Association between serum concentration of parathyroid hormone and left ventricle ejection fraction , and markers of heart failure and inflammation in ST elevation myocardial infarction patients treated with primary percutaneous coronary intervention

Background/Aim. Previous studies have shown increased serum concentration of parathyroid hormone (PTH) in acute myocardial infarction and heart failure. In this study we examined the relationships between parathyroid hormone status and biochemical markers of myocardial injury and heart failure, as well as electrocardiographic (ECG) and echocardiographic indicators of infarction size and heart failure. Methods. In 390 consecutive patients with ST segment elevation myocardial infarction (STEMI), average age 62 ± 12 years, laboratory analysis of serum concentrations of creatine kinase MB isoenzyme (CK-MB), C-reactive protein (CRP) and intact PTH and plasma concentration of brain natriuretic peptide (BNP) were done during the first three days after admission. All patients were treated with primary percutaneous coronary intervention (PCI). Exclusion criterion was  severe renal insufficiency (glomerular filtration rate ≤ 30 mL/min). Serum concentration of PTH was measured on the 1st, 2nd and, in some cases, on the 3rd morning after admission and maximum level of PTH was taken for analysis. Patient cohort was divided into four groups according to quartiles of PTH maximum serum concentration (I ≤ 4.4 pmol/L; II > 4.4 pmol/L and < 6.3 pmol/L; III ≥ 6.3 pmol/L and < 9.2 pmol/L; IV ≥ 9.2 pmol/L). Selvester’s ECG score, left ventricle ejection fraction and wall motion index (WMSI) were determined at discharge between 5–14 days after admission. Results. We found that LVEF at discharge significantly decreased (p < 0.001) and WMSI at discharge and ECG Selvester ́s score significantly increased across the quartiles of PTH max. level (p < 0.001 for both parameters). BNP, CRP and CK-MB isoenzyme level significantly increased across the quartiles of PTH max. level (p < 0.001; p < 0.001 and p = 0.004, retrospectively). Conclusion. The patients in the 4th quartile of PTH had significantly lower LVEF and higher WMSI and Selvester’s ECG score at discharge. This group of patients also had higher levels of BNP, CRP and CK-MB in blood in the early course of STEMI.


Introduction
Parathyroid hormone (PTH) has some cardiovascular effects which can be important for response to acute myocardial injury and acute heart failure [1][2][3][4] .Through the receptors on smooth mucle cells, PTH induces systemic arterial and coronary vasodilatation [5][6][7] and through the receptors on cardiomyocytes it produces chronotropic and inotropic effect on the heart [5][6][7] .It is one of the main messengers for the mobilization and homing of bone marrow derived stem cells which can partly regenerate the damaged myocardial muscle [8][9][10][11] .
The serum concentration of PTH increases in acute ST elevation myocardial infarction (STEMI) 12,13 and can even predict mortality in critically ill patients 14 .Cathecholamine stress and autonomic nervous system are probably the main inducers of the increased PTH release in circulation during acute myocardial infarction [15][16][17] .Large myocardial infarction causes haemodynamic compromise and huge reaction of supra-adrenal gland and sympatic nervous system which activate several hormonal systems including PTH which play an important role in the struggle to maintain sufficient circulation and perfusion of the vital organs 18 .
We have previously shown that PTH can be a marker of acute heart failure in patients with STEMI treated with primary percutaneous coronary intervention (PCI).The aim of this study is to establish correlations between serum concentration of PTH and several parameters which are associated with the prognosis of STEMI patients such as Selvester's ECG score, left ventricular ejection fraction (LVEF), wall motion score index (WMSI), and conventional biomarkers of heart failure, brain natriuretic peptide (BNP), C-reactive protein (CRP) and creatine kinase MB isoenzyme (CK-MB).

Study population and design
In this study, we included 390 consecutive patients admitted to the Coronary Care Unit of the Military Medical Academy (MMA) in Belgrade between Decembar 2008 and June 2015 because of the STEMI.The diagnosis of STEMI was established according to current guidelines of the European Society of Cardiology (ESC) and the American College of Cardiology/American Heart Association (ACC/AHA) (typical chest pain lasting > 20 minutes, electrocardiographic (ECG) changes consisting of ST-segment elevation in at least two contiguous precordial leads ≥ 2 mm in men over the age of 40 years, ≥ 2.5 mm in men below the age of 40 years, ≥ 1.5 mm in women in leads V2-V3 and/or ≥ 1.0 mm in other leads, or horizontal or descending ST depression ≥ 0.5 mm and/or T inversion ≥ 0.1 mV in V1-V3 precordial leads with prominent R wave or R/S ratio > 1 with hypokinesis or akinesis of the posterior left ventricle wall at admission echocardiography examination, confirmed with plasma CK-MB or troponin serum concentration elevation.All patients were treated with primary PCI (less than 12 hours after beginning of the chest pain) with adjunctive drug therapy and according to the ESC and the ACC/AHA guidelines.There was no age limit for study enrollment.
At admission, detailed medical history was taken for all patients, especially with regard to risk factors for ischemic heart disease and a complete physical examination with 12-lead ECG.Urgent laboratory analysis were also done for all patients at admission, including troponins and CK-MB.CK-MB was taken every 6 hours during the first 24 hours and maximum concentration was taken for analysis.Blood samples for PTH, BNP, CRP were taken from an antecubital vein at 8 am, i.e. before a meal.PTH serum concentration was measured on the first and second morning after admission, if the second measurement was higher than the first one, the third measurement was done.The highest concentration was taken for analysis.CRP was taken on the first and second morning and highest concentration was taken for analysis.BNP was taken on the first morning after admission.Echocardiographic assessment was done before discharge for all patients, usually on the days 5 to 8 of hospitalization.
The main exclusion criterion was low creatinine clearance (less than 30 mL/min).Beside renal dysfunction, other exclusion criteria were the presence of known malignant, infectious or autoimmune disease and death during the first 24 hours of the first hospitalization day.
The study was conducted according to the Declaration of Helsinki and was approved by the MMA Ethical Committee.Written informed consent was obtained from all participating patients.

Clinical and echocardiographic assesment
For all patents detailed history of risk factors for coronary artery disease was taken and complete physical examination at the admission to asses hemodynamic stability.

Coronary angiography
All coronary angiograms were done in MMA.Angiographic thrombolysis in miocardial infarction (TIMI) flow grade of the infarction artery was estimated before and after completion of PCI according to four grades of flow according to standard TIMI criteria 19 .Multivessel disease was defined as 70% or greater stenoses in at least one major epicardial artery and 50% or greater stenoses in at least one other major coronary artery 20 .All angiograms were reviewed by two independent interventional cardiologists.

Laboratory testing
Creatine kinase MB was determined in the serum of patients by immunoinhibition method on the commercial Dimension Clinical Chemistry System (Siemesn Heathcare Diagnostics), at admission and every 6 hours during the next 24 hours.C-reactive protein extended range was determined in the serum of patients with a particle enhanced turbidimetric immunoassay on commercial Dimension system on the first and second day in the morning before a meal.Brain natriuretic peptide was detemined in plasma by chemiluminescence immunoassay (ADVIA Centaur XP analyzer; Siemens Medical Solutions, Fernwald, Germany) on the first day of hospitalization in the morning before a meal.Intact PTH serum levels was determined from the venous blood sample withdrawn on the first, second and third (if the patient had the second level of PTH lower than the first one and was clinically stable, we did not take the 3rd sample) morning after admission, before a meal (15±8 hours from the admission).Intact PTH was measured in fresh serum during 4 hours from sampling by a commercial two-site sandwich immunoassay using chemiluminometric detection technology.Intact PTH was measured on ADVIA Centaur analyzer (Siemens Medical Solutions, Fernwald, Germany).The reference range from the test is 1.60-7.00pmol/L and intra-assay coefficient of variation is 2.7%.

Stastitical analysis
In the study we used the methods of descriptive statistics: continuous variables are presented as a mean with standard deviation (SD), or as a median with interquartile ran-ge (IQR) depending on the distribution of data.Categorical variables are reported as counts with percentages.According to the quartiles of maximum PTH serum concentration, the patients were split into 4 groups.Differences between the distribution of categorical variables among the 4 groups of patients were estimated by the χ 2 test.Differences in age, systolic blood pressure and heart rate were calculated with two-way ANOVA.The differences among the levels of LVEF, WMSI, plasma levels of BNP, serum levels of CK-MB and CRP and Selvester's score were compared across the quartiles of PTH maximum with Kruskal Wallis test.P value less than 0.05 was considered significant.The differences between quartile 1 and 2, quartile 2 and 3 and quartile 3 and 4 for all variables were tested by the Mann-Whitnney test (p value less than 0.05 was also considered significant).All analyses were performed by using the SPSS version 21 (SPSS Inc, Chicago, IL, USA).
We divided all patients in quartiles according to serum concentration of parathyroid hormone (I ≤ 4.4 pmol/L; II > 4.4 pmol/L and < 6.3 pmol/L; III ≥ 6.3 pmol/L and < 9.2 pmol/L; IV ≥ 9.2 pmol/L).The demographic and clinical characteristics of the patient population are shown in Table 1.

The demographic and clinical characteristics of the patients
We studied 390 patients and three quarters of them were men (p = 0.050).There was a statistically significant difference between quartiles of the patients by the age (58 ± 11 vs. 60 ± 12 vs.63 ± 12 vs.67 ± 12) respectively p < 0.001.Also, there was a significant difference among quartiles of the patients in the data of arterial hypertension (p = 0.038) and diabetes mellitus (p = 0.008).With the higher PTH max.level, the incidence of hypertension was higher.However, information about diabetes was questionable because diabetes was less common in the 2nd quartile of PTH max.which is probably an incidental finding.We did not find a significant difference between quartiles of the patients in the data of active smoking (p = 0.166) and hypercholesterolemia (p = 0.688).
There were significantly larger number of patients with Killip class greater than I in the 4th quartile of PTH max.level than in the 1st (11.5% vs. 1.0%; p < 0.001).In accordance with that data, we found that heart rate on the admission was significantly higher in the 4th quartile of PTH max.level than in the 1st quartile (84.9 ± 24.7 beats/min vs. 74.2± 18.8 beats/min; p = 0.001), but, on the contrary, systolic blood pressure on the admission showed no significant difference among quartiles of PTH max.level (132.2 ± 23.Every seventh patient had a previous myocardial infarction, i.e. 56 (14.4%) patients and we found that the number of patients with a previous myocardial infarction was significantly higher in the quartile 4 (p = 0.021).
The time from symptom onset until reperfusion occured was defined as total ischemic time (TIT).It was significantly different among quartiles of PTH max.level (p = 0.002).In the 1st quartile of PTH max.TIT was 3.00 (IQR 2.00-6.00)hours and in the 4th quartile TIT was 5.00 (IQR 3.00-9.00)hours.

Procedure related characteristics of the patients
As described in the methodology of this study, all patients were treated with primary PCI.About two thirds of the patients had multivessel disease, i.e. 256 (65.8%) patients.There were statistically significant differences among quartiles of the patients according to the presence of multivessel disease (52, 13.4% vs. 65, 16.7% vs. 72, 18.5% vs. 67, 17.2%; p = 0.017).Also, we analyzed which artery was most commonly infarction related artery (IRA).Infarct related artery in almost half of the cases was left anterior descending (LAD) artery, i.e. in 170 (43.6%) patients LAD was IRA.Right coronary artery (RCA) was IRA in 157 (40.3%) patients, left circumflex artery (LCx) was IRA in 61 (15.6%) patients and left main (LM) coronary artery in 2 (0.5%) patients.Statistically significant differences among quartiles of the patients according to the IRA were not found (p = 0.739).
TIMI flow grade of the infarction-related artery was assessed before and after PCI by two interventional cardiologist.Before PCI, majority of the patients (76.2%) had TIMI flow grade 0 or 1 and no statistically significant differences among quartiles of the patients were found (p = 0.799).Majority of patients (81.5%) had TIMI flow grade 3 after PCI and no statistically significant differences among quartiles of the patients according to TIMI flow grade after PCI were found (p = 0.001).
Majority of patients (86.4%) had stent implantation during PCI and there were no statistically significant differences among quartiles according to the stent implantation (p = 0.102).Onequarter of the patients received glycoprotein (GP) inhibitors before PCI with no statistically significant differences among quartiles (p = 0.898).All patients received oral antiplatelet therapy with aspirin and a P2Y 12 receptor blocker.Majority of the patients received clopidogrel (82.3%) and ticagrelor was  used in 17.7% of all patients.There were no statisticaly significant differences found among quartiles of the patients according to the oral antiplatetet therapy (p = 0,120).

Relation between BNP, CRP and CK-MB with quartiles of PTH
Brain natriuretic peptide level significantly increased in the 4th quartile of PTH level (p < 0.001; Figure 4).Medians with IQR for BNP are: for the 1st quartile 199.49pg/mL (87.43-296.55 pg/mL), for the 2nd quartile 163.90 pg/mL (80.20-320.00pg/mL), for the 3rdt quartile 251.50 pg/ml (111.30-449.10pg/mL) and for the 4th quartile 580.63 pg/ml (232.33-1007.90pg/mL).Thus, the patients in all 4 quartiles had median BNP level higher than a cut-off point recommended by the ESC guidelines for acute heart failure.
There was also significant correlation serum PTH maximum levels and serum creatinine concentrations at admission (Figure 7).However, there were no significant differences among the values of LVEF, WMSI, Selvester's score and CK-MB across the quartiles of creatinine (data not shown).This means that PTH has independent from creatinine level, an association with mentioned parameters.

Analysis of the statistical significance of differences among the individual quartiles for the ECG, echocardiography and biochemical markers of prognosis of acute myocardial infarction
When we analyzed whether there was a statistically significant difference (Mann-Whitney test) between the individual quartiles of the above listed markers of prognosis in acute myocardial infarction, we noticed that there was no statistically significant difference between quartiles 1 and 2, nor 2 and 3, but only between quartiles 3 and 4 of PTH max.levels for all of these markers except for CK-MB max.concentration (Table 2).The 4th quartile of PTH max.serum concentration, therefore, had significantly higher levels of all markers of poor prognosis in acute myocardial infarction (Figures 1-6).For CK-MB max.concentration, we did not find a statistically significant difference between the 1st and 2nd or between the 2nd and 3rd or between the 3rd and 4th quartile, but this does not mean that there was no difference between the 4th and the 1st quartile or the 3rd and the 1st quartile, and therefore, as stated above, there was a statistically significant increase in CK-MB max.concentration with higher quartiles of PTH max.

Discussion
In our patients with STEMI, who were treated with primary PCI, PTH maximum levels, which were on the upper limit of reference range and above this limit, were significantly associated with markers of larger infact size and heart failure.Half of the study patients were in the 3rd and 4th quartile of PTH levels (the upper limit of reference range and above this limit) and all of them had the clinical, ECG, echocardiographic and biochemical markers of larger myocardial infarction size and heart failure.
Clinically, patients in the 3rd and 4th quartile of PTH max.had higher Killip class at admission.They also had a  history of previous myocardial infarction and a longer total ischemic time.On coronary angiography, patients in the 3rd and 4th quartile of PTH max.level had significantly higher incidence of multivessel and TIMI flow after PCI in these patients was significantly less frequently grade 3. Accordingly, echocardiographic prognostic factors in myocardial infarction correlated with the PTH serum level, ejection fraction significantly decreased and WMSI significantly increased across the quartiles of PTH max.level.Selvester´s ECG score was shown to correlate with infarction size.In our study Selvester´s ECG score was significantly higher in higher PTH max.quartiles.The most widely used biochemical prognostic markers in acute myocardial infarction are CKMB, CRP and BNP.All these three markers in our study correlated with the PTH level and increased across the quartiles of PTH max.level.

Possible pathogenesis of PTH level increase in acute myocardial infarction (AMI)
Several studies have shown that there is an increase in PTH serum level in acute myocardial infarction.In study of Joborn et al. 13 serum concentration of PTH was increased in early course of acute myocadial infarction (AMI) as compared to the reference day number 7. In the same period, mean values of total and ionized calcium did not change significantly, but PTH correlated negatively with serum calcium.Conversely, PTH correlated positively with plasma and platelets epinephrine.That is one possible explanation for significant elevation of PTH in large AMI.It is well known that AMI increases sympathoadrenal activity 15 .In vivo and in vitro studies have shown that epinephrine can directly stimulate secretion of PTH and indirectly by lowering plasma total and ionized calcium 16,17 .Carlstedt et.al. 14 reported that PTH was stronger predictor of mortality than APACHE II score in patients in emergency department.The highest PTH levels were observed in patients with myocardial infarction and congestive heart failure.The reason for this observation remained unclear.Hypocalcaemia was not found in these patients and there was no clear association with proinflammatory cytokines.They also assumed that catecholamines could be responsible for elevation of PTH.
To the best of our knowledge, there is only one study of PTH secretion in acute heart failure.Sugimoto et al. 20 inclu-ded in a study 266 patients admitted for acute decompensated heart failure (HF) without acute coronary syndrome.The authors in this study, contrary to the findings in chronic heart failure, found that the low-normal levels of PTH were associated with higher 1-year all-cause mortality.They concluded that the PTH was somehow necessary in the acute heart failure.In experimental studies it was demonstrated that PTH exerted vasodilating effect on blood vessels and positive chronotropic and inotropic effect on the heart 7 .There is evidence that this might be beneficial in heart failure even when PTH level increase is small and close to the upper limit of the normal range 21 .Also, since the authors of this study excluded from the trial the patients with acute coronary syndrome, where it was observed in the earlier, as well as in our study that PTH serum concentration was elevated, it could be concluded that ischemic myocardium in some way contributes to the increased secretion of PTH.In experimatal studies of the application of PTH in myocardial infarction, PTH contributes to mobilization and homing of stem cells from bone marrow in ischaemic myocardium and has a regenerative role [8][9][10][11] .There is a need to investigate whether PTH serum concentrations in myocardial infarction is sufficient for this effect.
Selvester's ECG score is an ECG metod for estimating myocardial infarction size and thus provides prognostic information after myocardial infarction 22 .We used simplified Selve-ster´ score of 37 criteria, 29 point system 23 .Selvester´s score kept the same predictive value in the era of PCI as it used to in the era of thrombolytic therapy.Roubin et al. 23 showed that QRS score correlated well with survival rate, ejection fraction and Killip class.As the score increased, survival rates and ejection fraction decreased.In a study of Tjandrawidjaja et al. 24 with STEMI patients treated with primary PCI, higher QRS scores were associated with male gender, higher heart rate, worse Killip class, noninferior infarction location, greater ST-segment deviation, and longer times to reperfusion and also with impaired culprit artery flow before and after PCI and more frequent multivessel disease.These findings are consistent with our findings; Selvester QRS score was higher with higher serum PTH concentration and that group of patients had higher Killip class, longer ischemic time, faster heart rate on admission and also poorer TIMI flow after PCI and more often multivessel disease.
After AMI, LVEF is of a prognostic significance.It has been shown in numerous studies that ejection fraction below Vol.75, No 2 30-40% is strong predictor of all-cause cardiovascular mortality and sudden cardiac death (SCD) [25][26][27] .Also, there is a good correlation between LVEF and infarction size 28,29 .Pride et al. 28 showed that there was a linear relation between infarction size and LVEF only for moderate to large infarcts, but not for small infarcts.In our study, patients in the 4th quartile of PTH max.level had median LVEF 40%, therefore patients with PTH serum level above the upper limit of the normal range had the EF that indicated worse prognosis and larger infarction size.
LVEF is a marker of global LV systolic function, whereas WMSI allows regional wall motion analysis, i.e. evaluation of LV dysfunction.Similar to the LVEF, WMSI is a strong predictor of all-cause mortality after AMI 27 .Mortality increases exponentially with decreasing LVEF, whereas it increases linearly with increasing WMSI 27 .In the study of Eek et al. 29 a good correlation was found between infarction size and WMSI and global longitudinal strain.They found that wall motion score index > 1.30 accurately identified patients with substantial infarction (≥ 12% of myocardium).In our study, 4th quartile of PTH max.level had median WMSI 1.68, indicating in that way a larger infarction size and worse prognosis.
In acute STEMI, different biomarkers are used in short term and long disease prognosis 30 .We investigated association of PTH with three most commonly used biomarkers: CK-MB which indicates myocardial necrosis, CRP which is a marker of inflammation and BNP which is elevated mainly in response to left ventricular overload, but also in conditions of myocardial ischemia.
It was shown that BNP had predictive value for adverse events in STEMI infarction as well as in non-STEMI and unstable angina pectoris.Similarly, both of these markers are used in different studies of its prognostic value in acute coronary syndrome.Richards et al. 31 examined the predictive value of BNP, NT-proBNP and radionuclide LVEF for adverse events (death, heart failure and new myocardial infarction) in AMI.LVEF and the B-type natriuretic peptides were proved to be powerful independent predictors for adverse outcomes and the combination of NT-proBNP (or BNP) with LVEF (< 40%) substantially improved risk stratification.Besides, investigators concluded that both B-type peptides had similar utility as prognostic markers when measured early in the course of a broad spectrum of acute coronary syndromes.Velders et al. 32 evaluated the prognostic value of high-sensitivity cardiac troponin T, NT-proBNP and growth differentiation factor-15 (GDF-15) in STEMI treated with primary PCI.They concluded that biomarkers provided additional prognostic value for CVD beyond clinical risk factors and extent of coronary artery disease with NT-proBNP and GDF-15 being most valuable.In these studies, BNP/NT-pro BNP were measured at admission or in the first 24 hours up to 96 hours after the onset of symptoms depending on the type of acute coronary syndrome.We measured BNP value in 24 hours from the onset of symptoms.We found that the BNP plasma concentration significally increased with higher quartiles of PTH max.level.Interestingly, median value of BNP in the 1st quartile was 199.49pg/mL (IQR 87.43-296.55 pg/mL) which is a high level, i.e. 100 pg/mL is recommended cut-off value for acute onset of heart failure.The 1st quartile, however, involves a stable patients with smaller infarction size.This could be explained by the role of ischemia on BNP release from ventricular myocardium 33,34 .
CRP is well established risk factor in the pathogenesis of atherosclerosis.The role of CRP in acute myocardial infarction was investigated in several studies.Sano et al. 35 showed that elevated CRP serum concentration within 6 hours after the onset of symptoms of AMI might reflect the inflammatory activity of a ruptured plaque.Later in the course of AMI, elevated serum CRP levels may be caused by a inflammatory response to myocardial necrosis.Lagrand et al. 36 have concluded in experimatal study that CRP localizes in infracted, necrotis tissue and promotes local complement activation and subsequently tissue damage.Nikfardjam et al. 37 found that elevated CRP level on admission in patients with AMI predicted short term and long term mortality.Ohlmann et al. 38 in their study of patients with STEMI treated with primary PCI found that plasma concentrations of CRP measured 48 hours and 72 hours after PCI correlated with infarction size.Admission CRP level as well as level at 48 hours after PCI predicted 6-month mortality.They found that CRP level in this patients reached a peak value after a median interval of 49 hours after the admission.Sanchis et al. 39 have also found that CRP level increased after admission and reached its peak after 48 hours.It could be concluded, that CRP level in AMI depends on time from the pain onset until admission 40 and reperfusion therapy.We measured CRP on the first and second day after admission and a peak CRP serum value was reached around 48 hours after admission, what is in concordance with previous studies.We found that CRP level was significantly higher with higher PTH max.quartiles.
There is a number of studies which confirmed correlation between serum levels of CK-MB and infarction size and prognosis after AMI.Most of these studies are from the time before the thrombolytic therapy or from the thrombolytic therapy era 41,42 .Only Nienhuis et al. 43 showed that peak CK-MB was independent predictor of LVEF and 1-year mortality in patients after primary PCI for STEMI.In current guidelines, troponin is the preferred biomarker to use in patients with acute coronary syndrome (ACS), but CK-MB is considered as the best alternative when troponin assay is not avilable.We used CK-BM because of better availability of this assay in our hospital.In our study the 4th quartile of PHT max.level had significantly higher CK-MB level (median value 237.00 IU/L, interquartile range 132.50-437.00IU/L).This finding is very similar to finding of Nienhuis et al. 43 where CK value in the 3rd quartile was > 281 IU/L.

Study limitation
The present study is part of our larger study of PTH concentration and kinetics in STEMI.The relationship of PTH and other factors of mineral metabolism was described in our previous paper.In this paper we wanted to point out association of PTH and clinical, echocardiographic and biochemical markers of infarction size and heart failure.We didn´t take biochemical markers on admission, although in some studies this was done.This was not always possible to make and, beside that, total ischemic time was significantly different among quartiles of patients and since biochemical markers are dependent on this time, we decided to take samples for biochemical markers on the 1st, 2nd and 3rd day after the admission and to take maximum level for analysis as it was done in some other studies.

Conclusion
Patients with STEMI and elevated concentration of PTH (the lower cut-off for the 4th quartile of PTH was 9.2 pmol/L) in the early phase of had several markers of worse prognosis, high Selvester's ECG score, low LVEF, increased WMSI, and higher blood concentrations of BNP, CRP and CK-MB.

R
E F E R E N C E S 1. Ogino K, Burkhoff D, Bilezikian JP.The hemodynamic basis for the cardiac effects of parathyroid hormone (PTH) and PTHrelated protein.Endocrinology 1995; 136 (7): 3024−30.2. Conway DR, Kim D, Djuricin G, VanDenburgh A, Jacobs HK, Rosel TJ, et al.The effect of parathyroid hormone on the acutely ischemic myocardium.Am Surg 1990; 56(8): 463−7.ejection fraction for risk stratifiortality intervention and left ventricular ejection fraction Selvester´s ECG score was done as an ECG metod for estimating myocardial infarction size.We used simplified score of 37 criteria, 29 point system for scoring ECG at discharge.