Long-Term Prognostic Value of Mitral Regurgitation in Patients With

ST-Segment Elevation Myocardial Infarction Treated by Primary

Percutaneous Coronary Intervention
Manuel López-Pérez, MDa, Rodrigo Estévez-Loureiro, PhDa,b,*, Ángela López-Sainz, MDa,
David Couto-Mallón, MDa, María Rita Soler-Martin, PhDa, Alberto Bouzas-Mosquera, PhDa,
Jesús Peteiro, PhDa, Gonzalo Barge-Caballero, MDa, Oscar Prada-Delgado, MDa,
Eduardo Barge-Caballero, PhDa, Jorge Salgado-Fernández, MDa, Ramón Calviño-Santos, MDa,
José Manuel Vázquez-Rodríguez, PhDa, Pablo Piñón-Esteban, MDa, Guillermo Aldama-López, MDa,
Nicolás Vázquez-González, MDa, and Alfonso Castro-Beiras, PhDa

The presence of mitral regurgitation (MR) is associated with an impaired prognosis in

patients with ischemic heart disease. However, data with regard to the impact of this
condition in patients with ST-segment elevation myocardial infarction (STEMI) treated by
means of primary percutaneous coronary intervention (PPCI) are lacking. Our aim was to
assess the effect of MR in the long-term prognosis of patients with STEMI after PPCI. We
analyzed a prospective registry of 1,868 patients (mean age 62 – 13 years, 79.9% men) with
STEMI treated by PPCI in our center from January 2006 to December 2010. Our primary
outcome was the composite end point of all-cause mortality or admission due to heart
failure during follow-up. After exclusions, 1,036 patients remained for the final analysis.
Moderate or severe MR was detected in 119 patients (11.5%). Those with more severe MR
were more frequently women (p <0.001), older (p <0.001), and with lower ejection fraction
(p <0.001). After a median follow-up of 2.8 years (1.7 to 4.3), a total of 139 patients (13.4%)
experienced our primary end point. There was an association between the unfavorable
combined event and the degree of MR (p <0.001). After adjustment for relevant con-
founders, moderate or severe MR remained as an independent predictor of the combined
primary end point (adjusted hazard ratio [HR] 3.14, 95% confidence interval [CI] 1.57 to
6.27) and each event separately (adjusted HR death 3.1, 95% CI 1.34 to 7.2; adjusted HR
heart failure 3.3, 95% CI 1.16 to 9.4). In conclusion, moderate or severe MR detected early
with echocardiography was independently associated with a worse long-term prognosis in
patients with STEMI treated with PPCI. Ó 2014 Elsevier Inc. All rights reserved. (Am J
Cardiol 2014;113:907e912)

It has been consistently proved that mitral regurgitation
(MR) after myocardial infarction (MI) conveys a poorer
prognosis, and the presence of MR has been linked to an
increased risk of death and heart failure (HF).1e9 However,
information regarding the role of MR in prognosis of pa-
tients with ST-segment elevation myocardial infarction
(STEMI) treated by means of primary percutaneous coro-
nary intervention (PPCI) remains scarce. PPCI is currently
the preferred reperfusion strategy in patients with STEMI10
and it has shown an impact on the severity of ischemic
MR.11,12 The presence of acute ischemic MR is a severe
complication associated with increased in-hospital mortal-
ity.13 However, consistent data addressing the influence of
MR among survivors of a reperfused STEMI are lacking
and those published present conflicting outcomes.14,15 The
purpose of our study was to investigate the effect of residual
MR in the long-term prognosis of patients with STEMI
treated by PPCI.

a
Cardiology Department, Complejo Hospitalario Universitario A
Coruña, A Coruña, Spain and bInterventional Cardiology Unit, Division of
Cardiology, Complejo Asistencial Universitario de León, Fundación
Investigación Sanitaria de León (FISLeon), León, Spain. Manuscript
received October 17, 2013; revised manuscript received and accepted
November 23, 2013.
This work was supported by a grant from the Spanish Cardiovascular
Network RECAVA, Instituto de Salud Carlos III, Ministerio de Ciencia e
Innovación (Madrid, Spain).
See page 911 for disclosure information.
*Corresponding author: Tel: (þ34) 987237400; fax: (þ34) 987233322.
E-mail address: roiestevez@hotmail.com (R. Estévez-Loureiro).
Methods
The study cohort consisted of patients with STEMI. The
Galician Health Service has developed an active program to
offer PPCI to the majority of the population: the PROgrama
GALlego de atencion al Infarto Agudo de Miocardio
(PROGALIAM). Details of this program have been
described previously.16e19 All patients presenting with
typical chest pain lasting at least 30 minutes with ST-
segment elevation
1 mm in
2 contiguous leads (or
reciprocal ST depression
1 mm in leads V1 or V2) or left
bundle branch block within the first 12 hours after the
beginning of symptoms were eligible for PPCI. Baseline

0002-9149/14/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. www.ajconline.org
http://dx.doi.org/10.1016/j.amjcard.2013.11.050
908 The American Journal of Cardiology (www.ajconline.org)

Table 1 severe MRs were analyzed altogether, following previously

Clinical characteristics by mitral regurgitation (MR) severity published studies.1,6
Variable MR The study end point was a composite of all-cause mor-
tality after hospital discharge and development of new-onset
No (n ¼ 462) Mild Moderate or p Value
HF during follow-up. Mortality was defined as death by any
(n ¼ 455) Severe (n ¼ 119)
cause and was obtained from hospital records. CV mortality
Age (yrs) 59  13 63  13 69  11 <0.001 was collected as well and defined as mortality related with a
Women 69 (15) 105 (23) 34 (29) <0.001 precise CV cause (infarct, arrhythmia, cardiogenic shock, or
Hypertension 187 (40) 220 (48) 63 (53) 0.006 end-stage HF). HF was considered as readmission to the
Diabetes mellitus 57 (12) 89 (20) 26 (22) 0.002 hospital for management of HF, using for the diagnosis the
Current smokers 231 (50) 162 (36) 18 (15) <0.001 current guidelines.21 Data were identified using medical
Dyslipidemia 175 (38) 187 (41) 48 (40) 0.30
records and discharge summaries.
Cardiac arrest 7 (2) 5 (1) 1 (1) 0.42
Killip III and IV 9 (2) 19 (4) 12 (8) 0.003
Results as presented as mean  SD for continuous nor-
MI location mally distributed variables, as median (interquartile range)
Anterior 198 (43) 198 (44) 52 (44) 0.50 for continuous nonnormally distributed data, and as per-
Inferior 229 (50) 231 (51) 58 (49) 0.47 centages for categorical variables. Analysis of normality
Previous MI 34 (7) 34 (8) 8 (7) 0.51 was performed with the Kolmogorov-Smirnov and Shapiro-
PreCABG 7 (2) 3 (1) 3 (3) 0.09 Wilk tests. Characteristics were compared across groups
Stroke or TIA 10 (2) 16 (4) 4 (3) 0.21 with chi-square test or Fisher’s exact test, as required, for
Number of vessels 0.02 categorical variables and analysis of variance or Kruskal-
1-Vessel disease 243 (53) 227 (50) 47 (40) Wallis nonparametric test for continuous variables. Survival
2-Vessel disease 123 (27) 131 (29) 41 (35)
curves were constructed using the Kaplan-Meier method
3-Vessel disease 67 (29) 84 (19) 25 (21)
TIMI 3 after PPCI 266 (92) 246 (90) 62 (88) 0.396
and compared by the log-rank test. Cox proportional hazard
modeling was used to determine the risk of death or HF
Data are expressed as mean  SD for normally distributed data or according to the different degrees of MR. A model adjusted
number (%) for categorical variables. by age, gender, left ventricular ejection fraction, multivessel
Hypertension: serial blood pressure measurements >140/90 mm Hg or coronary disease, final Thrombolysis In Myocardial Infarc-
the use of antihypertensive therapy. Dyslipemia: low-density lipoprotein tion flow in the responsible artery, Killip class at admission,
cholesterol
130 mg/dl, total cholesterol
200 mg/dl, or the use of statin
anterior infarct, previous MI, previous coronary artery
treatment.
PreCABG ¼ previous coronary artery bypass graft; TIA ¼ transient
bypass grafting, and diabetes was used to address the effect
ischemic attack; TIMI ¼ Thrombolysis In Myocardial Infarction. of MR degrees on our primary end point. To better depict
the effect of the MR degrees on clinical events, a Cox
regression analysis using moderate and severe MR as indi-
characteristics including cardiovascular (CV) risk factors, vidual degrees and comparing them with no or mild MR was
medical history, or the use of CV drugs were recorded from carried out as well. p Values <0.05 were considered sig-
the patient directly or from the medical records if necessary. nificant. All analyses were performed with SPSS 20.0 sta-
Patients who died during their index hospitalization, tistical package for Windows (SPSS 20.0, Chicago, Illinois).
those who presented with mechanical complications, other
severe valvulopathy, or those with organic MR (defined as
Results
an intrinsic valve disease including severe calcified mitral
valve, primary leaflet or chordal pathology, endocarditis, or From January 2006 to December 2010, a total of 1,868
chronic rheumatic disease) were excluded from the study consecutive patients with STEMI were treated by PPCI at
protocol. The study was designed and performed in accor- the Complejo Hospitalario Universitario A Coruña, of
dance with the regulations of the institutional ethical com- whom 1,069 had an echocardiogram performed before
mittee. All patients gave written informed consent. discharge, available for analysis. Forty-three patients were
All patients with STEMI during the study period underwent also excluded because of in-hospital death, 27 because of
a transthoracic echocardiogram before hospital discharge. organic MR, and 7 because of mechanical complication or
Echocardiograms were performed and analyzed by expert other severe valvulopathy. After exclusions, the study
echocardiographic cardiologists in our hospital (the interven- population comprised 1,036 patients. The median time be-
tional hospital) and in the other 3 nonepercutaneous coronary tween PPCI and the echocardiography was 4 days (inter-
intervention centers of our region. The images were digitally quartile range 2 to 6). No trace of MR was detected in 462
recorded for off-line analysis in Xcelera workstation (Philips patients (44.6%), mild degree of MR was present in 455
Medical Systems, Amsterdam, The Netherlands). Data were patients (43.9%), and moderate or severe MR in 119 pa-
used unaltered from the original echocardiographic report tients (11.5%; moderate MR 90 patients [8.7%] and severe
without knowledge of patients’ outcomes. The severity of MR MR 29 patients [2.8%]).
was assessed during routine clinical interpretation according to Baseline clinical and demographic characteristics, strati-
current guidelines.20 For this purpose, color flow Doppler was fied by the severity of MR, are listed in Table 1. Patients
used as initial evaluation, adding supportive signs and quan- with greater degrees of MR were more likely to be older,
titative parameters. The MR was classified into 4 strata as none women, and to show history of diabetes, hypertension, and
(grade 0), mild (grade 1þ), moderate (grade 2þ to 3þ), and smoking habit. They presented also with higher Killip class
severe (grade 4þ). For the study purposes, moderate and and more frequent multivessel coronary artery disease. The
 Coronary Artery Disease/Mitral Regurgitation and Prognosis After STEMI 909

Table 2
Echocardiographic characteristics by mitral regurgitation (MR) severity
Variable MR

No (n ¼ 462) Mild (n ¼ 455) Moderate or Severe (n ¼ 119) p Value

Left ventricular ejection fraction (%) 57  10 53  11 46  14 <0.001

Left ventricular end-diastolic diameter (cm) 4.8  0.6 4.9  0.6 5.2  0.8 <0.001
Left ventricular end-systolic diameter (cm) 3.2  0.6 3.4  0.7 3.8  1.0 <0.001
E Doppler mitral/E0 tissue Doppler mitral 8.4  3.3 11.5  5.5 13.6  6.9 0.006

Data are expressed as mean  SD.

Figure 1. Cox analysis survival curves (adjusted by covariates) depicting the role of MR in the primary end point. (A) Effect of moderate or severe MR on
survival free of death or admission due to HF. (B) Contribution of moderate and severe MR in the occurrence of the primary outcome. Note that even moderate
MR is independently related to worse outcome on follow-up.

rest of the baseline characteristics were balanced between
groups.
With regard to echocardiographic data, patients with
increasing degree of MR presented with significantly lower
left ventricular ejection fraction, higher left ventricular di-
ameters, and E/E0 ratio (Table 2).
During a median follow-up of 2.8 years (range 1.7 to 4.3),
the primary event occurred in 139 patients (13.4%; 79 pa-
tients during in this time, of which CV cause was diagnosed
in 50 of them, and 60 patients needed to be readmitted due to
HF). The risk of developing the primary end point was higher
in patients with moderate or severe MR compared with those
with mild or no MR (34.5% vs 14.1% vs 7.4%; p <0.001).
Kaplan-Meier analysis showed an association between the
unfavorable combined event and the degree of MR. In fact,
the survival free of death or HF at median follow-up for
patients with no MR, mild MR, and moderate or severe MR
were 95%, 90%, and 70%, respectively (p value <0.001).
After adjustment for relevant confounders, moderate or
severe MR remained as an independent predictor of death or
HF (hazard ratio [HR] 3.14, 95% confidence interval [CI]
1.57 to 6.27, p ¼ 0.001; Figure 1). In addition to MR, other
independent factors of the combined outcome were age, fe-
male gender, left ventricular ejection fraction, previous MI,
previous coronary artery bypass grafting, and Killip class III
or IV at admission (Table 3). When analyzing separately each
end point of the combined event, the same Cox proportional
hazard model showed that moderate or severe MR was a
significant predictor of mortality (HR 3.11, 95% CI 1.34 to
7.2, p ¼ 0.008) and readmission for the treatment of HF (HR
3.3, 95% CI 1.16 to 9.42, p ¼ 0.026; Figure 2). Similar results
were obtained when CV mortality was studied. Thereby
higher degrees of MR persisted as an independent predictor
of the CV combined end point (HR 3.83, 95% CI 1.66 to 8.8,
p ¼ 0.002) and CV mortality (HR 6.06, 95% CI 1.59 to
23.08, p ¼ 0.008) in the multivariable analysis.
Likewise, when the degrees of MR were split into none,
mild, moderate, and severe, the moderate MR by itself
proved to be an independent predictor of the combined
adverse outcome in the multivariable model (HR 2.56, 95%
CI 1.2 to 5.44, p ¼ 0.015) as well as severe MR (HR 5.68,
95% CI 2.21 to 14.57, p <0.001; Figure 1). Also, moderate
MR alone was independently related with CV death (HR
4.49, 95% CI 1.1 to 18.38, p ¼ 0.037). The relation between
the categories of MR and the individual components of the
primary outcome are shown in Figure 2.
Discussion
To our knowledge, the present study comprises the
largest series analyzed to determine the role of MR detected
by echocardiogram during the index hospitalization in the
910 The American Journal of Cardiology (www.ajconline.org)

Table 3 HF. Even moderate degrees of MR seem to impair the

Independent predictors of combined event of death or heart failure in natural history of this subgroup of patients.
patients with ST-segment elevation myocardial infarction treated with Data regarding the prevalence of MR in patients suffering
primary percutaneous coronary intervention
from ischemic heart disease are controversial because the
Variable HR 95% CI p Value method of quantification and the timing of MR evaluation
are different across literature. Furthermore, in most of these
MR
Mild 1.11 0.57e2.18 0.75
studies, patients with STEMI are not included or are under-
Moderate or severe 3.14 1.57e6.27 0.001 represented. Earlier angiographic studies showed MR in 13%
Age 1.04 1.02e1.06 0.001 to 18% patients within the first 12 hours after MI5,14 and
Female sex 1.96 1.14e3.38 0.02 Lamas et al4 reported a prevalence of 19% within the 16 days
Left ventricular 0.93 0.91e0.95 <0.001 after MI. However, the latest echocardiographic series
ejection fraction founded a much greater prevalence. This might be related to
Previous MI 2.49 1.23e5.03 0.01 an increased sensitivity of the technique to detect MR. Bursi
Previous CABG 3.44 1.01e11.7 0.048 et al1 observed ischemic MR in 50% of patients within
Killip class III and IV 3.08 1.4e6.81 0.006 30 days after MI, whereas other authors evidenced a preva-
CABG ¼ coronary artery bypass graft. lence of up to 57% during the index hospitalization.2,3,15 In

Figure 2. Cox regression survival curves of the effect of MR on the single components of primary outcome. (A and C) Effect of moderate or severe MR on the
occurrence of the events death or admission due to HF. (B and D) Contribution of moderate and severe MR in the isolated components of the primary outcome.

long-term prognosis of patients with STEMI treated with our study, any degree of MR was detected in 55% of patients,
PPCI. Our data suggest that moderate or severe MR is an which is consistent with the latest publications, and reflects
independent predictor of all-cause mortality, CV death, and the magnitude of this entity in patients with STEMI.
 Coronary Artery Disease/Mitral Regurgitation and Prognosis After STEMI
The role of MR in the prognosis of patients with
ischemic heart disease has been previously addressed. It has
been shown that MR is an independent risk factor of
adverse outcome in a postepercutaneous coronary inter-
vention population,9 in those undergoing coronary artery
bypass grafting,22 and in patients who have experienced an
MI.1e8 However, the group of patients with STEMI has
been poorly represented in these studies making it difficult
to extrapolate these results to this specific population.
Previous reports of the role of MR after STEMI have shown
conflicting results. In a subanalysis of the Controlled
Abciximab and Device Investigation to Lower Late An-
gioplasty Complications trial, Pellizzon et al14 reported that
any degree of MR, detected on the left ventriculogram
during the PPCI, is an independent predictor of 1-year
mortality. This finding may be related to a lower sensitivity
for detecting mitral insufficiency, selecting thus, more se-
vere cases with poorer outcome. However, more recently
Uddin and coworkers15 showed no relation between MR
and death after adjustment by multiple confounders. In the
latter trial, the echocardiogram was the technique used to
assess the presence of MR. Our study sheds light into this
poorly depicted field by demonstrating that MR is a com-
mon finding after STEMI and is independently linked to
long-term mortality and HF.
The relation between MR and CV outcome may offer
several explanations. First, as it can be derived from the
analysis, those patients with more severe degrees of MR had
lower ejection fraction, higher filling pressures, and were
more frequently women. In this sense, MR could be
considered a marker of greater myocardial damage or a
condition associated with a specific risk population.23 On
the other hand, the presence of MR may be directly related
to ventricular remodeling with chronic volume overload,
progressive deterioration of myocardial function, and
appearance of adverse events. In this sense, the fact that
moderate MR is linked to an impaired outcome supports this
hypothesis.
Taking into account our results, those patients who
develop at least moderate MR after STEMI should be
monitored closely and they may require specific treatments
for MR. Several strategies can be applied to this entity.
Medical treatments such as angiotensin-converting enzyme
inhibitors or b blockers are widely used in the ischemic
heart disease to prevent remodeling process; however, their
role as a specific treatment for MR is limited.4,24 Likewise,
PPCI itself has proved to reduce the degree of acute
ischemic MR in selected cases,11,12 although it is unknown
whether it plays a role in the long term. Surgical treatment of
secondary MR is still a matter of debate because it has
yielded conflicting results. This is because of the lack of
clear survival benefit and the high recurrence rate of sig-
nificant MR 1 year after surgery, even with modern annu-
loplasty techniques.25e27 Novel strategies such as cardiac
resynchronization, which significantly reduced MR due to
reverse left ventricular remodeling,28 or percutaneous edge-
to-edge mitral valve repair29,30 may impact the prognosis in
this pathology. Therefore, it seems that the optimal treat-
ment for this specific high-risk group of patients is still
debatable and new studies will be necessary to clarify this
issue.
911
Several limitations should be considered regarding our
research. First, we used semiquantitative evaluation of MR in
most of our patients reflecting “real-world” experience in a
routine examination, which may result in misclassification.
In any case, this trouble would only bias our results to an
underestimation of the true effect of MR on prognosis. Sec-
ond, the MR quantification was performed during the index
hospitalization in the early postinfarction period. There are
no complete data concerning the follow-up, so the long-term
changes of the ischemic MR severity and how this can affect
the prognosis are not known. Hence, this study could not
determine the real natural history of ischemic MR in patients
with STEMI as a dynamic lesion closely related with the
ventricular remodeling timing. Further research with an
extensive follow-up will clarify this question. Third, the
possibility that MR was present before the STEMI cannot be
excluded, even if patients with organic MR are excluded.
Accordingly, some results may be not related with the
ischemic event.
Disclosures
Dr. Rodrigo Estévez-Loureiro has been awarded the “Rio
Hortega” research grant from the Ministry of Science and
Innovation, Instituto de Salud Carlos III, Madrid, Spain. The
other authors have no conflicts of interest to disclose.
1. Bursi F, Enriquez-Sarano M, Nkomo VT, Jacobsen SJ, Weston SA,
Meverden RA, Roger VL. Heart failure and death after myocardial
infarction in the community: the emerging role of mitral regurgitation.
Circulation 2005;111:295e301.
2. Hillis GS, Moller JE, Pellikka PA, Bell MR, Casaclang-Verzosa GC,
Oh JK. Prognostic significance of echocardiographically defined mitral
regurgitation early after acute myocardial infarction. Am Heart J
2005;150:1268e1275.
3. Aronson D, Goldsher N, Zukermann R, Kapeliovich M, Lessick J,
Mutlak D, Dabbah S, Markiewicz W, Beyar R, Hammerman H, Reisner
S, Agmon Y. Ischemic mitral regurgitation and risk of heart failure after
myocardial infarction. Arch Intern Med 2006;166:2362e2368.
4. Lamas GA, Mitchell F, Flaker GC, Smith SC, Gersh BJ, Basta L, Moye
L, Braunwald E, Pfeffer MA. Clinical significance of mitral regurgi-
tation after acute myocardial infarction. Survival and Ventricular
Enlargement Investigators. Circulation 1997;96:827e833.
5. Lehmann KG, Francis CK, Dodge HT. Mitral regurgitation in early
myocardial infarction. Incidence, clinical detection, and prognostic
implications. TIMI Study Group. Ann Intern Med 1992;117:10e17.
6. Grigioni F, Enriquez-Sarano M, Zehr KJ, Bailey KR, Tajik AJ.
Ischemic mitral regurgitation: long-term outcome and prognostic im-
plications with quantitative Doppler assessment. Circulation 2001;103:
1759e1764.
7. Barzilai B, Davis VG, Stone PH, Jaffe AS. Prognostic significance of
mitral regurgitation in acute myocardial infarction. The MILIS Study
Group. Am J Cardiol 1990;65:1169e1175.
8. Feinberg MS, Schwammentha El, Shlizerman L, Porter A, Hod H,
Friemark D, Matezky S, Boyko V, Mandelzweig L, Vered Z, Behar S,
Sagie A. Prognostic significance of mild mitral regurgitation by color
Doppler echocardiography in acute myocardial infarction. Am J Car-
diol 2000;86:903e907.
9. Pastorius CA, Henry TD, Harris KM. Long-term outcomes of patients
with mitral regurgitation undergoing percutaneous coronary interven-
tion. Am J Cardiol 2007;100:1218e1223.
10. Van de Werf F, Bax J, Betriu A, Blomstrom-Lundqvist C, Crea F, Falk
V, Filippatos G, Fox K, Huber K, Kastrati A, Rosengren A, Steg PG,
Tubaro M, Verheugt F, Weidinger F, Weis M. Management of acute
myocardial infarction in patients presenting with persistent ST-segment
elevation: the Task Force on the Management of ST-Segment Elevation
Acute Myocardial Infarction of the European Society of Cardiology.
Eur Heart J 2008;29:2909e2945.
912 The American Journal of Cardiology (www.ajconline.org)
11. Heuser RR, Maddoux GL, Goss JE, Ramo BW, Raff GL, Shadoff N.
Coronary angioplasty for acute mitral regurgitation due to myocardial
infarction. A nonsurgical treatment preserving mitral valve integrity.
Ann Intern Med 1987;107:852e855.
12. Shawl FA, Forman MB, Punja S, Goldbaum TS. Emergent coronary
angioplasty in the treatment of acute ischemic mitral regurgitation:
long-term results in five cases. J Am Coll Cardiol 1989;14:986e991.
13. Thompson CR, Buller E, Sleeper LA, Antonelli TA, Webb JG, Jaber
WA, Abel JG, Hochman JS. Cardiogenic shock due to acute severe
mitral regurgitation complicating acute myocardial infarction: a report
from the SHOCK Trial Registry. SHould we use emergently revascu-
larize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol
2000;36:1104e1109.
14. Pellizzon GG, Grines CL, Cox DA, Stuckey T, Tcheng JE, Garcia E,
Guagliumi G, Turco M, Lansky AJ, Griffin JJ, Cohen DJ, Aymong E,
Mehran R, O’Neill WW, Stone GW. Importance of mitral regurgitation
inpatients undergoing percutaneous coronary intervention for acute
myocardial infarction: the Controlled Abciximab and Device Investi-
gation to Lower Late Angioplasty Complications (CADILLAC) trial.
J Am Coll Cardiol 2004;43:1368e1374.
15. Uddin AM, Henry TD, Hodges JS, Haq Z, Pedersen WR, Harris KM.
The prognostic role of mitral regurgitation after primary percutaneous
coronary intervention for acute ST-elevation myocardial infarction.
Catheter Cardiovasc Interv 2012;80:779e786.
16. Estevez-Loureiro R, Calvino-Santos R, Vazquez JM, Barge-Caballero
E, Salgado-Fernandez J, Pineiro M, Freire-Tellado M, Varela-Portas J,
Martinez L, Gomez S, Rodriguez JA, Vazquez N, Castro-Beiras A.
Safety and feasibility of returning patients early to their originating
centers after transfer for primary percutaneous coronary intervention.
Rev Esp Cardiol 2009;62:1356e1364.
17. Estevez-Loureiro R, Calvino-Santos R, Vazquez-Rodriguez JM, Marzoa-
Rivas R, Barge-Caballero E, Salgado-Fernandez J, Aldama-Lopez G,
Barreiro-Diaz M, Varela-Portas J, Freire-Tellado M, Vazquez-Gonzalez N,
Castro-Beiras A. Direct transfer of ST-elevation myocardial infarction
patients for primary percutaneous coronary intervention from short
and long transfer distances decreases temporal delays and improves short-
term prognosis: the PROGALIAM Registry. Euro Intervention 2010;6:
343e349.
18. Barge-Caballero E, Vazquez-Rodriguez JM, Estevez-Loureiro R,
Barge-Caballero G, Rodriguez-Vilela A, Calvino-Santos R, Salgado-
Fernandez J, Aldama-Lopez G, Pinon-Esteban P, Campo-Perez R,
Rodriguez-Fernandez JA, Vazquez-Gonzalez N, Muniz-Garcia J,
Castro-Beiras A. Prevalence, etiology and outcome of catheterization
laboratory false alarms in patients with suspected ST-elevation
myocardial infarction. Rev Esp Cardiol 2010;63:518e527.
19. Prada-Delgado O, Estevez-Loureiro R, Calvino-Santos R, Barge-Ca-
ballero E, Salgado-Fernandez J, Pinon-Esteban P, Vazquez-Rodriguez
JM, Aldama-Lopez G, Flores-Rios X, Soler-Martin MR, Vazquez-
Gonzalez N, Castro-Beiras A. Safety and efficacy of femoral vascular
closure devices in patients undergoing primary percutaneous coronary
intervention for ST-elevation myocardial infarction. Am Heart J
2011;161:1207e1213.
20. Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD,
Levine RA, Nihoyannopoulos P, Otto CM, Quinones MA, Rakowski
H, Stewart WJ, Waggoner A, Weissman NJ. Recommendations for
evaluation of the severity of native valvular regurgitation with two-
dimensional and Doppler echocardiography. J Am Soc Echocardiogr
2003;16:777e802.
21. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats
TG, Jessup M, Konstam MA, Mancini DM, Michl K, Oates JA, Rahko
PS, Silver MA, Stevenson LW, Yancy CW, Antman EM, Smith SC,
Adams CD, Anderson JL, Faxon DP, Fuster V, Halperin JL, Hiratzka
LF, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B. ACC/
AHA 2005 guideline update for the diagnosis and management of
chronic heart failure in the adult: a report of the American College of
Cardiology/American Heart Association Task Force on Practice
Guidelines (Writing Committee to Update the 2001 Guidelines for the
Evaluation and Management of Heart Failure): developed in collabo-
ration with the American College of Chest Physicians and the Inter-
national Society for Heart and Lung Transplantation: endorsed by the
Heart Rhythm Society. Circulation 2005;112:e154ee235.
22. Trichon BH, Glower DD, Shaw LK, Cabell CH, Anstrom KJ, Felker
GM, O’Connor CM. Survival after coronary revascularization, with
and without mitral valve surgery, in patients with ischemic mitral
regurgitation. Circulation 2003;108(Suppl 1):II103eII110.
23. Benamer H, Tafflet M, Bataille S, Escolano S, Livarek B, Fourchard V,
Caussin C, Teiger E, Garot P, Lambert Y, Jouven X, Spaulding C.
Female gender is an independent predictor of in-hospital mortality after
STEMI in the era of primary PCI: insights from the greater Paris area
PCI Registry. Euro Intervention 2011;6:1073e1079.
24. Levine RA, Schwammenthal E. Ischemic mitral regurgitation on the
threshold of a solution: from paradoxes to unifying concepts. Circu-
lation 2005;112:745e758.
25. Wu AH, Aaronson KD, Bolling SF, Pagani FD, Welch K, Koelling
TM. Impact of mitral valve annuloplasty on mortality risk in patients
with mitral regurgitation and left ventricular systolic dysfunction. J Am
Coll Cardiol 2005;45:381e387.
26. Hung J, Papakostas L, Tahta SA, Hardy BG, Bollen BA, Duran CM,
Levine RA. Mechanism of recurrent ischemic mitral regurgitation after
annuloplasty: continued LV remodeling as a moving target. Circulation
2004;110:II85eII90.
27. McGee EC, Gillinov AM, Blackstone EH, Rajeswaran J, Cohen G,
Najam F, Shiota T, Sabik JF, Lytle BW, McCarthy PM, Cosgrove DM.
Recurrent mitral regurgitation after annuloplasty for functional
ischemic mitral regurgitation. J Thorac Cardiovasc Surg 2004;128:
916e924.
28. Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E,
Kocovic DZ, Packer M, Clavell AL, Hayes DL, Ellestad M, Trupp RJ,
Underwood J, Pickering F, Truex C, McAtee P, Messenger J. Cardiac
resynchronization in chronic heart failure. N Engl J Med 2002;346:
1845e1853.
29. Franzen O, Baldus S, Rudolph V, Meyer S, Knap M, Koschyk D,
Treede H, Barmeyer A, Schofer J, Costard-Jackle A, Schluter M,
Reichenspurner H, Meinertz T. Acute outcomes of MitraClip therapy
for mitral regurgitation in high-surgical-risk patients: emphasis on
adverse valve morphology and severe left ventricular dysfunction. Eur
Heart J 2010;31:1373e1381.
30. Franzen O, van der Heyden J, Baldus S, Schluter M, Schillinger W,
Butter C, Hoffmann R, Corti R, Pedrazzini G, Swaans MJ, Neuss M,
Rudolph V, Surder D, Grunenfelder J, Eulenburg C, Reichenspurner H,
Meinertz T, Auricchio A. MitraClipÒ therapy in patients with end-
stage systolic heart failure. Eur J Heart Fail 2011;13:569e576.