| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 1996;94:1269-1275.)
© 1996 American Heart Association, Inc.
Articles |
Alternation in the Coronary Blood Flow Velocity Pattern in Patients With No Reflow and Reperfused Acute Myocardial Infarction
the Division of Cardiology, Sakurabashi Watanabe Hospital, Osaka, and The First Department of Medicine, Osaka University School of Medicine (T. Masuyama, M.H.), Suita, Japan.
Correspondence to Hiroshi Ito, MD, Division of Cardiology, Sakurabashi Watanabe Hospital, 2-4-32 Umeda, Kita-ku, Osaka 530, Japan.
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Background Experimental and clinical evidence indicates that myocardial ischemia often damages the coronary microvasculature ("no-reflow" phenomenon). In this study, we examined the effect of this phenomenon on the coronary blood flow velocity pattern in patients with reperfused acute myocardial infarction.
Methods and Results We measured coronary blood flow velocity after coronary angioplasty in 42 patients with acute myocardial infarction using a Doppler guidewire. Myocardial contrast echocardiography (MCE) was also performed before and after angioplasty. Thirty-one patients showed good contrast reperfusion (MCE reflow), whereas the other 11 showed no reflow (MCE no reflow). Peak velocity and duration of systolic coronary flow were significantly less in patients with MCE no reflow than in those with MCE reflow (8±4 versus 17±10 cm/s and 207±79 versus 289±55 ms, respectively; P<.01). Early systolic retrograde flow was frequently observed in patients with MCE no reflow, whereas it was observed in only 1 patient among those with MCE reflow (95% versus 3%; P<.001). Although peak diastolic flow velocity was similar between the two subsets, diastolic deceleration rate was significantly higher in patients with MCE no reflow than in those with MCE reflow (107±76 versus 56±31 cm/s2; P<.01).
Conclusions The coronary flow velocity pattern in patients with the no-reflow phenomenon was characterized by the appearance of systolic retrograde flow, diminished systolic antegrade flow, and rapid deceleration of diastolic flow. Thus, the Doppler guidewire allows us to assess the presence of microvascular dysfunction in AMI.
Key Words: ultrasonics • circulation • reperfusion • myocardial infarction • microcirculation
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Coronary reperfusion therapy is widely performed to restore blood flow to the previously ischemic myocardium in patients with AMI. Several studies,1 2 3 4 5 however, have demonstrated that angiographically successful recanalization of the infarct-related artery does not necessarily guarantee adequate myocardial salvage in patients. We previously used MCE to show that a substantial no-reflow phenomenon is observed in about one fourth of patients with acute anterior myocardial infarction despite angiographically successful coronary recanalization.4 Little or no functional improvement was obtained in patients with no reflow on MCE.4 MCE, however, cannot be widely performed in patients with AMI, mainly because of technical limitations. On the other hand, recent clinical studies6 7 8 suggest that slow radio-contrast runoff observed in the infarct-related artery (TIMI grade 2 flow) after coronary intervention is possibly caused by microvascular dysfunction and is considered a sign that is compatible with the no-reflow phenomenon. Thus, microvascular dysfunction is likely to influence coronary flow dynamics, but there has been no systematic study to clarify the relation between microvascular damage and coronary flow dynamics in patients.
A recently developed Doppler guidewire (a 0.014-in guidewire with a 12-MHz Doppler transducer at the end) allows us to assess flow dynamics in the epicardial coronary artery during coronary intervention. Several studies have documented its usefulness in assessing changes in coronary flow velocity patterns proximal or distal to the coronary stenosis,9 10 11 12 13 monitoring coronary blood flow during angioplasty,10 11 14 15 and measuring coronary flow reserve13 16 17 18 in patients with ischemic heart disease. However, the blood flow velocity pattern of the infarct-related artery after coronary recanalization, especially in relation to the severity of coronary microvascular dysfunction, remains unknown.
In the present study, we used a Doppler guidewire to investigate coronary blood flow velocity patterns after coronary angioplasty in patients with AMI and to correlate these patterns with the no-reflow phenomenon assessed with MCE. We also studied the mechanism of slow radio-contrast filling (TIMI grade 2) in the infarct-related artery after angioplasty from the viewpoint of coronary flow dynamics.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Population
Between October 1993 and July 1994, 55 patients had successful coronary angioplasty after they were diagnosed with a first AMI and underwent MCE and coronary flow measurement by use of the Doppler guidewire. The diagnosis of AMI was based on chest pain that was
30 minutes' duration, ST-segment elevation of 2 mm in at least two contiguous ECG leads, more than a threefold increase in serum creatine kinase levels, and TIMI flow grade 0 or 1 at the initial coronary angiography. Thirteen patients were excluded for various reasons, including poor echocardiographic image (4 patients), unsuccessful angioplasty (2 patients), incomplete Doppler guidewire study (5 patients), and severe congestive heart failure (2 patients). Exchange of the balloon system was the main reason for the incomplete Doppler guidewire studies. No patient underwent thrombolytic therapy with recombinant tissue plasminogen activator before emergent catheterization. The culprit lesion was in the left anterior descending artery in 28 patients, in the left circumflex artery in 4, and in the right coronary artery in 10. Thirty-three patients subsequently developed Q-wave infarction and the other 9 manifested non-Q-wave AMI. The study protocol was approved by the ethics committee of our hospital. One of the investigators obtained informed consent from each patient before cardiac catheterization.
Study Protocol
Aspirin (243 mg) was given orally 30 minutes before coronary angiography. Intravenous heparin (10 000 U) was given before angiography according to our standard protocol. Coronary angiography was performed by the right femoral approach by use of Judkins' technique. After completion of the diagnostic coronary angiography and left ventriculography, MCE was performed as previously reported.4 In brief, we injected 2 mL sonicated ioxaglate (Hexabrix-320, Tanabe) containing microbubbles of a mean size of 12 µm into the left coronary artery while two-dimensional echocardiograms were recorded by use of a commercially available mechanical sector scanner (model SAL-38B, Toshiba; carrier frequency of 3.5 MHz). Recorded MCE images were the parasternal short-axis view at the mid-papillary muscle level and the apical two-chamber view. MCE was repeated with injection into the right coronary artery. All MCE images were recorded on 1.25-cm VHS videotape.
After positioning an 8F guiding catheter into the coronary ostium, we inserted a 0.014-in Doppler guidewire (Flowire, Cardiometrics) into an appropriately sized balloon catheter and positioned them at the appropriate site for angioplasty. The tip of the Doppler guidewire was positioned distal to the second diagonal branch in the left anterior descending coronary artery, distal to the obtuse marginal branch in the circumflex artery, or in the atrioventricular branch in the right coronary artery. After the position for measuring flow velocity was optimized, we performed coronary angioplasty in a routine manner using appropriately sized (2- to 3.5-mm) angioplasty balloon catheters advanced over the Doppler guidewire. Coronary blood flow velocity was recorded continuously on a 1.25-cm VHS videotape with audio output throughout the angioplasty procedure.
Angioplasty was repeated to reduce the degree of residual stenosis in all regions of the infarct-related artery vessel to <25% with restoration of flow. Final recording of coronary velocity was performed a mean of 10 minutes after the last balloon inflation to avoid the influence of possible reactive hyperemia. After that, coronary angiography was performed to determine TIMI flow grade at 30 frames/s. Then, MCE was repeated by use of the same procedure mentioned above.
Analysis of Echocardiographic Data
An experienced echocardiographer analyzed the MCE images with a commercially available image-analyzing system (color cardiology workstation, TomTec Imaging). The apical two-chamber view was analyzed in patients with anterior myocardial infarction, and the short-axis view at the papillary muscle level was analyzed in those with inferior- or posterior-wall myocardial infarction. Two independent observers with no knowledge of the clinical data analyzed the MCE images as previously reported.4 In cases of disagreement, consensus was established by a third observer. Contrast perfusion defects in the end-diastolic image before and after coronary recanalization were defined as the area at risk and the area of no-reflow phenomenon, respectively. We standardized the area of the no-reflow phenomenon by establishing its ratio to the risk area. When the ratio exceeded 25%, myocardial reperfusion in the corresponding segment was considered incomplete (MCE no reflow). If this ratio was 
25%, we considered myocardial reperfusion adequate (MCE reflow).
Analysis of Coronary Blood Flow Velocity Pattern
The coronary blood flow velocity spectrum recorded a mean of 10 minutes after the last balloon inflation was used for analysis. The coronary flow velocity spectrum recorded on the videotape was digitized by use of an off-line personal computer. The digitized velocity spectrum during systole was provided for the following parameters: peak and mean antegrade systolic velocity (cm/s), FDs (ms), and systolic antegrade coronary flow volume (mL), which was calculated as a product of the systolic antegrade flow velocity integral (cm), heart rate (bpm), and coronary cross-sectional area (cm2) determined angiographically from the diameter of the infarct-related artery at the site of the tip of the Doppler guidewire. These parameters were calculated as the mean of at least five continuous cardiac cycles. Because rapid retrograde flow (peak velocity 10 cm/s, duration 60 ms) was observed in early systole in some patients, the prevalence of this abnormal systolic retrograde flow was compared between patients with and without MCE no reflow.
The digitized velocity spectrum during diastole was provided for the following parameters: peak and mean diastolic velocity (cm/s), diastolic flow duration (ms), and diastolic coronary flow volume (mL) calculated as a product of diastolic velocity integral (cm), heart rate (bpm), and coronary cross-sectional area (cm2). The rate of decline in flow velocity in diastole was calculated as the diastolic deceleration rate (m/s2). The ratios of systolic to diastolic peak velocities and coronary forward flow volumes (peak systolic/diastolic velocity and systolic/diastolic coronary flow volume) were also calculated.
Analysis of Catheterization Data
Two radiologists with no knowledge of patient data evaluated the antegrade radio-contrast flow of the infarct-related artery on the final coronary angiogram using the TIMI criteria. The TIMI flow grades have been defined elsewhere.8 19 In four cases of disagreement, a third radiologist, who also was blinded to patient data, determined the TIMI grade. The percent coronary diameter stenosis of the infarct-related artery was also quantified by use of a validated technique. To elucidate the underlying mechanism of TIMI grade 2 reflow, we analyzed the dynamics of radio-contrast filling in the infarct-related artery. Two independent observers evaluated runoff of radio contrast in systole and diastole. Backward movement or cessation of runoff was judged as an abnormal finding in both the systolic and diastolic phases. There were no disagreements in terms of this judgment. We graded collateral channels using previously reported criteria.20
Reproducibility of Coronary Flow Measurement
Ten studies were randomly selected for evaluation of reproducibility of results in coronary flow measurement. One observer digitized the coronary flow velocity spectrum without knowledge of the previous measurement, which had been made more than 1 week previously (intraobserver variability). Intraobserver variation was 5% (1.5±1.2%). Similarly, two independent observers digitized the velocity spectrum in a blinded fashion and tested the interobserver variability. Interobserver variability was 6% (1.7±1.6%).
Statistics
Continuous values were expressed as mean±SD. Comparisons of variables between two groups were made by one-way ANOVA and Scheffe's F test for factor analysis. Categorical variables between two groups were compared with the use of the 
2 test. Statistical differences were considered significant at a value of P<.05 (two sided).
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Coronary Flow Velocity Patterns After Angioplasty
A substantial amount of area with no reflow was found within the risk area in 11 (26%) of 42 patients by MCE (MCE no reflow); the remaining 31 patients were classified as having MCE reflow. Characteristics of the two subsets are described in Table 1
. Figs 1 and 2 show MCE images and coronary flow velocity spectrums in patients with MCE reflow and MCE no reflow, respectively. The coronary flow velocity pattern in the patient with MCE reflow appears normal and is quite different from the patient with MCE no reflow. The coronary flow velocity spectrum in the patient with MCE no reflow seems to be characterized by low systolic antegrade flow velocity, appearance of early systolic retrograde flow, and a steep deceleration slope of the diastolic flow velocity. Fig 3 shows the coronary velocity pattern in another case of MCE no reflow. In this case, retrograde flow was observed throughout the systolic phase, and antegrade flow appeared only in diastole.
|
|
|
|
Systolic peak and mean velocities were significantly lower in patients with MCE no reflow than in those with MCE reflow (Table 2). FDs was significantly shorter in patients with MCE no reflow than in those with MCE reflow. Therefore, systolic antegrade flow volume tended to be lower in patients with MCE no reflow than in those with MCE reflow. We frequently observed early systolic retrograde flow in patients with MCE no reflow (91%, or 10 of 11 patients), whereas this abnormal flow was observed in only 1 (3%) of the 31 patients with MCE reflow. Therefore, the appearance of early systolic retrograde flow predicted MCE no reflow with high sensitivity (91%) and specificity (97%).
|
Regarding diastolic coronary flow velocity pattern, there was no significant difference in peak or mean velocity between the two subsets (Table 2
). The duration of diastolic antegrade flow, however, was shorter in patients with MCE no reflow than in those with MCE reflow. The systolic to diastolic peak velocity ratio and flow ratio were significantly lower in patients with MCE no reflow than in those with MCE reflow. The diastolic deceleration rate was significantly higher in patients with MCE no reflow than in those with MCE reflow, which indicates that coronary flow velocity decreases more rapidly during diastole in patients with MCE no reflow than in those with MCE reflow.
Relation Between TIMI Flow Grading and Coronary Flow Dynamics
We investigated the relation between TIMI flow grade and coronary flow dynamics. TIMI grade 2 reflow was observed in 9 of 11 patients with MCE no reflow after angioplasty (no reflow/TIMI-2), and the other 2 patients manifested TIMI grade 3 reflow (no reflow/TIMI-3). All patients with MCE reflow manifested TIMI grade 3 reflow (reflow/TIMI-3). Abnormal radio-contrast runoff (retrograde or stopped) was observed in all patients with no reflow/TIMI-2 during systole, whereas no patients with no reflow/TIMI-3 or reflow/TIMI-3 manifested this abnormal radio-contrast runoff. In diastole, abnormal radio-contrast runoff was not observed in any of these subsets. Thus, TIMI grade 2 reflow is highly associated with early retrograde flow in systole.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Microvascular Dysfunction and Coronary Blood Flow Velocity Pattern
Several studies9 10 11 12 demonstrated that a Doppler guidewire is useful for evaluation of the physiological significance of coronary stenosis. Blood flow distal to the critical coronary stenosis is systolic dominant, and therefore, the diastolic to systolic velocity ratio is significantly lower than the normal flow velocity pattern.9 10 11 12 However, the coronary blood flow velocity pattern observed in patients with MCE no reflow despite the absence of residual coronary stenosis was quite different from that observed in patients with coronary stenosis. In patients with substantial no-reflow phenomenon, the coronary blood flow velocity pattern is characterized by a reduction in systolic antegrade flow, the appearance of abnormal retrograde flow in early systole, and rapid deceleration of the diastolic flow velocity. The diastolic to systolic velocity ratio or flow ratio was even higher in patients with MCE no reflow than in those with MCE reflow. To our knowledge, this is the first report to elucidate that a distinct coronary flow pattern is associated with lack of reperfusion, which also appears to be correlated with TIMI grade 2 reflow.
The precise mechanisms of the alterations in the coronary blood flow velocity pattern may not be fully explained by the variables examined in the present study. It is well known that microvascular impedance significantly affects total coronary resistance in patients without severe coronary stenosis.3 In patients with MCE no reflow, the coronary microvasculature is profoundly damaged, and it seems probable that microvascular impedance increases21 22 23 and the intramyocardial blood pool decreases. The reduction in postprocedural coronary systolic flow velocity in patients with MCE no reflow may be explained primarily by an increase in microvascular impedance.
The early systolic retrograde flow found in patients with MCE no reflow was different from the collateral flow observed during balloon inflation.24 25 Experimental study26 has demonstrated that small early systolic reverse flow ("slosh") is detected in the peripheral coronary artery, such as the septal branch, even in normal subjects and that this reverse flow is caused by the milking effect produced by the contracting myocardium. However, this systolic retrograde flow should be different from that observed in the present study, because this "slosh" can no longer be detected in the major epicardial coronary artery. The early systolic retrograde flow identified in the present study possibly may be explained by an increase in microvascular impedance (Fig 4). The coronary microvasculature would be diffusely obstructed in patients with MCE no reflow. Increased myocardial stress during systole, even in the infarct region, would usually squeeze the intramyocardial blood, which is pooled during diastole, into the coronary venous circulation in normal subjects and in patients with MCE reflow. In patients with MCE no reflow, however, the pooled blood in the myocardium might not be smoothly squeezed into the venous circulation during systole because of the diffuse obstruction of microvasculature and, thus, would be pushed back to the epicardial coronary artery to produce early systolic retrograde flow. Because of this abnormal retrograde flow, the FDs was shorter in patients with MCE no reflow than in those with MCE reflow.
|
In diastole, the coronary blood flow predominantly fills the intramyocardial blood pool and partially runs through the coronary microcirculation into the venous circulation in normal subjects and in AMI patients with MCE reflow (Fig 4). In patients with MCE no reflow, the coronary microvasculature is profoundly damaged, which results in considerable reduction of the intramyocardial blood pool. The coronary blood flow should rapidly fill the residual intramyocardial blood pool and the distal coronary pressure should increase in the very early phase in diastole. Therefore, the coronary flow rapidly decreases its velocity in mid- to late diastole in patients with MCE no reflow, resulting in a decrease in duration of the diastolic antegrade flow.
The blood flow dynamics in a recanalized coronary artery may also depend on several other complex, interrelated factors, such as myocardial mass supplied by the infarct-related artery, vasodilator reserve, the extent of reperfusion injury, and hemodynamics (preload, afterload, and heart rate). Although the MCE no reflow group exhibited a larger infarction than the MCE reflow group,4 8 27 there were no differences in most of the hemodynamic variables, such as systolic and diastolic blood pressures and pulmonary capillary wedge pressure, between the two subsets in the present study.
Relation Between TIMI Grade and Coronary Flow Dynamics
Recent studies have suggested that TIMI grade 2 reflow is caused by the microvascular dysfunction of the ischemic region8 28 and may be regarded as reperfusion failure29 30 in AMI. However, the underlying mechanisms of slow radio-contrast filling in the infarct-related artery remain unknown. We initially speculated that slow movement of radio contrast throughout the cardiac cycle might contribute to TIMI grade 2 reflow. However, the present study clearly showed the to-and-fro features of the epicardial coronary blood flow in patients with TIMI grade 2 reflow: a rapid decrease in the diastolic antegrade flow velocity and a subsequent rapid retrograde flow in early systole. We investigated the relation between radio-contrast motion and coronary flow velocity dynamics in patients with TIMI grade 2 reflow. In fact, all patients with TIMI grade 2 reflow showed abnormal runoff of radio-contrast medium, such as retrograde movement or cessation of motion, during systole. Such abnormal radio-contrast runoff was not found during diastole in any patient. If systolic retrograde movement of radio contrast is found in patients with TIMI grade 2 reflow after coronary intervention, it would indicate microvascular dysfunction rather than the presence of a flow-restricting lesion in the epicardial coronary artery.
On the other hand, abnormal runoff of radio-contrast medium was not observed in patients with MCE reflow or those with no reflow/TIMI-3. Because of the small population of patients with no reflow/TIMI-3, we cannot fully elucidate the difference in radio-contrast runoff between TIMI grades 2 and 3 in patients with MCE no reflow. Visual judgment of radio-contrast runoff may well be affected by several factors, such as heart rate, size of the coronary artery, injection speed, and volume of the contrast medium.
Study Limitations
The coronary flow velocity pattern may alter with the position of the tip of the guidewire. Because time is limited in an emergent setting such as that in the present study, we could not measure flow velocity at multiple positions in the infarct-related artery. In the present study, the Doppler guidewire was positioned and flow velocity was measured only at a position distal to the culprit lesion. We did not measure coronary flow reserve with intracoronary administration of adenosine or papaverine, although we believe this measurement might be useful in patients with reperfused AMI.31 However, the purpose of the present study was to derive the parameters from the coronary flow velocity spectrum that identify patients with advanced microvascular damage, and we found a characteristic flow velocity pattern specific to microvascular damage even without administration of adenosine or papaverine.
Hyperemia after coronary reflow might influence the coronary flow velocity spectrum. In animals, the hyperemic increase in coronary flow continues for several hours,32 33 and coronary perfusion may dynamically change within a few hours34 35 to days36 after prolonged coronary occlusion. Because of the emergency situation, we could not monitor coronary blood flow continuously for several hours after reperfusion in any patient.
The coronary blood flow velocity pattern differs between the right and left coronary arteries.37 Systolic blood flow velocity is relatively augmented, and a systolic-predominant flow velocity pattern is even observed in the right coronary artery. The difference in the coronary flow velocity pattern is explained by the fact that the right coronary artery perfuses the right ventricular branch. We positioned the tip of the Doppler guidewire in the atrioventricular branch in the present study, and therefore, the effect on the examined coronary artery could be minimized.
Clinical Implications
The present study revealed that monitoring coronary blood flow velocity by use of a Doppler guidewire is a promising method to detect the no-reflow phenomenon in patients with reperfused AMI. This approach is more easily applied than MCE in acute patients. Among the characteristic parameters observed in patients with MCE no reflow, the appearance of early systolic retrograde flow is the most remarkable sign to identify patients with severe microvascular dysfunction. In our previous study,27 patients with MCE no reflow showed poor functional outcomes and high frequency of left ventricular remodeling, as well as complications such as prolonged congestive heart failure, malignant arrhythmia, and pericardial effusion after coronary reflow. Therefore, the use of a Doppler guidewire could provide helpful information for determining therapeutic strategy in patients with AMI.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
The authors gratefully acknowledge the excellent technical assistance of Yuzo Sakagami, Masakazu Ueda, Naoki Jonishi, and Hideshi Shimokawa and the excellent secretarial assistance of Rie Nishizawa.
Received December 12, 1995; revision received April 3, 1996; accepted April 15, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Schofer J, Mont R, Mathey DG. Scintigraphic evidence of the `no reflow' phenomenon in human beings after coronary thrombolysis. J Am Coll Cardiol. 1985;5:593-598.[Abstract]
2. Bates ER, Krell MJ, Dean EN, O'Neill WW, Vogel RA. Demonstration of the `no-reflow' phenomenon by digital coronary arteriography. Am J Cardiol. 1986;57:177-178.[Medline] [Order article via Infotrieve]
3. Nicklas JM, Diltz EA, O'Neill WW, Bourdillon PDV, Walton JA Jr, Bertram P. Quantitative measurement of coronary flow during medical revascularization (thrombolysis or angioplasty) in patients with acute infarction. J Am Coll Cardiol. 1987;10:284-289.[Abstract]
4.
Ito H, Tomooka T, Sakai N, Yu H, Higashino Y, Fujii K, Masuyama T, Kitabatake A, Minamino T. Lack of myocardial perfusion immediately after successful thrombolysis: a predictor of poor recovery of left ventricular function in anterior myocardial infarction. Circulation. 1992;85:1699-1705.
5.
Ragosta M, Camarano G, Kaul S, Powers ER, Sarembock IJ, Gimple LW. Microvascular integrity indicates myocellular viability in patients with recent myocardial infarction: new insights using myocardial contrast echocardiography. Circulation. 1994;89:2562-2569.
6.
Piana RN, Paik GY, Moscucci M, Cohen DJ, Gibson CM, Kugelmass AD, Carrozza JP Jr, Kunt RE, Baim DS. Incidence and treatment of `no-reflow' after percutaneous coronary intervention. Circulation. 1994;89:2514-2518.
7. Shani J, Feld H, Frankel R, Hollander G. Reversal of the no-reflow phenomenon with intracoronary verapamil during coronary angioplasty for acute myocardial infarction. Circulation. 1992;86(suppl I):I-852. Abstract.
8.
Ito H, Okamura A, Iwakura K, Masuyama T, Hori M, Takiuchi S, Negoro S, Nakatsuchi Y, Taniyama Y, Higashino Y, Fujii K, Minamino T. Myocardial perfusion patterns related to Thrombolysis In Myocardial Infarction perfusion grades after coronary angioplasty in patients with acute anterior wall myocardial infarction. Circulation. 1996;93:1993-1999.
9. Ofili EO, Labovitz AJ, Kern MJ. Coronary flow velocity dynamics in normal and diseased arteries. Am J Cardiol. 1993;71:3D-9D.[Medline] [Order article via Infotrieve]
10. Segal J, Kern MJ, Scott NA, King SB, Doucette JW, Heuser RR, Ofili E, Siegel R. Alteration of phasic coronary artery flow velocity in humans during percutaneous coronary angioplasty. J Am Coll Cardiol. 1992;20:276-286.[Abstract]
11. Ofili EO, Kern MJ, Labovitz AJ, St. Vrain JA, Segal J, Aguirre FV, Castello R. Analysis of coronary blood flow velocity dynamics in angiographically normal and stenosed arteries before and after endolumen enlargement by angioplasty. J Am Coll Cardiol. 1993;21:308-316.[Abstract]
12. Kern MJ, Flynn MS, Caracciolo EA, Bach RG, Donohue TJ, Aguirre FV. Use of translesional coronary flow velocity for interventional decisions in a patient with multiple intermediately severe coronary stenosis. Cathet Cardiovasc Diagn. 1993;29:148-153.[Medline] [Order article via Infotrieve]
13. Deychak YA, Segal J, Reiner JS, Rohrbeck SC, Thompson MA, Lundergan CF, Ross AM, Wasserman AG. Doppler guide wire flow-velocity indexes measured distal to coronary stenoses associated with reversible thallium perfusion defects. Am Heart J. 1995;129:219-227.[Medline] [Order article via Infotrieve]
14. Kern MJ, Aguirre FV, Donohue TJ, Bach RG, Caracciolo EA, Flynn MS, Wolford T, Moore JA. Continuous coronary flow velocity monitoring during coronary interventions: velocity trend patterns associated with adverse events. Am Heart J. 1994;128:426-434.[Medline] [Order article via Infotrieve]
15. Anderson HV, Kirkeeide RL, Krishnaswami A, Weigelt LA, Revana M, Weisman HF, Willerson JT. Cyclic flow variations after coronary angioplasty in humans: clinical and angiographic characteristics and elimination with 7E3 monoclonal antiplatelet antibody. J Am Coll Cardiol. 1994;23:1031-1037.[Abstract]
16. Deychak YA, Segal J, Reiner JS, Nachnani S. Doppler guide wire-derived coronary flow reserve distal to intermediate stenoses used in clinical decision making regarding intervention therapy. Am Heart J. 1994;128:178-181.[Medline] [Order article via Infotrieve]
17. Joye JD, Schulman DS, Lasorda D, Farah T, Donohue BC, Reichek N. Intracoronary Doppler guide wire versus stress single-photon emission computed tomographic thallium-201 imaging in assessment of intermediate coronary stenoses. J Am Coll Cardiol. 1994;24:940-947.[Abstract]
18. Deychak YA, Segal J, Reiner JS, Rohrbeck SC, Thompson MA, Lundergan CF, Ross AM, Wasserman AG. Doppler guide wire flow-velocity indexes measured distal to coronary stenoses associated with reversible thallium perfusion defects. Am Heart J. 1995;129:219-227.
19.
Chesebro JH, Knatterud G, Roberts R, and the TIMI Investigators. Thrombolysis In Myocardial Infarction (TIMI) trial, phase I: a comparison between intravenous plasminogen activator and intravenous streptokinase. Circulation. 1987;76:142-154.
20. Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Cardiol. 1985;5:587-592.[Abstract]
21. Engler RL, Schmid-Schoenbein G, Pavelec SR. Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. Am J Pathol. 1974;111:98-111.[Abstract]
22.
Frame LH, Powell WJ Jr. Progressive perfusion impairment during prolonged low flow myocardial ischemia in canine myocardium. Circ Res. 1976;39:269-276.
23.
Gorman MW, Sparks HVJ. Progressive coronary vasoconstriction during relative ischemia in dogs. Circ Res. 1982;51:411-420.
24. Oflili E, Kern J, Tatineni S, Deligonul U, Aguirre F, Serota H, Labovit AJ. Detection of coronary collateral flow by a Doppler-tipped guide wire during coronary angioplasty. Am Heart J. 1991;122:221-225.[Medline] [Order article via Infotrieve]
25. Kern MJ, Donohue TJ, Bach R, Aguirre FV, Caracciolo EA, Ofili EO. Quantitating coronary collateral flow velocity in patients during coronary angioplasty using a Doppler guidewire. Am J Cardiol. 1993;71:34D-40D.[Medline] [Order article via Infotrieve]
26. Goto M, Kimura A, Tsujioka K, Kajiya F. Characteristics of coronary artery inflow and its significance in coronary pathophysiology. Biorheology. 1993;30:323-331.[Medline] [Order article via Infotrieve]
27.
Ito H, Maruyama A, Iwakura K, Takiuchi S, Masuyama T, Hori M, Higashino Y, Fujii K, Minamino T. Clinical implications of `no-reflow' phenomenon: a predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction. Circulation. 1996;93:223-228.
28. Piana RN, Paik GY, Moscucci M, Cohen DJ, Gibson CM, Kugelmass AD, Carrozza JP, Kuntz RE, Baim DS. Incidence and treatment of `no-reflow' after percutaneous coronary intervention. Circulation. 1994;89:2514-2518.
29. Karagounis L, Sorensen SG, Menlove RL, Moreno F, Anderson JL, for the TEAM-2 Investigators. Does Thrombolysis In Myocardial Infarction (TIMI) perfusion grade 2 represent a mostly patent artery or mostly occluded artery? Enzymatic and electrocardiographic evidence from the TEAM-2 study. J Am Coll Cardiol. 1992;19:1-10.[Abstract]
30.
Keiman NS, White HD, Ohman EM, Ross AM, Woodlief LH, Califf RM, Holmes DR, Bates E, Pfisterer M, Vahanian A, Topol EJ, for the GUSTO Investigators. Mortality within 24 hours of thrombolysis for myocardial infarction: the importance of early reperfusion. Circulation. 1994;90:2658-2665.
31.
Suryapranata H, Zijlstra F, MacLeod DC, van den Brand M, de Feyter PJ, Serruys PW. Predictive value of reactive hyperemic response on reperfusion on recovery of regional myocardial function after coronary angioplasty in acute myocardial infarction. Circulation. 1994;89:1109-1117.
32.
Heyndrickx GR, Amano J, Patrick TA, Manders WT, Rogers G, Rosendorf C, Vatner SF. Effects of coronary artery reperfusion on regional myocardial blood flow and function in conscious baboons. Circulation. 1985;71:1029-1037.
33.
Kitakaze M, Hori M, Tamai J, Iwakura K, Koretsune Y, Kagiya T, Iwai K, Kitabatake A, Inoue M, Kamada T. 
1-Adrenoceptor activity regulates release of adenosine from the ischemic myocardium in dogs. Circ Res. 1987;60:631-639.
34.
Ambrosio G, Weisman HF, Mannisi JA, Becker LC. Progressive impairment of regional myocardial perfusion after initial restoration of postischemic blood flow. Circulation. 1989;80:1846-1861.
35.
Villanueva FS, Glasheen WP, Sklenar J, Kaul S. Characterization of spatial patterns of flow within the reperfused myocardium by myocardial contrast echocardiography: implication in determining extent of myocardial salvage. Circulation. 1993;88:2596-2606.
36.
Knabb RM, Bergmann SR, Fox KA, Sobel BE. The temporal patterns of recovery of myocardial perfusion and metabolism delineated by positron emission tomography after coronary thrombolysis. J Nucl Med. 1987;28:1563-1570.
37. Heller LI, Silver KH, Villegas BJ, Balcom SJ, Weiner BH. Blood flow velocity in the right coronary artery: assessment before and after angioplasty. J Am Coll Cardiol. 1994;24:1012-1017.[Abstract]
This article has been cited by other articles:
 |
|
 |
|
  Authors/Task Force Members, F. Van de Werf, J. Bax, A. Betriu, C. Blomstrom-Lundqvist, F. Crea, V. Falk, G. Filippatos, K. Fox, K. Huber, et al. Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology: Eur. Heart J., December 1, 2008; 29(23): 2909 - 2945. [Full Text] [PDF]
|
|
|
|
 |
|
 T Takahashi, Y Hiasa, Y Ohara, S Miyazaki, K Mahara, R Ogura, H Miyajima, K Yuba, N Suzuki, S Hosokawa, et al. Acute hyperglycaemia prevents the protective effect of pre-infarction angina on microvascular function after primary angioplasty for acute myocardial infarction Heart, November 1, 2008; 94(11): 1402 - 1406. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Hadjiloizou, J. E. Davies, I. S. Malik, J. Aguado-Sierra, K. Willson, R. A. Foale, K. H. Parker, A. D. Hughes, D. P. Francis, and J. Mayet Differences in cardiac microcirculatory wave patterns between the proximal left mainstem and proximal right coronary artery Am J Physiol Heart Circ Physiol, September 1, 2008; 295(3): H1198 - H1205. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Hirsch, R. Nijveldt, J. D.E. Haeck, A. M. Beek, K. T. Koch, J. P.S. Henriques, R. J. van der Schaaf, M. M. Vis, J. Baan Jr, R. J. de Winter, et al. Relation between the assessment of microvascular injury by cardiovascular magnetic resonance and coronary Doppler flow velocity measurements in patients with acute anterior wall myocardial infarction. J. Am. Coll. Cardiol., June 10, 2008; 51(23): 2230 - 2238. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. E. Rochitte Microvascular obstruction the final frontier for a complete myocardial reperfusion. J. Am. Coll. Cardiol., June 10, 2008; 51(23): 2239 - 2240. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Karatasakis, E. Leontiadis, E. Papadakis, N. Koutsogiannis, G. Athanassopoulos, K. Spargias, D. Poldermans, S. E. Karagiannis, and D. V. Cokkinos Transthoracic Doppler echocardiography assessment of left anterior descending artery flow in patients with previous anterior myocardial infarction Eur J Echocardiogr, May 1, 2008; 9(3): 363 - 367. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Heper, M. E. Korkmaz, and A. Kilic Reperfusion Arrhythmias: Are They Only a Marker of Epicardial Reperfusion or Continuing Myocardial Ischemia After Acute Myocardial Infarction? Angiology, January 1, 2008; 58(6): 663 - 670. [Abstract] [PDF]
|
|
|
|
|
|
A. Saraste, J. W Koskenvuo, M. Saraste, J. Parkka, J. Toikka, A. Naum, H. Ukkonen, J. Knuuti, J. Airaksinen, and J. Hartiala Coronary artery flow velocity profile measured by transthoracic Doppler echocardiography predicts myocardial viability after acute myocardial infarction Heart, April 1, 2007; 93(4): 456 - 457. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M Kato, K Dote, S Sasaki, K Goto, H Takemoto, S Habara, and D Hasegawa Myocardial performance index for assessment of left ventricular outcome in successfully recanalised anterior myocardial infarction Heart, May 1, 2005; 91(5): 583 - 588. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y Ohara, Y Hiasa, T Takahashi, K Yamaguchi, R Ogura, T Ogata, K Yuba, K Kusunoki, S Hosokawa, K Kishi, et al. Relation between the TIMI frame count and the degree of microvascular injury after primary coronary angioplasty in patients with acute anterior myocardial infarction Heart, January 1, 2005; 91(1): 64 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. P. Furber, F. Prunier, H. C. P. Nguyen, S. Boulet, S. Delepine, and P. Geslin Coronary Blood Flow Assessment After Successful Angioplasty for Acute Myocardial Infarction Predicts the Risk of Long-Term Cardiac Events Circulation, December 7, 2004; 110(23): 3527 - 3533. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Iwakura, H. Ito, S. Kawano, A. Okamura, K. Tanaka, Y. Nishida, Y. Maekawa, and K. Fujii Assessing myocardial perfusion with the transthoracic Doppler technique in patients with reperfused anterior myocardial infarction: comparison with angiographic, enzymatic and electrocardiographic indices Eur. Heart J., September 1, 2004; 25(17): 1526 - 1533. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. B. Feinstein The powerful microbubble: from bench to bedside, from intravascular indicator to therapeutic delivery system, and beyond Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H450 - H457. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Gibson, J. Karha, S. A. Murphy, J. A. de Lemos, D. A. Morrow, R. P. Giugliano, M. T. Roe, R. A. Harrington, C. P. Cannon, E. M. Antman, et al. Association of a pulsatile blood flow pattern on coronary arteriography and short-term clinical outcomes in acute myocardial infarction J. Am. Coll. Cardiol., April 7, 2004; 43(7): 1170 - 1176. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Bax, R. J. de Winter, C. E. Schotborgh, K. T. Koch, M. Meuwissen, M. Voskuil, R. Adams, K. J. J. Mulder, J. G. P. Tijssen, and J. J. Piek Short- and Long-Term recovery of left ventricular function predicted at the time of primary percutaneous coronary intervention in anterior myocardial infarction J. Am. Coll. Cardiol., February 18, 2004; 43(4): 534 - 541. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Takeuchi, Y. Nohtomi, H. Yoshitani, C. Miyazaki, K. Sakamoto, and J. Yoshikawa Enhanced coronary flow velocity during intra-aortic balloon pumping assessed by transthoracic doppler echocardiography J. Am. Coll. Cardiol., February 4, 2004; 43(3): 368 - 376. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N Ikeda, T Yasu, N Kubo, S Hashimoto, Y Tsuruya, M Fujii, M Kawakami, and M Saito Nicorandil versus isosorbide dinitrate as adjunctive treatment to direct balloon angioplasty in acute myocardial infarction Heart, February 1, 2004; 90(2): 181 - 185. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Kaul and H. Ito Microvasculature in Acute Myocardial Ischemia: Part II: Evolving Concepts in Pathophysiology, Diagnosis, and Treatment Circulation, January 27, 2004; 109(3): 310 - 315. [Full Text] [PDF]
|
|
|
|
|
|
S. Lee, Y. Otsuji, S. Minagoe, S. Hamasaki, K. Toyonaga, M. Negishi, M. Tsurugida, H. Toda, and C. Tei Noninvasive Evaluation of Coronary Reperfusion by Transthoracic Doppler Echocardiography in Patients With Anterior Acute Myocardial Infarction Before Coronary Intervention Circulation, December 2, 2003; 108(22): 2763 - 2768. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R Hoffmann, P Haager, W Lepper, A Franke, and P Hanrath Relation of coronary flow pattern to myocardial blush grade in patients with first acute myocardial infarction Heart, October 1, 2003; 89(10): 1147 - 1151. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T Hozumi, Y Kanzaki, Y Ueda, A Yamamuro, T Takagi, T Akasaka, S Homma, K Yoshida, and J Yoshikawa Coronary flow velocity analysis during short term follow up after coronary reperfusion: use of transthoracic Doppler echocardiography to predict regional wall motion recovery in patients with acute myocardial infarction Heart, October 1, 2003; 89(10): 1163 - 1168. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Ito and K. Yamamoto Prognostic significance of coronary blood flow velocity patterns in patients with reperfused acute myocardial infarction and TIMI-2 flow: Reply J. Am. Coll. Cardiol., July 2, 2003; 42(1): 182 - 183. [Full Text] [PDF]
|
|
|
|
|
|
L. J. Feldman, P. Coste, A. Furber, P. Dupouy, M. S. Slama, J.-P. Monassier, C. Tron, A. Lafont, M. Faraggi, D. Le Guludec, et al. Incomplete Resolution of ST-Segment Elevation Is a Marker of Transient Microcirculatory Dysfunction After Stenting for Acute Myocardial Infarction Circulation, June 3, 2003; 107(21): 2684 - 2689. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y Nohtomi, M Takeuchi, K Nagasawa, K Arimura, K Miyata, K Kuwata, T Yamawaki, S Kondo, A Yamada, and S Okamatsu Persistence of systolic coronary flow reversal predicts irreversible dysfunction after reperfused anterior myocardial infarction Heart, April 1, 2003; 89(4): 382 - 388. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Yamamuro, T. Akasaka, K. Tamita, K. Yamabe, M. Katayama, T. Takagi, and S. Morioka Coronary Flow Velocity Pattern Immediately After Percutaneous Coronary Intervention as a Predictor of Complications and In-Hospital Survival After Acute Myocardial Infarction Circulation, December 10, 2002; 106(24): 3051 - 3056. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Yamamoto, H. Ito, K. Iwakura, S. Kawano, M. Ikushima, T. Masuyama, T. Ogihara, and K. Fujii Two different coronary blood flow velocity patterns in thrombolysis in myocardial infarction flow grade 2 in acute myocardial infarction: Insight into mechanisms of microvascular dysfunction J. Am. Coll. Cardiol., November 20, 2002; 40(10): 1755 - 1760. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Lepper, G. T. j Sieswerda, A. Franke, N. Heussen, O. Kamp, C. C. de Cock, E. R. Schwarz, P. Voci, C. A. Visser, P. Hanrath, et al. Repeated assessment of coronary flow velocity pattern in patients with first acute myocardial infarction J. Am. Coll. Cardiol., April 17, 2002; 39(8): 1283 - 1289. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. H. Rezkalla and R. A. Kloner No-Reflow Phenomenon Circulation, February 5, 2002; 105(5): 656 - 662. [Full Text] [PDF]
|
|
|
|
|
|
T. Reffelmann and R. A Kloner The "no-reflow" phenomenon: basic science and clinical correlates Heart, February 1, 2002; 87(2): 162 - 168. [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Taylor, A. Bobik, M. C. Berndt, D. Ramsay, and G. Jennings Experimental Rupture of Atherosclerotic Lesions Increases Distal Vascular Resistance: A Limiting Factor to the Success of Infarct Angioplasty Arterioscler Thromb Vasc Biol, January 1, 2002; 22(1): 153 - 160. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E Eeckhout and M.J Kern The coronary no-reflow phenomenon: a review of mechanisms and therapies Eur. Heart J., May 1, 2001; 22(9): 729 - 739. [PDF]
|
|
|
|
|
|
G. Destro, P. Marino, E. Barbieri, A. Zorzi, G. Brighetti, M. Maines, M. Carletti, and P. Zardini Postinfarctional remodeling: increased dye intensity in the myocardial risk area after angioplasty of infarct-related coronary artery is associated with reduction of ventricular volumes J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1239 - 1245. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Matetzky, T. Sharir, M. Domingo, M. Noc, K.-Y. Chyu, S. Kaul, N. Eigler, P. K. Shah, and B. Cercek Elevated Troponin I Level on Admission Is Associated With Adverse Outcome of Primary Angioplasty in Acute Myocardial Infarction Circulation, October 3, 2000; 102(14): 1611 - 1616. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Morishima, T. Sone, K. Okumura, H. Tsuboi, J. Kondo, H. Mukawa, H. Matsui, Y. Toki, T. Ito, and T. Hayakawa Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1202 - 1209. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K G OLDROYD Identifying failure to achieve complete (TIMI 3) reperfusion following thrombolytic treatment: how to do it, when to do it, and why it's worth doing Heart, August 1, 2000; 84(2): 113 - 115. [Full Text] [PDF]
|
|
|
|
|
|
T. Wakatsuki, M. Nakamura, T. Tsunoda, H. Toma, T. Degawa, T. Oki, and T. Yamaguchi Coronary flow velocity immediately after primary coronary stenting as a predictor of ventricular wall motion recovery in acute myocardial infarction J. Am. Coll. Cardiol., June 1, 2000; 35(7): 1835 - 1841. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Akasaka, K. Yoshida, T. Kawamoto, S. Kaji, Y. Ueda, A. Yamamuro, T. Takagi, and T. Hozumi Relation of Phasic Coronary Flow Velocity Characteristics With TIMI Perfusion Grade and Myocardial Recovery After Primary Percutaneous Transluminal Coronary Angioplasty and Rescue Stenting Circulation, May 23, 2000; 101(20): 2361 - 2367. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Marzilli, E. Orsini, P. Marraccini, and R. Testa Beneficial Effects of Intracoronary Adenosine as an Adjunct to Primary Angioplasty in Acute Myocardial Infarction Circulation, May 9, 2000; 101(18): 2154 - 2159. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. J. Feldman, D. Himbert, J.-M. Juliard, G. J. Karrillon, H. Benamer, P. Aubry, O. Boudvillain, P. Seknadji, M. Faraggi, and P. G. Steg Reperfusion syndrome: relationship of coronary blood flow reserve to left ventricular function and infarct size J. Am. Coll. Cardiol., April 1, 2000; 35(5): 1162 - 1169. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Matetzky, M. Novikov, L. Gruberg, D. Freimark, M. Feinberg, D. Elian, I. Novikov, E. Di Segni, O. Agranat, Y. Har-Zahav, et al. The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA J. Am. Coll. Cardiol., December 1, 1999; 34(7): 1932 - 1938. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Wakatsuki, T. Oki, K. Sakabe, H. Shinohara, J. Ikata, T. Tabata, A. Nishikado, S. Ito, and T. Yamaguchi Coronary Flow Velocity Immediately After Reperfusion Reflects Myocardial Microcirculation in Canine Models of Acute Myocardial Infarction Angiology, November 1, 1999; 50(11): 919 - 928. [Abstract] [PDF]
|
|
|
|
|
|
T. Kawamoto, K. Yoshida, T. Akasaka, T. Hozumi, T. Takagi, S. Kaji, and Y. Ueda Can Coronary Blood Flow Velocity Pattern After Primary Percutaneous Transluminal Coronary Angiography Predict Recovery of Regional Left Ventricular Function in Patients With Acute Myocardial Infarction? Circulation, July 27, 1999; 100(4): 339 - 345. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Matetzky, D. Freimark, P. Chouraqui, I. Novikov, O. Agranat, B. Rabinowitz, E. Kaplinsky, and H. Hod The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1326 - 1330. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. N. James Complex Causes of Fatal Myocardial Infarction Circulation, September 2, 1997; 96(5): 1696 - 1700. [Abstract] [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||