Download Identification of Microvascular Obstruction Christopher M. Kramer

Identification of Microvascular Obstruction
Christopher M. Kramer MD
University of Virginia Health System
After acute myocardial infarction (MI), even with optimal early reperfusion either with
primary angioplasty and stenting or thrombolysis, there may be reperfusion injury due to
inflammatory processes that lead to capillary destruction and regions of microvascular no-reflow
or microvascular obstruction (MO). These regions can be visualized by CMR as regions of low
signal in the first few minutes after contrast infusion [1]. See Figure 1. These regions are low
signal because contrast does not arrive there due to the severe microvascular damage. These are
imaged most commonly with inversion recovery gradient echo imaging [2], but can also be
demonstrated on steady state free precession cine imaging after gadolinium infusion[3]. The
latter imaging strategy has been shown to correlate with findings on first pass-contrast enhanced
perfusion imaging and inversion recovery gradient echo imaging[3]. These regions are generally
subendocardial and are surrounded by regions of late gadolinium enhancement. MO is an
important determinant of recovery of local contractile function, subsequent post-infarct left
ventricular (LV) remodeling, as well as cardiovascular outcome for the post-MI patient.
The prevalence of MO depends on the population studied and ranges from 46%[4] to as
high as 90%[5]. In general, the larger the infarct as visualized by late gadolinium enhancement,
the greater the prevalence of MO[6]. Predictors of MO include inflammatory status (C-reactive
protein and leukocyte levels) and creatine kinase levels[5], as well as time to reperfusion[7].
Time delay to reperfusion has been shown to be a predictor of both infarct transmurality and
MO[7]. Pre-infarction angina has been shown to be an independent determinant and is protective
against MO[5].
Regional[6] and global[5] left ventricular function is worse in regions and patients with
MO after MI. Animal studies have shown that the extent of MO is better at predicting LV
remodeling or an increase in LV volumes than overall infarct size[8]. Regions with MO are those
that are truly nonviable. However, in clinical studies LV remodeling after reperfused myocardial
infarction is predicted by transmurality of infarction as well as by MO, although infarct
transmurality may be a more powerful predictor[9, 10]. Regions with MO demonstrate no
improvement in function during the first few weeks after MI[2] and in patients followed for as
long as 5 months post-MI, these regions demonstrate wall thinning and no functional
recovery[11]. Infarct involution has been demonstrated in the first few weeks after MI with
shrinkage of regions of late gadolinium enhancement by 25-30%[2, 12]. This infarct involution
is more pronounced in infarcts with regions of MO[2]. MO is not seen late after MI. This is
likely due to the fact that infarcts with MO show greater apoptosis and cellular loss, leading to
involution, wall thinning, and infarct expansion.
MO has important prognostic implications in the post-MI patient. Wu et al demonstrated
in a study of 44 patients studied for 16±5 months that patients with MO had a 45%
cardiovascular event rate during that time period as compared to 9% for those without MO[13].
Similarly, Hombach et al followed 89 patients for a year after reperfused MI and showed that
predictors of major adverse cardiac events (MACE) were end-diastolic volume, ejection fraction
(EF) and MO. MO was a more powerful predictor of survival than was infarct size. Thus, MO
may be the single most important prognostic indicator in the post- MI patient.
Figure 1. Late gadolinium enhanced
inversion recovery gradient echo
image from a patient on day 3 after
acute anteroseptal myocardial
infarction. There is a large transmural
anteroseptal infarct as demonstrated
by late gadolinium enhancement. At
the subendocardial core of the infarct
region is a region of microvascular
obstruction (dark zone) where
contrast never reaches due to the
microvascular damage.
References
1 Judd RM, Lugo-Olivieri C, Arai M, Kondo T, Croisille P, Lima JA, Mohan V, Becker LC,
Zerhouni EA: Physiological basis of myocardial contrast enhancement in fast magnetic
resonance images of 2-day-old reperfused canine infarcts. Circulation 1995;92:1902-1910.
2 Choi CJ, Haji-Momenian S, DiMaria JM, Epstein FH, Rogers WJ, Kramer CM: Infarct
involution and improved function during healing of acute myocardial infarction: the role of
microvascular obstruction. J Cardiovasc Magn Reson 2004;6:915-923.
3 Raff GL, O'Neill WW, Gentry RE, Dulli A, Bis KG, Shetty AN, Goldstein JA:
Microvascular Obstruction and Myocardial Function after Acute Myocardial Infarction:
Assessment by Using Contrast-enhanced Cine MR Imaging. Radiology 2006;240:529-536.
4 Hombach V, Grebe OC, Merkle N, Waldenmaier S, Hoeher M, Kochs M, Woehrle J,
Kestler HA: Sequelae of acute myocardial infarction regarding cardiac structure and
function and their prognostic significanace as assessed by magnetic resonance imaging. Eur
Heart J 2005;26:545-557.
5 Jesel L, Morel O, Ohlmann P, Germain P, Faure A, Jahn C, Coulbois PM, Chauvin M,
Bareiss P, Roul G: Role of pre-infarction angina and inflammatory status in the extent of
microvascular obstruction detected by MRI in myocardial infarction patients treated by
PCI. Int J Cardiol 2007;121:139-147.
6 Bogaert J, Kalaantzi M, Rademakers FE, Dymarkowski S, Janssens S: Determinants and
impact of microvascular obstruction in successfully reperfused ST-segment elevation
myocardial infarction. Assessment by magnetic resonance imaging. Eur Radiol
2007;17:2572-2580.
7 Tarantini G, Cacciavillani L, Corbetti F, Ramondo A, Marra MP, Bacchiega E, Napodano
M, Bilato C, Razzolini R, Iliceto S: Duration of Ischemia Is a Major Determinant of
Transmurality and Severe Microvascular Obstruction After Primary Angioplasty: A Study
Performed With Contrast-Enhanced Magnetic Resonance. J Am Coll Cardiol
2005;46:1229-1235.
8 Gerber BL, Rochitte CE, Melin JA, McVeigh ER, Bluemke DA, Wu KC, Becker LC, Lima
JAC: Microvascular Obstruction and Left Ventricular Remodeling Early After Acute
Myocardial Infarction. Circulation 2000;101:2734-2741.
9 Tarantini G, Razzolini R, Cacciavillani L, Bilato C, Sarais C, Corbetti F, Perazzolo Marra
M, Napodano M, Ramondo A, Iliceto S: Influence of Transmurality, Infarct Size, and
Severe Microvascular Obstruction on Left Ventricular Remodeling and Function After
Primary Coronary Angioplasty. Am J Cardiol 2006;98:1033-1040.
10 Shapiro MD, Nieman K, Nasir K, Nomura CH, Sarwar A, Ferencik M, Abbara S, Hoffman
U, Gold HK, Jang IK, Brady TJ, Cury RC: Utility of Cardiovascular Magnetic Resonance
to Predict Left Ventricular Recovery After Primary Percutaneous Coronary Intervention for
Patients Presenting With Acute ST-Segment Elevation Myocardial Infarction. Am J
Cardiol 2007;100:211-216.
11 Baks T, van Geuns RJ, Biagini E, Wielopolski P, Mollet NR, Cademartiri F, van der
Giessen WJ, Krestin GP, Serruys PW, Duncker DJ, de Feyter PJ: Effects of Primary
Angioplasty for Acute Myocardial Infarction on Early and Late Infarct Size and Left
Ventricular Wall Characteristics. J Am Coll Cardiol 2006;47:40-44.
12 Ingkanisorn WP, Rhoads KL, Aletras AH, Kellman P, Arai AE: Gadolinium delayed
enhancement cardiovascular magnetic resonance correlates with clinical measures of
myocardial infarction. J Am Coll Cardiol 2004;43:2253-2259.
13 Wu KC, Zerhouni EA, Judd RM, Lugo-Olivieri CH, Barouch LA, Schulman SP,
Blumenthal RS, Lima JAC: Prognostic significance of microvascular obstruction by
magnetic resonance imaging in patients with acute myocardial infarction. Circulation
1998;97:765-772.