European Journal of Cardiovascular Medicine

Magnesium is the second most ample intracellular cation after potassium and the fourth most common plentiful cation in the body[1-3]It serves as a cofactor for 325 enzyme systems, including specific vasoactive mediators [4].Magnesium is involved in many physiological processes in our body such as : cardiac excitability, neuromuscular transmission, serving as a cofactor for DNA and protein synthesis, oxidative phosphorylation, vasomotor tone, blood pressure regulation, and bone formation and intracellular signaling [1-3]. In an adult human, Total body magnesium is approximately 24 grams with 99% existing intracellularly in bone (53%), muscle (27%), and soft tissue (19%). [1,2] And only 1% of total body magnesium exists in the extracellular space [1,2] . Normal total serum concentration is in the range of 1.7-2.6mg/dl (0.7-1.1mmol/L).[1]. This range of serum magnesium represents only 0.3% of total body magnesium and may not accurately give back the total magnesium status[2,5]. Serum magnesium level is due to active balance between intestinal transport, bone transport, and renal exchange [1]. Hypertension is a condition marked by elevation in the systolic blood pressure (SBP) and/or diastolic blood pressure (DBP).[5,6] . Mills K T et al. postulated that Hypertension is a condition with SBP ≥ 140 mmHg and/or DBP ≥ 90 mmHg.[8,9]. In 2017, the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines redefined hypertension in adults as systolic BP ≥130 mmHg and/or diastolic BP ≥80 mmHg.[10,11]

Many clinical trials have shown low magnesium levels has significant undesirable effect on blood pressure.[12-17].Although magnesium has been shown to modulate blood pressure regulation to some extent, the exact mechanism of altered magnesium metabolism in hypertensive individuals remains unclear.[12].

The conventional hypothetical mechanism of effect of magnesium on blood pressure is that magnesium acts as a natural calcium antagonist on most types of calcium channels in vascular smooth muscles, reducing arterial blood pressure via lowering of peripheral and cerebral vascular resistance. [12] There are so many studies carried out to see the relationship between serum magnesium level and blood pressure. Collectively, these studies have revealed contradictory results for the relationship between serum magnesium levels and blood pressure, with some studies showing negative association,[13-17,18,20,23,24]

and others showing no association[19,21,22,25,26]or a positive association.[19]

This study is aimed to observe the magnesium level among hospitalized adult male and female who are hypertensive in medicine general wards, in the tertiary care hospital in Dahod district Gujrat state, India.

Source of Data Data were obtained from hypertensive patients admitted to the male and female general medicine wards of Zydus Medical College and Hospital, Dahod, Gujarat, India. Hospital admission registers and electronic medical records were reviewed to identify eligible participants during the study period.

Study Design This was an observational cross‑sectional study designed to assess serum magnesium levels among hospitalized hypertensive patients.

Study Location The investigation was carried out in the Department of Biochemistry in collaboration with the Male and Female Medicine Wards at Zydus Medical College and Hospital, Dahod, Gujarat, India.

Study Duration The study covered the period from 1 January 2022 through 30 November 2023.

Sample Size A total of 85 hypertensive patients were enrolled—51 male and 34 female participants per ward—selected to meet the calculated sample size requirements for adequate power.

Inclusion Criteria

• Patients aged 35–65 years.
• Established diagnosis of hypertension according to hospital records.
• Admission under general male or female medicine wards during the study period.
• Provision of written informed consent.

Exclusion Criteria

• Age below 35 years or above 65 years.
• History of epilepsy or cerebrovascular disease.
• Use of magnesium‑containing supplements or medications within the previous month.
• Chronic kidney disease (stage III or higher) or other conditions known to alter magnesium metabolism.

Procedure and Methodology After obtaining informed consent, approximately 2 mL of venous blood was drawn under strict aseptic precautions using plain vacutainer tubes. Samples were allowed to clot at room temperature for 30 minutes and then centrifuged at 3,000 rpm for 10 minutes to separate serum.

Sample Processing Serum aliquots were transferred into labeled cryovials and stored at 4 °C if not immediately processed. All assays were performed within 6 hours of sample collection to minimize pre‑analytical variation.

Estimation of Serum Magnesium Serum magnesium concentrations were measured using the Xylidyl Blue colorimetric method with commercially available assay kits (Transasia Biomedical Ltd, India). Analyses were conducted on the Erba XL 640 fully automated biochemistry analyzer under standard laboratory operating procedures. Calibration and daily quality control were maintained using Biorad control materials at two levels to ensure assay precision and accuracy.

Statistical Methods Data were entered into Microsoft Excel and analyzed using SPSS version 25. Continuous variables (serum magnesium levels) were expressed as means ± standard deviations. Categorical data (incidence of hypomagnesemia) were presented as percentages. The prevalence of low magnesium (< 1.70 mg/dL) was calculated separately for males and females. Comparisons between groups were performed using the chi‑square test for proportions. A p‑value < 0.05 was considered statistically significant.

Data Collection Demographic and clinical data (age, sex, duration of hypertension, concurrent medications) were extracted from patient case sheets and the hospital information system. Laboratory results were directly downloaded from the analyzer’s database. All data were anonymized and recorded on pre‑designed data collection forms.

Table 1: Distribution of Female patients according to Serum Magnesium level

Table 1 shows that among 34 hypertensive female inpatients, 8.82 % had serum magnesium levels at or below 1.70 mg/dL, whereas the majority (91.17 %) fell within the normal range of 1.70–3.60 mg/dL.

Table 2: Distribution of Male patients according to Serum Magnesium level

Table 2 indicates that of the 51 hypertensive male patients, only 3.92 % were hypomagnesemic (≤ 1.70 mg/dL), while 96.07 % maintained normal magnesium levels.

Table 3: Comparison of table 1 and table 2

No significant difference found in Mg levels of hypertensive male and hypertensive female (p>0.05)

Table 3, the mean serum magnesium concentration for males was 2.10 ± 0.289 mg/dL compared with 2.04 ± 0.315 mg/dL for females; this small difference was not statistically significant (p = 0.364), suggesting similar magnesium status in hypertensive patients regardless of gender.

The present cross‑sectional study aimed to elucidate the relationship between serum magnesium levels and essential hypertension in hospitalized patients. Serum total magnesium was selected as the principal biomarker of magnesium status because it correlates closely with ionized magnesium^[28,29] and intracellular magnesium concentrations^[30], while exhibiting low intra‑individual and temporal variability^[30]. By measuring serum magnesium in male and female hypertensive inpatients, our investigation contributes to the ongoing debate regarding magnesium’s role in blood pressure regulation.

Contrary to the prevailing hypothesis that hypomagnesemia predisposes to elevated blood pressure, we observed no significant reduction in serum magnesium among our hypertensive cohort. The mean serum magnesium values of 2.10 ± 0.289 mg/dL in males and 2.04 ± 0.315 mg/dL in females did not differ significantly (p = 0.364), and only a small fraction of patients—3.92 % of males and 8.82 % of females—had levels at or below the 1.70 mg/dL threshold. These findings mirror those of Kozielec et al.^[20] and Ifeanyi‑Chukwu et al. ^[3], both of which reported no statistically significant differences in serum magnesium between patients experiencing hypertensive crises and control groups.

Our results stand in contrast to several studies that have demonstrated lower serum or erythrocyte magnesium levels in hypertensive individuals compared to normotensive controls^{[12,13,14,15]}. Such investigations have often described a strong inverse association between magnesium status and blood pressure^[19,23,24], while others have even reported positive correlations^[20,31]. The discrepancy between our findings and those of these studies may stem from differences in study design, sample characteristics, dietary magnesium intake, or unmeasured confounders affecting magnesium metabolism.

Importantly, a number of large‑scale and methodologically rigorous analyses have also failed to confirm a clear link between serum magnesium and hypertension. Han et al.^[24], in a meta‑analysis of prospective cohort studies, found no significant association between circulating magnesium levels and subsequent changes in blood pressure. Similarly, Abigail May Khan et al.^[22], using data from 3,531 middle‑aged participants in the Framingham Heart Study Offspring Cohort, reported no relationship between baseline serum magnesium and incident hypertension over eight years or cardiovascular disease over twenty years. These community‑based findings suggest that a single measurement of serum magnesium may not capture the long‑term magnesium dynamics relevant to blood pressure control.

Interventional studies provide further nuance. Patki et al.^[32] conducted a double‑blind, randomized, controlled crossover trial in 37 adults with mild hypertension over 32 weeks. While potassium supplementation alone produced a significant reduction in blood pressure (p < 0.001), the addition of magnesium did not confer any additional antihypertensive benefit. This outcome aligns with the logistic regression analysis reported by Ifeanyi‑Chukwu et al.^[3], who found no significant impact of serum magnesium on systolic or diastolic blood pressure among patients in hypertensive crisis.

Collectively, these negative findings indicate that serum magnesium may not play a major, independent role in the regulation of blood pressure among hypertensive patients. Nevertheless, our study has limitations. The relatively modest sample size and lack of detailed dietary and medication histories may have constrained our ability to detect subtle associations. Additionally, the use of a single serum measurement does not account for diurnal or longer‑term variations in magnesium status. Future research employing larger cohorts, repeated magnesium assessments, and comprehensive dietary intake data will be necessary to conclusively define the role of magnesium in hypertension pathogenesis.

In this observational cross‑sectional study of 85 hypertensive inpatients at a tertiary care hospital in Dahod, Gujarat, serum total magnesium levels were generally within the normal reference range for both male and female patients. Only a small proportion—3.92 % of males and 8.82 % of females—exhibited hypomagnesemia (≤ 1.70 mg/dL). The mean serum magnesium concentrations (2.10 ± 0.29 mg/dL in males and 2.04 ± 0.32 mg/dL in females) did not differ significantly between genders, indicating no meaningful disparity in magnesium status among hypertensive individuals.

These findings are consistent with earlier studies reporting no significant difference in magnesium levels between hypertensive and normotensive populations, and contrast with other research showing lower magnesium levels in hypertensive patients. Moreover, large‑scale prospective analyses and randomized trials have generally failed to demonstrate a clear blood pressure–lowering effect of magnesium supplementation.

Overall, our data suggest that serum magnesium may not have a major, independent role in blood pressure regulation among hospitalized hypertensive patients. However, limitations such as a single time‑point measurement of magnesium, lack of dietary intake information, and a moderate sample size underscore the need for further research. Future studies with serial magnesium assessments, comprehensive dietary and medication profiling, and larger, community‑based cohorts will be essential to determine whether more subtle or context‑specific interactions between magnesium status and blood pressure exist. Until such evidence is available, routine screening for serum magnesium deficiency solely as a hypertension management strategy is not supported.

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