Latent plaque rupture in a patient undergoing stenting for acute coronary syndrome and diffuse coronary disease: A case report and review of literature

2006 ◽  
Vol 67 (2) ◽  
pp. 241-245 ◽  
Author(s):  
Tomomi Koizumi ◽  
Andrew M. Wilson ◽  
David A. Clark ◽  
Peter J. Fitzgerald
Keyword(s):  
Acute Coronary Syndrome ◽  
Case Report ◽  
Coronary Disease ◽  
Plaque Rupture ◽  
Review Of Literature ◽  
Coronary Syndrome

Cardiac cephalgia presenting as acute coronary syndrome: A case report and review of literature

2017 ◽  
Vol 14 (2) ◽  
pp. 119
Author(s):  
Biswajit Majumder ◽  
PritamKumar Chatterjee ◽  
KN Sudeep ◽  
Sandip Ghosh
Keyword(s):  
Acute Coronary Syndrome ◽  
Case Report ◽  
Review Of Literature ◽  
Coronary Syndrome ◽  
Cardiac Cephalgia

scholarly journals Acute Coronary Syndrome (ACS) in Polycythemia Vera: A Case Report with Review of Literature

CARDIAC ◽  
2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Abhishek Shah ◽  
Charan Reddy KV ◽  
Abhay Bhave ◽  
Prakash Sanzgiri
Keyword(s):  
Acute Coronary Syndrome ◽  
Case Report ◽  
Polycythemia Vera ◽  
Review Of Literature ◽  
Coronary Syndrome

scholarly journals Abolishment of high-risk left lateral accessory pathway by myocardial infarction: a blessing in disguise? A case report

2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Jim O’Brien ◽  
Nikola Kozhuharov ◽  
Shui Hao Chin ◽  
Mark Hall
Keyword(s):  
Atrial Fibrillation ◽  
Acute Coronary Syndrome ◽  
Case Report ◽  
High Risk ◽  
Coronary Sinus ◽  
Refractory Period ◽  
Accessory Pathway ◽  
Coronary Syndrome ◽  
Electrophysiology Study ◽  
Anomalous Coronary

Abstract Background Antegradely conducting left lateral accessory pathways are a risk for supraventricular tachycardias and pre-excited atrial fibrillation. Rarely, an anomalous coronary sinus can cause difficulty in locating the pathway. The left circumflex coronary artery and obtuse marginal branches supply the posterolateral left ventricle. We describe a case report of a high-risk accessory pathway associated with an anomalous coronary sinus which, between successive electrophysiology studies, was obliterated by a felicitous acute coronary syndrome in the left circumflex territory. Case summary A 49-year-old male with palpitations and manifest pre-excitation was referred for electrophysiology study. Initial study revealed a high-risk left lateral accessory pathway with antegrade effective refractory period of 240 ms and rapidly conducting pre-excited atrial fibrillation. The coronary sinus could not be cannulated to localize the pathway. Coronary angiography and cardiac computed tomography showed an anomalous coronary sinus emptying into the right atrial free wall and patent coronaries. While awaiting repeat electrophysiology study, the patient suffered an acute coronary syndrome with immediate loss of previously visible pre-excitation on electrocardiogram, and underwent stenting of an occluded marginal branch of the circumflex. Repeat electrophysiology study demonstrated a now low-risk accessory pathway (effective refractory period 390 ms). Since infarction, the patient’s palpitations have fully settled with all subsequent electrocardiograms devoid of manifest pre-excitation. Discussion Left lateral accessory pathways, which can associate with an anomalous coronary sinus, derive from tissue similar to normal ventricular myocardium and are vulnerable to ischaemic insults in the area subtended by the circumflex artery.

Macrophage infiltrates in coronary plaque erosion portend a worse cardiovascular outcome in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R.A Montone ◽  
V Vetrugno ◽  
M Camilli ◽  
M Russo ◽  
M.G Del Buono ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Vulnerable Plaque ◽  
Cardiac Death ◽  
Cox Regression ◽  
Plaque Rupture ◽  
Culprit Lesion ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Plaque Erosion

Abstract Background Plaque erosion (PE) is responsible for at least one-third of acute coronary syndrome (ACS). Inflammatory activation is considered a key mechanism of plaque instability in patients with plaque rupture through the release of metalloproteinases and the inhibition of collagen synthesis that in turns lead to fibrous cap degradation. However, the clinical relevance of macrophage infiltration has never been investigated in patients with PE. Purpose In our study, we aimed at assessing the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) at the culprit site in ACS patients with PE, evaluating their clinical and OCT correlates, along with their prognostic value. Methods ACS patients undergoing OCT imaging and presenting PE as culprit lesion were retrospectively selected. Presence of MØI at culprit site and in non-culprit segments along the culprit vessel was assessed. The incidence of major adverse cardiac events (MACEs), defined as the composite of cardiac death, recurrent myocardial infarction and target vessel revascularization (TVR), was assessed [follow-up median (interquartile range, IQR) time 2.5 (2.03–2.58) years]. Results We included 153 patients [median age (IQR) 64 (53–75) years, 99 (64.7%) males]. Fifty-one (33.3%) patients presented PE with MØI and 102 (66.7%) PE without MØI. Patients having PE with MØI compared with PE patients without MØI had more vulnerable plaque features both at culprit site and at non-culprit segments. In particular, culprit lesion analysis demonstrated that patients with PE with MØI had a significantly thinner fibrous cap [median (IQR) 100 (60–120) μm vs. 160 (95–190) μm, p<0.001], higher prevalence of thrombus [41 (80.4%) vs. 64 (62.7%), p=0.028], lipid plaque [39 (76.5%) vs. 50 (49.0%), p<0.001], TCFA [20 (39.2%) vs. 14 (13.7%), p=0.001], and a higher maximum lipid arc [median [IQR] 250.0° (177.5°-290.0°) vs. 190.0° (150.0°-260.0°), p=0.018) at the culprit lesion compared with PE without MØI. MACEs were significantly more frequent in PE with MØI patients compared with PE without MØI [11 (21.6%) vs. 6 (5.9%), p=0.008], mainly driven by a higher risk of cardiac death and TVR. At multivariable Cox regression model, PE with MØI [HR=2.95, 95% CI (1.09–8.02), p=0.034] was an independent predictor of MACEs. Conclusion Our study demonstrates that among ACS patients with PE the presence of MØI at culprit lesion is associated with a more aggressive phenotype of coronary atherosclerosis with more vulnerable plaque features, along with a worse prognosis at a long-term follow-up. These findings are of the utmost importance in the era of precision medicine because clearly show that macrophage infiltrates may identify patients with a higher cardiovascular risk requiring more aggressive secondary prevention therapies and a closer clinical follow-up. Prognosis Funding Acknowledgement Type of funding source: None

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