ABSTRACT
The incidence of supraventricular tachycardia (SVT) is approximately 35 cases per 100,000 patients with a prevalence of 2.25 cases per 1,000. This dysrhythmia originates at or above the atrioventricular node and is defined by a narrow complex QRS (<120 msec) at a rate of >100 beats/min. The effects of vitamin B12 deficiency on sympathetic and parasympathetic systems may cause heart rate variability and autonomic dysfunction. In patients with SVT, the underlying mechanism may be further exacerbated by vitamin B12 deficiency or induced by the deficiency. We describe a case series of three patients with no known comorbidity who presented to our department with SVT. Their SVTs were terminated using the modified Valsalva maneuver. All three patients were incidentally found to be severely deficient in vitamin B12 and had hyperhomocysteinemia. They were discharged on medications and dietary advice to increase vitamin B12 levels. Correcting vitamin B12 deficiency and hyperhomocysteinemia could play a preventive role in patients at risk for SVT. Our case series demonstrates a plausible association between vitamin B12 deficiency and SVT occurrence in previously healthy individuals with no known comorbid conditions.
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Keywords: Supraventricular tachycardia; Vitamin B12; Homocysteine; Case reports
INTRODUCTION
Supraventricular tachycardia (SVT) is a dysrhythmia originating at or above the atrioventricular node and is defined by a narrow complex QRS (<120 msec) at a rate of >100 beats/min. Anxiety, palpitations, chest discomfort, lightheadedness, syncope, or dyspnea are the most common symptoms that patients may present with. Shock, signs of heart failure, lightheadedness, or exercise intolerance may be present in some cases [
1]. The most common causes of SVT are coronary artery disease, heart valve disease, heart failure, anemia, thyroid disease, diabetes, illicit drug use, caffeine intake, emotional stress, excessive alcohol consumption, and smoking [
2].
According to the Food Safety and Standards Authority of India, preventable micronutrient deficiency is widespread in the Indian population [
3]. A water-soluble vitamin, vitamin B
12 (cobalamin), is naturally present only in animal foods and available as a dietary supplement and a prescription medication (cyanocobalamin). Vitamin B
12 is a vital precursor for the development, myelination, and function of the central nervous system; formation of healthy red blood cells; and the synthesis of DNA [
4]. Cobalamin plays a vital role in DNA synthesis and in the metabolic conversion of homocysteine to methionine. Deficient vitamin B
12 levels result in homocysteine accumulation in the bloodstream, a condition known as hyperhomocysteinemia (hHcy) that is associated with increased oxidative stress, endothelial dysfunction, and prothrombotic state, all of which can affect cardiovascular function [
5]. Studies have demonstrated a positive correlation of homocysteine levels with atherosclerosis and coronary artery disease [
6,
7]. Autonomic dysfunction also plays a major role in the development of SVT [
8], and vitamin B
12 deficiency causes autonomic dysfunction and failure [
9]. In patients with SVT, the underlying mechanism may be further exacerbated by vitamin B
12 deficiency and high homocysteine levels, resulting in increased susceptibility to dysrhythmia and thrombotic events. Previous studies have also reported a strong association between vitamin B
12 deficiency and atrial fibrillation [
10,
11]. Herein, we describe a series of three patients who presented to our emergency department (ED) with SVT and had no known comorbid conditions. They were found to be severely deficient in vitamin B
12 and had hHcy. Their SVT was managed in the ED, after which they were discharged with dietary recommendations and calcium channel blockers.
CASE REPORT
Ethics statement
All study procedures were conducted in accordance with the principles of the Declaration of Helsinki. The next of kin of all three patients gave us consent to publish their cases.
Case presentation 1
A 40-year-old male patient with no medical history came to the ED with uneasiness on the right side of the chest and sweating for 30 minutes before arrival to the ED. On arrival to the ED, his heart rate was 213/min, blood pressure (BP) was 130/90 mmHg, respiratory rate (RR) was 24/min, oxygen saturation was 97% on room air, body temperature was 97.1 °F, and random blood sugar level was 90 mg/dL. On primary and secondary examinations, tachycardia on auscultation was the only significant finding.
An electrocardiogram (ECG) was performed, which suggested SVT. The modified Valsalva maneuver was performed, and the SVT reverted to normal sinus rhythm. The patient had no previous comorbid conditions and was a pure vegetarian since birth. His incidental biochemical findings revealed a vitamin B12 level of 70 pg/mL and a homocysteine level of 69 µmol/L, whereas serum folate level was 10.96 ng/mL.
After obtaining a cardiology consultation, the patient was discharged on oral diltiazem 20 mg once a day, supplementation, and dietary advice from the ED itself. Vital findings at the time of discharge were heart rate 95/min, BP 110/70 mmHg, RR 16/min, and oxygen saturation 98% on room air. He returned to our hospital after 6 months with the same complaints and was diagnosed with an SVT with a heart rate of 205/min. The SVT was reverted using the modified Valsalva maneuver. On further history-taking, he denied following the dietary and supplementation advice but had been diligently taking diltiazem. Repeat tests for vitamin B12 and homocysteine showed levels of 100 pg/mL and 33.8 µmol/L, respectively, and the serum folate level was 13.61 ng/mL. The patient intended to be followed up in the cardiology outpatient department and was hence discharged with dietary and supplementation advice again and to continue oral diltiazem.
Case presentation 2
A 64-year-old female patient with no medical history came to the ED with dry cough and shortness of breath since 1 day before. She was a vegetarian who did not even consume eggs. On arrival to the ED, she had a heart rate of 160/min, BP of 140/80 mmHg, RR of 24/min, oxygen saturation of 94% on room air, random blood sugar level of 160 mg/dL, and body temperature of 98.6 °F. On examination, no obvious abnormality was found.
Her ECG was diagnostic of SVT. The modified Valsalva maneuver was performed, and the SVT reverted to normal sinus rhythm with a heart rate of 105/min. The patient’s incidental vitamin B12 and homocysteine levels were 114 pg/mL and 19.5 µmol/L, respectively. Two-dimensional echocardiography showed negative findings for any structural abnormality. Other blood investigations revealed a N-terminal pro–B-type natriuretic peptide level of 177 pg/mL, D-dimer level of 232 ng/mL, Troponin I level of 0.01 ng/mL, creatine kinase MB (CKMB) level of 3.4 ng/mL, and a hemoglobin level of 12.9 g/dL. Deranged vitamin B12 and homocysteine levels were the only positive findings for the patient.
After obtaining a cardiology consultation, she was admitted to the Cardiac Care Unit due to her elderly status. She was managed conservatively and discharged after 2 days in a stable condition on ivabradine 5 mg prescribed by the cardiology team.
Case presentation 3
A 46-year-old male patient with no medical history came to the ED with palpitations and chest uneasiness since 15 to 20 minutes before arrival to the ED. He was a vegetarian who consumed eggs on an occasional basis. On arrival to the ED, he had a heart rate of 216/min, BP of 130/90 mmHg, RR of 28/min, oxygen saturation of 100% on room air, body temperature 98 °F, and random blood sugar level of 135 mg/dL. On examination, no obvious abnormality was detected.
ECG was used to diagnose SVT. After performing the modified Valsalva maneuver, the SVT reverted to normal sinus rhythm. Laboratory data revealed the following: vitamin B
12 level 89 pg/mL, folate level 3.91 ng/mL, homocysteine level 120.9 µmol/L, hemoglobin level 15.6 g/dL, Troponin I level 0 ng/mL, and CKMB level 0.9 ng/mL. The patient was advised for admission for further investigation by the cardiology team, but he decided to leave against medical advice. However, he was counseled regarding the deficiency and the increased risk of cardiovascular events due to his severely high homocysteine levels. He was provided dietary (to increase egg consumption if he cannot consume red meat) and supplementation advice and discharged in a stable condition. None of the three patients were followed up in the cardiology outpatient department.
Table 1 shows the vitamin B
12 and homocysteine levels of all three patients.
DISCUSSION
Our case series emphasizes a possible association of SVT with vitamin B
12 deficiency and homocysteine. Strict vegetarians who experience vitamin B
12 deficiency must take supplements enriched with vitamin B
12 [
5]. Vitamin B
12 deficiency and hHcy have been implicated in various cardiovascular complications due to their impact on vascular and endothelial health. In fact, hHcy has been investigated as a risk factor for arterial and venous thrombosis, as well as dysrhythmias, due to its negative effect on endothelial cells and its role in promoting inflammation and coagulation. In particular, endothelial dysfunction is critical in the pathophysiology of dysrhythmias, such as SVT, where disrupted cardiac electrical signaling may develop due to vascular inflammation and oxidative stress, which are associated with increased homocysteine levels [
12]. Acute treatment of SVT is based on the patient’s hemodynamic stability. The vagal maneuver and pharmaceutical therapy are recommended for hemodynamically stable patients. Standard guidelines for the management of SVT mention that adenosine should be the first medication therapy if vagal maneuvers fail to terminate SVT [
13]. Vagal maneuvers have demonstrated a wide range of success rates in terminating SVT, ranging from 19% to 54%.
In hemodynamically unstable patients, cardioversion is the first choice of treatment. Moreover, calcium channel blockers and beta blockers may be used in patients with frequent atrial and ventricular premature beats. Verapamil (0.075–0.15 mg/kg iv) or diltiazem (0.25 mg/kg) has also been shown to terminate SVT in 64% to 98% of patients [
14].
SVT is caused by certain known medical conditions such as heart failure or other heart diseases, lung disease, thyroid disease, Wolff-Parkinson-White syndrome, congenital conditions, and previous heart surgeries. Other documented triggers for SVT include stress, excess caffeine or alcohol intake, anxiety, smoking, tobacco chewing, and stimulant drugs such as cocaine [
15].
Vitamin B
12 deficiency is found in >20% of older adults aged >60 years. Vitamin B
12 is the most important precursor for the myelination process during the development of the nervous system. Therefore, myelination deficiency due to low levels of vitamin B
12 in the nerve terminals innervating the heart and arteries may cause abnormalities in heart rate regulation and vascular dynamics, resulting in cardiac autonomic neuropathy [
16]. Vitamin B
12 plays a vital role in cardiovascular disease. Vitamin B
12 affects the levels of homocysteine metabolism along with folate and vitamin B
6 in converting homocysteine into methionine. Increased levels of homocysteine have also been identified as an independent risk factor for cardiovascular disease, as high homocysteine levels can cause endothelial dysfunction, arterial damage, and increased clotting risk [
17]. Vitamin B
12 also plays a vital role in maintaining homocysteine homeostasis, which exerts a direct impact on reducing cardiovascular events [
18]. As mentioned earlier, vitamin B
12 deficiency results in autonomic dysfunction and failure, which may cause dysrhythmias [
8,
9]. In fact, Yilmaz et al. [
19] reported low levels of vitamin B
12 as a significant indicator of arrhythmogenic susceptibility in healthy individuals. Furthermore, hHcy was found to exhibit a linear correlation with cardiac autonomic system dysfunction in patients with obstructive sleep apnea syndrome [
20]. In a retrospective study, Liakos et al. [
18] found that the incidence of sustained, paroxysmal, and all-type atrial fibrillation had a direct association with homocysteine levels and an inverse association with vitamin B
12 levels.
India is a country where vegetarian and plant-based diets are prevalent. Vitamin B
12 deficiency is commonly caused by dietary deficiency, lack of intrinsic factors (e.g., pernicious anemia), gastrointestinal tract surgeries, and prolonged use of medications such as metformin and proton pump inhibitors [
21,
22]. Moreover, due to a largely vegetarian population, vitamin B
12 deficiency is endemic in India. In fact, Mahalle et al. [
23] found that 86.7% of their study patients were deficient in vitamin B
12 and had suffered from coronary artery disease. Singla et al. [
24] also reported a 47% prevalence of vitamin B
12 deficiency in a North Indian population. Even children are not spared from this deficiency in India. Shalini et al. [
25] found vitamin B
12 deficiency rates of 31% in adolescents, 17.3% in school children, and 13.8% in preschool children.
Vitamin B
12 deficiency also causes megaloblastic anemia, glossitis, fatigue, peripheral neuropathy, neural tube defect, and infertility and has also been associated with depression, cardiovascular disease, atrial fibrillation, and Alzheimer dementia [
23,
24,
26-
28].
All patients in our series were vegetarian, which may have been the trigger for the cascade of cardiac autonomic nervous system dysfunction suffered by them. Patient 1 who was taking standard drug therapy but did not follow the dietary and supplementation advice returned to our ED with SVT and was again found to have vitamin B12 deficiency and high homocysteine levels. Remarkably, none of the patients were examined for serum methylmalonic acid (a sensitive marker for vitamin B12 deficiency) as the test is not readily available, and only a subset was evaluated for folate levels.
Although some causes of SVT (structural abnormality, electrolyte imbalance, and thyroid dysfunction) were not excluded in our cases, our series of patients who were previously apparently healthy and had no known comorbid conditions did demonstrate a plausible association between vitamin B12 deficiency and SVT occurrence. To the best of our knowledge, there have been no reports on the association of SVTs with vitamin B12 deficiency or hHcy.
In conclusion, it would be advisable for emergency physicians to be aware of nutritional deficiencies in such patients, especially with no known comorbid conditions. Vitamin B12 and homocysteine examinations may be considered a baseline assessment in unexplained SVT cases, although further large-scale prospective studies are essential before establishing clinical guidelines. Correct dietary advice comprising the intake of eggs and red meat as well as supplementation may be provided to patients found to be deficient in vitamin B12. Multicentric trials may be conducted to confirm a stronger relationship between SVT, vitamin B12 deficiency, and high homocysteine levels.
NOTES
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Authors’ contributions
Conceptualization: AV. Formal analysis: AV. Investigation: all authors. Methodology: AV. Writing - original draft: AV. Writing - review & editing: SR, MS, VC, SJ. All authors read and approved the final manuscript.
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Conflicts of interest
None.
-
Funding
None.
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Acknowledgments
The views expressed in the submitted article are the authors’ own and are not an official position of the institution.
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Data availability
Not applicable.
Table 1.Vitamin B12 and homocysteine levels of the patients
Table 1.
|
Variable |
Vitamin B12 (pg/mL) |
Homocysteine (µmol/L) |
|
Reference range |
120–914 |
6.0–15.0 |
|
Patient 1 |
70 |
69.0 |
|
Patient 2 |
114 |
19.5 |
|
Patient 3 |
89 |
120.9 |
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