Atrial Fibrillation and Hypertension: Mechanistic, Epidemiologic, and
                        Treatment Parallels

Ogunsua, Adedotun; Shaikh, Amir Y.; Ahmed, Mohamed; McManus, David D.

doi:10.14797/mdcj-11-4-228

Cited by 68 publications

(54 citation statements)

References 68 publications

(70 reference statements)

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“…Cardiac remodeling, especially the structural remodeling, is a key result of AF [2]. Cardiac fibroblasts activation and aberrant fibroblast signaling can lead to cardiac fibrosis and heart injury [3].…”

Section: Introductionmentioning

confidence: 99%

miR-21 enhances cardiac fibrotic remodeling and fibroblast proliferation via CADM1/STAT3 pathway

Cao

Shi

2017

BMC Cardiovasc Disord

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BackgroundCardiac fibrosis play a key role in the atrial fibrillation pathogenesis but the underlying potential molecular mechanism is still understood. However, potential mechanisms for miR-21 upregulation and its role in cardiac fibrosis remain unclear. The controls cell proliferation and processes fundamental to disease progression.MethodsIn this study, immunohistochemistry, real-time RT-PCR, cell transfection, cell cycle, cell proliferation and Western blot were used, respectively.ResultsHere we have been demonstrated that the tumor suppressor cell adhesion molecule 1 (CADM1) is the potential target of miR-21. Our study revealed that miR-21 regulation of CADM1 expression, which was decreased in cardiac fibroblasts and fibrosis tissue. The cardiac fibroblasts transfected with miR-21 mimic promoted miR-21 overexpression enhanced STAT3 expression and decreased CADM1 expression. Nevertheless, the cardiac fibroblasts transfected with miR-21 inhibitor obtained the opposite expression result. Furthermore, downexpression of miR-21 suppressed cardiac fibroblast proliferation.ConclusionsThese results suggested that miR-21 overexpression promotes cardiac fibrosis via STAT3 signaling pathway by decrease CADM1 expression, indicating miR-21 as an important signaling molecule for cardiac fibrotic remodeling and AF.

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Section: Introductionmentioning

confidence: 99%

miR-21 enhances cardiac fibrotic remodeling and fibroblast proliferation via CADM1/STAT3 pathway

Cao

Shi

2017

BMC Cardiovasc Disord

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“…Over the last few decades, dramatic changes have occurred in how patients with AMI are diagnosed and treated. More sensitive troponin assays, early percutaneous revascularization and newer therapeutic options for medical management, have favorably reshaped the prognosis of patients with AMI [6]. Moreover, economic factors, including pay-for-performance and public reporting of adverse outcomes, as well as quality improvement programs have helped achieve better patient-related outcomes [7].…”

Section: Introductionmentioning

confidence: 99%

Relation of Atrial Fibrillation in Acute Myocardial Infarction to In-Hospital Complications and Early Hospital Readmission

Kundu

O’Day

Shaikh

et al. 2016

The American Journal of Cardiology

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Atrial fibrillation (AF) is a common complication of acute myocardial infarction (AMI) and contributes to high rates of in-hospital adverse events. However, there are few contemporary studies examining rates of AF in the contemporary era of AMI or the impact of new-onset AF on key in-hospital and post-discharge outcomes. We examined trends in AF among 6,384 residents of Worcester, Massachusetts who were hospitalized with confirmed AMI during 7 biennial periods between 1999 and 2011. Multivariate logistic regression analysis was used to examine associations between occurrence of AF and various in-hospital and post-discharge complications. The overall incidence of AF complicating AMI was 10.8%. Rates of new-onset AF increased from 1999 to 2003 (9.8% to 13.2%), and declined thereafter. In multivariable adjusted models, patients developing new-onset AF following AMI were at higher risk for inhospital stroke [Odds Ratio (OR) 2.5, 95% Confidence Interval (CI) 1.6–4.1], heart failure [OR 2.0, 95% CI 1.7 to 2.4], cardiogenic shock [OR 3.7, 95% CI 2.8–4.9] and death [OR 2.3, 95% CI 1.9 to 3.0] than patients without AF. Development of AF during hospitalization for AMI was associated with higher rates of readmission within 30-days after discharge [21.7% vs. 16.0%], but no significant difference was noted in early post-discharge 30-day all-cause mortality rates [8.3% vs. 5.1%]. In conclusion, new-onset AF following AMI is strongly related to in-hospital complications of AMI as well as higher short-term readmission rates.

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“…5 To better understand the causal pathway between hypertension and AF, researchers have examined relations between AF and state-of-the-art measures of arterial stiffness, wave reflection, pulsatile hemodynamic load, and endothelial dysfunction. Studies have reported that various measures of vascular structure and function [6][7][8][9] -including carotid-femoral pulse wave velocity (CFPWV), augmentation index, and central pulse pressure (CPP)-and measures of endothelial dysfunction, AF, as well as several other manifestations of cardiovascular disease.…”

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confidence: 99%

Relations of Arterial Stiffness and Brachial Flow–Mediated Dilation With New-Onset Atrial Fibrillation

et al. 2016

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The relations of measures of arterial stiffness, pulsatile hemodynamic load, and endothelial dysfunction to atrial fibrillation (AF) remain poorly understood. To better understand the pathophysiology of AF, we examined associations between noninvasive measures of vascular function and new-onset AF. The study sample included participants aged ≥45 years from the Framingham Heart Study offspring and third-generation cohorts. Using Cox proportional hazards regression models, we examined relations between incident AF and tonometry measures of arterial stiffness (carotid–femoral pulse wave velocity), wave reflection (augmentation index), pressure pulsatility (central pulse pressure), endothelial function (flow-mediated dilation), resting brachial arterial diameter, and hyperemic flow. AF developed in 407/5797 participants in the tonometry sample and 270/3921 participants in the endothelial function sample during follow-up (median 7.1 years, maximum 10 years). Higher augmentation index (hazard ratio, 1.16; 95% confidence interval, 1.02–1.32; P =0.02), baseline brachial artery diameter (hazard ratio, 1.20; 95% confidence interval, 1.01–1.43; P =0.04), and lower flow-mediated dilation (hazard ratio, 0.79; 95% confidence interval, 0.63–0.99; P =0.04) were associated with increased risk of incident AF. Central pulse pressure, when adjusted for age, sex, and hypertension (hazard ratio, 1.14; 95% confidence interval, 1.02–1.28; P =0.02) was associated with incident AF. Higher pulsatile load assessed by central pulse pressure and greater apparent wave reflection measured by augmentation index were associated with increased risk of incident AF. Vascular endothelial dysfunction may precede development of AF. These measures may be additional risk factors or markers of subclinical cardiovascular disease associated with increased risk of incident AF.

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Atrial Fibrillation and Hypertension: Mechanistic, Epidemiologic, and Treatment Parallels

Cited by 68 publications

References 68 publications

miR-21 enhances cardiac fibrotic remodeling and fibroblast proliferation via CADM1/STAT3 pathway

miR-21 enhances cardiac fibrotic remodeling and fibroblast proliferation via CADM1/STAT3 pathway

Relation of Atrial Fibrillation in Acute Myocardial Infarction to In-Hospital Complications and Early Hospital Readmission

Relations of Arterial Stiffness and Brachial Flow–Mediated Dilation With New-Onset Atrial Fibrillation

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