|
|
||||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Cardiovascular Division (Drs. Hatada, Kamihata, Nakamura, Takahashi, Yuasa, and Iwasaka), Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan; and the Department of Clinical Laboratory Medicine (Dr. Sugiura), Kochi Medical School, Kochi, Japan.
Correspondence to: Kengo Hatada MD, CCU, Kansai Medical University Hospital, 1015 Fumizono-cho, Moriguchi-City, Osaka 570-8507, Japan; e-mail: hatada{at}takii.kmu.ac.jp
| Abstract |
|---|
|
|
|---|
Design: Consecutive case series analysis.
Setting: Coronary-care unit in a university hospital.
Patients: Two hundred sixty-four consecutive patients with ST-elevation acute MIs who had successful primary percutaneous transluminal coronary angioplasty.
Interventions: Coronary angiography on hospital admission and serial echocardiography.
Measurements and results: The status of infarct-related artery flow before primary angioplasty was evaluated on hospital admission. Left ventricular wall motion and pericardial effusions were studied by echocardiography. One hundred ninety patients had total occlusions (Thrombolysis in Myocardial Infarction [TIMI] flow grade, 0 to 1) in the infarct-related artery (group 1), and 74 patients had antegrade flow (TIMI flow grade, 2 to 3) [group 2] before undergoing primary angioplasty procedures. When group 1 was subdivided into two groups (for the presence and absence of collateral flow), the patients with total occlusions and no collateral flow had a higher incidence of left ventricular aneurysmal wall motion (11% vs 1%, respectively; p = 0.03) and pericardial friction rub (15% vs 3%, respectively; p = 0.03) than did those in group 2. Moreover, those patients with total occlusions and no collateral flow had higher incidences of pericardial effusion (34% vs 17%, respectively; p = 0.02; and 34% vs 9%, respectively; p < 0.01) and in-hospital mortality (8% vs 1%, respectively; p = 0.04; and 8% vs 1%, respectively; p = 0.06) than did those patients in the other two groups.
Conclusions: Despite successful primary angioplasty, the absence of antegrade flow in the infarct-related artery and collateral flow to the infarct zone before angioplasty resulted in a higher incidence of in-hospital complications.
Key Words: acute myocardial infarction echocardiography in-hospital complications primary angioplasty residual coronary flow
| Introduction |
|---|
|
|
|---|
| Materials and Methods |
|---|
|
|
|---|
22
after undergoing primary PTCA
(ie, they experienced an angiographic "no-reflow"
phenomenon or technical failure including coronary dissections), and 7
other patients were excluded because they experienced an acute
reocclusion and had undergone a repeat PTCA. Therefore, this report is
based on the remaining 264 patients. The research protocol was approved
by the institutional review board of the Kansai Medical University
Hospital.
Clinical Evaluation
A primary PTCA was performed when a patient had experienced
chest pains for
30 min and had ST-segment elevation (ie,
0.1 MV above the TP-segment measured 80 ms after the J point) in
more than two contiguous leads on serial electrocardiograms and at
least twice the normal elevation in serum creatine kinase levels with
MB isoenzyme of
5%. Each patient was monitored continuously in the
coronary-care unit. Major arrhythmias noted during the hospital stay
included transient atrial fibrillation and third-degree
atrioventricular block requiring temporary pacing during the first 3
days after the patients admission to the hospital. Careful
auscultation was performed at least twice daily. Pericardial rub was
considered to be a scratchy, grating, or creaking noise heard in
systole, mid-diastole, and presystole or in any one of these phases.
The detection of pericardial rub within 3 days after hospital admission
was considered to be diagnostic of infarction-associated pericarditis.
A history of hypertension was defined as previously prescribed
antihypertensive therapy, diastolic readings that were more than twice
those previously documented that were
95 mm Hg, or systolic
readings that were more than twice those previously documented that
were
160 mm Hg. Patients were divided into smokers or
nonsmokers (ie, those who had never smoked). Patients were
defined as having non-insulin-dependent diabetes mellitus if diabetes
(of the adult-onset variety) had been documented and therapy had been
initiated before the onset of the acute MI. Patients without a previous
diagnosis of hypercholesterolemia or diabetes mellitus were examined by
blood samples of serum cholesterol and HbA1C, which were taken after an
overnight fast on the third to seventh day in the hospital.
Coronary Angiography and Primary PTCA
After informed consent was obtained, the patients were taken to
the cardiac catheterization laboratory as soon as possible to undergo
an emergency coronary angiogram that was performed using the Judkins
method. The status of the culprit lesion in the infarct-related
coronary artery before primary PTCA was visually evaluated by staff
cardiologists according to the work of Chesebro and
colleagues.2
A total occlusion was defined as TIMI flow
grade 0 to 1, and a subtotal occlusion was defined as TIMI flow grade 2
to 3 before a revascularization procedure was performed. PTCA was
attempted whenever there was total or subtotal occlusion in the
infarct-related artery (TIMI flow grade 0 to 2) with the use of
exchangeable guidewire systems. Successful PTCA was defined as a
50% diameter of stenosis of the infarct-related artery after
reflow. After catheterization, patients were admitted to the
coronary-care unit for intensive monitoring. The culprit lesion was
successfully dilated in all patients. An IV infusion of heparin was
maintained for 3 to 5 days after its bolus injection at hospital
admission, with the dose adjusted to achieve a therapeutic level of
anticoagulation. Angiographically visible collaterals were graded as
follows: 0, no visible filling of any collateral channels; 1,
collateral filling of branches of the vessel to be dilated without any
dye reaching the epicardial segment of that vessel (that is, right
coronary artery injection showing retrograde filling of septal branches
to their origin from the left anterior descending artery, without
visualization of the latter occluded artery); 2, partial collateral
filling of the epicardial segment of the vessel being dilated; and 3,
complete collateral filling of the vessel being dilated.10
Collateral channels were graded from the initial angiography, and a
patient was considered to have collateral flow to the infarct-related
artery if the collateral perfusion grade was 2 or 3. Angiograms were
analyzed by three experienced angiographers who did not have knowledge
of the patients clinical findings.
Echocardiography
Two-dimensional echocardiography was performed with a
phased-array sector scanner (model SSD 870; Aloka Co, Ltd; Tokyo,
Japan). All classic views were recorded on videotape for subsequent
analysis by observers who were unaware of the patients clinical data.
The presence of pericardial effusion was assessed
24 h after the
PTCA with the method described by Horowitz et al.11
An
epicardial-pericardial separation that persisted throughout the cardiac
cycle (D-pattern) was considered to be diagnostic of pericardial
effusion. An analysis of the left ventricular wall motion was performed
in 11 segments that were assessed by long-axis and short-axis images
obtained on the day of hospital admission,12
and the
number of segments with advanced asynergy (akinesis or dyskinesis) was
calculated. Left ventricular aneurysmal wall motion was defined by
serial observations of two-dimensional echocardiography during
hospitalization (< 24 h, 3 days, and 7 days after the PTCA) as an
area of myocardium that was dyskinetic in systole with distinct
diastolic deformity and preserved adjacent wall motion.13
The left ventricular aneurysmal wall motion was classified as present
if aneurysmal wall motion was diagnosed in at least one of these
studies. Doppler echocardiography was performed when pericardial rub
was first detected in order to rule out mitral regurgitation caused by
papillary muscle dysfunction.
Statistical Analysis
Results are reported as the mean ± SD. Statistical analysis
between the two groups was performed by Students t test
for continuous variables and Fishers Exact Test for discrete
variables. The comparison of three discrete variables was made by
2 analysis and Sheffe-type multiple
comparison. One-way layout analysis of variance and a Bonferroni
multiple comparison were used to compare the three groups. All
calculated p values are two-tailed. A p value < 0.05 was considered
to be significant.
| Results |
|---|
|
|
|---|
|
|
|
| Discussion |
|---|
|
|
|---|
The incidence of total occlusion of the infarct-related coronary artery in the early phase of an MI in the present study was approximately 72%, which is consistent with that found in a previous report.14 We found that current smokers were more common (61%) in group 1 compared to group 2. Although the mechanisms leading to acute MI are still incompletely understood, intracoronary thrombus formation plays a greater role in the pathophysiology of abrupt coronary occlusion.15 Smokers have higher fibrinogen and factor VII levels as well as impaired endothelial function.16 17 18 19 In addition, increased plasma epinephrine concentrations associated with enhanced platelet aggregation and adhesion and higher incidences of vasoconstriction have been observed in smokers,20 all of which would tend to predispose them to plaque rupture leading to total coronary occlusion.
The patients with no coronary blood supply to the infarct zone before primary PTCA (ie, the occlusion of the infarct-related coronary artery without collateral flow [group 1b]) had a significantly higher incidence of pericardial effusion compared to those with coronary flow to the infarct zone (group 1a and group 2). Pericardial effusion is still a common clinical sign after primary PTCA (21%)21 and is associated with more extensive myocardial damage.21 22 23 24 Although there was no significant difference in the number of left ventricular segments with advanced asynergy among the three groups, patients in group 1b had a significantly higher incidence of pericardial rub and aneurysmal wall motion than those in group 2. An earlier report21 from our laboratory found that patients with pericardial effusion and a pericardial rub had more severe transmural myocardial damage and a higher in-hospital mortality rate. Thus, patients in group 1b had more severe transmural myocardial damage as a result of the absence of coronary perfusion to the jeopardized myocardium before the achievement of coronary recanalization.
Despite there being no significant difference in the elapsed time from the onset of the MI to PTCA, the patients in group 1b had a higher in-hospital mortality rate compared to the other two groups. Although the survival rate of patients who have experienced MIs has improved by the use of mechanical reperfusion, further study is necessary to evaluate combining pharmacologic therapy (to open the infarct artery early) with mechanical reperfusion, because those patients with no coronary perfusion to the infarct zone might benefit from early thrombolytic therapy to prevent the risk of left ventricular pump failure, which leads to a poor prognosis.
Study Limitations
Two limitations of our study should be addressed. First, because
this study excluded those patients who had experienced technically
unsuccessful PTCAs, including the angiographic no-reflow phenomenon
after primary PTCA, we are unable to document whether our data hold up
in all patients who have undergone primary PTCAs. However, angiographic
no-reflow after angioplasty has been shown to be an adverse clinical
sign of poor left ventricular functional recovery and cardiac
death.24
25
Therefore, the present study still provides
one of the clinical signs differentiating the patients outcomes in
the reperfusion era.
Second, infarct expansion, which can play an important role in the left ventricular remodeling, has been considered to begin within hours of an acute transmural MI and usually reaches a peak within 7 to 14 days.26 The diagnosis of left ventricular aneurysmal wall motion in our study was performed by serial echocardiographic observations, but the remodeling is also caused by the dilatation of the viable portion of the ventricle and process for months or years thereafter.27 Although the incidence of aneurysmal wall motion has decreased after successful PTCA,28 29 30 our data may have underestimated the number of patients with the aneurysmal wall motion.
| Conclusion |
|---|
|
|
|---|
| Footnotes |
|---|
Received for publication January 3, 2001. Accepted for publication May 2, 2001.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
T. Sugiura, S. Nakamura, Y. Kudo, T. Okumiya, F. Yamasaki, and T. Iwasaka Clinical Factors Associated With Persistent Pericardial Effusion After Successful Primary Coronary Angioplasty Chest, August 1, 2005; 128(2): 798 - 803. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |