Development Of Left Ventricular Aneurysm Research Articles

Utilidade do Nível de NT-Pro-BNP no Plasma à Internação em Predizer a Formação de Aneurisma do Ventrículo Esquerdo após Infarto Agudo do Miocárdio com Elevação do Segmento ST

BackgroundLeft ventricular aneurysm (LVA) is an important complication of acute myocardial infarction. In this study, we investigated the role of N- Terminal pro B type natriuretic peptide level to predict the LVA development after acute ST-segment elevation myocardial infarction (STEMI).MethodsWe prospectively enrolled 1519 consecutive patients with STEMI. Patients were divided into two groups according to LVA development within the six months after index myocardial infarction. Patients with or without LVAs were examined to determine if a significant relationship existed between the baseline N- Terminal pro B type natriuretic peptide values and clinical characteristics. A p-value < 0.05 was considered statistically significant.ResultsLVA was detected in 157 patients (10.3%). The baseline N- Terminal pro- B type natriuretic peptide level was significantly higher in patients who developed LVA after acute MI (523.5 ± 231.1 pg/mL vs. 192.3 ± 176.6 pg/mL, respectively, p < 0.001). Independent predictors of LVA formation after acute myocardial infarction was age > 65 y, smoking, Killip class > 2, previous coronary artery bypass graft, post-myocardial infarction heart failure, left ventricular ejection fraction < 50%, failure of reperfusion, no-reflow phenomenon, peak troponin I and CK-MB and NT-pro BNP > 400 pg/mL at admission.ConclusionsOur findings indicate that plasma N- Terminal pro B type natriuretic peptide level at admission among other variables provides valuable predictive information regarding the development of LVA after acute STEMI.

Features of renal macrophage infiltration in patients with myocardial infarction

Purpose. To characterise phenotypic heterogeneity of renal macrophage infiltration and its relationships with clinical and medical history data in patients who died at different times after myocardial infarction (MI).Material and Methods. We analyzed the material (kidney sections) collected from patients (n = 30) who died from type 1 MI. Renal macrophage infiltration was assessed by the immunohistochemistry method using antibodies to CD68, CD80, CD163, CD206, and stabilin-1.Results. The study included patients with MI aged 74.8 ± 9.8 years. ST-segment elevation myocardial infarction (STEMI) was diagnosed in 87% of patients; the creatinine level was 115.1 ± 79 μmol/L at admission to hospital. The study showed a significant heterogeneity of macrophage phenotypes in renal tissue: the counts of CD163+, CD68+, CD206+, CD80+, and stabilin-1+ cells were 55 (27; 55), 30 (27; 56), 4 (2; 6), 3 (2; 5), and 2 (1; 3) per field of view, respectively. The CD163+ and CD68+ macrophages were predominant cell types in patients who died within three days after MI onset (p &lt; 0.05). In case of fatal outcome that occurred after three days of MI, the count of CD163+ cells was the highest and exceeded the number of СD68+ cells, which, nevertheless, prevailed over other cell phenotypes (p &lt; 0.05). Starting from day 4 of MI, the counts of CD206+ cells decreased from 6 (5; 8) to 2 (1; 2) similarly to a decrease in CD80+ count from 5 (3; 5) to 2 (1; 2) (p &lt; 0.05). The rate of adverse cardiovascular complications and the severity of coronary lesions were associated with CD80+ and CD206+ cell counts; the development of left ventricular aneurysm was associated with the numbers of stabilin-1+ and CD163+ cells.Conclusion. Renal macrophage infiltration was characterized by a pronounced cellular heterogeneity that depended on the timing of death after MI. The CD163+ and CD68+ cells predominated at the early stages of MI; the CD163+ cells were predominant at the later stages. The CD80+ and CD206+ cell counts changed quantitatively, decreasing from day 4 of MI. The presence of multiple correlation relationships between the cells of macrophage lineage in the kidneys and the development of adverse cardiovascular complications in patients with MI provides rationale for further studies.

Correlations between morphological features of intracoronary thrombi and left ventricular structure and function in patients with ST-segment elevation myocardial infarction

The majority of cases of acute ST-elevation myocardial infarction (STEMI) are caused by the rupture of an atherosclerotic plaque and subsequent thrombus formation. The study of clot structure may be important for the prediction of further course of the disease. The study included 100 patients with STEMI who underwent primary percutaneous coronary intervention (PCI) with manual thromboaspiration within the first 12 hours after the onset of symptoms. Sufficient aspiration material for histological examination was obtained in 97 patients. These intracoronary thrombi were investigated macroscopically and microscopically. Subsequently, correlations between morphological structure of thrombi and structural and functional features of the myocardium after revascularization were analyzed. Pathological QS pattern was detected in 45 (46.39±5.06%) patients. Peripheral infiltration of intracoronary thrombus with neutrophils was the only morphological feature associated with the presence of QS (r= -0.36; p&lt;0.001). The mean left ventricular ejection fraction (LVEF) measured during echocardiography was 48.34±9.39%. Positive and significant correlation was found between LVEF and peripheral infiltration of intracoronary thrombus with neutrophils (r=0.37; p&lt;0.001), while negative correlation was found between LVEF and presence of microchannels within the clot (r= -0.27; p&lt;0.01). The mean total segmental left ventricular contractility index at the time of hospital discharge was 1.38 [1.25; 1.63]. This index negatively correlated with neutrophil infiltration (r= -0.37; p&lt;0.001), and positively – with the presence of microchannels in the obtained clot samples (r=0.26; p=0.01). Signs of left ventricular aneurysm formation before discharge from the hospital were found in 15 (15.46±3.67%) patients. A significant negative correlation was found between this parameter and the presence of peripheral neutrophil infiltration of intracoronary thrombi (r= -0.32; p&lt;0.01). The presence of peripheral infiltration of intracoronary thrombi with neutrophil leukocytes was associated with better left ventricular systolic function and less likely hood of development of left ventricular aneurysm or electrocardiographic QS pattern. The formation of microchannels within the clot was associated with poorer recovery of systolic cardiac function.

The relationship between post-procedural platelet count and left ventricular aneurysm in patients with acute anterior ST-segment elevation myocardial infarction following primary percutaneous coronary intervention.

Left ventricular aneurysm (LVA) relates to worse prognosis in patients with myocardial infarction despite successful reperfusion treatment. There is no evidence that early detectable biomarkers can predict the risk for the future development of LVA. The aim of our study was to investigate the possible predictive value of periprocedural haematological parameters for LVA. A total of 281 patients with acute anterior ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (pPCI) were enrolled. Haematological parameters were measured on admission before pPCI and between 8 and 12 h after pPCI, separately. The development of LVA was evaluated at one-year follow-up. The patients were then divided into two groups: an LVA group and a non-LVA group. Univariate and multivariate logistic regression analyses were performed to find the predictors of LVA. A total of 34 (12.1%) patients developed LVA at one-year follow-up after pPCI. Multivariate analyses revealed that a 10 × 109/L increase in platelet count 12 h after pPCI (odds ratio [OR] 1.092, 95% confidence interval [CI] 1.015-1.188, p = 0.039), peak cardiac troponin I (OR 1.107, 95% CI 1.003-1.215, p = 0.000), and left ventricular ejection fraction (OR 0.853, 95% CI 0.772-0.943, p = 0.002) were independent risk factors for LVA. For the prediction of LVA, platelet count 12 h after pPCI at a cut-off value > 197 × 109/L yielded a receiver operating characteristic-area under the curve (ROC-AUC) of 0.635 (82.3% sensitivity, 44.1% specificity). Platelet count after pPCI was significantly associated with the development of LVA in anterior STEMI patients and may be available for early risk stratification of future LVA formation.

The effect of thrombolytic therapy on left ventricular aneurysm formation in acute myocardial infarction: relationship to successful reperfusion and vessel patency.

Although there is increasing evidence for the beneficial effect of thrombolytic therapy on global left ventricular (LV) function in acute myocardial infarction (AMI), the data concerning the early effect of thrombolytic therapy on the incidence of left ventricular aneurysm (LVA) formation and its relationship to clinical and angiographic determinants are limited. The study aimed to determine the independent factors involved in the development of LVA and to evaluate whether thrombolytic therapy has any preventive effect on the development of LVA in AMI. In all, 350 consecutive patients suffering from a first attack of AMI were included. Of these, 205 who arrived within 12 h of onset of symptoms received thrombolytic therapy (thrombolytic group) and the remaining 145 patients served as control group. All patients received aspirin and maximal-dose anticoagulation with intravenous heparin therapy. Early successful reperfusion was assessed by enzymatic and electrocardiographic evidence, and late vessel patency was evaluated according to Thrombolysis in Myocardial Infarction (TIMI) classification. Patients with TIMI grade 2 or 3 flow were considered to have vessel patency. The overall incidence of LVA was 11.7% (41/350), and no statistical difference was found between the incidence of LVA between the two groups (11.7 vs. 11.7%, p>0.05). However, the patients receiving thrombolytic therapy and exhibiting a patent infarct-related artery (PIRA) (n = 125, 61%), had a significantly reduced incidence of LVA compared with those who did not (7.2 vs. 18.8%, p= 0.015). In univariate analysis, vessel patency, proximal left anterior descending artery (LAD) stenosis, total LAD occlusion, multivessel disease, and hypertension were found to be important factors in LVA formation after AMI. After adjustment for other clinical and angiographic variables, total LAD occlusion (odds ratio [OR] 3.62,95% confidence interval [CI] 2.45-8.42, p = 0.0014), absence of PIRA (OR 2.92, 95% CI 1.41-09, p = 0.0037) and proximal LAD stenosis (OR 2.11, 95% CI 1.05-4.71, p = 0.045) remained the independent determinants of LVA formation after AMI. Our data indicate that not all patients who received thrombolytic therapy, but only those with PIRA had evidently reduced the incidence of LVA. Patients with total LAD occlusion, with proximal LAD stenosis, and without PIRA were found to have increased risk for formation of LVA after AMI. These findings indicate that the presence of vessel patency has a preventive effect on LVA formation in AMI.

Determinants of left ventricular aneurysm formation after anterior myocardial infarction: A clinical and angiographic study

To determine factors involved in left ventricular aneurysm formation after transmural anterior myocardial infarction, 79 patients with a first myocardial infarction who underwent cardiac catheterization within 6 months of infarction were evaluated. Patients who had received thrombolytic therapy were excluded. Patients were divided into four groups depending on the status of the left anterior descending artery and the presence or absence of a left ventricular aneurysm: Group I (n = 25): aneurysm with occluded left anterior descending artery; Group II (n = 27): no aneurysm and occluded left anterior descending artery; Group III (n = 23): no aneurysm and patent left anterior descending artery; and Group IV (n = 4): aneurysm with patent left anterior descending artery. Single vessel disease was more common in Group I (aneurysm) compared with Groups II and III (no aneurysm) (chi 2(4) = 12.8; probability value equal to 0.012). Collateral blood supply in the presence of an occluded left anterior descending artery was significantly less in Group I (aneurysm) compared with Group II (no aneurysm) (0.9 versus 2.4, p less than 0.001). The extent of coronary artery disease and collateral blood supply in Groups I and II were directly related (p = 0.012). Neither age, sex nor risk factors for coronary disease correlated with aneurysm formation. At a mean follow-up of 48 months, no differences were observed in the incidence of recurrent angina, new myocardial infarction, embolic events or sudden death. More patients in Group II underwent coronary artery bypass surgery. Total occlusion of the left anterior descending artery in association with inherent poor collateral blood supply is a significant determinant of aneurysm formation after anterior myocardial infarction. Multivessel disease with either good collateral circulation or a patent left anterior descending artery is uncommonly associated with the development of left ventricular aneurysm.

Left Ventricular Mural Thrombus

The identification of mural thrombus in patients with left ventricular aneurysm and mural thrombus probably warrants consideration of long-term anticoagulation. In patients with acute, large, anterior or anteroapical, transmural myocardial infarctions, serial noninvasive examinations are warranted to define a group of patients at high risk for the development of left ventricular aneurysm and/or mural thrombus. Anticoagulants should be considered in patients in whom mural thrombi develop as a complication of their infarction. Patients with congestive cardiomyopathy should be considered for long-term anticoagulation. These recommendations are all tempered by the realization that the use of anticoagulant therapy is not without its own risks. The decision to anticoagulate must be balanced against each individual patient's suitability for such therapy and the individual likelihood of the development of side effects.

Left ventricular mural thrombus

The identification of mural thrombus in patients with left ventricular aneurysm and mural thrombus probably warrants consideration of long-term anticoagulation. In patients with acute, large, anterior or anteroapical, transmural myocardial infarctions, serial noninvasive examinations are warranted to define a group of patients at high risk for the development of left ventricular aneurysm and/or mural thrombus. Anticoagulants should be considered in patients in whom mural thrombi develop as a complication of their infarction. Patients with congestive cardiomyopathy should be considered for long-term anticoagulation. These recommendations are all tempered by the realization that the use of anticoagulant therapy is not without its own risks. The decision to anticoagulate must be balanced against each individual patient's suitability for such therapy and the individual likelihood of the development of side effects.

Left ventricular aneurysm without coronary arterial obstruction or occlusion

The most common cause of left ventricular aneurysm is severe obstruction or occlusion of a major coronary artery. Among the last 2,500 patients studied in our laboratory with selective coronary cinearteriography and left ventriculography, we found 9 with unquestionable evidence of left ventricular aneurysm and no or minimal coronary arterial obstruction. Eight of the nine patients had a history of previous myocardial infarction and classic electrocardiographic changes. We believe that in these patients coronary arterial obstruction had led to the development of left ventricular aneurysm. Later, complete or partial regression of the coronary obstruction ensued, leaving a normal or a minimally compromised vascular lumen.