Helicobacter pylori and myocardial infarction: one final push for the truth?

2001 ◽  
Vol 5 (4) ◽  
pp. 165-166
Author(s):  
D.S.G. Conway ◽  
G.Y.H. Lip
BMJ ◽  
1999 ◽  
Vol 319 (7218) ◽  
pp. 1157-1162 ◽  
Author(s):  
J. Danesh ◽  
L. Youngman ◽  
S. Clark ◽  
S. Parish ◽  
R. Peto ◽  
...  

2003 ◽  
Vol 33 (7) ◽  
pp. 267-272 ◽  
Author(s):  
A. G. Fraser ◽  
R. K. Scragg ◽  
B. Cox ◽  
R. T. Jackson

2016 ◽  
Vol 64 (4) ◽  
pp. 940-941
Author(s):  
N Vyas ◽  
H Alkhawam ◽  
E Saker ◽  
R Sogomonian ◽  
RA Ching Companioni ◽  
...  

IntroductionHelicobacter pylori (HP) infection is known to target the gastrointestinal system and is associated with extra gastrointestinal manifestations, but there is limited literature on cardiac associations. The most supported pathogenesis uses chronic inflammation as a risk factor causing atherosclerosis resulting in cardiovascular disease. Our aim is to evaluate whether there is an association between HP infection and acute myocardial infarction (AMI) and coronary artery disease (CAD).MethodWe performed a retrospective single center study at our medical center from 2005 to 2014 consisting of 1,671 patients who underwent Coronary Angiography (CA). We divided these patients into two groups based on CA reports. Patients with CAD defined as left main stenosis of ≥50% or any stenosis of ≥70% versus normal coronaries. We reviewed each patient chart to determine the prevalence of positive serum HP IgG antibody. Smoking, hypertension, dyslipidemia and obesity were also considered in each group.ResultsOf 1,671 patients, 1,237 had evidence of CAD vs 434 with normal coronary arteries. Twelve percent of CAD patients were found to have seropositive HP (SPHP) versus 1% in the control group (OR: 7.3, 95% CI: 3.5–15, p<0.0001) as depicted in figure 1. When we looked at the CAD group and compared SPHP patients to seronegative HP (SNHP) patients we found a greater amount of multiple coronary vessels disease in the SPHP group (OR: 1.4, 95% CI: 1.1–2, P=0.04). With regards to AMI, 30% of the SPHP group presented with AMI versus 10% seen in the SNHP group (OR: 4.3, 95% CI: 3–6.5, p<0.0001). In the CAD group with SPHP there was more hyperlipidemia and a higher BMI than in the CAD SNHP group (p<0.0001 and <0.0001, respectively), but there was no statistical difference between the two groups for the risk factors of smoking, hypertension and diabetes.ConclusionAccording to this study, the results showed a correlation with SPHP patients and CAD. Patients with HP seropositivity also tend to have multiple coronary artery vessel disease. In addition, our results also confirmed that there is an association between with HP infection and AMI. We hypothesize that the associated maybe secondary to inflammatory reaction associated with HP. Additional studies with larger sample groups are needed to investigate the possible role of this pathogen as a risk factor for heart disease.Abstract ID: 35 Figure 1Twelve percent of CAD patients were found to have seropositive HP (SPHP) versus 1% in the control group (OR: 7.3, 95% CI: 3.5–15, p<0.0001).


2021 ◽  
Vol 231 ◽  
pp. 105-109
Author(s):  
Jonatan Wärme ◽  
Martin Sundqvist ◽  
Katarina Mars ◽  
Layth Aladellie ◽  
Sven-Christian Pawelzik ◽  
...  

2001 ◽  
Vol 313 (1-2) ◽  
pp. 87-94 ◽  
Author(s):  
Katsuko Hara ◽  
Yutaka Morita ◽  
Hiroshi Kamihata ◽  
Toshiji Iwasaka ◽  
Hakuo Takahashi

1998 ◽  
Vol 114 ◽  
pp. A253
Author(s):  
P.P. Parravicini ◽  
R. Pellicano ◽  
R. Bigi ◽  
N. Gandolfo ◽  
G. Baduini ◽  
...  

1999 ◽  
Vol 82 (07) ◽  
pp. 14-18 ◽  
Author(s):  
Francesco Zito ◽  
Augusto Di Castelnuovo ◽  
Andria D’Orazio ◽  
Riccardo Negrini ◽  
Domenico De Lucia ◽  
...  

SummaryThe contribution of Helicobacter pylori (HP) infection to the risk of myocardial infarction was evaluated. The role of fibrinogen and its genetic control as a possibile mechanism by which HP may influence myocardial infarction risk was explored in this context. A case-control study was performed in 101 patients with myocardial infarction and in 101 controls.HP infection was associated with an increased risk of myocardial infarction independently for confounding variables (OR 4.1, CI95: 1.8-9.4). HP infection was significantly associated with higher levels of fibrinogen, both in cases and in controls. Furthermore, there was an additive effect of HP infection and B2 allele of BclI fibrinogen poly-morphism in increasing fibrinogen levels. HP infection showed a stronger effect on the risk of myocardial infarction in B2 allele carriers (OR 7.6, CI95: 1.8-31.6) as compared to subjects carrying the B1B1 genotype (OR 3.3, CI95: 1.2-9.2).We showed that a previous HP infection is a risk factor for myocardial infarction. An increase in fibrinogen levels is a possible mechanism by which HP may act. Concomitant conditions, like a genetic predisposition in increasing fibrinogen levels, seem to further increase the effect of HP on myocardial infarction risk.


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