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Eur J Cardiothorac Surg 2001;20:217-218
© 2001 Elsevier Science NL
Letter to the Editor |
a Gastroenterology Endocrinology and Metabolism Division, St. George's Hospital, London, UK
b Cardio-thoracic Centre, Broadgreen University Hospital, Liverpool, UK
Received 18 December 2000; received in revised form 3 April 2001; accepted 6 April 2001.
Corresponding author. Tel.: +44-208-725-5747; fax: +44-208-725-3270
e-mail: apoullis{at}sghms.ac.uk
In 1899 a spiral like bacteria was isolated from human stomachs. In 1989 it was named Helicobacter pylori (H. pylori) because of its helical appearance and the pylorus of the stomach is the commonest site of isolation [1].
H. pylori has been implicated as having a pathological role in a variety of gastrointestinal disease from peptic ulcers to gastric cancer. Epidemiological studies have linked H. pylori with ischaemic heart disease (IHD) [2]. This association is stronger with the more virulent cytotoxin associated gene-A (Cag A) strain [3].
H. pylori is the commonest chronic infection in humans; 30–60% of middle aged adults in European countries have serological evidence of infection. It is acquired in childhood and persists unless treated. The mode of transmission is unknown but proposed routes include oral–oral and faecal–oral.
Aspirin is the most commonly prescribed cardiovascular drug. While aspirin and H. pylori independently cause the majority of peptic ulcers their interaction remains controversial. A review of the seven studies investigating their interaction has given conflicting results. Three found no additional risk in treating H. pylori infected patients with non-steroidal anti-inflammatory drugs (NSAIDs), three found possible evidence that infection may protect against NSAID induced ulcers and one reported infection doubles the risk of bleeding peptic ulcers in patients treated with NSAIDs [4]. In post coronary artery bypass grafting patients treated with aspirin after three months 24% have endoscopic evidence of erosions or ulcers, H. pylori infection is associated with 64% of these lesions [5]. It is unclear whether screening and eradication is of benefit in these patients to reduce gastrointestinal bleeds.
Atrial fibrillation is the commonest indications for long-term anticoagulation and gastro-intestinal bleeding the main complications of this. No trials have been undertaken to address whether screening for infection and eradication prior to anticoagulation reduces this risk.
Anticoagulation of patients with mechanical heart valve prosthesis is essential subsequent gastro-intestinal bleeding is a major cause of morbidity and mortality. In a study of 150 patients anticoagulated following prosthetic valve surgery 21.6% of H. pylori positive patients were subsequently hospitalised due to an upper gastro-intestinal bleed. None of the H. pylori negative patients had hospital admissions due to bleeding episodes [6]. An intervention study is required to confirm that eradication therapy in patients who are H. pylori positive does protect them from gastrointestinal bleeding following anticoagulation.
The most widely used regimen to eradicate H. pylori is the combination of a proton pump inhibitor (PPI), amoxycillin and clarithromycin. This combination has important interactions with commonly used cardiac drugs. Clarithromycin and omeprazole enhance the effect of warfarin. PPI's and Clarithromycin may increase the plasma concentration of digoxin and Clarithroycin increases the risk of myopathy in patients on simvastatin.
Since its discovery H. pylori has been associated with an increasing number of diseases. Its weak association with IHD, predisposition to ulcer formation and treatment interactions with cardiac drugs has brought this bacteria to the attention of the cardiac surgeon. As it is easily treated it is essential that research is carried out to clearly define which populations should be screened and treated for this common infection.
References
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