scholarly journals ST-segment elevation myocardial infarction in a patient with anomalous origin of left circumflex coronary artery

2015 ◽  
Vol 11 (4) ◽  
pp. 120-123 ◽  
Author(s):  
Masahiro Yamamoto ◽  
Kenichi Tsujita ◽  
Kenshi Yamanaga ◽  
Naohiro Komura ◽  
Kenji Sakamoto ◽  
...  
2017 ◽  
Vol 44 (5) ◽  
pp. 320-325 ◽  
Author(s):  
Diab Ghanim ◽  
Fabio Kusniec ◽  
Wadi Kinany ◽  
Dahud Qarawani ◽  
David Meerkin ◽  
...  

The prevalence of the left circumflex coronary artery (LCx) as the culprit vessel in ST-segment-elevation myocardial infarction (STEMI) is reportedly lowest among that of the 3 main epicardial arteries, and has not been described for non-STEMI (NSTEMI) and stable angina pectoris. We sought to define the distribution of culprit arteries in these clinical presentations and suggest mechanisms for the differences. We reviewed 189 coronary angiograms of patients with STEMI, 203 with NSTEMI, and 548 with stable angina (n=940), and compared distributions of stenotic and culprit coronary arteries (lesions prompting intervention). Obstructive coronary lesions (≥50% narrowing) were more prevalent in the left anterior descending coronary artery (LAD) (36%–38%) and similar in the LCx and right coronary artery (RCA) (27%–29%), regardless of clinical presentation (P <0.01). In NSTEMI and stable angina, culprit vessels and total obstructive disease had the same distribution. In STEMI, however, a culprit LCx was significantly less prevalent (17%) than was total obstructive disease (27%; P <0.01), or a culprit LAD (47%) or RCA (34%) (both P <0.001). In our computed tomographic angiographic model of coronary longitudinal strain (percentage of shortening), LCx strain was only 1.5% ± 2.4%, versus 9.5% ± 2.9% for LAD strain and 10.1% ± 3.9% for RCA strain. In STEMI, LCx plaques seem less prone to rupturing. Culprit and total disease distributions are similar in NSTEMI and angina, suggesting a different ischemic pathophysiology in these presentations. Lower LCx longitudinal strain might contribute to reduced plaque rupture in STEMI.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Ilias Nikolakopoulos ◽  
Bernardo B. C. Lopes ◽  
Evangelia Vemmou ◽  
Judit Karacsonyi ◽  
João Cavalcante ◽  
...  

2013 ◽  
Author(s):  
R Scott Wright ◽  
Joseph G Murphy

Patients with coronary artery disease (CAD) present clinically when their disease enters an unstable phase known as an acute coronary syndrome (ACS), in which the cap of a previously stable atheromatous coronary plaque ruptures or erodes, which in turn activates a thrombotic cascade that may lead to coronary artery occlusion, myocardial infarction (MI), cardiogenic shock, and patient death. There are nearly 2 million episodes of ACS in the United States annually; it is the most common reason for hospitalization with CAD and is the leading cause of death in the developed world. ACS patients include those with unstable angina (UA), non–ST segment elevation myocardial infarction (non-STEMI), and ST segment elevation myocardial infarction (STEMI) and patients who die suddenly of an arrhythmia precipitated by coronary occlusion. The distinction among various ACS subgroups reflects varying characteristics of clinical presentation (presence or absence of elevated cardiac biomarkers) and the type of electrocardiographic (ECG) changes manifested on the initial ECG at the time of hospitalization. This chapter focuses on UA and non-STEMI. A graph outlines mortality risks faced by patients with varying degrees of renal insufficiency. An algorithm describes the suggested management of patients admitted with UA or non-STEMI. Tables describe the risk stratification of the patient with chest pain, categories of Killip class, examination findings of a patient with high-risk ACS, diagnosis of MI, causes of troponin elevation other than ischemic heart disease, initial risk stratification of ACS patients, and long-term medical therapies and goals in ACS patients. This review contains 2 highly rendered figures, 11 tables, and 76 references.


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