Prognostic significance of cardiac magnetic resonance imaging: Update 2010

Cardiac magnetic resonance imaging (CMR) has become an indispensible imaging technique for the diagnosis and treatment of patients with cardiovascular diseases. Technical advances in the past have rendered CMR unique in the evaluation of cardiovascular anatomy, physiology, and pathophysiology due to its unique ability to produce high resolution tomographic images of the human heart and vessels in any arbitrary orientation, with soft tissue contrast that is superior to competing imaging modalities without the use of ionizing radiation. CMR imaging is the gold standard for assessing left and right ventricular function and for detecting myocardial tissue abnormalities like edema, infarction, or scars. For prognostic reasons abnormal structure and dysfunction of the heart, and the detection of myocardial ischemia and/or myocardial scars are the main targets for CMR imaging. In this review we briefly describe the prognostic significance of several CMR imaging techniques and special CMR parameters in patients with coronary artery disease (CAD), with cardiomyopathies, and with chronic heart failure. Myocardial ischemia proved to be a strong predictor of an adverse outcome in patients with CAD. Microvascular obstruction in acute myocardial infarction is a new and independent parameter of negative left ventricular remodeling and a worse prognosis. Myocardial scars in patients with CAD and unrecognized myocardial infarction heralds a negative outcome. Scar in patients with dilated or hypertrophic cardiomyopathy are a strong predictor of both life-threatening ventricular tachyarrhythmias and prognosis. CMR imaging may improve the assessment of inter- and intraventricular dyssynchrony and provide prognostic information by detecting myocardial scars. (Cardiol J 2010; 17, 6: 549-557

Systemic Embolization and Myocardial Infarction due to Clinically Unrecognized Left Atrial Myxoma

Myxomas are the most common primary tumors of the heart. We report an extraordinary severe case of left atrial myxoma, presenting with stroke, myocardial infarction, and multiple arterial embolism including aorta, splenic and renal arteries, and several peripheral arteries. The patient had previously been diagnosed with systemic vasculitis, a typical but less common finding caused by multiple emboli mimicking vasculitis. The myxoma was removed and atrial septum reconstruction was performed. In summary, early diagnostic differentiation of myxoma from vasculitis is critical, and immediate surgical removal of myxoma is required as the probability of thromboembolic complications increases over time

Cardiac magnetic resonance imaging derived quantification of myocardial ischemia and scar improves risk stratification and patient management in stable coronary artery disease

Background: Quantification of myocardial ischemia and necrosis might ameliorate prognostic models and lead to improved patient management. However, no standardized consensus on how to assess and quantify these parameters has been established. The aim of this study was to quantify these variables by cardiac magnetic resonance imaging (CMR) and to establish possible incremental implications in cardiovascular risk prediction. Methods: This study is a retrospective analysis of patients with known or suspected coronary artery disease (CAD) referred for adenosine perfusion CMR was performed. Myocardial ischemia and necrosis were assessed and quantified using an algorithm based on standard first-pass perfusion imaging and late gadolinium enhancement (LGE). The combined primary endpoint was defined as cardiac death, non-fatal myocardial infarction, and stroke. Results: 845 consecutive patients were enrolled into the study. During the median follow-up of 3.64 [1.03; 10.46] years, 61 primary endpoints occurred. Patients with primary endpoint showed larger extent of ischemia (10.7 ± 12.25% vs. 3.73 ± 8.29%, p < 0.0001) and LGE (21.09 ± 15.11% vs. 17.73 ± 10.72%, p < 0.0001). A risk prediction model containing the extent of ischemia and LGE proved to be superior in comparison to all other models (χ² increase: from 39.678 to 56.676, integrated discrimination index: 0.3851, p = 0.0033, net reclassification index: 0.11516, p = 0.0071). The ben­eficial effect of revascularization tended to be higher in patients with greater extents of ischemia, though statistical significance was not reached. Conclusions: Quantification of myocardial ischemia and LGE was shown to significantly improve existing risk prediction models and might thus lead to an improvement in patient management

Ivabradine Reduces Chemokine-Induced CD4-Positive Lymphocyte Migration

Aims. Migration of CD4-positive lymphocytes into the vessel wall is a critical step in atherogenesis. Recent data suggest that ivabradine, a selective I(f)-channel blocker, reduces atherosclerotic plaque formation in apolipoprotein E-deficient mice, hitherto nothing is known about the mechanism by which ivabradine modulates plaque formation. Therefore, the present study investigated whether ivabradine regulates chemokine-induced migration of lymphocytes. Methods and results. Stimulation of CD4-positive lymphocytes with SDF-1 leads to a 2.0 ± 0.1 fold increase in cell migration (P < .01; n = 7). Pretreatment of cells with ivabradine reduces this effect to a maximal 1.2 ± 0.1 fold induction at 0.1 µmol/L ivabradine (P < .01 compared to SDF-1-treated cells, n = 7). The effect of ivabradine on CD4-positive lymphocyte migration was mediated through an early inhibition of chemokine-induced PI-3 kinase activity as determined by PI-3 kinase activity assays. Downstream, ivabradine inhibits activation of the small GTPase Rac and phosphorylation of the Myosin Light Chain (MLC). Moreover, ivabradine treatment reduces f-actin formation as well as ICAM3 translocation to the uropod of the cell, thus interfering with two important steps in T cell migration. Conclusion. Ivabradine inhibits chemokine-induced migration of CD4-positive lymphocytes. Given the crucial importance of chemokine-induced T-cell migration in early atherogenesis, ivabradine may be a promising tool to modulate this effect