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With the introduction of high sensitivity troponin-T (hs-TnT) assay, clinicians face more patients with 'positive' results but without myocardial infarction. Repeated hs-TnT determinations are warranted to improve specificity. The aim of this study was to compare diagnostic accuracy of three different interpretation rules for two hs-TnT results taken 6 h apart. After adjusting for clinical differences, hs-TnT results were recoded according to the three rules. Rule1: hs-TnT >13 ng/L in at least one determination. Rule2: change of >20 % between the two measures. Rule3: change >50 % if baseline hs-TnT 14-53 ng/L and >20 % if baseline >54 ng/L. The sensitivity, specificity and ROC curves were compared. The sensitivity analysis was used to generate post-test probability for any test result. Primary outcome was the evidence of coronary critical stenosis (CCS) on coronary angiography in patients with high-risk chest pain. 183 patients were analyzed (38.3 %) among all patients presenting with chest pain during the study period. CCS was found in 80 (43.7 %) cases. The specificity was 0.62 (0.52-0.71), 0.76 (0.66-0.84) and 0.83 (0.74-0.89) for rules 1, 2 and 3, respectively (P < 0.01). Sensitivity decreased with increasing specificity (P < 0.01). Overall diagnostic accuracy did not differ among the three rules (AUC curves difference P = 0.12). Sensitivity analysis showed a 25 % relative gain in predicting CCS using rule 3 compared to rule 1. Changes between two determinations of hs-TnT 6 h apart effectively improved specificity for CCS presence in high-risk chest pain patients. There was a parallel loss in sensitivity that discouraged any use of such changes as a unique way to interpret the new hs-TnT results.

Aims: The anatomical correlates of perfusion defect (PD) at myocardial contrast echocardiography (MCE) in the subacute phase of ST-elevation myocardial infarction (STEMI) are currently unknown. The study aimed at assessing whether, in the subacute phase of STEMI, within MCE PD microvessels are anatomically damaged or if some vasodilation can be still elicited and if the PD correlates with the extent of myocardial necrosis., Methods and Results: Twenty-two post-percutaneous coronary intervention (PCI) patients underwent MCE 7 ± 1 days after STEMI, at baseline and after adenosine (ADN) administration. An area of completely non-opacified myocardium, corresponding to the area of the PD, was quantitated by planimetry. The area of the PD on MCE was compared with biochemical and imaging measures of myocardial necrosis: cardiac Troponin T peak (cTnT peak) and hyperenhanced area at gadolinium-enhanced cardiac magnetic resonance (Gd-CMR), respectively. After vasodilator stimulus, the area of the PD remained significantly unchanged when compared with the baseline value (P = 0.09 vs. baseline). The MCE index correlated at baseline with cTnT peak and Gd-CMR assessments of myocardial necrosis (P < 0.001). Also after ADN infusion, correlations between PD and extent of myocardial necrosis were similar to that assessed at baseline., Conclusion: When assessed in the subacute phase of STEMI, the extent of the PD on MCE represents an area of both myocardial and microvascular necrosis.

Background: After ST-elevation myocardial infarction (STEMI), microvascular obstruction (MVO) can be assessed using semiquantitative angiographic "blush" scores subject to interoperator variability. Quantitative Blush Evaluator (QuBE) is a free computer-calculated algorithm that evaluates myocardial blush on a continuous scale with improved reproducibility. We aimed to compare QuBE with cardiovascular magnetic resonance (CMR) in detecting MVO and its severity., Methods: Fifty-two STEMI treated with successful primary percutaneous coronary intervention were enrolled. Quantitative Blush Evaluator and electrocardiographic sum ST-segment resolution were blindly calculated. All patients underwent CMR 4 to 7 days after STEMI for assessment of infarct size (IS), myocardial salvage index, MVO (both as first-pass MVO and delayed-enhancement MVO [DE-MVO]), and presence of intramyocardial hemorrhage on T2-weighted sequences., Results: Quantitative Blush Evaluator values were inversely related to IS (R = -0.4, P = .008), DE-MVO (R = -0.7, P < .001), and first-pass MVO (R = -0.4, P = .002) and positively related to myocardial salvage index (R = 0.4, P = .007). Moreover, patients with intramyocardial hemorrhage had significantly lower QuBE values (3.9, 3.5-8.0 vs 12.2, 8.2-16.0, P = .001) than those without. At receiver operating characteristic curve analysis, QuBE accounted for an area under the curve of 0.88 (95% CI 0.7-0.9, P = .001) for both DE-MVO and hemorrhage detection and performed significantly better than ST resolution., Conclusions: Quantitative Blush Evaluator score correlates with IS and microvascular dysfunction by CMR and can be considered as an accurate tool for the assessment of MVO in clinical practice. Quantitative Blush Evaluator is a useful quantitative angiographic technique for the assessment of myocardial reperfusion after STEMI., (Copyright © 2011 Mosby, Inc. All rights reserved.)

Aims: Microvascular damage (MD) occurring soon after primary percutaneous coronary intervention (PPCI) may reverse or remain sustained within the first week after ST-elevation myocardial infarction (STEMI). We investigated the incidence, determinants, and long-term clinical relevance of MD reversal after PPCI., Methods and Results: Serial two-dimensional echocardiograms (2DE) and a myocardial contrast study were obtained within 24 h of PPCI (T1) and at pre-discharge (T2) in 110 successfully re-perfused STEMI patients. Six months 2DE and 2-year clinical follow-up were obtained. After PPCI myocardial re-perfusion was normal at T1 only in 40 patients (36%, 'normal reflow'), recovered at T2 in 33 (30%, 'reversible MD'), and remained abnormal in 37 (34%, 'sustained MD'). At follow-up, normal reflow and reversible MD were coupled with a significant reduction in the infarct area, decrease in cardiac volumes, and a slight non-significant improvement in systolic function. Conversely, in the sustained MD group, the infarct area did not change and cardiac volumes significantly increased with a parallel worsening in systolic function. By multivariate analysis, independent predictors of reversible MD were: absence of family history of coronary artery disease (CAD), younger age, shorter time to re-perfusion, and absence of diabetes. The 2-year combined events rate was significantly lower in reversible MD (log-rank test P= 0.03) compared with sustained MD patients., Conclusions: In STEMI patients treated according to the current guidelines, MD frequently occurs soon after re-perfusion but it is reversible in ~50% of cases and it is associated with a favourable functional and clinical outcome. Family history of CAD, aging, time to re-perfusion, and diabetes are independent predictors of MD reversibility.

Assessment of myocardial "blush" by either Myocardial Blush Grade or TIMI Myocardial Perfusion Grade, is the angiographic method currently preferred to confirm myocardial tissue-level perfusion after primary percutaneous intervention. This review focuses on the utility of angiographic "blush" as a simple, widely available, and virtually costless technique for the immediate diagnosis of microvascular impairment at the time of acute catheterization. We comprehensively outline the available evidence behind the "blush," its use in clinical practice, and draw comparisons with other new technologies for assessment of microvascular integrity., (Copyright © 2010 Mosby, Inc. All rights reserved.)

Aims: To ascertain whether the presence of left ventricular (LV) hypertrophy in patients with ST-segment elevation myocardial infarction (STEMI) influences microvascular dysfunction and LV remodelling at 6 months of follow-up., Methods and Results: Fifty-six consecutive STEMI patients successfully treated with primary or rescue percutaneous coronary intervention underwent conventional two-dimensional and myocardial contrast echocardiography within 24 h and at 6 months. Left ventricular mass, end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction, and wall motion score index (WMSI) were measured. Left ventricular hypertrophy was defined as LV mass index >116 g/m(2) in men and >104 g/m(2) in women. In order to evaluate the potential influence of microvascular dysfunction on LV remodelling, myocardial perfusion was semiquantitatively scored by contrast score index (CSI). Patients with LV hypertrophy had higher EDV and ESV both at 24 h and at 6 months, compared with patients without LV hypertrophy (P < 0.05). No significant changes over time were observed in both groups. Both WMSI and CSI were similar between groups at 24 h and at follow-up, but improved in both groups over time (P < 0.05)., Conclusion: Left ventricular hypertrophy does not appear to influence the development of post-acute myocardial infarction LV remodelling. Hypertrophic and non-hypertrophic left ventricles showed the same extent and temporal improvement in regional contractile function and microvascular perfusion.

In the setting of acute myocardial infarction, early and adequate reopening of an infarct-related artery is not necessarily followed by a complete restoration of myocardial perfusion. This condition is usually defined as 'no-reflow'. The pathophysiology of no-reflow is multifactorial since extravascular compression, microvascular vasoconstriction, embolization during percutaneous coronary intervention, and platelet and neutrophil aggregates are involved. In the clinical arena, angiographic findings and easily available clinical parameters can predict the risk of no-reflow. More recently, several studies have demonstrated that biomarkers, especially those related to the pathogenetic components of no-reflow, could also have a prognostic role in the prediction and in the full understanding of the multiple mechanisms of this phenomenon. Thus, in this article, we investigate the role of several biomarkers on admission in predicting the occurrence of no-reflow following successful percutaneous coronary intervention.

Aims: To study coronary microvascular dysfunction as possible pathogenetic mechanism in Apical Ballooning Syndrome (ABS)., Methods and Results: Fifteen ABS patients (all women, 68 +/- 14 years) underwent myocardial contrast echocardiography at baseline during adenosine infusion (140 microg/kg/min) and at 1-month follow-up and compared with a group of anterior ST-elevation myocardial infarction (STEMI) patients with similar clinical characteristics. Myocardial perfusion was assessed by contrast score index (CSI) and endocardial length of contrast defect (contrast defect length, CDL), whereas myocardial dysfunction by wall motion score index (WMSI), endocardial length of contractile dysfunction (wall motion defect length, WMDL), and LV ejection fraction (LVEF). At baseline, no difference in myocardial perfusion and dysfunction were present between the two groups. During adenosine challenge, while no changes were observed in STEMI group, in ABS patients CSI, CDL, WMSI, and WMDL significantly decreased compared with baseline (P < 0.001 vs. baseline for all parameters) and LVEF significantly increased (P = 0.01 vs. baseline). At 1-month follow-up, myocardial perfusion and dysfunction completely recovered in ABS patients (P < 0.001 vs. baseline for all parameters), whereas no significant changes were observed in STEMI group., Conclusion: Our data strongly suggest that in ABS, irrespectively of its underlying aetiology, acute and reversible coronary microvascular vasoconstriction could represent a common pathophysiological mechanism.

In a variable proportion of patients presenting with ST-segment elevation myocardial infarction, ranging from 5% to 50%, primary percutaneous coronary intervention achieves epicardial coronary artery reperfusion but not myocardial reperfusion, a condition known as no-reflow. Of note, no-reflow is associated with a worse prognosis at follow-up. The phenomenon has a multifactorial pathogenesis including: distal embolization, ischemia-reperfusion injury, and individual predisposition of coronary microcirculation to injury. Moreover, it is spontaneously reversible in some patients, thus suggesting that it might be amenable to treatment also when we fail to prevent it. Several recent studies have shown that biomarkers and other easily available clinical parameters can predict the risk of no-reflow and can help in the assessment of the multiple mechanisms of the phenomenon. Several therapeutic strategies have been tested for the prevention and treatment of no-reflow. In particular, thrombus aspiration before stent implantation prevents distal embolization and has been recently shown to improve myocardial perfusion and clinical outcome as compared with the standard procedure. However, it is conceivable that the relevance of each pathogenetic component of no-reflow is different in different patients, thus explaining the occurrence of no-reflow despite the use of mechanical thrombus aspiration. Thus, in this review article, for the first time, we propose a personalized management of no-reflow on the basis of the assessment of the prevailing mechanisms of no-reflow operating in each patient.

Background: Heart rate, measured as beat-to-beat intervals, is not constant and varies in time. This property is known as heart rate variability (HRV) and it has been investigated in several diseases, including myocardial infarction (MI). The main hypothesis is that HRV embed some physiological processes that are characteristics of regulatory systems acting on cardiovascular system. It is possible to quantify such a complex behaviour starting from RR intervals properties itself with the idea that any event affecting the cardiac regulatory system significantly will disrupt and change HRV. In this article, we first review different methodologies previously published to calculate HRV indexes. We then searched literature for studies published on HRV and MI and we derive a metanalysis where published data allow calculation of composite outcomes., Material and Methods: Articles considered eligible for metanalysis were original retrospective/prospective studies investigating HRV after myocardial infarction, reporting follow up for mortality or significant cardiac complications. Random effect model was used to assessed for homogeneity and calculate composite outcome and its 95% confidence interval (CI)., Results: 21 studies were identified as eligible for subsequent analysis. Among these studies 5 large trials were eligible for metanalysis: "they included 3489 total post-MI patient with an overall mortality of 125/577 (21.7%) in patients with standard deviation of RR intervals (SDNN) less than 70 msec compared to 235/2912 (8.1%) in patients with SDNN > 70 msec". Metanalysis demonstrates that, after a MI, patients with SDNN below 70 msec on 24 hours ECG recording have almost 4 times more chance to die in the next 3 years., Conclusion: Results from metanalysis and other studies considered (but not included in the analysis) are consistent with the final finding, that a disrupted HRV dynamic (low SDNN) is associated with higher adverse outcome. In this perspective, although data are strongly positive for a direct relationship between SDNN and mortality after MI, SDNN value must be considered carefully on a single patient. The primary purpose of the metanalysis was to address whether studies conducted on HRV and MI were consistent rather than established a cut-off for SDNN. HRV is simple, non invasive and relatively not expensive to obtain.

Aims: Few data are available on the extent and prognostic value of reverse left ventricular remodelling (r-LVR) after ST-elevation acute myocardial infarction (STEMI). We sought to evaluate incidence, major determinants, and long-term clinical significance of r-LVR in a group of STEMI patients treated with primary percutaneous coronary intervention (PPCI). In particular, the role of preserved microvascular flow within the infarct zone in inducing r-LVR has been investigated., Methods and Results: Serial echocardiograms (2DE) and myocardial contrast study were obtained within 24 h of coronary recanalization (T1) and at pre-discharge (T2) in 110 reperfused STEMI patients. Follow-up 2DE was scheduled after 6 months (T3). Two-year clinical follow-up was obtained. Reverse remodelling was defined as a reduction >10% in LV end-systolic volume (LVESV) at 6 months follow-up. r-LVR occurred in 39% of study population. At multivariable analysis, independent predictors of r-LVR were an effective microvascular reflow within the infarct zone, the in-hospital improvement of myocardial perfusion, an initial large LVESV, and a short time to reperfusion. Cox analysis identified r-LVR as the only independent predictor of 2-year event-free survival. Combined events rate was significantly higher among patients without compared to those with r-LVR (log-rank test P < 0.05)., Conclusion: r-LVR frequently occurs in STEMI patients treated with PPCI and it is an important predictor of favourable long-term outcome. A preserved microvascular perfusion within the infarct zone is the major determinant of r-LVR.

Background: Intensive statin therapy can lower the risk of recurrence of major cardiac events in patients with acute coronary syndromes. This could be related to the ability of statins to increase levels of Endothelial Progenitor Cells (EPCs), which were demonstrated to be favorably associated with a better prognosis and post-infarction left ventricular remodeling in patients with ischemic heart disease., Aim of the Study: First, to evaluate, in a randomized clinical trial, the effect of an intensive vs a standard treatment with statins on EPC mobilization in patients undergoing a successful primary or rescue percutaneous coronary intervention; secondary, to evaluate whether left ventricular remodeling could be influenced by statin therapy through EPC mobilization., Methods: Forty ST-segment elevation myocardial infarction (STEMI) patients undergoing a successful primary or rescue PCI were randomized to receive atorvastatin 80 mg immediately after the admission (Intensive Treatment, IT) or atorvastatin 20 mg from the day of the discharge (Standard Treatment, ST). CD34+/KDR+ EPC count by flow cytometry and left ventricular function by 2-D Echo were measured on admission, at discharge and at 4 months follow up., Results: We found that EPC count was similar in the two groups of patients both on admission and at discharge. At follow up, however, EPC count was higher in patients randomized to IT compared to patients randomized to ST (7.59+/-7.30 vs 3.04+/-3.93, p=0.04). However, LV volumes, ejection fraction and wall motion score index were similar in both groups., Conclusions: An intensive statin treatment after primary or rescue PCI is associated with a higher EPC count at follow up as compared to standard treatment. This beneficial effect did not translate in an improvement of LV function.

Objectives: We sought to evaluate the value of the extent of microvascular damage as assessed with myocardial contrast echocardiography (MCE) in the prediction of left ventricular (LV) remodeling after ST-segment elevation myocardial infarction (STEMI) as compared with established clinical and angiographic parameters of reperfusion., Background: Early identification of post-percutaneous coronary intervention microvascular dysfunction may help in tailoring appropriate pharmacological interventions in high-risk patients. The ideal method to establish effective microvascular reperfusion after percutaneous coronary intervention remains to be determined., Methods: A total of 110 patients with first successfully reperfused STEMI were enrolled in the AMICI (Acute Myocardial Infarction Contrast Imaging) multicenter study. After reperfusion, peak creatine kinase, ST-segment reduction, and Thrombolysis In Myocardial Infarction (TIMI) and myocardial blush grade were calculated. We evaluated perfusion defects with MCE by using continuous infusion of Sonovue (Bracco, Milan, Italy) in real-time imaging. The endocardial length of contrast defect (CD) on day 1 after reperfusion was calculated. Wall motion score index, the extent of wall motion abnormalities, LV end-diastolic volume, and ejection fraction after reperfusion and at follow-up also were calculated., Results: Of 110 patients, 25% evolved in LV remodeling and 75% did not. Although peak creatine kinase, ST-segment reduction >70%, and myocardial blush grade were not different between groups, in patients exhibiting LV remodeling, TIMI flow grade 3 was less frequent (p < 0.001), wall motion score index was greater (p < 0.001), and CD was greater (p < 0.001). At multivariate analysis, only TIMI flow grade <3 and CD with a cutoff of >25% were independently associated with LV remodeling. Among patients with TIMI flow grade 3, CD was the only independent variable associated with LV remodeling., Conclusions: Among patients with TIMI flow grade 3, the extent of microvascular damage, detected and quantitated by MCE, is the most powerful independent predictor of LV remodeling after STEMI as compared with persistent ST-segment elevation and myocardial blush grade.

Background: In the thrombolytic era, persistence of ST-segment elevation was considered a marker of left ventricular (LV) aneurysm. ST-segment elevation may still be found persistently raised after successful primary percutaneous coronary intervention (PCI). Echocardiographic correlates of this finding, however, are still poorly known., Methods and Results: 82 consecutive patients with first ST-segment elevation myocardial infarction and successful PCI were divided into patients with persistent ST-segment elevation at discharge (sum of ST >4 mm) (n = 33) and those without persistent ST-segment elevation (n = 49). Conventional and myocardial contrast echocardiography were performed at discharge and at 6 months. At discharge, LV aneurysm was more common in patients with persistent ST elevation (27% vs 8%, p<0.005). Similarly, the wall motion score index was higher (2.5 vs 2.0, p<0.005) and microvascular damage larger (2.3 vs 1.8, p<0.005) in patients with persistent ST-segment elevation. At 6 months' follow-up, LV volumes were similar in the two groups., Conclusions: After primary PCI, persistent ST-segment elevation is associated with LV aneurysm formation in 30% of cases, it is not associated with significantly larger LV dilatation but with larger microvascular damage and dysfunctioning risk area.

Intracoronary injection of bone marrow stem cells seems to improve left ventricular (LV) function after acute myocardial infarction (AMI). Granulocyte colony-stimulating factor (G-CSF) could improve myocardial function and perfusion noninvasively through mobilization of stem cells into peripheral blood, although previous clinical trials have produced controversial results. Forty-one patients with large anterior wall AMI at high risk of unfavorable remodeling were randomized 1:2 to G-CSF (10 microg/kg/day for 5 days) or to conventional therapy. All patients underwent successful primary or rescue percutaneous coronary intervention. LV function was assessed by echocardiography before G-CSF administration, > or =5 days after AMI, and at follow-up. Only patients with a LV ejection fraction <50% at baseline were enrolled in the study. After a median follow-up of 5 months (range 4 to 6) patients treated with G-CSF exhibited improvement in LV ejection fraction, from 40 +/- 6% to 45 +/- 6% (p = 0.068) in the absence of LV dilation (LV end-diastolic volume from 147 +/- 33 to 144 +/- 46 ml at follow-up, p = 0.77). In contrast, patients treated conventionally exhibited significant LV dilation (LV end-diastolic volume from 141 +/- 35 to 168 +/- 41 ml, p = 0.002) in the absence of change in LV ejection fraction (from 38 +/- 6% to 38 +/- 8%, p = 0.95). However, when comparing patients treated with G-CSF with controls, variations in these parameters were significantly different at 2-way analysis of variance (p = 0.04 for LV end-diastolic volume, p = 0.02 for LV ejection fraction). In conclusion, G-CSF prevents unfavorable LV remodeling and improves LV function in patients with large anterior wall AMI and decreased LV ejection fraction after successful percutaneous coronary intervention.

Background: Recent data show that percutaneous coronary intervention (PCI) in patients with stable postthrombolytic ST-segment elevation myocardial infarction (STEMI) is better than no PCI or ischemia-guided PCI. These results still have to find a pathophysiologic explanation. We hypothesized that complete mechanical recanalization of infarct-related artery improves clinical benefits of thrombolysis as a result of more preserved and better perfused coronary microcirculation. To test this hypothesis, we studied a selected STEMI population presenting very early after symptom onset in whom successful infarct-related artery reperfusion was obtained by thrombolysis followed or not by elective PCI within 24 hours, and we compared these 2 groups with those underwent primary PCI., Methods: This study analyzed 96 patients with STEMI randomized within 3 hours from symptom onset to primary PCI (group A, n = 36), tenecteplase followed within 24 hours by PCI (group B, n = 30), or to tenecteplase alone (group C, n = 30). Microvascular perfusion was assessed by myocardial contrast echocardiography. Regional contrast score, endocardial length and area of contrast defect on day 2 (T1) and at predischarge (T2), left ventricular end-diastolic volume, regional wall motion score, extent of wall motion abnormalities, and ejection fraction at T1, T2, and at 3 months' follow-up were calculated., Results: Baseline clinical and angiographic characteristics were not statistically different between groups. The extent of microvascular damage and of myocardial salvage was similar in primary PCI-treated or in invasively treated patients after lytic administration. Conversely, group C patients, although treated very early with fibrinolytic therapy, showed higher extent of microvascular damage and infarct size and a more depressed left ventricular function after reperfusion and at follow-up., Conclusions: Our data suggest that early PCI after lysis is more effective in preserving myocardial perfusion and function than lysis alone and may be a helpful alternative when primary PCI is not available.

Background: Recent studies have shown that microvascular dysfunction after myocardial infarction is a dynamic phenomenon., Aims: To evaluate the implications of dynamic changes in microvascular dysfunction on contractile recovery and left ventricular remodelling, and to identify the ideal timing of assessment of such microvascular dysfunction., Methods and Results: In 39 patients with a first myocardial infarction who underwent successful percutaneous coronary intervention, microvascular dysfunction was studied by myocardial contrast echocardiography (MCE) at 24 h, 1 week and 3 months after the procedure. Real-time MCE was performed by contrast pulse sequencing and intravenous Sonovue. 14 patients exhibited left ventricular remodelling at 3 months (>20% increase in left ventricular end-diastolic volume, group B), whereas 25 did not (group A). Microvascular dysfunction was similar in the two groups at 24 h and improved in group A only, being significantly better than that of group B at 1 week (p<0.05) and 3 months (p<0.005). Improvement in microvascular dysfunction was not associated with improvement in wall motion in the same segments. With multivariate analysis including all echocardiographic variables, microvascular dysfunction at 1 week was found to be the only independent predictor of left ventricular remodelling (p<0.01). With a cut-off value of 1.4, 1-week microvascular dysfunction predicts left ventricular remodelling with sensitivity and specificity of 73%., Conclusions: Improvement in microvascular dysfunction occurs early after myocardial infarction, although it is not associated with a parallel improvement in wall motion but is beneficial in preventing left ventricular remodelling. Accordingly, 1-week microvascular dysfunction is a powerful and independent predictor of left ventricular remodelling.

Background: Information on the accuracy of both magnetic resonance imaging (MRI) and myocardial contrast echocardiography (MCE) for the identification of perfusion defects in patients with acute myocardial infarction is limited. We evaluated the accuracy of MRI and MCE, using Single Photon Emission Computed Tomography (SPECT) imaging as reference technique., Methods: Fourteen consecutive patients underwent MCE, MRI and 99mTc-MIBI SPECT after acute myocardial infarction to assess myocardial perfusion. MCE was performed by Harmonic Power Angio Mode, with end-systolic triggering 1:4, using i.v. injection of Levovist. First-pass and delayed enhancement MRI was obtained after i.v administration of Gadolinium-DTPA. At MCE, homogeneous perfusion was considered as normal and absent or "patchy" perfusion as abnormal. At MRI, homogenous contrast enhancement was defined as normal whereas hypoenhancement at first-pass followed by hyperenhancement or persisting hypoenhancement in delayed images was defined as abnormal., Results: At MCE 153 (68%) of segments were suitable for analysis compared to 220 (98%) segments at MRI (p<0.001). Sensitivity, specificity and accuracy of MCE for segmental perfusion defects in these 153 segments were 83, 73 and 77%, respectively. Sensitivity, specificity and accuracy of MRI were 63, 82, and 77%, respectively. MCE and MRI showed a moderate agreement with SPECT (k: 0.52 and 0.46, respectively). The agreement between MCE and MRI was better (k: 0.67) that the one of each technique with SPECT., Conclusion: MCE and MRI may be clinically useful in the assessment of perfusion defects in patients with acute myocardial infarction, even thought MCE imaging may be difficult to obtain in a considerable proportion of segments when the Intermittent Harmonic Angio Mode is used.

Aims: Recent data suggest that the administration of bone marrow-derived stem cells (BMSC) might improve myocardial perfusion and left ventricular (LV) function after acute myocardial infarction (AMI). The aim of this study was to assess spontaneous mobilization of BMSC expressing the haematopoietic and endothelial progenitor cell-associated antigen CD34+ after AMI and its relation to post-infarction remodelling., Methods and Results: Peripheral blood concentration of CD34+ BMSC was measured by flow cytometry in 54 patients with AMI, 26 patients with chronic stable angina (CSA), and 43 normal healthy subjects. In patients with AMI, LV function was measured by 2D-echocardiography. Eighteen AMI patients were reassessed at 1 year. BMSC concentration was higher in patients with AMI (mean peak value: 7.04+/-6.27 cells/microL), than in patients with CSA (3.80+/-2.12 cells/microL, P=0.036) and in healthy controls (1.87+/-1.52 cells/microL, P<0.001). At multivariable analysis statin use (P<0.001), primary percutaneous intervention (P=0.048) and anterior AMI (P=0.05) were the only independent predictors of increased BMSC mobilization after AMI. In the 28 patients without subsequent acute coronary events reassessed at 1 year follow-up, CD34+ cell concentration was an independent predictor of global and regional improvement of LV function (r=0.52, P=0.004 and r=-0.41, P=0.03, respectively)., Conclusion: AMI is followed by enhanced spontaneous mobilization of BMSC, in particular, in patients on statin therapy and following a primary percutaneous intervention. More importantly persistent spontaneous mobilization of BMSC might contribute to determine a more favourable post-AMI remodelling.

Objective: To identify in humans the temporal patterns of no reflow and their functional implications., Methods: 24 patients with first acute myocardial infarction and successful coronary recanalisation by recombinant tissue-type plasminogen activator (n = 15) or primary percutaneous transluminal coronary angioplasty (n = 9) were studied by myocardial contrast echocardiography within 24 hours of recanalisation and at one month's follow up. Myocardial contrast echocardiography was performed by intermittent harmonic power Doppler and intravenous Levovist. The regional contrast score index (CSI) was calculated within dysfunctioning myocardium. Videointensity was measured (dB) within risk and control areas and their ratio was calculated., Results: In 8 patients reflow was observed at 24 hours and persisted at one month. Conversely in 16 patients areas of no reflow were detectable at 24 hours. At one month, no reflow was spontaneously reversible in 9 patients (mean (SD) CSI and videointensity ratio improved from 2.5 (0.5) to 1.4 (0.6) and from 0.6 (0.1) to 0.7 (0.1), respectively; p < 0.05) and was sustained in the remaining 7 patients (CSI and videointensity ratio remained unchanged from 2.6 (0.6) to 2.6 (0.5) and from 0.5 (0.2) to 0.5 (0.2), respectively; NS). Left ventricular function improved significantly in patients with reflow and reversible no reflow. Volumes were enlarged only in patients with sustained no reflow., Conclusions: No reflow detected at 24 hours may be sustained or spontaneously reversible at one month. Such reversibility of the phenomenon is associated with preserved left ventricular volumes and function. Clarification of the mechanisms of delayed reversibility may lead to tailored treatment of no reflow even in the subacute phase of myocardial infarction.

Successfully reopening the infarct-related artery after acute myocardial infarction (MI) is currently achieved more frequently than before due to efficient therapeutic strategies, including new thrombolytic drugs and percutaneous transluminal coronary angioplasty. Successful reopening does not necessarily mean reperfusion; in fact the "no-reflow" phenomenon can occur. This phenomenon is due to functional and anatomic alterations, including microcirculation. Experimental and clinical studies have demonstrated that microvascular integrity is a fundamental prerequisite for ensuring viability after an acute MI. Often, studies have also shown that myocardial contrast echocardiography is a technique capable of detecting functional and anatomic conditions of microcirculation after ischemic reperfusion, and thus myocardial contrast echocardiography can be used for viability detection after acute MI.

Objective: To report a case of eosinophilic myocarditis with remarkable initial clinical manifestations and outcome., Material and Methods: A 67-year-old woman with hypertension and a history of asthma and drug hypersensitivity was referred to our institution with a diagnosis of acute myocardial infarction on the basis of severe chest pain, ST elevation on an electrocardiogram, and a slight increase in cardiac enzymes. Further diagnostic studies were performed., Results: Echocardiography disclosed left ventricular dysfunction in conjunction with apical asynergy, thinning, and thrombus. The eosinophil count in the peripheral blood was increased only slightly. Coronary angiography showed normal arteries and prompted the performance of endomyocardial biopsy, which revealed active eosinophilic myocarditis. After corticosteroid therapy, global and regional left ventricular function returned to normal., Conclusion: This unusual clinical picture and outcome demonstrate that eosinophilic myocarditis may simulate acute myocardial infarction and should be considered in patients with a history of allergies or acute left ventricular dysfunction, even in the absence of pronounced eosinophilia in the peripheral blood. With appropriate medical therapy, recovery for these patients can be complete.

Aims: The study was set up to evaluate the functional role of post-infarct preserved microvascular integrity. Low dose dobutamine echocardiography and myocardial contrast echocardiography were used to study patients before hospital discharge who had suffered a recent myocardial infarction and had a patent infarct-related artery (TIMI flow grade 3)., Method: In the dysfunctioning infarct area, the wall motion score index was calculated at baseline, during the dobutamine infusion and at the 3 month follow-up echocardiogram; contrast echocardiography was performed at the time of coronary angiography, before hospital discharge., Results: In patients with more than 50% of the dysfunctioning infarct area opacified at contrast echocardiography (group A), regional wall motion score index decreased, compared to baseline, during the dobutamine infusion (1.97 +/- 0.78 vs 2.5 +/- 0.35 at baseline; P < 0.001) and at follow-up echocardiography (1.83 +/- 0.63 vs 2.5 +/- 0.35 at baseline; P < 0.001). In patients with less extensive microvascular integrity as revealed by contrast echocardiography (group B), regional wall motion score index did not decrease from baseline during either the dobutamine infusion (2.73 +/- 0.21 vs 2.81 +/- 0.20 at baseline; P = ns), or at follow-up (2.81 +/- 0.20 vs 2.81 +/- 0.20 at baseline; P = ns)., Conclusion: In patients with post-infarct dysfunctioning myocardium but a patent infarct-related artery, microvascular integrity, as assessed by myocardial contrast echocardiography, is an indicator of myocardial viability in terms of preserved contractile reserve, as demonstrated by dobutamine infusion and functional recovery at follow-up.

The purpose of this study was to evaluate, in postinfarction dysfunctioning myocardium, the relative potential of myocardial contrast and low-dose dobutamine echocardiography in detecting myocardial viability, and the relation between microvascular integrity, contractile reserve, and functional recovery at follow-up. Twenty-four patients with recent myocardial infarction were studied before hospital discharge with low-dose dobutamine and myocardial contrast echocardiography. In the dysfunctioning infarct area, wall motion score index was calculated at baseline, during low-dose dobutamine, and at 3-month follow-up. Revascularization of the infarct-related artery was performed if clinically indicated. Eighteen patients (group A) had myocardial enhancement of the dysfunctioning infarct area at myocardial contrast echocardiography of >50%, whereas the remaining patients (group B) had an increase of < or = 50%. Wall motion score index was similar at baseline in groups A and B (2.6 +/- 0.4 and 2.8 +/- 0.2; p = NS), but it improved during low-dose dobutamine and at follow-up only in group A (1.9 +/- 0.9 and 1.9 +/- 0.7, respectively; p <0.001 vs baseline). In group B, wall motion score index was 2.7 +/- 0.4 with low-dose dobutamine and 2.8 +/- 0.2 at follow-up (p = NS vs rest). In identifying viable myocardial segments, myocardial contrast echo had 100% sensitivity and 46% specificity, whereas low-dose dobutamine echo had 71% sensitivity and 88% specificity. Thus, microvascular integrity after acute myocardial infarction is a fundamental prerequisite for ensuring myocardial contractile reserve and regional functional recovery. Myocardial contrast and low-dose dobutamine echocardiography have different, but complementary, diagnostic characteristics in detecting myocardial viability.

Myocardial contrast echocardiography is a technique used in experimental and clinical settings in order to visualize the pattern of intramyocardial perfusion. In the acute phase of myocardial infarction, regional absence of flow during myocardial contrast echocardiography delineates the area at risk of necrosis, while the definitive non-perfused area expresses infarct size. Reopening the infarct-related artery, which may be achieved spontaneously by thrombolysis or percutaneous transluminal coronary angioplasty, is not a reliable indicator of intramyocardial reperfusion. If myocardial ischaemia due to coronary occlusion has been sufficiently prolonged and severe, not only myocyte viability, but also microvascular integrity is lost. Myocardial contrast echocardiography, using intracoronary injection of sonicated contrast medium, gives information about microvascular integrity and the effective presence of intramyocardial reflow. Anatomical integrity of microvasculature does not necessarily imply preserved function, and thus the microvessel vasodilating reserve may also be impaired. Myocardial contrast echocardiography has the potential to assess alterations in microvascular function, showing, in the myocardial area with reduced coronary reserve, a relatively reduced increase in echocontrast signal intensity when an intravenous vasodilator agent is administered.

Left ventricular recovery of dysfunctioning but viable myocardium can occur only in tissue in which both myocardial contractile reserve and microvascular integrity are preserved. Recent studies have demonstrated that both inotropic stimulating echo tests and myocardial contrast echocardiography can be used to assess myocardial viability in post-myocardial infarction patients. Therefore we performed a transesophageal and myocardial contrast echocardiographic evaluation of post-myocardial infarction patients to assess: the respective accuracy of post-extrasystolic potentiation and low-dose dobutamine (5 and 10 mcg) during transesophageal echocardiography in eliciting contractile reserve, and the potential of myocardial contrast echocardiography in predicting later functional recovery. Results of our studies showed comparable effects of low-dose dobutamine (5 mcg) and post-extrasystolic potentiation in increasing myocardial thickening while low-dose dobutamine (10 mcg) had a greater potential in eliciting residual contractility. Lastly, myocardial contrast echocardiography provided a clear spectrum of intramyocardial perfusion patterns in dysfunctioning areas but did not accurately correlate with later functional recovery as better predicted by low-dose dobutamine in the same segments. In conclusion, these methods represent the preferred choice of studying the perfusion-contraction match in viable myocardium thus playing an important role in prognostic and therapeutic strategies in myocardial infarction patients.

Myocardial contrast echocardiography is a technique used in experimental and clinical settings in order to visualize the pattern of intramyocardial perfusion. In the acute phase of myocardial infarction, regional absence of flow during myocardial contrast echocardiography delineates the area at risk of necrosis, while the definitive non-perfused area expresses infarct size. Reopening the infarct-related artery, which may be achieved spontaneously by thrombolysis or percutaneous transluminal coronary angioplasty, is not a reliable indicator of intramyocardial reperfusion. If myocardial ischaemia due to coronary occlusion has been sufficiently prolonged and severe, not only myocyte viability, but also microvascular integrity is lost. Myocardial contrast echocardiography, using intracoronary injection of sonicated contrast medium, gives information about microvascular integrity and the effective presence of intramyocardial reflow. Anatomical integrity of microvasculature does not necessarily imply preserved function, and thus the microvessel vasodilating reserve may also be impaired. Myocardial contrast echocardiography has the potential to assess alterations in microvascular function, showing, in the myocardial area with reduced coronary reserve, a relatively reduced increase in echocontrast signal intensity when an intravenous vasodilator agent is administered.(Eur Heart J 1996; 17: 344–353) [ABSTRACT FROM PUBLISHER]

The article presents case of a 75 year old man who was admitted to coronary care unit with anterolateral ST elevation myocardial infarction. After intravenous treatment with aspirin and nitrates, the patient underwent urgent coronary angiography that documented occlusion of the proximal left anterior descending coronary artery (LAD) with TIMI 0 flow. During the procedure "dual LAD" anatomy was documented with a bifurcation of the LAD into a large septal branch and a large diagonal branch. Twelve hours after percutaneous coronary intervention, a myocardial contrast echo study was performed using a Sequoia ultrasound machine and intravenous SonoVue. The patient had a large area of microvascular obstruction at the level of the apex, septum, and posterolateral wall.

An abstract of the article "Persistent and Reversible no Reflow: Predictors and Functional Evolution" by L. Galiuto and colleagues are presented.

An abstract of the article "Predictive value of myocardial contrast echocardiography in the identification of contractile reserve after acute myocardial infarction: role of timing of assessment" by L. Galiuto and colleageus is presented.