Transient Marked Myocardial Thickening after Reperfused Myocardial Infarction Causing Refractory Heart Failure.
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ABSTRACT:
SUBMITTER: Miura T
PROVIDER: S-EPMC7175793 | biostudies-literature | 2020 Apr
REPOSITORIES: biostudies-literature
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Transient Marked Myocardial Thickening after Reperfused Myocardial Infarction Causing Refractory Heart Failure.
Miura Toshiya T Araki Masaru M Onoue Takeshi T Tsuda Yuki Y Sonoda Shinjo S Otsuji Yutaka Y
CASE (Philadelphia, Pa.) 20191031 2
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Project description:Penetrating chest trauma can cause a wide variety of cardiac injuries, including myocardial contusion, damage to the interventricular septum, laceration of the coronary arteries, and free-wall rupture. Herein, we describe the case of a 21-year-old man who presented with congestive heart failure, which was secondary to an old myocardial infarction and complicated by the delayed formation of a ventricular septal defect. All of these conditions were attributable to multiple gunshot wounds that the patient had sustained 6 months earlier. Left ventricular angiography showed an apical aneurysm; a large, muscular, ventricular septal defect; and 19 gunshot pellets in the chest wall. Three months after aneurysmectomy and surgical closure of the septal defect, the patient had recovered fully and was asymptomatic.This case reaffirms the fact that substantial cardiac injuries can appear months after chest trauma. The possibility of traumatic ventricular septal defect should be considered in all multiple-trauma patients who develop a new heart murmur, even when overt chest-wall injury is absent.
| S-EPMC3298914 | biostudies-literature
Project description:Tyro3, AXL, and MerTK (TAM) receptors are activated in macrophages in response to tissue injury and as such have been proposed as therapeutic targets to promote inflammation resolution during sterile wound healing, including myocardial infarction. Although the role of MerTK in cardioprotection is well characterized, the unique role of the other structurally similar TAMs, and particularly AXL, in clinically relevant models of myocardial ischemia/reperfusion infarction (IRI) is comparatively unknown. Utilizing complementary approaches, validated by flow cytometric analysis of human and murine macrophage subsets and conditional genetic loss and gain of function, we uncover a maladaptive role for myeloid AXL during IRI in the heart. Cross signaling between AXL and TLR4 in cardiac macrophages directed a switch to glycolytic metabolism and secretion of proinflammatory IL-1β, leading to increased intramyocardial inflammation, adverse ventricular remodeling, and impaired contractile function. AXL functioned independently of cardioprotective MerTK to reduce the efficacy of cardiac repair, but like MerTK, was proteolytically cleaved. Administration of a selective small molecule AXL inhibitor alone improved cardiac healing, which was further enhanced in combination with blockade of MerTK cleavage. These data support further exploration of macrophage TAM receptors as therapeutic targets for myocardial infarction.
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Project description:Background and objectivesAcute myocardial infarction-related heart failure (HF) is associated with poor outcome. This study was designed to investigate the usefulness of global longitudinal strain (GLS), global circumferential strain (GCS) and mean longitudinal strain of left anterior descending artery territory (LSant) measured by 2-dimensional speckle tracking echocardiography (2D STE) in prediction of acute anterior wall ST-segment elevation myocardial infarction (ant-STEMI)-related HF.MethodsA total of 171 patients with ant-STEMI who underwent successful primary coronary intervention and had available 2D STE data were enrolled. Patients were divided into 3 groups: in-hospital HF, post-discharge HF, and no-HF groups.ResultsIn-hospital and post-discharge HF developed in 39 (22.8%) and 13 (7.6%) of patients, respectively and 113 patients (69.6%) remained without HF. Multivariate analysis showed that GLS was the only factor significantly associated with the development of in-hospital HF. For post-discharge HF, LSant was the only independent predictor. Other echocardiographic or laboratory parameters did not show independent association with the development of ant-STEMI-related HF.ConclusionsGLS is a powerful echocardiographic parameter related to development of in-hospital HF and LSant was significantly associated with post-discharge HF in patients with successfully reperfused ant-STEMI.
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Project description:Heart diseases remain the major cause of death worldwide. Advances in pharmacological and biomedical management have resulted in an increasing proportion of patients surviving acute heart failure (HF). However, many survivors of HF in the early stages end up increasing the disease to chronic HF (CHF). HF is an established frequent complication of myocardial infarction (MI), and numerous influences including persistent myocardial ischemia, shocked myocardium, ventricular remodeling, infarct size, and mechanical impairments, as well as hibernating myocardium trigger the development of left ventricular systolic dysfunction following MI. Macrophage population is active in inflammatory process, yet the clear understanding of the causative roles for these macrophage cells in HF development and progression is actually incomplete. Long ago, it was thought that macrophages are of importance in the heart after MI. Also, though inflammation is as a result of adverse HF in patients, but despite the fact that broad immunosuppression therapeutic target has been used in various clinical trials, no positive results have showed up, but rather, the focus on proinflammatory cytokines has proved more benefits in patients with HF. Therefore, in this review, we discuss the recent findings and new development about macrophage activations in HF, its role in the healthy heart, and some therapeutic targets for myocardial repair. We have a strong believe that there is a need to give maximum attention to cardiac resident macrophages due to the fact that they perform various tasks in wound healing, self-renewal of the heart, and tissue remodeling. Currently, it has been discovered that the study of macrophages goes far beyond its phagocytotic roles. If researchers in future confirm that macrophages play a vital role in the heart, they can be therapeutically targeted for cardiac healing.
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Project description:PurposeNitric oxide (NO) is constitutively produced and released from the endothelium and several blood cell types by the isoform 3 of the NO synthase (NOS3). We have shown that NO protects against myocardial ischemia/reperfusion (I/R) injury and that depletion of circulating NOS3 increases within 24 h of ischemia/reperfusion the size of myocardial infarction (MI) in chimeric mice devoid of circulating NOS3. In the current study we hypothesized that circulating NOS3 also affects remodeling of the left ventricle following reperfused MI.MethodsTo analyze the role of circulating NOS3 we transplanted bone marrow of NOS3-/- and wild type (WT) mice into WT mice, producing chimerae expressing NOS3 only in vascular endothelium (BC-/EC+) or in both, blood cells and vascular endothelium (BC+/EC+). Both groups underwent 60 min of coronary occlusion in a closed-chest model of reperfused MI. During the 3 weeks post MI, structural and functional LV remodeling was serially assessed (24 h, 4 d, 1 w, 2 w and 3 w) by echocardiography. At 72 hours post MI, gene expression of several extracellular matrix (ECM) modifying molecules was determined by quantitative RT-PCR analysis. At 3 weeks post MI, hemodynamics were obtained by pressure catheter, scar size and collagen content were quantified post mortem by Gomori's One-step trichrome staining.ResultsThree weeks post MI, LV end-systolic (53.2±5.9 μl; ***p≤0.001; n = 5) and end-diastolic volumes (82.7±5.6 μl; *p<0.05; n = 5) were significantly increased in BC-/EC+, along with decreased LV developed pressure (67.5±1.8 mm Hg; n = 18; ***p≤0.001) and increased scar size/left ventricle (19.5±1.5%; n = 13; **p≤0.01) compared to BC+/EC+ (ESV: 35.6±2.2 μl; EDV: 69.1±2.6 μl n = 8; LVDP: 83.2±3.2 mm Hg; n = 24; scar size/LV13.8±0.7%; n = 16). Myocardial scar of BC-/EC+ was characterized by increased total collagen content (20.2±0.8%; n = 13; ***p≤0.001) compared to BC+/EC+ (15.9±0.5; n = 16), and increased collagen type I and III subtypes.ConclusionCirculating NOS3 ameliorates maladaptive left ventricular remodeling following reperfused myocardial infarction.
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Project description:BackgroundAntecedent hypertension is associated with poor outcome in patients with ST-elevation myocardial infarction (STEMI). Whether differences in myocardial salvage, infarct size and microvascular injury contribute to the adverse outcome is unknown. We investigated the association between antecedent hypertension and cardiovascular magnetic resonance (CMR) parameters of myocardial salvage and damage in a multicenter CMR substudy of the AIDA-STEMI trial (Abciximab Intracoronary versus intravenously Drug Application in ST-elevation myocardial infarction).MethodsWe analyzed 792 consecutive STEMI patients reperfused within 12 h after symptom onset. Patients underwent CMR imaging for assessment of myocardial salvage, infarct size and microvascular obstruction within 10 days after infarction. Major adverse cardiac events (MACE) were recorded at 12-month follow-up.ResultsAntecedent hypertension was present in 540 patients (68 %) and was associated with a significantly increased baseline risk profile (advanced age, higher body mass index, higher incidence of diabetes, hypercholesterolemia, previous angioplasty and multivessel disease, p < 0.001 for all). MACE were more frequent in patients with hypertension as compared to patients without hypertension (45 [8 %] vs. 8 [3 %], p < 0.01). Antecedent hypertension remained an independent predictor of MACE after multivariate adjustment (hazard ratio 3.42 [confidence interval 1.45-8.08], p < 0.01). There was, however, no significant difference in the area at risk, infarct size, myocardial salvage index, extent of microvascular obstruction, and left ventricular ejection fraction between the groups (all p > 0.05).ConclusionDespite a higher rate of MACE in contemporary reperfused STEMI patients with antecedent hypertension, there was no difference in reperfusion efficacy, infarct size and reperfusion injury as visualized by CMR.Trial registrationNCT00712101 .
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Project description:The use of a large number of cardiovascular biomarkers, meant to complement the use of the electrocardiogram, echocardiography cardiac imaging, and clinical symptom assessment, has become a routine in clinical diagnosis, differential diagnosis, risk stratification, and prognosis and guides the management of patients with suspected cardiovascular diseases. There is a broad consensus that cardiac troponin and natriuretic peptides are the preferred biomarkers in clinical practice for the diagnosis of the acute coronary syndrome and heart failure, respectively, while the roles and possible clinical applications of several other potential biomarkers are still under study. This review mainly focuses on the recent studies of the roles and clinical applications of troponin and natriuretic peptides, which seem to be the best-validated markers in distinguishing and predicting the future cardiac events of patients with suspected cardiovascular diseases. Additionally, the review briefly discusses some of the large number of potential markers that may play a more prominent role in the future.
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Project description:The regulation of bone vasculature by chronic diseases, such as heart failure is unknown. Here, we describe the effects of myocardial infarction and post-infarction heart failure on the bone vascular cell composition. We demonstrate an age-independent loss of type H endothelium in heart failure after myocardial infarction in both mice and humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium, showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1β production partially prevented the post-myocardial infarction loss of type H vasculature in mice. These results provide a rationale for using anti-inflammatory therapies to prevent or reverse the deterioration of bone vascular function in ischemic heart disease.
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Project description:Background Type 2 myocardial infarction (T2MI) is common and associated with high cardiovascular event rates. However, the relationship between T2MI and heart failure (HF) is uncertain. Methods and Results We identified patients with T2MI at a large tertiary hospital between October 2017 and May 2018. Patient characteristics, causes of T2MI, and subsequent HF hospitalizations were determined by physician chart review. We identified 359 patients with T2MI over the study period; 184 patients had a history of HF. Among patients with ejection fraction (EF) assessment (N=180), the majority had preserved EF (N=107; 59.4%), followed by reduced EF (N=54; 30.0%), and mid-range EF (N=19; 10.6%). Acute HF was the most common cause of T2MI (20.9%). Of those whose T2MI was precipitated by HF (N=75), the mean EF was 53.0±16.8% and 16 (21.3%) were de novo diagnoses of HF. Among patients with T2MI who were discharged alive with available follow-up (N=289), 5.5% were hospitalized with acute HF within 30 days, 17.3% within 180 days, and 22.1% within 1 year. In subgroup analyses, among patients with T2MI with prevalent or new HF (N=161), the rate of HF hospitalization at 1 year was 34.2%, considerably higher than those with T2MI and no HF diagnosis at discharge (7.0%; N=9/128). Conclusions Index presentations of HF or worsening chronic HF represent the most common causes of T2MI. ≈1 in 5 patients with T2MI will be readmitted for HF within 1 year of their event. Strategies to prevent HF events after a T2MI are needed.
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Project description: Not available
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