Electrocardiographic Changes Due to Pyridoxine Deficiency EDUARDO MALMIERCA, JORGE POLO, and JORGE R. CASTRO* From the Fundacion ´ Jim´enez D´ıaz, Madrid and the *Hospital General de Guadalajara, Spain
MALMIERCA, E., ET AL.: Electrocardiographic Changes Due to Pyridoxine Deficiency. A young woman presented with marked alterations in the ECG without cardiological symptoms or evidence of structural heart disease after further evaluation. There was evidence of vitamin deficiency and the ECG normalized after 10 days of treatment with vitamins. Similar alterations have been described in several experimental studies with rats, but this is the first case reported in humans. (PACE 2003; 26:1289–1291) pyridoxine, vitamin B6 , electrocardiogram
Introduction Pyridoxine deficiency can cause several alterations in many organs. With regard to the heart, it has been well described that hypertrophic cardiomyopathy due to vitamin B6 deficiency and ischemic alterations caused by the excess of serum homocysteine levels are also associated with this deficiency. The patient had important electrocardiographic (ECG) alterations without any of the heart lesions described in this type of hypovitaminosis. Case report A 35-year-old woman was admitted to the hospital because of tetraparesis. Her past medical history was unremarkable. She was homeless since age 17 years and she usually ate only white bread. A progressive paresis of the four limbs had settled over the last 6 months and when she was brought to the hospital, she could not walk and could hardly bring food to her mouth. The paresis was symmetrical and started in the distal areas, progressing proximally. No respiratory involvement was noted and no other symptoms were recorded in the anamnesis. The general examination was normal except for a rhythmic tachycardia. In the neurological examination a flaccid tetraparesis was confirmed along with a marked sensitive impairment. An ECG was performed (Fig. 1), showing a T wave inversion and an ST-segment depression in most leads. No cardiological symptoms were recorded after being specifically asked. Serum levels of potassium, sodium, calcium, and magnesium were all normal. Sequential determinations of cardiac enzymes were made over 24 hours
Address for reprints: Eduardo Malmierca, M.D., Fundacion ´ Jim´enez D´ıaz, Avd. Reyes Catolicos 2, 28040 Madrid, Spain. ´ Fax: 915504922; e-mail:
[email protected] Received July 16, 2002; revised August 23, 2002; accepted October 4, 2002.
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and an echocardiogram was performed, being both normal. The final diagnosis of her neurological problem was polineuropathy due to vitamin deficiency. Normal vitamin B12 and folate levels were found in peripheral blood. Therapy with oral vitamin B complex (B1 , B6 , B12, and folate) was started. No additional treatments were given. Similar abnormalities in the ECG were registered in three occasions after the first one. Ten days after starting therapy the ECG normalized (Fig. 2). During hospital admission her neurological symptoms did not significantly improve and the patient was lost for follow-up after discharge.
Discussion Vitamin B6 deficiency has been related to several heart alterations. It is well known the association with hypertrophic cardiomyopathy. It has also been postulated how this deficiency can be responsible for a higher risk of ischemic events because it rises the levels of homocysteine in serum. None of these two conditions were the case in the patient. The echocardiogram disclosed no evidence of hypertrophy nor alterations in contractility which, in addition to the finding of normal cardiac enzymes on sequential measurements in a young woman without known cardiovascular risk factors, reasonably rules out ischemia as the cause of the ECG abnormalities. Thus, no other diagnostic techniques, like stress test, were performed. Between the first ECG and the one performed 10 days later, the only intervention was the administration of vitamins B1 , B6 , B12, and folate. Vitamin B12 and folate were measured before therapy was started, and they were both normal. Therefore, the authors think that none of these two vitamins were responsible for the changes seen in the ECG. The lack of neurological improvement during hospital admission is not surprising, as these patients usually need a longer time for recovery.
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Figure 1. Electrocardiogram recording before the multivitamin therapy.
Vitamin B1 and pyridoxine were not measured as there were no available tests. There are no references in the medical literature relating vitamin B1 and ECG alterations. Few experimental works with rats correlate pyridoxine deficiency and ECG changes.1−7 In 1979 Mulvaney and Seronde1 published a study using 18 rats that received a diet totally deficient in pyridoxine. After
a mean time of 77 days their ECG changed. The most common changes were a shorter PR interval, transient atrioventricular block, irregular sinus rhythm, wandering pacemaker, and diffuse T wave inversion. Those ECG changes returned to normal after 2 weeks of treatment with vitamin B6 . Although vitamin B6 deficiency has been associated with bradycardia,2 some other studies1
Figure 2. Electrocardiogram recording 10 days after starting the multivitamin therapy.
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ECG CHANGES DUE TO PYRIDOXINE DEFICIENCY
have shown no differences in heart rate. In the case under discussion the patient presented with tachycardia. There are enough similarities between the changes seen in the ECG in experimental works and the changes in the ECG of the present patient. Furthermore, those changes reverted after treat-
ment with vitamins in a similar way to what is described in rats. As serum vitamin B12 and folate levels were normal in the patient and thiamine (vitamin B1 ) deficiency has never been reported to cause ECG alterations, the authors think pyridoxine deficiency was responsible for the ECG changes found in their patient.
References 1. Mulvaney DA, Seronde J. Electrocardiographic changes in vitamin B6 deficient rats. Cardiovasc Res 1979; 3:506–513. 2. Valora N, Fidanza A. Alterazioni elettrocardiografiche nel ratto in carenza di piridossina. Boll Soc Ital Biol Sper 1963; 39:1521– 1524. 3. Valora N, Floridi S, Mei V. Electrocardiographic changes in the rat induced by high doses of the coenzymatic forms of several vitamins of the B group. Boll Ital Biol Sper 1983; 59:834–838. 4. Ceriani T, Ventura U, Molina V, et al. Effect of pyridoxine defi-
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ciency on rat intracellular cardiac action potentials. Plugers Arch ¨ 1972; 336:237–248. 5. Seronde J. Crdiac lesions and related findings in young vitamin B6 deficient rats. J Nutrition 1960; 72:53–65. 6. Agnew LRC. Cardiac, renal and hepatic hypertrophy in pyridoxine deficient rats. Proc Soc Exp Biol Med 1955; 90:452–453. 7. Maggizatelli R, Pietrobono P. The importance of vitamin B6 in the prevention of electrocardiographic changes induced by hypoxia. Acta Anaesthesiol 1967; 18(Suppl. 2):1–10.
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