The Internet Journal of Thoracic and Cardiovascular Surgery™ ISSN: 1524-0274

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Prevalence of Hyperhomocyseinemia in Patients requiring Coronary Artery Bypass

O. Stanger
Div. Of Cardiac Surgery
1st University Clinic of Surgery Physical Address

Th. Lang
Div. Of Laboratory Medicine I
1st University Clinic of Surgery Physical Address

L. Salaymeh
Div. Of Cardiac Surgery
1st University Clinic of Surgery Physical Address

H. Rabl
Div. Of General Surgery
1st University Clinic of Surgery Physical Address

B. Rigler
Div. Of Cardiac Surgery
1st University Clinic of Surgery Physical Address

Citation: O. Stanger, T. Lang, L. Salaymeh, H. Rabl & B. Rigler : Prevalence of Hyperhomocyseinemia in Patients requiring Coronary Artery Bypass . The Internet Journal of Thoracic and Cardiovascular Surgery. 1997 Volume 2 Number 1

Keywords: surgery | medicine | cardiac | heart | vascular | chest | heart-lung machine | cardio-pulmonary | bypass surgery | aneurysm | aorta | vessel | cardiothoracic | thoracic | cardiopulmonary bypass | valve | carotid

 


Purpose

Hyperhomocysteinemia has been suggested as an independent risk factor for premature atherosclerosis 1,2 and is associated with an elevated risk for thromboembolic events 3 and a higher mortality ratio in patients with Coronary Artery

Disease (CAD) 4.

Biochemistry

Homocysteine is a sulfur-containing amino acid formed during the metabolism of methionine (itself being an essential protein and consumed with food,-mainly meat and cheese products). Two major pathways regulate the metabolism of homocysteine:

    Remethylation of homocysteine to methionine is catalysed by methionine-synthase and requires folic acid and vitamin B12 as essential co-factors. Transsulfuration of homocysteine to cystathione (and cysteine) is catalysed by the vitamin B6-dependent enzyme cystathionine-ß-synthase. Deficits of the vitamins mentioned are associated with elevated homocysteine levels in plasma and may increase the risk of atherosclerosis and thromboembolic events. 5

Methods

85 male patients (mean age 49.2 ± 5.1years) with angiographically confirmed Coronary Artery Disease (CAD) were included in this study. Inclusion and exclusion criterias have been described earlier elsewhere3. All patients were expecting Coronary Artey Bypass Grafting (CABG) within one week at the time of investigation. Total plasma homocysteine (tHcy) concentrations were assessed in a fasting state and 6 hours after administration of an oral methionine-loading-test (0.1 g methionine / kg / body weight), using HPLC with fluoresence detection. Increase of fasting and post-load tHcy-levels were related to vitamin B12- and folate concentrations.

Results

In this study population, a total of 32 patients (37%) had pathological homocysteine values. Fasting hyperhomocysteinemia (tHcy > 15m mol/l) was detected in 19 patients, with a mean value of 19.98 (15.36-22.99). The oral methionine-loading-test identified additional 13 patients (+40%) with a mean value of 53.13 (40.01-79.75). These patients had normal fasting levels and required the methionine-loading-test for positive identification. The increase of tHcy (fasting / post-load) showed an inverse correlation with plasma folate concentrations, but not with plasma vitamin B12 levels.

Conclusions

Prevalence of hyperhomocysteinemia is high,- 37% in this study group (compared to 5-7%, that can be expected in the general population 6,7). The methionine-loading-test identified 40% of the patients with pathological tHcy values, and is therefore a useful tool in searching for hyperhomocysteinemia. High post-load increase of homocysteine is associated with low folate concentrations, not with vitamin B12 levels. Available prospective studies (max. follow-up 5 years) document the inverse relation-ship between tHcy- levels and clinical outcome in CAD-patients 4,6. However, whether the easy and effective tHcy- lowering therapy through vitamin supplementation can slow the progression of CAD requires further investigation and long-term prospective studies.

References

1. Clarke R, Daly L, Robinson K, Naughten E, Cahalane S, Fowler B, Graham I Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med 1991; 324: 1149-55.(back to text) (s)

2. McCully KS Homocysteine and vascular disease. Nat Med 1996; 2: 386-9 (back to text) (s)

3. Welch GN, Loscalzo J. Mechanisms of Disease: Homocysteine and Athero- thrombosis. N Engl J Med 1998; 338: 1042-50. (back to text) Welch GN, Loscalzo J Mechanisms of Disease: Homocysteine and Athero- thrombosis. N Engl J Med 1998; 338: 1042-50. (back to text) (s)

4. Nygard O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med 1997; 337: 230-6. (back to text) (s)

5. Dalery K, Lussier-Cacan S, Selhub J, Davignon J, Latour Y, Genest J Homocysteine and Coronary Artery Disease in French Canadian Subjects: Relation With Vitamins B12, B6, Pyridoxal Phosphate, and Folate. Am J Cardiol 1995; 75: 1107-1111. (back to text) (s)

6. Ueland PM et al, Plasma homocysteine, a risk factor for vascular disease: plasma levels in health, disease and drug therapy J lab Clin Med 1989; 114: 473- 501) (back to text) (s)

7. Arnesen E, Refsum H, Bonaa KH, Ueland PM, Forde OH, Nordrehaug JE Serum total homocysteine and coronary heart disease. Int J Epidemiol 1995; 24: 704-9. (back to text) (s)

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