5 RESULTS
5.6 Association of serum magnesium with all CVD outcomes
5.6.1 Association with CVD and CVD death
From the previous analysis LDL, fiber, aspirin medication, date of examination, alcohol intake, diabetes were found to be the potential confounders for CVD incidence and CVD mortality. Based on this result multivariate Cox hazard analysis was done for both CVD and CVD death adjusting for potential confounders.
Table 6: Hazard ratio of CVD incidence (n =1582) by total serum magnesium concentration, both adjusted and unadjusted for confounders
Variables (unit) HR (95% CI) P-value
Serum magnesium (mg/l) 0.98 (0.95, 1.02) 0.36 Diabetes (yes, no) 2.07 (1.71, 2.51) <0.001 LDL-chol (mmol/l) 1.15 (1.10, 1.21) < 0.001
Fiber (g/d) 0.99 (0.98, 0.10) 0.002
Aspirin medication (yes, no) 1.41 (1.16, 1.72) 0.001 Date of examination (year) 0.97 (0.94, 1.00) 0.11 Alcohol /week (g/d) 1.00 (1.00, 1.00) 0.16 Unadjusted serum
magnesium (mg/l)
0.99 (0.95, 1.02) 0.41
Table 7: Hazard ratio of CVD death (n = 491) by total serum magnesium concentration, both adjusted and unadjusted for confounders
Variables (unit) HR (95% CI) P- value
Serum magnesium (mg/l) 0.91 (0.85, 0.96) 0.001 Diabetes (yes, no) 2.98 (2.27, 3.89) <0.001
LDL-chol (mmol/l) 1.16 (1.07, 1.27) 0.001
Fiber (g/d) 0.98 (0.97, 0.99) 0.005
Aspirin medication (yes, no) 1.48 (1.06, 2.07) 0.02 Date of examination (year) 0.94 (0.88, 0.10) 0.04 Alcohol /week (g/d) 1.00 (1.00, 1.00) <0.001 Unadjusted serum
magnesium (mg/l)
0.89 (0.84, 0.94) <0.001
Q1, Q2, Q3, Q4: fourths of serum magnesium concentration
We found that with an increase in a unit serum magnesium concentration, risk of CVD death decreased by 9% (HR: 0.91, 95% CI: 0.85, 0.96) after adjusting for all other confounders. The result was almost the same also for unadjusted serum magnesium concentration.
Both adjusted and unadjusted serum magnesium concentration were not found to have association with CVD incidence. However diabetes was strongly associated with both CVD incidence and death.
Table 8: Hazard ratio of CVD incidence (n = 1582) by quartiles of serum magnesium LDL-chol (mmol/l) 1.15 (1.10, 1.21) <0.001
Fiber (g/d) 0.99 (0.98, 0.10) 0.002
Aspirin medication (yes, no) 1.41 (1.16, 1.72) 0.001 Date of examination (year) 0.98 (0.95, 1.00) 0.16 Alcohol /week (g/d) 1.00 (1.00, 1.00) 0.15 Q1, Q2, Q3, Q4: fourths of serum magnesium concentration
Table 9: Hazard ratio of CVD death (n = 491) by quartiles of serum magnesium concentration, adjusted for confounders
Aspirin medication (yes, no) 1.51 (1.08, 2.11) 0.01 Date of examination (year) 0.95 (0.89, 1.00) 0.06 Alcohol /week (g/d) 1.00 (1.00, 1.00) <0.001 Q1, Q2, Q3, Q4: fourths of serum magnesium concentration
All quartiles of serum magnesium concentration were significantly inversely associated with CVD death. Men in the highest quartile of serum magnesium concentration had the lowest risk (HR: 0.74, 95% CI: 0.57, 0.95) of CVD death compared to the men in the lowest quartile.
LDL, fiber, aspirin medication, date of examination, diabetes were all found to be associated with CVD mortality.
After adjusting for confounders, quartiles of serum magnesium were not associated with the risk of CVD incidence.
5.6.2 Association with CHD incidence and mortality
From the above analysis LDL, aspirin medications, date of examination year, diabetes were found to be the confounders of both CHD incidence and CHD death. Whereas fiber was found to be the confounding variable for only CHD incidence and alcohol intake was found to be the confounding variable for CHD death
Table 10: Hazard ratio of CHD incidence (n = 930) by serum magnesium concentration, both adjusted and unadjusted for confounders
Variables (unit) HR (95% CI) P- value
Serum magnesium (mg/l) 1.00 (0.96, 1.04) 0.95 Diabetes (yes, no) 2.65 (2.12, 3.33) <0.001 LDL-Chol (mmol/l) 1.28 (1.21, 1.37) <0.001 Aspirin medication (yes, no) 1.74 (1.37, 2.21) <0.001
Fiber (g/d) 0.99 (0.98, 1.00) 0.06
Date of examination (year) 0.96 (0.92, 1.00) 0.06 Unadjusted serum
magnesium (mg/l)
1 (0.96, 1.04) 0.94
Table 11: Hazard ratio of CHD death (n = 332) by serum magnesium concentration, both adjusted and unadjusted for confounders
Variables (unit) HR (95% CI) P- value
Serum magnesium (mg/l) 0.91 (0.85, 0.98) 0.01 Diabetes (yes, no) 3.43 (2.51, 4.69) <0.001 LDL-Chol (mmol/l) 1.25 (1.13, 1.39) <0.001 Aspirin medication (yes, no) 1.57 (1.05, 2.33) 0.03 Alcohol intake (g/d) 1.00 (1.00, 1.00) 0.003 Date of examination (year) 0.95 (0.88, 1.02) 0.13 Unadjusted serum
magnesium (mg/l)
0.89 (0.83, 0.95) 0.001
Total serum magnesium concentration was strongly associated with CHD mortality but was not found to be associated with CHD incidence after adjusting for potential confounders. The findings were similar also for unadjusted serum magnesium concentration. Increase in serum magnesium concentration by 1 unit, decreased the risk of CHD death by 9% after adjusting for all the potential confounders. All other confounders except date of examination were found to be strongly associated with CHD incidence and death.
Table 12: Hazard ratio for CHD incidence (n = 930) by quartiles of serum magnesium, adjusted for confounders
Variables (unit) HR (95%CI) P- value
Q1 (<18.85mg/l) 1 (ref)
Q2 (18.86-19.85mg/l) 0.86 (0.72, 1.04) 0.13 Q3 (19.86-20.87mg/l) 1.06 (0.88, 1.27) 0.55
Q4 (>20.88mg/l) 0.95 (0.79, 1.14) 0.59
Diabetes (yes, no) 2.65 (2.11, 3.32) <0.001 LDL-Chol (mmol/l) 1.29 (1.21, 1.37) <0.001 Aspirin medication (yes, no) 1.74 (1.37, 2.21) <0.001 Date of examination (year) 0.96 (0.92, 1.00) 0.08
Fiber (g/d) 0.99 (0.98, 1.00) 0.06
Q1, Q2, Q3, Q4: fourths of serum magnesium concentration
Table 13: Hazard ratio for CHD death (n = 332) by quartiles of serum magnesium, adjusted for confounders
Variables (unit) HR (95%CI) P- value
Q1 (<18.85mg/l) 1
Q2 (18.86-19.85mg/l) 0.71(0.53, 0.96) 0.03
Q3 (19.86-20.87mg/l) 0.70 (0.52, 0.95) 0.02
Q4 (>20.88mg/l) 0.72 (0.53, 0.97) 0.03
Diabetes (yes, no) 3.44 (2.52, 4.70) <0.001 LDL-Chol (mmol/l) 1.25 ( 1.13, 1.39) <0.001 Aspirin medication (yes, no) 1.6 (1.07, 2.37) 0.02 Alcohol intake/week (g/d) 1.00 (1.00, 1.00) 0.001 Date of examination (year) 0.95 (0.88, 1.02) 0.17 Q1, Q2, Q3, Q4: fourths of serum magnesium concentration
All the fourths of serum magnesium concentration were strongly associated with CHD death after adjusting for all the confounders. However the risk of death due to CHD did not vary much among the quartiles of serum magnesium concentration. Fourths of serum magnesium concentration were not found to be associated with CHD incidence.
5.6.3 Association with AMI
From the previous analysis LDL cholesterol, fiber, aspirin medication, date of examination year, and diabetes were derived as the confounders for AMI.
Table 14: Hazard ratio of AMI (n = 732) by total serum magnesium concentration, both adjusted and unadjusted for confounders
Variables (unit) HR (95% CI) P- value
Serum magnesium (mg/l) 1.00 (0.95, 1.04) 0.88
Diabetes (yes, no) 3.1 (2.45, 3.92) <0.001
LDL-chol (mmol/l) 1.33 (1.24, 1.43) <0.001
Fibre (g/d) 0.99 (0.98, 1.00) 0.03
Aspirin medication (yes, no) 1.48 (1.12, 1.95) 0.005 Date of examination (year) 0.96 (0.92, 1.01) 0.09 Unadjusted serum
magnesium (mg/l)
0.99 (0.95, 1.04) 0.83
Total serum magnesium concentration when unadjusted was not found to be associated with risk of AMI. The result was same also when adjusted for its confounders. Instead all other confounders except date of examination were found to be strongly associated with AMI.
Table 15: Hazard ratio of AMI (n = 732) by quartiles of serum magnesium concentration, adjusted for confounders
Variables (unit) HR (95%CI) P- value
Q1 (<18.85mg/l) 1 (ref)
Q2 (18.86-19.85mg/l) 0.79 (0.64, 0.98) 0.03
Q3 (19.86-20.87mg/l) 1.01 (0.83, 1.24) 0.90
Q4 (>20.88mg/l) 0.96 (0.78, 1.18) 0.69
Diabetes (yes, no) 3.07 (2..42, 3.88) <0.001
LDL-chol (mmol/l) 1.33 (1.24, 1.43) <0.001
Fiber (g/d) 0.99 (0.98, 1.0) 0.03
Aspirin medication (yes, no) 1.49 (1.13, 1.96) 0.005 Date of examination (year) 0.96 (0.92, 1.01) 0.13 Q1, Q2, Q3, Q4: fourths of serum magnesium concentration
Serum magnesium only in the seconds, comparing to the lowest quartile was associated with risk of AMI. There was 21% decrease in the risk of AMI among men belonging to second quartile than in the lowest quartile of serum magnesium concentration after adjusting for fiber, aspirin medication and date of examination year, diabetes. Adjusted LDL (HR: 1.33; 95% CI:
1.24, 1.43), diabetes (HR: 3.07, 95% CI: 2.42, 3.88) and aspirin medication (HR: 1.49, 95%
CI: 1.13, 1.96) were found to increase the risk of occurrence of AMI.
5.6.4 Association with SCD or SCA
LDL, fiber, aspirin medication, alcohol intake, diabetes were found to be the potential confounders for sudden cardiac death or sudden cardiac arrest from the various analyses done above.
Table 16: Hazard ratio SCD24 or cardiac arrest (n = 232) by total serum magnesium concentration, both adjusted and unadjusted for confounders
Variables HR (95% CI) P- value
Serum magnesium (mg/l) 0.91 (0.84, 0.99) 0.13 Diabetes (yes, no) 3.00 (2.03, 4.44) <0.00 LDL-chol (mmol/l) 1.24 (1.09, 1.39) <0.001
Fiber (g/d) 0.99 (0.97, 1.01) 0.31
Aspirin medication (yes, no) 1.46 (0.91, 2.34) 0.08 Alcohol /week (g/d) 1.00 (1.00, 1.00) 0.01 Unadjusted serum
magnesium (mg/l)
0.92 (0.84, 0.99) 0.03
Increase in serum magnesium concentration by 1 unit decreased the risk of SCD by 8% when it was not adjusted for it confounder. After further adjustment, total serum magnesium concentration was not found to be associated with SCD24. Also LDL and diabetes were significant risk factors for SCD whereas alcohol intake neither increased nor decreased the risk of SCD.
Table 17: Hazard ratio SCD24 or cardiac arrest (n = 232) by quartiles of serum magnesium concentration, adjusted for confounders
Variables (unit) HR (95% CI) P- value
Q1 (<18.85mg/l) 1 (ref)
Q2 (18.86-19.85mg/l) 0.69 (0.47, 0.99) 0.05 Q3 (19.86-20.87mg/l) 0.82 (0.58, 1.17) 0.28 Q4 (>20.88mg/l) 0.76 (0.53, 1.09) 0.13 Diabetes (yes, no) 2.99 (2.02, 4.42) <0.001 LDL-chol (mmol/l) 1.24 (1.10, 1.10) <0.001
Fiber (g/d) 0.99 (0.97, 1.01) 0.31
Aspirin medication (yes, no) 1.54 (0.96, 2.46) 0.07 Alcohol /week (g/d) 1.00 (1.00, 1.00) 0.004 Q1, Q2, Q3, Q4: fourths of serum magnesium concentration
Adjusted multivariate cox proportional hazard showed that men in the second quartile (0.69, 95% CI: 0.47, 0.99) of serum magnesium concentration had significant lower risk of SCD compared to the lowest quartile of serum magnesium concentration.
5.6.5 Associations with stroke, ischemic stroke and hemorrhagic stroke
From the above analysis we found that only diabetes was significantly associated with both serum magnesium and outcome variable stroke and ischemic stroke, i.e only diabetes was found as the confounder for both ischemic and hemorrhagic stroke. Fiber was found to be the potential confounder for hemorrhagic stroke.
Table 18: Hazard ratio of stroke (n = 226) by total serum magnesium concentration, both adjusted and unadjusted for confounder
Stroke HR (95% CI) P- value
Serum magnesium (mg/l) 0.96 (0.88, 1.04) 0.341 Diabetes (yes, no) 2.69 (1.8, 4.02) <0.001 Unadjusted serum magnesium
(mg/l)
0.93 (0.86, 1.02) 0.11
Table 19: Hazard ratio of ischemic stroke (n = 182) by total serum magnesium concentration, both adjusted and unadjusted for confounder
Table 20: Hazard ratio of hemorrhagic stroke (n = 47) by total serum magnesium concentration, adjusted for confounder
There was not found any significant association between total serum magnesium concentration (both adjusted and unadjusted) and the occurrence of stroke, ischemic stroke, and hemorrhagic stroke (Table.18, 19, 20). However the respective confounding variable fiber was found to be associated for slight decrease in the risk of hemorrhagic stroke and diabetes was found to be associated with increase in risk of stroke and ischemic stroke after adjustment of serum magnesium
Table 21: Hazard ratio of stroke (n = 226) by quartiles of serum magnesium, adjusted for confounder
Table 22: Hazard ratio of ischemic stroke (n = 182) by quartiles of serum magnesium, adjusted for confounder
Variables (unit) HR (95% CI) P- value
Q1(<18.85mg/l) 1 (ref)
Q2 (18.86-19.85mg/l) 1.0 (0.66, 1.50) 0.99
Q3 (19.86-20.87mg/l) 1.08 (0.72, 1.62) 0.72
Q4 (>20.88mg/l) 0.88 (0.58, 1.35) 0.57
Diabetes (yes, no) 3.09 (2.01, 4.75) <0.001
Variables (unit) HR (95% CI) P- value
Q1(<18.85mg/l) 1 (ref)
Q2 (18.86-19.85mg/l) 0.89 (0.62, 1.29) 0.55 Q3 (19.86-20.87mg/l) 1.08 (0.75, 1.55) 0.67 Q4 (>20.88mg/l) 0.86 (0.59, 1.25) 0.43 Diabetes (yes, no) 2.75 (1.84, 4.11) <0.001
Table 23: Hazard ratio of hemorrhagic stroke (n = 47) by quartiles of serum magnesium, adjusted for confounder
Variables (unit) HR (95% CI) P- value
Q1(<18.85mg/l) 1 (ref)
Q2 (18.86-19.85mg/l) 0.78 (0.34, 1.81) 0.56
Q3 (19.86-20.87mg/l) 1.18 (0.55, 2.52) 0.67
Q4 (>20.88mg/l) 0.75 (0.32, 1.74) 0.50
Fiber (g/d) 0.95 (0.91, 0.99) 0.01
There was not any association between quartiles of serum magnesium concentration and stroke, ischemic stroke and hemorrhagic stroke after adjusting for confounders.
6 DISCUSSION
In this prospective cohort of Finnish men, change in total serum magnesium concentration by a unit, was associated with lower risk of CVD, CHD and SCD mortality when unadjusted. But after adjusting for the potential confounders, total serum magnesium concentration was found to be associated only with CVD and CHD mortality. When compared to the quartiles of serum magnesium concentration, highest serum magnesium concentration was very strongly associated with the lower risk of CVD and CHD mortality. Men with highest serum magnesium concentration had 26% lower risk of CVD death and 28% lower risk of CHD death after adjusting for its potential confounders. Total serum magnesium concentration was not associated with non-fatal CVD, CHD and AMI after controlling for their risk factors. But there was found significant decrease in risk of non-fatal AMI and fatal SCD in the second quartile compared to the lowest quartile of serum magnesium concentration. Serum magnesium concentration was not found to be associated with stroke, ischemic stroke, and hemorrhagic stroke at any condition.
There are conflicting results in many previous studies regarding the association between magnesium and all the outcome events. There are many studies based on dietary magnesium intake which has either gone against or in a support of our study findings (Guasch-Ferre et al.
2014; Stevanovic et al. 2011; Al-Delaimy et al. 2004). These studies based on dietary measures might be influenced by residual confounding or recall bias. And also diet or food rich in magnesium may contain other nutrient factors which might have influenced the CVD outcomes and its risk factors. There are only few studies which have examined the association between serum magnesium and CVD events. Similar to our result serum magnesium was not found to be associated with CVD (Khan et al. 2010). A prospective study showed no significant association with serum magnesium concentration and stroke after adjusting for potential confounders (Ohira et al. 2009). Consistent with other studies result there was not found any association between serum magnesium concentration and stroke after adjusting for potential confounders. In our study there was seen significant lower risk of SCD when unadjusted but when it was adjusted for confounders there was not seen any association between total serum magnesium concentration and SCD. When divided into fourths there was
seen a significant lowest risk of SCD in the second lowest quartile of serum magnesium concentration. Though the result supported the finding of other studies that serum magnesium is associated with lower risk of SCD it did not support other studies finding stating that there is the lowest risk of SCD in the highest serum magnesium concentration (Chiuve et al. 2011;
peacock et al. 2010). Similar to other studies serum magnesium concentration was strongly associated with fatal CHD but not with CHD incidence (Ford 1999; Chiuve et al. 2013). In contrast few studies have shown no effect of magnesium on CHD. Similar to serum magnesium concentration many studies showed the association between dietary intake of magnesium and risk of cardiovascular events (Lian et al. 2011; Al-Delaimy et al. 2004).
Magnesium is an intracellular cation, so serum magnesium may not represent the total body magnesium stores (Jahnen-Dechent and Ketteler 2012). However measurement of serum magnesium is the easiest, cheapest and most common laboratory measurement and also serum magnesium concentration can be correlated with the intracellular magnesium.
Magnesium affects the movement of sodium, potassium and calcium (Swaminathan 2003), which may lead to affect in the cardiovascular system resulting in increased risk. However in our study there was not seen any significant correlation between serum magnesium concentration and calcium and potassium. Magnesium and many CVD outcomes were found to be associated with hypertension, diabetes, and alcohol (Ma et al. 1995; Romani 2008). Thus one of the important finding of this study was the exploration of factors that might affect the association between magnesium and cardiovascular events. We found that alcohol intake, fiber, aspirin medication, date of examination, diabetes were statistically affecting both the serum magnesium concentration and CVD mortality. Diabetes was one of the variables which was found to be strongly associated with the change in magnesium level as renal magnesium wasting and osmotic diuresis causes magnesium depletion. In contrast magnesium depletion also affects insulin secretion and insulin resistance (Takaya et al. 2004). Also diabetes independently was a very strong factor predicting almost 200% increased risk of CVD outcomes except hemorrhagic stroke. However even after adjusting for these potential confounders, serum magnesium remained strongly associated with CVD mortality. There was no association between total serum magnesium concentration and CVD after adjustment for all
the biomarkers. These results suggest that magnesium can protect fatal CVD. Clinical trials also had shown both protective and no effect of magnesium infusion in patient to prevent from arrhythmias (Roffe et al.1994; Gyamlani et al. 2000). Thus further clinical trials are needed to know antithrombotic effect of magnesium to prevent AMI.
7 STRENGTHS AND LIMITATIONS OF THE STUDY
The strength of this study is that it is a prospective population based study that includes reliable sample size at baseline and follow up. We had reliable definitions of all the outcome variables as they were based on ICD-10 diagnoses. The outcomes were based on the diagnosis available from the National Hospital Discharge Registry, the National Causes of Death Registry and FINMONICA registry which are very reliable sources of information. The level of magnesium was based on the measurement of serum magnesium concentration present in the body. The method used to measure serum magnesium concentration was atomic absorption spectrometry. Hence it has high level of accuracy.
The study also has few limitations like the study only includes male population so it cannot be generalized to women. Serum magnesium represents very small part of total body magnesium so it may not reflect if there is really a deficiency of magnesium in our body which is increasing or decreasing the risk of CVD events.
8 CONCLUSION
In conclusion there was strong relation between serum magnesium concentration and CVD, CHD mortality. Increase in serum magnesium concentration decreased the occurrence of fatal CVD and CHD. Total serum magnesium concentration was found to be associated with SCD only when it was unadjusted. However total serum magnesium concentrations was not found to be associated with incidence of CVD, CHD, AMI and stroke risk both before and after adjusting for its potential confounders. But serum magnesium concentration when divided into
fourths showed significant decrease in risk in the second quartile of AMI incidence and SCD and in all fourths of fatal CVD and CHD when compared to the lowest quartile.
However, further studies including clinical and randomized controlled trials are needed to clearly state the importance of magnesium and to recommend magnesium rich food stating its protective effect for cardiovascular outcomes.
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