Letters to the Editor

Acute plaque rupture and myocardial stunning in patient with normal coronary arteriography

Acute ST-elevation myocardial infarction in patients with normal coronary arteries has previously been described, but coronary angiography in these patients was performed after the acute phase of the infarction. It is possible that these patients did not have normal angiograms during the acute phase (transient coronary thrombosis or spasm were usually suspected to be the cause). Information on the prevalence of truly normal coronary angiograms during the acute phase of a suspected ST-elevation myocardial infarction is lacking.

The PRimary Angioplasty in patients transferred from General community hospitals to specialized PTCA Units with or without Emergency thrombolysis-1 (PRAGUE-1) and PRAGUE-2 studies enrolled 1150 patients with ST-elevation acute myocardial infarction, in whom 625 coronary angiograms were performed within 2 h of the initial electrocardiogram. A simultaneous registry included an additional 379 coronary angiograms performed during the ST-elevation phase of a suspected myocardial infarction. Thus, a total of 1004 angiograms were retrospectively analyzed. A normal coronary angiogram was defined as one with the absence of any visible angiographic signs of atherosclerosis, thrombosis or spontaneous spasm.

Normal coronary angiograms were obtained for 26 patients (2.6%). Among these, the diagnosis at discharge was a small myocardial infarction in seven patients (0.7%), acute (peri)myocarditis in five patients, dilated cardiomyopathy in four patients, hypertension with left ventricular hypertrophy in three patients, pulmonary embolism in two patients and misinterpretation of the electrocardiogram (ie, no cardiac disease) in five patients. Seven patients with small infarctions underwent angiography within 30 min to 90 min of complete relief of the signs of acute ischemia, and thus, angiograms during pain were not taken. None of the 898 patients catheterized during ongoing symptoms of ischemia had a normal coronary angiogram. Spontaneous coronary spasm as the only cause (without underlying coronary atherosclerosis) for the evolving infarction was not seen among these 898 patients. Thus, the causes of the seven small infarcts in patients with normal angiograms remain uncertain.

The observed prevalence of normal coronary angiography in patients presenting with acute chest pain and ST elevations was 2.6%. Most of these cases were misdiagnoses, not infarctions. A normal angiogram during a biochemically confirmed infarction is extremely rare (0.7%) and was not seen during the ongoing symptoms of ischemia.

On a déjà décrit des infarctus du myocarde avec surélévation du segment ST chez des patients aux artères coronaires saines, mais la coronarographie avait été effectuée après la phase aiguë de l’infarctus. Est-il possible que la coronarographie n’ait pas été normale pendant la phase aiguë (on présumait généralement une thrombose coronaire transitoire ou des spasmes). On ne possède pas d’information sur la prévalence d’une coronarographie vraiment normale pendant la phase aiguë d’une présomption d’infarctus du myocarde avec surélévation du segment ST.

Dans le cadre des études PRAGUE-1 et PRAGUE-2 sur l’angioplastie primaire de patients transférés d’un hôpital général à une unité spécialisée de coronaropathie percutanée transluminale, on a enrôlé 1 150 patients ayant un infarctus aigu du myocarde avec surélévation du segment ST, chez qui 625 coronarographies ont été effectuées dans les deux heures suivant le premier électrocardiogramme. Un registre simultané contenait 379 autres coronarographies exécutées pendant la phase de surélévation du segment ST d’une présomption d’infarctus du myocarde. Ainsi, au total, 1 004 coronarographies ont fait l’objet d’une analyse rétrospective. Une coronarographie normale était définie comme un examen ne comportant aucun signe angiographique visible d’artériosclérose, de thrombose ou de spasme spontané.

On a obtenu des coronarographies normales auprès de 26 patients (2,6%). De ce nombre, à leur congé, sept patients avaient un diagnostic de petit infarctus du myocarde (0,7%) au congé, cinq patients, une (péri)myocardite, quatre patients, une myocardiopathie dilatée, trois patients, une hypertension accompagnée d’une hypertrophie ventriculaire gauche, deux patients, une embolie pulmonaire et cinq patients, une mauvaise interprétation de l’électrocardiogramme (c’est-à-dire, pas de maladie cardiaque). Les sept patients ayant un petit infarctus ont subi une angiographie de 30 à 90 minutes après le soulagement complet des signes d’ischémie aiguë, et non pendant la douleur. Aucun des 898 patients ayant subi un cathétérisme pendant des symptômes d’ischémie ne présentait de coronarographie normale. Chez ces 898 patients, on n’a observé aucun cas de spasme coronaire spontané (sans artériosclérose coronarienne sousjacente) expliquant l’infarctus en évolution. Ainsi, les causes des petits infarctus chez les sept patients ayant une angiographie normale ne sont pas claires.

On a observé une prévalence de 2,6% de coronarographies normales chez les patients ayant des douleurs thoraciques aiguës et une surélévation du segment ST. La plupart de ces cas étaient des mauvais diagnostics et non des infarctus. Il est extrêmement rare de constater une coronarographie normale pendant un infarctus confirmé biologiquement (0,7%), et on n’en a pas observé pendant les symptômes continus d’ischémie.

Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features—arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve—, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism.

OBJECTIVES

This study was designed to identify potential differences between the intravascular ultrasound (IVUS) characteristics of spontaneously ruptured and nonruptured coronary plaques.

BACKGROUND

The identification of vulnerable plaques in vivo may allow targeted prevention of acute coronary events and more effective evaluation of novel therapeutic approaches.

METHODS

Intravascular ultrasound was used to identify 29 ruptured plaques in arteries containing another nonruptured plaque in an adjacent segment. Intravascular ultrasound characteristics of these plaques were compared with plaques of computer-matched controls without evidence of plaque rupture. Plaque distribution was assessed by measuring the eccentricity of lumen location (inside the total vessel). Lumen cross-sectional area narrowing was calculated as [1 − (target/reference lumen area)] × 100%. A remodeling index was calculated as lesion/reference arterial area (>1.05 = compensatory enlargement, <0.95 = shrinkage).

RESULTS

Among the three groups of plaques, there was no significant difference in quantitative angiographic parameters, IVUS reference dimensions and IVUS lumen cross-sectional area narrowing. There was a difference in plaque distribution; lumen location by IVUS was significantly more eccentric in ruptured than in nonruptured (p = 0.002) and control plaques (p < 0.0001). The arc of disease-free vessel wall was larger in ruptured than in control plaques (p < 0.0001). The remodeling pattern of ruptured and nonruptured plaques differed significantly from that of the control plaques (p = 0.0001 and 0.003); compensatory enlargement was found in 66%, 48%, and 17%, whereas shrinkage was found in 7%, 10% and 48%, respectively.

CONCLUSIONS

Intravascular ultrasound assessment of plaque distribution and vascular remodeling may help to classify plaques with the highest probability of spontaneous rupture.

Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction; however, in milder forms it may result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. The present report summarizes the available morphologic evidence for coronary microembolization in patients who died of coronary artery disease, especially sudden death. The report then goes on to address the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes and heart failure. Finally, the report presents the available clinical evidence for coronary microembolization, highlights its key features-arrhythmias, contractile dysfunction, infarctlets and reduced coronary reserve-and addresses prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism. Copyright © 2001 by W.B. Saunders Company

Progress in Cardiovascular Diseases, Vol. 44, No. 3, (November/December) 2001: pp 217-230