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The Journal of Physiology Sep 2022Hypertensive heart disease (HHD) increases risk of ventricular tachycardia (VT) and ventricular fibrillation (VF). The roles of structural vs. electrophysiological...
Hypertensive heart disease (HHD) increases risk of ventricular tachycardia (VT) and ventricular fibrillation (VF). The roles of structural vs. electrophysiological remodelling and age vs. disease progression are not fully understood. This cross-sectional study of cardiac alterations through HHD investigates mechanistic contributions to VT/VF risk. Risk was electrically assessed in Langendorff-perfused, spontaneously hypertensive rat hearts at 6, 12 and 18 months, and paced optical membrane voltage maps were acquired from the left ventricular (LV) free wall epicardium. Distributions of LV patchy fibrosis and 3D cellular architecture in representative anterior LV mid-wall regions were quantified from macroscopic and microscopic fluorescence images of optically cleared tissue. Imaging showed increased fibrosis from 6 months, particularly in the inner LV free wall. Myocyte cross-section increased at 12 months, while inter-myocyte connections reduced markedly with fibrosis. Conduction velocity decreased from 12 months, especially transverse to the myofibre direction, with rate-dependent anisotropy at 12 and 18 months, but not earlier. Action potential duration (APD) increased when clustered by age, as did APD dispersion at 12 and 18 months. Among 10 structural, functional and age variables, the most reliably linked were VT/VF risk, general LV fibrosis, a measure quantifying patchy fibrosis, and non-age clustered APD dispersion. VT/VF risk related to a quantified measure of patchy fibrosis, but age did not factor strongly. The findings are consistent with the notion that VT/VF risk is associated with rate-dependent repolarization heterogeneity caused by structural remodelling and reduced lateral electrical coupling between LV myocytes, providing a substrate for heterogeneous intramural activation as HHD progresses. KEY POINTS: There is heightened arrhythmic risk with progression of hypertensive heart disease. Risk is related to increasing left ventricular fibrosis, but the nature of this relationship has not been quantified. This study is a novel systematic characterization of changes in active electrical properties and fibrotic remodelling during progression of hypertensive heart disease in a well-established animal disease model. Arrhythmic risk is predicted by several left ventricular measures, in particular fibrosis quantity and structure, and epicardial action potential duration dispersion. Age alone is not a good predictor of risk. An improved understanding of links between arrhythmic risk and fibrotic architectures in progressive hypertensive heart disease aids better interpretation of late gadolinium-enhanced cardiac magnetic resonance imaging and electrical mapping signals.
Topics: Action Potentials; Animals; Arrhythmias, Cardiac; Cross-Sectional Studies; Fibrosis; Multimodal Imaging; Pericardium; Rats; Rats, Inbred SHR; Tachycardia, Ventricular; Ventricular Fibrillation
PubMed: 35984854
DOI: 10.1113/JP282526 -
International Journal of Nanomedicine 2012Myocardial infarction (MI) is characterized by heart-wall thinning, myocyte slippage, and ventricular dilation. The injury to the heart-wall muscle after MI is... (Review)
Review
Myocardial infarction (MI) is characterized by heart-wall thinning, myocyte slippage, and ventricular dilation. The injury to the heart-wall muscle after MI is permanent, as after an abundant cell loss the myocardial tissue lacks the intrinsic capability to regenerate. New therapeutics are required for functional improvement and regeneration of the infarcted myocardium, to overcome harmful diagnosis of patients with heart failure, and to overcome the shortage of heart donors. In the past few years, myocardial tissue engineering has emerged as a new and ambitious approach for treating MI. Several left ventricular assist devices and epicardial patches have been developed for MI. These devices and acellular/cellular cardiac patches are employed surgically and sutured to the epicardial surface of the heart, limiting the region of therapeutic benefit. An injectable system offers the potential benefit of minimally invasive release into the myocardium either to restore the injured extracellular matrix or to act as a scaffold for cell delivery. Furthermore, intramyocardial injection of biomaterials and cells has opened new opportunities to explore and also to augment the potentials of this technique to ease morbidity and mortality rates owing to heart failure. This review summarizes the growing body of literature in the field of myocardial tissue engineering, where biomaterial injection, with or without simultaneous cellular delivery, has been pursued to enhance functional and structural outcomes following MI. Additionally, this review also provides a complete outlook on the tissue-engineering therapies presently being used for myocardial regeneration, as well as some perceptivity into the possible issues that may hinder its progress in the future.
Topics: Animals; Cells, Cultured; Guided Tissue Regeneration; Humans; Injections, Intralesional; Minimally Invasive Surgical Procedures; Myocardial Ischemia; Myocytes, Cardiac; Pericardium; Tissue Engineering; Tissue Scaffolds
PubMed: 23271906
DOI: 10.2147/IJN.S37575 -
Frontiers in Endocrinology 2021In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity... (Review)
Review
In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the "cytokine storm" and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.
Topics: Adipose Tissue; Angiotensin-Converting Enzyme 2; COVID-19; Cardiomyopathies; Heart Diseases; Humans; Inflammation; Intra-Abdominal Fat; Obesity; Pericardium; Prognosis; SARS-CoV-2; Serine Endopeptidases
PubMed: 34484128
DOI: 10.3389/fendo.2021.726967 -
Stem Cell Research & Therapy May 2015Engineered bioimplants for cardiac repair require functional vascularization and innervation for proper integration with the surrounding myocardium. The aim of this work...
Engineered bioimplants for cardiac repair require functional vascularization and innervation for proper integration with the surrounding myocardium. The aim of this work was to study nerve sprouting and neovascularization in an acellular pericardial-derived scaffold used as a myocardial bioimplant. To this end, 17 swine were submitted to a myocardial infarction followed by implantation of a decellularized human pericardial-derived scaffold. After 30 days, animals were sacrificed and hearts were analyzed with hematoxylin/eosin and Masson's and Gallego's modified trichrome staining. Immunohistochemistry was carried out to detect nerve fibers within the cardiac bioimplant by using βIII tubulin and S100 labeling. Isolectin B4, smooth muscle actin, CD31, von Willebrand factor, cardiac troponin I, and elastin antibodies were used to study scaffold vascularization. Transmission electron microscopy was performed to confirm the presence of vascular and nervous ultrastructures. Left ventricular ejection fraction (LVEF), cardiac output (CO), stroke volume, end-diastolic volume, end-systolic volume, end-diastolic wall mass, and infarct size were assessed by using magnetic resonance imaging (MRI). Newly formed nerve fibers composed of several amyelinated axons as the afferent nerve endings of the heart were identified by immunohistochemistry. Additionally, neovessel formation occurred spontaneously as small and large isolectin B4-positive blood vessels within the scaffold. In summary, this study demonstrates for the first time the neoformation of vessels and nerves in cell-free cardiac scaffolds applied over infarcted tissue. Moreover, MRI analysis showed a significant improvement in LVEF (P = 0.03) and CO (P = 0.01) and a 43 % decrease in infarct size (P = 0.007).
Topics: Animals; Coronary Vessels; Immunohistochemistry; Magnetic Resonance Imaging; Myocardial Infarction; Myocardium; Neovascularization, Pathologic; Pericardium; S100 Proteins; Swine; Tissue Scaffolds; Tubulin; Ventricular Function, Left
PubMed: 26205795
DOI: 10.1186/s13287-015-0101-6 -
TheScientificWorldJournal Nov 2007During heart development, cells of the primary and secondary heart field give rise to the myocardial component of the heart. The neural crest and epicardium provide the... (Review)
Review
During heart development, cells of the primary and secondary heart field give rise to the myocardial component of the heart. The neural crest and epicardium provide the heart with a considerable amount of nonmyocardial cells that are indispensable for correct heart development. During the past 2 decades, the importance of epicardium-derived cells (EPDCs) in heart formation became increasingly clear. The epicardium is embryologically formed by the outgrowth of proepicardial cells over the naked heart tube. Following epithelial-mesenchymal transformation, EPDCs form the subepicardial mesenchyme and subsequently migrate into the myocardium, and differentiate into smooth muscle cells and fibroblasts. They contribute to the media of the coronary arteries, to the atrioventricular valves, and the fibrous heart skeleton. Furthermore, they are important for the myocardial architecture of the ventricular walls and for the induction of Purkinje fiber formation. Whereas the exact signaling cascades in EPDC migration and function still need to be elucidated, recent research has revealed several factors that are involved in EPDC migration and specialization, and in the cross-talk between EPDCs and other cells during heart development. Among these factors are the Ets transcription factors Ets-1 and Ets-2. New data obtained with lentiviral antisense constructs targeting Ets-1 and Ets-2 specifically in the epicardium indicate that both factors are independently involved in the migratory behavior of EPDCs. Ets-2 seems to be especially important for the migration of EPDCs into the myocardial wall, and to subendocardial positions in the atrioventricular cushions and the trabeculae. With respect to the clinical importance of correct EPDC development, the relation with coronary arteriogenesis has been noted well before. In this review, we also propose a role for EPDCs in cardiac looping, and emphasize their contribution to the development of the valves and myocardial architecture. Lastly, we focus on the congenital heart anomalies that might be caused primarily by an epicardial developmental defect.
Topics: Animals; Heart Defects, Congenital; Humans; Morphogenesis; Myocytes, Cardiac; Pericardium; Proto-Oncogene Protein c-ets-1; Proto-Oncogene Protein c-ets-2
PubMed: 18040540
DOI: 10.1100/tsw.2007.294 -
Heart Rhythm Feb 2021The absence of strategies to consistently and effectively address nonparoxysmal atrial fibrillation by nonpharmacological interventions has represented a long-standing... (Review)
Review
The absence of strategies to consistently and effectively address nonparoxysmal atrial fibrillation by nonpharmacological interventions has represented a long-standing treatment gap. A combined epicardial/endocardial ablation strategy, the hybrid Convergent procedure, was developed in response to this clinical need. A subxiphoid incision is used to access the pericardial space facilitating an epicardial ablation directed at isolation of the posterior wall of the left atrium. This is followed by an endocardial ablation to complete isolation of the pulmonary veins and for additional ablation as needed. Experience gained with the hybrid Convergent procedure during the last decade has led to the development and adoption of strategies to optimize the technique and mitigate risks. Additionally, a surgical and electrophysiology "team" approach including comprehensive training is believed critical to successfully develop the hybrid Convergent program. A recently completed randomized clinical trial indicated that this ablation strategy is superior to an endocardial-only approach for patients with persistent atrial fibrillation. In this review, we propose and describe best practice guidelines for hybrid Convergent ablation on the basis of a combination of published data, author consensus, and expert opinion. A summary of clinical outcomes, emerging evidence, and future perspectives is also given.
Topics: Atrial Fibrillation; Catheter Ablation; Endocardium; Heart Conduction System; Heart Rate; Humans; Pericardium; Practice Guidelines as Topic; Recurrence
PubMed: 33045430
DOI: 10.1016/j.hrthm.2020.10.004 -
Pediatric Reports Jan 2021Congenital pericardial cysts are rare anomalies caused by the failure of fetal lacunae to coalesce into pericardial coelom. In this article a 9-year-old boy admitted...
Congenital pericardial cysts are rare anomalies caused by the failure of fetal lacunae to coalesce into pericardial coelom. In this article a 9-year-old boy admitted with complain of palpitation in daily activities. The electrocardiography detected sinus tachycardia of 150 beats per minute with normal axis. Although chest X ray were normal, echocardiography showed an abnormal mass that compressed the posterior wall of left ventricle. The mass was extrinsic and confined to the pericardium. After midsternotomy, a huge cyst was found and totally excised. The complications of pericardial cyst can be significant, and the diagnosis relies on a careful examination and radiographic findings.
PubMed: 33467404
DOI: 10.3390/pediatric13010007 -
Journal of Biomechanics Jun 1996Recent research suggests that left ventricular torsion is an important indicator of cardiac function. We used two theoretical models to study the mechanics of this...
Recent research suggests that left ventricular torsion is an important indicator of cardiac function. We used two theoretical models to study the mechanics of this phenomenon: a compressible cylinder and an incompressible ellipsoid of revolution. The analyses of both models account for large- strain passive and active material behavior, with a muscle fiber angle that varies linearly from endocardium to epicardium. Relative to the end- diastolic configuration, the predicted torsion exhibits several experimentally observed features, including a peak near end systole, rapid untwisting during isovolumic relaxation, and increased twist near the apex. The magnitude of the twist is sensitive to the fiber architecture, the ventricular geometry, and the compressibility and contractility of the myocardium. In particular, the model predicts that the systolic twist increases with increasing compressibility, contractility, and wall thickness, while it decreases with increasing cavity volume. The peak twist approximately doubles (from about 0.02 to 0.04 rad cm(-1)) with a doubling of myocardial compressibility or with a change in the endocardial/epicardial muscle fiber angles from 90/ -90 degrees to 60/ -60 degrees. The twist is less sensitive to changes in contractility and ventricular geometry. These findings provide a basis for interpreting measurements of ventricular torsion in the clinical setting.
Topics: Animals; Biomechanical Phenomena; Cardiac Volume; Computer Simulation; Diastole; Dogs; Endocardium; Forecasting; Heart Ventricles; Models, Cardiovascular; Muscle Fibers, Skeletal; Myocardial Contraction; Pericardium; Rotation; Systole; Ventricular Function; Ventricular Function, Left
PubMed: 9147971
DOI: 10.1016/0021-9290(95)00129-8 -
BMC Cardiovascular Disorders May 2021We examined the relationship between epicardial fat thickness (EFT) measured by echocardiography and left ventricular diastolic function parameters in a Beijing...
BACKGROUND
We examined the relationship between epicardial fat thickness (EFT) measured by echocardiography and left ventricular diastolic function parameters in a Beijing community population.
METHODS
We included 1004 participants in this study. Echocardiographic parameters including E and A peak velocity, the early diastolic velocities (e') of the septal and lateral mitral annulus using tissue doppler imaging, E/e', and EFT were measured. EFT1 was measured perpendicularly on the right ventricular free wall at end diastole in the extension line of the aortic root. EFT2 was the maximum thickness measured perpendicularly on the right ventricular free wall at end diastole. Multivariable linear regression was used to analyze the relationship between EFT and the mean e' and E/e'.
RESULTS
The mean age of the participants was 63.91 ± 9.02 years, and 51.4% were men. EFT1 and EFT2 were negatively correlated with lateral e', septal e', and mean e' (p < 0.05), and the correlation coefficient for EFT1 and EFT2 and mean e' was - 0.138 and - 0.180, respectively. EFT1 and EFT2 were positively correlated with lateral E/e', septal E/e', and mean E/e' (p < 0.05), and the correlation coefficient for EFT1 and EFT2 and mean e' was 0.100 and 0.090, respectively. Multivariable egression analysis showed that EFT2 was independently and negatively associated with e' mean (β = - 0.078 [95% confidence interval = - 0.143, - 0.012, p = 0.020]). There were no interactions between EFT2 and any covariates, including age or heart groups, sex, BMI, or presence of hypertension, diabetes, or coronary heart disease, in relation to left ventricular diastolic dysfunction.
CONCLUSIONS
EFT2 was negatively and independently associated with e' mean, which suggests that more attention to this type of adipose fat is required for cardiovascular disease therapy.
Topics: Adipose Tissue; Adiposity; Adult; Aged; Beijing; Diastole; Echocardiography, Doppler; Female; Humans; Male; Middle Aged; Pericardium; Predictive Value of Tests; Prevalence; Risk Factors; Ventricular Dysfunction, Left; Ventricular Function, Left
PubMed: 34049490
DOI: 10.1186/s12872-021-02071-w -
Indian Journal of Thoracic and... Sep 2021Constrictive pericarditis is a great mimic and has posed a diagnostic dilemma since its first description 300 years ago as "Concretio Cordis." It can mimic restrictive...
Constrictive pericarditis is a great mimic and has posed a diagnostic dilemma since its first description 300 years ago as "Concretio Cordis." It can mimic restrictive cardiomyopathy, endomyocardial fibrosis, and chronic liver and renal disease. This would perhaps be the first clinical report of constriction in patients undergoing cardiac transplantation. We report two distinct cases with cardiomyopathy requiring cardiac transplantation and the clinical implications of concomitant pericardial constriction. While the first case mimics a natural "cardiac support device," which addresses ventricular remodeling in heart failure by reducing the wall stress, the second case is a case in point against the use of "biological pericardial membrane-like the bovine pericardium," as a pericardial substitute.
PubMed: 34511768
DOI: 10.1007/s12055-021-01157-6