Rupture In Myocardial Infarction Research Articles

Successful occlusion of ventricular septal rupture in myocardial infarction under the guidance of echocardiography

IntroductionThe traditional treatment of myocardial infarction with ventricular septal rupture is surgical treatment. For the elderly patients with cardiac insufficiency, surgical treatment is very risky. The successful treatment of this case by interventional occlusion is a new method. No relevant literature reports have been found.CaseA 77-year-old man with a past medical history of old myocardial infarction presented to the physician with sudden onset of palpitation and shortness of breath. Echocardiography showed thinning of the interventricular septum near the apex and bulging toward the right ventricular side with “paradoxical motion”, on which a rupture of about 8 mm in diameter was seen. CDFI: left ventricular blood shunted to the right ventricle through the rupture.Echocardiographic diagnosis: old left ventricular anteroseptal myocardial infarction with ventricular septal rupture. Due to the older age of the patient and reduced left ventricular function, surgical repair of the ventricular septal rupture site was more difficult. After multidisciplinary discussion, it was agreed that the patient could not afford thoracotomy and was not suitable for thoracotomy, and echocardiography guided interventional occlusion of the ruptured interventricular septum could be performed.ConclusionTransesophageal echocardiography-guided interventional occlusion of myocardial infarction with ventricular septal rupture in elderly patients with cardiac insufficiency is a new attempt, the successful treatment of this case shows that this method is feasible, for some patients is an appropriate treatment.

Left ventricular free wall rupture in myocardial infarction: A retrospective analysis from a single tertiary center.

ObjectiveLeft ventricular free wall rupture (LVFWR) is a rare but severe complication of acute myocardial infarction (AMI). During the era of pre-thrombolysis, autopsies revealed an incidence of approximately 8%.MethodThe objective of this retrospective study was to analyze the current incidence of LVFWR and to identify predictors by comparing the AMI-cohort with LVFWR to those without. The control group involved a random selection of one in every ten patients who presented with acute myocardial infarction between 2005 and 2014.ResultA total of 5143 patients with AMI were treated at the Central Hospital, Bad Berka (71% men, median age 68 years). Out of these, seven patients with LVFWR were identified with an overall incidence of 0.14%. Clinically, LVFWR patients presented late to admission since symptom onset (median 24 h vs. 6.1 h; p < 0.0001), were more likely in cardiogenic shock (28.6% vs. 3.2%; p = 0.02) and were usually accompanied by emergency physicians (71.4% vs. 20.7%; p = 0.006). Higher troponin T (median 8.6 vs. 0.5 ng/ml; p < 0.0002), higher CRP (median 50 vs. 0.5 mg/l; p = 0.05) as well as a lower hematocrit-values (0.33 vs. 0.42; p = 0.04) were observed. All LVFWR patients were operated (100% vs. 1.6%; p < 0.001). The patients had lower rates of beta-blocker treatment (57.1% vs. 95.8%; p = 0.003). The 30-day mortality was significantly higher (42.9% vs. 6.8%; p = 0.01).ConclusionCompared to the thrombolytic era, the current incidence of LVFWR with AMI, who reach the hospital alive, is significantly lower. However, 30-day mortality continues to be high.

Hepatokine \u03b11-Microglobulin Signaling Exacerbates Inflammation and Disturbs Fibrotic Repair in Mouse Myocardial Infarction

Acute cardiac rupture and adverse left ventricular (LV) remodeling causing heart failure are serious complications of acute myocardial infarction (MI). While cardio-hepatic interactions have been recognized, their role in MI remains unknown. We treated cultured cardiomyocytes with conditioned media from various cell types and analyzed the media by mass spectrometry to identify α1-microglobulin (AM) as an Akt-activating hepatokine. In mouse MI model, AM protein transiently distributed in the infarct and border zones during the acute phase, reflecting infiltration of AM-bound macrophages. AM stimulation activated Akt, NFκB, and ERK signaling and enhanced inflammation as well as macrophage migration and polarization, while inhibited fibrogenesis-related mRNA expression in cultured macrophages and cardiac fibroblasts. Intramyocardial AM administration exacerbated macrophage infiltration, inflammation, and matrix metalloproteinase 9 mRNA expression in the infarct and border zones, whereas disturbed fibrotic repair, then provoked acute cardiac rupture in MI. Shotgun proteomics and lipid pull-down analysis found that AM partly binds to phosphatidic acid (PA) for its signaling and function. Furthermore, systemic delivery of a selective inhibitor of diacylglycerol kinase α-mediated PA synthesis notably reduced macrophage infiltration, inflammation, matrix metalloproteinase activity, and adverse LV remodeling in MI. Therefore, targeting AM signaling could be a novel pharmacological option to mitigate adverse LV remodeling in MI.

P3674New candidate genes for plaque rupture in myocardial infarction

P3674New candidate genes for plaque rupture in myocardial infarction

Time dependent apoptotic rates in the evolving coronary thrombus mass of myocardial infarction patients

AimTo study the rate of apoptotic cell death in the process of thrombus evolution after plaque rupture in myocardial infarction. MethodsParaffin embedded thrombosuction aspirates of 63 patients were stained with haematoxylin & eosin (H&E) to assess histologically the age of the thrombi: fresh (intact blood cells; <1day old), lytic (necrosis; 1–5days old) or organized (ingrowth of cells; >5days old). Presence of plaque constituents (atheroma including foam cells, cholesterol crystals calcifications and fibrous cap tissue) was also recorded. Immunohistochemical (double) stains with anti-caspase-3-antibody were used to visualize apoptosis and the cells involved. For the latter caspase-3 antibody was combined with cell-specific markers MPO (granulocytes), CD68 (macrophages), CD34 (endothelial cells), SMA-1 (smooth muscle cells) and a Feulgen stain (DNA). Second, the rate of apoptosis was evaluated in relation to the age of the thrombi. Platelet apoptosis was further evaluated with the use of TEM. ResultsFrom a total of 63 aspirates, plaque constituents were found in 33 of the aspirates, and in 15 of them lipid rich plaque tissue was the sole component. Age classification of all thrombus containing aspirates (n=48) resulted in 12 fresh (25%), 18 lytic (37.5%) and 18 organized (37.5%) thrombi. Apoptosis was more extensive in lytic thrombi than in fresh or organized thrombi (P<0.0001). Plaque-containing aspirates showed more apoptosis than aspirates without plaque (P<0.05). Immuno staining with caspase-3 antibody in combination with cell-specific markers showed that apoptosis was most extensive in MPO+ granulocytes. Caspase-3-positive platelets (CD61+ anucleate particles) were most abundant in lytic thrombi. Apoptosis in platelets was confirmed by ultrastructure. ConclusionThis study demonstrated a significant association between thrombus age and occurrence of apoptosis of granulocytes and also platelets, with highest rates in (fragile) lytic thrombi. We propose that apoptotic cell death in athero thrombosis could potentially serve as a biomarker for thrombus instability.

Polymorphism in the chemokine receptor 7 gene (CCR7) is associated with previous myocardial infarction in patients undergoing elective coronary angiography.

Coronary artery disease (CAD) remains a major cause of death in developed countries. Both environmental and, less known, genetic factors contribute to progression of CAD to myocardial infarction (MI). Immune system is activated in patients with CAD through dendritic cells (DCs), which present plaque antigens to T lymphocytes. Production of proinflammatory cytokines by activated T cells contributes to plaque rupture in MI. Chemokine receptor 7 (CCR7) on DCs is required for their chemotaxis from plaque to lymph nodes. This makes possible an interaction of DCs with T lymphocytes and initiation of specific immune response. We hypothesized that single nucleotide polymorphisms (SNPs) in CCR7 gene locus are associated with previous MI in patients with CAD. To test this hypothesis, we genotyped six SNPs from the CCR7 gene locus in 300 consecutive patients, admitted for elective coronary angiography. We performed univariate-, multivariate- (including potential confounders) and haplotype-based tests of association of SNPs with previous MI and results of angiography. Allele A of rs17708087 SNP was associated with previous MI. This association remained significant after adjustment for age, sex, smoking, hypercholesterolaemia and drugs used by patients (odds ratio 2.13, 95% confidence interval: 1.13-3.86). Therefore, we conclude that CCR7 gene locus harbours a polymorphism that modifies risk of MI in patients with CAD. Replication of this association could be sought in a prospective cohort of initially healthy individuals.

High sensitivity cytokine detection in acute coronary syndrome reveals up-regulation of Interferon Gamma and Interleukin-10 post Myocardial Infarction

Inflammation is an important element in the development and destabilization of atherosclerotic plaque. Using a high sensitivity multiplex assay, previously untested in the context of atherosclerotic disease, we determined serum concentrations of GM-CSF, IFNgamma, IL-1beta, IL-2, IL-10, IL-12p70, TNF alpha, IL-6, and IL-8 in 48 Myocardial Infarction (MI) patients, 14 Unstable Angina (UA) patients and 12 healthy controls. IFNgamma levels were significantly higher in MI compared to UA (p=0.0091) and Control groups (p=0.0014). IL-10 also showed higher expression levels between MI, UA groups and Controls (p=0.0299).This up-regulation may reflect the extent of plaque instability and/or rupture in MI patients.Our observations provide evidence that IFNgamma and IL-10 merit further investigation in atherosclerotic disease states as potential markers of disease and therapeutic targets.

Cardiac rupture: histological study of ruptured and non-ruptured myocardial infarcts (author's transl)

178 myocardial infarcts with wall rupture and 116 without were studied histologically. Mean morphological age of the infarct was 3.7 in the ruptured and 2.9 days in the non-ruptured cases. 57.7% of patients had died within the first 24 hours from a non-ruptured infarct. Death rate within the first 24 hours after infarction was 57.7% among the non-ruptured cases, 25.8% among those with rupture. 23.1% of infarcts had ruptured between the third and fourth day. Only 5.1% of patients with non-ruptured infarcts had died on the third or fourth day. Transmural infarction was present in 71.7% of those that had ruptured. The ruptured channel in general ran through the middle of the necrotic-infarcted, leucocyte-infiltrated myocardium. Infarct recurrence was demonstrated in 20% of ruptured and 73% of non-ruptured infarcts. Morphological comparison indicated that transmural infarction and marked leucocytic reaction in a not previously infarct-damaged myocardium are the main causes for rupture in myocardial infarction.

The complex dynamics of stroke onset and progression

The aim of this article is to discuss the dynamic nature of cerebrovascular ischemia. Acute risk factors are superimposed on chronic risk factors to precipitate plaque rupture in myocardial infarction. The interaction between external triggers, such as stress, with internal triggers, such as vasoconstriction, is mediated to a large part by the autonomic nervous system. Numerous algorithms have been developed to describe physiological time-series data, for example heartbeat variability, and reveal complex structure that has diagnostic and prognostic significance. Much of this structure is mediated by the autonomic nervous system. Recent data on stroke triggers, carotid stenosis, transient ischemic attack, and infarct expansion suggest a similar need for detailed physiological measurement and non-linear dynamics in order to understand stroke onset and progression. The picture emerging is that stroke arises as a result of multiple processes with different time constants. The nature and timing of interventions should be tailored to these complex interacting processes. This will require more frequent and varied physiological measurement accompanied by non-linear analytical methods. This new approach, which stresses complex within-subject measurements, will likely make 'one size fits all' solutions to stroke care untenable.

Fatigue and plaque rupture in myocardial infarction

Plaque rupture plays a role in the majority of acute coronary syndromes. Rupture has been associated with stress concentrations, which are affected by tissue properties and anatomy. In this study rupture was not approached as an acute syndrome, but rather as the culmination of a chronic injury or fatigue process. The aim of our study was to investigate the impact of anatomy, tissue properties, and blood pressure on a fatigue mechanism. Incremental crack propagation was dynamically simulated based on evolving stress distributions. Stresses were resolved by a finite element solver, using vessel stiffness properties derived from in vivo data. Plaque fatigue crack growth per pressure pulse was estimated using an adapted Paris-relation. It was demonstrated that cracks begin at the lumen wall at areas of stress concentration, depending on the shape of the lumen, thickness of the fibrous cap and stiffness of the plaque components. Mean or pulse pressure did not affect initiation location. Cracks extended radially and grew at a rate that was highly dependent on both mean and pulse pressure and on lipid stiffness. Rupture rate depended on blood pressure and lipid stiffness. It was concluded that a fatigue mechanism in a pulsatile cardiovascular pressure environment reconciles clinical evidence of acute plaque rupture at seemingly low stress levels, and it could provide a framework for developing strategies to create a biomechanically benign environment which is least conducive to plaque rupture.

Medical Management of Selected Patients With Left Ventricular Free Wall Rupture During Acute Myocardial Infarction

Objectives. This study sought to evaluate the effects of prolonged rest and blood pressure control on survival of patients in whom left ventricular free wall rupture (LVFWR) was strongly suspected.Background. Left ventricular free wall rupture in myocardial infarction is often fatal, and only a few patients may undergo operation. However, survival without surgical repair has not yet been evaluated.Methods. Eighty-one consecutive patients with a first transmural acute myocardial infarction in Killip class I or II who presented with acute hypotension due to cardiac tamponade, with electromechanical dissociation (EMD) in 72, were prospectively evaluated. Patients with early recovery were managed with prolonged bed rest and blood pressure control with beta-blockade as tolerated.Results. Forty-seven patients died within 2 h of acute tamponade, and autopsy in 21 showed LVFWR in all. In 15 others, an emergency surgical repair resulted in 2 survivors. The remaining 19 patients, 10 with EMD, had early recovery with dobutamine and colloid solution, and 15 required pericardiocentesis. Shortly thereafter, these 19 patients still showed a paradoxic pulse ≥20 mm Hg, relevant pericardial effusion (24 ± 7 mm [mean ± SD]) and comparable elevation of right and left ventricular filling pressures (15.8 ± 3.9 and 15.9 ± 3.8 mm Hg, respectively). Subsequent management included bed rest (8.2 ± 4.8 days) and control of systolic blood pressure (≤120 mm Hg) with beta-adrenergic blocking agents as tolerated (n = 12). Four patients died, and autopsy in three revealed a rupture that was sealed in two. A sealed rupture was also seen at thoracotomy in 2 other patients who, like the remaining 13, survived for 52.5 ± 35.2 months.Conclusions. Long-term survival of selected patients with prompt hemodynamic recovery after LVFWR is possible without surgical repair. Prolonged bed rest and blood pressure control are likely to contribute favorably to their initial outcome.(J Am Coll Cardiol 1997;29:512–8)

Reliability of electromechanical dissociation in the diagnosis of left ventricular free wall rupture in acute myocardial infarction: J. Figueras, A. Curos, J. Cortadellas, J. Soler-Soler. Unitat Coronaria, Hospital General Vall d'Hebron, Barcelona, Spain. Am Heart J 1996;131:861–4

Objectives. This study sought to evaluate the effects of prolonged rest and blood pressure control on survival of patients in whom left ventricular free wall rupture (LVFWR) was strongly suspected.Background. Left ventricular free wall rupture in myocardial infarction is often fatal, and only a few patients may undergo operation. However, survival without surgical repair has not yet been evaluated.Methods. Eighty-one consecutive patients with a first transmural acute myocardial infarction in Killip class I or II who presented with acute hypotension due to cardiac tamponade, with electromechanical dissociation (EMD) in 72, were prospectively evaluated. Patients with early recovery were managed with prolonged bed rest and blood pressure control with beta-blockade as tolerated.Results. Forty-seven patients died within 2 h of acute tamponade, and autopsy in 21 showed LVFWR in all. In 15 others, an emergency surgical repair resulted in 2 survivors. The remaining 19 patients, 10 with EMD, had early recovery with dobutamine and colloid solution, and 15 required pericardiocentesis. Shortly thereafter, these 19 patients still showed a paradoxic pulse ≥20 mm Hg, relevant pericardial effusion (24 ± 7 mm [mean ± SD]) and comparable elevation of right and left ventricular filling pressures (15.8 ± 3.9 and 15.9 ± 3.8 mm Hg, respectively). Subsequent management included bed rest (8.2 ± 4.8 days) and control of systolic blood pressure (≤120 mm Hg) with beta-adrenergic blocking agents as tolerated (n = 12). Four patients died, and autopsy in three revealed a rupture that was sealed in two. A sealed rupture was also seen at thoracotomy in 2 other patients who, like the remaining 13, survived for 52.5 ± 35.2 months.Conclusions. Long-term survival of selected patients with prompt hemodynamic recovery after LVFWR is possible without surgical repair. Prolonged bed rest and blood pressure control are likely to contribute favorably to their initial outcome.(J Am Coll Cardiol 1997;29:512–8)

Infiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction

In the early 1960s, complete serial section studies through the whole thrombosed segment of occluded coronary arteries of myocardial infarction patients autopsied in St Louis, Mo, showed that all of the occluding thrombi had been caused by fissures of the surface of the underlying atherosclerotic plaques, fissures through which blood sometimes entered the plaque interior before they were sealed by the thrombi.1 Because essentially similar findings have since been made in Germany,2 Great Britain,3 Denmark,4 and Russia (A. Vichert, personal communication, 1985) and the same scenario was found to be responsible for cerebral artery thrombosis,5 it now seems certain that thrombosis in human atherosclerotic arteries is always triggered by a disruption …

Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction.

Erosion and rupture of coronary atheromas are the events preceding the vast majority of acute coronary syndromes. The shoulder regions of atheromas, the sites at which erosion or rupture is most likely to occur, are the sites at which mast cells accumulate. These cells are filled with neutral proteases capable of triggering extracellular matrix degradation via activation of matrix metalloproteinases. To obtain more direct evidence for the participation of mast cells in the acute coronary syndromes, we quantified the numbers of mast cells at eroded or ruptured sites of coronary atheromas in patients who died of myocardial infarction. In specimens of coronary arteries from 20 patients who had died of acute myocardial infarction, the site of atheromatous erosion or rupture was identified. The specimens were stained with monoclonal antibodies against the two major proteases of mast cells, tryptase and chymase, and against macrophages, T lymphocytes, and smooth muscle cells. At the immediate site of erosion or rupture, mast cells amounted to 6% of all nucleated cells, in the adjacent atheromatous area to 1%, and in the unaffected intimal area to 0.1%. The proportions of these mast cells that were activated, ie, had been stimulated to degranulate and release some of their tryptase and chymase contents, were 86% at the site of erosion or rupture, 63% in the adjacent atheromatous area, and 27% in the unaffected intima. At the site of erosion or rupture, the numbers of macrophages and T lymphocytes were also increased, but the number of smooth muscle cells was decreased. The accumulation of activated mast cells (200-fold more than in the unaffected coronary intima) at the site of atheromatous erosion or rupture suggests that in thrombotic coronary occlusion the role played by mast cells is significant.

A clinicopathological analysis of cardiac rupture following acute myocardial infarction in elderly patients

In all autopsied cases from January 1980 to June 1988 (56-102 years old, 243 men and 307 women), cardiac rupture death was observed in 14 cases out of 68 deaths of acute myocardial infarction in our hospital. Cardiac rupture occurred in 2, 4, 3, and 5 cases in their 60's, 70's, 80's, and 90' respectively, and 4 in men and 10 in women. Complaints of chest pain were present in 4 cases. Cerebrovascular disease was present in 9 cases and hypertension in 7. In 9 cases, the thickness of the ruptured wall was over 14 mm. The location of the ruptured lesion was the anterior wall in 4 cases, anteroseptal in 3, anterolateral in 1, lateral in 1, posterior in 1, and apical in 1. In conclusion, the incidence of cardiac rupture was higher in female than in males, and in silent myocardial infarction than in painful one. The location of rupture was frequently in the anterior or lateral wall. Aging and hypertension would not be a worsening factor in the pathogenesis of cardiac rupture in myocardial infarction, but cerebrovascular disease might be a risk factor in respect to masking occurrence of myocardial infarction.

Doppler echocardiographic features of ventricular septal rupture in myocardial infarction

Doppler echocardiography was used to evaluate the features of interventricular septal rupture in six patients with acute myocardial infarction and to substantiate the hemodynamic data and morphologic findings at surgery or autopsy. Although echocardiographic visualization of the septal rupture was obtained in only two of the six patients, unusual Doppler flow signals were detected in the apical portion of the right ventricle in all six patients. Five patients had unusual flow signals during both systole and diastole; one had such signals only during systole. The location of these unusual flow signals coincided with the site of septal rupture confirmed at surgery or autopsy. The pattern of the flow signals in one cardiac cycle was very similar to that of the pressure difference between the left and right ventricular cavities. These findings indicate that the unusual flow signals represent the left to right shunt flows resulting from septal rupture. In conclusion, Doppler echocardiography may be a very useful tool for diagnosing interventricular septal rupture easily and noninvasively in patients with acute myocardial infarction.