Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography.

Bertrand, Michel E.; Lablanche, Jean M.; Tilmant, Pierre Y.; Thieuleux, F.; Delforge, M R; Carré, A; Asseman, Philippe; Berzin, B; Libersa, C; Laurent, J.

doi:10.1161/01.cir.65.7.1299

Cited by 464 publications

(219 citation statements)

References 33 publications

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“…We suggest that ergonovine provocation testing is useful in identifying patients with DCM and coronary vasospasm, in whom atrial fibrillation is frequently associated and cardiac performance is improved by anti-vasospastic agents. Prevalence of provoked coronary vasospasm in patients with DCM: The prevalence of coronary vasospasm in patients with DCM reported by Bertrand, et al 10) is lower than that in our study (0% vs 33%). However, differences in coronary vasospastic responses after recent myocardial infarction in Japanese and Caucasian patients has been described by Pristipino,et al 11) They reported that the Continuous values are median (25th/75th percentile).…”

Section: Discussioncontrasting

confidence: 78%

Effects of Anti-vasospastic Agents in Japanese Patients with Dilated Cardiomyopathy and Coronary Vasospasm.

et al. 2002

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SUMMARYThe pathogenesis of dilated cardiomyopathy (DCM) is unknown, but clinical evidence suggests that coronary vasospasm is associated with the development of DCM in some cases. In the present study, we aimed to clarify the prevalence of coronary vasospasm in patients with DCM, the characteristics of patients with DCM and coronary vasospasm, and the effects of anti-vasospastic agents on patients with DCM and coronary vasospasm. This study included 18 consecutive patients with DCM who underwent cardiac catheterization with ergonovine provocation testing. The patient was diagnosed as having coronary vasospasm if ergonovine induced coronary vasoconstriction ≥75% diameter narrowing was observed compared to the diameter after nitroglycerin administration. Six (33%) patients were found to have coronary vasospasm and anti-vasospastic agents were added after the cardiac catheterization. The prevalence of atrial fibrillation in the patients with DCM and coronary vasospasm was greater than that in DCM without coronary vasospasm [67% vs 8% (P<0.05)]. The left ventricular end-diastolic dimension decreased from 61 mm (56/64) to 55 mm (53/56) (median, 25th/75th percentile, P<0.05) and the left ventricular ejection fraction increased from 36% (32/40) to 47% (46/48) (median, 25th/ 75th percentile, P<0.05) after the administration of anti-vasospastic agents and 4 of the 6 patients improved symptomatically. Therefore, ergonovine provocation testing is useful in identifying patients with DCM and coronary vasospasm, in whom cardiac performance is expected to be improved with anti-vasospastic agent therapy. DCM patients with atrial fibrillation may be a clue for identifying patients with coronary vasospasm. (Jpn Heart J 2002; 43: 333-342)

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Section: Discussioncontrasting

confidence: 78%

Effects of Anti-vasospastic Agents in Japanese Patients with Dilated Cardiomyopathy and Coronary Vasospasm.

et al. 2002

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“…Spasm was also provoked in 38% of a group with resting, mostly nocturnal, angina. 41 The most common ECG abnormality in this group was ST-segment elevation during angina, and almost half of the group had normal or nonsignificant coronary artery disease. Thus, the characteristic clinical entity of unstable angina was not specifically described in the study by Bertrand et al…”

Section: Discussionmentioning

confidence: 79%

Vasoreactivity of the culprit lesion in unstable angina.

et al. 1994

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BACKGROUND Although abnormal vasoconstriction may be involved in the pathogenesis of the acute coronary syndromes, the vasoreactivity of the lesion responsible for unstable angina (culprit lesion) has not been directly investigated. It is also unknown if enhanced vasoreactivity is found downstream to this lesion or extends to uninvolved coronary arteries. METHODS AND RESULTS We studied seven unstable angina patients whose condition had sufficiently stabilized to allow ergometric bicycle exercise and a cold pressor test to be performed as provocative stimuli during coronary arteriography. We measured the luminal diameter of the culprit lesion, a normal-appearing distal segment, and the segment of an uninvolved coronary artery using quantitative coronary angiography. Seven stable angina patients served as controls. Antianginal medications were tapered and interrupted. The culprit lesion constricted significantly with exercise and the cold pressor test compared with a stable angina control lesion. The culprit lesion measured 1.41 +/- 0.07 mm at baseline and diminished to 1.09 +/- 0.07 mm with exercise (P = .001). It measured 1.26 +/- 0.07 mm before the cold pressor test and diminished to 1.09 +/- 0.03 mm with this test (P = .015). In contrast, the profile of the stable lesion in the stable angina control group differed significantly (P = .006). Its luminal diameter measured 1.42 +/- 0.17 mm at baseline and 1.48 +/- 0.21 mm with exercise (P = NS). It measured 1.57 +/- 0.18 mm before and 1.55 +/- 0.18 mm with the cold pressor test (P = NS). There were no significant changes to these stimuli in the uninvolved coronary artery segments in unstable angina and in the distal segments in both unstable and stable angina patients. CONCLUSIONS This study demonstrates increased vasoreactivity of the culprit lesion in unstable angina compared with a control lesion in stable angina. The lack of an effect either in the uninvolved coronary artery or downstream to the culprit lesion suggests that systemic neurohumoral or seeding mechanisms are not operative. This abnormal vasoreactivity might predispose to, or be a marker for, the recurrence of acute ischemia at this site.

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“…The prevalence of VSA in a known coronary patient is probably underestimated. Bertrand et al [5] found a coronary spasm in 13.8% of patients with mixed angina, more often encountered in our practice, while Hamilton et al emphasized that in 1999, only six tests of ergonovine provocations were carried out for 1,240 coronary explorations [6]. Lanza et al reported a diagnosis delay of more than six months in more than 30% of the cases in 2007, in a prospective series of 202 patients with VSA, and concluded that its diagnosis was too frequently neglected with a risk of cardiac events [2].…”

Section: Discussionmentioning

confidence: 99%

Prinzmetal or Vasospastic Angina in a Young Woman: An Under-Diagnosed Pathology

Js¹,

Dioum²,

Mb³

et al. 2017

J Clin Exp Cardiolog

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Vasospastic angina is considered rare but its prevalence is probably underestimated, especially in the case of atheromatous coronary lesions. Its diagnosis remains important because of its poor prognosis and its therapeutic features. We report a clinical case illustrating the issue of vasospastic angina's diagnosis. Diagnostic ways such as coronary spasm challenge tests must be adapted to the evolution of the techniques and the use of coronary angiography nowadays, in particular the preferential use of the radial pathway especially in women with a smaller radial caliber compared to men. Clinical CaseWe report through this clinical observation the issue of the diagnosis of vasospastic angina or Prinzmetal's angina (VSA).Mrs. GV, 41 years old, had as a cardiovascular risk factor an active smoking at the rate of 15 packs-year and a family history of coronary heart disease. She was admitted to the emergency department for a stable angina evolving for three weeks with episodes at rest.Biology noted an elevation of ultra-sensitive troponins to 220 ng/l. The electrocardiogram was normal, echocardiography noted moderate hypokinesis of left ventricle contractility in apical anterior, apex and anterior territories.The coronary angiography performed by right radial artery access with a 5 french catheter concluded to intermediate coronary lesions at 50% in the distal part of the left main coronary artery (LMCA), encompassing the origin of the left circumflex artery (LCA) and left anterior descending artery or LAD (Classification Medina 1-0-0), and a lesion of 50% in the distal portion of the middle right coronary artery or RCA (Figures 1 and 2).The measurement of the coronary reserve by Fractional Flow Reserve [FFR] towards the three axes was respectively 0.82 to the LAD, 0.83 to the circumflex artery and 0.92 to the right coronary artery.Drug therapy including beta-blockers, aspirin, clopidogrel, statins and a nitroglycerin transdermal patch was initiated. The patient was advised on the need for good control of cardiovascular risk factors, specially smoking cessation.Three days later, she presented a new recurrence of identical chest pain that occurred at rest for 10 minutes, leading her back to the emergency room.At rest, the electrocardiogram showed electrical modifications like repolarization disorders of biphasic T-type in V1 and V2 precordial leads; getting normal on the following electrocardiograms. Troponins were increased to 327 ng/l.The control coronary angiography performed again by the right radial artery access without injection of vasodilator, did not find an evaluative lesion. The methylergometrine testing was positive with the reappearance of chest pain, T-wave negativity in V1 lead (Figure 3) and spastic occlusion of the proximal LAD (Figure 4), regressive after intra-coronary injection of 3 milligrams of isosorbide dinitrate (Figures 5 and 6).

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Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography.

Cited by 464 publications

References 33 publications

Effects of Anti-vasospastic Agents in Japanese Patients with Dilated Cardiomyopathy and Coronary Vasospasm.

Effects of Anti-vasospastic Agents in Japanese Patients with Dilated Cardiomyopathy and Coronary Vasospasm.

Vasoreactivity of the culprit lesion in unstable angina.

Prinzmetal or Vasospastic Angina in a Young Woman: An Under-Diagnosed Pathology

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