Example of Therapeutic Advances in Cardiovascular Disease format
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Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format
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Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format Example of Therapeutic Advances in Cardiovascular Disease format
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open access Open Access

Therapeutic Advances in Cardiovascular Disease — Template for authors

Publisher: SAGE
Categories Rank Trend in last 3 yrs
Cardiology and Cardiovascular Medicine #73 of 317 up up by 85 ranks
Pharmacology (medical) #73 of 246 up up by 57 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 92 Published Papers | 439 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 12/06/2020
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Related Journals

open access Open Access

Springer

Quality:  
High
CiteRatio: 5.1
SJR: 1.063
SNIP: 0.959
open access Open Access

Springer

Quality:  
High
CiteRatio: 6.5
SJR: 1.108
SNIP: 1.077
open access Open Access

SAGE

Quality:  
Good
CiteRatio: 4.3
SJR: 0.787
SNIP: 0.865
open access Open Access

Wiley

Quality:  
Good
CiteRatio: 4.2
SJR: 0.818
SNIP: 0.742

Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

A measure of average citations received per peer-reviewed paper published in the journal.

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

4.8

45% from 2019

CiteRatio for Therapeutic Advances in Cardiovascular Disease from 2016 - 2020
Year Value
2020 4.8
2019 3.3
2018 3.3
2017 2.5
2016 2.5
graph view Graph view
table view Table view

1.164

94% from 2019

SJR for Therapeutic Advances in Cardiovascular Disease from 2016 - 2020
Year Value
2020 1.164
2019 0.599
2018 0.537
2017 0.535
2016 0.5
graph view Graph view
table view Table view

1.22

72% from 2019

SNIP for Therapeutic Advances in Cardiovascular Disease from 2016 - 2020
Year Value
2020 1.22
2019 0.709
2018 0.728
2017 0.51
2016 0.537
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 45% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has increased by 94% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 72% in last years.
  • This journal’s SNIP is in the top 10 percentile category.
Therapeutic Advances in Cardiovascular Disease

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SAGE

Therapeutic Advances in Cardiovascular Disease

The journal is aimed at clinicians and researchers from the cardiovascular disease field and will be a forum for all views and reviews relating to this discipline.Topics covered will include: arteriosclerosis, cardiomyopathies, coronary artery disease, diabetes, heart failure,...... Read More

Medicine

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Last updated on
11 Jun 2020
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ISSN
1753-9447
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Impact Factor
Medium - 0.817
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Open Access
No
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Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
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Bibliography Name
SageV
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Citation Type
Numbered (Superscripted)
25
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Bibliography Example
Blonder GE, Tinkham M and Klapwijk TM. Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 1982; 25(7): 4515–4532. URL 10.1103/PhysRevB.25.4515.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1177/1753944717711379
Metabolic syndrome: pathophysiology, management, and modulation by natural compounds.
Yogita Rochlani1, Naga Venkata Pothineni2, Swathi Kovelamudi2, Jawahar L. Mehta2

Abstract:

Metabolic syndrome (MetS) represents a cluster of metabolic abnormalities that include hypertension, central obesity, insulin resistance, and atherogenic dyslipidemia, and is strongly associated with an increased risk for developing diabetes and atherosclerotic and nonatherosclerotic cardiovascular disease (CVD). The pathogen... Metabolic syndrome (MetS) represents a cluster of metabolic abnormalities that include hypertension, central obesity, insulin resistance, and atherogenic dyslipidemia, and is strongly associated with an increased risk for developing diabetes and atherosclerotic and nonatherosclerotic cardiovascular disease (CVD). The pathogenesis of MetS involves both genetic and acquired factors that contribute to the final pathway of inflammation that leads to CVD. MetS has gained significant importance recently due to the exponential increase in obesity worldwide. Early diagnosis is important in order to employ lifestyle and risk factor modification. Here, we review the epidemiology and pathogenesis of MetS, the role of inflammation in MetS, and summarize existing natural therapies for MetS. read more read less

Topics:

Metabolic syndrome (54%)54% related to the paper
View PDF
478 Citations
Journal Article DOI: 10.1177/1753944708096379
Cardiovascular disease in chronic kidney disease.
Anita M. Saran1, Thomas D. DuBose1

Abstract:

The presence of kidney disease, manifested by low glomerular filtration rates (GFR) and/or large amounts of protein in the urine, is independently associated with increased rates of cardiovascular disease (CVD). The severity of kidney disease is associated with graded increases in risk for CVD and death. Chronic kidney diseas... The presence of kidney disease, manifested by low glomerular filtration rates (GFR) and/or large amounts of protein in the urine, is independently associated with increased rates of cardiovascular disease (CVD). The severity of kidney disease is associated with graded increases in risk for CVD and death. Chronic kidney disease (CKD) should be recognized and treatment initiated early to maximize the chances for slowing nephropathy progression and reducing proteinuria. We recommend screening for CKD in all patients with CVD, including computing an estimated GFR and evaluating for proteinuria using a spot urine albumin:creatinine ratio. Aggressive management of traditional cardiovascular risk factors should be employed in this high-risk population, specifically rigorous hypertension control (including the use of angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blocking agents (ARB)), management of hyperglycemia, hyperlipidemia and smoking cessation. Further studies are needed to identify the unique renal failure-related (non-traditional) risk factors that contribute to accelerated atherosclerosis in this population and performance of randomized trials to assess the effects of cardiovascular interventions in individuals with CKD. read more read less

Topics:

Kidney disease (67%)67% related to the paper, Renal function (61%)61% related to the paper, Nephropathy (61%)61% related to the paper, Proteinuria (55%)55% related to the paper, Population (53%)53% related to the paper
View PDF
222 Citations
open accessOpen access Journal Article DOI: 10.1177/1753944708094227
Preeclampsia and future cardiovascular risk: formal risk factor or failed stress test?
Iasmina M. Craici1, Steven J. Wagner1, Vesna D. Garovic1

Abstract:

It is estimated that 10% of pregnancies are affected by hypertension worldwide. Approximately one-half of all hypertensive pregnancy disorders are due to preeclampsia, a pregnancy-specific disorder, its distinctive feature being either sudden onset, or worsening of pre-existing proteinuria. It has become increasingly recogniz... It is estimated that 10% of pregnancies are affected by hypertension worldwide. Approximately one-half of all hypertensive pregnancy disorders are due to preeclampsia, a pregnancy-specific disorder, its distinctive feature being either sudden onset, or worsening of pre-existing proteinuria. It has become increasingly recognized that women with a history of preeclampsia are at increased risk for future cardiovascular disease (CVD), but the mechanisms of this increase in risk are unclear. One possible explanation is that these two conditions share several common metabolic abnormalities as risk factors, including obesity, insulin resistance, and lipid abnormalities that may lead to preeclampsia and CVD at different times of a woman's life. Recent studies have revealed that, similar to CVD, several mediators of endothelial cell dysfunction are up-regulated in preeclampsia. Free radical derived oxidative stress, various inflammatory markers, including neutrophil response, C-reactive protein, and leukocyte adhesion, may contribute to endothelial dysfunction in both preeclampsia and coronary atherosclerosis. Alternatively, preeclampsia itself may induce metabolic and vascular changes that may increase the overall future risk for CVD in affected women. Therefore, at present, it remains unclear whether preeclampsia is a formal risk factor for CVD, or identifies women at increased risk for CVD later in life. Pending large-scale studies aiming to examine the causality of this association, women with a history of preeclampsia should be counseled regarding their increased risks for hypertension and other cardiovascular sequelae later in life, followed closely and treated aggressively for modifiable CVD risk factors. read more read less

Topics:

Risk factor (56%)56% related to the paper, Preeclampsia (53%)53% related to the paper, Eclampsia (52%)52% related to the paper, Risk assessment (50%)50% related to the paper
View PDF
172 Citations
open accessOpen access Journal Article DOI: 10.1177/1753944719870084
6-minute walking test: a useful tool in the management of heart failure patients:

Abstract:

Reduced functional ability and exercise tolerance in patients with heart failure (HF) are associated with poor quality of life and a worse prognosis. The 6-minute walking test (6MWT) is a widely available and well-tolerated test for the assessment of the functional capacity of patients with HF. Although the cardiopulmonary ex... Reduced functional ability and exercise tolerance in patients with heart failure (HF) are associated with poor quality of life and a worse prognosis. The 6-minute walking test (6MWT) is a widely available and well-tolerated test for the assessment of the functional capacity of patients with HF. Although the cardiopulmonary exercise test (a maximal exercise test) remains the gold standard for the evaluation of exercise capacity in patients with HF, the 6MWT (submaximal exercise test) may provide reliable information about the patient's daily activity. The current review summarizes the value of 6MWT in patients with HF and identifies its usefulness and limitations in everyday clinical practice in populations of HF. We aimed to investigate potential associations of 6MWD with other measures of functional status and determinants of 6MWD in patients with HF as well as to review its prognostic role and changes to various interventions in these patients. read more read less

Topics:

Functional ability (56%)56% related to the paper
View PDF
129 Citations
open accessOpen access Journal Article DOI: 10.1177/1753944715597623
ACE2 and vasoactive peptides: novel players in cardiovascular/renal remodeling and hypertension

Abstract:

The renin-angiotensin system (RAS) is a key component of cardiovascular physiology and homeostasis due to its influence on the regulation of electrolyte balance, blood pressure, vascular tone and cardiovascular remodeling. Deregulation of this system contributes significantly to the pathophysiology of cardiovascular and renal... The renin-angiotensin system (RAS) is a key component of cardiovascular physiology and homeostasis due to its influence on the regulation of electrolyte balance, blood pressure, vascular tone and cardiovascular remodeling. Deregulation of this system contributes significantly to the pathophysiology of cardiovascular and renal diseases. Numerous studies have generated new perspectives about a noncanonical and protective RAS pathway that counteracts the proliferative and hypertensive effects of the classical angiotensin-converting enzyme (ACE)/angiotensin (Ang) II/angiotensin type 1 receptor (AT1R) axis. The key components of this pathway are ACE2 and its products, Ang-(1-7) and Ang-(1-9). These two vasoactive peptides act through the Mas receptor (MasR) and AT2R, respectively. The ACE2/Ang-(1-7)/MasR and ACE2/Ang-(1-9)/AT2R axes have opposite effects to those of the ACE/Ang II/AT1R axis, such as decreased proliferation and cardiovascular remodeling, increased production of nitric oxide and vasodilation. A novel peptide from the noncanonical pathway, alamandine, was recently identified in rats, mice and humans. This heptapeptide is generated by catalytic action of ACE2 on Ang A or through a decarboxylation reaction on Ang-(1-7). Alamandine produces the same effects as Ang-(1-7), such as vasodilation and prevention of fibrosis, by interacting with Mas-related GPCR, member D (MrgD). In this article, we review the key roles of ACE2 and the vasoactive peptides Ang-(1-7), Ang-(1-9) and alamandine as counter-regulators of the ACE-Ang II axis as well as the biological properties that allow them to regulate blood pressure and cardiovascular and renal remodeling. read more read less

Topics:

Angiotensin II (58%)58% related to the paper, Cardiovascular physiology (54%)54% related to the paper, Renin–angiotensin system (51%)51% related to the paper, Kidney (51%)51% related to the paper
View PDF
124 Citations
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Frequently asked questions

1. Can I write Therapeutic Advances in Cardiovascular Disease in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Therapeutic Advances in Cardiovascular Disease guidelines and auto format it.

2. Do you follow the Therapeutic Advances in Cardiovascular Disease guidelines?

Yes, the template is compliant with the Therapeutic Advances in Cardiovascular Disease guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in Therapeutic Advances in Cardiovascular Disease?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the Therapeutic Advances in Cardiovascular Disease citation style.

4. Can I use the Therapeutic Advances in Cardiovascular Disease templates for free?

Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for Therapeutic Advances in Cardiovascular Disease.

5. Can I use a manuscript in Therapeutic Advances in Cardiovascular Disease that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper Therapeutic Advances in Cardiovascular Disease that you can download at the end.

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SciSpace's Therapeutic Advances in Cardiovascular Disease is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

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12. Is Therapeutic Advances in Cardiovascular Disease's impact factor high enough that I should try publishing my article there?

To be honest, the answer is no. The impact factor is one of the many elements that determine the quality of a journal. Few of these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Therapeutic Advances in Cardiovascular Disease?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Therapeutic Advances in Cardiovascular Disease. The table below indicates the level of access a journal has as per Sherpa Romeo's archiving policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

14. What are the most common citation types In Therapeutic Advances in Cardiovascular Disease?

The 5 most common citation types in order of usage for Therapeutic Advances in Cardiovascular Disease are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

15. How do I submit my article to the Therapeutic Advances in Cardiovascular Disease?

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16. Can I download Therapeutic Advances in Cardiovascular Disease in Endnote format?

Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Therapeutic Advances in Cardiovascular Disease Endnote style according to Elsevier guidelines.

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