absent in the majority of these 24 patients with idiopathic mitral valve prolapse syndrome.
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http://dx.doi.org/10.1002/ccd.1810040308 | DOI Listing |
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