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Pharmacological Research Aug 2008Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible... (Review)
Review
Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll-like receptor-mediated pathways, the complement cascade and reactive oxygen generation induce nuclear factor (NF)-kappaB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming growth factor (TGF)-beta plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.
Topics: Animals; Chemokines; Complement System Proteins; Cytokines; Heart; Humans; Immune System; Immunity, Innate; Myocardial Infarction; NF-kappa B; Neutrophils; Reactive Oxygen Species; Regeneration; Signal Transduction
PubMed: 18620057
DOI: 10.1016/j.phrs.2008.06.007 -
Stroke Jan 2020Background and Purpose- To test the hypothesis that covert brain infarcts (CBIs) are more likely to be located in noneloquent brain areas compared with clinical strokes...
Background and Purpose- To test the hypothesis that covert brain infarcts (CBIs) are more likely to be located in noneloquent brain areas compared with clinical strokes and that CBI etiological subtypes carry a differential risk of vascular events compared with people without CBI. Methods- We used brain magnetic resonance imaging from 1290 stroke-free participants in the NOMAS (Northern Manhattan Study) to evaluate for CBI. We classified CBI as cardioembolic (ie, known atrial fibrillation), large artery atherosclerosis (extracranial and intracranial), penetrating artery disease, and cryptogenic (no apparent cause). CBI localized in the nonmotor areas of the right hemisphere were considered noneloquent. We then evaluated risk of events by CBI subtype with adjusted Cox proportional models. Results- At the time of magnetic resonance imaging, 236 participants (18%) had CBI (144 [61%] distal cryptogenic, 29 [12%] distal cardioembolic, 26 [11%] large artery atherosclerosis, and 37 [16%] penetrating artery disease). Smaller (per mm, odds ratio, 0.8 [0.8-0.9]) and nonbrain stem infarcts (odds ratio, 0.2 [0.1-0.6]) were more likely to be covert. During the follow-up period (10.4±3.1 years), 398 (31%) died (162 [13%] of vascular death) and 117 (9%) had a stroke (99 [85%]) were ischemic. Risks of events varied by CBI subtype, with the highest risk of stroke (hazard ratio, 2.2 [1.3-3.7]) and vascular death (hazard ratio, 2.24 [1.29-3.88]) noted in participants with intracranial large artery atherosclerosis-related CBI. Conclusions- CBI can be classified into subtypes that have differential outcomes. Certain CBI subtypes such as those related to intracranial large artery atherosclerosis have a high risk of adverse vascular outcomes and could warrant consideration of treatment trials.
Topics: Aged; Atrial Fibrillation; Brain Infarction; Brain Ischemia; Cerebral Infarction; Female; Humans; Infarction; Intracranial Arteriosclerosis; Male; Middle Aged; Risk Factors; Stroke
PubMed: 31766980
DOI: 10.1161/STROKEAHA.119.026068 -
Circulation. Cardiovascular Imaging Aug 2017The purpose of this systematic review is to provide a clinically relevant, disease-based perspective on myocardial strain imaging in patients with acute myocardial... (Review)
Review
The purpose of this systematic review is to provide a clinically relevant, disease-based perspective on myocardial strain imaging in patients with acute myocardial infarction or stable ischemic heart disease. Cardiac magnetic resonance imaging uniquely integrates myocardial function with pathology. Therefore, this review focuses on strain imaging with cardiac magnetic resonance. We have specifically considered the relationships between left ventricular (LV) strain, infarct pathologies, and their associations with prognosis. A comprehensive literature review was conducted in accordance with the PRISMA guidelines. Publications were identified that (1) described the relationship between strain and infarct pathologies, (2) assessed the relationship between strain and subsequent LV outcomes, and (3) assessed the relationship between strain and health outcomes. In patients with acute myocardial infarction, circumferential strain predicts the recovery of LV systolic function in the longer term. The prognostic value of longitudinal strain is less certain. Strain differentiates between infarcted versus noninfarcted myocardium, even in patients with stable ischemic heart disease with preserved LV ejection fraction. Strain recovery is impaired in infarcted segments with intramyocardial hemorrhage or microvascular obstruction. There are practical limitations to measuring strain with cardiac magnetic resonance in the acute setting, and knowledge gaps, including the lack of data showing incremental value in clinical practice. Critically, studies of cardiac magnetic resonance strain imaging in patients with ischemic heart disease have been limited by sample size and design. Strain imaging has potential as a tool to assess for early or subclinical changes in LV function, and strain is now being included as a surrogate measure of outcome in therapeutic trials.
Topics: Biomechanical Phenomena; Echocardiography; Female; Humans; Magnetic Resonance Imaging, Cine; Male; Middle Aged; Myocardial Contraction; Myocardium; Predictive Value of Tests; Prognosis; Recovery of Function; Reproducibility of Results; ST Elevation Myocardial Infarction; Stress, Mechanical; Ventricular Function, Left
PubMed: 28733364
DOI: 10.1161/CIRCIMAGING.117.006498 -
Abdominal Radiology (New York) Jun 2023Infarcts and ischemia of abdominal organs may present with acute abdominal pain, and early diagnosis is crucial to prevent morbidity and mortality. Unfortunately, some... (Review)
Review
Infarcts and ischemia of abdominal organs may present with acute abdominal pain, and early diagnosis is crucial to prevent morbidity and mortality. Unfortunately, some of these patients present in poor clinical conditions to the emergency department, and imaging specialists are crucial for optimal outcomes. Although the radiological diagnosis of abdominal infarcts is often straightforward, it is vital to use the appropriate imaging modalities and correct imaging techniques for their detection. Additionally, some non-infarct-related abdominal pathologies may mimic infarcts, cause diagnostic confusion, and result in delayed diagnosis or misdiagnosis. In this article, we aimed to outline the general imaging approach, present cross-sectional imaging findings of infarcts and ischemia in several abdominal organs, including but not limited to, liver, spleen, kidneys, adrenals, omentum, and intestinal segments with relevant vascular anatomy, discuss possible differential diagnoses and emphasize important clinical/radiological clues that may assist radiologists in the diagnostic process.
Topics: Humans; Abdomen; Abdomen, Acute; Diagnostic Imaging; Abdominal Pain; Infarction; Ischemia
PubMed: 36933024
DOI: 10.1007/s00261-023-03877-2 -
AJNR. American Journal of Neuroradiology Jan 2017Acute stroke presentation and outcome depend on both ischemic infarct volume and location. We aimed to determine the association between acute ischemic infarct topology...
BACKGROUND AND PURPOSE
Acute stroke presentation and outcome depend on both ischemic infarct volume and location. We aimed to determine the association between acute ischemic infarct topology and lesion volume and stroke severity at presentation and discharge.
MATERIALS AND METHODS
Patients with acute ischemic stroke who underwent MR imaging within 24 hours of symptom onset or last seen well were included. Infarcts were segmented and coregistered on the Montreal Neurological Institute-152 brain map. Voxel-based analyses were performed to determine the distribution of infarct lesions associated with larger volumes, higher NIHSS scores at admission and discharge, and greater NIHSS/volume ratios.
RESULTS
A total of 238 patients were included. Ischemic infarcts involving the bilateral lentiform nuclei, insular ribbons, middle corona radiata, and right precentral gyrus were associated with larger infarct volumes (average, 76.7 ± 125.6 mL versus 16.4 ± 24.0 mL, P < .001) and higher admission NIHSS scores. Meanwhile, brain stem and thalami infarctions were associated with higher admission NIHSS/volume ratios. The discharge NIHSS scores were available in 218 patients, in whom voxel-based analysis demonstrated that ischemic infarcts of the bilateral posterior insular ribbons, middle corona radiata, and right precentral gyrus were associated with more severe symptoms at discharge, whereas ischemic lesions of the brain stem, bilateral thalami, and, to a lesser extent, the middle corona radiata were associated with higher ratios of discharge NIHSS score/infarct volume.
CONCLUSIONS
Acute ischemic infarcts of the insulae, lentiform nuclei, and middle corona radiata tend to have larger volumes, more severe presentations, and worse outcomes, whereas brain stem and thalamic infarcts have greater symptom severity relative to smaller lesion volumes.
Topics: Aged; Aged, 80 and over; Cerebral Infarction; Female; Hospitalization; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Patient Discharge; Severity of Illness Index
PubMed: 27758775
DOI: 10.3174/ajnr.A4970 -
Annals of Thoracic and Cardiovascular... 2013Treatment for postinfarction ventricular septal defect has been improving for several decades. Aggressive resection of the infarcted myocardium (infarctectomy and... (Review)
Review
Treatment for postinfarction ventricular septal defect has been improving for several decades. Aggressive resection of the infarcted myocardium (infarctectomy and closure technique) and preserving infarcted myocardium (infarct exclusion technique) have been technically modified. Recent improvement includes use of surgical glue, using an additional patch for infarct exclusion, septal exclusion, sandwich technique via right or left ventricular approach, and endovascular repair. This field still has room for cardiac surgeons to improve surgical strategy and technique.
Topics: Cardiac Surgical Procedures; History, 19th Century; History, 20th Century; History, 21st Century; Humans; Myocardial Infarction; Postoperative Complications; Risk Factors; Time Factors; Treatment Outcome; Ventricular Septal Rupture
PubMed: 23575001
DOI: 10.5761/atcs.ra.12.02201 -
Conformational and thermal characterization of left ventricle remodeling post-myocardial infarction.Biochimica Et Biophysica Acta.... Jun 2017Adverse cardiac remodeling after myocardial infarction (MI) causes impaired ventricular function and heart failure. Histopathological characterization is commonly used...
Adverse cardiac remodeling after myocardial infarction (MI) causes impaired ventricular function and heart failure. Histopathological characterization is commonly used to detect the location, size and shape of MI sites. However, the information about chemical composition, physical structure and molecular mobility of peri- and infarct zones post-MI is rather limited. The main objective of this work was to explore the spatiotemporal biochemical and biophysical alterations of key cardiac components post-MI. The FTIR spectra of healthy and remote myocardial tissue shows amides A, I, II and III associated with proteins in freeze-died tissue as major absorptions bands. In infarcted myocardium, the spectrum of these main absorptions was deeply altered. FITR evidenced an increase of the amide A band and the distinct feature of the collagen specific absorption band at 1338cm in the infarct area at 21days post-MI. At 21days post-MI, it also appears an important shift of amide I from 1646cm to 1637cm that suggests the predominance of the triple helical conformation in the proteins. The new spectra bands also indicate an increase in proteoglycans, residues of carbohydrates in proteins and polysaccharides in ischemic areas. Thermal analysis indicates a deep increase of unfreezable water/freezable water in peri- and infarcted tissues. In infarcted tissue is evidenced the impairment of myofibrillar proteins thermal profile and the emergence of a new structure. In conclusion, our results indicate a profound evolution of protein secondary structures in association with collagen deposition and reorganization of water involved in the scar maturation of peri- and infarct zones post-MI.
Topics: Animals; Male; Mice; Muscle Proteins; Myocardial Infarction; Myocardium; Protein Structure, Secondary; Spectroscopy, Fourier Transform Infrared; Ventricular Remodeling
PubMed: 28245984
DOI: 10.1016/j.bbadis.2017.02.025 -
JACC. Cardiovascular Imaging Feb 2023Adverse LV remodeling post-ST-segment elevation myocardial infarction (STEMI) is associated with a poor prognosis, but the underlying mechanisms are not fully...
BACKGROUND
Adverse LV remodeling post-ST-segment elevation myocardial infarction (STEMI) is associated with a poor prognosis, but the underlying mechanisms are not fully understood. Diffusion tensor (DT)-cardiac magnetic resonance (CMR) allows in vivo characterization of myocardial architecture and provides unique mechanistic insight into pathophysiologic changes following myocardial infarction.
OBJECTIVES
This study evaluated the potential associations between DT-CMR performed soon after STEMI and long-term adverse left ventricular (LV) remodeling following STEMI.
METHODS
A total of 100 patients with STEMI underwent CMR at 5 days and 12 months post-reperfusion. The protocol included DT-CMR for assessing fractional anisotropy (FA), secondary eigenvector angle (E2A) and helix angle (HA), cine imaging for assessing LV volumes, and late gadolinium enhancement for calculating infarct and microvascular obstruction size. Adverse remodeling was defined as a 20% increase in LV end-diastolic volume at 12 months.
RESULTS
A total of 32 patients experienced adverse remodeling at 12 months. Compared with patients without adverse remodeling, they had lower FA (0.23 ± 0.03 vs 0.27 ± 0.04; P < 0.001), lower E2A (37 ± 6° vs 51 ± 7°; P < 0.001), and, on HA maps, a lower proportion of myocytes with right-handed orientation (RHM) (8% ± 5% vs 17% ± 9%; P < 0.001) in their acutely infarcted myocardium. On multivariable logistic regression analysis, infarct FA (odds ratio [OR]: <0.01; P = 0.014) and E2A (OR: 0.77; P = 0.001) were independent predictors of adverse LV remodeling after adjusting for left ventricular ejection fraction (LVEF) and infarct size. There were no significant changes in infarct FA, E2A, or RHM between the 2 scans.
CONCLUSIONS
Extensive cardiomyocyte disorganization (evidenced by low FA), acute loss of sheetlet angularity (evidenced by low E2A), and a greater loss of organization among cardiomyocytes with RHM, corresponding to the subendocardium, can be detected within 5 days post-STEMI. These changes persist post-injury, and low FA and E2A are independently associated with long-term adverse remodeling.
Topics: Humans; ST Elevation Myocardial Infarction; Stroke Volume; Magnetic Resonance Imaging, Cine; Contrast Media; Ventricular Function, Left; Predictive Value of Tests; Gadolinium; Myocardial Infarction; Percutaneous Coronary Intervention; Ventricular Remodeling
PubMed: 36412993
DOI: 10.1016/j.jcmg.2022.04.002 -
NeuroImage. Clinical 2022The integration of somatosensory, ocular motor and vestibular signals is necessary for self-location in space and goal-directed action. We aimed to detect remote changes...
OBJECTIVE
The integration of somatosensory, ocular motor and vestibular signals is necessary for self-location in space and goal-directed action. We aimed to detect remote changes in the cerebral cortex after thalamic infarcts to reveal the thalamo-cortical connections necessary for multisensory processing and ocular motor control.
METHODS
Thirteen patients with unilateral ischemic thalamic infarcts presenting with vestibular, somatosensory, and ocular motor symptoms were examined longitudinally in the acute phase and after six months. Voxel- and surface-based morphometry were used to detect changes in vestibular and multisensory cortical areas and known hubs of central ocular motor processing. The results were compared with functional connectivity data in 50 healthy volunteers.
RESULTS
Patients with paramedian infarcts showed impaired saccades and vestibular perception, i.e., tilts of the subjective visual vertical (SVV). The most common complaint in these patients was double vision or vertigo / dizziness. Posterolateral thalamic infarcts led to tilts of the SVV and somatosensory deficits without vertigo. Tilts of the SVV were higher in paramedian compared to posterolateral infarcts (median 11.2° vs 3.8°). Vestibular and ocular motor symptoms recovered within six months. Somatosensory deficits persisted. Structural longitudinal imaging showed significant volume reduction in subcortical structures connected to the infarcted thalamic nuclei (vestibular nuclei region, dentate nucleus region, trigeminal root entry zone, medial lemniscus, superior colliculi). Volume loss was evident in connections to the frontal, parietal and cingulate lobes. Changes were larger in the ipsilesional hemisphere but were also detected in homotopical regions contralesionally. The white matter volume reduction led to deformation of the cortical projection zones of the infarcted nuclei.
CONCLUSIONS
White matter volume loss after thalamic infarcts reflects sensory input from the brainstem as well the cortical projections of the main affected nuclei for sensory and ocular motor processing. Changes in the cortical geometry seem not to reflect gray matter atrophy but rather reshaping of the cortical surface due to the underlying white matter atrophy.
Topics: Cerebral Cortex; Cerebral Infarction; Humans; Thalamus; Vestibule, Labyrinth; White Matter
PubMed: 35139478
DOI: 10.1016/j.nicl.2022.102953 -
PloS One 2020We hypothesized that admission insular infarcts could be associated with early neurological deterioration (END) in acute minor stroke with large vessel occlusion.
BACKGROUND AND PURPOSE
We hypothesized that admission insular infarcts could be associated with early neurological deterioration (END) in acute minor stroke with large vessel occlusion.
METHODS
Using acute and follow-up diffusion-weighted imaging (DWI), we assessed insular involvement including the percent insular ribbon infarction (PIRI) scores and follow-up lesion patterns in acute minor stroke (NIHSS ≤5) with MCA/ICA occlusion. Follow-up lesion patterns were classified as swelling, new lesions, or infarct growth. END was defined as any increase in the NIHSS score.
RESULTS
Among 166 patients (age: 66±12 y, 60.8% male), 82 (49.4%) had insular lesions on baseline DWI, and 64 (38.6%) had PIRI scores ≥2. On follow-up DWI, infarct growths, new lesions, and swelling were observed in 34.9%, 69.9%, and 29.5% of patients. Infarct growths were significantly more frequent in patients with insular infarcts (43.9%), especially those with a PIRI score of 2 (54.8%), than in patients without insular infarcts (p = 0.02). While END was not significantly different in patients with and without insular lesions, insular lesions were independently associated with infarct growths (OR 2.18, 95% CI 1.12-4.26, p = 0.02) and END due to infarct growth (OR 2.54, 95% CI 1.12-5.76, p = 0.03), particularly in those with PIRI scores ≥2.
CONCLUSION
In acute minor stroke with MCA/ICA occlusion, insular lesions on admission DWI, especially in patients with PIRI scores ≥2, were more likely to exhibit infarct growth and END due to infarct growth. This finding may help identify patients with higher risks of clinical worsening following acute minor stroke with large vessel occlusion.
Topics: Adult; Aged; Aged, 80 and over; Diffusion Magnetic Resonance Imaging; Female; Humans; Infarction, Middle Cerebral Artery; Male; Middle Aged; Retrospective Studies; Severity of Illness Index
PubMed: 32160209
DOI: 10.1371/journal.pone.0229836