Regional myocardial perfusion abnormalities on xenon-133 imaging in patients with angina pectoris and normal coronary arteries

Korhola, O; Valle, M; Frick, M. H.; Wiljasalo, M; Riihimäki, E

doi:10.1016/s0002-9149(77)80088-x

Cited by 36 publications

(8 citation statements)

References 23 publications

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“…[21][22][23][24] The exact etiopathogenesis of this syndrome X, however, remains unknown. Convincing evidence of abnormal hemoglobin-oxygen dissociation,29 hyperdynamic left ventricular contraction resulting in increased myocardial oxygen consumption,3o,31 abnormal pain perception,32 and increased sympathetic activity33 as a cause of angina is lacking.…”

Section: Discussionmentioning

confidence: 99%

Slow Coronary Flow: A Distinct Angiographic Subgroup in Syndrome X

Goel¹,

Gupta²,

Agarwal³

et al. 2001

Angiology

127

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Patients evaluated for chest pain with angiographically normal coronary arteries are usually labelled syndrome X. A portion of these patients may not have a cardiac cause for their symptoms. The authors aimed to study a subset within this group who showed the phenomenon of slow coronary flow (SCF) as evidenced by a slow antegrade progression of the dye on the coronary arteriogram to see if this could be used as a marker of myocardial ischemia. This observational study included 207 patients being evaluated for suspected coronary artery disease and found to have normal coronary angiograms. SCF was seen in 49 of these patients (23.7%) while the remaining 158 (76.3%) had normal coronary flow (NCF), as detected by the corrected thrombosis in myocardial infarction (TIMI) frame count method (TIMI frame count more than 2 SD of normal). Forty of the 49 patients (82%) in the SCF group had classical angina as compared with only 51 of the 158 patients (32%) in the NCF group (p<0.01). Also, a definitively positive exercise test was observed more commonly in the SCF group than in the NCF group (71% vs 42%, p < 0.01). The authors conclude that SCF patients constitute a definite subset within the wide spectrum of syndrome X and that the phenomenon of SCF could be used as a marker for myocardial ischemia.

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Section: Discussionmentioning

confidence: 99%

Slow Coronary Flow: A Distinct Angiographic Subgroup in Syndrome X

Goel¹,

Gupta²,

Agarwal³

et al. 2001

Angiology

127

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“…'0 However, others have found many such patients to have abnormal exercise electrocardiograms, 11-18, 23 abnormal lactate metabolism during infusion of isoproterenol or atrial pacing,'l 14, 17. 19-1, 23 [24][25][26] and abnormal left ventricular function in patients with chest pain and angiographically normal coronary arteries. '8 27.…”

mentioning

confidence: 99%

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

et al. 1985

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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,

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“…Despite the presence of both chest pain and an abnormal exercise test in all 9 patients, no myocardial perfusion abnormalities were observed in any patient. By contrast, Korhola et al (1977), using a semi-selective method of injecting xenon-133, reported that 50 per cent of their patients with normal coronary angiograms, positive exercise tolerance tests, and chest pain had perfusion abnormalities on resting myocardial scintigrams, with associated reduced flow rates in the region involved. They recorded very high flow rates at rest so that the 'underperfused' regions actually had flows in the normal range.…”

Section: Discussionmentioning

confidence: 98%

Regional myocardial blood flow in patients with chest pain syndromes and normal coronary arteriograms.

Green¹,

Cohn²,

Holman³

et al. 1978

Heart

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To evaluate possible disorders of regional myocardial blood flow in patients with chest pain syndromes and normal coronary arteriograms, we studied 21 patients with intracoronary injections of Xenon-133. Thirteen patients were restudied during an intervention: 6 patients received glyceryl trinitrate and 7 patients had contrast agent-induced hyperaemia. Patients were divided into 3 clinical groups: 7 patients had classic angina, 7 patients had a mixture of typical and atypical chest pain, and 7 patients had entirely atypical pain. A wide range of normal values for regional myocardial blood flow at rest was noted (41 to 128 ml/min per 100 g, with an average regional myocardial blood flow of 77 ml/min per 100 g ± 7 (mean ± SEM)). There were no significant differences between the 3 groups.With contrast hyperaemia, regional myocardial blood flow increased 164 per cent, while with glyceryl trinitrate, it decreased 31 per cent. Again, there was no statistical difference among the groups. Regional abnormalities offlow (> 15% difference between distal quadrants) were noted in 3 of 34 measurements. Two patients had heterogeneity of flow at rest by quadrant analysis but no focal perfusion abnormalities detected by functional imaging. Interestingly, both patients had positive exercise tests. Another patient had regional differences only during contrast-induced hyperaemia. Our findings suggest that most patients with chest pain syndromes and normal coronary arteriograms-even those with classic angina-do not have significant measurable myocardial perfusion abnormalities.The pathophysiology of angina pectoris is usually related to myocardial ischaemia secondary to significant luminal obstruction of the proximal coronary arteries (Zoll et al., 1951). Occasionally, however, patients will present with the typical or quasi-typical symptoms of angina, yet have entirely normal coronary arteriograms and no other recognised cause of myocardial ischaemia (valvular heart disease, hypertension, arteritides, etc.). Some patients with typical (and even atypical) angina may also have evidence of abnormal myocardial function compatible with ischaemia-such as myocardial lactate production with stress (Arbogast and Bourassa, 1972;Boudoulas et al., 1974) and electrocardiographic ST segment depression on exercise testing (Dwyer et al., 1969;Kemp et al., 1973)-others show abnormal left ventricular performance-such as a rise in left 'Supported by USPHS Grants.

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Regional myocardial perfusion abnormalities on xenon-133 imaging in patients with angina pectoris and normal coronary arteries

Cited by 36 publications

References 23 publications

Slow Coronary Flow: A Distinct Angiographic Subgroup in Syndrome X

Slow Coronary Flow: A Distinct Angiographic Subgroup in Syndrome X

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

Regional myocardial blood flow in patients with chest pain syndromes and normal coronary arteriograms.

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