DOI:10.2214/AJR.07.2518
AJR 2008; 191:73-79
© American Roentgen Ray Society
No-Reflow Phenomenon in Cardiac MRI: Diagnosis and Clinical Implications
Víctor Pineda1,
Xavier Merino1,
Susana Gispert1,
Patricia Mahía2,
Bruno Garcia2 and
Rosa Domínguez-Oronoz1
1 Department of Radiology, Unitat de Ressonància Magnètica,
Hospital General Vall d'Hebron, Pg. De la Vall d'Hebron 119-129, 08035
Barcelona, Spain.
2 Cardiology Department, Hospital General Vall d'Hebron, Barcelona, Spain.
Received May 6, 2007;
accepted after revision January 28, 2008.
Address correspondence to V. Pineda
(victor{at}pineda.com.es).
Abstract
OBJECTIVE. The purposes of this study were to depict the first-pass,
delayed contrast enhancement and regional myocardial wall motion abnormalities
of no-reflow phenomenon MRI and to review the major mechanisms and
significance of this phenomenon in the clinical setting.
CONCLUSION. Contrast-enhanced MRI is a useful noninvasive technique
for determining the presence of microvascular obstruction. No-reflow
phenomenon has important prognostic implications, and knowledge of the
physiologic mechanism is important to understanding the distribution patterns
of enhancement in correlation with the underlying pathologic process.
Keywords: cardiovascular imaging • delayed contrast enhancement • MRI
Introduction
The benefits of early revascularization in patients with acute myocardial
infarction (AMI) is unquestionable. Early reperfusion of ischemic myocardium
with thrombolytic therapy or angioplasty limits the size of the infarct,
preserves left ventricular function, and improves survival among AMI patients
[1]. Contrary to what might be
expected, however, the ischemic territory may not be properly reperfused even
though blood flow in the previously occluded coronary artery has been
reestablished. This no-reflow phenomenon is defined as deficient reperfusion
of previously ischemic tissue even though the lumen of the artery that
irrigates the territory has been opened. Proper recovery of myocardial
perfusion depends on adequate perfusion of the epicardial vessels and on
microvascularization (Fig. 1).
Patients with no-reflow phenomenon have morphologic and functional
microvascular alterations that result in a myocardial perfusion defect despite
establishment of thrombolysis in myocardial infarction grade 3 blood flow
[2] in the epicardial
vasculature. That is, correct coronary recanalization is not synonymous with
myocardial reperfusion.
Mechanisms of No-Reflow Phenomenon
The pathophysiologic mechanisms of no-reflow phenomenon are likely
multifactorial. The final result is a microvascular lesion secondary to the
initial ischemic injury and the reperfusion injury. Distal microembolization
after angioplasty or thrombolytic therapy may also contribute to no-reflow
phenomenon.
The decrease in tissue perfusion due to occlusion of a coronary artery
decreases phosphocreatinine level, decreases aerobic metabolism, and initiates
anaerobic metabolism and generation of several toxic metabolites. Persistence
of the perfusion defect leads to irreversible structural damage and tissue
death. If reperfusion is achieved before the injury becomes irreversible, the
cells can recover. Nevertheless, some myocardial cells sustain even greater
injury once the flow is reestablished. Reperfusion injury has been related to
the sudden increase in oxygen and calcium that occurs after revascularization
of an occluded vessel [3]. The
reintroduction of oxygen and calcium accelerates the injury occurring with
reperfusion and leads to generation of free radicals; mitochondrial
dysfunction; and infiltration of inflammatory cells, humoral factors that
mediate inflammation, and the products of glucose and fatty acid
metabolism.
The macroscopic findings associated with no-reflow phenomenon include
myocardial necrosis and diffuse tissue hemorrhage. The microscopic findings
include cellular and intercellular edema, endothelial damage, and neutrophil
infiltration [4]. These
findings have been attributed to various mechanisms, such as capillary
plugging by leukocytes or erythrocytes, endothelial cell swelling and
protrusion, perivascular edema, postreperfusion vascular dysfunction,
small-vessel spasm, and compression of the microvascular bed due to myocardial
cell swelling or contracture
[5].
Diagnosis of No-Reflow Phenomenon
Because of the negative prognostic implications of no-reflow phenomenon, it
is important to correctly identify the patients affected. MRI with standard
gadolinium chelates has proved useful for detection of the presence of
no-reflow phenomenon in patients with revascularized AMI. The no-reflow zone
is characterized by persistent first-pass hypoenhancement caused by reduced
blood flow. This persistent hypoperfusion on first-pass contrast-enhanced
images after satisfactory reperfusion therapy is due to microvascular
obstruction that impedes delivery of contrast medium (Fig.
2A,
2B,
2C,
2D). First-pass perfusion
imaging is performed with a multislice T1-weighted turbo FLASH sequence.
Acquisition is performed immediately after injection of a 0.05- to 0.1-mmol/kg
bolus of gadolinium followed by saline solution.
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Fig. 2C —58-year-old man with acute myocardial infarction. Short-axis
(C) and four-chamber (D) gradient-echo first-pass perfusion MR
images (TR/TE, 203/1.06; flip angle, 50°). Segmental images obtained soon
after angioplasty show perfusion defect (arrow) in lateral wall
despite restored blood flow in circumflex coronary artery.
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Fig. 2D —58-year-old man with acute myocardial infarction. Short-axis
(C) and four-chamber (D) gradient-echo first-pass perfusion MR
images (TR/TE, 203/1.06; flip angle, 50°). Segmental images obtained soon
after angioplasty show perfusion defect (arrow) in lateral wall
despite restored blood flow in circumflex coronary artery.
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In experimental studies, the location and extent of microvascular
obstruction have been correlated with the perfusion defects found on
first-pass MRI
[6–8].
In these studies, the spatial locations of hypoenhancement on MR images
obtained with radioactive microspheres and thioflavin stain have correlated
closely with no-reflow regions. Hypoenhancement during first-pass imaging can
be caused by severe stenosis of a hypoperfused coronary artery already at rest
or by impaired microvascular blood flow in infarcted regions. To establish a
diagnosis of no-reflow phenomenon, in which the perfusion alteration is
attributed to deficient microvascularization, thrombolysis in myocardial
infarction grade 3 flow must have been achieved in the epicardial vessel (Fig.
3A,
3B,
3C,
3D,
3E,
3F).
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Fig. 3C —62-year-old woman with acute myocardial infarction.
Four-chamber gradient-echo first-pass perfusion MR images (TR/TE, 203/1.06;
flip angle, 50°) in multiple temporal phases soon after angioplasty show
incomplete apical tissue reperfusion despite restoration of thrombolysis in
myocardial infarction grade 3 flow in LAD.
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Fig. 3D —62-year-old woman with acute myocardial infarction.
Four-chamber gradient-echo first-pass perfusion MR images (TR/TE, 203/1.06;
flip angle, 50°) in multiple temporal phases soon after angioplasty show
incomplete apical tissue reperfusion despite restoration of thrombolysis in
myocardial infarction grade 3 flow in LAD.
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Fig. 3E —62-year-old woman with acute myocardial infarction.
Four-chamber gradient-echo first-pass perfusion MR images (TR/TE, 203/1.06;
flip angle, 50°) in multiple temporal phases soon after angioplasty show
incomplete apical tissue reperfusion despite restoration of thrombolysis in
myocardial infarction grade 3 flow in LAD.
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Fig. 3F —62-year-old woman with acute myocardial infarction.
Four-chamber gradient-echo first-pass perfusion MR images (TR/TE, 203/1.06;
flip angle, 50°) in multiple temporal phases soon after angioplasty show
incomplete apical tissue reperfusion despite restoration of thrombolysis in
myocardial infarction grade 3 flow in LAD.
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The status of microvascularization can be assessed with a delayed phase
contrast-enhanced MRI viability study. Because of the biologic characteristics
of necrotic myocardium, contrast medium is retained in the nonviable tissue.
In acutely infarcted myocardium, the myocytic membranes are ruptured, allowing
rapid distribution of gadolinium chelates into both the intravascular and
extracellular spaces. Cellular degradation in the infarcted region increases
the permeability and enlargement of the extravascular space with increased
distribution volume for the extracellular contrast agent. Thus gadolinium
chelates wash out of infarcted tissue more slowly than out of healthy
myocardium. Therefore, the necrotic territory exhibits late gadolinium
enhancement on T1-weighted images
[9,
10]. Presence of late
enhancement in the necrotic myocardial tissue indicates proper patency of
microvascularization. In contrast, when there is a lack of reperfusion due to
microvascular impairment, gadolinium cannot reach the central area (core) of
the reperfused infarcted area. Absence of late enhancement in the necrotic
myocardial core indicates microvascularization obstruction (Fig.
4A,
4B). These hypoenhanced areas
are always surrounded by areas of hyperenhancement and should not be confused
with nonnecrotic myocardium. Myocardial delayed enhancement is performed
10–15 minutes after injection with a T1-weighted multishot inversion
recovery prepared gradient-echo sequence with the appropriate inversion time
for nulling the signal intensity of normal myocardium
[9].
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Fig. 4A —54-year-old man with revascularized acute myocardial
infarction. Short-axis gradient-echo first-pass perfusion segmental MR image
(TR/TE, 450/1.26; flip angle, 50°) shows perfusion defect in inferolateral
wall (arrow) after epicardial reperfusion, indicating no reflow.
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Fig. 4B —54-year-old man with revascularized acute myocardial
infarction. Short-axis delayed-enhancement inversion recovery gradient-echo MR
image (450/1.26; inversion time, 300 milliseconds; flip angle, 50°) shows
hypoenhanced area (arrow) within hyperenhanced myocardium. Finding is
consistent with microvascular obstruction.
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Delayed phase contrast-enhanced MRI is less sensitive than first-pass MRI
[11] because small no-reflow
zones become rapidly enhanced owing to diffusion of extracellular contrast
medium from surrounding regions with intact microvessels (Fig.
5A,
5B). No-reflow phenomenon is
characterized by dynamic changes, particularly in the phase immediately after
postcoronary recanalization
[12]. These very early changes
can be dynamically influenced by reactive hyperemia or transient plugging by
microthrombi and neutrophils, as well as by microvascular spasm. Thus, in some
patients, microvascularization obstruction reverses spon taneously. For this
reason, in the subacute phase areas of hypoenhancement due to no-reflow
phenomenon can become hyperenhanced on delayed contrast-enhanced MRI because
subacute and chronic infarcts also exhibit late hyperenhancement. In subacute
and chronic infarcts, the interstitial space between collagen fibers is
greater than the interstitial space between myocytes of normal myocardium. The
concentration of gadolinium chelates in the scar is greater than in normal
myocardium and appears hyperenhanced on delayed phase contrast-enhanced MRI
(Fig. 6A,
6B).
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Fig. 5A —46-year-old man with revascularized acute myocardial
infarction. Short-axis gradient-echo first-pass segmental perfusion MR image
(TR/TE, 203/1.06; flip angle, 50°) obtained after angioplasty shows
perfusion defect in anterior wall (arrow), indicating no reflow.
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Fig. 5B —46-year-old man with revascularized acute myocardial
infarction. Short-axis delayed-enhancement inversion recovery gradient-echo MR
image (450/1.26; inversion time, 280 milliseconds; flip angle, 50°)
obtained 10 minutes after contrast administration shows nontransmural
infarction and small perfusion defect has become hyperenhanced
(arrow) owing to diffusion of extracellular contrast medium from
surrounding regions.
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Fig. 6A —59-year-old woman with reperfused anterior infarction.
Four-chamber delayed-enhancement inversion recovery gradient-echo MR image
(TR/TE, 450/1.26; inversion time, 300 milliseconds; flip angle, 50°) shows
transmural apical necrosis. Dark area within infarct core represents
microvascular obstruction (arrow).
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Fig. 6B —59-year-old woman with reperfused anterior infarction.
Four-chamber delayed-enhancement inversion recovery gradient-echo MR image
(450/1.26; inversion time, 270 milliseconds; flip angle, 50°) obtained
after 6-month follow-up period shows dark area has become hyperenhanced
(arrow).
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High signal intensity on T2-weighted images is common in patients with
no-reflow phenomenon and represents areas of myocardial edema, which is known
to contribute to microvascular injury owing to compression (Fig.
7A,
7B). This finding, however, is
nonspecific and also is seen in patients with AMI and no evidence of reflow
deficit. Patients with distal microemboli can have MRI findings consistent
with no-reflow phenomenon because distal coronary embolization is associated
with limited myocardial perfusion (Fig.
8A,
8B,
8C,
8D).
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Fig. 7A —55-year-old man with revascularized acute myocardial
infarction. Two-chamber delayed-enhancement inversion recovery gradient-echo
MR image (TR/TE, 450/1.26; inversion time; 250 milliseconds; flip angle,
50°) shows transmural infarct with black core (arrow)
corresponding to no reflow. Small apical thrombus (arrowhead) is
evident.
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Fig. 7B —55-year-old man with revascularized acute myocardial
infarction. Two-chamber T2-weighted MR image (700/49) shows high signal
intensity in infarcted region consistent with myocardial edema
(arrow). Pericardial thickening (arrowhead) caused by
epistenocardiac pericarditis is evident.
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Fig. 8B —62-year-old man with acute myocardial infarction. Angiogram
obtained after stent placement shows restored LAD artery flow (arrow)
with persistent black dot of contrast material (arrowhead) in distal
LAD artery indicating distal microembolization.
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Fig. 8C —62-year-old man with acute myocardial infarction. Two-chamber
(C) and four-chamber (D) delayed-enhancement inversion recovery
gradientecho MR images (TR/TE, 450/1.26; inversion time, 300 milliseconds;
flip angle, 50°) depict apical hypoenhanced area (arrow) caused
by microvascular injury surrounded by hyperenhanced area of infarct.
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Fig. 8D —62-year-old man with acute myocardial infarction. Two-chamber
(C) and four-chamber (D) delayed-enhancement inversion recovery
gradientecho MR images (TR/TE, 450/1.26; inversion time, 300 milliseconds;
flip angle, 50°) depict apical hypoenhanced area (arrow) caused
by microvascular injury surrounded by hyperenhanced area of infarct.
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Methods other than MRI can be used to assess microcirculation. A suspected
diagnosis can be made with ECG evidence of persistent ST-segment elevation
after revascularization. Conventional coronary angiography may show slow
anterograde flow in the revascularized vessel. Myocardial perfusion defects
secondary to microvascular injury also can be detected with PET,
99mTc methoxyisobutyl isonitrile SPECT, and myocardial contrast
echocardiography
[13–15].
Intracoronary Dop pler sonography shows decreased systolic anterograde flow
and rapid deceleration of diastolic flow. The advantage of MRI is that it
facilitates precise assessment of myocardial microvascularization, viability,
and segmental motion in a single examination. Contrast-enhanced cine MRI has
been described [16] as a
useful technique that reduces examination time and allows dynamic
visualization of microvascularization obstruction.
Clinical Implications of No-Reflow Phenomenon
No-reflow phenomenon after thrombolysis or angioplasty occurs in
approximately 40% of patients with AMI
[17,
18] and is associated with
greater myocardial injury
[19]. No-reflow phenomenon is
generating increasing interest because of the extensive current use of early
revascularization techniques in AMI. The disparity between epicardial and
microvascular revascularization produced in patients with no reflow is an
important cause of therapeutic failure. When the prognostic implications of
no-reflow phenomenon are taken into account, early recognition of this
phenomenon provides important prognostic information and offers the
opportunity to establish therapeutic measures for reducing its detrimental
effects.
No-reflow phenomenon can be clinically silent or manifest as angina,
hemodynamic instability, or conduction alterations. Studies
[18,
20] have shown that evidence
of microvascularization obstruction on MRI is predictive of left ventricular
remodeling and poor functional recovery (Fig.
9A,
9B,
9C,
9D,
9E). The mechanisms by which
no-reflow phenomenon influences left ventricular remodeling are unknown. They
may be related to an adverse effect on ventricular geometry and segmental
function, causing increased ventricular remodeling. The extent of
microvascular obstruction tissue may be related to reduced local myocardial
deformation and dysfunction of uninfarcted adjacent myocardium in the early
healing phase [21].
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Fig. 9A —67-year-old man with revascularized acute myocardial
infarction. Four-chamber delayed-enhancement inversion recovery gradient-echo
MR image (TR/TE, 450/1.26; inversion time, 280 milliseconds; flip angle,
50°) obtained after revascularization shows no-reflow area
(arrow) in apical septal wall.
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Fig. 9B —67-year-old man with revascularized acute myocardial
infarction. Steady-state free precession four-chamber cine MR image (3.6/1.8;
flip angle, 55°) obtained after revascularization shows absence of apical
septal wall thickening (arrow, C).
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Fig. 9C —67-year-old man with revascularized acute myocardial
infarction. Steady-state free precession four-chamber cine MR image (3.6/1.8;
flip angle, 55°) obtained after revascularization shows absence of apical
septal wall thickening (arrow, C).
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Fig. 9D —67-year-old man with revascularized acute myocardial
infarction. Follow-up four-chamber cine MR images (3.6/1.8; flip angle,
55°) obtained 6 months after B and C show left ventricular
remodeling and no improvement in wall motion (arrow, E).
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Fig. 9E —67-year-old man with revascularized acute myocardial
infarction. Follow-up four-chamber cine MR images (3.6/1.8; flip angle,
55°) obtained 6 months after B and C show left ventricular
remodeling and no improvement in wall motion (arrow, E).
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Therapy for no-reflow phenomenon may not necessarily reduce the size of the
area of myocardial necrosis because the microvascularization lesion is located
within the area of necrosis. Nevertheless, reducing microvascular injury may
improve the arrival of blood to the necrotic area, facilitating healing of the
infarct and reducing the magnitude of ventricular remodeling. Because
no-reflow phenomenon is associated with lengthy coronary occlusion and large
infarct size, revascularization of the occluded coronary artery as soon as
possible is likely to reduce the incidence of no-reflow phenomenon. Several
strategies for the management of no-reflow phenomenon are being investigated.
One of these approaches is based on decreasing leukocyte proliferation and the
release of oxygen radicals with the glycoprotein IIb/IIIa receptor inhibitor
abciximab [22]. Other
potential therapeutic approaches are based on drugs with vasodilating
activity, such as adenosine and calcium antagonists (verapamil) and adenosine
triphosphate–sensitive potassium ion channel activators
(nicorandil).
Conclusion
Although the clinical benefits of early revascularization in AMI patients
are indisputable, in some cases, myocardial hypoperfusion persists because of
the no-reflow phenomenon. This phenomenon is due to an alteration in
microvascularization and is associated with a poorer prognosis after AMI
revascularization. MRI is useful for noninvasive assessment of
microvascularization, which is likely to improve the outcome of management of
AMI.
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Abstract
Introduction
