Improvement Of Regional Contractility Research Articles

Invited Commentary

The inability to predict the response of the left ventricle to myocardial revascularization and mitral valve repair in ischemic mitral regurgitation (MR) patients remains problematic. Morgan and colleagues [1Morgan A.E. Zhang Y. Tartibi M. et al.Ischemic mitral regurgitation: abnormal strain overestimates nonviable myocardium.Ann Thorac Surg. 2018; 105: 1754-1762Abstract Full Text Full Text PDF Scopus (10) Google Scholar] compared the ability of tagged cardiac magnetic resonance imaging (MRI) and late gadolinium-enhanced (LGE) MRI to determine the amount of nonviable myocardium in patients with ischemic MR. Their hypothesis was that strain measurements using tagged cardiac MRI overestimate the amount of nonviable myocardium in ischemic MR when compared with LGE MRI, suggesting that much of the myocardium deemed nonviable by strain measurements is actually viable but nonfunctional (ie, stunned or hibernating). This is a critical issue because it is believed that the degree of stunned myocardium in patients with ischemic MR correlates not only with functional myocardial recovery due to revascularization but also with the degree of ventricular remodeling and, thus, the success or failure of mitral valve surgery in these patients. Although LGE MRI is helpful in identifying nonviable myocardium, it is not necessarily as helpful in determining the response of viable myocardium to surgery for ischemic MR. Gadolinium chelate distributes in the extracellular space but does not cross the intact cell membrane. Through a combination of increased extracellular volume and slower washout kinetics, there is a relative accumulation of gadolinium in areas of necrosis, fibrosis, and inflammation in the late washout phase. LGE MRI depends on this relative accumulation of gadolinium in areas of damaged myocardium, but it may miss areas of diffuse fibrosis and underestimate the true extent of nonviable muscle. Grapsa and colleagues [2Grapsa J. Zimbarra Cabrita I. Jakaj G. et al.Strain balance of papillary muscles as a prerequisite for successful mitral valve repair in patients with mitral valve prolapse due to fibroelastic deficiency.Eur Heart J Cardiovasc Imaging. 2015; 16: 53-61Crossref PubMed Scopus (3) Google Scholar], using 3-D echo speckle-tracking, showed that a disproportionate increase in the deformation of the papillary muscles is a predictor of recurrent MR following mitral valve annuloplasty and that global longitudinal deformation depends on the degree of mitral regurgitation. The amount of deformation of the mitral apparatus in patients with only minor degrees of MR was zero. It would be instructive to include tagged cardiac MRI and LGE MRI in a group of patients with ischemia and no MR to compare with patients with ischemic MR. Pasque and associates used MRI-based multiparametric strain data calculated from 15,300 grid points per patient in normal volunteers and in ischemic patients with and without MR [3Lancaster T.S. Kar J. Cupps B.P. et al.Topographic mapping of left ventricular regional contractile injury in ischemic mitral regurgitation.J Thorac Cardiovasc Surg. 2017; 154: 149-158.e1Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar]. They showed that ischemic MR is caused by dysfunction of the subpapillary ventricular wall and that the free ventricular wall segments outside the subpapillary regions showed the same strain patterns in ischemic MR patients and in ischemic patients without MR. The relationships between nonviability, functional recovery, and response to surgical intervention for ischemic MR are not yet clear. What is needed now are studies comparing these types of preoperative measurements in patients with ischemic MR with similar postoperative measurements on the same patients that might clarify the preoperative parameters that are truly capable of predicting postoperative outcomes. Perhaps we would then have a better understanding of precisely how to treat ischemic MR in individual patients. Ischemic Mitral Regurgitation: Abnormal Strain Overestimates Nonviable MyocardiumThe Annals of Thoracic SurgeryVol. 105Issue 6PreviewTherapy for moderate ischemic mitral regurgitation remains unclear. Determination of myocardial viability, a necessary prerequisite for an improvement in regional contractility, is a likely key factor in determining response to revascularization alone. Myocardial strain has been proposed as a viability measure but has not been compared with late gadolinium enhancement (LGE) cardiac magnetic resonance imaging. We hypothesized that abnormal strain overestimates nonviable left ventricular (LV) segments measured with LGE and that ischemia and mechanical tethering by adjacent transmural myocardial infarction (TMI) also decreases strain in viable segments. Full-Text PDF

Ischemic Mitral Regurgitation: Abnormal Strain Overestimates Nonviable Myocardium

Therapy for moderate ischemic mitral regurgitation remains unclear. Determination of myocardial viability, a necessary prerequisite for an improvement in regional contractility, is a likely key factor in determining response to revascularization alone. Myocardial strain has been proposed as a viability measure but has not been compared with late gadolinium enhancement (LGE) cardiac magnetic resonance imaging. We hypothesized that abnormal strain overestimates nonviable left ventricular (LV) segments measured with LGE and that ischemia and mechanical tethering by adjacent transmural myocardial infarction (TMI) also decreases strain in viable segments. Sixteen patients with mild or greater ischemic mitral regurgitation and 7 healthy volunteers underwent cardiac magnetic resonance imaging with noninvasive tags (complementary spatial modulation of magnetization [CSPAMM]), LGE, and stress perfusion. CSPAMM images were post-processed with harmonic phase and circumferential and longitudinal strains were calculated. Viability was defined as the absence of TMI on LGE (hyperenhancement >50% of wall thickness). The borderzone was defined as any segment bordering TMI. Abnormal strain thresholds (±1 to 2.5 SDs from normal mean) were compared with TMI, ischemia, and borderzone. 7.4% of LV segments had TMI on LGE, and more than 14.5% of LV segments were nonviable by strain thresholds (p < 0.005). In viable segments, ischemia impaired longitudinal strain (least perfused one-third of LV segments:-0.18 ± 0.08 versus most perfused:-0.22 ± 0.1, p = 0.01) and circumferential strain (-0.12 ± 0.1 versus-0.16 ± 0.08, p < 0.05). In addition, infarct proximity impaired longitudinal strain (-0.16 ± 0.11 borderzone versus-0.18 ± 0.09 remote, p= 0.05). Impaired LV strain overestimates nonviable myocardium compared with TMI on LGE. Ischemia and infarct proximity also decrease strain in viable segments.

Percutaneous Treatment of Chronic Total Coronary Occlusions Improves Regional Hyperemic Myocardial Blood Flow and Contractility: Insights From Quantitative Cardiovascular Magnetic Resonance Imaging

We sought to investigate temporal changes in contractility and hyperemic and resting myocardial blood flow (MBF) in dependent and remote myocardium after percutaneous coronary intervention (PCI) of chronic total occlusions (CTOs) by using cardiovascular magnetic resonance (CMR) imaging. Data about the physiological consequences of revascularization of CTOs are limited. The use of CMR allows investigation of the regional effects of revascularization on MBF and left ventricular contractility. We prospectively recruited 3 patient groups: 17 patients scheduled for CTO PCI, 17 scheduled for PCI of a stenosed but nonoccluded coronary artery (non-CTO), and 6 patients with CTO who were not scheduled for revascularization. All patients undergoing PCI underwent CMR imaging <24 h before PCI, with repeat CMR imaging 24 h and 6 months after PCI. Each CMR scan consisted of cine, perfusion, and delayed enhancement imaging. Regional hyperemic and resting MBF, wall thickening, and transmural extent of infarction were calculated. In both intervention groups, hyperemic MBF in treated segments increased 24 h after PCI compared with baseline: CTO group, 2.1 +/- 0.2 ml/min/g versus 1.4 +/- 0.2 ml/min/g (p < 0.01); non-CTO group, 2.5 +/- 0.2 ml/min/g versus 1.6 +/- 0.2 ml/min/g (p < 0.01). This improvement persisted 6 months after PCI (p < 0.01 for both groups). Contractility in treated segments was improved at 24 h and 6 months after CTO PCI but only at 6 months after non-CTO PCI. In both intervention groups, treated segments no longer had reduced MBF or contractility compared with remote segments. In patients with untreated CTO segments, MBF and wall thickening did not improve at follow-up. Successful CTO PCI increases hyperemic MBF as early as 24 h after the procedure, with a greater and earlier improvement in regional contractility than after non-CTO PCI, despite a greater likelihood of irreversible injury in CTO segments.

689 Improvement of regional contractility after autologous bone marrow cell transplantation in patients with left ventricular dysfunction due to acute myocardial infarction

In patients with an irreversible left ventricular dysfunction due to acute myocardial infarction, autologous transplantation of mononuclear bone marrow cells induced an improvement of regional, as well as global left ventricle function.

Analysis of First-Pass and Delayed Contrast-Enhancement Patterns of Dysfunctional Myocardium on MR Imaging

The purpose of the study was to analyze first-pass and delayed contrast-enhancement patterns of dysfunctional myocardial regions on MR imaging after injection of gadopentetate dimeglumine to predict myocardial viability in patients with coronary artery disease. Twelve patients with wall motion abnormalities and related coronary artery disease revealed by conventional coronary angiography underwent MR imaging at 1.5-T before and 3 months after revascularization therapy. Short-axis images were acquired using a cine gradient-echo sequence. Each slice was divided into eight segments. Overall, 73 segments with impaired contractility were imaged during the first-pass and 14 +/- 2 min after injection of 0.05-mmol/kg gadopentetate dimeglumine at a flow of 3 ml/sec using a T1-weighted turbo fast low-angle shot sequence. Improved systolic wall thickening 3 months after revascularization served as the criterion of viability. At study entry, 26 dysfunctional segments showed delayed hyperenhancement compared with the adjacent functional segments within the same slice, and 47 did not reveal hyperenhancement. After revascularization, 25 (96%) of the 26 hyperenhanced segments did not recover function, whereas 39 (83%) of the 47 segments without hyperenhancement showed mechanical improvement. Segment-related sensitivity and specificity for the correlation of lack of delayed hyperenhancement with myocardial viability were 39 (98%) of 40 and 25 (76%) of 33, respectively. Hypoenhancement during first-pass did not serve as a reliable criterion of viability. Evidence of delayed hyperenhancement of dysfunctional myocardium may be used to predict lack of mechanical improvement or nonviability, whereas the lack of hyperenhancement can be correlated with improvement of regional contractility or viability after revascularization.

Evaluating signal intensity of movement-impaired myocardial segments in MR delayed images after administration of Gd-DTPA. Correlation of regional increase in contraction after revascularization

The aim of the study was to correlate delayed contrast enhancement of dysfunctional regions of the myocardium after injection of Gd-DTPA with the improvement of regional contractility 3 months after revascularization. Eleven patients with coronary artery disease and wall motion abnormalities underwent MR imaging before and 3 months after revascularization therapy (PTCA or CABG). Short-axis images were acquired using a cine gradient echo sequence. After revascularization, a representative slice was analyzed 14 +/- 1 min after injection of 0.1 mmol/kg Gd-DTPA using a T1-weighted turbo fast low-angle shot sequence. Improved systolic wall thickening 3 months after revascularization served as criterion of viability and was correlated with delayed contrast enhancement patterns. After revascularization, 6 patients showed complete recovery of the dysfunctional area, 1 patient partial recovery, and 4 patients remained unchanged. All 4 patients with persisting wall motion abnormalities, 1/6 patients with recovery and the patient with partial recovery revealed a delayed enhancement. Three months after revascularization, delayed enhancement of dysfunctional myocardium is evident in patients without regional wall motion improvement, while the lack of delayed enhancement correlates with improvement of regional contractility.