Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve.

Abstract

Thirty-three patients with chest pain despite angiographically normal coronary arteries underwent both coronary flow studies during pacing and resting and exercise gated blood pool scintigraphy. During atrial pacing after administration of ergonovine, those patients developing their typical chest pain demonstrated significantly lower great cardiac vein flow (97 ± 31 vs 150 + 33 ml/ min, p < .001), higher coronary resistance (1.27 -+-0.43 vs 0.77 ± 0.18 mm Hg/ml/min, p < .005), and less lactate consumption (30.5 ± 22.0 vs 69.7 + 41.1 mM * ml/min, p < .005) and a higher left ventricular end-diastolic pressure after pacing (20 + 4 vs 12 ± 1, p < .001) compared with those without pain and in the absence of significant luminal narrowing of the epicardial coronary arteries. The 26 patients with abnormal vasodilator reserve demonstrated reduced left ventricular ejection fraction during exercise (58 ± 8%) compared with the seveni patients with appropriate vasodilator reserve (66 ± 4%, p < .05) and with a group of 52 control patients of similar age and sex distribution and free of known heart disease (66 ± 10%, p < .001). In addition, 12 of the 26 patients with abnormal vasodilator reserve demonstrated exercise-induced regional wall motion abnormalities. Many of these patients also manifested impaired left ventricular diastolic filling at rest compared with the control subjects (peak filling rate 2.6 + 0.7 vs 3.2 -+ 0.7 end-diastolic volume/sec, p < .005). Thus, patients with chest pain resulting from abnormal vasodilator reserve demonstrate abnormalities of left ventricular systolic and diastolic function suggestive of myocardial ischemia. Circulation 71, No. 2, 218-226, 1985. MUCH DEBATE has focused on whether or not patients with chest pain despite normal epicardial coronary arteries truly experience myocardial ischemia. I6 Several investigators have found that many of these patients clearly have a noncardiac cause of their pain, including esophageal,7 8 chest wall,9 and psychosomatic causes.'0 However, others have found many such patients to have abnormal exercise electrocardiograms, 11-18,

Acute effects of nitrates on exercise testing in patients with syndrome X. Clinical and pathophysiological implications.

“…[11][12][13] Our data show that in patients with effort angina and exercise-induced ischemic ST-segment depression, the response to sublingual nitrates of exercise testing can be useful to predict the presence or the absence of obstructive coronary lesions. Indeed, in our study groups There are several possible explanations for the negative effects of nitrates in patients with syndrome X.…”

Thallium-201 stress imaging in hypertensive patients.

“…37 Some of these patients have been shown to have true myocardial ischemia, as judged by myocardial lactate production during pacing-induced stress. 38 In summary, this study indicates that in a mixed population of patients referred for thallium-201 exercise testing, those with a low likelihood of coronary artery disease and hypertension were more likely to have abnormal thallium-201 test results than were their normotensive counterparts. The diagnostic accuracy of routine exercise treadmill exercise testing has been shown to be enhanced when performed in conjunction with radionuclide studies.…”

Airway hyperresponsiveness in patients with microvascular angina. Evidence for a diffuse disorder of smooth muscle responsiveness.

“…[3][4][5][6]8 Because these studies have been performed in patients with angiographically normal appearing coronary arteries and because the coronary vasoconstrictor response to ergonovine involves arterial segments too small to be reliably imaged angiographically, we have termed this syndrome "microvascular angina. "8 Because the coronary vasoconstrictor response to ergonovine during pacing stress is one of the hallmarks of this disorder of coronary flow, we prospectively used this coronary hemodynamic response to separate patients with microvascular angina from those in whom no flow abnormality could be demonstrated.…”

“…The protocol for this study has been described by us previously. [3][4][5][6]8 Briefly, after basal measurements of flow, rapid atrial pacing was performed to a heart rate of 150 beats/ min for 4 minutes in all patients and followed by measurements of great cardiac vein flow and computation of coronary resistance (mean systemic blood pressure divided by flow). After abrupt termination of pacing, ergonovine 0.15 mg was administered intravenously over 2 minutes, with resumption of pacing 2 minutes later at a rate of 150 beats/min for an additional 4 minutes with repeat great cardiac vein flow measurement and coronary resistance computation.…”

“…(Circulation 1990;82:2011-2017 Approximately 10-30% of patients with anginalike chest pain exhibit no large vessel coronary artery disease at catheterization and have no other myocardial or valvular cause for the pain.1,2 We have found that many of these patients have a dynamic abnormality in coronary flow caused by increased coronary resistance of vessels too small to be imaged angiographically and have applied the term "microvascular angina" to denote this syndrome. [3][4][5][6][7][8] Many patients with microvascular angina experience breathlessness during physical or emotional stress. However, the severity of myocardial ischemia during stress appears relatively mild and unlikely to explain this symptom.…”