The no-reflow phenomenon: State of the art

SummaryPrimary percutaneous coronary intervention (PCI) is the best available reperfusion strategy for acute ST-segment elevation myocardial infarction (STEMI), with nearly 95% of occluded coronary vessels being reopened in this setting. Despite re-establishing epicardial coronary vessel patency, primary PCI may fail to restore optimal myocardial reperfusion within the myocardial tissue, a failure at the microvascular level known as no-reflow (NR). NR has been reported to occur in up to 60% of STEMI patients with optimal coronary vessel reperfusion. When it does occur, it significantly attenuates the beneficial effect of reperfusion therapy, leading to poor outcomes. The pathophysiology of NR is complex and incompletely understood. Many phenomena are known to contribute to NR, including leukocyte infiltration, vasoconstriction, activation of inflammatory pathways and cellular oedema. Vascular damage and haemorrhage may also play important roles in the establishment of NR. In this review, we describe the pathophysiological mechanisms of NR and the tools available for diagnosing it. We also describe the microvasculature and the endothelial mechanisms involved in NR, which may provide relevant therapeutic targets for reducing NR and improving the prognosis for patients

Cardioprotective effects of shock wave therapy: A cardiac magnetic resonance imaging study on acute ischemia-reperfusion injury

IntroductionCardioprotection strategies remain a new frontier in treating acute myocardial infarction (AMI), aiming at further protect the myocardium from the ischemia-reperfusion damage. Therefore, we aimed at investigating the mechano-transduction effects induced by shock waves (SW) therapy at time of the ischemia reperfusion as a non-invasive cardioprotective innovative approach to trigger healing molecular mechanisms.MethodsWe evaluated the SW therapy effects in an open-chest pig ischemia-reperfusion (IR) model, with quantitative cardiac Magnetic Resonance (MR) imaging performed along the experiments at multiple time points (baseline (B), during ischemia (I), at early reperfusion (ER) (∼15 min), and late reperfusion (LR) (3 h)). AMI was obtained by a left anterior artery temporary occlusion (50 min) in 18 pigs (32 ± 1.9 kg) randomized into SW therapy and control groups. In the SW therapy group, treatment was started at the end of the ischemia period and extended during early reperfusion (600 + 1,200 shots @0.09 J/mm2, f = 5 Hz). The MR protocol included at all time points LV global function assessment, regional strain quantification, native T1 and T2 parametric mapping. Then, after contrast injection (gadolinium), we obtained late gadolinium imaging and extra-cellular volume (ECV) mapping. Before animal sacrifice, Evans blue dye was administrated after re-occlusion for area-at-risk sizing.ResultsDuring ischemia, LVEF decreased in both groups (25 ± 4.8% in controls (p = 0.031), 31.6 ± 3.2% in SW (p = 0.02). After reperfusion, left ventricular ejection fraction (LVEF) remained significantly decreased in controls (39.9 ± 4% at LR vs. 60 ± 5% at baseline (p = 0.02). In the SW group, LVEF increased quickly ER (43.7 ± 11.4% vs. 52.4 ± 8.2%), and further improved at LR (49.4 ± 10.1) (ER vs. LR p = 0.05), close to baseline reference (LR vs. B p = 0.92). Furthermore, there was no significant difference in myocardial relaxation time (i.e. edema) after reperfusion in the intervention group compared to the control group: ΔT1 (MI vs. remote) was increased by 23.2±% for SW vs. +25.2% for the controls, while ΔT2 (MI vs. remote) increased by +24.9% for SW vs. +21.7% for the control group.DiscussionIn conclusion, we showed in an ischemia-reperfusion open-chest swine model that SW therapy, when applied near the relief of 50′ LAD occlusion, led to a nearly immediate cardioprotective effect translating to a reduction in the acute ischemia-reperfusion lesion size and to a significant LV function improvement. These new and promising results related to the multi-targeted effects of SW therapy in IR injury need to be confirmed by further in-vivo studies in close chest models with longitudinal follow-up

166 Balloon aortic valvuloplasty in unstable and critically ill patients: analysis of three strategies

AimThanks to improved technology and the advent of transcatheter aortic valve implantation (TAVI), balloon aortic valvuloplasty (BAV) has reappared in the management of high risk patients with severe aortic stenosis in a critical clinical state in three different therapeutic strategies: 1) palliative care [A] 2) bridge to surgery [B] 3) bridge to TAVI [C]. Our main objective was to assess the safety, the effiency and the pertinence of BAV.MethodsThirty six patients with severe aortic stenosis and prohibitive surgical risk (logistic Euroscore>15% or severe commorbidities) underwent 39 BAV: 8 in strategy A, 20 in strategy B, 11 in strategy C. 3 patients underwent a second BAV due to early restenosis.ResultsThere was a significant improvement of the hemodynamic parameters after BAV: the peak to peak transaortic gradient was reduced by 56% (47mmHg vs 30mmHg; p<0.001) and index valve area was increased by 48% (0.35 vs 0.52cm2/m2; p<0.001). There was no severe procedural complication (no death due to procedure, no massive aortic insuffisiency, no tamponade). Two patients (5.1%) needed a pacemaker implantation for postprocedure atrioventricular block and 6 patients (15.4%) had moderate bleeding of the femoral artery site. The mortality and follow up for the three strategies are summarized in the table.ConclusionBAV is a safe and efficient transient therapeutic strategy for patients with severe aortic stenosis with prohibitive surgical risk. BAV appears to be more pertinent in bridge to surgery or brige to TAVI than in palliative care. For patients in critical clinical state, BAV stabilizes the hemodynamic status and allows the assessment of anatomical selection criteria for TAVIStratégy A(n=8)Stratégy B(n=20)Stratégy C(n=11)Age (mean, min-max)80 (61–94)73 (44–85)81 (60–87)Mean logistic Euroscore (%)4822.644.2Death n (%)6 (75)8 (40)5 (45)Cardiovascular death n (%)4 (50)3 (15)2 (18)Time of occurrence (days, min-max)12 (0–47)66 (0–130)155 (10–316)Aortic valve replacement n (%)-14 (70)-TAVI n (%)--2 (18

Determination of the myocardial area at risk after reperfused acute myocardial infarction with different imaging techniques: cardiac magnetic resonance imaging, multidetector computed tomography and histopathological validation

International audiencen.

Myocardial T1-mapping for early detection of left ventricular myocardial fibrosis in systemic sclerosis

International audiencen.

Atrial septum fat deposition and atrial anatomy assessed by cardiac magnetic resonance: relationship to atrial electrophysiology

To assess the prevalence of fat deposition in the atrial septum with and its relationship with 12-lead electrocardiogram (ECG) atrial parameters (PR interval, P wave duration) and the presence of atrial fibrillation

Effect of Cyclosporine on Left Ventricular Remodeling After Reperfused Myocardial Infarction

ObjectivesThis study examined the effect of a single dose of cyclosporine administered at the time of reperfusion on left ventricular (LV) remodeling and function by cardiac magnetic resonance 5 days and 6 months after myocardial infarction.BackgroundIn a human study, administration of cyclosporine at the time of acute reperfusion was associated with a smaller infarct size.MethodsTwenty-eight patients of the original cyclosporine study had an acute (at 5 days) and a follow-up (at 6 months) cardiac magnetic resonance study to determine LV volumes, mass, ejection fraction, myocardial wall thickness in infarcted and remote noninfarcted myocardium, and infarct size.ResultsThere was a persistent reduction in infarct size at 6 months in the cyclosporine group compared with the control group of patients (29 ± 15 g vs. 38 ± 14 g; p = 0.04). There was a significant reduction of LV end-systolic volume (and a trend for LV end-diastolic volume; p = 0.07) in the cyclosporine group compared with the control group, both at 5 days and 6 months after infarction. There was no significant difference between the 2 groups in either global LV mass or regional wall thickness of the remote noninfarcted myocardium at 5 days or 6 months. Attenuation of LV dilation and improvement of LV ejection fraction by cyclosporine at 6 months were correlated with infarct size reduction.ConclusionsCyclosporine used at the moment of acute myocardial infarction reperfusion persistently reduces infarct size and does not have a detrimental effect on LV remodeling. These results are preliminary and must be supported by further studies. (Ciclosporin A and Acute Myocardial Infarction; NCT00403728

Beta-blocker management in patients admitted for acute heart failure and reduced ejection fraction: a review and expert consensus opinion

The role of the beta-adrenergic signaling pathway in heart failure (HF) is pivotal. Early blockade of this pathway with beta-blocker (BB) therapy is recommended as the first-line medication for patients with HF and reduced ejection fraction (HFrEF). Conversely, in patients with severe acute HF (AHF), including those with resolved cardiogenic shock (CS), BB initiation can be hazardous. There are very few data on the management of BB in these situations. The present expert consensus aims to review all published data on the use of BB in patients with severe decompensated AHF, with or without hemodynamic compromise, and proposes an expert-recommended practical algorithm for the prescription and monitoring of BB therapy in critical settings