Variant Angina of Prinzmetal with Normal Coronary Arteriograms

Cheng, Tsung O.; Bashour, Tali T.; Kelser, George A.; Weiss, Lowell; Bacos, James M.

doi:10.1161/01.cir.47.3.476

Cited by 213 publications

(52 citation statements)

References 10 publications

(1 reference statement)

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“…In about half of VA patients, coronary angiography shows normal coronary arteries (NCAs). 4,5 CSX, on the other hand, is characterized by angina occurring predominantly during effort, ST-segment depression suggesting subendocardial ischemia during exercise stress test and normal coronary arteries during angiography. Coronary microvascular dysfunction (CMVD) is believed to be responsible for angina in most of these patients.…”

Section: Introductionmentioning

confidence: 99%

Combination of Variant and Microvascular Angina

Infusino

Lanza

Sestito

et al. 2009

Clinical Cardiology

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Prinzmetal's variant angina (VA) and cardiac syndrome X (CSX) are two distinct, usually easily recognizable, forms of angina syndromes, caused by epicardial spasm, usually responsible for transient transmural myocardial ischemia at rest and by coronary microvascular dysfunction (CMVD), usually responsible for effort induced subendocardial ischemia, respectively. In this article we report clinical evidence in three patients of the simultaneous occurrence of angina episodes typical of both VA and CSX, suggesting that common pathogenetic factors may be responsible for clinical manifestations both of functional macrovascular and microvascular coronary artery abnormalities in some angina patients. Copyright © 2009 Wiley Periodicals, Inc.

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Section: Introductionmentioning

confidence: 99%

Combination of Variant and Microvascular Angina

Infusino

Lanza

Sestito

et al. 2009

Clinical Cardiology

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“…On the other hand, exercise-induced ST-segment elevation has been reported in patients with variant angina. [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] Most have no evidence of left ventricular dysfunction and some have no fixed coronary stenoses. 27 Finally, Bruce et al28 noted ST-segment elevation during exercise testing in 0.5% of asymptomatic, presumably healthy subjects.…”

mentioning

confidence: 99%

Clinical and angiographic correlates of exercise-induced ST-segment elevation. Increased detection with multiple ECG leads.

Waters¹,

Chaitman²,

Bourassa³

et al. 1980

Circulation

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SUMMARY ST-segment elevation was observed in 47 of 720 patients who underwent treadmill exercise testing using 14 ECG leads 1 day before coronary arteriography. This abnormality was detected in lead V. in only 13 of 47 patients (28%) and in lead CM5 in only nine of 47 patients (19%). In 36 patients previous myocardial infarction (27 anterior, nine inferior) was diagnosed on the resting ECG; in all cases the ST-segment elevation during exercise occurred in leads with Q waves. In 34 of 36 patients (94%) a corresponding left ventricular wall motion abnormality was present, usually (33 of 36, 92%) a dyskinetic or akinetic segment. All but two of the 36 patients had a coronary stenosis > 70% in the artery perfusing the involved region.Ten of the 11 patients with no ECG evidence of myocardial infarction had documented variant angina. In all 10 cases ST-segment elevation during exercise occurred in the same ECG leads as during spontaneous resting attacks. All 10 had normal left ventricular angiograms and only three had a coronary stenosis 2 70%. A large perfusion defect corresponding to the site of ST-segment elevation and not present at rest was detected in each of the six who had exercise thallium-201 scans. Four patients retested during treatment with nifedipine did not develop angina, ST changes or perfusion defects.These findings suggest that exercise-induced ST-segment elevation is probably caused directly by a segmental wall motion abnormality in patients with previous myocardial infarction, but by coronary artery spasm in patients with variant angina.THE CLINICAL SIGNIFICANCE of ST-segment depression during exercise testing is well understood.' In contrast, the mechanism for exercise-induced STsegment elevation, a more unusual finding, is controversial and the associated clinical and angiographic features vary widely from one study to another.2`9 Many authors2' 5-8 conclude that localized left ventricular dysfunction, which is present in nearly all of these patients,2 accounts for ST-segment elevation during exercise; however, others1 3, 4suggest that severe myocardial ischemia is the cause, because most patients also have critical coronary stenoses. On the other hand, exercise-induced ST-segment elevation has been reported in patients with variant angina. 10 At our institution 720 patients have undergone clinical evaluation and treadmill exercise testing with 14 ECG leads on the day before coronary and left ventricular angiography. The primary purpose of this study was to examine the clinical and angiographic features of the patients in this population who developed ST-segment elevation during exercise. In addition, we have compared the sensitivity of different ECG leads in detecting this abnormality. Methods Patient SelectionMaximal treadmill exercise tests using a 14-lead ECG system were performed on 720 consecutive patients 1 day before coronary and left ventricular angiography. Those with unstable angina, associated valvular, cardiomyopathic or congenital heart disease, overt heart failure or limiting ort...

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“…The development of coronary arteriography provided a clue to confirm that spasm was indeed an important, if not predominant, factor in variant angina. [2][3][4][5][6][7][8] Although aortocoronary bypass surgery has been widely accepted in the treatment of patients with coronary artery disease, its role is controversial in variant angina. A review of the literature9' 10 has shown poor results with coronary artery grafting: persistence of spontaneous pain in spite of patent grafts, high incidence of occlusion of the grafts or postoperative myocardial infarction.…”

Section: In 1959mentioning

confidence: 99%

Surgical treatment of variant angina: use of plexectomy with aortocoronary bypass.

Bertrand¹,

Lablanche²,

Rousseau³

et al. 1980

Circulation

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SUMMARY Aortocoronary bypass surgery, widely accepted in the treatment of patients with coronary artery disease, is controversial in the management of variant angina. Persistence of attacks, occlusion of the graft or postoperative infarction have been described and could be explained by a persistent spasm frequently observed in variant angina that might occlude the distal part of the grafted vessel.It has been suggested that plexectomy might be added to the aortocoronary graft procedure in order to prevent the spasm. Our study includes 35 patients with variant angina who had surgery. They were divided into two groups. Group 1 (n = 13) had aortocoronary bypass alone; the patients in group 2 had plexectomy in addition to the myocardial revascularization. The average follow-up period was 37 months in group 1 and 20 months in group 2. The results were assessed by clinical study, stress testing, control of patency of the grafts and provocative test with an ergot alkaloid (methergine).Despite the difficulties of evaluating the effects of the various treatments in these patients with a wide spontaneous variability of symptoms, these data suggest that a complete plexectomy associated with aortocoronary bypass gives better results (86%) than bypass alone (61%) in variant angina. The recurrence rate of attacks was lower (5%) when plexectomy was associated with bypass than with bypass alone (18%

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Variant Angina of Prinzmetal with Normal Coronary Arteriograms

Cited by 213 publications

References 10 publications

Combination of Variant and Microvascular Angina

Combination of Variant and Microvascular Angina

Clinical and angiographic correlates of exercise-induced ST-segment elevation. Increased detection with multiple ECG leads.

Surgical treatment of variant angina: use of plexectomy with aortocoronary bypass.

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