Circulation Impact Factor Reaches New High
Circulation’s impact factor was 11.164 in 2003—the highest it has ever been. The journal has ranked highest in cardiovascular journals since it began weekly publication in 1998 under the direction of Editor James T. Willerson, MD.
A journal’s impact factor is based on 2 elements: the numerator, which is the number of citations in the current year to any items published in a journal in the previous 2 years, and the denominator, which is the number of substantive articles (source items) published in the same 2 years (CMAJ. 1999;161:979–980OpenUrl).
For comparison purposes, the impact factor for the New England Journal of Medicine was 34.833; for Science, 29.162; Nature, 21.65; the Journal of the American Medical Association, 21.455; Lancet, 18.316; the Annals of Internal Medicine, 12.427; Circulation Research, 10.117; the Journal of the American College of Cardiology, 7.599; Arteriosclerosis, Thrombosis and Vascular Biology, 6.791; the European Heart Journal, 5.997; Stroke, 5.233; and Cardiovascular Research, 5.164.
For Dr Willerson, whose editorship of the journal Circulation ends this month, the latest impact factor demonstrates the credibility of his vision for the journal. Under his leadership, Circulation added sections specifically for the practicing cardiologist, online pages (including Cardiovascular News), Rapid Track Articles, Cardiology Patient Pages, Clinician Update, Rapid Access Articles, and Mini-Review: Expert Opinions. He took the journal online during his tenure and made it possible for authors to submit their research articles online and for reviewers to submit their opinions in the same manner—all of which sped up the submission and review process dramatically. The numbers of manuscripts submitted to the journal reached a monthly high of 738 in December 2003.
“I am confident that the future of Circulation will be equally successful under the leadership of Joseph Loscalzo, MD, PhD,” said Dr Willerson. “Circulation has become the most prominent journal in the cardiovascular world, and I anticipate that it will remain so because of the strength of the research world in that field and the leadership that Dr Loscalzo will provide.”
Clopidogrel Resistance Marks Recurrent Risks
Approximately 25% of patients who undergo stenting for acute ST-segment–elevation myocardial infarction are resistant to the antiplatelet effects of clopidogrel, which is used to prevent subsequent cardiovascular events, said researchers in the June 29, 2004, issue of the journal Circulation (Circulation. 2004;109:3171–3175OpenUrl).
In this study, researchers led by Shlomi Matetzky, MD, of the Heart Institute of Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel, divided 60 consecutive acute myocardial infarction patients who had undergone primary percutaneous intervention with stenting into 4 groups according to platelet aggregation scores. Patients in the first quartile were resistant to the effects of clopidogrel. Platelet aggregation was reduced 69% in quartile 2, 58% in quartile 3, and 33% in quartile 4. During 6 months of follow-up, 40% of patients in quartile 1 had a recurrent cardiovascular event. By comparison, only 1 patient in quartile 2 and none in quartiles 3 and 4 had a recurrent cardiovascular event during the same period.
Although the study is merely observational and the researchers noted that limitation, they wrote, “Clopidogrel resistance occurs in a significant percentage of STEMI [ST-segment–elevation myocardial infarction] patients and is associated with a higher risk of recurrent cardiovascular events. The question of whether increased doses of clopidogrel might overcome this resistance in nonresponsive patients warrants further investigation.”
Plasma Brain Natriuretic Peptide Poor Detector of Systolic or Diastolic Dysfunction
Plasma brain natriuretic peptide (BNP) would be a poor screening test for preclinical systolic or diastolic function in the population, requiring echocardiograms in 10% to 40% of the population screened, with most of the tests turning out negative, said researchers in this week’s issue of the journal Circulation (Circulation. 2004;109:3176–3181OpenUrl). At the same time, the test would miss between 10% and 60% of those who had the disorders, according to the researchers led by Margaret M. Redfield, MD, of the Mayo Clinic and Foundation in Rochester, Minn.
The physicians in the study measured BNP, systolic and diastolic ventricular function, and other clinical parameters in 2042 residents of Olmsted County, Minn. The subjects were randomly selected from those aged 45 years or older.
The best values for determining risk of systolic or diastolic function varied with the age and sex of the subjects tested. However, none of them were adequate to provide a test with the specificity and sensitivity needed to screen a population. The authors wrote that the results of their study, along with results of other studies, “suggest that BNP is considerably less accurate for detection of milder degrees of systolic dysfunction, which is more common and also associated with increased risk. A screening tool that does not reliably detect milder levels of systolic dysfunction would limit ability to impact events. Lastly, high false-positive rates may lead to poor physician acceptance, which would limit use of screening.”
Estrogen-Receptor Gene Polymorphism Associated With Increased Risk of Myocardial Infarction
The estrogen receptor 1 (ESR1) haplotype created by the c.454-397T_C (PvuII) and c.454-351A_G (XbaI) polymorphisms, when carried by postmenopausal women, appears to increase the risk of myocardial infarction and ischemic heart disease independently of known risk factors for cardiovascular disease, said researchers from Erasmus Medical Center, Rotterdam, the Netherlands, in the June 23, 2004, issue of the Journal of the American Medical Association (JAMA. 2004;291:2969–2977OpenUrlCrossRefPubMed). No similar association was seen in men.
A total of 2617 women and 3971 men from The Rotterdam Study, a population-based cohort study of participants aged 55 years or more, were enrolled in the study. Approximately 29% of the women and 28.2% of the men were homozygous for the ESR1 haplotype 1, and 49% of women and 50% of men were heterozygous. Twenty-two percent of women and 21.4% of men did not carry the suspect alleles.
During the follow-up period of 7 years, on average, 285 subjects suffered an acute myocardial infarction and 440 had an ischemic heart disease event. Of these, 97 were fatal. Adjusting for known risk factors, women who were homozygous and heterozygous carriers for haplotype 1 had an increased risk of myocardial infarction compared with those who did not carry the mutation. A similarly increased risk was seen for ischemic heart disease in women.
The authors wrote, “In interpreting the clinical implications of these results, we must consider that 78% of the population carries the ESR1 haplotype 1 risk allele and that heterozygous and homozygous carriers of haplotype 1 have a 2-fold increased risk of IHD [ischemic heart disease]. Perhaps we should view this not as a ‘risk’ allele but consider the noncarriers as having a protective allele, which implies that noncarriers (22% of the population) have a 50% reduced risk. In conclusion, this population-based prospective cohort study shows a significant 2-fold increased risk of myocardial infarction, as well IHD events, in postmenopausal women who carry ESR1 haplotype 1 (c.454-397 T allele and c.454-351 A allele). The association was not explained by known cardiovascular risk factors such as age, previous myocardial infarction, BMI [body mass index], age at menopause, use of hormone therapy, blood pressure, smoking, diabetes, and cholesterol level, suggesting that haplotype 1 is an independent risk factor for IHD. Furthermore, our results also suggest that postmenopausal women who carry ESR1 haplotype 1 have not only an increased risk of having an IHD event but also an increased risk of death from such an event.”
Folate Therapy May Increase Risk of In-Stent Restenosis
Folate therapy (folic acid, vitamin B6, and vitamin B12 given after coronary stenting) may increase the risk of restenosis in the stent and the subsequent need for a repeat revascularization, said researchers from Germany and the Netherlands in a report in the June 24, 2004, issue of The New England Journal of Medicine (N Engl J Med. 2004;350:2673–2681OpenUrlCrossRefPubMed).
In this study, 636 patients who had undergone successful coronary stenting were assigned to receive 1 mg folic acid, 5 mg vitamin B6, and 1 mg vitamin B12 intravenously, followed by oral doses of the compounds daily or placebo for 6 months.
At 6 months, researchers led by Helmut Lange, MD, of the Kardiologische Praxis, Klinikum Links der Weser, Heart Center, Bremen, Germany, assessed minimal luminal diameter, late loss, and restenosis by quantitative coronary angiography. They found that the mean minimal luminal diameter was significantly smaller in the group that underwent folate therapy compared with the placebo group (1.59 versus 1.74 mm). Late luminal loss was greater in the folate group than in the placebo group, and restenosis was more common in the folate group compared with placebo. In fact, restenosis occurred in 34.5% of the restenosis group and only 26.5% of the placebo group. More patients in the folate group had to undergo repeat target-vessel revascularization (15.8%) versus the placebo group (10.6%).
The groups in which folate therapy did not have a negative effect included women, patients with diabetes, and those with very high homocysteine levels. The authors wrote, “Our data do not provide any evidence that folate therapy for the primary or secondary prevention of coronary artery disease is potentially harmful, since the folate group did not have an increased incidence of death or infarction. Our data cannot be interpreted to mean that multivitamin supplementation should be discontinued in patients after coronary stenting. The oral dose of folate that we used—1.2 mg—is three times the recommended daily dose for vitamin supplements. If, however, physicians decide to administer folate therapy to patients with coronary artery disease and moderate hyperhomocysteinemia even before the results of prospective prevention studies are known, they should exercise caution in the use of this therapy for patients who have just received a stent.”
I began writing the news for Circulation in 1998. The ride has been a whirlwind of learning, meeting new people, and watching the field of cardiology expand into the molecular, gene therapy, and a host of new drugs. I am thrilled that it has reached the heights with its new impact factor, and I know it will continue to improve as the years go by. This is the last Cardiovascular News I will write in this format. I hope the readers have enjoyed it as much as I.