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American Journal of Cardiovascular Drugs — Template for authors

Publisher: Springer

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Guideline source

Categories	Rank	Trend in last 3 yrs
Cardiology and Cardiovascular Medicine	#68 of 317	-
Pharmacology (medical)	#64 of 246	down by 12 ranks

Journal quality:

High

Last 4 years overview: 197 Published Papers | 1008 Citations

Indexed in: Scopus

Last updated: 11/07/2020

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Insights

General info

Related Journals

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Therapeutic Advances in Cardiovascular Disease

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Quality:

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CiteRatio: 4.8

SJR: 1.164

SNIP: 1.22

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CiteRatio: 6.5

SJR: 1.108

SNIP: 1.077

Open Access

Journal of Cardiovascular Pharmacology and Therapeutics

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CiteRatio: 4.3

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SNIP: 0.865

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Quality:

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CiteRatio: 4.2

SJR: 0.818

SNIP: 0.742

Journal Performance & Insights

Impact Factor

CiteRatio

Determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

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

2.674

4% from 2018

Impact factor for American Journal of Cardiovascular Drugs from 2016 - 2019
Year	Value
2019	2.674
2018	2.578
2017	2.643
2016	2.768

Graph view

5.1

9% from 2019

CiteRatio for American Journal of Cardiovascular Drugs from 2016 - 2020
Year	Value
2020	5.1
2019	4.7
2018	4.6
2017	5.4
2016	4.7

Graph view

Insights

Impact factor of this journal has increased by 4% in last year.
This journal’s impact factor is in the top 10 percentile category.

Insights

CiteRatio of this journal has increased by 9% in last years.
This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

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.

1.063

24% from 2019

SJR for American Journal of Cardiovascular Drugs from 2016 - 2020
Year	Value
2020	1.063
2019	0.854
2018	0.903
2017	0.951
2016	0.927

Graph view

0.959

16% from 2019

SNIP for American Journal of Cardiovascular Drugs from 2016 - 2020
Year	Value
2020	0.959
2019	0.824
2018	0.853
2017	1.029
2016	0.921

Graph view

Insights

SJR of this journal has increased by 24% in last years.
This journal’s SJR is in the top 10 percentile category.

Insights

SNIP of this journal has increased by 16% in last years.
This journal’s SNIP is in the top 10 percentile category.

American Journal of Cardiovascular Drugs

Guideline source: View

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Springer

American Journal of Cardiovascular Drugs

American Journal of Cardiovascular Drugs - The ultimate guide to prevention and management of cardiovascular disease. Promoting rational therapy and effective patient management within the discipline of cardiology, the journal covers all aspects of the management of cardiovascular disorders, particularly the place of newer and established drugs and devices. American Journal of Cardiovascular Drugs includes current opinion on contentious issues and emerging areas and definitive reviews on a broad range of topics relating to the optimum management of cardiovascular disorders. Read Less

Medicine

Last updated on	11 Jul 2020
ISSN	1175-3277
Impact Factor	Medium - 0.886
Acceptance Rate	60%
Open Access	Yes
Sherpa RoMEO Archiving Policy	Green
Endnote Style	Download Available
Bibliography Name	SPBASIC
Citation Type	Author Year (Blonder et al, 1982)
Bibliography Example	Beenakker CWJ (2006) Specular andreev reflection in graphene. Phys Rev Lett 97(6):067,007, URL 10.1103/PhysRevLett.97.067007

Top papers written in this journal

Open access • Journal Article • DOI: 10.2165/0129784-200808060-00004 •

Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism

Beatrice A. Golomb¹, Marcella A. Evans¹, •

01 Jan 2008 - American Journal of Cardiovascular Drugs

Abstract:

HMG-CoA reductase inhibitors (statins) are a widely used class of drug, and like all medications, have potential for adverse effects (AEs). Here we review the statin AE literature, first focusing on muscle AEs as the most reported problem both in the literature and by patients. Evidence regarding the statin muscle AE mechanis... HMG-CoA reductase inhibitors (statins) are a widely used class of drug, and like all medications, have potential for adverse effects (AEs). Here we review the statin AE literature, first focusing on muscle AEs as the most reported problem both in the literature and by patients. Evidence regarding the statin muscle AE mechanism, dose effect, drug interactions, and genetic predisposition is examined. We hypothesize, and provide evidence, that the demonstrated mitochondrial mechanisms for muscle AEs have implications to other nonmuscle AEs in patients treated with statins. In meta-analyses of randomized controlled trials (RCTs), muscle AEs are more frequent with statins than with placebo. A number of manifestations of muscle AEs have been reported, with rhabdomyolysis the most feared. AEs are dose dependent, and risk is amplified by drug interactions that functionally increase statin potency, often through inhibition of the cytochrome P450 3A4 system. An array of additional risk factors for statin AEs are those that amplify (or reflect) mitochondrial or metabolic vulnerability, such as metabolic syndrome factors, thyroid disease, and genetic mutations linked to mitochondrial dysfunction. Converging evidence supports a mitochondrial foundation for muscle AEs associated with statins, and both theoretical and empirical considerations suggest that mitochondrial dysfunction may also underlie many nonmuscle statin AEs. Evidence from RCTs and studies of other designs indicates existence of additional statin-associated AEs, such as cognitive loss, neuropathy, pancreatic and hepatic dysfunction, and sexual dysfunction. Physician awareness of statin AEs is reportedly low even for the AEs most widely reported by patients. Awareness and vigilance for AEs should be maintained to enable informed treatment decisions, treatment modification if appropriate, improved quality of patient care, and reduced patient morbidity. read more

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670 Citations

Journal Article • DOI: 10.2165/1153161-S0-000000000-00000 •

Markers of inflammation and cardiovascular disease: clinical applications of C-reactive protein determination.

Vicente Bertomeu Martínez, J. Ramón González-Juanatey

01 Jan 2009 - American Journal of Cardiovascular Drugs

Abstract:

C-reactive protein (CRP) is produced by the macrophages in the liver and adipocytes and is integrated in the acute-phase response pathway. Being a nonspecific marker of inflammation, it increases in response to inflammation. The results of recent studies that have analyzed the role of CRP have not yet influenced current clini... C-reactive protein (CRP) is produced by the macrophages in the liver and adipocytes and is integrated in the acute-phase response pathway. Being a nonspecific marker of inflammation, it increases in response to inflammation. The results of recent studies that have analyzed the role of CRP have not yet influenced current clinical practice. When used in combination with other established biomarkers for the prediction of the first major cardiovascular event or death, CRP does not improve the risk stratification obtained with the current guidelines. The reduction of CRP levels itself or as a statin-related pleiotropic effect has been assessed in different scenarios, including the acute phase of myocardial infarction; secondary prevention of cardiovascular diseases; special patient populations, such as diabetic patients; and finally in a primary prevention study (JUPITER [Justification for the Use of statins in primary Prevention: an Intervention Trial Evaluating Rosuvastatin]). Risk stratification in all the examined scenarios was related to serum LDL-C levels; in other words, the degree of cardiovascular risk was always lipid dependent. read more

384 Citations

Journal Article • DOI: 10.2165/00129784-200707030-00004 •

Endogenous and Exogenous Cardiac Glycosides and their Mechanisms of Action

Wilhelm Schoner¹, Georgios Scheiner-Bobis¹ •

01 Jan 2007 - American Journal of Cardiovascular Drugs

Abstract:

Cardiac glycosides have been used for decades to treat congestive heart failure The recent identification of cardiotonic steroids such as ouabain, digoxin, marinobufagenin, and telocinobufagin in blood plasma, adrenal glands, and hypothalamus of mammals led to exciting new perspectives in the pathology of heart failure and ar... Cardiac glycosides have been used for decades to treat congestive heart failure The recent identification of cardiotonic steroids such as ouabain, digoxin, marinobufagenin, and telocinobufagin in blood plasma, adrenal glands, and hypothalamus of mammals led to exciting new perspectives in the pathology of heart failure and arterial hypertension Biosynthesis of ouabain and digoxin occurs in adrenal glands and is under the control of angiotensin II, endothelin, and epinephrine released from cells of the midbrain upon stimulation of brain areas sensing cerebrospinal Na(+) concentration and, apparently, the body's K(+) content Rapid changes of endogenous ouabain upon physical exercise may favor the economy of the heart by a rise of intracellular Ca(2)(+) levels in cardiac and atrial muscle cells According to the sodium pump lag hypothesis, this may be accomplished by partial inhibition of the sodium pump and Ca(2+) influx via the Na(+)/Ca(2+) exchanger working in reverse mode or via activation of the Na(+)/K(+)-ATPase signalosome complex, generating intracellular calcium oscillations, reactive oxygen species, and gene activation via nuclear factor-kappaB or extracellular signal-regulated kinases 1 and 2 Elevated concentrations of endogenous ouabain and marinobufagenin in the subnanomolar concentration range were found to stimulate proliferation and differentiation of cardiac and smooth muscle cells They may have a primary role in the development of cardiac dysfunction and failure because (i) offspring of hypertensive patients evidently inherit elevated plasma concentrations of endogenous ouabain; (ii) such elevated concentrations correlate positively with cardiac dysfunction, hypertrophy, and arterial hypertension; (iii) about 40% of Europeans with uncomplicated essential hypertension show increased concentrations of endogenous ouabain associated with reduced heart rate and cardiac hypertrophy; (iv) in patients with advanced arterial hypertension, circulating levels of endogenous ouabain correlate with BP and total peripheral resistance; (v) among patients with idiopathic dilated cardiomyopathy, high circulating levels of endogenous ouabain and marinobufagenin identify those individuals who are predisposed to progressing more rapidly to heart failure, suggesting that endogenous ouabain (and marinobufagenin) may contribute to toxicity upon digoxin therapy In contrast to endogenous ouabain, endogenous marinobufagenin may act as a natriuretic substance as well It shows a higher affinity for the ouabain-insensitive alpha(1) isoform of Na(+)/K(+)-ATPase of rat kidney tubular cells and its levels are increased in volume expansion and pre-eclampsia Digoxin, which is synthesized in adrenal glands, seems to counteract the hypertensinogenic action of ouabain in rats, as do antibodies against ouabain, for example, (Digibind) and rostafuroxin (PST 2238), a selective ouabain antagonist It lowers BP in ouabain- and adducin-dependent hypertension in rats and is a promising new class of antihypertensive medication in humans read more

220 Citations

Journal Article • DOI: 10.2165/11587580-000000000-00000 •

Thiazolidinediones and risk of heart failure in patients with or at high risk of type 2 diabetes mellitus: A meta-analysis and meta-regression analysis of placebo-controlled randomized clinical trials

Adrian V. Hernandez¹, Ali Usmani², •

01 Jan 2011 - American Journal of Cardiovascular Drugs

Abstract:

Recent meta-analyses of randomized clinical trials (RCTs) demonstrated a higher risk of heart failure (HF) with the use of thiazolidinediones (TZDs). However, this effect may have been diluted by including active controls. Also, it is uncertain whether the risk of HF is similar with rosiglitazone and pioglitazone. This study ... Recent meta-analyses of randomized clinical trials (RCTs) demonstrated a higher risk of heart failure (HF) with the use of thiazolidinediones (TZDs). However, this effect may have been diluted by including active controls. Also, it is uncertain whether the risk of HF is similar with rosiglitazone and pioglitazone. This study quantified the risks of HF with the use of TZDs in patients with or at high risk of developing type 2 diabetes mellitus (DM), and evaluated differential effects by type of TZD. Secondarily, we evaluated risks of peripheral edema. We performed a systematic review and meta-analysis of placebo-controlled RCTs evaluating the effect of rosiglitazone or pioglitazone on investigator-reported HF and edema. Articles published before 31 December 2009 were searched in MEDLINE, The Web of Science, and Scopus, and the data were extracted by three investigators. RCTs with ≥100 patients and ≥3 months of follow-up were included. We quantified the effect of TZDs as odds ratios (ORs) by using the Mantel-Haenzel and alternative models. We further evaluated the risk of serious/severe HF, and the effect of several trial characteristics on HF risk by subgroup analysis and meta-regression analysis. 29 trials (n = 20254) were evaluated. TZDs were significantly associated with HF (TZD 360/6807 [5.3%] vs placebo 234/6328 [3.7%], OR 1.59; 95% CI 1.34, 1.89; p<0.00001). The risk of HF was higher with rosiglitazone than with pioglitazone (2.73 [95% CI 1.46, 5.10] vs 1.51 [1.26, 1.81]; p = 0.06). TZDs were associated with a similar risk of serious/severe HF (OR 1.47; 95% CI 1.16, 1.87; p = 0.002). Use of TZDs was also associated with edema (OR 2.04; 95% CI 1.85, 2.26; p<0.00001). HF and edema risks were consistent using Peto and random effects models. Risks of HF were significantly high for the subgroups of trials including patients with or at high risk for type 2 DM, and for the subgroup of trials with ≥12 months of follow-up. Meta-regression analysis showed that trials with lower overall baseline risk had higher HF risks. In placebo-controlled trials of adult patients with or at high risk for type 2 DM, TZD therapy is significantly and consistently associated with a higher risk of HF. The risk of serious/severe HF is also increased with the use of TZDs. HF risks are similar to those of meta-analyses combining active- and placebo-controlled trials. The benefit/risk profile of TZDs should be considered when treating diabetic patients with or without prior HF. read more

196 Citations

Journal Article • DOI: 10.2165/00129784-200505060-00005 •

Beyond low-density lipoprotein: addressing the atherogenic lipid triad in type 2 diabetes mellitus and the metabolic syndrome.

Richard W. Nesto¹ •

01 Jan 2005 - American Journal of Cardiovascular Drugs

Abstract:

The metabolic syndrome and type 2 diabetes mellitus are both becoming more prevalent, and both increase the risk of cardiovascular disease. Many patients are not receiving appropriate treatment for the type of dyslipidemia that commonly occurs in these disorders--the so-called 'atherogenic lipid triad' of high serum triglycer... The metabolic syndrome and type 2 diabetes mellitus are both becoming more prevalent, and both increase the risk of cardiovascular disease. Many patients are not receiving appropriate treatment for the type of dyslipidemia that commonly occurs in these disorders--the so-called 'atherogenic lipid triad' of high serum triglyceride levels, low serum high-density lipoprotein cholesterol (HDL-C) levels, and a preponderance of small, dense, low-density lipoprotein cholesterol (LDL-C) particles. All of the processes involved in atherogenesis can be exacerbated by insulin resistance and/or the metabolic syndrome. Hypertriglyceridemia is a strong predictor of coronary heart disease. There is also an inverse relationship between serum levels of HDL-C and triglycerides in diabetic patients, with low serum HDL-C levels possibly representing an independent risk factor for cardiovascular disease. Small, dense, LDL-C particles are also highly atherogenic as they are more likely to form oxidized LDL and are less readily cleared. Insulin resistance, which is central to the metabolic syndrome and type 2 diabetes mellitus, leads to high levels of very low-density lipoprotein (VLDL), which contain a high concentration of triglycerides, resulting in high serum triglyceride levels and low serum HDL-C levels. Even though modification of the atherogenic lipid triad is probably one of the most effective methods of reducing cardiovascular risk, therapy for diabetic dyslipidemia is often directed to first lowering serum LDL-C levels with a HMG-CoA reductase inhibitor. This may leave substantial excess risk for cardiovascular disease in patients with these types of dyslipidemia. The results of recent trials evaluating HMG-CoA reductase inhibitors have been mixed, with two showing no significant effect on cardiovascular outcomes in subgroups of diabetic patients. The recent CARDS (Collaborative Atorvastatin Diabetes Study) showed that atorvastatin can reduce cardiovascular events in a trial specifically designed for a diabetic population, though the population had to have at least one other risk factor in addition to diabetes mellitus. Fibric acid derivatives, such as fenofibrate, bezafibrate and gemfibrozil, are potentially well suited to the treatment of dyslipidemia that is generally associated with type 2 diabetes mellitus and the metabolic syndrome, as they are usually more effective than HMG-CoA reductase inhibitors for normalizing serum levels of HDL-C and triglycerides. Promising results have been obtained from several trials of fibric acid derivatives including the BIP (Bezafibrate Infarction Prevention) study and the VA-HIT (Veterans Affairs Cooperative Studies Program HDL-C Intervention Trial; gemfibrozil). The FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) trial, a clinical outcomes trial specifically designed to evaluate fenofibrate in a large population of patients with type 2 diabetes mellitus, many of whom have the metabolic syndrome, is underway. The FIELD trial results should shed light on the efficacy and safety of fenofibrate in reducing cardiovascular morbidity in diabetic and metabolic syndrome patients and on the safety profile of combination therapy with fenofibrate and a HMG-CoA reductase inhibitor. read more

191 Citations

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13. What is Sherpa RoMEO Archiving Policy for American Journal of Cardiovascular Drugs?

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 American Journal of Cardiovascular Drugs. 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:

Pre-prints as being the version of the paper before peer review and
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 American Journal of Cardiovascular Drugs?

The 5 most common citation types in order of usage for American Journal of Cardiovascular Drugs are:.

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

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American Journal of Cardiovascular Drugs — Template for authors

Related Journals

Journal Performance & Insights

Impact Factor

CiteRatio

2.674

5.1

Insights

Insights

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

1.063

0.959

Insights

Insights

American Journal of Cardiovascular Drugs

American Journal of Cardiovascular Drugs

Top papers written in this journal

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