Comparison of morphologic findings obtained by optical coherence tomography in acute coronary syndrome caused by vasospasm and chronic stable variant angina
Abstract:This study used optical coherence tomography (OCT) to evaluate morphologic changes in vasospastic lesions, which can cause acute coronary syndrome (ACS) or chronic stable VA. Thirty-nine patients (52.4 ± 9.0 years, 33 males) with vasospasm-induced ACS who presented with chest pain and displayed transient ST segment elevation on electrocardiography were included in the ACS group. Forty-one patients (49.3 ± 7.7 years, 33 males) who presented with chronic stable variant angina were included in the VA group. The c… Show more
“…Moreover, the OCT data supported the CAS findings; this indicates that focal CS was associated with a thicker intima-media layer with a lipid-rich plaque. Our findings are consistent with our previous IVUS report [11] or the findings of other previous reports [7,[28][29][30]. Focal CS is caused by local hyperreactivity to a generalized constrictor stimulus in mild atherosclerosis [25].…”
These results indicate that the presence of atherosclerotic plaques at the spasm site is likely to be related to the occurrence of a focal vasospasm. This may support the difference of features between focal CS and diffuse CS and contribute to precise treatment for each spasm type.
“…Moreover, the OCT data supported the CAS findings; this indicates that focal CS was associated with a thicker intima-media layer with a lipid-rich plaque. Our findings are consistent with our previous IVUS report [11] or the findings of other previous reports [7,[28][29][30]. Focal CS is caused by local hyperreactivity to a generalized constrictor stimulus in mild atherosclerosis [25].…”
These results indicate that the presence of atherosclerotic plaques at the spasm site is likely to be related to the occurrence of a focal vasospasm. This may support the difference of features between focal CS and diffuse CS and contribute to precise treatment for each spasm type.
“…[ 26 , 27 ] Recently, some investigators found intimal erosion and lumen irregularities on optical coherence tomography in patients with CV and acute coronary syndromes. [ 28 , 29 ] Therefore, another form of atherosclerosis has been suggested in spastic arteries. [ 30 ] The structural changes in the epicardial coronary arteries can be visualized using intracoronary imaging techniques; however, microvascular changes can be assessed indirectly such as with hyperemic microvascular resistance.…”
Rationale:Although transient reduction in the left ventricular ejection fraction is characteristic of Takotsubo cardiomyopathy, little is known about the time-course changes of myocardial deformation in coronary vasospasm-related Takotsubo cardiomyopathy.Patient concerns:We retrospectively analyzed the time-course changes in left ventricle, right ventricle, and left atrium strain values in a patient with coronary vasospasm-related Takotsubo cardiomyopathy. We found that not only left ventricular strain but also left atrial strain was abnormal during acute Takotsubo cardiomyopathy due to coronary vasospasm. Right ventricular free wall strain was normal.Diagnoses:Coronary vasospasm-related Takotsubo cardiomyopathy.Interventions:A serial echocardiographic study.Outcomes:The left ventricular strain was still subnormal despite a normalized left ventricular ejection fraction 2 months later. The left atrial strain was normal when the left ventricular ejection fraction normalized.Lessons:From this limited experience, it is suggested that echocardiographic myocardial deformation analysis can provide more information than the standard ejection fraction in evaluating myocardial contractile function.
“…It is possible that coronary a peripheral thrombus or the plaque composition causes occlusion, myocardial microcirculation disorders, cardiac syncope, and ischemia-reperfusion injury (e.g., freedom injury, vascular endothelial tissue injury, inflammatory cell infiltration, and myocardial edema) [ 23 , 24 ]. With the development of coronary and myocardial perfusion and coronary morphology evaluation tools, an increasing number of studies show that micro-thrombi (15 ~ 100μm) caused by unstable plaque ruptures in the intervention process play a very important role in the mechanism of myocardial reperfusion [ 25 , 26 ].…”
ObjectiveTo study the mechanism of the no-reflow phenomenon using coronary angiography (CAG) and intravascular ultrasound (IVUS).MethodsA total of 120 patients with acute myocardial infarction (AMI) who successfully underwent indwelling intracoronary stent placement by percutaneous coronary intervention (PCI). All patients underwent pre- and post-PCI CAG and pre-IVUS. No-reflow was defined as post-PCI thrombolysis in myocardial infarction (TIMI) grade 0, 1, or 2 flow in the absence of mechanical obstruction. Normal reflow was defined as TIMI grade 3 flow. The pre-operation reference vascular area, minimal luminal cross-sectional area, plaque cross-sectional area, lesion length, plaque volume and plaque traits were measured by IVUS.ResultsThe no-reflow group was observed in 14 cases (11.6%) and normal blood-flow group in 106 cases (89.4%) based on CAG results. There was no statistically significant difference in the patients’ medical history, reference vascular area (no-flow vs. normal-flow; 15.5 ± 3.2 vs. 16.2 ± 3.3, p> 0.05) and lesion length (21.9 ± 5.1 vs. 19.5 ± 4.8, p> 0.05) between the two groups. No-reflow patients had a longer symptom onset to reperfusion time compared to normal blood-flow group [(6.6 ± 3.1) h vs (4.3 ± 2.7) h; p< 0.05] and higher incidence of TIMI flow grade< 3 (71.4% vs 49.0%, p< 0.05). By IVUS examination, the no-reflow group had a significantly increased coronary plaque area and plaque volume compared to normal blood-flow group [(13.7 ± 3.0) mm2 vs (10.2 ± 2.9) mm2; (285.4 ± 99.8) mm3 vs (189.7 ± 86.4) mm3; p< 0.01]. The presence of IVUS-detected soft plaque (57.1% vs. 24.0%, p< 0.01), eccentric plaque (64.2% vs. 33.7%, p< 0.05), plaque rupture (50.0% vs. 21.2%, p< 0.01), and thrombosis (42.8% vs. 15.3%) were significantly more common in no-reflow group.ConclusionThere was no obvious relationship between the coronary risk factors and no-reflow phenomenon. The symptom onset to reperfusion time, TIMI flow grade before stent deployment, plaque area, soft plaques, eccentric plaques, plaque rupture and thrombosis may be risk factors for the no-reflow phenomenon after PCI.
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