Download The Potential Impact of Primary Percutaneous

The Potential Impact of Primary
Percutaneous Coronary Intervention on
Ventricular Septal Rupture Complicating
Acute Myocardial Infarction*
Hon-Kan Yip, MD; Chih-Yuan Fang, MD; Kuei-Ton Tsai, MD;
Hsueh-Wen Chang, PhD; Kuo-Ho Yeh MD; Morgan Fu, MD; and
Chiung-Jen Wu, MD
Background: Recent data suggest that the risk of acquired ventricular septal defect (VSD), a
complication of acute myocardial infarction (AMI), could be reduced using thrombolytic therapy.
There are, however, still no available data regarding the potential impact of primary percutaneous coronary intervention (PCI) on AMI-related VSD in a clinical setting. The purposes of this
study were to delineate the incidence and the potential risk factors of AMI-related VSD in the
Chinese population, and to determine whether primary PCI could reduce such risk.
Methods and results: From May 1993 through March 2003, a total of 1,321 patients with AMI (for
< 12 h) underwent primary PCI in our hospital. Of these 1,321 patients, 3 patients (0.23%)
developed VSD after undergoing a primary PCI, with a mean (ⴞ SD) time of occurrence of
25.3 ⴞ 12.2 h. During the same period, a total of 616 consecutive, unselected patients with early
AMI [ie, > 12 h and < 7 days] or recent myocardial infarction (MI) [ie, > 8 days and < 30 days]
who had not received thrombolytic therapy underwent elective PCI. Of these 616 patients, 18
(2.9%) had VSD either on presentation or during hospitalization, with a mean time of occurrence
of 71.1 ⴞ 64.2 h. Clinical variables were utilized to statistically analyze the potential risk factors.
Univariate analysis demonstrated that the enrollment variables strongly related to this complication were advanced age, hypertension, nonsmokers, anterior infarction, female gender, and
lower body mass index (BMI) [all p < 0.005]. Using multiple stepwise logistic regression analysis,
the only variables independently related to VSD were advanced age, female gender, anterior
infarction, and low BMI (all p < 0.05). The in-hospital mortality rate was significantly higher in
patients with this complication than in patients without this complication (47.6% vs 8.0%;
p < 0.0001). The incidence of this complication was significantly lower in patients with AMI who
underwent primary PCI than in those with early or recent MI who underwent elective PCI (3.0%
vs 0.23%, respectively; p ⴝ 0.0001).
Conclusion: Primary PCI had a striking impact on reducing the incidence of VSD after AMI
compared to elective PCI in patients who did not receive thrombolytic therapy. Advanced age,
female gender, anterior infarction, and low BMI had potentially increased the risk of this
catastrophic complication after AMI in this Chinese population.
(CHEST 2004; 125:1622–1628)
Key words: coronary angioplasty; myocardial infarction; ventricular septal rupture
Abbreviations: AMI ⫽ acute myocardial infarction; BMI ⫽ body mass index; GUSTO ⫽ Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries; MI ⫽ myocardial infarction;
PCI ⫽ percutaneous coronary intervention; TIMI ⫽ thrombolyis in myocardial infarction; VSD ⫽ ventricular septal
defect
hile ventricular septal defect (VSD) is an unW common
mechanical complication after acute
myocardial infarction (AMI) and has a reported
incidence during the prethrombolytic era of 1 to
2%,1,2 it carries an extremely high mortality rate
either with or without surgical intervention.1–5 Pre-
*From the Divisions of Cardiology (Drs. Yip, Fang, Yeh, Fu, and
Wu) and Cardiovascular Surgery (Dr. Tsai), Chang Gung Memorial Hospital, Kaohsiung; and the Department of Biological
Sciences (Dr. Chang), National Sun Yat-Sen University, Kaohsiung,
Taiwan, ROC.
Manuscript received May 30, 2003; revision accepted November
6, 2003.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail:
[email protected]).
Correspondence to: Chiung-Jen Wu, MD, Division of Cardiology,
Department of Internal Medicine, Chang Gung Memorial Hospital,
Kaohsiung, 123 Ta Pei Rd, Niao Sung Hsiang, Kaohsiung Hsien,
83301, Taiwan, ROC; e-mail: [email protected]
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Clinical Investigations
vious studies2,6 – 8 have demonstrated that this complication typically occurs during the first week after
AMI, usually with a mean time of 3 to 5 days from
symptom onset. Investigators also have demonstrated that this complication occurs more often in
patients of advanced age,5 of female gender,1,5,9,10
with total occlusion of the infarct-related artery,5,10,11
and with absence of a previous MI.1,12 The impact of
thrombolytic therapy on AMI-related VSD had not
been well-established until recently from the Global
Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries
(GUSTO)-I trial.5 Their study5 demonstrated that
thrombolytic therapy provided the additional benefits of reduced risk of AMI-related VSD. Surprisingly, the effects of primary percutaneous coronary
intervention (PCI) on reducing the risk of AMIrelated VSD has not been well-established.
Therefore, we analyzed the pooled data and compared patients with AMI (ie, ⬍ 12 h) who were
undergoing primary PCI and patients with early
myocardial infarction (MI) [⬎ 12 h and ⱕ 7 days] or
recent MI (ⱖ 8 days and ⬍ 30 days) who had not
undergone thrombolytic therapy but were undergoing elective PCI in our hospital, in order to delineate
the baseline and clinical variables associated with this
complication In addition, we tried to identify the
prevalence of VSD after AMI in a Chinese popula-
tion. Finally, the aim of this study was to evaluate the
value of primary PCI in reducing the incidence of
this complication.
Materials and Methods
Patient Population
From May 1993 through March 2003, primary PCI was
performed in 1,321 consecutive and unselective patients of any
age who presented with AMI (ie, ⬍ 12 h). Of these 1,321
patients, 3 (0.23%) developed VSD after primary PCI. During
the same period, a total of 616 consecutive unselected patients
with early MI or recent MI who had not received thrombolytic
therapy underwent elective PCI. Of these 616 patients, 18 (2.9%)
were found to have VSD either on presentation or during
hospitalization. Figure 1 illustrates the excluded and eligible
patients for primary or elective PCI.
Procedure and Protocol
Before stents were available in our country, balloon angioplasty
was performed in these patients. However, after stents were
available in our country, stent implantation was strongly encouraged unless the infarct-related artery had heavy calcification, a
reference lumen diameter of ⬍ 2.5 mm, or a stent-like result at
the treatment site after balloon angioplasty. Left ventriculograms,
which were immediately performed after angioplasty, were recorded for 30° right anterior oblique and 60° left anterior oblique
views.
Echocardiography was routinely performed in each patient
Figure 1. Flow diagram illustrating the excluded patients and eligible patients undergoing PCI.
CABG ⫽ coronary artery bypass surgery; LM ⫽ left main coronary artery; tPA ⫽ tissue plasminogen
activator; * ⫽ PCI not performed; † ⫽ patients transferred to our hospital from other local hospitals
after receiving thrombolytic therapy.
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either before or after undergoing cardiac catheterization. However, echocardiography was performed before cardiac catheterization when the presence of a heart murmur (observed by
physical examination) complicating the MI was suggested.
The routine medical treatment of these patients was as follows.
First, the patient was pretreated with aspirin (324 mg) and was
given a bolus of 5,000 U heparin. This was followed by an IV
heparin drip, which was adjusted to keep the activated partial
thromboplastin time at 1.5 to 2 times the normal values. Before
angioplasty, an additional bolus of heparin was given to achieve
an activated clotting time of ⱖ 300 s. Tirofiban has been available
in our country since August 2000. Therefore, it was given to 406
patients in our study. Patients were treated with ticlopidine (250
mg bid) for at least 2 weeks if stent deployment was performed.
Aspirin (100 mg po daily) was administered indefinitely to each
patient. All other medications, nitrates, ␤-blockers, diuretics, and
angiotensin-converting enzyme inhibitors were used as needed in
the patients.
Results
Baseline Clinical Characteristics of the Patients
Relevant patient baseline characteristics are summarized in Table 1. There were no significant differences in terms of the presence of diabetes mellitus,
hypercholesterolemia, and previous MI between patients with and without VSD. However, patients with
VSD had significantly higher incidences of hypertension, and more of these patients were nonsmokers
than were patients without this complication. Furthermore, patients with VSD were significantly older
and thinner than patients without this complication.
Moreover, the incidence of occurrence in female
patients was significantly higher in patients with VSD
than in patients without it.
Definitions
AMI was defined as typical chest pain lasting for ⬎ 30 min with
ST-segment elevation of ⬎ 1 mm in two consecutive precordial
or inferior leads, or typical chest pain lasting for ⬎ 30 min with a
new onset of complete left bundle branch block. Early MI was
defined as an AMI that developed at ⬎ 12 h and ⱕ 7 days in a
patient with a history of typical chest pain (with or without an
elevation of creatine kinase levels and a creatine kinase-MB
fraction of ⬎ 4%), and series changes in ECGs followed by
echocardiographic and angiographic findings of regional hypokinesis of the left ventricle. Recent MI was defined as an AMI that
developed at ⱖ 8 days and ⬍ 30 days in patients with a history of
typical chest pain, and series changes in ECGs followed by
echocardiographic and angiographic findings of regional hypokinesis of the left ventricle.
Body mass index (BMI) was defined as the weight in kilograms
divided by the square of the height in meters (kg/m2). VSD was
first suggested by physical examination findings. It was subsequently confirmed using echocardiography, and by a significant
step-up of oxygen saturation between the right atrium and the
pulmonary artery using a Swan-Ganz catheter, left ventriculogram, and operative findings. When VSD was found on presentation, we tried to review the source in medical records. Multivessel coronary artery disease was defined by a stenosis of
⬎ 50% in two or more major epicardial coronary arteries.
Clinical and Angiographic Findings and
In-Hospital Mortality Rate
Relevant clinical and angiographic results and
in-hospital mortality are summarized in Table 2.
There were no significant differences in terms of
pre-TIMI flow grades, presence of multivessel disease, or intercoronary collaterals between patients
with and without VSD. However, the incidence of
the left anterior descending artery as an infarctrelated artery and the incidence of the total occlusion of the left anterior descending artery were
significantly higher in patients with VSD than in
patients without it. Furthermore, the incidences of
cardiogenic shock and mortality rate were significantly higher in patients with VSD than in patients
without it.
Operations were performed in the three patients
who underwent primary PCI and later developed
VSD. One patient died in the hospital due to multiorgan failure, and the other two patients were discharged from the hospital uneventfully and have
Data Collection
Detailed in-hospital and follow-up data, including age, sex,
coronary risk factors, present or absent congestive heart failure
on presentation, Killip score on hospital admission, reperfusion
time, preintervention and postintervention thrombolysis in myocardial infarction (TIMI) flow grades, angiographic results, number of diseased vessels, and number in-hospital adverse events,
were obtained. These data were collected prospectively and were
entered into a computerized database.
Statistical Analysis
Data were expressed as the mean ⫾ SD. Continuous variables
were compared using the Wilcoxon rank sum test. Categoric
variables were compared using the ␹2 test or Fisher exact test.
Stepwise logistic regression analysis was used to determine
independent determinants of VSD complicating AMI. Statistical
analysis was performed using a statistical software package (SAS
for Windows, version 8.2; SAS Institute; Cary, NC). A probability
value of ⬍ 0.05 was considered to be statistically significant.
Table 1—Baseline Characteristics of Patients With and
Without VSD*
Variables
Age, yr
Female sex
Hypertension
Diabetes mellitus
Smoking
Hypercholesterolemia
Anterior infarction
Previous myocardial
infarction
BMI, kg/m2
VSD
(n ⫽ 21)
No VSD
(n ⫽ 1,916)
p Value
74.1 ⫾ 5.4
76.2 (16)
81.0 (17)
28.6 (6)
9.5 (2)
38.1 (8)
85.7 (18)
9.5 (2)
61.5 ⫾ 11.7
17.1 (327)
48.6 (931)
28.0 (536)
56.8 (1089)
43.4 (832)
54.9 (1052)
9.6 (183)
⬍0.0001
⬍0.0001
0.003
0.93
⬍0.0001
0.99
0.004
0.99
21.9 ⫾ 3.3
25.6 ⫾ 4.1
⬍0.0001
*Values given as mean ⫾ SD or No. %, unless otherwise indicated.
(No. of patients).
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Clinical Investigations
Table 2—Clinical and Angiographic Findings, and InHospital Mortality in Patients With and Without VSD*
Variables
Pre-TIMI flow
ⱕ 1 flow
ⱖ 2 flow
Multivessel disease
LAD artery infarction
Total occlusion of LAD
artery
Collateral circulation
Cardiogenic shock
In-hospital mortality
VSD
(n ⫽ 21)
No VSD
(n ⫽ 1,916)
57.1 (12)
42.9 (9)
52.4 (11)
85.7 (18/21)
52.4 (11)
70.8 (1,356)
27.0 (518)
58.1 (1,114)
56.3 (1,079)
29.1 (558)
28.6 (6)
57.1 (12)
47.6 (10)
32.2 (616)
10.9 (209)
8.0 (153)
p Value
Primary PCI Elective PCI
p Value
In-hospital mortality
33.3 (1/3)
Timing of VSD occurrence 25.3 ⫾ 12.2
Incidence of VSD
0.23 (3/1321)
0.64
0.006
0.018
*Values given as mean ⫾ SD or % (No. of patients), unless otherwise
indicated.
0.75
⬍0.0001
⬍0.0001
survived to the present. Three of the 18 patients who
had early or recent MI complicated by VSD refused
operations and died in the hospital. The other 15
patients underwent the operation. Six of these 15
patients died in the hospital after their operation.
The other patients were discharged from the hospital
uneventfully. There was no statistically significant
difference in in-hospital mortality between patients
who had later VSD after primary PCI (33.3% [1 of 3
patients]) and patients with early or recent MI
complicated by VSD (50% [9 of 18 patients];
p ⫽ 1.0). However, patients who had received medical treatment had a statistical tendency for a significantly higher in-hospital mortality rate (100% [3 of 3
patients]) than did patients who had received surgical treatment (38.7% [7 of 18 patients]; p ⫽ 0.09).
50 (9/18)
1.0
71.1 ⫾ 64.2
0.06
2.9 (18/616) ⬍ 0.0001
Timing of Occurrence and Incidences of
Ventricular Septal Rupture Among Patients With
AMI, Early MI, or Recent MI
AMI-related VSD developed in patients who underwent primary PCI at a mean time of 25.3 ⫾ 12.2 h
(range, 12 to 36 h). On the other hand, VSD developed
in patients with early or recent MI who had not
received thrombolytic therapy, and they underwent
elective PCI at a mean time of 71.1 ⫾ 64.2 h (range,
12 h to 12 days). The timing of the occurrence of VSD
had a statistical tendency of significant shortening in
patients with AMI who underwent primary PCI than in
patients with early or recent MI who underwent elective PCI (p ⫽ 0.06). Univariate analysis demonstrated
that the incidence of VSD in patients with AMI who
underwent primary PCI was significantly lower (0.23%
[3 of 1,321 patients]) than that in patients with early or
recent MI who underwent elective PCI (2.9% [18 of
616 patients]; p ⬍ 0.0001).
Discussion
Independent Predictors of Ventricular Septal
Rupture
Independent determinants of VSD are summarized in Table 3. Multiple stepwise logistic regression
analysis of enrolled baseline and clinical variables
demonstrated that only advanced age, female gender, anterior infarction, and low BMI were significant independent predictors of VSD after MI.
Table 3—Multiple Stepwise Logistic Regression
Analysis of Independent Predictors of VSD*
Variables
OR
95% CI
p Value
Advanced age
Female sex
Infarct location (anterior vs
nonanterior)
BMI
1.11
7.41
4.35
1.05–1.18
2.55–21.53
1.21–14.3
0.0005
⬍0.0001
0.016
1.30
1.12–1.52
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Variables
0.20
*Values given as mean ⫾ SD or % (No. of patients), unless otherwise
indicated. LAD ⫽ left anterior descending.
*CI ⫽ confidence interval; OR ⫽ odds ratio.
Table 4 —Comparison of Impact of Primary PCI vs
Elective PCI on Mortality, Timing of Occurrence, and
Incidence of VSD in Patients With MI*
0.0004
Potential Impact of Primary PCI on AMI
Complicated by Ventricular Septal Rupture
In the present study, one of the important findings
was that, when compared with those patients who
did not receive thrombolytic therapy who underwent
elective PCI, primary PCI markedly reduced the
incidence of AMI-related VSD. The results from the
GUSTO-I trial5 also demonstrated that thrombolytic
therapy reduced the potential risk of AMI-related
VSD. Our findings were consistent with the results
from GUSTO-I trial.5 Results from our present and
recent studies,13 and from other current data,5,14 –17
suggest the concept that early and complete restoration of the infarct-related artery by either thrombolytic therapy or primary PCI minimizes the effects of
ischemic insult on the myocardium, preserves left
ventricular function, reduces later VSD, and ultimately improves the overall survival of patients
with AMI.
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1625
Incidence, Timing, Possible Mechanisms, and
Predisposed Factors of Ventricular Septal Rupture
Complicating AMI
In the present study, we found that the incidence
of AMI-related VSD was 2.9% (18 of 616 patients) in
our population of patients who did not receive
thrombolytic therapy and underwent elective PIC.
Our findings are comparable with those of previous
studies from the prethrombolytic era1,2 and suggested that the incidence of AMI-related VSD would
have no racial differences between Chinese and
western populations.1,2
It has been stated that VSD usually occurred at a
mean time of 3 to 5 days from symptom onset in the
prethrombolytic era.2,6 – 8 In contrast, most VSDs
associated with early thrombolytic therapy occur at a
peak incidence time within 24 h after treatment.5
The results of the present study demonstrated that
the mean time of VSD was 3 days in those patients
whose presentation was delayed and who underwent
elective PCI. Our data were comparable with those
of previous studies in the prethrombolytic era.2,6 – 8
Additionally, in our study one valuable finding was
that the mean time of occurrence of AMI-related
VSD after primary PCI had a statistical tendency of
being earlier than that of the elective PCI group. Our
present findings were comparable with those from
our recent report13 regarding the timing of free wall
rupture after AMI in those patients undergoing
primary PCI and with those of other current studies,1,2,5,18,19 which suggested that the time sequence
of AMI-related VSD or free wall rupture in patients
who had received various strategic treatments was
different, as shown following thrombolytic therapy,
mechanical reperfusion therapy (ie, primary PCI),
and conventional therapy.
Previous studies2,6 –12,18 –22 and our clinical observations have increased our understanding, leading us
to speculate that the pathogenesis of a VSD may be
a sequence of several mechanisms and preexisting
predisposed factors acting together. First, an extensive and complete infarct area is a prerequisite for
the cardiac rupture. This could be explained by the
fact that after an MI, the infarct area usually showed
a paradoxical motion during systole. This paradoxical
motion was more vigorous in the larger infarct
interventricular septal area, which in turn, led to a
potential risk for rupture of the septum. This could
explain that the incidences of left anterior descending artery infarctions and the angiographic findings
that totally occluded left anterior descending artery
were significantly higher in patients with VSD than
in patients without VSD complicating AMI.5 This
could also explain why anterior placement of the MI
was an independent determinant of VSD in the
present study. Second, the synergistic effect of BP
and expansion thinning of the interventricular septal
area plays another important role in VSD. The
results of a previous study20 have demonstrated that
infarct-area thinning occurs in patients with infarct
expansion before resorption has occurred. The more
extensive the infarction, the greater the expansion
cavity dilatation of the left ventricle. Furthermore,
high BP increased the wall tension, intramural
stretching, and tearing of myocardial fibers during
systole. Consequently, the left ventricular dilatation
and wall remodeling were accelerated. The LaPlace
law (ie, that wall stress is directly proportional to
intracavity pressure and its radius, and is inversely
proportional to wall thickness) may, at least in part,
explain why AMI-related VSD or free wall rupture
was more likely to occur in patients with a history of
hypertension in previous studies5,13,18 and in our
present study. Third, we suggest that VSD complicating AMI may be due to an insult of “reperfusion
injury.” Successful reperfusion in the infarct-related
artery would accelerate the rate of the inflammatory
and healing processes, and would aggravate the
absorption rate of necrotic tissue in the infarct area
by increasing the transportation of inflammatory
cells and proteolytic enzymes. This in turn, leads to
thinning and softening of the necrotic zone, and to
decreased tensile strength of the myocardial fibers.
This could explain why VSD complicated by AMI
usually occurs earlier in patients who have undergone primary PCI than in the prethrombolytic era.
Moreover, beyond those mechanisms mentioned
above, several possible additional ones, including the
extension of myocardial hemorrhage weakening and
the dissection of the necrotizing zone,18,19 the diminishing of myocardial collagen content,23 and the
digestion of collagen by collagenases24,25 and plasmin,26 also have been suggested to accelerate the
occurrence of cardiac rupture during thrombolytic
therapy. In other words, it is not surprising that
AMI-related VSD would develop early in the course
of thrombolytic therapy rather than during primary
PCI reperfusion.
Advanced age has been found to be an increased
risk factor for adverse outcomes after AMI.5,13,27 The
risks increased proportionally with advancing age,
and primary angioplasty did not alter the relationship
between adverse outcomes after AMI and being
elderly.27 In the present study, old age was found to
be an independent predictor of AMI-related VSD.
However, the cause of the high incidence of cardiac
rupture in the elderly remains undefined and may
perhaps be due to the disparity between left ventricular compliance in the aged and the age-related
structural changes of the ventricular myocardium.
Morbidity and mortality rates after AMI have been
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Clinical Investigations
reported28 to be higher in women than in men.
Recently, in patients with coronary artery disease
undergoing PCI, lean patients were reported29 to be
at increased risk for in-hospital complications and
cardiac death. In the present study, female gender
and lower BMI were two of the most important
independent predictors of AMI-related VSD. The
results of our study were consistent with those of
other studies,5,28,29 and suggested that female gender
and lean body mass are universal risk factors for the
occurrence of untoward cardiac events during PCI.
Formidable Challenges for Management of
Ventricular Septal Rupture
Despite improvements in medical therapy and in
percutaneous and surgical techniques, the mortality
rate due to VSD complicating AMI remains extremely high.5 In the present study, we found that
more than half of the patients with VSD presented
with cardiogenic shock and that 47.6% of the patients with this complication died in the hospital. Our
findings were consistent with those in another report.5 Although surgical intervention significantly
improved the survival rate compared with conservative treatment in patients with this catastrophic
complication, an in-hospital mortality rate of nearly
40.0% was observed after surgical intervention in the
present study. This suggested that further therapeutic and management research is still required in
patients with such a clinical condition.
There were several limitations to this study. First,
the number of patients in the present study, although it is one of the largest series reported in the
intervention era, was relatively small and had limited
statistical power. Second, only three patients with
AMI complicated by VSD were found in the primary
PCI era. Therefore, the timing of the occurrence of
AMI-related VSD had only a statistical tendency of
significant shortening in patients with AMI undergoing primary PCI when compared with patients with
early or recent MI undergoing elective PCI
(p ⫽ 0.06), which could have been due to a type-2
error. Furthermore, the clinical symptoms and signs
in patients with AMI-related VSD mostly had an
insidious presentation. Progressive dyspnea, worsening congestive heart failure, and pansystolic heart
murmur found during physical examination were the
usual initial presentations. Therefore, a bias regarding the exact timing of the occurrence could not be
completely ruled out. Finally, some patients may
have died before arriving at our hospital or could not
be diagnosed on presentation. Therefore, the true
incidence of AMI-related VSD may have been underestimated in our study. Furthermore, the mean
time of occurrence of VSD in these patients may be
www.chestjournal.org
earlier than 71.1 h. Hence, caution should be used
when extrapolating the results of this study for use as
a reference in the management of patients in the
same clinical setting.
In conclusion, our study demonstrated that the
incidence of VSD complicating AMI was comparable
between the Chinese and western populations.1,2
VSD may be the consequence of several mechanisms
acting together with predisposed factors, including
hypertension, female gender, low BMI, advanced
age, and anterior infarction. When compared with
those patients who did not receive thrombolytic
therapy and underwent elective PIC, primary PCI
markedly reduced the incidence of AMI-related VSD.
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Clinical Investigations