Intravascular Ultrasound

(Abstract no. 199)

AS-199From the Intragastric to Extragastric Role of HelicobacterPylori: Implications on Metabolic Syndromes. Afzalur Rahman1,Habib Sadat Chaudhury1, Mark Cope2, Shafique Sarker3,Tim Garvey2, Mohammad Khaled2, AKM Mohibullah1. 1NationalInstitute of Cardiovascular Diseases (NICVD), Dhaka, Bangladesh;2Department of Nutrition Sciences, University of Alabama atBirmingham, Birmingham, USA; 3International Centre forDiarrhoeal Disease Research, Bangladesh (ICDDR,B), Dhaka,Bangladesh.

Background: Interests and investigations have been mounting in re-cent years to implicate inflammation with atherosclerosis. Interestingly,incidence of chronic diseases, particularly diabetes mellitus (DM) andcoronary artery disease (CAD) is significantly higher among AsianIndians. Coincidently, �85% of Asian Indians in the Indian subconti-nent have also been found to contract Helicobacter pylori (HP) infec-tion during their childhood. This prompted us to investigate if inflam-mation as induced by this chronic infection has any role in thepathogenesis of CAD in Asian Indians living in Bangladesh. Furtherinvestigations were, therefore, undertaken to examine if HP infectionwith its virulent strain cytotoxic-associated gene A (CagA), could beimplicated in insulin resistance (IR) and/or insulin secretion, along withother metabolic syndromes, such as obesity, in terms of body massindex (BMI) and lipid profile.

Methods: This study was conducted at the National Institute ofCardiovascular Diseases with approval from the Ethical Review Com-mittee of the University of Dhaka. HP (CagA) subjects who underwentcoronary angiography for the first time and were found to have coro-nary artery narrowing �50% were considered as HP�ve cases (n �21), whereas subjects without CAD and with and without HP weregrouped as HP�ve (n � 20) and HP-ve (n � 21) controls, respec-tively. The IgG antibodies to HP were measured by the enzyme-linked immunosorbent assay (ELISA) method and CagA, by West-ern blot analysis. Thromboxane B (TXB) was estimated using anenzyme immunoassay kit. IR was determined by the HomeostasisModel Assessment (HOMA-IR) according to the formula: HOMA-IR � (fasting glucose [millimoles per liter] � fasting insulin [mil-liunits per liter])/22.5. Insulin secretion was calculated as theHOMA-B (�) cell index according to the equation: HOMA-B �(fasting insulin [milliunits per liter] � 20)/(fasting glucose [milli-moles per liter] � 3.5).

Results: Differences occurred among the groups involvingHOMA-B, HOMA-IR, fasting glucose, high-density lipoprotein(HDL), and TXB (Table). TXB, an index of inflammation for CAD inparticular, did not show any significant variation with BMI. It is,however, significantly higher in the HP�ve cases (Figure 1). The bloodlevel of thromboxane was significantly higher in HP CagA�ve than theCagA�ve subjects, with and without CAD. HP�ve cases have asignificantly lower level of HDL than the HP-ve normal control (Figure2). HP�ve controls also have lower HDL levels than the �ve controls.IR is significantly higher in the HP�ve cases than both the controlgroups (Figure 3).

TABLE 2 Comparative statistics (p values).

HP�ve Controlsvs HP�ve Controls

HP-ve Controlsvs HP�ve Cases

HP�ve Controlsvs HP�ve Cases

Demographics — — —Age 0.09 0.85 0.05Metabolic Features — — —BMI 0.70 0.71 0.98HOMA-B (ISD) — — —HOMA-IR 0.84 — —Fasting Glucose — — —Triglycerides 0.25 0.38 0.77Total Cholesterol 0.45 0.08 0.33HDL — — 0.43LDL 0.41 0.47 0.14Inflammatory Marker — — —B (TXB) 0.88 — —

Conclusion: (1) Inflammation in HP (CagA)–infected subjects hasa positive trend with increased adiposity in terms of BMI; (2) inflam-mation is significantly higher in the HP (CagA)–infected subjects; (3)

The American Journal of Cardiology� APRIL 22–24 2009 ANGIOPLASTY SUMMIT ABSTRACTS/E-Poster 85B

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ABSTRACTS

Wednesday, April 22 - Friday, April 24, 2009 (E-Poster Abstract Zone)

HP (CagA) was found to modify the level of HDL by lowering it inthe human subjects; (4) fasting glucose levels in the HP (CagA)–infected subjects are significantly higher; (5) IR is significantlyhigher in the HP (CagA)–infected CAD patients; and (6) insulinsecretion dysfunction appears to be significantly higher in the HP

(CagA)–infected subjects with and without CAD, observed for thefirst time, to our knowledge. The above findings warrant prospectiveclinical studies to eradicate HP (CagA) in infected subjects toinvestigate if this bacterium is indeed associated with metabolicdysfunctions as observed in this study.

86B The American Journal of Cardiology� APRIL 22–24 2009 ANGIOPLASTY SUMMIT ABSTRACTS/E-Poster

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ABSTRACTS

Wednesday, April 22 - Friday, April 24, 2009 (E-Poster Abstract Zone)