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ACC/AHA 2008 Performance Measures for Adults With ST-Elevation and Non–ST-Elevation Myocardial Infarction

ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease
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J Am Coll Cardiol, 2001; 37:1239-1245
© 2001 by the American College of Cardiology Foundation
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CLINICAL STUDY

Postinfarctional remodeling: increased dye intensity in the myocardial risk area after angioplasty of infarct-related coronary artery is associated with reduction of ventricular volumes

Gianni Destro, MD*, Paolo Marino, MD{dagger}, Enrico Barbieri, MD, FACC*, Andrea Zorzi, MD*, Giovanna Brighetti, MD*, Massimiliano Maines, MD*, Monica Carletti, MD* and Piero Zardini, MD*

* Division of Cardiology, University of Verona, Verona, Italy
{dagger} Cardiology Service, University of Verona, Verona, Italy

Manuscript received August 7, 2000; revised manuscript received November 22, 2000, accepted December 21, 2000.

Reprint requests and correspondence: Dr. Gianni Destro, Division of Cardiology, University of Verona, P. le Stefani, 1, 37126 Verona, Italy


   Abstract
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 Abstract
Methods
 Results
 Discussion
 Conclusions and clinical...
 References
 
OBJECTIVES

We sought to evaluate if angiographic dye videointensity of the risk area during percutaneous transluminal coronary angioplasty (PTCA) of the infarct-related artery (IRA) relates to remodeling.

BACKGROUND

Poor reflow after myocardial infarction (MI) predicts worse ventricular remodeling.

METHODS

Fifty-three patients with a first anterior MI and isolated disease of the left anterior descending (LAD), who underwent "primary" (n = 14), "rescue" (n = 7) or "late" (after 10 ± 4 days, n = 32) PTCA, were retrospectively selected. In 10 patients prospectively collected, we assessed Doppler flow velocities and Doppler flow reserve (DFR), relating them to the videointensity technique. Coronary stenosis and TIMI flow were determined, and echocardiographic volumes (end-diastolic and end-systolic volume indexes) and regional asynergy were computed before hospital discharge (baseline) and at six months. Assuming higher peak videointensity reflects greater myocardial blood volume, a 1- to 5-point (poor-optimal) perfusion scale was devised.

RESULTS

The correlation of Doppler peak velocity and DFR with videointensity was significant (r = 0.58, p = 0.007 and r = 0.71, p < 0.001, respectively). Patients were subdivided into group A (increased videointensity post-PTCA ≥1.5 points, n = 29) and group B (unchanged videointensity, n = 24). Analysis of variance showed a time-group interaction for end-diastolic volume index (–4.6 ± 23% vs. +22 ± 22%, p = 0.003) and end-systolic volume index (–3.05 ± 11.1% vs. +4.1 ± 12.5%, p = 0.027). There was no interaction for changes in LAD stenosis (p = 0.39) and TIMI flow after PTCA (p = 0.27), or regional asynergy at six months (p = 0.31).

CONCLUSIONS

Angiographic dye videointensity in the risk area correlates with Doppler peak velocity and DFR, and its increase after PTCA of IRA has a limiting effect on ventricular volumes, independent of coronary stenosis resolution, changes in Thrombolysis In Myocardial Infarction (TIMI) flow or extent of regional asynergy.

Abbreviations and Acronyms
  ANOVA = analysis of variance
  CK-MB = creatine kinase-MB
  CPK-MB = creatine phosphokinase-MB
  DFR = Doppler flow reserve
  IRA = infarct-related coronary artery
  LAD = left anterior descending
  MI = myocardial infarction
  PTCA = percutaneous transluminal coronary angioplasty
  ROI = region of interest
  SD = standard deviation
  TIMI = Thrombolysis In Myocardial Infarction

Patency of the infarct-related coronary artery (IRA) does not always correlate with the presence of myocardial perfusion in the related territory, as shown in studies using myocardial contrast echocardiography (1,2) or, more recently, angiographic dye contrast (3,4). An ischemic episode may damage coronary microvasculature, so that flow to the infarcted myocardium is reduced or absent (low-flow or no-reflow phenomenon) (5). If myocardial perfusion is related to microvascular integrity and viability (6), it may be the key to predicting postinfarction changes in regional function and ventricular volumes. The present study addresses the topic of ventricular remodeling and myocardial perfusion in the risk area, using an angiographic method based on dye videointensity during left main coronary injection of dye contrast, before and after percutaneous transluminal coronary angioplasty (PTCA) of the IRA. Moreover, in 10 patients we investigated the relation between videointensity and Doppler coronary flow pattern, a well-established technique (7) in which Doppler velocities may be used to assess microvascular dysfunction (8,9) and coronary flow reserve to predict functional myocardial recovery (10) after an acute myocardial infarction (MI).


   Methods
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Study patients.   Clinical criteria for inclusion in our study were 1) admission to the Coronary Care Unit due to diagnosis of a first acute MI based on typical chest pain of <6 h duration, characteristic electrocardiographic signs (ST segment elevation in the anterior leads), subsequent rise and fall of isoenzyme creatine phosphokinase (CPK)-MB; 2) execution of a PTCA during the acute phase of MI ("primary" or "rescue" according to clinical indications), or of a "late" PTCA (10 ± 4 days after MI) after a coronary angiography showing a Thrombolysis In Myocardial Infarction (TIMI) 0 or 1 flow in the left anterior descending coronary artery (LAD), without critical lesions of the right coronary artery or the left circumflex; 3) execution of two-dimensional echocardiography before discharge from the hospital (baseline) to evaluate left ventricular volumes, ejection fraction and wall motion abnormalities; and 4) clinical and echocardiographic follow-up (including a bicycle ergometer test) within four to six months. Patients with previous angina, MI, valvular disease or left ventricular hypertrophy were excluded.

Patient population.   From patients admitted to the Coronary Care Unit over the previous 3 years, we selected 53 patients (mean age, 55.9 ± 10.6 years, 5 women); 21 had PTCA during acute MI (14 "primary" and 7 "rescue"), and 32 had "late" PTCA, all with good results (reduction of coronary stenosis by >50% after PTCA). None of these patients underwent stent positioning during the PTCA procedure. In the group who had PTCA in the acute phase, "rescue" PTCA was performed in seven patients because of the absence of clinical signs of myocardial reperfusion (persistence of chest pain and persistent electrocardiographic changes) after systemic thrombolysis with recombinant tissue-type plasminogen activator. Fourteen patients underwent "primary" PTCA because of cardiogenic shock (n = 5), young age (<50 years, n = 4) or cardiopulmonary resuscitation (n = 1). Four patients with large MI (as detected by ECG and/or echocardiography) were admitted to the hospital during routine operating hours of the catheterization laboratory and so had the chance to undergo immediate PTCA, with the aim of reducing infarct size and preserving left ventricular function (11). Thirty-two patients underwent successful systemic thrombolysis with recombinant tissue-type plasminogen activator in the acute phase, and then were consecutively admitted to the coronary angiography unit after 10 ± 4 days, irrespective of ischemia or viability in the infarcted region. In all these patients who had a critical stenosis (>75%) of the proximal-mid tract of LAD, "late" PTCA was performed at the discretion of the referring physician.

Quantitative coronary arteriography.   Cineangiographic film from the catheterization laboratory was copied onto a VHS videotape using a video projector (Cipro, Siemens, Erlangen, Germany). Images of the LAD were analyzed using a computer system (Cardio 500, Version 2.0, Kontron Instruments, Munich, Germany), selecting two orthogonal projections (right anterior oblique 30° and left anterior oblique 60°) at end-diastole. These images were digitized onto a 512 x 512-pixel matrix with maximal spatial resolution of 0.13 mm/pixel using an 8-bit gray scale with 256 shades of gray. An automated operator interactive program was used to analyze the stenotic segment and the angiographic catheter (to obtain the magnification factor), and to calculate the absolute minimal luminal cross-sectional area and relative values (percentage area stenosis) (12,13).

Analysis of echocardiographic ventriculogram.   A quantitative analysis of the two-dimensional echocardiographic images was made using a semiautomatic computer system (Cardio 500, Kontron Instruments). Briefly, the endocardial boundary of the left ventricular cavity was identified and traced by means of a light-pen system, in the four- and two-chamber views from electrocardiographic-gated images frozen at end-diastole (onset of QRS complex) and at end-systole (the subsequent frame with the smallest left ventricular cavity area) (14). The end-diastolic and end-systolic volumes and ejection fraction were then computed using a modified Simpson’s rule technique (15). Regional wall motion was evaluated by using the centerline method, with the endocardial excursion measured along 100 chords constructed perpendicular to a centerline drawn midway between the end-diastolic and the end-systolic contours and normalized for heart size (16). The extent of regional dysfunction was quantified according to the number of chords with percentage shortening falling below the mean, –2 SDs, of that detected in a group of 15 normal subjects (14).

Analysis of myocardial videointensity.   Our study applied a semiquantitative analysis of myocardial videointensity, based on the assumption that higher peak intensity of dye contrast in a region of interest (ROI) reflects greater myocardial blood volume (considered as an index of regional myocardial perfusion) (12,13,17–20) and using the hyperemic stimulus induced by transient coronary occlusion due to thrombus or balloon inflation during PTCA (21). In brief, image sequences of the LAD during a standard dye (Iopamiro 70, Bracco, Italy) contrast manual injection (7 ml over 3 to 4 s) obtained in a 90° left lateral projection were digitized onto a 512 x 512-pixel matrix. End-diastolic frames were selected and a polygonal ROI (size 1,325 pixels) was identified in the muscular region of the anterolateral profile of the left ventricle. Analysis was carried out from the frames before vessel visualization (precontrast myocardial intensity) to the point where contrast intensity was clearly diminishing, so as to include the frame with the maximal contrast intensity (peak contrast intensity). By subtracting the first of these values from the second, a corrected peak myocardial contrast intensity was obtained in gray pixel units (absolute values). To avoid excessive data scattering, these absolute values were converted to categorical values using a 5-point scale rising by 3 gray-scale pixel units increments and plateauing for absolute values exceeding 12 pixel units (12,13). In this way, a 1 to 5 (poor-optimal) categorical point scale was obtained, and used as an index of myocardial perfusion. Reproducibility was assessed by repeating measurements of myocardial videointensity pre-PTCA and immediately post-PTCA (precontrast and peak) in all patients.

Doppler coronary flow velocities and reserve.   In 10 patients who had "late" PTCA, we obtained informed consent to determine coronary flow velocities and Doppler flow reserve (DFR). A Doppler-tipped angioplasty guidewire (Flowire, Cardiometrics, Mountain View, California) was positioned in the LAD, with the tip distal to the coronary stenosis. Doppler flow velocity spectra were analyzed on line to determine time-averaged peak velocity (7). We determined peak velocity at baseline and after intracoronary bolus of adenosine 18 µg, and DFR was calculated as the ratio of maximal hyperemic peak velocity to baseline peak velocity. The DFR in these 10 patients was computed before and after PTCA.

Statistics.   Data are expressed as mean ± 1 SD. Differences in means between patient groups were assessed by t tests for paired or unpaired data as indicated. Repeated measurement analysis of variance (ANOVA) (two-way ANOVA) was used to assess the time change in hemodynamic and angiographic variables, with the effect of PTCA on muscle videointensity (improved vs. no change) as between patient factor. Contingency table analysis was performed for categorical variables. Linear regression was used to relate Doppler flow velocities and DFR to videointensity. Multivariate analysis was also performed to predict six-month changes in ventricular volumes. A p value < 0.05 was considered to be statistically significant.


   Results
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Discussion
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 References
 
In this population of patients, after PTCA there was a significant reduction in coronary stenosis (from 97.6 ± 5% to 50 ± 17.1%, p < 0.001), and a significant increase in TIMI flow grade (22) (from 1.2 ± 0.8 to 2.5 ± 0.7, p < 0.001) and in muscular videointensity (from 1.3 ± 0.8 to 3.1 ± 1.7 points, p < 0.001). Over the next six months, follow-up showed no variations in ventricular volumes (end-diastolic volumes: from 67.2 ± 17.2 to 68.8 ± 15.9 ml/m2, p = 0.63; end-systolic volumes: from 40.6 ± 13.4 to 40.7 ± 10.4 ml/m2, p = 0.94) or ejection fraction (from 40.0 ± 3.8% to 41.0 ± 10.4%, p = 0.63).

Doppler coronary flow velocities and reserve.   There was a significant correlation between DFR and coronary stenosis (r = 0.78; p < 0.001). After PTCA (Table 1), basal and peak Doppler flow velocities and DFR significantly improved. Moreover, these variations in Doppler parameters were in line with corresponding increments in videointensity values. In fact, there was a good relation of videointensity with peak flow velocity (r = 0.58; p = 0.007) and Doppler reserve (r = 0.71, p < 0.001). A borderline relation was found with baseline flow velocity (r = 0.46; p = 0.041).


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  		Table 1 Changes in Doppler Flow Velocities and Coronary Flow Reserve in 10 Patients With "Late" Percutaneous Transluminal Coronary Angioplasty

 
Videointensity as discriminating factor between patients.   Plotting changes (before and after PTCA) in muscular videointensity versus changes in cross-sectional area (Fig. 1) according to the 95% confidence intervals of the densitometric (± 1.5 gray scale points) and quantitative coronary angiographic reproducibility (± 5%), the population of patients divided into two separate groups: 29 patients with increased muscular videointensity (group A) after PTCA, and 24 patients without such improvement (group B), although the changes in the coronary cross-sectional area in the two groups overlapped.



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  		Figure 1 Individual changes in muscle videointensity (y-axis) versus changes in minimal descending coronary cross-sectional area (x-axis) before and immediately after percutaneous transluminal coronary angioplasty (PTCA). The 95% confidence intervals (dashed lines) of the densitometric and quantitative angiographic reproducibility are also shown. Twenty-nine patients showed increased muscle videointensity (open circles) after PTCA (group A), while 24 did not (group B, unchanged videointensity, black circles), although the coronary cross-sectional areas of the two groups overlapped.

 
Clinical characteristics, therapeutic regimens and PTCA details were comparable in the two groups (Table 2). The ANOVA analysis (Table 3) showed that after PTCA there was a comparable increase in coronary cross-sectional area in both groups (+49.34 ± 11.5%, +2.19 ± 0.78 mm2 in group A vs. +45.5 ± 20.2%, +2.09 ± 1.08 mm2 in group B, interaction respectively, p = 0.39 and p = 0.71). Changes in videointensity, however, were significantly different (videointensity being the selection criteria), with an increment of +3.13 ± 0.83 gray scale categorical points in group A as compared with +0.16 ± 0.8 gray scale points in group B (interaction: p < 0.001), although increment of TIMI flow was equivalent in the two groups (+1.4 ± 0.8 in group A vs. +1.1 ± 1.07 in group B, interaction: p = 0.27).


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  		Table 2 Comparison of Clinical, Instrumental and Therapeutic Data in Group A (Increased Videointensity) and in Group B (Unchanged Videointensity)

 

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  		Table 3 Hemodynamic and Echocardiographic Variables at Baseline and at 6 Months for Group A (Improved Videointensity) and Group B (Unchanged Videointensity): Coronary Stenosis, Videointensity and TIMI Flow Are Pre-PTCA and Post-PTCA

 
In the 10 patients with estimation of Doppler flow velocity pattern, five had increased videointensity (group A) and five had unchanged videointensity (group B) (Table 4). The ANOVA analysis showed that after PTCA, there was an increase in Doppler velocities and DFR in both groups ("time effect" for DFR: p < 0.001) which was greater ("group effect," p = 0.06) in the A group than in the B group (Table 4), but without a significant "interaction effect" (p = 0.11).


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  		Table 4 Subdivision of 10 Patients in Whom Doppler Flow Velocities and Reserve Were Computed Into Group A (Increased Videointensity) and Group B (Unchanged Videointensity)

 
Effect of increased muscular videointensity on left ventricular remodeling.   End-diastolic volumes in the two groups showed a significant time-perfusion interaction (–4.2 ± 14.5% in group A vs. +8.6 ± 17.4% in group B, p = 0.003) (Table 3), with a similar trend for end-systolic volumes (–3.05 ± 11.1% in group A vs. +4.1 ± 12.5% in group B, p = 0.027). However, there was no interaction between groups in the extent of regional asynergy over the study period (group A: –4.5 ± 15 chords; group B: +0.1 ± 12 chords, p = 0.31).

The beneficial effect of increased videointensity on the remodeling process was evident also after the patient population had been subdivided according to timing of PTCA ("primary/rescue" PTCA [n = 21] vs. "late" PTCA [n = 32]) (Fig. 2), although a significant interaction effect could be demonstrated for the diastolic volume only in the "primary/rescue" PTCA group (p = 0.005). On the average, ventricular volumes were smaller in this group compared with the "late" PTCA group, although extent of regional asynergy at baseline (39.9 ± 5.6 vs. 40.1 ± 10.3 chords, p = 0.62), creatine kinase (CK)-MB peak (256 ± 236.6 vs. 298 ± 271.1 U/liter, p = 0.27) and time to CPK-MB peak (14.2 ± 7.2 vs. 16.5 ± 7.8 h, p = 0.45) did not differ.



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  		Figure 2 Increased videointensity and left ventricular (LV) volumes (mean value ± SEM) in the "primary/rescue" percutaneous transluminal coronary angioplasty (PTCA) group (left graph) and in the "late" PTCA group (right graph). A trend for a beneficial effect from increased videointensity was evident in all subgroups, but it reached statistical significance only for the diastolic volume in the "primary/rescue" PTCA group. Ventricular volumes were, on the average, larger in the "late" PTCA group.

 
Multiple linear regression analysis.   A multivariate analysis was performed to verify the role of changes in cross-sectional stenosis, TIMI flow grading, muscle videointensity, regional asynergy and ejection fraction in predicting 6-month changes in ventricular volumes. Changes in end-diastolic volume correlated with videointensity (p = 0.01); this was true even when patients were grouped according to the timing of PTCA (p = 0.015 for "primary/rescue;" p = 0.040 for "late" PTCA). Changes in end-systolic volume index correlated with ejection fraction (p = 0.022) and videointensity (p = 0.05). No correlations were found for the other variables.


   Discussion
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 Methods
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Conclusions and clinical...
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Left ventricular remodeling is the final result of chronic changes in shape and structure and is characterized by progressive enlargement (23–26), a process in which the infarct size and the perfusion status of the IRA (27–29) are considered to be the most important factors. In recent years, clinicians’ attention has been focused (1–4) on the role of microcirculation preserved within the infarcted area, which is able to influence postinfarctional remodeling. In the present study, the mere status of myocardial perfusion, under the same conditions of vessel patency and extent of regional dysfunction, was used as the discriminating factor between patients.

Videointensity and coronary Doppler flow pattern.   Being considered as an index of myocardial perfusion (8), Doppler peak flow velocity has been found to be significantly increased in patients reperfused after PTCA of IRA during an acute MI (8,9), whereas DFR has been used to predict (as an index of viability) recovery of regional myocardial function (10). Thus, videointensity seems to be related to maximal myocardial blood flow (8), but also to myocardial viability and vascular integrity (10,30). Analyzing differences between groups A and B (increased vs. unchanged videointensity) before PTCA, the baseline and peak velocities were slightly higher in the B group (Table 4). After the resolution of coronary stenosis, in the two groups there was a significant increase in Doppler velocities, videointensity and DFR (greater in group A) (Table 4). The absence of an "interaction effect," besides the small number of patients in both groups, may be due to the increased basal flow velocities detected after PTCA in group A which, in turn, may reflect an increased number of functional vascular segments (8). Increased peak velocity, in the same group, may also reflect a greater myocardial blood flow secondary to an increased reserve of vasodilation, as suggested by increased videointensity.

Microvascular integrity, myocardial viability and their impact on left ventricular function.   In animal models of MI, myocellular necrosis has been associated with loss of microvasculature (5). Further zones of myocardium, located within the borders of necrosis, can show no reperfusion (no or low-reflow phenomenon) despite a patent IRA, as an expression of microvascular injury (6). A series of studies using myocardial contrast echocardiography (1,2,31) and angiographic dye contrast (3,4) demonstrated that the absence of reperfused zones in the risk areas promoted left ventricular remodeling with an increase in ventricular volumes, a decline in ejection fraction and worse mortality. However, degree of residual stenosis of the IRA differed across the various studies (32). In the present study, patients had different levels of videointensity, but under the same condition of coronary stenosis resolution and extent of regional wall motion abnormalities.

The exact mechanisms that connect such a reserve of vasodilation to a restraining effect on ventricular volumes in the absence of a significant recruitment of regional systolic function is unclear, but likely linked to factors capable of counteracting diastolic wall stress through the beneficial effect of blood-filled myocardial microcirculation (11,28,33). Unfortunately, in our patients, no data from tests unveiling myocardial reserve of contractility were available. It should be recognized, however, that these tests could underestimate the extent of viable myocardium, because reserve of contractility relates to the integrity of the inner layers of muscle and not to the "transmural" reserve of microcirculation (34–37).

Timing of coronary revascularization: "primary/rescue" versus "late" PTCA.   The beneficial effect of increased videointensity on the 6-month remodeling process was evident also after the patient population had been subdivided according to timing of PTCA (Fig. 2), although a significant interaction effect could be demonstrated for the diastolic volume only in the "primary/rescue" PTCA group. Smaller ventricular volumes in this group were also found, as compared with "late" PTCA, both at baseline and after six months (Fig. 2). Some recent studies comparing patients who underwent systemic thrombolysis with primary angioplasty have shown a reduction in mortality, myocardial ischemia and reinfarction in the angioplasty group, with an improved ejection fraction at discharge (38–40). It is possible that, beyond reperfusion, early resolution of a critical residual coronary stenosis already in the acute phase of MI after PTCA can favorably affect subsequent ventricular remodeling, avoiding stunning and/or hibernating phenomena, and providing earlier benefit to myocardial microcirculation as compared with systemic thrombolysis and "late" PTCA (41,42). In any case, the distribution of "primary/rescue" versus "late" PTCA in the perfused and nonperfused groups was comparable (Table 3), so that any possibly different effect on ventricular remodeling should have been balanced.


   Conclusions and clinical implications
Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions and clinical...
References
 
In the present study performed using an angiographic videodensitometric technique before and after PTCA of the IRA, it was possible to analyze perfusion of the related muscular territory. Dye videointensity showed a good relation with Doppler peak velocity and DFR, providing support for its use to assess myocardial perfusion in humans. Patients with increased videointensity after PTCA in comparison with nonperfused patients, showed a contrary trend toward a reduction in ventricular volumes over time, under the same final conditions of coronary patency and extent of regional dysfunction. The detection of increased muscle perfusion that is not followed by improved regional wall motion, suggests that selection of post-MI patients who might benefit from coronary revascularization in a perspective of counteracting ventricular remodeling, might be larger than what originally considered, giving further support to the concept of the "open artery hypothesis" (43).


   References
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 References
 

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