Updates on Acute Coronary Syndrome

Eisen, Alon; Giugliano, Robert P.; Braunwald, Eugene

doi:10.1001/jamacardio.2016.2049

Cited by 162 publications

(130 citation statements)

References 78 publications

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“…Significant progress in prevention of coronary artery disease (CAD) has led to a decrease in the incidence of myocardial infarction (MI) (1). However, recent reports highlight that the reduction in the rate of MI has not extended to young adults, and young women in particular continue to have worse cardiovascular outcomes than men (2,3).…”

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confidence: 99%

Cardiovascular Risk and Statin Eligibility of Young Adults After an MI

Singh

Collins

Gupta

et al. 2018

Journal of the American College of Cardiology

167

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BACKGROUND Despite significant progress in primary prevention, the rate of MI has not declined in young adults. OBJECTIVES The purpose of this study was to evaluate statin eligibility based on the 2013 American College of Cardiology/American Heart Association guidelines for treatment of blood cholesterol and 2016 U.S. Preventive Services Task Force recommendations for statin use in primary prevention in a cohort of adults who experienced a first-time myocardial infarction (MI) at a young age. METHODS The YOUNG-MI registry is a retrospective cohort from 2 large academic centers, which includes patients who experienced an MI at age ≤50 years. Diagnosis of type 1 MI was adjudicated by study physicians. Pooled cohort risk equations were used to estimate atherosclerotic cardiovascular disease risk score based on data available prior to MI or at the time of presentation. RESULTS Of 1,685 patients meeting inclusion criteria, 210 (12.5%) were on statin therapy prior to MI and were excluded. Among the remaining 1,475 individuals, the median age was 45 years, there were 294 (20%) women, and 846 (57%) had ST-segment elevation MI. At least 1 cardiovascular risk factor was present in 1,225 (83%) patients. The median 10-year atherosclerotic cardiovascular disease risk score of the cohort was 4.8% (interquartile range: 2.8% to 8.0%). Only 724 (49%) and 430 (29%) would have met criteria for statin eligibility per the 2013 American College of Cardiology/American Heart Association guidelines and 2016 U.S. Preventive Services Task Force recommendations, respectively. This finding was even more pronounced in women, in whom 184 (63%) were not eligible for statins by either guideline, compared with 549 (46%) men (p < 0.001). CONCLUSIONS The vast majority of adults who present with an MI at a young age would not have met current guideline-based treatment thresholds for statin therapy prior to their MI. These findings highlight the need for better risk assessment tools among young adults.

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mentioning

confidence: 99%

Cardiovascular Risk and Statin Eligibility of Young Adults After an MI

Singh

Collins

Gupta

et al. 2018

Journal of the American College of Cardiology

167

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“…Chest pain suggestive of ACS is a common cause of presentation with poor prognosis in the emergency department [1, 2]. Diagnosis based on 18-lead ECG and traditional cardiac necrosis biomarkers including troponin recognizes less than half of the patients with MI.…”

Section: Discussionmentioning

confidence: 99%

“…However, their utility in detecting patients with unstable angina but without typical ECG or enzyme changes is very limited. The development of coronary plaque is a major precipitating factor in the triggering of ACS [2]. The traditional biomarkers that reflect myocardial necrosis represent the severe and late stages of ACS and may not serve as indicators for all subtype patients with ACS in a clinical practice.…”

Section: Introductionmentioning

confidence: 99%

Association of Circulating IGFBP1 Level with the Severity of Coronary Artery Lesions in Patients with Unstable Angina

et al. 2017

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Aims. Local IGFBP1 level was reported to affect the development of coronary artery plaque. This study investigated the association of circulating IGFBP1 level with the severity of coronary artery lesions in patients with unstable angina. Materials and Methods. In 112 consecutive patients with clinically diagnosed unstable angina, admitted from July 2014 to July 2015, we studied the correlations of circulating IGFBP1 and the severity of coronary artery disease (CAD). Results. All patients underwent scheduled coronary angiography, and 67 cases were diagnosed with critical and 45 with noncritical CAD. Of the 67 critical CAD patients, 41 (61.19%) presented with multivessel and 26 (38.81%) with single-vessel lesions. IGFBP1 levels were higher in patients with multivessel than those with single-vessel lesions. Moreover, the IGFBP1 level was positively correlated with the GRACE score. Among clinical variables, the IGFBP1 level was correlated with HDL-C. IGFBP1 alone (cutoff 20.86 ng/ml) demonstrated a sensitivity of 0.448 and specificity of 0.933 in predicting CAD. Combination of IGFBP1 and HDL-C had a sensitivity of 0.821 and specificity of 0.800 in predicting CAD. Conclusions. Circulating IGFBP1 level positively correlated with the severity of CAD. IGFBP1, when combined with HDL-C, might be useful in screening for high risk CAD patients.

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“…Currently, combination therapy of antiplatelet agents (aspirin plus an inhibitor of P2Y12 receptor) or even triple therapy (based on antiplatelet drugs plus anticoagulant agents) may be considered because of high risk of thromboembolism in patient affected by arterial thrombosis (i.e patients affected by atrial fibrillation undergoing coronary stent implantation). In the last decade newer antiplatelet drugs have proven their efficacy in combination with aspirin in reducing major cardiovascular events in patients presenting with acute coronary syndrome [53,54].…”

Section: The Parmacological Modulation Of the Two Sides Of Thrombosismentioning

confidence: 99%

The Two Faces of Thrombosis: Coagulation Cascade and Platelet Aggregation. Are Platelets the Main Therapeutic Target?

Cimmino¹,

Fischetti²,

Golino³

2017

J Thrombo Cir

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Acute thrombus formation is the pathophysiological substrate underlying several clinical conditions, such as acute coronary syndrome (ACS) and stroke. Activation of coagulation cascade is a key step of the thrombotic process: vessel injury results in exposure of the glycoprotein tissue factor (TF) to the flowing blood. Once exposed, TF binds factor VII/VIIa (FVII/FVIIa) and in presence of calcium ions, it forms a tertiary complex able to activate FX to FXa, FIX to FIXa, and FVIIa itself. The final step is thrombin formation at the site of vessel injury with subsequent platelet activation, fibrinogen to fibrin conversion and ultimately thrombus formation.Platelets are the key cells in primary hemostasis. For years they have been considered only as cell fragments participating to primary hemostasis and onto which coagulation factors are assembled in the process of thrombus formation. However, recent advances in platelets pathophysiology have shown that these cells are able to regulate their gene and protein expression, make de novo protein synthesis, and release different mediators with paracrine effects that may interfere with different cell functions.Pharmacological modulation of both side of thrombosis, coagulation cascade and platelet activation, is of great clinical importance. Several clinical trials have clearly shown the efficacy of anticoagulation and/or anti platelet aggregation in different thrombotic disorders. This article aims at reviewing the recent advancements on the two faces of thrombosis focusing on the emerging role of platelets not only as clot-forming components, but highlighting their involvement in the inflammatory-immune system, as well as in modulation of different cell functions.

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Updates on Acute Coronary Syndrome

Cited by 162 publications

References 78 publications

Cardiovascular Risk and Statin Eligibility of Young Adults After an MI

Cardiovascular Risk and Statin Eligibility of Young Adults After an MI

Association of Circulating IGFBP1 Level with the Severity of Coronary Artery Lesions in Patients with Unstable Angina

The Two Faces of Thrombosis: Coagulation Cascade and Platelet Aggregation. Are Platelets the Main Therapeutic Target?

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