Angina, Unstable – ABC CARDIOL

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Editorial

Legumain – Another Piece in the Complex Puzzle of Atherosclerotic Plaque Formation and Vulnerability

The atherosclerotic plaque formation process in the arterial walls is a very complex process. Plaque development occurs due to an interplay between endothelial cells, smooth muscle cells, and immune cells. There is an increase in endothelial permeability and activation of signaling molecules, including inflammatory mediators and cell adhesion molecules. Moreover, circulating lipoproteins (particularly low-density lipoproteins – LDL) can cross the endothelial layer and be deposited in the intimal space, where they undergo oxidative changes (oxLDL), increasing the local inflammatory response. Furthermore, monocytes mature into macrophages, being recruited via attractant chemokines, and while they attempt to clear oxLDL via phagocytosis, they are converted into foam cells and ultimately undergo necrosis. In addition, vascular smooth muscle cells (VSMCs) proliferate and migrate from the media to the intima, leading to intimal hyperplasia, and these cells organize and deposit extracellular matrix, forming a fibrous cap. Erosion or rupture of the fibrous cap will lead to thrombotic occlusion or distal embolism, resulting in ischemia.

In this process, matrix metalloproteinases (MMPs) play an important role. MMPs are a family of zinc-dependent endoproteases that are secreted by endothelial cells, VSMCs, fibroblasts, osteoblasts, macrophages, neutrophils, and lymphocytes. During stable atherosclerotic plaque development, MMP-2 cleaves the endogenous nitric oxide synthase, causing endothelial dysfunction and facilitating infiltration of LDL into the intima. Then, MMP-2 expressed by activated platelets promotes monocyte transmigration into the intima . MMP-2 also facilitates oxLDL-induced VSMCs migration to the intima, forming the fibrous cap. Therefore, it can induce migration and proliferation of VSMCs, enhancing plaque stability. However, MMP-2 levels are higher in unstable than in stable atherosclerotic plaque, indicating that MMP-2 plays a role in plaque vulnerability and propensity to rupture. They participate in the degradation of the extracellular matrix (ECM), which will cause thinning of the plaque fibrous cap, becoming more prone to rupture.

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Anatomopathological Session

Case 5/2016 – A 56-Year-old Man Hospitalized for Unstable Angina, who Presented Recurrence of Precordial Pain and Cardiac Arrest with Pulseless Electrical Activity

Desiderio Favarato et al. Paulo Sampaio Gutierrez

Clinical aspects

This is a 56-year-old man with a recent onset of angina and three-vessel lesions on coronary cineangiography, who presented with dyspnea and, a few hours later, cardiorespiratory arrest with intense ST segment elevation.

Angina is the initial manifestation in half of the patients with coronary artery disease. Even when stable, i.e., without changes in the triggering events or intensity, a duration of the episodes longer than 3 months doubles the risk of cardiovascular events.^,

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Original Article

Correlation between C-Reactive Protein in Peripheral Vein and Coronary Sinus in Stable and Unstable Angina

Weverton Ferreira Leite et al. José Antonio Franchini Ramires Luiz Felipe Pinho Moreira Célia Maria Cassaro Strunz José Armando Mangione

Background:

High sensitivity C-reactive protein (hs-CRP) is commonly used in clinical practice to assess cardiovascular risk. However, a correlation has not yet been established between the absolute levels of peripheral and central hs-CRP.

Objective:

To assess the correlation between serum hs-CRP levels (mg/L) in a peripheral vein in the left forearm (LFPV) with those in the coronary sinus (CS) of patients with coronary artery disease (CAD) and a diagnosis of stable angina (SA) or unstable angina (UA).

Methods:

This observational, descriptive, and cross-sectional study was conducted at the Instituto do Coração, Hospital das Clinicas, Faculdade de Medicina, Universidade de São Paulo, and at the Hospital Beneficência Portuguesa de Sao Paulo, where CAD patients referred to the hospital for coronary angiography were evaluated.

Results:

Forty patients with CAD (20 with SA and 20 with UA) were included in the study. Blood samples from LFPV and CS were collected before coronary angiography. Furthermore, analysis of the correlation between serum levels of hs-CRP in LFPV versus CS showed a strong linear correlation for both SA (r = 0.993, p < 0.001) and UA (r = 0.976, p < 0.001) and for the entire sample (r = 0.985, p < 0.001).

Conclusion:

Our data suggest a strong linear correlation between hs-CRP levels in LFPV versus CS in patients with SA and UA.

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Artigo Original

Causality analysis of the relationship between bleeding and lethality in Acute Coronary Syndromes

Luis Cláudio Lemos Correia et al. Michael Sabino Mariana Brito Guilherme Garcia … Mateus Viana J. Péricles Esteves Márcia R. Noya

BACKGROUND: Hemorrhagic events in Acute Coronary Syndromes (ACS) have been independently associated with death in international multicenter registries. However, that association has not been tested in Brazil and the true causal relationship between bleeding and death has not been completely shown. OBJECTIVE: To test the following hypotheses: (1) major bleeding is an independent predictor of in-hospital death in ACS; (2) the relationship between those two endpoints is causal. METHODS: This study included patients meeting predefined criteria of unstable angina, non-ST-segment elevation myocardial infarction or ST-segment elevation myocardial infarction. Major bleeding during hospitalization was defined according to the Bleeding Academic Research Consortium (types 3 or 5). Logistic regression and analysis of the sequence of events were used to assess the association between bleeding and death. RESULTS: Of the 455 patients studied, 29 experienced major bleeding (6.4%; 95% CI = 4.3-9.0%). They had in-hospital mortality of 21%, as compared with 5.6% of those not experiencing bleeding (RR = 4.0; 95% CI = 1.8-9.1; P = 0.001). After adjusting for the propensity score, major bleeding remained as a predictor of in-hospital death (OR = 3.34; 95% CI = 1.2-9.5; P = 0.02). Of the 29 patients who experienced bleeding, six died. However, the detailed analysis of the sequence of events showed causal relationship only in one case. CONCLUSION: (1) Major bleeding is an independent predictor of in-hospital death in ACS; (2) the role of bleeding as a risk marker overcomes that as a risk factor for death. This conclusion should be seen as a hypothesis generator to be confirmed by larger-sample studies. (Arq Bras Cardiol. 2012; [online].ahead print, PP.0-0)

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Artigo Original

NT-proBNP levels in patients with non-ST-segment elevation acute coronary syndrome

Luiz Ricardo A. Castro et al. Maria Clara N. Alencar Márcia M. Barbosa Maria do Carmo P. Nunes … José Ronaldo Cardoso Antonio Luiz P. Ribeiro

BACKGROUND: Non-ST-segment elevation acute coronary syndrome is associated with elevation of brain natriuretic peptide and markers of myocardial necrosis, although its relationship with the TIMI score and left ventricular function are largely unknown. OBJECTIVE: To evaluate the correlation between plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) and markers of myocardial necrosis [creatine phosphokinase muscle-brain fraction (CK-MB) and troponin I], TIMI risk score and left ventricular ejection fraction in patients with non-ST-segment elevation acute coronary syndrome. METHODS: Eighty-seven patients with non-ST-segment elevation acute coronary syndrome were divided into two groups: 37 (42.5%) with unstable angina and 50 (57.5%) with non-ST-segment elevation myocardial infarction. RESULTS: Left ventricular ejection fraction more than 40% was found in 86.2% of the total sample. Serum levels of NT-proBNP was higher in patients with non-ST elevation myocardial infarction than in those with unstable angina (p<0.001). Increased levels of NT-proBNP were associated with increases in troponin I (rs=0.425, p<0.001), peak CK-MB (rs=0.458, p<0.001) and low left ventricular ejection fraction (rs=-0.345, p=0.002); no correlation was found with the TIMI risk score (rs=0.082, p=0.44). Multivariate analysis revealed that left ventricular ejection fraction and troponin I levels were independently correlated with NT-proBNP levels (p=0.017 and p=0.002, respectively). CONCLUSION: Increased levels of NT-proBNP in patients with non-ST-segment elevation acute coronary syndrome are not related exclusively to low left ventricular ejection fraction, but can also be caused by the presence of myocardial ischemia and necrosis.

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Artigo Original

Preinfarction angina and in-hospital outcome of elderly patients with acute myocardial infarction

Chiu Wen Shian et al. Sandro Gonçalves de Lima Brivaldo Markman Filho

BACKGROUND: Preinfarction angina (PIA) may be a marker of ischemic preconditioning. A decrease in infarct size, ventricular remodeling, congestive heart failure, cardiogenic shock or death was demonstrated in the presence of preinfarction angina. These findings were more evident in adults, but not in the elderly. OBJECTIVE: To assess the relationship between PIA and the clinical course of elderly patients with acute myocardial infarction (AMI). METHODS: This was a case-series study with a comparison group. A total of 36 patients with ST-segment elevation AMI were included in the study and divided into two groups: group A (21 patients with PIA) and group B (15 patients without PIA). RESULTS: Mean age of the study population was 70.5 years, and there was a predominance of males (73%). Mean body mass index was 25.3 Kg/m2. Hypertension was present in 77.8%, diabetes in 27.8% and dyslipidemia in 32.4%. Type-A chest pain was reported by 71.4% of patients, and the majority of them (72.2%) were in Killip class I. Clinical endpoints for groups A and B were as follows: postinfarction angina 9.5% versus 20%, p = 0.630; heart failure 23.8% versus 13.3%, p = 0.674; urgent revascularization 4.8% versus 6.7%, p = 1; and cardiac arrhythmia 0% versus 6.7%, p = 0.417. There was no case of reinfarction, cardiogenic shock or death within 30 days of follow up in either group. CONCLUSION: In this case series, preinfarction angina was not associated with better clinical course in elderly patients with AMI.

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Legumain – Another Piece in the Complex Puzzle of Atherosclerotic Plaque Formation and Vulnerability

Case 5/2016 – A 56-Year-old Man Hospitalized for Unstable Angina, who Presented Recurrence of Precordial Pain and Cardiac Arrest with Pulseless Electrical Activity

Clinical aspects

Correlation between C-Reactive Protein in Peripheral Vein and Coronary Sinus in Stable and Unstable Angina

Background:

Objective:

Methods:

Results:

Conclusion:

Causality analysis of the relationship between bleeding and lethality in Acute Coronary Syndromes

NT-proBNP levels in patients with non-ST-segment elevation acute coronary syndrome

Preinfarction angina and in-hospital outcome of elderly patients with acute myocardial infarction

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