<i>Background</i>. Circular RNAs (circRNAs) were known to be related to the pathogenesis of many diseases through competing endogenous RNA (ceRNA) regulatory mechanisms. However, the function of circRNA in coronary artery disease (CAD) remains unclear. In this study, we aim to construct a circRNA-related competing endogenous RNA (ceRNA) network in CAD. <i>Methods</i>. The gene expression profiles of CAD were obtained from Gene Expression Omnibus datasets. Bioinformatics analysis was performed to construct a ceRNA regulatory network, from which the hub genes involved were identified through protein-protein interaction (PPI) networks leading to the identification of the circRNA-miRNA-hub gene subnetwork. In addition, function enrichment analysis was performed to detect the potential biological mechanism in which circRNA might be involved. <i>Results</i>. A total of 115 DEcircRNAs (differentially expressed circRNAs), 17 DEmiRNAs (differentially expressed microRNAs), and 790 DEmRNAs (differentially expressed mRNAs) were identified between CAD and control groups from microarray datasets. Functional enrichment analysis showed that DEmRNAs were significantly involved in inflammation-related pathways and ubiquitin-protein ligase binding. After identifying 20 DEcircRNA-DEmiRNA pairs and 561 DEmiRNA-DEmRNA pairs, we obtained a circRNA-miRNA-mRNA regulatory network. PPI network analysis showed that eight hub genes were closely related to CAD, leading to the identification of a circRNA-miRNA-hub gene subnetwork consisting of nine circRNAs (hsa_circ_0020275, hsa_circ_0020387, hsa_circ_0020417, hsa_circ_0045512, hsa_circ_0047336, hsa_circ_0069094, hsa_circ_0071326, hsa_circ_0071330, and hsa_circ_0085340), four miRNAs (hsa-miR-136-5p, hsa-miR-376c-3p, hsa-miR-411-5p, and hsa-miR-654-5p), and eight mRNAs (MKRN1, UBE2H, UBE2W, UBE2D1, UBE2F, BE2J1, ZNRF1, and SIAH2). In addition, we discovered these hub genes were enriched in the ubiquitin-mediated proteolysis pathway, suggesting circRNAs may be involved in the pathogenesis of CAD through this pathway. <i>Conclusions</i>. This study may deepen our understanding of the potential role of circRNA-miRNA-mRNA regulation network in CAD and suggest novel diagnostic biomarkers and therapeutic targets for CAD.

Zebo Zhang

Haiyan Qian

Li Wang

Zhenbo Tao

Keai Cheng

Kaiyue Wang

Yanqing Xie

Lina Zhang

Construction of a circRNA-miRNA-mRNA Regulatory Network for Coronary Artery Disease by Bioinformatics Analysis

<i>Background</i>. Trimethylamine-N-oxide (TMAO) has been shown to be an important player in cardiovascular disease (CVD) by promoting vascular inflammation and endothelial dysfunction. We recently found that exosomes (Exos) released from TMAO-activated hepatocytes (TMAO-Exos) could significantly induce inflammation and endothelial dysfunction. However, understandings of how are the Exos secreted by hepatocytes, where are they distributed <i>in vivo</i>, and what effects will they have on vascular inflammation remain limited. The present study aimed to explore the hub genes involved in the production of TMAO-Exos and their distributions <i>in vivo</i> and effects on inflammation. <i>Methods</i>. The transcriptome profiles of primary rat hepatocytes stimulated with TMAO were obtained from the GSE135856 dataset in the Gene Expression Omnibus repository, and the hub genes associated with Exos were screened and verified by qPCR. Next, Exos derived from TMAO-treated hepatocytes were isolated using differential centrifugation and given intravenously to mice. After 24&#x2009;h, the distributions of DiI-labelled Exos were visualized with a fluorescence microscope, and the levels of proinflammatory genes in the aorta were detected by qPCR. <i>Results</i>. <i>Phgdh</i>, <i>Mdh</i>2, <i>Echs</i>1, <i>Rap</i>2<i>a</i>, <i>Gpd</i>1<i>l</i>, and <i>Slc3a</i>2 were identified as hub genes that may be involved in the production of TMAO-Exos. And TMAO-Exos were found to be efficiently taken up by cardiomyocytes, hepatocytes, and endothelial cells in the aorta and gastrocnemius muscle. Furthermore, TMAO-Exos, but not control-Exos, could significantly promote the mRNA expressions of <i>Tnf</i>, <i>Icam</i>1, <i>Sele</i>, and <i>Cox-</i>2 in the aorta. <i>Conclusions</i>. We provided clues about how TMAO may stimulate hepatocytes to produce Exos and further offered evidence that Exos secreted by TMAO-treated hepatocytes could be widely distributed <i>in vivo</i> and promote vascular inflammation.

Xiang Liu

Jiazichao Tu

Ziqin Zhou

Bingxin Huang

Jianrong Zhou

Jimei Chen

TMAO-Activated Hepatocyte-Derived Exosomes Are Widely Distributed in Mice with Different Patterns and Promote Vascular Inflammation

<i>Objectives</i>. In a cohort of type 2 diabetic (T2D) patients who underwent baseline cardiac magnetic resonance (CMR) and biomarker testing, during a median follow-up of 6 years, we aimed to determine longitudinal changes in the phenotypic expression of heart disease in diabetes, report clinical outcomes, and compare baseline clinical characteristics and CMR findings of patients who experienced major adverse cardiovascular events (MACE) to those remaining MACE free. <i>Background</i>. T2D increases the risk of heart failure (HF) and cardiovascular mortality. The long-term impact of T2D on cardiac phenotype in the absence of cardiovascular disease and other clinical events is unknown. <i>Methods</i>. Patients with T2D (<i>n</i>&#x2009;&#x3d;&#x2009;100) with no history of cardiovascular disease or hypertension were recruited at baseline. Biventricular volumes, function, and myocardial extracellular volume fraction (ECV) were assessed by CMR, and blood biomarkers were taken. Follow-up CMR was repeated in those without interim clinical events after 6 years. <i>Results</i>. Follow-up was successful in 83 participants. Of those, 29 experienced cardiovascular/clinical events (36&#x0025;). Of the remaining 59, 32 patients who experienced no events received follow-up CMR. In this cohort, despite no significant changes in blood pressure, weight, or glycated hemoglobin, significant reductions in biventricular end-diastolic volumes and ejection fractions occurred over time. The mean ECV was unchanged. Baseline plasma high-sensitivity cardiac troponin T (hs-cTnT) was significantly associated with a change in left ventricular (LV) ejection fraction. Patients who experienced MACE had higher LV mass and greater LV concentricity than those who remained event free. <i>Conclusions</i>. T2D results in reductions in biventricular size and systolic function over time even in the absence of cardiovascular/clinical events.

Amrit Chowdhary

Nicholas Jex

Sharmaine Thirunavukarasu

Amanda MacCannell

Natalie Haywood

Altaf Almutairi

Lavanya Athithan

Manali Jain

Thomas Craven

Arka Das

Noor Sharrack

Christopher E. D. Saunderson

Anshuman Sengupta

Lee Roberts

Peter Swoboda

Richard Cubbon

Klaus Witte

John Greenwood

Sven Plein

Eylem Levelt

Prospective Longitudinal Characterization of the Relationship between Diabetes and Cardiac Structural and Functional Changes

Cancer survivors suffer a higher risk of coronary artery atherosclerosis (CAA). Whether cancer patients had increased baseline CAA burden prior to cardiotoxic therapy remains unclear. We conducted a case-control study, and 286 consecutive patients were finally included. Among these patients, 181 had newly diagnosed cancer and 105 had nonmalignant diseases. Cancer was confirmed by biopsy. The severity of CAA was determined by coronary angiography and evaluated using the percentage of stenosis or Gensini scoring (GS). Patients with cancer versus cancer-free controls were older (OR = 1.052, 95% CI: 1.021–1.084, <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M1" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><path id="g113-113" d="M570 304C570 398 525 448 414 448C385 448 343 445 312 434L329 511L321 518C297 504 262 482 244 460L233 411C195 397 159 381 128 358L135 332C160 347 189 360 224 373L111 -147C97 -210 84 -218 17 -231L13 -257L254 -247L259 -218L233 -216C183 -212 177 -202 189 -142L218 -1C238 -10 266 -12 283 -12C351 3 429 48 483 105C543 168 570 242 570 304ZM482 289C482 161 380 33 304 33C278 33 248 51 233 69L303 396C326 400 352 403 369 403C428 403 482 380 482 289Z"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><path id="g117-91" d="M512 -3V55L134 254V256L512 456V514L75 281V230L512 -3Z"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="28.184pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 28.184 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><path id="g113-49" d="M241 635C89 635 35 457 35 312C35 153 89 -12 240 -12C390 -12 443 166 443 312C443 466 390 635 241 635ZM238 602C329 602 354 454 354 312C354 172 330 22 240 22C152 22 124 173 124 313S148 602 238 602Z"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><path id="g113-47" d="M113 -12C146 -12 170 11 170 46C170 78 146 103 114 103S58 78 58 46C58 11 82 -12 113 -12Z"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,44.289,0)"><path id="g113-50" d="M384 0V27C293 34 287 42 287 114V635C232 613 172 594 109 583V559L157 557C201 555 205 550 205 499V114C205 42 199 34 109 27V0H384Z"/></g></svg>),</span></span> more commonly male (OR = 0.048, 95% CI: 1.004–2.676, <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M2" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><path id="g117-34" d="M535 323V373H52V323H535ZM535 138V188H52V138H535Z"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="28.184pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 28.184 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><path id="g113-53" d="M456 178V225H360V632H320C217 496 115 347 20 206V178H280V106C280 40 276 34 189 27V0H445V27C364 34 360 39 360 106V178H456ZM280 225H82C149 335 214 431 278 520H280V225Z"/></g><g transform="matrix(.013,0,0,-0.013,44.289,0)"><path id="g113-57" d="M249 635C141 635 70 555 70 471C70 401 114 353 179 316C143 294 106 267 90 252C68 231 45 202 45 157C45 50 130 -12 237 -12C322 -12 435 52 435 169C435 256 372 304 303 343C349 374 375 398 383 407C401 429 411 458 411 487C411 569 344 635 249 635ZM238 603C285 603 337 567 337 482C337 422 310 385 276 358C205 393 145 426 145 500C145 552 179 603 238 603ZM248 20C183 20 125 70 125 163C125 218 158 268 206 300C284 261 355 217 355 143C355 66 308 20 248 20Z"/></g></svg>),</span></span> and more severely exposed to smoking (OR = 1.020, 95% CI: 1.007–1.033, <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M3" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><use xlink:href="#g117-34"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="28.184pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 28.184 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,44.289,0)"><path id="g113-52" d="M285 378C315 398 338 416 353 432C373 451 384 474 384 503C384 579 325 635 236 635H235C182 635 136 610 108 579L65 516L85 496C110 533 150 575 205 575C258 575 300 543 300 481C300 407 232 369 141 339L147 310C163 315 188 321 211 321C268 321 338 284 338 192C338 94 288 40 217 40C160 40 119 68 93 91C85 98 77 97 69 91C60 84 47 71 46 58C44 46 48 35 62 22C75 10 116 -12 162 -12C234 -12 424 62 424 224C424 297 373 359 285 376V378Z"/></g></svg>).</span></span> Cancer patients were significantly more commonly complicated by ≥90% coronary stenosis than the gender- and age-matched cancer-free controls (9/93 versus 1/93, OR = 4.875, 95% CI: 1.024–23.213, <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M4" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><use xlink:href="#g117-34"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="28.184pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 28.184 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-53"/></g><g transform="matrix(.013,0,0,-0.013,44.289,0)"><path id="g113-56" d="M447 623H65C61 580 56 530 47 475H76C100 541 106 550 172 550H388C308 376 196 170 91 -1L98 -12L172 -2C268 204 360 408 455 611L447 623Z"/></g></svg>).</span></span> After adjustment for age, gender, hypertension, diabetes, smoking history, blood glucose, and total cholesterol, cancer was significantly associated with high GS (adjusted OR = 2.208, 95% CI: 1.077–4.524, <span class="inline_break"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="18.973pt" style="vertical-align:-3.42938pt" id="M5" height="11.7782pt" version="1.1" viewBox="-0.0498162 -8.34882 18.973 11.7782"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g><g transform="matrix(.013,0,0,-0.013,11.342,0)"><use xlink:href="#g117-34"/></g></svg><span class="irelop"/><span class="nowrap"><svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" width="28.184pt" style="vertical-align:-3.42938pt" height="11.7782pt" version="1.1" viewBox="22.555183800000002 -8.34882 28.184 11.7782"><g transform="matrix(.013,0,0,-0.013,22.605,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,28.845,0)"><use xlink:href="#g113-47"/></g><g transform="matrix(.013,0,0,-0.013,31.809,0)"><use xlink:href="#g113-49"/></g><g transform="matrix(.013,0,0,-0.013,38.049,0)"><use xlink:href="#g113-52"/></g><g transform="matrix(.013,0,0,-0.013,44.289,0)"><use xlink:href="#g113-50"/></g></svg>).</span></span> Our study demonstrated that cancer patients had increased CAA burden prior to cardiotoxic therapy. Further study is necessary to investigate the link between CAA and cancer.

Junyi Guo

Peng Fang

Wei Shi

Pengcheng Luo

Shengqi Huo

Dan Yan

Moran Wang

Dewei Peng

Lintong Men

Sheng Li

Jiagao Lv

Li Lin

Preexisting Cardiovascular Risk Factors and Coronary Artery Atherosclerosis in Patients with and without Cancer

<i>Objectives</i>. To compare right ventricular thickness (RVT) and deformation of cardiac amyloidosis (CA) and hypertrophic cardiomyopathy (HCM) patients. <i>Methods</i>. Sixty CA (mean age 58 ± 10 years; 33 males (55%)) and sixty HCM patients (mean age 55 ± 14 years; 27 males (45%)) were retrospectively enrolled. RVT, global radical peak strain (GRPS), global longitudinal peak strain (GLPS), and global circumferential peak stain (GCPS) were analyzed. To determine the cutoff values of the RVT and RV strain parameters for distinguishing CA from HCM, the areas under the receiver operating characteristic curve (AUCs) were analyzed. <i>Results</i>. RVT of CA patients was significantly thicker than that of HCM patients (7.8 ± 2.1 vs 5.9 ± 1.3, <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M1" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><path id="g113-113" d="M570 304C570 398 525 448 414 448C385 448 343 445 312 434L329 511L321 518C297 504 262 482 244 460L233 411C195 397 159 381 128 358L135 332C160 347 189 360 224 373L111 -147C97 -210 84 -218 17 -231L13 -257L254 -247L259 -218L233 -216C183 -212 177 -202 189 -142L218 -1C238 -10 266 -12 283 -12C351 3 429 48 483 105C543 168 570 242 570 304ZM482 289C482 161 380 33 304 33C278 33 248 51 233 69L303 396C326 400 352 403 369 403C428 403 482 380 482 289Z"/></g></svg> &lt; 0.001). Moreover, significantly decreased RV-GRPS (12.1 ± 6.9 vs 23.5 ± 12.1, <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M2" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> &lt; 0.001), RV-GCPS (−3.4 ± 2.2 vs −5.6 ± 3.5, <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M3" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> &lt; 0.001), and RV-GLPS (−4.6 ± 2.3 vs −11.1 ± 4.9, <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M4" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> &lt; 0.001) were observed in CA patients compared with HCM patients. RVT and RV strain demonstrate comparable diagnostic accuracy in differentiating CA from HCM. In particular, RV-GLPS combined with RVT showed the best performance for discriminating CA from HCM (AUC = 0.92, 95% CI: 0.85 to 0.96, <svg xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg" style="vertical-align:-3.42943pt" id="M5" height="10.2124pt" version="1.1" viewBox="-0.0498162 -6.78297 7.83752 10.2124" width="7.83752pt"><g transform="matrix(.013,0,0,-0.013,0,0)"><use xlink:href="#g113-113"/></g></svg> = 0.0001). <i>Conclusions</i>. Right ventricular myocardial thickness and deformation of CA patients was more severe than HCM patients. RV-GLPS combined with RVT presents an excellent diagnostic performance in distinguishing CA and HCM.

Hui Liu

Peng Bai

Hua-Yan Xu

Zhen-Lin Li

Chun-Chao Xia

Xiao-Yue Zhou

Liang-Geng Gong

Ying-Kun Guo

Distinguishing Cardiac Amyloidosis and Hypertrophic Cardiomyopathy by Thickness and Myocardial Deformation of the Right Ventricle

<i>Background</i>. Acute coronary syndrome (ACS) causes pathophysiological changes in exercise capacity, N-terminal part of pro-brain natriuretic peptide (NT-proBNP), and adiponectin that impact the course of coronary artery disease and clinical outcomes after cardiac rehabilitation (CR). However, the serial changes and the relationship between the changes in these parameters for a prolonged term remain uninvestigated. <i>Methods</i>. Eighty-one patients with ACS underwent a three- or four-week CR program after acute care and were followed up for 12 months. Exercise capacity on a cycle ergometer and blood levels of NT-proBNP and adiponectin were determined before and after CR as well as at the 12-month follow-up. <i>Results</i>. Exercise capacity increased from 100&#x2009;watts (in median) before CR to 138 watts after CR and 150 watts at 12 months. The NT-proBNP level (526&#x2009;pg/ml before CR) remained almost unchanged after CR (557 pg/ml) and then decreased at 12 months (173&#x2009;pg/ml). The adiponectin level (14.5&#x2009;<i>&#xb5;</i>g/ml before CR) increased after CR (16.0&#x2009;<i>&#xb5;</i>g/ml) and at 12 months (17.2&#x2009;<i>&#xb5;</i>g/ml). There was no significant correlation among the changes in these parameters at each observation time point. <i>Conclusion</i>. During the observation period from before CR to the 12-month follow-up, exercise capacity, NT-proBNP, and adiponectin underwent significant changes; however, these changes were independent from each other and not correlated linearly, and they provide complementary information in clinical practice. Thus, all these parameters should be included and determined at different time points for a prolonged period of time.

Hong Jin

Yuefei Liu

Bernd Schweikert

Harry Hahman

Lei Wang

Armin Imhof

Rainer Muche

Wolfgang K&#xf6;nig

J&#xfc;rgen M. Steinacker

Serial Changes in Exercise Capacity, NT-proBNP, and Adiponectin in Patients with Acute Coronary Syndrome before and after Phase II Rehabilitation as well as at the 12-Month Follow-Up

About this journal

<p><em>Cardiology Research and Practice</em> publishes original research articles and&nbsp;review articles&nbsp;focusing on the diagnosis and treatment of cardiovascular diseases, including hypertension, arrhythmia, heart failure, and vascular disease.</p>


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<p>Dr. Terrence Ruddy is Director of Nuclear Cardiology at the University of Ottawa Heart Institute, and Professor of Medicine and Radiology at the University of Ottawa. His research is in SPECT and PET imaging techniques in cardiovascular disease.</p>


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Cardiology Research and Practice - Table of contents 2022

Cardiology Research and Practice | Hindawi

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Cardiology Research and Practice publishes original research articles and review articles focusing on the diagnosis and treatment of cardiovascular diseases, including hypertension, arrhythmia, heart failure, and vascular disease.

Cardiology Research and Practice