Multiple Infections and Subsequent Cardiovascular Events in the Heart Outcomes Prevention Evaluation (HOPE) Study

Śmieja, Marek; Gnarpe, Judy; Lonn, Eva; Gnarpe, Håkan; Olsson, Gunnar; Yi, Qilong; Džavík, Vladimir; McQueen, Matthew; Yusuf, Salim

doi:10.1161/01.cir.0000044940.65226.1f

Cited by 131 publications

(101 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, a prospective nested case-control study found that H. pylori-IgG positivity is not associated with the risk of myocardial infarction or stroke in middle-aged Japanese individuals 45) . Additionally, neither CagA-negative nor CagApositive H. pylori infection has been shown to be associated with an increased risk of myocardial infarction and stroke in Germany 44) , consistent with the results obtained from other countries, including England 47) , Greece 46) , Canada 48) and China 49) . The discrepancies reported concerning the association between H. pylori HP: Helicobacter pylori, CIMT: carotid intima-media thickness, AMI: acute myocardial infarction, CHD: coronary heart disease, IHD: ischemic heart disease, IS: ischemic stroke, UBT: urea breath test.…”

Section: Potential Mechanisms Through Which H Pylori May Contribute supporting

confidence: 88%

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

Yang

Lü

2014

JAT

View full text Add to dashboard Cite

Accumulating evidence implicates Helicobacter pylori (H. pylori) infection in the pathogenesis of certain diseases localized outside the stomach, particularly those characterized by persistent and lowgrade systematic inflammation. Recently, the role of H. pylori infection in the development of atherosclerosis and its clinical complications has received attention. Atherosclerosis is a high-cost disease, and acute events resulting from this condition rank first among morbidity and mortality statistics in most industrialized countries. Atherosclerosis is a multifactorial disorder, and traditional risk factors explain only 50% of its etiology. Therefore, identifying new risk factors for atherosclerosis is necessary. Serological studies indicate that chronic H. pylori infection, especially that with more virulent strains, may predispose patients to the onset of atherosclerosis and related adverse clinical events, and PCR studies have detected H. pylori DNA in atherosclerotic plaques, although this finding remains controversial. If this association were to be confirmed, its importance to public health would be substantial, as the eradication of H. pylori is more straightforward and less costly than the longterm treatment of other risk factors. This review investigates the potential relationship between H. pylori infection and atherosclerosis from both epidemiological and pathogenic perspectives and characterizes the potential mechanisms underlying this correlation.

show abstract

Section: Potential Mechanisms Through Which H Pylori May Contribute supporting

confidence: 88%

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

Yang

Lü

2014

JAT

View full text Add to dashboard Cite

show abstract

“…However, CMV did predict secondary risk (death/myocardial infarction) in patients with pre-existing coronary artery disease especially in those with elevated C-reactive protein or interleukin-6 (IL-6) (27,28). Similar results were obtained in the HOPE (Heart Outcomes and Prevention Evaluation) study showing that out of the four pathogens tested (Cpn, Hpyl, hepatitis A, CMV) only CMV serostatus was predictive of cardiovascular events (29). The association with CMV seems to be more pronounced in connection with rapidly progressing atherosclerotic processes such as coronary restenosis after angioplasty or vascular surgery (18), and this observation might be of relevance to CAV in view of its rapid time course.…”

Section: Seroepidemiological Studiessupporting

confidence: 53%

The Role of Viruses in Cardiac Allograft Vasculopathy

Valantine

2004

American Journal of Transplantation

View full text Add to dashboard Cite

Considerable evidence suggests a role for viruses in transplant arteriosclerosis (TA), including observational data, experimental models and therapeutic trials implicating human cytomegalovirus (HCMV) in the progression to TA. In pediatric heart transplant patients, adenoviral genome in endomyocardial biopsies (EMB) is an important predictor of TA and graft loss. During CMV viremia, EMBs from adult patients demonstrate endothelialitis and vascular smooth muscle cell proliferation. These changes are predictors of subsequent diffuse TA. HCMV immediate early proteins (IE-1 and IE-2) increase the constitutive expression of intercellular adhesion molecule-1 (ICAM-1) independent of other intracellular cytokines. Likewise, viral chemokines such as US28 have been implicated in vascular disease because of their ability to induce smooth muscle cell migration. Recent data suggests that CMV might accelerate TA through its ability to abrogate the vascular protective effects of the endothelium-derived nitric oxide system (eNOS). Confirmation of causality requires clinical trials demonstrating that antiviral agents such as ganciclovir inhibit TA. Such studies in patients though limited to retrospective analyses, suggest that ganciclovir prophylaxis early after heart transplantation reduces the risk of TA. These observations emphasize the need for randomized controlled clinical trials to confirm a causal role for CMV (and other viruses) in TA.

show abstract

“…Adjusted risk for the seropair with the highest risk for posttransplantation CMV disease (donor-positive/recipientnegative) approached but did not reach our chosen level of statistical significance (P ϭ 0.03). In accordance with these unadjusted risk estimates, CMV infection has been linked with atherosclerotic risk among heart transplant recipients (35) and general patients without transplants (36). As approximately 15% of serologic pairing information was missing, failure to detect an independent association of CMV seropairing with PTMI may reflect misclassification error, which tends to reduce the estimated statistical significance of effects.…”

Section: Predictors Of Ptmimentioning

confidence: 65%

Incidence and Predictors of Myocardial Infarction after Kidney Transplantation

Lentine¹,

Brennan²,

Schnitzler³

2005

Journal of the American Society of Nephrology

313

235

View full text Add to dashboard Cite

The risk and predictors of post-kidney transplantation myocardial infarction (PTMI) are not well described. Registry data collected by the United States Renal Data System were used to investigate retrospectively PTMI among adult first renal allograft recipients who received a transplant in 1995 to 2000 and had Medicare as the primary payer. PTMI events were ascertained from billing and death records, and participants were followed for up to 3 yr after transplant or until the end of observation (December 31, 2000 R ecent studies demonstrate that myocardial infarction (MI) and renal dysfunction form a "high-risk combination" (1,2). Patients with mild chronic renal insufficiency faced more than twofold higher death rates after MI than those with normal renal function in one center's experience (2), and post-MI mortality increases explosively among ESRD patients on dialysis (1,2). Although kidney transplantation may reduce the risk for MI and improve post-MI survival (1,3), mortality rates after hospitalization for acute coronary syndromes among renal allograft recipients remain sobering, ranging from approximately 24% at 1 yr (1,4), to 30 to 38% at 2 yr (1,4,5), to Ͼ45% at 5 yr (1,4). Furthermore, as a leading cause of death (and thus graft loss) in patients with functioning renal transplants (6), posttransplantation MI (PTMI) has important implications for allograft longevity in this population.Several investigations have approached estimation of the incidence and predictors of MI after kidney transplantation by modeling primary hospital discharge diagnoses (5,7). These studies are limited by the quantity of available information for many clinical variables and, in not ascertaining other presentations including secondary diagnoses and fatal MI, underestimate risk. Candidate risk factors for PTMI include characteristics of the recipient, the kidney donor, transplantation management, and transplant course. Renal allograft recipients have a higher prevalence of "traditional" Framingham atherosclerotic vascular disease risk factors, including advanced age, diabetes, hypertension, and dyslipidemia (8). Time on dialysis before transplantation (9), donor history of hypertension (10), immunosuppressive regimen (11), quality of allograft function (12), and posttransplantation diabetes (13,14) also are implicated as mediators of cardiovascular risk in this population. Along with current uncertainty for the magnitude of PTMI incidence rates, the independent predictive values of putative posttransplantation cardiovascular risk factors for PTMI specifically, potential for risk modification, and the spectrum of clinical consequences after this complication are not yet known.Prompted by the limited available evidence on the risk and outcomes of PTMI, we undertook a retrospective study of a large cohort of recent kidney transplant recipients recorded in the United States Renal Data System (USRDS). We aimed to quantify the risk for PTMI in all presentations, identify clinically relevant risk factors, and estimate the impact of thi...

show abstract

Multiple Infections and Subsequent Cardiovascular Events in the Heart Outcomes Prevention Evaluation (HOPE) Study

Cited by 131 publications

References 31 publications

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

The Role of Viruses in Cardiac Allograft Vasculopathy

Incidence and Predictors of Myocardial Infarction after Kidney Transplantation

Contact Info

Product

Resources

About