Search

OBJECTIVES: This study compared the prognostic value of a noncontrast CMR risk score for the composite of all-cause death, nonfatal myocardial infarction, and new congestive heart failure.BACKGROUND: A cardiovascular magnetic resonance (CMR) risk score including left ventricular ejection fraction (LVEF), myocardial infarct (MI) size, and microvascular obstruction (MVO) was recently proposed to risk-stratify patients with ST-segment elevation myocardial infarction (STEMI).METHODS: The Eitel CMR risk score and GRACE (Global Registry of Acute Coronary Events) score were used as a reference (Score 1: acute MI size ≥19% LV, LVEF ≤47%, MVO >1.4% LV and GRACE score). MVO was replaced by intramyocardial hemorrhage (IMH) in Score 2 (acute MI size ≥19% LV, LVEF ≤47%, IMH, and GRACE score). Score 3 included only LVEF ≤45%, IMH, and GRACE score.RESULTS: There were 370 patients in the derivation cohort and 234 patients in the validation cohort. In the derivation cohort, the 3 scores performed similarly and better than GRACE score to predict the 1-year composite endpoint with C-statistics of 0.83, 0.83, 0.82, and 0.74, respectively. In the validation cohort, there was good discrimination and calibration of score 3, with a C-statistic of 0.87 and P = 0.71 in a Hosmer-Lemeshow test for goodness of fit, on the 1-year composite outcome. Kaplan-Meier curves for 5-year composite outcome showed that those with LVEF ≤45% (high-risk) and LVEF >45% and IMH (intermediate-risk) had significantly higher cumulative events than those with LVEF >45% and no IMH (low-risk), log-rank tests: P = 0.02 and P = 0.03, respectively. The HR for the high-risk group was 2.3 (95% CI: 1.1-4.7) and for the intermediate-risk group was 2.0 (95% CI: 1.0-3.8), and these remained significant after adjusting for the GRACE score.CONCLUSIONS: This noncontrast CMR risk score has performance comparable to an established risk score, and patients with STEMI could be stratified into low risk (LVEF >45% and no IMH), intermediate risk (LVEF >45% and IMH), and high risk (LVEF ≤45%). (A Trial of Low-dose Adjunctive alTeplase During prIMary PCI [T-TIME]; NCT02257294) (Detection and Significance of Heart Injury in ST Elevation Myocardial Infarction [BHF MR-MI]; NCT02072850).

Background: Cut off values for change in left ventricular end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) by cardiovascular magnetic resonance following ST-segment–elevation myocardial infarction have recently been proposed and 4 patterns of LV remodeling were described. We aimed to assess their long-term prognostic significance. Methods: A prospective cohort of unselected patients with ST-segment–elevation myocardial infarction with paired acute and 6-month cardiovascular magnetic resonance, with the 5-year composite end point of all-cause death and hospitalization for heart failure was included. The prognosis of the following groups (group 1: reverse LV remodeling [≥12% decrease in LVESV]; group 2: no LV remodeling [changes in LVEDV and LVESV Results: Two hundred eighty-five patients were included with a median follow-up was 5.8 years. The composite end point occurred in 9.5% in group 1, 12.3% in group 2, 7.1% in group 3, and 24.2% in group 4. Group 4 had significantly higher cumulative event rates of the composite end point (log-rank test, P =0.03) with the other 3 groups showing similar cumulative event rates (log-rank test, P =0.51). Cox proportional hazard for group 2 (hazard ratio, 1.3 [95% CI, 0.6–3.1], P =0.53) and group 3 (hazard ratio, 0.6 [95% CI, 0.2–2.3], P =0.49) were not significantly different but was significantly higher in group 4 (hazard ratio, 3.0 [95% CI, 1.2–7.1], P =0.015) when compared with group 1. Conclusions: Patients with ST-segment–elevation myocardial infarction developing adverse LV remodeling at 6 months, defined as ≥12% increase in both LVESV and LVEDV by cardiovascular magnetic resonance, was associated with worse long-term clinical outcomes than those with adverse LV remodeling with compensation, reverse LV remodeling, and no LV remodeling, with the latter 3 groups having similar outcomes in a cohort of stable reperfused patients with ST-segment–elevation myocardial infarction. Registration URL: http://www.clinicaltrials.gov . Unique identifier: NCT02072850.

Supplemental Digital Content is available in the text., The rationale for our study was to investigate the pathophysiology of microvascular injury in patients with acute ST-segment–elevation myocardial infarction in relation to a history of hypertension. We undertook a cohort study using invasive and noninvasive measures of microvascular injury, cardiac magnetic resonance imaging at 2 days and 6 months, and assessed health outcomes in the longer term. Three hundred twenty-four patients with acute myocardial infarction (mean age, 59 [12] years; blood pressure, 135 [25] / 79 [14] mm Hg; 237 [73%] male, 105 [32%] with antecedent hypertension) were prospectively enrolled during emergency percutaneous coronary intervention. Compared with patients without antecedent hypertension, patients with hypertension were older (63 [12] years versus 57 [11] years; P

Purpose To investigate the prognostic value of circumferential left ventricular (LV) strain measured by using cardiac MRI for prediction of major adverse cardiac events (MACE) following an acute ST-segment-elevation myocardial infarction (STEMI). Materials and Methods Participants with acute STEMI were prospectively enrolled from May 11, 2011, to November 22, 2012. Cardiac MRI was performed at 1.5 T during the index hospitalization. Displacement encoding with stimulated echoes (DENSE) and feature tracking of cine cardiac MRI was used to assess circumferential LV strain. MACE that occurred after discharge were independently assessed by cardiologists blinded to the baseline observations. Results A total of 259 participants (mean age, 58 years ± 11 [standard deviation]; 198 men [mean age, 58 years ± 11] and 61 women [mean age, 58 years ± 12]) underwent cardiac MRI 2.2 days ± 1.9 after STEMI. Average infarct size was 18% ± 13 of LV mass and circumferential strain was -13% ± 3 (DENSE method) and -24% ± 7 (feature- tracking method). Fifty-one percent (131 of 259 participants) had presence of microvascular obstruction. During a median follow-up period of 4 years, 8% (21 of 259) experienced MACE. Area under the curve (AUC) for DENSE was different from that of feature tracking (AUC, 0.76 vs 0.62; P = .03). AUC for DENSE was similar to that of initial infarct size (P = .06) and extent of microvascular obstruction (P = .08). DENSE-derived strain provided incremental prognostic benefit over infarct size for prediction of MACE (hazard ratio, 1.3; P.01). Conclusion Circumferential strain has independent prognostic importance in study participants with acute ST-segment-elevation myocardial infarction. Published under a CC BY 4.0 license. Online supplemental material is available for this article. See also the editorial by Kramer in this issue.

Background Invasive measures of microvascular resistance in the culprit coronary artery have potential for risk stratification in acute ST‐segment–elevation myocardial infarction. We aimed to investigate the pathological and prognostic significance of coronary thermodilution waveforms using a diagnostic guidewire. Methods and Results Coronary thermodilution was measured at the end of percutaneous coronary intervention, (PCI) and contrast‐enhanced cardiac magnetic resonance imaging (MRI) was intended on day 2 and 6 months later to assess left ventricular (LV) function and pathology. All‐cause death or first heart failure hospitalization was a pre‐specified outcome (median follow‐up duration 1469 days). Thermodilution recordings underwent core laboratory assessment. A total of 278 patients with acute ST‐segment elevation myocardial infarction EMI (72% male, 59±11 years) had coronary thermodilution measurements classified as narrow unimodal (n=143 [51%]), wide unimodal (n=100 [36%]), or bimodal (n=35 [13%]). Microvascular obstruction and myocardial hemorrhage were associated with the thermodilution waveform pattern ( P =0.007 and 0.011, respectively), and both pathologies were more prevalent in patients with a bimodal morphology. On multivariate analysis with baseline characteristics, thermodilution waveform status was a multivariable associate of microvascular obstruction (odds ratio [95% confidence interval]=5.29 [1.73, 16.22];, P =0.004) and myocardial hemorrhage (3.45 [1.16, 10.26]; P =0.026), but the relationship was not significant when index of microvascular resistance (IMR) >40 or change in index of microvascular resistance (5 per unit) was included. However, a bimodal thermodilution waveform was independently associated with all‐cause death and hospitalization for heart failure (odds ratio [95% confidence interval]=2.70 [1.10, 6.63]; P =0.031), independent of index of microvascular resistance>40, ST‐segment resolution, and TIMI (Thrombolysis in Myocardial Infarction) Myocardial Perfusion Grade. Conclusions The thermodilution waveform in the culprit coronary artery is a biomarker of prognosis and may be useful for risk stratification immediately after reperfusion therapy.

The aim of this study was to mechanistically investigate associations among cigarette smoking, microvascular pathology, and longer term health outcomes in patients with acute ST-segment elevation myocardial infarction (MI).The pathophysiology of myocardial reperfusion injury and prognosis in smokers with acute ST-segment elevation MI is incompletely understood.Patients were prospectively enrolled during emergency percutaneous coronary intervention. Microvascular function in the culprit artery was measured invasively. Contrast-enhanced magnetic resonance imaging (1.5-T) was performed 2 days and 6 months post-MI. Infarct size and microvascular obstruction were assessed using late gadolinium enhancement imaging. Myocardial hemorrhage was assessed with T2* mapping. Pre-specified endpoints included: 1) all-cause death or first heart failure hospitalization; and 2) cardiac death, nonfatal MI, or urgent coronary revascularization (major adverse cardiovascular events). Binary logistic regression (odds ratio [OR] with 95% confidence interval [CI]) with smoking status was used.In total, 324 patients with ST-segment elevation MI were enrolled (mean age 59 years, 73% men, 60% current smokers). Current smokers were younger (age 55 ± 11 years vs. 65 ± 10 years, p 0.001), with fewer patients with hypertension (52 ± 27% vs. 53 ± 41%, p = 0.007). Smokers had better TIMI (Thrombolysis In Myocardial Infarction) flow grade (≥2 vs. ≤1, p = 0.024) and ST-segment resolution (none vs. partial vs. complete, p = 0.010) post-percutaneous coronary intervention. On day 1, smokers had higher circulating C-reactive protein, neutrophil, and monocyte levels. Two days post-MI, smoking independently predicted infarct zone hemorrhage (OR: 2.76; 95% CI: 1.42 to 5.37; p = 0.003). After a median follow-up period of 4 years, smoking independently predicted all-cause death or heart failure events (OR: 2.20; 95% CI: 1.07 to 4.54) and major adverse cardiovascular events (OR: 2.79; 95% CI: 2.30 to 5.99).Smoking is associated with enhanced inflammation acutely, infarct-zone hemorrhage subsequently, and longer term adverse cardiac outcomes. Inflammation and irreversible myocardial hemorrhage post-MI represent mechanistic drivers for adverse long-term prognosis in smokers. (Detection and Significance of Heart Injury in ST Elevation Myocardial Infarction. [BHF MR-MI]; NCT02072850).

No abstract available.

The index of microvascular resistance (IMR) predicts presence of microvascular obstruction (MVO) on cardiovascular magnetic resonance (CMR) imaging & prognosis in acute STEMI, but discordance between IMR & MVO occurs in about one third of cases. We studied the predictive value of a new parameter

Supplemental Digital Content is available in the text., The natural history and pathophysiological significance of tissue remodeling in the myocardial remote zone after acute ST-elevation myocardial infarction (STEMI) is incompletely understood. Extracellular volume (ECV) in myocardial regions of interest can now be measured with cardiac magnetic resonance imaging. Patients who sustained an acute STEMI were enrolled in a cohort study (BHF MR-MI [British Heart Foundation Magnetic Resonance Imaging in Acute ST-Segment Elevation Myocardial Infarction study]). Cardiac magnetic resonance was performed at 1.5 Tesla at 2 days and 6 months post STEMI. T1 modified Look-Locker inversion recovery mapping was performed before and 15 minutes after contrast (0.15 mmol/kg gadoterate meglumine) in 140 patients at 2 days post STEMI (mean age: 59 years, 76% male) and in 131 patients at 6 months post STEMI. Remote zone ECV was lower than infarct zone ECV (25.6±2.8% versus 51.4±8.9%; P

Aims Coronary guidewire-based diagnostic assessments with hyperemia may cause iatrogenic complications. We assessed the safety of guidewire-based measurement of coronary physiology, using intravenous adenosine, in patients with an acute coronary syndrome. Methods We prospectively enrolled invasively managed STEMI and NSTEMI patients in two simultaneously conducted studies in 6 centers (NCT01764334; NCT02072850). All of the participants underwent a diagnostic coronary guidewire study using intravenous adenosine (140 μg/kg/min) infusion for 1–2 min. The patients were prospectively assessed for the occurrence of serious adverse events (SAEs) and symptoms and invasively measured hemodynamics were also recorded. Results 648 patients (n = 298 STEMI patients in 1 hospital; mean time to reperfusion 253 min; n = 350 NSTEMI in 6 hospitals; median time to angiography from index chest pain episode 3 (2, 5) days) were included between March 2011 and May 2013. Two NSTEMI patients (0.3% overall) experienced a coronary dissection related to the guidewire. No guidewire dissections occurred in the STEMI patients. Chest symptoms were reported in the majority (86%) of patient's symptoms during the adenosine infusion. No serious adverse events occurred during infusion of adenosine and all of the symptoms resolved after the infusion ceased. Conclusions In this multicenter analysis, guidewire-based measurement of FFR and IMR using intravenous adenosine was safe in patients following STEMI or NSTEMI. Self-limiting symptoms were common but not associated with serious adverse events. Finally, coronary dissection in STEMI and NSTEMI patients was noted to be a rare phenomenon.

Background: The pathophysiological basis of reperfusion injury in smokers is incompletely understood. Methods: Patients with acute STEMI were prospectively enrolled during emergency PCI, and categorized according to a current smoking status (yes/no). Contrast-enhanced MRI at 1.5T was acquired 2

Background Infarct size assessed early after acute ST-segment elevation myocardial infarction (STEMI) can overestimate the true extent of infarction, limiting its usefulness as a prognostic biomarker. Myocardial strain derived from displacement encoding with stimulated echoes (DENSE) cardiovascular magnetic resonance (CMR) provides information on myocardial contractility with high precision and accuracy. We hypothesised that the prognostic value of peak circumferential strain is higher than infarct size. Methods In a prospective, single centre study, participants underwent 1·5T CMR 2 days and 6 months after myocardial infarction. The 5-SD technique was used to quantify late gadolinium enhancement (LGE) as proportion of left ventricular mass. Mid-left ventricular DENSE acquisitions were analysed using postprocessing software. During longer-term follow-up, major adverse cardiac events (MACE) were independently assessed by masked cardiologists. Participants provided written informed consent and ethics approval was given (reference 10/S0703/28). This study is registered with ClinicalTrials.gov, number NCT02072850. Findings 300 patients underwent CMR (mean age 58·6 years [SD 13·2], 237 men [79%], 118 anterior myocardial infarction [39%], 30 with diabetes [10%], 284 with normal flow [Thrombolysis in Myocardial Infarction grade 3] after percutaneous coronary intervention [95%]). 259 of these patients had DENSE acquired, of whom 21 (8%) experienced a MACE at 3 years' follow-up. DENSE and baseline LGE had reasonable power for prediction of adverse events (area under the curve [AUC] DENSE 0·712, p=0·001; AUC LGE 0·644, p=0·028). For MACE (receiver operating characteristic analysis), optimal cut-offs for peak circumferential strain using DENSE was −10·51%, and LGE 24·05 g. Cox-regression analysis showed that DENSE (hazard ratio 1·175, 95% CI 0·036–1·334; p=0·012) offered an incremental prognostic benefit over LGE (1·040, 1·010–1·070; p=0·008) to predict MACE. Interpretation DENSE-derived peak circumferential strain offers an incremental prognostic benefit over infarct size revealed by LGE to predict MACE; a cut-off of −10·51% can identify STEMI patients at higher risk of events. This is the first time, to our knowledge, that CMR-derived strain has been shown to provide prognostic utility in patients with STEMI. Funding This research was supported by project grants from the Chief Scientist Office (SC01), Medical Research Scotland (343 FRG), and the British Heart Foundation (BHF-PG/14/64/31043).

Background The clinical significance of infarct extracellular volume (ECV) post-STEMI is unknown. ECV can be estimated by cardiac magnetic resonance imaging (CMR) using T1 MOLLI maps. We measured infarct ECV in STEMI survivors, and assessed the relationships between ECV and markers of MI severity. Methods STEMI survivors were enrolled in a single-centre cohort study (BHF MR-MI study – NCT02072850). Culprit artery flow was described by thrombus in myocardial infarction (TIMI) classification. CMR was performed at 1.5 Tesla (Siemens MAGNETOM Avanto) 2-days and 6-months post-MI, including T1-mapping with MOLLI before and 15-minutes after contrast (0.15 mmol/kg gadoterate meglumine). ECV was analysed by outlining regions-of-interest (ROIs) in infarcted myocardium, including microvascular obstruction, and left ventricular (LV) blood pool. ECV was calculated as the relaxation rate (R1=1/T1) for myocardium and LV blood pool before vs. after contrast, corrected for haematocrit. ECV was compared with TIMI-flow pre- and post-percutaneous coronary intervention (PCI) and ST-segment resolution. A reduction in ST-segment voltage of ≥70% was considered complete ST-resolution and Results 201 STEMI patients (age 58 ± 11 years; 156 (77%) male) were enrolled. Infarct ECV was similar at baseline and follow-up (51.3 ± 9.5% vs. 50.3 ± 12.0%, p = 0.1). Pre-PCI, 131 (65%) patients had TIMI-flow 0 and 70 (35%) had TIMI-flow 1–3. Post-PCI, 3 (1.5%) patients had TIMI-flow 0 and 198 (98.5%) had TIMI-flow 2–3. TIMI-flow 0 pre-PCI was associated with higher infarct ECV at baseline (p Conclusion Preserved culprit artery flow and complete ST-resolution are associated with lower infarct ECV at baseline and follow-up. Clinical and electrocardiographic markers of MI severity are predictors of interstitial expansion in the infarct zone in STEMI patients.

Background Myocardial haemorrhage is a prognostically important complication of acute ST-elevation myocardial infarction (STEMI). Persistence of haemoglobin degradation products within infarct scar tissue and the potential clinical significance have not been investigated. Methods and Results Patients who sustained an acute STEMI were enrolled in a cohort study (BHF MR-MI; ClinicalTrials.gov: NCT02072850). 211 patients (mean (SD) age 57 (11) years, 77% male) had evaluable T2* cardiac magnetic resonance (CMR) imaging (1.5 Tesla) 2 days 6 months post-MI. Myocardial haemorrhage was defined as a hypointense infarct core with T2* signal de novo haemorrhage after the first CMR scan. Clinical associates of a persistent hypointense core at 6 months included hypertension (odds ratio (95% confidence interval) 0.28 (0.08, 0.95); p = 0.040), heart rate (1.08 (1.03, 1.13); p = 0.001), systolic blood pressure (1.06 (1.01, 1.12); p = 0.015), neutrophil count (2.19 (1.01, 4.74); p = 0.048), left anterior descending as culprit artery (9.26 (1.26, 67.99); p = 0.029), infarct size (1.10 (1.03, 1.17); p = 0.004) and initial haemorrhage size (1.34 (1.06, 1.66); p = 0.012). A hypointense infarct core with T2*-mapping at 6 months was associated with worsening LV end-diastolic volume (regression coefficient (95% confidence interval) 15.43 (1.35, 29.50); p = 0.032) and worsening left ventricular ejection fraction (-4.15 (-7.40, -0.89); p = 0.013). Conclusion Persistence of haemoglobin degradation products at 6 months post-STEMI is common and prognostically important.

Background The natural history of persistent myocardial oedema after ST-elevation myocardial infarction (STEMI) is uncertain. Methods and ResultsPatients who sustained an acute STEMI were enrolled in a cohort study (BHF MR-MI; ClinicalTrials.gov: NCT02072850). Cardiac magnetic resonance (CMR) imaging with T2-mapping of myocardial oedema was performed at 1.5 Tesla 2 days and 6 months post-MI. Myocardial oedema was defined as infarct signal intensity (S. I.) >2 standard deviations from the mean S. I. within a remote reference region. 283 STEMI patients (mean (SD) age 59 (12) years, 75% male) were enrolled. Infarct size was 18 (13)% of left ventricular (LV) mass. At 2 days, infarct zone T2 (ms) was higher than remote zone T2 (62.9 (5.2) vs. 49.7 (2.1); p Conclusion Persistence of oedema within the infarct zone affected the majority of patients at 6 months post-STEMI, and was associated with the initial severity of STEMI and adverse LV remodelling.

Background Myocardial extracellular volume (ECV) can be estimated by cardiac magnetic resonance imaging (CMR) using pre- and post-contrast T1 MOLLI maps. The age and sex associations with myocardial ECV in healthy mid-life adults are uncertain. Methods Healthy adults without any history of cardiovascular disease or treatment underwent contrast-enhanced CMR at 1.5 Tesla (Siemens MAGNETOM Avanto). T1 mapping with MOLLI was performed before and 15 min after contrast (0.15 mmol/kg gadoterate meglumine). ECV was estimated in regions (AHA 16-segment LV model) and for the whole left ventricular (LV) myocardium (all regions). ECV was calculated as the difference in relaxation rate (R1=1/T1) for myocardium and LV blood pool before vs. after gadolinium contrast administration, corrected for haematocrit (HCT). LV segments which were not evaluable due to artefact were excluded from analysis. Results 114 segments were assessed from 19 subjects (mean age 61 ± 12 years; 10 (53%) male). 21 (18%) segments were excluded due to blood pool artefact or signal drop-out in the pre-contrast T1 MOLLI scan. All segments were evaluable in the post-contrast T1 MOLLI scans. The remaining segments for each subject were averaged to give an overall ECV (global LV). The mean ECV for all subjects was 25.6 ± 2.9%. There was no overall segmental variation in ECV. ECV in females was higher than in males (27.6 ± 3.1% vs. 23.9 ± 1.3%; P = 0.003) The percentage difference was 14.5%. ECV was higher in septal segments in females (anteroseptal: 28.0 ± 3.3% vs. 24.2 ± 1.5%; P = 0.004; inferoseptal: 27.3 ± 3.8% vs. 23.5 ± 1.6%; P = 0.011), whereas no differences were observed for other segments (Table 1). Conclusion In this preliminary analysis, myocardial ECV was higher in women than in men, which was attributable to higher ECV in the septum in females. This sex difference merits further study. If these results are confirmed by other studies, then sex-specific reference ranges for ECV would seem appropriate.

Background The clinical significance of extracellular volume (ECV) expansion in infarcted myocardium post-STEMI is unknown. Myocardial ECV can be estimated by cardiac magnetic resonance imaging (CMR) using T1 MOLLI maps before and after contrast. We repeatedly measured infarct ECV in STEMI survivors, and assessed the relationships between ECV, peak troponin T and baseline infarct size. Methods Acute STEMI survivors were enrolled in a single-centre cohort study (BHF MR-MI study – NCT02072850). Contrast-enhanced CMR was performed at 1.5 Tesla (Siemens MAGNETOM Avanto) 2 days and 6 months post-MI. T1 mapping with MOLLI was performed before and 15 min after contrast (0.15 mmol/kg gadoterate meglumine). ECV analysis was performed by outlining regions of interest (ROIs) in infarcted myocardium and left ventricular (LV) blood pool. ROIs were representative of the infarct including microvascular obstruction. ECV was calculated as the relaxation rate (R1=1/T1) for myocardium and LV blood pool before vs. after contrast, corrected for haematocrit. Infarct size was measured using late gadolinium images and expressed as a percentage of LV mass. Infarct ECV at baseline and follow up was compared with peak troponin T measured at presentation and infarct size at baseline. Peak troponin T was log-transformed to improve normality and linearity. Results 201 STEMI patients (mean age 58 ± 11 years; 156 (77%) male) were enrolled. Infarct ECV was similar at baseline and follow-up (51.3 ± 9.5% vs. 50.3 ± 12.0%, p = 0.097). Peak troponin T was widely variable (4256.7 ug/L ± 4020.8 ug/L). Peak troponin T was positively associated with infarct ECV at baseline (p Conclusion High peak troponin T and a large infarct size are predictors of higher infarct ECV at baseline and follow-up. Infarct ECV is associated with clinical and MRI measures of MI severity in survivors of STEMI.

Objective. Emerging evidence suggests an important role for mast cells in vein graft failure. This study addressed the hypothesis that perivascular mast cells regulate in situ vascular inflammatory and proliferative responses and subsequent vein graft neointimal lesion formation, using an optimized local mast cell reconstitution method.\ud \ud Methods and Results. Neointimal hyperplasia was induced by insertion of a vein graft into the right carotid artery in wild type and mast cell deficient KitW−sh/W−sh mice. In some experiments, mast cells were reconstituted systemically (tail vein injection of bone marrow-derived mast cells) or locally (directly into the right neck area) prior to vein grafting. Vein graft neointimal lesion formation was significantly (P < 0.05) reduced in KitW−sh/W−sh mice. Mast cell deficiency reduced the number of proliferating cells, and inhibited L-selectin, CCL2, M-CSF and MIP-3α expression in the vein grafts. Local but not systemic mast cell reconstitution restored a perivascular mast cell population that subsequently promoted neointimal formation in mast cell deficient mice.\ud \ud Conclusion. Our data demonstrate that perivascular mast cells play a key role in promoting neointima formation by inducing local acute inflammatory and proliferative responses. These results suggest that ex vivo intraoperative targeting of mast cells may have therapeutic potential for the prevention of pathological vein graft remodeling.