Helicobacter pylori: a new cardiovascular risk factor?

There is increasing evidence that certain microbial agents may have an etiopathogenic role in the development of atherothrombosis. Helicobacter pylori, a bacterium that causes peptic ulcer disease, has been suggested as one of the microbes involved in the development of atherothrombosis. This hypothesis is based on the following observations: a) a higher prevalence of Helicobacter pylori infection in patients with coronary artery disease, myocardial infarction, or cerebrovascular disease; b) the coincidence of Helicobacter pylori infection and cardiovascular risk factors, such as serum cholesterol and triglyceride concentrations and plasma fibrinogen; c) Helicobacter pylori seropositivity correlates with acute-phase proteins associated with higher risk of coronary disease, such as C-reactive protein, and d) controversial PCR studies indicating the presence of Helicobacter pylori in atheromas. Analysis of the scientific evidence suggests that Helicobacter pylori infection could indirectly contribute to the development and severity of atherothrombosis and cardiovascular disease.     

Homocysteine in inflammatory bowel disease: a risk factor for thromboembolic complications?

OBJECTIVE: Patients with inflammatory bowel disease (IBD) are at increased risk for thromboembolic events. Hyperhomocysteinemia, which is an established risk factor for arterial as well as venous thrombosis, may be more prevalent in IBD because of vitamin deficiencies. METHODS: In this retrospective study, we studied the concentrations of total homocysteine (tHcy), cobalamin, folate, and pyridoxine in 231 consecutive patients with IBD, of whom 16 patients had a history of venous thrombosis, and nine a history of arterial thrombosis. Age- and gender-matched healthy volunteers served as controls (n = 102). RESULTS: Homocysteine concentrations in patients were higher (12.3 micromol/L [range 4.6-51.3] vs 11.1 micromol/L [range 3.9-27.6], p = 0.001) and hyperhomocysteinemia tended to be more prevalent in patients than in the controls (11.1% vs 5%, p = 0.07). Folate, cobalamin, creatinine, and pyridoxine concentrations were correlated with tHcy. Folate deficiency was infrequently encountered in IBD patients (4.3%). The tHcy concentration in patients with a history of venous or arterial thrombosis was not higher than in patients without a history of thrombosis (12.7 micromol/L [range 4.6-40.1] and 15.2 micromol/L (range 10.5-26.8) vs 12.3 micromol/L [range 10.5-26.8], not significant). Hyperhomocysteinemia was found in 18.8% of the patients with venous thrombosis, 11.1% of the patients with arterial thrombosis, and 10.5% of the patients without thrombosis (not significant). CONCLUSIONS: Hyperhomocysteinemia is a common phenomenon in IBD and correlates with serum folate, cobalamin, creatinine, and pyridoxine concentrations. No correlation between tHcy and a history of venous or arterial thromboembolic complications is found. Hyperhomocysteinemia does not seem to be a major contributory factor in the development of venous or arterial thrombosis in IBD patients.     

Homocysteine, a risk factor for coronary artery disease or not? A meta-analysis

This meta-analysis suggests that homocysteine may not be as harmful for the heart as it seems. At the same time, however, homocysteine may be an indicator for unhealthy lifestyles, and therefore, an important variable for cardiologists to take into account when assessing coronary artery disease.     

Homocysteine. The cardiovascular risk factor of the next millennium?

Several epidemiologic studies have demonstrated that hyperhomocysteinemia is a risk factor for arteriosclerosis in coronary, cerebral, peripheral and aortic arteries. This risk is independent of other cardiovascular risk factors, and it is dose related. However, prospective studies show contradictory findings. Hyperhomocysteinemia is also associated with a higher risk of venous thrombosis to which other coagulation disorders, such as factor V Leiden, could contribute. Hyperhomocysteinemia can be due to genetic defects in the enzymes that control homocysteine metabolism, and also to other factors, mainly nutritional (deficiencies in vitamin B6, vitamin B12, or folic acid). Dietary supplements of these vitamins reduce plasma homocysteine levels. Randomized clinical trials are still needed to demonstrate that reducing plasma homocysteine levels will reduce the risk for cardiovascular disease.     

Advanced glycoxidation. A new risk factor for cardiovascular disease?

Cardiovascular disease (CVD) is the leading cause of mortality worldwide. A large body of evidence both in vitro and in vivo suggests an important role for advanced glycoxidation end products (AGE) in the development or progression of CVD. AGE are a heterogenous group of molecules formed within the body during aging and, at an accelerated rate, in diabetes. AGE result from the nonenzymatic reaction of reducing sugars with proteins, lipids, and nucleic acids. Diet is considered an important exogenous source of highly reactive AGE. Recent studies have suggested a relationship between AGE and features of CVD. These findings together with the cardioprotective effects of anti-AGE agents demonstrate the causal relationship of AGE to the development and progression of CVD. Prospective outcome and controlled studies are needed to further support this relationship.     

Is obesity a new risk factor for gastritis?

Obesity has become a major concern among gastroenterologists due to its large influence on gastrointestinal and hepatic diseases: reflux esophagitis, pancreatitis, gallstone disease, liver fibrosis, and neoplastic tumors of the esophagus, pancreas, and colon. Studies of morbid obese subjects undergoing bariatric surgery have revealed that obesity is related with an increased prevalence of endoscopic and histologic gastritis. A recent study of health check-up subjects demonstrated an association of obesity with endoscopic gastritis and gastric ulcers. We recently investigated the underlying mechanisms of the effects of obesity on endoscopic gastritis in subjects undergoing health check-up examination, and demonstrated that adiponectin, a bioactive molecule released from visceral fat, could be a protective factor of endoscopic gastritis. We would like to propose a new category of gastritis, obesity-related gastritis, which could become dominant in the near future.     

Impaired glucose tolerance - a new risk factor?

This editorial refers to "Newly detected abnormal glucose tolerance:an important predictor of long term outcome after myocandialinfarction" by M. Bartnik on page 1990. Recently, a plethora of scientific papers have revealed theparallel impairment of carbohydrate metabolism in patients referredto hospitals along with acute ischaemic events.¹ The most recent,the Euro Heart Survey, reports the     

Ascending aorta or arch surgery: is previous cardiac surgery a risk factor?

Surgery on the ascending aorta +/- arch is a challenge. The risks involved in such operations after previous cardiac surgery were assessed in elective and emergency settings in a single institution. Over a 10-year period, 29 patients underwent replacement of the ascending aorta +/- arch following previous cardiac surgery. In 12 patients (41.4%), the procedure was carried out on an emergency basis. Thirteen had previous replacement of the ascending aorta and 16 had previous valve replacement with or without coronary artery bypass; 4 patients were undergoing a 3rd cardiac operation. Concomitant procedures included coronary artery bypass in 2, arch replacement in 4, and descending aortic replacement in one. The overall in-hospital mortality was 13.8% (4/29) vs. 12.4% (33/267) in primary procedures. Mortality in elective repeat surgery was 5.9% (1/17) vs. 25% (3/12) in emergency re-operations. The incidences of permanent stroke (3.4%) and renal failure (3.4%) were similar to first-time operations. Elective re-operation for ascending aorta +/- arch repair can be accomplished with acceptable mortality and morbidity. Outcomes in emergency cases carry a higher early mortality but still conform to contemporary expectations and are similar to emergency first-time aortic surgery.     

Homocysteine as a risk factor for cardiovascular disease: should we (still) worry about?

Cardiovascular disease (CVD) is the leading cause of death worldwide. CVD is causally related to "classical" risk factors such as elevated blood pressure, cholesterol, or glucose level and smoking. A causal role in the development of CVD is also suggested for numerous other factors, including an elevated plasma homocysteine concentration. Variation of homocysteinaemia is mainly due to genetic mutations and/or vitamin deficiency. The homocysteine concentration can be lowered with folate. Vitamin supplementation has thus been proposed in individuals with hyperhomocysteinaemia in order to reduce their CVD risk. On the other hand, population-based studies show little or no association between moderate hyperhomocysteinaemia and CVD risk. Nor has any randomised clinical trial clearly proven the efficacy of lowering the homocysteine concentration as a means of lowering the incidence of CVD. Hence at present it is inappropriate to recommend screening and treatment of hyperhomocysteinaemia in asymptomatic persons with or without other CVD risk. Until new evidence is available, clinicians should focus on better control of the "classical" risk factors for CVD.     

Non-alcoholic fatty liver disease: a new and important cardiovascular risk factor?

Non-alcoholic fatty liver disease (NAFLD) affects up to a third of the population worldwide and may confer increased cardiometabolic risk with consequent adverse cardiovascular outcomes independent of traditional cardiovascular risk factors and the metabolic syndrome. It is characterized almost universally by insulin resistance and is strongly associated with type 2 diabetes and obesity. Non-alcoholic fatty liver disease is a marker of pathological ectopic fat accumulation combined with a low-grade chronic inflammatory state. This results in several deleterious pathophysiological processes including abnormal glucose, fatty acid and lipoprotein metabolism, increased oxidative stress, deranged adipokine profile, hypercoaguability, endothelial dysfunction, and accelerated progression of atherosclerosis. This ultimately leads to a dysfunctional cardiometabolic phenotype with cardiovascular mortality representing the main mode of premature death in NAFLD. This review is aimed at introducing NAFLD to the clinical cardiologist by discussing in-depth the evidence to date linking NAFLD with cardiovascular disease, reviewing the likely mechanisms underlying this association, as well as summarizing from a cardiologist's perspective, current and potential future treatment options for this increasingly prevalent disease.     

A family history of Barrett's oesophagus: another risk factor?

Barrett's oesophagus and oesophageal adenocarcinoma, although increasingly common, have no known genetic cause. In this report we describe a family with a remarkable history of Barrett's oesophagus and adenocarcinoma. The index case is a 76-year-old man with adenocarcinoma arising within Barrett's oesophagus. Two of his three brothers, aged 68 and 78 years, also developed adenocarcinoma arising in Barrett's oesophagus and the remaining 67-year-old brother has severe dysplasia in biopsies from Barrett's oesophagus. The sons and daughters of the index case requested screening and all had histologically confirmed short-segment Barrett's oesophagus. This kindred appears to be genetically susceptible to Barrett's oesophagus and oesophageal adenocarcinoma. Pooling of data from this and other Barrett's families may allow successful linkage analysis.