Unstable Angina and Other Acute Coronary Syndromes

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.

2020 ◽  
Author(s):  
Fan-xin Kong ◽  
Meng Li ◽  
Chun-Yan Ma ◽  
Ping-ping Meng ◽  
Yong-huai Wang ◽  
...  

Abstract Background Loeffler’s endocarditis is an inflammatory cardiac condition of hypereosinophilic syndrome which rarely involves coronary artery. When coronary artery is involved, known as eosinophilic coronary periarteritis, the clinical presentation, electrocardiographic changes and troponin level are extremely nonspecific and may mimic acute coronary syndrome. It is very important to make differential diagnosis for ECPA in order to avoid the unnecessary further invasive coronary angiography. Case presentation We report a case with chest pain, ST-segment depression in electrocardiogram and increased troponin-I mimicking acute non-ST-segment elevation myocardial infarction. However, quick echocardiography showed endomyocardial thickening with normal regional wall motion, which corresponded to the characteristics of Loeffler’s endocarditis. Emergent blood analysis showed marked increase in eosinophils and computed tomography angiography found no significant stenosis of coronary artery. Manifestations of magnetic resonance imaging consisted with findings of echocardiography. Finally, the patient was diagnosed as Loeffler’s endocarditis and possible coronary spasm secondary to eosinophilic coronary periarteritis. Conclusion This case exhibits the crucial use of quick transthoracic echocardiography and the emergent hematological examination for differential diagnosis in such scenarios as often if electrocardiogram change mimicking myocardial infarction.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Tatsuo Haraki ◽  
Ryota Uemura ◽  
Shin-ichiro Masuda ◽  
Takeshi Lee

Spontaneous coronary artery dissection (SCAD) is a rare condition that may have a serious outcome because of acute coronary syndrome. The condition especially affects young women. We evaluated a middle-aged male patient with a non-ST segment elevation myocardial infarction caused by multivessel SCAD. The SCAD had occurred in the distal right coronary artery (RCA), the mid left anterior descending artery (LAD), and the distal LAD at the same time. His culprit lesion was in the distal RCA, but the SCAD had progressed more proximally within the RCA 12 days later with no clinical symptoms. We treated the mid LAD with implantation of a drug-eluting stent on admission and the SCAD had not progressed 12 days later. Moreover, the SCAD in the distal RCA and distal LAD healed spontaneously 12 days later. He had no recurrent attack, and all SCAD lesions of the RCA and LAD had completely healed 6 months later. Given that SCAD appears in various forms over the clinical course, a strategy of intervention needs careful consideration.


2021 ◽  
Vol 18 (3) ◽  
pp. 51-56
Author(s):  
Mădălina Badea ◽  
Ana-Maria Balahura ◽  
Daniela Bartoş

Abstract According to tradition, every year, at the Congress of the European Society of Cardiology new clinical guidelines, usefull for our daily pratice, are launched. This year a new guideline for the management of non-ST-segment elevation myocardial infarction (NSTEMI) was presented. Substantial resources had been invested to sustain the research efforts in order to improve the diagnosis and therapeutic tools for this disease. In this article we present the main differences between this guideline and the previous one, regarding the utility of the cardiac biomarkers, diagnosis and risk stratification algorithms, and last, but not least, medical and invasive treatment tools.


Angiology ◽  
2020 ◽  
pp. 000331972097923
Author(s):  
Mengqiu Wei ◽  
Hailin Pan ◽  
Kai Guo

Genome-wide association studies have shown that a disintegrin and metalloproteinase with thrombospondin motifs 9 (ADAMTS-9) is associated with the development of atherosclerosis. We assessed the level of ADAMTS-9 in patients with coronary artery disease (CAD) and its severity and prognosis. We selected 666 participants who underwent coronary angiography in our hospital and met the inclusion and exclusion criteria; participants included non-CAD patients, patients with stable angina pectoris (SAP), unstable angina, non-ST-segment elevation myocardial infarction, or ST-segment elevation myocardial infarction. The serum level of ADAMTS-9 was higher in patients with CAD than in non-CAD patients (37.53 ± 8.55 ng/mL vs 12.04 ± 7.02 ng/mL, P < .001) and was an independent predictor for CAD (odds ratio = 1.871, 95% CI: 1.533-2.283, P < .001). Subgroup analysis showed that compared with the SAP group, the acute coronary syndrome groups had higher serum levels of ADAMTS-9. In addition, the level of ADAMTS-9 was related to the SYNTAX score (r = 0.523, P < .001). Patients with acute myocardial infarction (AMI) with elevated levels of ADAMTS-9 had a higher risk of major adverse cardiovascular events (MACE) within 12 months than those with lower levels (log-rank = 4.490, P = .034). Plasma ADAMTS-9 levels may be useful for the diagnosis of CAD and as predictors of MACE in AMI patients.


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