Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 30.048
Filtrar
1.
Folia Med Cracov ; 61(2): 103-115, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34510168

RESUMO

I n t r o d u c t i o n: Mortality from myocardial infarction (MI) is determined by patients' ability to prevent it and, in case of its occurrence, to recognise its symptoms and call an ambulance immediately. There is scarce data on rural populations' knowledge of MI, even though they are disadvantaged in access to medical emergency services. Objective: The aim of the study was to investigate the rural patients' awareness of MI risk factors, symptoms, necessity of calling an ambulance in response to MI symptoms, and its determinants. Materials and Methods: An anonymous and voluntary survey was conducted among 194 patients and their caregivers with median age 68 years at a rural non-public healthcare facility in Poland. R e s u l t s: 60.3% perceive their knowledge of MI as insufficient. Only 26.3% were able to recognise all suggested MI risk factors. 44.8% did not know whether they are at risk of MI. Furthermore, 78% of respondents who had at least three MI risk factors were unaware of being at risk. 45.4% recognised at least three out of four suggested MI symptoms. 76.2% would call an ambulance in response to chest pain suggesting they have MI. Merely 80% were able to provide the emergency phone number. Moreover, among respondents who declared they would not call an ambulance, 38.7% were afraid of in-hospital COVID-19 infection or healthcare system collapse. C o n c l u s i o n s: Rural patients' knowledge of MI risk factors, symptoms, and proper response to them is insufficient. The problem is exacerbated by the COVID-19 pandemic. To improve survival in MI an education campaign is needed.


Assuntos
Serviços Médicos de Emergência , Conhecimentos, Atitudes e Prática em Saúde , Comportamento de Busca de Ajuda , Infarto do Miocárdio/fisiopatologia , População Rural , Idoso , COVID-19 , Dor no Peito , Gerenciamento Clínico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/epidemiologia , Infarto do Miocárdio/terapia , Polônia , Fatores de Risco , SARS-CoV-2
2.
Sci Rep ; 11(1): 15667, 2021 08 02.
Artigo em Inglês | MEDLINE | ID: mdl-34341436

RESUMO

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and is primarily characterised by a respiratory disease. However, SARS-CoV-2 can directly infect vascular endothelium and subsequently cause vascular inflammation, atherosclerotic plaque instability and thereby result in both endothelial dysfunction and myocardial inflammation/infarction. Interestingly, up to 50% of patients suffer from persistent exercise dyspnoea and a post-viral fatigue syndrome (PVFS) after having overcome an acute COVID-19 infection. In the present study, we assessed the presence of coronary microvascular disease (CMD) by cardiovascular magnetic resonance (CMR) in post-COVID-19 patients still suffering from exercise dyspnoea and PVFS. N = 22 patients who recently recovered from COVID-19, N = 16 patients with classic hypertrophic cardiomyopathy (HCM) and N = 17 healthy control patients without relevant cardiac disease underwent dedicated vasodilator-stress CMR studies on a 1.5-T MR scanner. The CMR protocol comprised cine and late-gadolinium-enhancement (LGE) imaging as well as velocity-encoded (VENC) phase-contrast imaging of the coronary sinus flow (CSF) at rest and during pharmacological stress (maximal vasodilation induced by 400 µg IV regadenoson). Using CSF measurements at rest and during stress, global myocardial perfusion reserve (MPR) was calculated. There was no difference in left ventricular ejection-fraction (LV-EF) between COVID-19 patients and controls (60% [57-63%] vs. 63% [60-66%], p = NS). There were only N = 4 COVID-19 patients (18%) showing a non-ischemic pattern of LGE. VENC-based flow measurements showed that CSF at rest was higher in COVID-19 patients compared to controls (1.78 ml/min [1.19-2.23 ml/min] vs. 1.14 ml/min [0.91-1.32 ml/min], p = 0.048). In contrast, CSF during stress was lower in COVID-19 patients compared to controls (3.33 ml/min [2.76-4.20 ml/min] vs. 5.32 ml/min [3.66-5.52 ml/min], p = 0.05). A significantly reduced MPR was calculated in COVID-19 patients compared to healthy controls (2.73 [2.10-4.15-11] vs. 4.82 [3.70-6.68], p = 0.005). No significant differences regarding MPR were detected between COVID-19 patients and HCM patients. In post-COVID-19 patients with persistent exertional dyspnoea and PVFS, a significantly reduced MPR suggestive of CMD-similar to HCM patients-was observed in the present study. A reduction in MPR can be caused by preceding SARS-CoV-2-associated direct as well as secondary triggered mechanisms leading to diffuse CMD, and may explain ongoing symptoms of exercise dyspnoea and PVFS in some patients after COVID-19 infection.


Assuntos
COVID-19 , Cardiomiopatia Hipertrófica , Circulação Coronária , Vasos Coronários , Angiografia por Ressonância Magnética , Microcirculação , Infarto do Miocárdio , Imagem de Perfusão do Miocárdio , SARS-CoV-2 , Adulto , Idoso , COVID-19/complicações , COVID-19/diagnóstico por imagem , COVID-19/fisiopatologia , Cardiomiopatia Hipertrófica/diagnóstico por imagem , Cardiomiopatia Hipertrófica/etiologia , Vasos Coronários/diagnóstico por imagem , Vasos Coronários/fisiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/diagnóstico por imagem , Infarto do Miocárdio/etiologia , Infarto do Miocárdio/fisiopatologia , Projetos Piloto
3.
Molecules ; 26(16)2021 Aug 18.
Artigo em Inglês | MEDLINE | ID: mdl-34443591

RESUMO

The development and progression of heart failure (HF) due to myocardial infarction (MI) is a major concern even with current optimal therapy. Resveratrol is a plant polyphenol with cardioprotective properties. Sacubitril/valsartan is known to be beneficial in chronic HF patients. In this study, we investigated the comparative and combinatorial benefits of resveratrol with sacubitril/valsartan alongside an active comparator valsartan in MI-induced male Sprague Dawley rats. MI-induced and sham-operated animals received vehicle, resveratrol, sacubitril/valsartan, valsartan alone or sacubitril/valsartan + resveratrol for 8 weeks. Echocardiography was performed at the endpoint to assess cardiac structure and function. Cardiac oxidative stress, inflammation, fibrosis, brain natriuretic peptide (BNP), creatinine and neutrophil gelatinase associated lipocalin were measured. Treatment with resveratrol, sacubitril/valsartan, valsartan and sacubitril/valsartan + resveratrol significantly prevented left ventricular (LV) dilatation and improved LV ejection fraction in MI-induced rats. All treatments also significantly reduced myocardial tissue oxidative stress, inflammation and fibrosis, as well as BNP. Treatment with the combination of sacubitril/valsartan and resveratrol did not show additive effects. In conclusion, resveratrol, sacubitril/valsartan, and valsartan significantly prevented cardiac remodeling and dysfunction in MI-induced rats. The reduction in cardiac remodeling and dysfunction in MI-induced rats was mediated by a reduction in cardiac oxidative stress, inflammation and fibrosis.


Assuntos
Aminobutiratos/farmacologia , Compostos de Bifenilo/farmacologia , Infarto do Miocárdio/patologia , Infarto do Miocárdio/fisiopatologia , Resveratrol/farmacologia , Valsartana/farmacologia , Remodelação Ventricular/efeitos dos fármacos , Animais , Combinação de Medicamentos , Interações Medicamentosas , Fibrose , Humanos , Masculino , Infarto do Miocárdio/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Função Ventricular Esquerda/efeitos dos fármacos
4.
Medicine (Baltimore) ; 100(29): e26627, 2021 Jul 23.
Artigo em Inglês | MEDLINE | ID: mdl-34398018

RESUMO

OBJECTIVE: Previous investigations yielded inconsistent results for diagnostic and prognostic predictive values of MicroRNAs (miRNAs) for acute myocardial infarction (AMI). METHODS AND RESULTS: We systematically searched on PubMed and Web of Science for articles explored association of miRNAs and AMI published from January 1989 to March 2019. For diagnostic studies, a summary of sensitivity, specificity, positive likelihood ratios (PLR), negative likelihood ratios (NLR), and diagnostic odds ratio (DOR), which indicated the accuracy of microRNAs in the differentiation of AMI and no AMI, were calculated from the true positive (TP), true negative (TN), false positive (FP), and false negative (FN) of each study. In addition, the summary receive-operating characteristics (SROC) curve was constructed to summarize the TP and FP rates. For follow-up study, we computed hazard ratios (HRs) and 95% confidence intervals (CIs) for individual clinical outcomes. The meta-analysis showed a sensitivity [0.72 (95% CI: 0.61--0.81)] and specificity [0.88 (95% CI: 0.79--0.94)] of miR-1 for AMI. In addition, miR-133 showed a sensitivity [0.73 (95% CI: 0.55--0.85)] and specificity [0.88 (95% CI: 0.74--0.95)] for AMI. Moreover, the present study showed a sensitivity [0.83 (95% CI: 0.74--0.89)] and specificity [0.96 (95% CI: 0.82--0.99)] of miR-208 for AMI. A significant association was found between miR-208 and mortality after AMI (HR 1.09, 95% CI 1.01--1.18). It also indicated a sensitivity [0.84 (95% CI: 0.70--0.92)] and specificity [0.97 (95% CI: 0.87--0.99)] of miR-499 for AMI. CONCLUSIONS: Circulating miR-1, miR-133, miR-208, and miR-499 showed diagnostic values in AMI.


Assuntos
MicroRNAs/análise , Infarto do Miocárdio/sangue , Valor Preditivo dos Testes , Área Sob a Curva , Biomarcadores/análise , Biomarcadores/sangue , Humanos , MicroRNAs/sangue , Infarto do Miocárdio/fisiopatologia , Razão de Chances , Prognóstico , Curva ROC
5.
Int J Mol Sci ; 22(16)2021 Aug 09.
Artigo em Inglês | MEDLINE | ID: mdl-34445255

RESUMO

One of the most important features of striated cardiac muscle is the excitability that turns on the excitation-contraction coupling cycle, resulting in the heart blood pumping function. The function of the heart pump may be impaired by events such as myocardial infarction, the consequence of coronary artery thrombosis due to blood clots or plaques. This results in the death of billions of cardiomyocytes, the formation of scar tissue, and consequently impaired contractility. A whole heart transplant remains the gold standard so far and the current pharmacological approaches tend to stop further myocardium deterioration, but this is not a long-term solution. Electrically conductive, scaffold-based cardiac tissue engineering provides a promising solution to repair the injured myocardium. The non-conductive component of the scaffold provides a biocompatible microenvironment to the cultured cells while the conductive component improves intercellular coupling as well as electrical signal propagation through the scar tissue when implanted at the infarcted site. The in vivo electrical coupling of the cells leads to a better regeneration of the infarcted myocardium, reducing arrhythmias, QRS/QT intervals, and scar size and promoting cardiac cell maturation. This review presents the emerging applications of intrinsically conductive polymers in cardiac tissue engineering to repair post-ischemic myocardial insult.


Assuntos
Arritmias Cardíacas , Materiais Biocompatíveis , Condutividade Elétrica , Infarto do Miocárdio , Miocárdio/metabolismo , Regeneração/efeitos dos fármacos , Tecidos Suporte/química , Animais , Arritmias Cardíacas/metabolismo , Arritmias Cardíacas/fisiopatologia , Arritmias Cardíacas/terapia , Materiais Biocompatíveis/química , Materiais Biocompatíveis/uso terapêutico , Humanos , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/fisiopatologia , Infarto do Miocárdio/terapia , Engenharia Tecidual
6.
Int J Mol Sci ; 22(16)2021 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-34445301

RESUMO

Angiotensin receptor neprilysin inhibitor (ARNI) treatment reduces functional mitral regurgitation (MR) to a greater extent than angiotensin receptor blocker (ARB) treatment alone, but the mechanism is unclear. We evaluated the mechanisms of how ARNI has an effect on functional MR. After inducing functional MR by left circumflex coronary artery occlusion, male Sprague Dawley rats (n = 31) were randomly assigned to receive the ARNI LCZ696, the ARB valsartan, or corn oil only (MR control). Excised mitral leaflets and left ventricle (LV) were analyzed, and valvular endothelial cells were evaluated focusing on molecular changes. LCZ696 significantly attenuated LV dilatation after 6 weeks when compared with the control group (LV end-diastolic volume, 461.3 ± 13.8 µL versus 525.1 ± 23.6 µL; p < 0.05), while valsartan did not (471.2 ± 8.9 µL; p > 0.05 to control). Histopathological analysis of mitral leaflets showed that LCZ696 strongly reduced fibrotic thickness compared to the control group (28.2 ± 2.7 µm vs. 48.8 ± 7.5 µm; p < 0.05). Transforming growth factor-ß and downstream phosphorylated extracellular-signal regulated kinase were also significantly lower in the LCZ696 group. Consequently, excessive endothelial-to-mesenchymal transition (EndoMT) was mitigated in the LCZ696 group compared to the control group and leaflet area was higher (11%) in the LCZ696 group than in the valsartan group. Finally, the MR extent was significantly lower in the LCZ696 group and functional improvement was observed. In conclusion, neprilysin inhibitor has positive effects on LV reverse remodeling and also attenuates fibrosis in MV leaflets and restores adaptive growth by directly modulating EndoMT.


Assuntos
Aminobutiratos/uso terapêutico , Compostos de Bifenilo/uso terapêutico , Insuficiência da Valva Mitral/tratamento farmacológico , Infarto do Miocárdio/tratamento farmacológico , Valsartana/uso terapêutico , Aminobutiratos/farmacologia , Antagonistas de Receptores de Angiotensina/farmacologia , Antagonistas de Receptores de Angiotensina/uso terapêutico , Animais , Compostos de Bifenilo/farmacologia , Células Cultivadas , Combinação de Medicamentos , Células Endoteliais/efeitos dos fármacos , Células Endoteliais/fisiologia , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/fisiopatologia , Humanos , Masculino , Valva Mitral/efeitos dos fármacos , Valva Mitral/patologia , Valva Mitral/fisiologia , Insuficiência da Valva Mitral/diagnóstico , Insuficiência da Valva Mitral/etiologia , Insuficiência da Valva Mitral/fisiopatologia , Infarto do Miocárdio/complicações , Infarto do Miocárdio/diagnóstico , Infarto do Miocárdio/fisiopatologia , Traumatismo por Reperfusão Miocárdica/complicações , Traumatismo por Reperfusão Miocárdica/diagnóstico , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica/fisiopatologia , Neprilisina/antagonistas & inibidores , Ratos , Ratos Sprague-Dawley , Valsartana/farmacologia , Função Ventricular Esquerda/efeitos dos fármacos , Remodelação Ventricular/efeitos dos fármacos
7.
Theranostics ; 11(16): 7984-7994, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34335975

RESUMO

Rationale: Acute myocardial infarction (MI) triggers a systemic inflammatory response including crosstalk along the heart-kidney axis. We employed radionuclide-based inflammation-targeted whole-body molecular imaging to identify potential cardio-renal crosstalk after MI in a translational setup. Methods: Serial whole-body positron emission tomography (PET) with the specific CXCR4 ligand 68Ga-Pentixafor was performed after MI in mice. Tracer retention in kidneys and heart was compared to hematopoietic organs to evaluate systemic inflammation, validated by ex vivo analysis and correlated with progressive contractile dysfunction. Additionally, 96 patients underwent 68Ga-Pentixafor PET within the first week after MI, for systems-based image analysis and to determine prognostic value for adverse renal outcome. Results: In mice, transient myocardial CXCR4 upregulation occurred early after MI. Cardiac and renal PET signal directly correlated over the time course (r = 0.62, p < 0.0001), suggesting an inflammatory link between organs. Ex-vivo autoradiography (r = 0.9, p < 0.01) and CD68 immunostaining indicated signal localization to inflammatory cell content. Renal signal at 7d was inversely proportional to left ventricular ejection fraction at 6 weeks after MI (r = -0.79, p < 0.01). In patients, renal CXCR4 signal also correlated with signal from infarct (r = 0.25, p < 0.05) and remote myocardium (r = 0.39, p < 0.0001). Glomerular filtration rate (GFR) was available in 48/96 (50%) during follow-up. Worsening of renal function (GFR loss >5 mL/min/1.73m2), occurred a mean 80.5 days after MI in 16/48 (33.3%). Kaplan-Meier analysis revealed adverse renal outcome for patients with elevated remote myocardial CXCR4 signal (p < 0.05). Multivariate Cox analysis confirmed an independent predictive value (relative to baseline GFR, LVEF, infarct size; HR, 5.27). Conclusion: Systems-based CXCR4-targeted molecular imaging identifies inflammatory crosstalk along the cardio-renal axis early after MI.


Assuntos
Coração/fisiopatologia , Rim/fisiopatologia , Infarto do Miocárdio/fisiopatologia , Animais , Complexos de Coordenação/farmacologia , Humanos , Inflamação/metabolismo , Inflamação/fisiopatologia , Masculino , Camundongos , Imagem Molecular/métodos , Infarto do Miocárdio/metabolismo , Miocárdio/metabolismo , Peptídeos Cíclicos/farmacologia , Tomografia por Emissão de Pósitrons/métodos , Receptores CXCR4/metabolismo , Volume Sistólico , Função Ventricular Esquerda , Remodelação Ventricular/fisiologia , Imagem Corporal Total/métodos
8.
Theranostics ; 11(16): 7755-7766, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34335962

RESUMO

Background: Myocardial infarction (MI) evokes an organized remodeling process characterized by the activation and transdifferentiation of quiescent cardiac fibroblasts to generate a stable collagen rich scar. Early fibroblast activation may be amenable to targeted therapy, but is challenging to identify in vivo. We aimed to non-invasively image active fibrosis by targeting the fibroblast activation protein (FAP) expressed by activated (myo)fibroblasts, using a novel positron emission tomography (PET) radioligand [68Ga]MHLL1 after acute MI. Methods: One-step chemical synthesis and manual as well as module-based radiolabeling yielded [68Ga]MHLL1. Binding characteristics were evaluated in murine and human FAP-transfected cells, and stability tested in human serum. Biodistribution in healthy animals was interrogated by dynamic PET imaging, and metabolites were measured in blood and urine. The temporal pattern of FAP expression was determined by serial PET imaging at 7 d and 21 d after coronary artery ligation in mice as percent injected dose per gram (%ID/g). PET measurements were validated by ex vivo autoradiography and immunostaining for FAP and inflammatory macrophages. Results: [68Ga]MHLL1 displayed specific uptake in murine and human FAP-positive cells (p = 0.0208). In healthy mice the tracer exhibited favorable imaging characteristics, with low blood pool retention and dominantly renal clearance. At 7 d after coronary artery ligation, [68Ga]MHLL1 uptake was elevated in the infarct relative to the non-infarcted remote myocardium (1.3 ± 0.3 vs. 1.0 ± 0.2 %ID/g, p < 0.001) which persisted to 21 d after MI (1.3 ± 0.4 vs. 1.1 ± 0.4 %ID/g, p = 0.013). Excess unlabeled compound blocked tracer accumulation in both infarct and non-infarct remote myocardium regions (p < 0.001). Autoradiography and histology confirmed the regional uptake of [68Ga]MHLL1 in the infarct and especially border zone regions, as identified by Masson trichrome collagen staining. Immunostaining further delineated persistent FAP expression at 7 d and 21 d post-MI in the border zone, consistent with tracer distribution in vivo. Conclusion: The simplified synthesis of [68Ga]MHLL1 bears promise for non-invasive characterization of fibroblast activation protein early in remodeling after MI.


Assuntos
Endopeptidases/metabolismo , Radioisótopos de Gálio/farmacologia , Proteínas de Membrana/metabolismo , Tomografia por Emissão de Pósitrons/métodos , Animais , Autorradiografia/métodos , Linhagem Celular Tumoral , Endopeptidases/fisiologia , Fibroblastos/metabolismo , Fibrose/diagnóstico por imagem , Radioisótopos de Gálio/metabolismo , Humanos , Masculino , Proteínas de Membrana/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Imagem Molecular/métodos , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/fisiopatologia , Miocárdio/patologia , Distribuição Tecidual/fisiologia , Tomografia Computadorizada por Raios X/métodos
9.
Nat Commun ; 12(1): 4808, 2021 08 10.
Artigo em Inglês | MEDLINE | ID: mdl-34376683

RESUMO

Myocardial regeneration is restricted to early postnatal life, when mammalian cardiomyocytes still retain the ability to proliferate. The molecular cues that induce cell cycle arrest of neonatal cardiomyocytes towards terminally differentiated adult heart muscle cells remain obscure. Here we report that the miR-106b~25 cluster is higher expressed in the early postnatal myocardium and decreases in expression towards adulthood, especially under conditions of overload, and orchestrates the transition of cardiomyocyte hyperplasia towards cell cycle arrest and hypertrophy by virtue of its targetome. In line, gene delivery of miR-106b~25 to the mouse heart provokes cardiomyocyte proliferation by targeting a network of negative cell cycle regulators including E2f5, Cdkn1c, Ccne1 and Wee1. Conversely, gene-targeted miR-106b~25 null mice display spontaneous hypertrophic remodeling and exaggerated remodeling to overload by derepression of the prohypertrophic transcription factors Hand2 and Mef2d. Taking advantage of the regulatory function of miR-106b~25 on cardiomyocyte hyperplasia and hypertrophy, viral gene delivery of miR-106b~25 provokes nearly complete regeneration of the adult myocardium after ischemic injury. Our data demonstrate that exploitation of conserved molecular programs can enhance the regenerative capacity of the injured heart.


Assuntos
MicroRNAs/genética , Infarto do Miocárdio/genética , Miócitos Cardíacos/metabolismo , Regeneração/genética , Animais , Animais Recém-Nascidos , Cardiomegalia/genética , Células Cultivadas , Ecocardiografia , Regulação da Expressão Gênica , Humanos , Hiperplasia/genética , Camundongos , Infarto do Miocárdio/patologia , Infarto do Miocárdio/fisiopatologia , Ratos , Reação em Cadeia da Polimerase Via Transcriptase Reversa
10.
Cardiovasc Ther ; 2021: 6628194, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34239606

RESUMO

Background: Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells. Methods: qRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells. Results: LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p. Conclusions: LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI.


Assuntos
Autoantígenos/biossíntese , MicroRNAs/biossíntese , Infarto do Miocárdio/fisiopatologia , RNA Longo não Codificante/biossíntese , Proteínas de Ligação a RNA/biossíntese , Animais , Apoptose , Sobrevivência Celular , Regulação para Baixo , Masculino , Camundongos Endogâmicos C57BL , Miócitos Cardíacos/metabolismo , Regulação para Cima
11.
Int J Mol Sci ; 22(13)2021 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-34281199

RESUMO

The current global prevalence of heart failure is estimated at 64.34 million cases, and it is expected to increase in the coming years, especially in countries with a medium-low sociodemographic index where the prevalence of risk factors is increasing alarmingly. Heart failure is associated with many comorbidities and among them, cancer has stood out as a contributor of death in these patients. This connection points out new challenges both in the context of the pathophysiological mechanisms involved, as well as in the quality of life of affected individuals. A hallmark of heart failure is chronic activation of the renin-angiotensin-aldosterone system, especially marked by a systemic increase in levels of angiotensin-II, a peptide with pleiotropic activities. Drugs that target the renin-angiotensin-aldosterone system have shown promising results both in the prevention of secondary cardiovascular events in myocardial infarction and heart failure, including a lower risk of certain cancers in these patients, as well as in current cancer therapies; therefore, understanding the mechanisms involved in this complex relationship will provide tools for a better diagnosis and treatment and to improve the prognosis and quality of life of people suffering from these two deadly diseases.


Assuntos
Isquemia Miocárdica/fisiopatologia , Neoplasias/fisiopatologia , Sistema Renina-Angiotensina/fisiologia , Aldosterona/metabolismo , Angiotensina II/metabolismo , Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/fisiopatologia , Humanos , Infarto do Miocárdio/fisiopatologia , Isquemia Miocárdica/metabolismo , Neoplasias/metabolismo , Renina/metabolismo
12.
Cardiovasc Ther ; 2021: 5530541, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34194542

RESUMO

Background: After myocardial infarction, anti-inflammatory macrophages perform key homeostatic functions that facilitate cardiac recovery and remodeling. Several studies have shown that lactate may serve as a modifier that influences phenotype of macrophage. However, the therapeutic role of sodium lactate in myocardial infarction (MI) is unclear. Methods: MI was established by permanent ligation of the left anterior descending coronary artery followed by injection of saline or sodium lactate. Cardiac function was assessed by echocardiography. The cardiac fibrosis area was assessed by Masson trichrome staining. Macrophage phenotype was detected via qPCR, flow cytometry, and immunofluorescence. Signaling proteins were measured by Western blotting. Results: Sodium lactate treatment following MI improved cardiac performance, enhanced anti-inflammatory macrophage proportion, reduced cardiac myocytes apoptosis, and increased neovascularization. Flow-cytometric analysis results reported that sodium lactate repressed the number of the IL-6+, IL-12+, and TNF-α+ macrophages among LPS-stimulated bone marrow-derived macrophages (BMDMs) and increased the mRNA levels of Arg-1, YM1, TGF-ß, and IL-10. Mechanistic studies revealed that sodium lactate enhanced the expression of P-STAT3. Furthermore, a STAT3 inhibitor eliminated sodium lactate-mediated promotion macrophage polarization. Conclusion: Sodium lactate facilitates anti-inflammatory M2 macrophage polarization and protects against MI by regulating P-STAT3.


Assuntos
Ativação de Macrófagos/efeitos dos fármacos , Macrófagos/efeitos dos fármacos , Infarto do Miocárdio/tratamento farmacológico , Infarto do Miocárdio/fisiopatologia , Lactato de Sódio/farmacologia , Animais , Anti-Inflamatórios/farmacologia , Apoptose/efeitos dos fármacos , Vasos Coronários/fisiopatologia , Modelos Animais de Doenças , Ecocardiografia , Mediadores da Inflamação/metabolismo , Macrófagos/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Miocárdio/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Fator de Transcrição STAT3/biossíntese , Transdução de Sinais/efeitos dos fármacos
13.
Medicine (Baltimore) ; 100(25): e26396, 2021 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-34160422

RESUMO

BACKGROUND: Cardiovascular diseases have become a prominent threat to public health and quality of life. In recent years, some studies have reported that ivabradine can improve the cardiac function and prognosis of patients with acute myocardial infarction (AMI). Therefore, we perform a protocol for systematic review and meta-analysis to evaluate the efficacy of ivabradine for treating AMI. METHODS: This protocol of systematic review and meta-analysis has been drafted under the guidance of the preferred reporting items for systematic reviews and meta-analyses protocols. We will search PubMed, Cochrane Library, Embase, Web of Science, and Medline databases for relevant studies. In addition, we will also collect 4 databases of China: China National Knowledge Infrastructure, China Biomedical Literature Database, China Science Journal Database, and Wan-fang Database. Risk of bias will be assessed using the Cochrane Handbook risk of bias assessment tool version (V.5.1.0). We will use STATA 16.0 software (Stata Corporation, College Station, TX) to perform data analysis. RESULTS: The results of this systematic review and meta-analysis will be published in a peer-reviewed journal. CONCLUSION: We hypothesized that ivabradine can reduce the resting heart rate and improve heart function in patients with AMI.


Assuntos
Ivabradina/administração & dosagem , Infarto do Miocárdio/tratamento farmacológico , Frequência Cardíaca/efeitos dos fármacos , Frequência Cardíaca/fisiologia , Humanos , Metanálise como Assunto , Infarto do Miocárdio/fisiopatologia , Descanso/fisiologia , Volume Sistólico/efeitos dos fármacos , Revisões Sistemáticas como Assunto , Resultado do Tratamento , Função Ventricular Esquerda/efeitos dos fármacos
14.
Pan Afr Med J ; 38: 302, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34178220

RESUMO

Acute myocardial infarction (AMI) is a major cause of death in a patient with systemic lupus erythematosus (SLE). Due to their chronic inflammatory state, patient with SLE has an increased risk of developing coronary artery disease. We report a case of a middle-aged woman with an acute myocardial infarction (AMI) caused by a right coronary artery (RCA) stenosis complicated with severe coronary artery spasm. Our patient has a history of long-standing SLE. Clinical expression of coronary artery disease (CAD) in SLE is the result of different pathophysiologic mechanism. From this case, we raise the importance of the clinician to be aware of the diverse pathophysiologic pathways involving a coronary artery in a patient with SLE.


Assuntos
Estenose Coronária/complicações , Vasoespasmo Coronário/complicações , Lúpus Eritematoso Sistêmico/complicações , Infarto do Miocárdio/etiologia , Adulto , Estenose Coronária/fisiopatologia , Vasoespasmo Coronário/fisiopatologia , Feminino , Humanos , Lúpus Eritematoso Sistêmico/fisiopatologia , Infarto do Miocárdio/fisiopatologia
15.
Am J Cardiol ; 152: 158-163, 2021 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-34120705

RESUMO

Type A acute aortic dissection (AAD) is a life-threatening disease. The use of contrast-enhanced computed tomography (CT) for diagnosing AAD has increased, and CT can provide pathophysiologic information on dissection such as intramural hematoma (IMH), longitudinal extent of dissection, and branch vessel involvement. However, the prognostic impact of these CT findings is poorly investigated. This multicenter registry included 703 patients with type A AAD. The longitudinal extent of dissection and IMH was determined on CT. Branch vessel involvement was defined as dissection extended into coronary, cerebral, and visceral arteries on CT. The evidence of malperfusion was defined based on clinical presentations. The primary endpoint was in-hospital death. Of 703 patients, 126 (18%) died during hospitalization. Based on contrast-enhanced CT findings, longitudinal extent of dissection was not associated with in-hospital death, while patients with IMH had lower in-hospital mortality than those without (13% vs 22%, p = 0.004). Coronary, cerebral, and visceral artery involvement on CT was found in 6%, 55%, and 32%. In patients with coronary artery involvement, 90% had clinical coronary malperfusion, while only 25% and 21% of patients with cerebral and visceral artery involvement had clinical evidence of corresponding organ malperfusion. Multivariable analysis showed evidence of malperfusion as a significant factor associated with in-hospital mortality. In conclusions, branch vessel involvement on CT was not always associated with end-organ malperfusion in patients with type A AAD, especially in cerebral and visceral arteries. Clinical evidence of malperfusion was significantly associated with in-hospital mortality beyond branch vessel involvement on CT.


Assuntos
Aneurisma Dissecante/diagnóstico por imagem , Aneurisma Dissecante/fisiopatologia , Aneurisma Aórtico/diagnóstico por imagem , Aneurisma Aórtico/fisiopatologia , Mortalidade Hospitalar , Injúria Renal Aguda/fisiopatologia , Idoso , Idoso de 80 Anos ou mais , Isquemia Encefálica/fisiopatologia , Artérias Carótidas/diagnóstico por imagem , Artéria Celíaca/diagnóstico por imagem , Transtornos da Consciência/fisiopatologia , Angiografia Coronária , Oclusão Coronária/diagnóstico por imagem , Oclusão Coronária/fisiopatologia , Vasos Coronários , Feminino , Humanos , Masculino , Artéria Mesentérica Superior/diagnóstico por imagem , Isquemia Mesentérica/fisiopatologia , Pessoa de Meia-Idade , Infarto do Miocárdio/fisiopatologia , Prognóstico , Sistema de Registros , Artéria Renal/diagnóstico por imagem , Índice de Gravidade de Doença , Tomografia Computadorizada por Raios X
16.
Am J Cardiol ; 152: 27-33, 2021 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-34130825

RESUMO

Scarce data exist on the prognostic impact of type 2 myocardial infarction (MI) in patients with AF. The Nationwide Readmission Database 2018 was queried for primary AF hospitalizations with and without type 2 MI. Complex samples multivariable logistic and linear regression models were used to determine the association between type 2 MI and outcomes (in-hospital mortality, index length of stay [LOS], hospital costs, discharge to nursing facility, and 30-day all-cause readmissions). Of 382,896 weighted primary AF hospitalizations included in this study, 7,375 (1.9%) had type 2 MI. AF with type 2 MI is associated with significantly higher in-hospital mortality (adjusted OR [aOR] 1.76; 95% CI 1.30 to 2.38), LOS (adjusted parameter estimate [aPE] 0.48; 95% CI 0.35 to 0.62), hospital costs (aPE 1307.75; 95% CI 986.05 to 1647.44), discharges to nursing facility (aOR 1.38; 95% CI 1.24 to 1.54), and 30-day all-cause readmissions (adjusted hazard ratio 1.17; 95% CI 1.07 to 1.27) compared to AF without type 2 MI. Heart failure, chronic kidney disease, neurologic disorders, and age (per year) were identified as independent predictors of mortality among AF patients with type 2 MI. In conclusion, type 2 MI in the setting of AF hospitalization is associated with high in-hospital mortality and increased resource utilization.


Assuntos
Fibrilação Atrial/terapia , Custos Hospitalares , Mortalidade Hospitalar , Infarto do Miocárdio/terapia , Idoso , Fibrilação Atrial/complicações , Fibrilação Atrial/economia , Estudos de Casos e Controles , Comorbidade , Feminino , Recursos em Saúde , Hospitalização/economia , Humanos , Tempo de Internação/economia , Tempo de Internação/estatística & dados numéricos , Masculino , Infarto do Miocárdio/complicações , Infarto do Miocárdio/economia , Infarto do Miocárdio/fisiopatologia , Casas de Saúde , Alta do Paciente/estatística & dados numéricos , Readmissão do Paciente/estatística & dados numéricos , Modelos de Riscos Proporcionais
17.
Cardiovasc Res ; 117(10): 2161-2174, 2021 08 29.
Artigo em Inglês | MEDLINE | ID: mdl-34114614

RESUMO

We review some of the important discoveries and advances made in basic and translational cardiac research in 2020. For example, in the field of myocardial infarction (MI), new aspects of autophagy and the importance of eosinophils were described. Novel approaches, such as a glycocalyx mimetic, were used to improve cardiac recovery following MI. The strategy of 3D bio-printing was shown to allow the fabrication of a chambered cardiac organoid. The benefit of combining tissue engineering with paracrine therapy to heal injured myocardium is discussed. We highlight the importance of cell-to-cell communication, in particular, the relevance of extracellular vesicles, such as exosomes, which transport proteins, lipids, non-coding RNAs, and mRNAs and actively contribute to angiogenesis and myocardial regeneration. In this rapidly growing field, new strategies were developed to stimulate the release of reparative exosomes in ischaemic myocardium. Single-cell sequencing technology is causing a revolution in the study of transcriptional expression at cellular resolution, revealing unanticipated heterogeneity within cardiomyocytes, pericytes and fibroblasts, and revealing a unique subpopulation of cardiac fibroblasts. Several studies demonstrated that exosome- and non-coding RNA-mediated approaches can enhance human induced pluripotent stem cell (iPSC) viability and differentiation into mature cardiomyocytes. Important details of the mitochondrial Ca2+ uniporter and its relevance were elucidated. Novel aspects of cancer therapeutic-induced cardiotoxicity were described, such as the novel circular RNA circITCH, which may lead to novel treatments. Finally, we provide some insights into the effects of SARS-CoV-2 on the heart.


Assuntos
Pesquisa Biomédica , Cardiologia , Proliferação de Células , Insuficiência Cardíaca/patologia , Infarto do Miocárdio/patologia , Traumatismo por Reperfusão Miocárdica/patologia , Miócitos Cardíacos/patologia , Regeneração , Animais , COVID-19/patologia , COVID-19/virologia , Comunicação Celular , Microambiente Celular , Exossomos/metabolismo , Exossomos/patologia , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/fisiopatologia , Humanos , Mitocôndrias Cardíacas/metabolismo , Mitocôndrias Cardíacas/patologia , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/fisiopatologia , Traumatismo por Reperfusão Miocárdica/metabolismo , Traumatismo por Reperfusão Miocárdica/fisiopatologia , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/virologia , Fenótipo , RNA não Traduzido/metabolismo , SARS-CoV-2/patogenicidade
18.
Crit Care ; 25(1): 217, 2021 06 24.
Artigo em Inglês | MEDLINE | ID: mdl-34167575

RESUMO

BACKGROUND: The viral load of asymptomatic SAR-COV-2 positive (ASAP) persons has been equal to that of symptomatic patients. On the other hand, there are no reports of ST-elevation myocardial infarction (STEMI) outcomes in ASAP patients. Therefore, we evaluated thrombus burden and thrombus viral load and their impact on microvascular bed perfusion in the infarct area (myocardial blush grade, MBG) in ASAP compared to SARS-COV-2 negative (SANE) STEMI patients. METHODS: This was an observational study of 46 ASAP, and 130 SANE patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention and thrombus aspiration. The primary endpoints were thrombus dimension + thrombus viral load effects on MBG after PPCI. The secondary endpoints during hospitalization were major adverse cardiovascular events (MACEs). MACEs are defined as a composite of cardiovascular death, nonfatal acute AMI, and heart failure during hospitalization. RESULTS: In the study population, ASAP vs. SANE showed a significant greater use of GP IIb/IIIa inhibitors and of heparin (p < 0.05), and a higher thrombus grade 5 and thrombus dimensions (p < 0.05). Interestingly, ASAP vs. SANE patients had lower MBG and left ventricular function (p < 0.001), and 39 (84.9%) of ASAP patients had thrombus specimens positive for SARS-COV-2. After PPCI, a MBG 2-3 was present in only 26.1% of ASAP vs. 97.7% of SANE STEMI patients (p < 0.001). Notably, death and nonfatal AMI were higher in ASAP vs. SANE patients (p < 0.05). Finally, in ASAP STEMI patients the thrombus viral load was a significant determinant of thrombus dimension independently of risk factors (p < 0.005). Thus, multiple logistic regression analyses evidenced that thrombus SARS-CoV-2 infection and dimension were significant predictors of poorer MBG in STEMI patients. Intriguingly, in ASAP patients the female vs. male had higher thrombus viral load (15.53 ± 4.5 vs. 30.25 ± 5.51 CT; p < 0.001), and thrombus dimension (4.62 ± 0.44 vs 4.00 ± 1.28 mm2; p < 0.001). ASAP vs. SANE patients had a significantly lower in-hospital survival for MACE following PPCI (p < 0.001). CONCLUSIONS: In ASAP patients presenting with STEMI, there is strong evidence towards higher thrombus viral load, dimension, and poorer MBG. These data support the need to reconsider ASAP status as a risk factor that may worsen STEMI outcomes.


Assuntos
COVID-19/complicações , Trombose Coronária/virologia , Coração/fisiopatologia , Microcirculação/fisiologia , Infarto do Miocárdio/fisiopatologia , Idoso , Análise de Variância , Infecções Assintomáticas/epidemiologia , COVID-19/epidemiologia , Estudos de Coortes , Angiografia Coronária/métodos , Trombose Coronária/epidemiologia , Ecocardiografia/métodos , Feminino , Humanos , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/epidemiologia
19.
Clin Interv Aging ; 16: 1139-1149, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34168437

RESUMO

Background: Silent myocardial infarction (SMI) accounts for more than half of all MIs, and common risk factors and pathophysiological pathways coexist between SMI and frailty. The risk of frailty among patients with SMI is not well established. This study aimed to examine the association between SMI and frailty. Methods and Results: This analysis included data from the Atherosclerosis Risk in Communities study. Patients without MI at baseline were eligible for inclusion. SMI was defined as electrocardiographic evidence of MI without clinical MI (CMI) after the baseline and until the fourth visit. Frailty was assessed during the fifth visit. A total of 4953 participants were included with an average age of 52.2±5.1 years. Among these participants, 2.7% (n=135) developed SMI, and 2.9% (n=146) developed CMI. After a median follow-up time of 14.7 (14.0-15.3) years, 6.7% (n=336) of the participants developed frailty. Patients with SMI and CMI were significantly more likely to become frail than those without MI (15.6% vs 6.2%, P<0.001 and 16.4% vs 6.2%, P<0.001, respectively). After adjusting for confounders, SMI and CMI were found to be independent predictors of frailty (odds ratio [OR]=2.243, 95% confidence interval [CI]=1.307-3.850, P=0.003 and OR=2.164, 95% CI=1.259-3.721, P=0.005, respectively). The association was consistent among the subgroups of age, sex, race, diabetes, and hypertension. Conclusion: In conclusion, both SMI and CMI were found to be associated with a higher risk of frailty. Future studies are needed to confirm the beneficial effects of screening for SMI as well as to implement standardized preventive treatment to reduce the risk of frailty. Clinical Trial Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT00005131.


Assuntos
Aterosclerose/epidemiologia , Fragilidade/epidemiologia , Infarto do Miocárdio/epidemiologia , Idoso , Aterosclerose/fisiopatologia , Eletrocardiografia/métodos , Fragilidade/fisiopatologia , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/fisiopatologia , Prognóstico , Medição de Risco , Fatores de Risco
20.
Nat Commun ; 12(1): 3964, 2021 06 25.
Artigo em Inglês | MEDLINE | ID: mdl-34172720

RESUMO

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-1ß 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.


Assuntos
Osso e Ossos/irrigação sanguínea , Células Endoteliais/patologia , Insuficiência Cardíaca/fisiopatologia , Infarto do Miocárdio/fisiopatologia , Idoso , Animais , Osso e Ossos/fisiopatologia , Estudos de Casos e Controles , Células Endoteliais/metabolismo , Feminino , Furanos/farmacologia , Genes myc , Insuficiência Cardíaca/etiologia , Células-Tronco Hematopoéticas/patologia , Humanos , Indenos/farmacologia , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Inflamação/patologia , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Pessoa de Meia-Idade , Infarto do Miocárdio/complicações , Infarto do Miocárdio/genética , Molécula-1 de Adesão Celular Endotelial a Plaquetas/metabolismo , Sulfonamidas/farmacologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...