A previously healthy woman about 50 years old with no previous medical history or coronary risk factors presented 30 minutes after the sudden onset of severe substernal chest pain. An ECG was recorded and interpreted within 13 minutes:
|Sinus rhythm. Intraventricular conduction delay with a QRS of 117 ms (really, incomplete LBBB)|
There are hyperacute T-waves in V4-V6, I and aVL, with reciprocal ST depression and T-wave in version in III and aVF. V4 shows a de Winter's T-wave, with some ST depression.
This is diagnostic of proximal LAD occlusion, and I activated the cath lab the moment I saw this ECG.
We gave clopidogrel 600 mg, aspirin, and a heparin bolus. There was time to get another ECG, 13 minutes later, before going to the cath lab:
Cath lab results
|Now there is evolution to ST elevation in V2-V6.|
The patient went to the cath lab and had a door to balloon time of 50 minutes, for a total symptom onset to balloon time of 80 minutes (very fast). There was complete occlusion of the proximal LAD which was opened and revealed a very large first diagonal
(this explains the predominance of V4-V6 on the ECG). After reperfusion, there was somewhat less "blush" (micovascular reperfusion
as demonstrated by slight opacification, by contrast, of the affected myocardium).
There was now TIMI-3 flow, and the patient was pain free
, but there was persistent ST elevation in lead V5 on the 6-lead monitor in the cath lab.
Therefore, in addition to thrombectomy, the interventionalist gave intra-coronary adenosine (a vasodilator) to try to improve distal microvascular flow. As is routine, he also gave intracoronary nitro. And, of course, he used an eptifibatide bolus and infusion to maximally inhibit platelets. He did not see any distal "cut off" of vessels in the distribution of the large diagonal or the LAD, but he suspected, based on the persistent ST elevation, that the patient had a significant shower of debris down the diagonal distribution. He states that "this probably occurred at the time of the acute vessel closure because we did not have any "no flow" or "slow flow" issues that developed acutely during the case."
Here was the post-cath ECG:
After cath, the troponin I was already 107 ng/mL at 5 hours after presentation, and peaked at 178 ng/mL (very large MI).
|Sinus rhythm and a narrower QRS.|
There is persistent ST elevation, and persistently upright T-waves (absence of reperfusion T-waves) in V4-V6. Though T-waves are inverted in aVL, they are not inverted in lead I, and there is persistent ST elevation in aVL.
The patient had a post cath ejection fraction of 36% and persistent chest pain for much of the day. Due to high risk of cardiogenic shock and dysrhythmia, ICU admission was warranted (usually not necessary for completely successful reperfusion).
Usually, a low ejection fraction in a patient with rapid restoration of TIMI-3 flow means that the patient has stunned myocardium that will recover. However, the absence of resolution of ST elevation here is consistent with poor microvascular reperfusion, as is the very high troponin I, and thus recovery of function is not likely to be excellent.
The pain did eventually resolve, but significant damage was done. For instance, the risk of sudden death from dysrhythmia is much higher than it would have been with good microvascular reperfusion, and she may need to go home on a temporary external automatic defibrillator
.2 days after presentation, here is the ECG:
|There is still persistent ST elevation in lateral leads, though now there is T-wave inversion. There is a new Q-wave in lead I.|
This patient had remarkably fast symptom onset to balloon time, and optimal reperfusion therapy, and yet did not get good reperfusion because of poor microvascular reperfusion (thought to be due mostly to downstream microvascular obstruction and/or vasoconstriction). About 2-5% of patients with successful PCI have no reflow. Absence of resolution of ST elevation on the ECG is the best indicator of no reflow. Suffice it to say that these patients have a much worse outcome than patients with good microvascular reperfusion.
It's etiology is not uniform for every patient. It is associated with, among other factors, clopidogrel resistance
. (We usually think of using Prasugrel or Ticagrelor to prevent re-occlusion; maybe we should be using these alternatives to clopidogrel to prevent "no reflow." The therapy of "No reflow" is based on vasodilators such as adenosine, verapamil, and nitroprusside, as well as on triple antiplatelet therapy; no single mechanical or pharmacologic therapy has proven consistently effective.Here is one review from 2010
.Here is another review from 2012
.Reperfusion on the ECG: Summary
I will leave the details for the below chapter from my book.
1. The ECG is the best predictor of reperfusion of the microvasculature, even better than angiographic assessment by TIMI flow. Notice that the interventionalist relied on the ECG to diagnose "no reflow" in this patient.
2. TIMI myocardial perfusion grading (TMP) flows 1-3 grade the amount of microvascular reperfusion seen on angiogram, called "blush". Absence of microvascular perfusion in the presence of good epicardial blood flow is called "no reflow."
3. "No reflow" is probably mostly caused by downstream showering emboli of platelet aggregates, and also by vasoconstriction.
4. After reperfusion, the first ECG marker of microvascular reperfusion is T-wave inversion
5. After reperfusion, the best ECG marker of microvascular reperfusion is resolution of ST segment elevation by at least 50% from maximum, and preferably, > 70% (or complete) resolution.
6. The ECG is far more reliable at gauging microvascular reperfusion than is resolution of chest pain.
The ECG in REPERFUSION AND REOCCLUSIONThis is Chapter 27 (Reperfusion and Reocclusion) from my book, The ECG in Acute MI. It is long, and has a detailed annotated bibliography. It comes from literature before 2002, but it is still accurate and almost everything you need to know (unless you are an interventionalist) about the ECG in Reperfusion and Reocclusion.
Arterial patency and microvascular circulation Reperfusion therapy is guided by the ongoing assessment of myocardial reperfusion. This depends on two factors: 1) reperfusion of the epicardial infarct-related artery (IRA); and 2) reperfusion of the microvascular circulation, which may be damaged by ischemia and reperfusion (the “no-reflow” phenomenon) and result in impeded capillary flow. Hemodynamic status and age are the best clinical prognostic indicators for AMI outcome. The best ECG indicator for AMI outcome is ST resolution or the lack thereof (318-322). The best overall predictor of failed myocardial reperfusion is a finding of < 50% recovery of ST segments from maximal elevation. However, the ECG cannot determine whether the cause of failed reperfusion is persistent arterial occlusion or microvascular damage. Angiography is necessary to assess and grade IRA patency and microvascular circulation and to guide subsequent therapy. Rescue PCI, which we define as PCI undertaken within 6 hours of the start of thrombolytic therapy, (323) should be strongly considered when clinicians have determined that thrombolytic reperfusion has failed and should be done immediately after transfer to a PCI facility if there is no ECG evidence of good reperfusion (324). This is especially true for a large AMI, as indicated by anterior location, high ST elevation, or ST deviation in numerous leads. A patent IRA with inadequate flow may be due to residual stenosis or abnormal microvascular circulation and may be treated with vasodilators, antiplatelet, and antithrombotic agents +/- PCI. TIMI grading of IRA patency IRA patency can only be definitively assessed by angiography. Angiographic assessments are then systematized by TIMI grading, as follows (325): · TIMI-1 = penetration of contrast without perfusion. These patients have persistent ST elevation and a poor prognosis and must be identified for rescue PCI · TIMI-2 = partial reperfusion. These patients may have resolution of ST elevation and a prognosis intermediate between TIMI 0/1 and TIMI 3 flow. · TIMI-3 = complete reperfusion. These patients usually (but not always) show ST resolution. TIMI-3 flow after reperfusion is associated with lower mortality and lower incidence of CHF (326, 327), but its prognostic value may not be independent of resolution of ST elevation (318). By outcome measures, a flow grade < TIMI-3 indicates failed reperfusion (26, 328). After reperfusion therapy for AMI, TIMI-3 flow is associated with a 30-42 day mortality of 3.6%, in contrast to TIMI-2 flow (6.6% mortality) and TIMI-0/1 flow (9.5% mortality) (327).
TIMI Frame Count
The TIMI frame count (TFC) further systematizes TIMI flow categorization. The TFC is the measure of the exact number of cineangiographic frames required for contrast to reach a defined distal segment of the IRA (see Background discussion under Angiographic Reperfusion Grades in the annotated bibliography of this chapter). TIMI myocardial perfusion grading of microvasculature TIMI flow and TFC are impacted by both the severity of the underlying stenosis and thrombus and by the microvasculature. Intact microvasculature is most accurately assessed by the appearance on an angiogram of diffuse and faint highlighting of the myocardium by contrast, known as “myocardial blush.” These assessments are systematized with TIMI myocardial perfusion grading (TMP), which is based on a scale from 0-3 as follows (319, 326, 329): · TMP grade 0 = no microvascular perfusion · TMP grade 1 = no clearance of contrast · TMP grade 2 = slow clearance of contrast · TMP grade 3 = normal clearance. An open coronary artery may have brisk TIMI-3 flow but have a TMP grade of 0 or 1 (326); patients with these findings show persistent ST elevation (318, 319, 329). TMP grade 3 is associated with a good prognosis, independent of TIMI flow.
ECG DIAGNOSIS OF REPERFUSION
ST segments in reperfusion
With a reperfused IRA AND intact microcirculation, ST segments usually fall rapidly and are near baseline within 3 hours of reperfusion (see Case 27-1). Approximately 80% of cases with IRA reperfusion manifest 50% ST recovery within 90 minutes. Most of the remaining 20% likely have microvascular injury with resultant poor capillary flow; their prognosis is as poor as patients with poor flow in the IRA (318, 319, 329). This contrasts with a non-reperfused IRA, in which ST segments fall gradually and plateau, with or without persistent elevation. Plateauing occurs as early as 6 to 12 hours, due to myocardial cell death (330). ST resolution is an accurate predictor of reperfusion, especially in patients whose ECG’s show ST elevation > 4 mm (331). During or shortly before reperfusion, ST segments often continue to rise before resolving, frequently with an increase in CP (156, 157, 332, 333, 334). Some patients experience “cyclic reperfusion,” in which there is reperfusion and subsequent reocclusion. This may occur with or without therapy. Cyclic reperfusion occurs in 25-30% of AMI before reperfusion therapy and can be detected with ST segment monitoring (335).
In reperfused AMI, terminal T-wave inversion often occurs rapidly(within 90 minutes) in the leads that manifested the greatest ST elevation on presentation, and before full ST resolution (156, 157). This contrasts with non-reperfused AMI, 90% of which show gradual T-wave inversion (over 48 to 72 hours), with a depth < 3 mm (94) (Fig. 8-3). If there is some myocardial injury, as measured by elevated troponin, expect terminal T-wave inversion to develop into deep and symmetric T-wave inversion over the first 48 hours after the onset of AMI (94) (see Case 27-2). Accordingly, early T-wave inversion (< 24 hours) is associated with greater IRA patency, better perfusion grade, and a more benign in-hospital course than later inversion (336). In some patients with very early reperfusion and very little or no myocardial cell death, as measured by troponin, there may be no T-wave inversion, very late inversion, or reversible inversion (94).
Q-wave and R-wave changes are not accurate markers of AMI reperfusion (337).
Monitoring for reperfusion may include observation of 5 elements, as follows: 1) ST resolution, or “recovery;” 2) terminal T-wave inversion; 3) resolution of CP; 4) reperfusion arrhythmias; and 5) biochemical markers.
ST segment resolution, or “recovery,” is the best marker for reperfusion (see Cases 27-1 and 27-2). ST segments may be monitored continuously or with static ECG’s every 5 minutes from the time of thrombolytic administration. If ST elevation is > 4 mm and there is NEITHER >/= 50% recovery at 60 minutes NOR terminal T-wave inversion, TIMI-3 flow is unlikely. Strongly consider rescue PCI. Continuous ST segment monitoring is the best method for monitoring ST segment changes (156, 159, 338, 339) (see Case 27-3). Commercial products are available. Select one lead with the greatest ST elevation, plot the ST segment elevation continuously, and observe for peaks and troughs. By convention, ST elevation is measured on continuous monitors at 80 ms after the J-point. See Table 27-1. · ST recovery >/= 50% from MAXIMAL ST elevation (peak level attained) within 60 minutes and without re-elevation is a very good predictor of reperfusion. These patients do not need early angiography or rescue PCI. ST recovery >/= 50% has a positive predictive value (PPV) for patency (TIMI-2 or -3 flow) of 87%. · ST recovery < 50%, consider rescue PCI. The negative predictive value (NPV) for occlusion (lack of recovery) is 71%; i.e., 71 % of patients who do not show ST recovery >/= 50% have closed arteries and 29% have TIMI 2-3 flow. These patients are candidates for rescue PCI. Most importantly, ST recovery < 50% with no terminal T-wave inversion indicates a TIMI flow of 0-2 with a PPV of 86%. TIMI-3 flow is true successful reperfusion. Of patients with persistent ST elevation (< 50% recovery), 14% have TIMI-3 flow but presumably continue to have ST elevation due to microvascular injury. · The higher the maximal or initial ST elevation, the more accurate the patency prediction (331). Although static ECG’s are inferior to continuous ST segment monitoring (339), if continuous monitoring is unavailable, recording static ECG’s every 5 minutes from the time of thrombolytic administration is a reasonable substitute (158). Use the single lead with the highest ST elevation and measure resolution from the maximal height. ST resolution > 50% at 60 minutes after treatment is a good indicator of reperfusion (158). Complete ST resolution assures reperfusion but occurs infrequently by 60 minutes after treatment (339). 2. Terminal T-wave inversion Terminal T-wave inversion within the first 90 minutes is a specific marker of reperfusion and is approximately 60% sensitive (156, 157, 158). If leads with ST elevation develop terminal T-wave inversion within 60 minutes of thrombolysis, reperfusion is highly likely. Because T-wave inversion usually indicates some myocardial injury, rapid ST resolution without any T-wave inversion may be evidence that reperfusion occurred before myocardial cell death; in such cases, biomarkers may not be elevated. Terminal T-wave inversion usually occurs before full resolution of the ST segment. Deep, symmetric T-wave inversion (> 3 mm) indicates reperfusion that is less recent than reperfusion indicated by terminal T-wave inversion (see Case 27-2). Terminal T-wave inversion undergoes further development into symmetric T-wave inversion (94). Deep, symmetric T-wave inversion need not be preceded by ST elevation, although there is usually no development of Q-waves without ST elevation. Symmetric T-wave inversion is generally present after full resolution of the ST segment. T-waves also eventually invert in persistently occluded vessels. T-wave inversion in the presence of deep Q-waves, especially QS-waves, may be a manifestation either of reperfusion late in the course of AMI or of a well-developed, non-reperfused AMI (94, 340). These inverted T-waves are usually < 3 mm, in contrast with inverted T-waves of reperfused AMI, which are > 3 mm (94). Such T-wave inversion may be evident at presentation if the patient presents late after onset (see Case 33-3). With posterior AMI, if the T-wave is upright before reperfusion and there is ST recovery, reperfusion usually results in precordial T-waves (especially V2) becoming fully upright and taller and wider than before AMI onset. This is a reciprocal view of posterior inverted T-waves. Reocclusion in this case is unlikely to result in T-wave inversion. If the T-wave is asymmetrically inverted before reperfusion, reperfusion usually results in T-waves pseudonormalizing (turning upright) and becoming taller and wider than before the onset of AMI; reocclusion generally results in re-inversion of T-waves. See Case 27-1. (See also: Cases 16-10 and 13-4). Two studies showed that complete relief of CP, often with an initial transient increase in pain, had a good PPV, with an 84% (339) to 96% (156) chance of reperfusion. However, relief of CP with neither any recovery of ST segments nor terminal T-wave inversion is unlikely to represent reperfusion. If CP resolves, record serial ECG’s; pursue rescue angioplasty if there is no ECG evidence of reperfusion. With spontaneous relief of CP, do not abort reperfusion unless accompanied by some amount of ST recovery: · With increased, unchanged, or < 25% ST elevation resolution, continue reperfusion therapy. · With 25%-50% resolution, or terminal T-wave inversion, record serial ECG’s or continuous monitoring and look for >/= 50% ST resolution. · With 50%-100% resolution, reperfusion therapy may be suspended, pending further assessment, especially continuous ST monitoring. Relief of CP has a poor NPV, in that persistent pain did not necessarily imply persistent occlusion (159, 339). 4. Reperfusion arrhythmias Occurrence of early accelerated idioventricular rhythm (AIVR) indicates reperfusion with 97% specificity but only 45% sensitivity (335). A sudden burst of ventricular tachycardia may also indicate reperfusion. 5. Biochemical markers of reperfusion Biochemical markers may also be useful in assessing reperfusion; see Chapter 29 for details. See Cases 27-1 to 27-3 for examples of reperfusion. (See also: Cases 6-4, 12-3, 16-10, 20-11, and 32-1).
A meta-analysis of randomized trials showed that rescue angioplasty performed in patients with failed reperfusion results in a decreased incidence of CHF, death, and recurrent MI, without significant adverse effects (324). These trials were performed withoutthe latest technology and with prolonged time intervals from thrombolysis to rescue. In this age of abciximab and stenting, we highly recommend rapid rescue PCI for failed reperfusion as evidenced by the above-mentioned ECG indicators or by persistent clinical instability. If TIMI-3 flow is present but TMP grade is low, treatment with vasodilators, antiplatelet, and antithrombotic agents is particularly important.
Once reperfusion is achieved, monitor ST segments for reocclusion. Symptoms are notreliable indicators of reocclusion and many recurrent AMI’s are asymptomatic (69, 89). If continuous monitoring is unavailable, record frequent static ECG’s every 30 to 60 minutes until stability is assured. At a minimum, record hourly ECG’s for several hours after reperfusion.
ECG manifestations of reocclusion
Each AMI has an “ischemic fingerprint,” such that reocclusion of the same vessel at the same location reproduces the same ECG findings (83, 190). Thus, reocclusion manifests the reverse of reperfusion on the ECG, as follows: · Initial rapid “pseudonormalization” of T-waves, in which inverted T-waves turn upright. · Subsequent re-elevation of ST segments. Caution: post-infarction regional pericarditis(PIRP) may mimic reocclusion (see Chapter 28) (94). This is characterized by gradual pseudonormalization of T-waves or persistent upright T-waves in the leads that had the greatest ST elevation at presentation. There is also gradual ST re-elevation, over 24-72 hours. PIRP lacks the typical diffuse ST elevation of nonspecific pericarditis. See Case 27-3 of reocclusion. (See also: Case 8-12, of pseudonormalization of symmetrically inverted T-waves; Case 13-4 of an inferoposterior AMI with reperfusion and reocclusion; and Case 3-3 of reocclusion a week after reperfusion).
Reocclusion after thrombolysis mandates either repeat thrombolysis or, preferably, rescue angiography +/- PCI.
Reperfusion: General background
Krucoff MW et al., Continuously updated 12-lead ST-segment recovery analysis for myocardial infarct artery patency assessment and its correlation with multiple simultaneous early angiographic observations, 1993. Methods: Krucoff et al. (341) performed angiography and continuous ST segment monitoring in 22 AMI patients. Findings: Forty-four episodes of arterial patency and multiple ST trend transitions in 11 of 22 patients after thrombolysis suggested cyclic changes in coronary flow before catheterization. Comment: These authors and others (158, 159) have shown repeatedly that ST recovery must be measured from maximal ST elevation for accurate assessment of reperfusion. Peak ST elevation may occur in the absence of or any time after thrombolytic therapy. Static ECG’s are less effective than continuous monitoring because ST segments may rise from baseline before actual reperfusion and fall again (or vice versa) to nearly the same level without detection.
Angiographic reperfusion grades, persistent ST elevation, and prognosis
Background: TIMI flow grade is a measurement of reperfusion of a coronary vessel and TMP flow grade is a measurement of myocardial microvascular perfusion. TFC is the measure of the exact number of cineangiographic frames required for contrast to reach a defined distal segment of the IRA. TFC is especially helpful to further categorize TIMI-2 and TIMI-3 flow. Normal mean TFC’s are: 36.2 +/- 2.6 for the LAD, 20.4 +/- 3.0 for the RCA, and 22.2 +/- 4.1 for the circumflex artery (342). To standardize TFC for all arteries, the TFC of the LAD is divided by 1.7 to give a “corrected” TFC (CTFC) (342). At 90 minutes after thrombolysis for STEMI in all locations. a CTFC of 0-13 is above normal blood flow and is associated with mortality of 0%. A CTFC of 14-40 is associated with mortality of 2.7%, and a CTFC > 40 is associated with mortality of 6.4% (343). Of patients with TIMI-3 flow, CTFC </= 20 vs. > 20 is associated with complication rates of 7.9% vs. 15.5%, respectively (343).
Van’t Hof et al., Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction, 1998. Methods: Van ‘t Hof et al. (320) studied ST resolution in 403 AMI patients with TIMI-3 flow after primary angioplasty. Findings: ST segments normalized in 51% of patients (ST < 0.1 mV). Partial normalization (30-70% of initial height) was associated with a relative risk (RR) of death of 3.6 (CI = 1.6-8.3) compared with full normalization(< 30% of initial height). Absence of resolution or increased ST elevation was associated with a RR of death of 8.7 (range = 3.7-20.1). Van’t Hof et al., Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade, 1998. Methods: Van ‘t Hof et al. (329) studied myocardial blush during primary angioplasty in 777 AMI patients. Findings: Angioplasty resulted in TIMI-3 flow in 89% of patients and in TIMI-0, -1, or -2 flow in 11%. Patients with TMP grades 3, 2, and 0/1 had: 1) CK infarct sizes of 757 IU/L, 1143 IU/L, and 1623 IU/L; 2) EF’s of 50%, 46%, and 39%; and 3) mortality (after a mean follow-up of 1.9 +/- 1.7 years) of 3%, 6%, and 23%, respectively. TMP grade predicted mortality independently of Killip class, TIMI grade flow, EF, and other clinical variables. TMP grade was the best predictor of 3-year mortality, with rates of 3%, 15%, and 37% for patients with grades 3 (19% of patients), 2, and 0/1, respectively. Among TMP grade 3 patients, ST elevation normalized in 65% and ST elevation decreased in an additional 28%. Gibson CM et al., Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs, 2000. Methods: Gibson et al. (326) studied 762 patients in the TIMI-10B trial, in which 854 patients with AMI were randomized to TNK-tPA or standard alteplase and underwent angiography at 90 minutes post-thrombolytic administration. Findings: TMP grade 3 myocardial perfusion was independently associated with low 30-day mortality of 2.0%, as compared to 3.5% for patients with TIMI-3 flow. The decreased risk was additive to the low risk of TIMI-3 flow, such that mortality was a mere 0.73% (1 of 137) for patients with TIMI-3 flow and TMP grade 3 perfusion compared to a 10.9% mortality (14 of 129) for those with both TIMI 0-2 and TMP 0/1 grading. Mortality was approximately the same for patients with: (1) both TIMI 0-2 flow and TMP grade 3 perfusion, presumably through collaterals; and (2) both TIMI-3 flow and TMP 0/1 perfusion.
ST recovery and prognosis
ST recovery can be a good prognostic indicator, even in the presence of an occluded vessel. Lack of ST recovery portends a poor prognosis, even with an open artery.
Claeys MJ, Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome, 1999.
Methods: Claeys et al. (319) studied 91 AMI patients with reperfusion after angioplasty.
Findings: Of 91 patients, 75 had TIMI-3 and 16 had TIMI-2 flow. Persistent ST elevation, defined as ST >/= 50% of the initial height, was observed in 33 (36%) patients and was associated with high one-year mortality (15% vs. 2%) and high total major adverse cardiac event rate (45% vs. 15%). Persistent ST elevation was the most important independent determinant of major adverse cardiac event rate, with an adjusted RR of 3.4, and both were attributed to impaired microvascular circulation.
Shah A et al., Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the "gold standard” for myocardial reperfusion treatment, 2000. Methods: Shah et al. (318) identified 258 AMI patients who underwent thrombolysis and then angiography in the TIMI-7 and GUSTO-1 trials (see Appendix). Patients were stratified according to TIMI 0-3 reperfusion and by ST resolution >/= 50% vs. < 50%. Findings: ST resolution WAS an independent predictor of the combined clinical outcome of death or CHF but TIMI flow grade was NOT. ST resolution among patients with TIMI grade 0-1 flow identified a group with a relatively benign clinical course. Dissman R et al., Early assessment of outcome by ST segment analysis after thrombolytic therapy in acute myocardial infarction, 1994. Methods: Dissman et al. (321) studied CK levels and EF’s in 77 AMI patients to correlate ST resolution and infarct size.
Findings: The enzyme-determined infarct size and the resulting EF correlated closely with complete (>70%), partial (30-70%), or no ST (<30 3="" 43="" 53="" 58="" and="" at="" complete="" ef="" for="" hours="" nbsp="" no="" o:p="" or="" partial="" patients="" post-thrombolysis.="" resolution="" respectively.="" s="" were="" with="">30>