Severity of Coronary Arterial Stenoses Responsible for Acute Coronary Syndromes

doi:10.1016/j.amjcard.2008.12.047

The American Journal of Cardiology

Volume 103, Issue 9, 1 May 2009, Pages 1183-1188

https://doi.org/10.1016/j.amjcard.2008.12.047 Get rights and content

Acute myocardial infarctions were generally believed to result from plaque rupture and thrombosis at the site of a “mild to moderate” coronary stenosis. To assess the severity of coronary stenoses that predisposed to acute coronary syndrome, the 317 patients prospectively included were (1) 102 patients with acute ST-elevation myocardial infarction (STEMI) referred for primary percutaneous coronary intervention (PCI), (2) 135 patients with non-STEMI or unstable angina pectoris (UAP) referred for semiurgent PCI, and (3) 80 patients with stable angina pectoris (SAP) admitted for elective PCI. Patients with STEMI were included if thrombus aspiration could restore normal antegrade coronary blood flow. After aspiration (but before PCI), a high-quality angiogram was obtained and the reference diameter, minimal luminal diameter, and percentage of diameter stenosis of the culprit lesion were quantified. In patients with non-STEMI/UAP and SAP, aspiration was not performed. Average diameter of stenosis was similar in patients with STEMI and those with SAP (66 ± 12% vs 65 ± 10%, respectively; p = NS), but was slightly larger in patients with non-STEMI/UAP (71 ± 12%; p <0.05 vs both STEMI and SAP). In patients with STEMI, only 11% of culprit stenoses were found to have diameter stenosis <50% after removal of the thrombus. In conclusion, most STEMIs occurred at the site of severe coronary stenosis. Diameter stenosis severity was <50% in a minority of cases.

Section snippets

Methods

A total of 317 patients belonging to the 3 groups defined according to clinical presentation were included in this prospective study of (1) 102 consecutive patients with STEMI referred for primary PCI, (2) 135 patients with non-STEMI or unstable angina pectoris (UAP) referred for semiurgent PCI, and (3) 80 patients with stable angina pectoris (SAP) admitted for elective coronary angioplasty.

The STEMI group consisted of patients strictly meeting the 4 criteria of (1) onset of symptoms ≥30

Results

Main clinical characteristics of the 3 groups of patients are listed in Table 1. Patients presenting with STEMI were significantly younger and had less arterial hypertension compared with patients with non-STEMI/UAP or SAP. Although left ventricular ejection fraction of patients with STEMI was on average in the normal range, it was still significantly lower than in the 2 other groups of patients.

Main angiographic data for the 3 groups are listed in Table 2. Incidences of left anterior

Discussion

In this study, angiographic assessment of lesion severity was objectively quantified in patients with acute myocardial infarction after aspiration of the occlusive thrombus. Data suggested that STEMI predominantly occurred at sites with angiographic diameter stenosis >50%. Only approximately 10% of patients with STEMI had a culprit lesion with diameter stenosis <50% after aspiration of thrombus material. Similarly, in patients with non-STEMI/UAP, in whom aspiration was not performed, diameter

References (30)

W. Ganz et al.
Intravenous streptokinase in evolving acute myocardial infarction
Am J Cardiol
(1984)
M. Schweiger et al.
Comparison of patients with <60% to >60% diameter narrowing of the myocardial infarct-related artery after thrombolysis
Am J Cardiol
(1994)
S. Iskander et al.
Risk assessment using single-photon emission computed tomographic technetium-99m sestamibi imaging
J Am Coll Cardiol
(1998)
M. Hamilos et al.
Differential effects of drug eluting stents on local endothelium dependent coronary vasomotion
J Am Coll Cardiol
(2008)
J.A. Ambrose et al.
Angiographic progression of coronary artery disease and the development of myocardial infarction
J Am Coll Cardiol
(1988)
D. Hackett et al.
Coronary stenoses before and after myocardial infarction
Am J Cardiol
(1989)
D. Giroud et al.
Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis at prior angiography
Am J Cardiol
(1992)
A. Moise et al.
Clinical and angiographic predictors of new total coronary occlusion in coronary artery disease: analysis of 313 nonoperated patients
Am J Cardiol
(1984)
K. Fujii et al.
Intravascular ultrasound profile analysis of ruptured coronary plaques
Am J Cardiol
(2006)
G.A. Rodriguez-Granillo et al.
In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis
J Am Coll Cardiol
(2005)

E.L. Alderman et al.

Five-year angiographic follow-up of factors associated with progression of coronary artery disease in the Coronary Artery Surgery Study (CASS)CASS Participating Investigators and Staff

J Am Coll Cardiol

(1993)

N. Pijls et al.

Percutaneous coronary intervention of functionally nonsignificant stenosis: 5-year follow-up of the DEFER Study

J Am Coll Cardiol

(2007)

M. Takano et al.

Angioscopic follow-up study of coronary ruptured plaques in nonculprit lesions

J Am Coll Cardiol

(2005)

W. Wijns et al.

What does the clinical cardiologist need from noninvasive cardiac imaging: is it time to adjust practices to meet evolving demands?

J Nucl Cardiol

(2007)

D.G. Mathey et al.

Intracoronary streptokinase thrombolytic recanalization and subsequent surgical bypass of remaining atherosclerotic stenosis in acute myocardial infarction: complementary combined approach effecting reduced infarct size, preventing reinfarction, and improving left ventricular function

Am Heart J

(1981)

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Dynamic natural morphologies and component changes in nonculprit subclinical atherosclerosis in patients with acute coronary syndrome at 1-year follow-up and clinical significance at 3-year follow-up
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Beta-blocker use was also associated with LR in our analysis, but due to a lack of relevant supporting research, our interpretation of this result remains cautious; we look forward to the confirmation of this finding in future studies with larger samples. Previous studies have alerted us to the need to pay attention to nonculprit lesions in patients with ACS, since these lesions promote an incidence of MACEs similar to that of culprit lesions that were not treated by PCI in the previous 3 years [23,47–49]. Currently, most culprit lesions in ACS patients are treated with PCI, so MACEs caused by nonculprit lesions have received increased attention.
We aimed to explore the dynamic natural morphologies and main components of nonculprit subclinical atherosclerotic changes underlying lesion regression (LR) or lesion progression (LP) in patients with acute coronary syndrome.
The primary endpoints were changes in percent atheroma volume (ΔPAV), normalized total atheroma volume (ΔTAVn) and each component in nonculprit subclinical atherosclerosis from baseline to 1 year measured by optical flow ratio (OFR) software. LR or LP was defined by an increase or decrease in PAV. Secondary endpoints included the correlation between changes in the lipid profile and ΔPAV/ΔTAVn and major adverse cardiac events (MACEs) related to nonculprit subclinical atherosclerosis at 3 years.
This was a subgroup analysis of our previous randomized trial with a total of 161 nonculprit lesions analysed. In the LR (approximately 55.3% of the lesions) group, ΔTAVn was positively correlated only with lipid ΔTAVn (r = 0.482, p < 0.001) but not fibrous and calcium ΔTAVn, and ΔPAV was positively correlated with lipid ΔPAV (r = 0.315, p = 0.003) but not fibrous and calcium ΔPAV. The percent reduction in low-density lipoprotein cholesterol (LDL-C) was an independent predictor of LR in multivariate logistic regression analysis (OR = 3.574, 95% CI: 1.125–11.347, p = 0.031). The incidence of MACEs related to nonculprit lesions at 3 years was higher in the LP group than the LR group (9.9% vs. 2.2%, p = 0.040).
LR of nonculprit subclinical atherosclerosis at 1-year follow-up was mainly caused by regression of the lipid component, which was correlated with the degree of LDL-C reduction and fewer MACEs at 3-year follow-up.
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This study sought to appraise the predictive value of major adverse cardiovascular events (MACE) by combined plaque morphology and computational physiology.
A total of 604 patients with acute coronary syndrome who underwent OCT imaging in ≥1 nonculprit vessel during index coronary angiography were retrospectively enrolled. A novel morphologic index, named the lipid-to-cap ratio (LCR), and a functional parameter to evaluate the physiologic significance of coronary stenosis from OCT, namely, the optical flow ratio (OFR), were calculated from OCT, together with classical morphologic parameters, like thin-cap fibroatheroma (TCFA) and minimal lumen area.
The 2-year cumulative incidence of a composite of nonculprit vessel–related cardiac death, cardiac arrest, acute myocardial infarction, and ischemia-driven revascularization (NCV-MACE) at 2 years was 4.3%. Both LCR (area under the curve [AUC]: 0.826; 95% CI: 0.793-0.855) and OFR (AUC: 0.838; 95% CI: 0.806-0.866) were superior to minimal lumen area (AUC: 0.618; 95% CI: 0.578-0.657) in predicting NCV-MACE at 2 years. Patients with both an LCR of >0.33 and an OFR of ≤0.84 had significantly higher risk of NCV-MACE at 2 years than patients in whom at least 1 of these 2 parameters was normal (HR: 42.73; 95% CI: 12.80-142.60; P < 0.001). The combination of thin-cap fibroatheroma and OFR also identified patients at higher risk of future events (HR: 6.58; 95% CI: 2.83-15.33; P < 0.001).
The combination of LCR with OFR permits the identification of a subgroup of patients with 43-fold higher risk of recurrent cardiovascular events in the nonculprit vessels after acute coronary syndrome.
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Coronary artery disease (CAD) burden for society is expected to steeply increase over the next decade. Improved feasibility and efficiency of preventive strategies is necessary to flatten the curve. Acute myocardial infarction (AMI) is the main determinant of CAD-related mortality and morbidity, and predominantly occurs in individuals with more advanced stages of CAD causing subclinical myocardial ischemia (obstructive CAD; OCAD). Unfortunately, OCAD can remain subclinical until its destructive presentation with AMI or sudden death. Current primary preventive strategies are not designed to differentiate between non-OCAD and OCAD and the opportunity is missed to treat individuals with OCAD more aggressively.
EARLY-SYNERGY is a multicenter, randomized-controlled clinical trial in individuals with coronary artery calcium (CAC) presence to study (1.) the yield of cardiac magnetic resonance stress myocardial perfusion imaging (CMR-MPI) for early OCAD diagnosis and (2) whether early OCAD diagnosis improves outcomes. Individuals with CAC score ≥300 objectified in 2 population-based trials (ROBINSCA; ImaLife) are recruited for study participation. Eligible candidates are randomized 1:1 to cardiac magnetic resonance stress myocardial perfusion imaging (CMR-MPI) or no additional functional imaging. In the CMR-MPI arm, feedback on imaging results is provided to primary care provider and participant in case of guideline-based actionable findings. Participants are followed-up for clinical events, healthcare utilization and quality of life.
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The past decades have seen tremendous progress on elucidating mechanisms leading to acute coronary syndrome and sudden cardiac death. Pathology and imaging studies have identified features of coronary atherosclerosis that precede acute coronary events. However, many factors influence the risk of adverse events from coronary atherosclerotic disease and available data support our transition from focusing on individual “vulnerable plaque,” coronary arterial stenosis, and inducible myocardial ischemia to understanding coronary heart disease as multifactorial, chronic disease. The concept of the vulnerable patient has evolved, with the atheroma burden, its metabolic activity, and the disposition to vascular thrombosis building a platform for assessing central aspects of coronary heart disease. In turn, this model has directed us to a focus on controlling the activity of atherosclerotic disease and on modifying the susceptibility of vascular thrombosis which has led to reduced morbidity and mortality from coronary heart disease.
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It has been believed that most acute coronary events result from the rupture of mildly stenotic plaques, based on studies in which angiographic information was available from many months to years before the event. However, serial studies in which angiographic data were available from the past as also within 1 to 3 months of myocardial infarction have clarified that nonobstructive lesions progressively enlarged relatively rapidly before the acute event occurred. Noninvasive computed tomography angiography imaging data have confirmed that lesions that did not progress voluminously over time rarely led to events, regardless of the extent of luminal stenosis or baseline high-risk plaque morphology. Therefore, plaque progression could be proposed as a necessary step between early, uncomplicated atherosclerosis and plaque rupture. On the other hand, it has been convincingly demonstrated that intensive lipid-lowering therapy (to a low-density lipoprotein cholesterol level of <70 mg/dl) halts plaque progression. Given the current ability to noninvasively detect the presence of early atherosclerosis, the importance of plaque progression in the pathogenesis of myocardial infarction, and the efficacy of maximum lipid-lowering therapy, it has been suggested that plaque progression is a modifiable step in the evolution of atherosclerotic plaque. A personalized approach based on the detection of early atherosclerosis can trigger the necessary treatment to prevent plaque progression and hence plaque instability. Therefore, this approach can redefine the traditional paradigm of primary and secondary prevention based on population-derived risk estimates and can potentially improve long-term outcomes.

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Coronary artery diseaseSeverity of Coronary Arterial Stenoses Responsible for Acute Coronary Syndromes

Section snippets

Methods

Results

Discussion

Am J Cardiol

Am J Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Nucl Cardiol

Intracoronary streptokinase thrombolytic recanalization and subsequent surgical bypass of remaining atherosclerotic stenosis in acute myocardial infarction: complementary combined approach effecting reduced infarct size, preventing reinfarction, and improving left ventricular function

Am Heart J

Coronary artery disease
Severity of Coronary Arterial Stenoses Responsible for Acute Coronary Syndromes