Usefulness of Hyponatremia in the Acute Phase of ST-Elevation

Myocardial Infarction as a Marker of Severity

Chiara Lazzeri, MD*, Serafina Valente, MD, Marco Chiostri, MD, Paola Attanà, MD,
Claudio Picariello, MD, and Gian Franco Gensini, MD
Whether hyponatremia (sodium <135 mEq/L) in the acute phase of ST-segment elevation
myocardial infarction is just a marker of “more ill” patients or decreased sodium concen-
tration is able to exert a direct adverse effect on the cardiovascular system is still unknown.
The aim of this study was to assess the prognostic impact, in the short and long terms, of
admission hyponatremia in 1,231 consecutive patients with ST-segment elevation myocar-
dial infarctions all submitted to primary percutaneous coronary intervention. In this series,
286 patients (23.2%) had sodium values <135 mEq/L. Patients with hyponatremia were
older (p ⴝ 0.018) and more frequently had diabetes (p ⴝ 0.040). Anterior myocardial
infarction was more frequent in patients with hyponatremia, who showed a higher inci-
dence of 3-vessel coronary artery disease and advanced Killip class. Higher mortality rates
were observed in patients with hyponatremia during intensive cardiac care unit stay and at
follow-up. On multivariate regression analysis, admission sodium concentration was not
independently related to early death, nor did it show any relations with long-term mortality
on Cox regression analysis. In conclusion, the main findings of the present investigation are
as follows: (1) hyponatremia is a common finding, being associated mainly with older age,
diabetes, and advanced Killip class; (2) patients with hyponatremia had higher rates of
in-hospital and long-term mortality; and (3) hyponatremia, also when assessed by means of
the propensity score model, was not independently associated with increased risk for death
in the short and long terms. These data therefore strongly suggest that the presence of
hyponatremia in the acute phase of ST-segment elevation myocardial infarction should be
considered a marker of more ill patients. © 2012 Elsevier Inc. All rights reserved. (Am J
Cardiol 2012;110:1419 –1424)

Hyponatremia (sodium ⬍135 mEq/L) in the acute phase
of ST-segment elevation myocardial infarction (STEMI)
has been identified as an independent predictor of short-
term mortality,1,2 long-term mortality, and rehospitalization
for heart failure.3 However, previous investigations were
performed in the thrombolytic era or included series of
heterogenous patients with STEMIs submitted either to
thrombolysis or percutaneous coronary intervention.
Whether hyponatremia is just a marker of “more ill” pa-
tients or decreased sodium concentration is able to exert a
direct adverse effect on the cardiovascular system is still
unknown. We assessed the prognostic impact, in the short
and long terms, of admission hyponatremia in 1,231 con-
secutive patients with STEMIs, all submitted to primary
percutaneous coronary intervention (PCI) and admitted to
our intensive cardiac care unit (ICCU).
Methods
From April 1, 2004, to December 31, 2010, 1,231 con-
secutive patients with STEMIs (within 12 hours of symptom
Intensive Cardiac Coronary Unit, Heart and Vessel Department,
Azienda Ospedaliero–Universitaria Careggi, Florence, Italy. Manuscript
received April 16, 2012; revised manuscript received and accepted July 5,
2012.
*Corresponding author: Tel: 39-55-7947518; fax: 39-55-7947518.
E-mail address: lazzeric@libero.it (C. Lazzeri).
onset)4 were admitted to our ICCU, which is located at a
tertiary center (at which primary PCI can be performed 24
hours a day, 7 days a week). In our hospital, in Florence,
Italy, the reperfusion strategy for patients with STEMIs is
represented by primary PCI.5– 8 Patients with STEMIs are
first evaluated by the medical emergency system staff in the
prehospital setting and then directly admitted to the cathe-
terization laboratory or transferred there after rapid stabili-
zation in the first aid department. After primary PCI, they
are admitted to our ICCU.
A successful procedure was defined as an infarct-related
artery stenosis ⬍20% associated with Thrombolysis In
Myocardial Infarction (TIMI) grade 3 flow. Failed PCI was
defined as resulting in TIMI grade 0 to 2 flow, regardless
residual stenosis.
The diagnosis of STEMI was based on the criteria of the
American College of Cardiology and American Heart As-
sociation.4,9
On ICCU admission, after PCI, in a fasting blood sam-
ple, the following parameters were measured: sodium (mil-
liequivalents per liter), glucose (grams per liter), glycosy-
lated hemoglobin (percentage),10 troponin I (nanograms/
milliliter), uric acid (milligrams per deciliter),11 N-terminal
pro– brain natriuretic peptide (picograms per milliliter),12
erythrocyte sedimentation rate, leukocyte count (thousands
per microliter), fibrinogen (milligrams per deciliter) and
high-sensitivity C-reactive protein positivity. Creatinine
(milligrams per deciliter) was also measured to calculate the

0002-9149/12/$ – see front matter © 2012 Elsevier Inc. All rights reserved. www.ajconline.org
http://dx.doi.org/10.1016/j.amjcard.2012.07.004
1420 The American Journal of Cardiology (www.ajconline.org)

Table 1
Clinical characteristics
Variable Serum Sodium (mEq/L) p Value

⬍135 ⱖ135
(n ⫽ 286) (n ⫽ 945)

Age (years) 68.4 ⫾ 11.9 66.3 ⫾ 12.9 0.018

Men/women 198 (69.2%)/88 (30.8%) 699 (74.0%)/246 (26.0%) 0.114
Body mass index (kg/m2) 25.7 ⫾ 3.3 26.4 ⫾ 3.7 0.007
Diabetes mellitus 85 (29.7%) 224 (23.7%) 0.040
Smoking 168 (58.7%) 598 (63.3%) 0.165
Chronic obstructive pulmonary disease 27 (9.4%) 77 (8.1%) 0.491
Previous PCI 48 (16.8%) 120 (12.7%) 0.078
Previous myocardial infarction 48 (16.8%) 126 (13.3%) 0.142
Hypertension 157 (54.9%) 501 (53.0%) 0.577
Symptoms-to-balloon time (minutes) 240 (180–350) 230 (160–300) 0.078
Acute myocardial infarction location 0.005
Anterior 175 (61.2%) 480 (50.8%)
Inferior 89 (31.1%) 393 (41.6%)
Other 22 (7.7%) 72 (7.6%)
Number of coronary arteries narrowed 0.048
1 96 (33.6%) 389 (41.2%)
2 101 (35.3%) 315 (33.3%)
3 89 (31.1%) 241 (25.5%)
Left main 14 (4.9%) 43 (4.6%) 0.808
Coronary artery bypass grafting 6 (2.1%) 24 (2.5%) 0.671
PCI failure 23 (8.1%) 54 (5.8%) 0.166
Killip class 0.012
I or II 243 (85.0%) 853 (90.3%)
III or IV 43 (15.0%) 92 (9.7%)
Length of stay (hours) 72 (48–96) 61 (48–79) 0.051
In-ICCU death 22 (7.7%) 36 (3.8%) 0.007
Follow-up death (n ⫽ 530) 52/237 (21.9%) 111/820 (13.5%) 0.002

Data are expressed as mean ⫾ SD, as number (percentage), or as median (interquartile range).

glomerular filtration rate (milliliters per minute per 1.73
square meters),13 on admission and at discharge. Glucose,
troponin I, and creatinine were measured 3 times a day, and
peak values were considered. Acute insulin resistance was
assessed using homeostasis model assessment, as previ-
ously described.6,14,15 Mild hyponatremia was defined as
sodium ⬍135 mEq/L.1,2
Transthoracic 2-dimensional echocardiography was per-
formed on ICCU admission to measure the left ventricular
ejection fraction (LVEF).
Ventilatory support (invasive and noninvasive ventila-
tion), ultrafiltration (continuous venous-venous ultrafiltra-
tion, continuous venovenous hemodiafiltration), and intra-
aortic balloon pump implantation were used when
needed.5,7,8
The primary end point was in-ICCU death and all-cause
death at follow-up.
The study protocol was in accordance with the Declara-
tion of Helsinki and approved by the local ethics committee.
Written informed consent was obtained from all patients
before enrollment.
Data were analyzed using SPSS version 17.0 (SPSS,
Inc., Chicago, Illinois). A p value ⬍0.05 was considered
statistically significant. Discrete variables are reported as
frequencies and percentages, and between-group compari-
sons were made using chi-square or Fisher’s exact tests,
when the expected value in almost 1 cell was ⬍5. Contin-
uous variables are reported as mean ⫾ SD or as median
(interquartile range) according to the shape of their distri-
bution, assessed using 1-sample Kolmogorov-Smirnov
tests; comparisons were performed using Student’s t tests or
Mann-Whitney U tests. A multivariate logistic regression
model was constructed to identify adjusted predictors of
in-ICCU death; candidate variables were carefully chosen
among those significantly different on univariate analysis
and/or clinically relevant, to avoid model overfitting. Model
calibration was assessed using the Hosmer-Lemeshow test.
Because several baseline characteristics of patients with
hyponatremia significantly differed from those with normal
sodium levels, a propensity analysis was carried out using a
nonparsimonious logistic regression to determine the prob-
ability of a patient to have serum sodium ⬍135 mEq/L. The
variables included in the propensity score model were age;
body mass index; glycemia; estimated glomerular filtration
rate (eGFR); leukocyte count; fibrinogen; previous PCI;
history of diabetes; coronary disease severity; myocardial
infarction location; Killip classification; treatment with di-
uretics, nitrates, and inotropes; mechanical ventilation; con-
tinuous renal replacement therapy; and intra-aortic balloon
pump implantation. The procedure selected 260 patients
with hyponatremia to be compared to 260 with normal
sodium levels; all baseline characteristics (except myocar-
dial infarction location) did not differ between the 2 sub-
groups.
 Coronary Artery Disease/Hyponatremia in STEMI 1421

Table 2
Laboratory data
Variable All Patients Serum Sodium (mEq/L) p Value
(n ⫽ 1,231)
⬍135 ⱖ135
(n ⫽ 286) (n ⫽ 945)

Admission glucose (mg/L) 133 (112–169) 140 (116–192) 130 (110–163) ⬍0.001
Peak glycemia (mg/L) 152 (127–197) 165 (134–232) 150 (125–189) ⬍0.001
Insulin (mU/L) 9.6 (5.5–17.7) 9.2 (5.0–20.3) 9.8 (5.7–17.3) 0.664
Homeostasis model assessment of insulin resistance positivity 116/720 (16.1%) 35/164 (21.3%) 81/556 (14.6%) 0.038
Glycosylated hemoglobin (%) 5.9 (5.6–6.4) 6.0 (5.7–7.0) 5.9 (5.6–6.4) 0.019
eGFR (ml/min/1.73 m2)
Admission 83.0 ⫾ 30.2 77.4 ⫾ 31.2 84.6 ⫾ 29.7 ⬍0.001
Nadir 69.9 ⫾ 25.9 62.6 ⫾ 27.6 72.2 ⫾ 25.0 ⬍0.001
Discharge 79.9 ⫾ 28.7 73.8 ⫾ 31.6 81.8 ⫾ 27.5 ⬍0.001
Microalbuminuria (mg/dl) 17.0 (6.4–55.0) 16.0 (6.4–73.2) 17.2 (6.4–53.8) 0.407
Peak troponin I (ng/ml) 82.7 (36.9–176.2) 95.5 (38.6–204.8) 79.2 (36.1–165.9) 0.116
N-terminal pro–brain natriuretic peptide (pg/ml) 1,306 (468–3,257) 1,722 (568–4,707) 1,140 (459–2,758) 0.002
Uric acid (mg/dl) 5.7 ⫾ 1.8 5.6 ⫾ 1.8 5.8 ⫾ 1.8 0.354
Erythrocyte sedimentation rate (mm/hour) 24 (12–41) 27 (14–49) 23 (12–38) 0.003
Leukocyte count (⫻103/␮l) 10.7 (8.8–13.7) 11.6 (9.4–14.6) 10.7 (8.7–13.4) 0.003
High-sensitivity C-reactive protein positivity 456/913 (49.9%) 119/227 (52.4%) 337/686 (49.1%) 0.389
Fibrinogen (mg/dl) 398 (335–479) 417 (337–523) 391 (334–468) 0.011

Data are expressed as median (interquartile range), as number (percentage), or as mean ⫾ SD.

Figure 1. The incidence of hyponatremia according to LVEF.

After the assessment of risk proportionality, a multivar-
iate Cox regression analysis was conducted to identify pre-
dictors of long-term death.
Results
In our series, 286 of 1,231 patients (23.2%) showed
sodium values ⬍135 mEq/L. Patients with hyponatremia
patients were older (p ⫽ 0.018) and more frequently had
diabetes (p ⫽ 0.040). Anterior wall myocardial infarction
was more frequent in patients with hyponatremia, who
showed a higher incidence of 3-vessel coronary artery dis-
ease and advanced Killip class. Higher mortality rates were
observed in patients with hyponatremic during the ICCU
stay and at follow-up (Table 1).
As listed in Table 2, patients with hyponatremia had
higher values of admission and peak glycemia (p ⬍0.001
and p ⬍0.001, respectively), homeostasis model assessment
of insulin resistance positivity (p ⫽ 0.038), and lower val-
ues of admission, nadir, and discharge eGFR (p ⬍0.001 for
all). Higher values of N-terminal pro– brain natriuretic pep-
tide were observed in patients with hyponatremia (p ⫽
0.002), as well as higher levels of erythrocyte sedimentation
rate (p ⫽ 0.003), leukocyte count (p ⫽ 0.003), and fibrin-
ogen (p ⫽ 0.011).
1422 The American Journal of Cardiology (www.ajconline.org)

Table 3
Devices
Variable All Patients Serum Sodium (mEq/L) p Value
(n ⫽ 1,231)
⬍135 ⱖ135
(n ⫽ 286) (n ⫽ 945)

Mechanical ventilation 91/1,215 (7.5%) 32/283 (11.3%) 59/932 (6.3%) 0.005

Noninvasive ventilation 70/1,192 (5.9%) 25/278 (9.0%) 45/914 (4.9%) 0.012
Continuous venovenous hemodiafiltration 47/283 (3.9%) 22/280 (7.9%) 25/933 (2.7%) ⬍0.001
Intra-aortic balloon pump 274/1,213 (22.6%) 83/282 (29.4%) 191/931 (20.5%) 0.002

Table 4
Medications
Variable Serum Sodium (mEq/L) p Value

⬍135 ⱖ135
(n ⫽ 286) (n ⫽ 945)

During ICCU stay

Aspirin 286 (100%) 943 (99.8%) 1.00*
Clopidogrel 280 (97.9%) 920 (97.4%) 0.605
Unfractionated heparin 282 (98.6%) 920 (97.4%) 0.223
Glycoprotein IIb/IIIa inhibitors 207 (72.4%) 684 (72.4%) 0.999
␤ blockers 241 (85.8%) 792 (84.3%) 0.538
Angiotensin-converting enzyme inhibitors 250 (89.3%) 849 (90.3%) 0.612
Angiotensin receptor blockers 4 (1.4%) 23 (2.5%) 0.307
Diuretics 218 (77.6%) 671 (71.4%) 0.041
Nitrates 155 (55.2%) 443 (47.1%) 0.018
Inotropes 53 (18.5%) 118 (12.5%) 0.010
At discharge n ⫽ 264 (22.5%) n ⫽ 909 (77.5%)
Aspirin 249 (94.3%) 872 (95.9%) 0.263
Clopidogrel 241 (91.3%) 849 (93.5%) 0.214
Unfractionated heparin 227 (86.0%) 757 (83.3%) 0.292
Glycoprotein IIb/IIIa inhibitors 232 (87.9%) 802 (88.2%) 0.877
␤ blockers 3 (1.1%) 28 (3.1%) 0.083
Angiotensin-converting enzyme inhibitors 158 (59.8%) 492 (54.1%) 0.100
Angiotensin receptor blockers 71 (26.9) 145 (16.0) ⬍0.001

* Fisher’s exact test.

In patients with admission LVEFs ⬍45%, the inci-
dence of hyponatremia was higher with respect to that
observed in patients with admission LVEFs ⬎45% (p ⫽
0.002; Figure 1).
As listed in Table 3, higher use of ventilatory support,
intra-aortic balloon pump implantation, and ultrafiltration
was observed in patients with hyponatremia.
During ICCU stay, inotropic agents (p ⫽ 0.041), nitrates
(p ⫽ 0.018), and diuretics (p ⫽ 0.010) were more frequently
used in patients with hyponatremia. At discharge, nitrates
were more frequently administered in patients with hypo-
natremia (p ⬍0.001) (Table 4).
On multivariate logistic regression analysis, the follow-
ing variables were independent predictors of in-ICCU mor-
tality (when adjusted for sodium values): age (per 1 year;
odds ratio [OR] 1.04, 95% confidence interval [CI] 1.01 to
1.08, p ⫽ 0.006), body mass index (per 1 kg/m2; OR 0.89,
95% CI 0.81 to 0.91, p ⫽ 0.016), admission glycemia (per
1 g/L; OR 2.27, 95% CI 1.68 to 3.07, p ⬍0.001), the LVEF
(per 1%; OR 0.92, 95% CI 0.90 to 0.95, p ⬍0.001), and
admission eGFR (per 1 ml/min/1.73 m2; OR 0.98, 95% CI
0.97 to 0.99, p ⫽ 0.006). The Hosmer-Lemeshow goodness-
of-fit test chi-square statistic was 9.8 (p ⫽ 0.277), and the
Nagelkerke pseudo-R2 value was 0.35.
At long-term follow-up, no difference was observed in
survival rate between patients with STEMIs with sodium
⬍135 mEq/L and those with sodium ⱖ135 mEq/L. On Cox
regression analysis, the following variables were indepen-
dently associated with long-term death: age (per 1 year;
hazard ratio 1.08, 95% CI 1.05 to 1.10, p ⬍0.001), eGFR
(per 1 ml/min/1.73 m2; hazard ratio 0.98, 95% CI 0.97 to
0.99, p ⫽ 0.002), and previous myocardial infarction (haz-
ard ratio 1.81, 95% CI 1.17 to 2.80, p ⫽ 0.008).
After adjustment for propensity score and baseline cova-
riates, hyponatremia was not associated with an increased
mortality rate in the short and long terms (for in-ICCU
death, patients with hyponatremia 6.5% vs those with nor-
mal sodium levels 5.0%, p ⫽ 0.452; for long-term death,
patients with hyponatremia 20.3% vs those with normal
sodium levels 17.9%, p ⫽ 0.524).
Discussion
The main findings of the present investigation, including
1,231 consecutive patients with STEMIs, all submitted to
 Coronary Artery Disease/Hyponatremia in STEMI
PCI, are as follows: (1) hyponatremia is a common finding,
being associated mainly with older age, diabetes, and ad-
vanced Killip class; (2) patients with hyponatremia showed
higher rates of in-hospital and long-term mortality; and (3)
hyponatremia, also when assessed using the propensity
score model, was not independently associated with in-
creased risk for death in the short and long terms. Our data
therefore strongly suggest that the presence of hyponatre-
mia, in the acute phase of STEMI, should be considered a
marker of more ill patients.
In 1979, Flear and Hilton16 observed excess in-hospital
deaths in patients with severe hyponatremia and acute
myocardial infarctions treated conservatively. In the fol-
lowing years, in the reperfusion era, several studies1–3
dealt with the prognostic impact of hyponatremia in acute
myocardial infarction. Goldberg et al1 observed that hy-
ponatremia on admission or early development of hypo-
natremia was an independent predictor of 30-day mortal-
ity in patients with acute STEMIs (in whom primary PCI
was performed in 22%). In a series of 978 patients with
STEMIs, the same group observed that admission hypo-
natremia was a predictor of long-term mortality and re-
admission for heart failure; PCI was performed in 26% of
the population.
Tang et al17 documented, in 1,620 patients with
STEMI, that hyponatremia was independently associated
with in-hospital death and heart failure; however, in their
series, reperfusion, by means either of thrombolysis or
PCI, was performed in 74% of the entire population. In a
retrospective analysis of 230 consecutive patients with
STEMI (in whom PCI was performed in 88.5%), patients
with hyponatremic in the acute phase showed increased
risk for worse in-hospital clinical outcomes.18 However,
in 1,858 patients with STEMIs treated with mechanical
reperfusion,2 admission hyponatremia was independently
associated with in-hospital death only in patients with
preserved LVEFs or proper kidney function.
Our investigation is the largest series of patients with
STEMIs who underwent PCI in whom the prognostic role
of admission hyponatremia has been assessed. In our
population, the presence of hyponatremia identifies a
subset of more ill patients, being characterized by older
age, advanced Killip class, and reduced LVEF, as previ-
ously described. These patients also showed higher in-
flammatory activation (as inferred by higher values of
erythrocyte sedimentation rate, fibrinogen, and high-sen-
sitivity C-reactive protein) and an altered glucose re-
sponse (as indicated by higher admission and peak gly-
cemia and an increased incidence of homeostasis model
assessment of insulin resistance positivity), all factors
known to be associated with adverse prognosis of STEMI
in the acute phase.
The novelty of our investigation is that admission hypo-
natremia, when adjusted by baseline covariates and when
assessed using the propensity score model, was not related
to death, in the short and long terms. This finding strongly
suggests that the presence of hyponatremia in the acute
phase of STEMI in patients who undergo PCI should be
considered a marker of more ill patients.
1423
1. Goldberg A, Hammerman H, Petcherski S, Zdorovyak A, Yalonetsky
S, Kapeliovich M, Agmon Y, Markiewicz W, Aronson D. Prognostic
importance of hyponatremia in acute ST-elevation myocardial infarc-
tion. Am J Med 2004;117:242–248.
2. Klopotowski M, Kruk M, Przyluski J, Kalinczuk L, Pregowski J,
Bekta P, Malek LA, Kepka C, Ciszewski A, Chmielak Z, Demkow M,
Karcz M, Witkowski A, Ruzyllo W. Sodium level on admission and
in-hospital outcomes of STEMI patients treated with primary angio-
plasty: the ANIN Myocardial Infarction Registry. Med Sci Monit
2009;15:477– 483.
3. Goldberg A, Hammerman H, Petcherski S, Nassar M, Zdorovyak A,
Yalonetsky S, Kapeliovich M, Agmon Y, Beyar R, Aronson W,
Markiewicz. Hyponatremia and long-term mortality in survivors of
acute ST-elevation myocardial infarction. Arch Intern Med 2006;166:
781–786.
4. European Association for Percutaneous Cardiovascular Interven-
tions, Wijns W, Kolh P, Danchin N, Di Mario C, Falk V, Folliguet
T, Garg S, Huber K, James S, Knuuti J, Lopez-Sendon J, Marco J,
Menicanti L, Ostojic M, Piepoli MF, Pirlet C, Pomar JL, Reifart N,
Ribichini FL, Schalij MJ, Sergeant P, Serruys PW, Silber S, Sousa
Uva M, Taggart D; ESC Committee for Practice Guidelines, Va-
hanian A, Auricchio A, Bax J, Ceconi C, Dean V, Filippatos G,
Funck-Brentano C, Hobbs R, Kearney P, McDonagh T, Popescu
BA, Reiner Z, Sechtem U, Sirnes PA, Tendera M, Vardas PE,
Widimsky P; EACTS Clinical Guidelines Committee, Kolh P, Alfi-
eri O, Dunning J, Elia S, Kappetein P, Lockowandt U, Sarris G,
Vouhe P, Kearney P, von Segesser L, Agewall S, Aladashvili A,
Alexopoulos D, Antunes MJ, Atalar E, Brutel de la Riviere A,
Doganov A, Eha J, Fajadet J, Ferreira R, Garot J, Halcox J, Hasin
Y, Janssens S, Kervinen K, Laufer G, Legrand V, Nashef SA,
Neumann FJ, Niemela K, Nihoyannopoulos P, Noc M, Piek JJ, Pirk
J, Rozenman Y, Sabate M, Starc R, Thielmann M, Wheatley DJ,
Windecker S, Zembala M. Guidelines on myocardial revasculariza-
tion: the Task Force on Myocardial Revascularization of the Euro-
pean Society of Cardiology (ESC) and the European Association
for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2010;31:2501–
2555.
5. Valente S, Lazzeri C, Vecchio S, Giglioli C, Margheri M, Bernardo P,
Comeglio M, Chiocchini S, Gensini GF. Predictors of in-hospital
mortality after percutaneous coronary intervention for cardiogenic
shock. Int J Cardiol 2007;114:176 –182.
6. Lazzeri C, Sori A, Chiostri M, Gensini GF, Valente S. Prognostic role
of insulin resistance as assessed by homeostatic model assessment
index in the acute phase of myocardial infarction in nondiabetic pa-
tients submitted to percutaneous coronary intervention. Eur J Anaes-
thesiol 2009;26:856 – 862.
7. Valente S, Lazzeri C, Chiostri M, Giglioli C, Zucchini M, Grossi F,
Gensini GF. Gender-related difference in ST-elevation myocardial
infarction treated with primary angioplasty: a single-centre 6-year
registry. Eur J Prev Cardiol 2012;19:233–240.
8. Valente S, Lazzeri C, Chiostri M, Sori A, Giglioli C, Salvadori C,
Gensini GF. Time of onset and outcome of cardiogenic shock in acute
coronary syndromes. J Cardiovasc Med (Hagerstown) 2008;9:1235–
1240.
9. Kushner FG, Hand M, Smith SC Jr, King SB III, Anderson JL,
Antman EM, Bailey SR, Bates ER, Blankenship JC, Casey DE Jr,
Green LA, Hochman JS, Jacobs AK, Krumholz HM, Morrison DA,
Ornato JP, Pearle DL, Peterson ED, Sloan MA, Whitlow PL,
Williams DO. 2009 focused updates: ACC/AHA guidelines for the
management of patients with ST elevation myocardial infarction
(updating the 2004 guideline and 2007 focused update) and ACC/
AHA/SCAI guidelines on percutaneous coronary intervention (up-
dating the 2005 guideline and 2007 focused update) a report of the
American College of Cardiology Foundation/American Heart As-
sociation Task Force on Practice Guidelines. J Am Coll Cardiol
2009;54:2205–2241.
10. Lazzeri C, Valente S, Chiostri M, Picariello C, Attanà P, Gensini GF.
The prognostic impact of glycated hemoglobin in diabetic ST-eleva-
tion myocardial infarction. Int J Cardiol 2011;151:250 –252.
11. Lazzeri C, Valente S, Chiostri M, Sori A, Bernardo P, Gensini GF.
Uric acid in the acute phase of ST elevation myocardial infarction
submitted to primary PCI: its prognostic role and relation with inflam-
1424 The American Journal of Cardiology (www.ajconline.org)
matory markers: a single center experience. Intern Emerg Med 2012;
7:33–39.
12. Valente S, Lazzeri C, Chiostri M, Giglioli C, Sori A, Tigli S, Gensini
GF. NT-proBNP on admission for early risk stratification in STEMI
patients submitted to PCI. Relation with extension of STEMI and
inflammatory markers. Int J Cardiol 2009;132:84 – 89.
13. Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF III, Feld-
man HI, Kusek JW, Eggers P, Van Lente F, Greene T, Coresh J;
CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration). A
new equation to estimate glomerular filtration rate. Ann Intern Med
2009;150:604 – 612.
14. Lazzeri C, Valente S, Chiostri M, Picariello C, Gensini GF. Cor-
relates of acute insulin resistance in the early phase of non-diabetic
ST-elevation myocardial infarction. Diab Vasc Dis Res 2011;8:
35– 42.
15. Lazzeri C, Valente S, Chiostri M, Picariello C, Gensini GF. Acute
glucose dysmetabolism in the early phase of ST-elevation myocardial
infarction: the age response. Diab Vasc Dis Res 2010;7:131–137.
16. Flear CT, Hilton P. Hyponatremia and severity and outcome of myo-
cardial infarction. BMJ 1979;1:1242–1246.
17. Tang Q, Hua Q. Relationship between hyponatremia and in-hospital
outcomes in Chinese patients with ST-elevation myocardial infarction.
Intern Med 2011;50:969 –974.
18. Havránek Š, Bělohlávek J, Škulec R, Kovárník T, Dytrych V, Linhart
A. Long-term prognostic impact of hyponatremia in the ST-elevation
myocardial infarction. Scand J Clin Lab Invest 2011;71:38 – 44.