ObjectivesT1 mapping allows quantitative myocardial assessment, but its value in clinical routine remains unclear. We investigated, whether the average native myocardial T1 value can be used as a diagnostic classifier between healthy and diffuse diseased myocardium.MethodsNative T1 mapping was performed in 54 persons with healthy hearts and in 150 patients with diffuse myocardial pathologies (coronary artery disease (CAD): n = 76, acute myocarditis: n = 19, convalescent myocarditis: n = 26, hypertrophic cardiomyopathy (HCM): n = 12, dilated cardiomyopathy (DCM): n = 17) at 1.5 Tesla in a mid-ventricular short axis slice using a modified Look-Locker inversion recovery (MOLLI) sequence. The average native myocardial T1 value was measured using dedicated software for each patient. The mean as well as the range of the observed average T1 values were calculated for each group, and compared using t-test. The ability of T1 mapping to differentiate between healthy and diffuse diseased myocardium was assessed using receiver operating characteristic analysis (ROC).ResultsThe mean T1 value of the group “healthy hearts” (955±34ms) differed significantly from that of the groups DCM (992±37ms, p<0.001), HCM (980±44ms, p = 0.035), and acute myocarditis (974±36ms, p = 0.044). No significant difference was observed between the groups “healthy hearts” and CAD (951±37ms, p = 0.453) or convalescent myocarditis (965±40ms, p = 0.240). The average native T1 value varied considerably within all groups (range: healthy hearts, 838-1018ms; DCM, 882-1034ms; HCM, 897-1043ms; acute myocarditis, 925-1025ms; CAD, 867-1082ms; convalescent myocarditis, 890-1071ms) and overlapped broadly between all groups. ROC analysis showed, that the average native T1 value does not allow for differentiating between healthy and diffuse diseased myocardium, except for the subgroup of DCM.ConclusionsThe average native T1 value in cardiac MR imaging does not allow differentiating between healthy and diffusely diseased myocardium in individual cases.

Our aim was to investigate acute effects of muscular counterpulsation (MCP) on hemodynamic parameters and to evaluate its safety in regard to myocardial integrity and interferences with implanted rhythm devices in patients with chronic heart failure (CHF). A total of 22 patients with CHF (16 male, 67.8 ± 9.5 years, New York Heart Association [NYHA] class II + III, left ventricular ejection fraction 29.6 ± 6.6%) were treated with MCP for 3 consecutive days for 45 min, while hemodynamic parameters were measured noninvasively by bioimpedance (Task Force Monitor). Laboratory control and a complete device testing were performed prior to the first and after the third treatment. In addition, continuous rhythm device interrogation was performed online during the first MCP application. During each application, a significant increase in cardiac output (CO; average change +2.08 ± 2.33 L/min, P < 0.05) was documented. This increase was due to a decrease of total peripheral resistance (-336 ± 530 dyn × s/cm(5) , P < 0.05), to an augmented stroke volume (+8.35 ±  20.86 mL, P = n.s.), and an increase in heart rate (+17.12 ± 21.12 bpm, P < 0.05). Cardiac markers and enzymes were within normal limits at all times and did not increase during treatment. MCP stimuli were monitored using surface electrocardiogram, and no abnormal sensing or pacing events occurred. MCP acutely improves CO in patients with stable CHF. No adverse influence on myocardial integrity was observed nor were any inappropriate sensing or pacing artifacts detected in patients with implanted rhythm devices.

Background: Heart failure is a complex clinical syndrome with growing prevalence and substantial impact on health care in the western world. Furthermore, mortality is enormous in these patients. Heart failure with reduced ejection fraction (HFrEF) may result from a variety of causes and delayed enhancement cardiovascular magnetic resonance imaging (DE-CMR) seems ideal to define the etiology thereof. A head to head, real-world comparison of clinical parameters, biomarkers and DE-CMR in this population has not yet been performed. Purpose: To evaluate the capability of DE-CMR compared to clinical parameters and biomarkers in acute decompensated HFrEF to define the etiology of heart failure. Methods: Consecutive patients hospitalized with acute decompensated heart failure and newly diagnosed reduced left ventricular function by echocardiography (EF≤45%) were included. Patients presenting with an acute coronary syndrome (ACS), preserved ejection fraction or contraindications to DE-CMR were excluded. All patients underwent DE-CMR within the index hospitalization. Results: 339 consecutive patients were included (mean age 60±15 years, 62% male gender) in this study, whereof 241 patients (71%) experienced symptoms within 30 days prior to hospitalization. 166 (49%) patients presented with an EF between 30 and 45%, whereas 173 patients (51%) showed an EF of less than 30%. Despite excluding patients with an ACS a priori, DE-CMR detected silent myocardial infarction in 61 patients (18%). There was no statistical difference between ischemic and non-ischemic cardiomyopathies in EF, clinical parameters and biomarkers. Flu-like symptoms were more common in non-ischemic heart failure patients (p<0.05). Conclusion:In patients with acute decompensated heart failure and reduced ejection fraction, clinical parameters and biomarkers do not differentiate nonischemic and ischemic causes of heart failure. Contrary, DE-CMR allows for accurate differentiaton thereof and further refining the etiology of heart failure. Thus,CMR facilitates patient management and impacts prognosis in the individual patient in a real-world setting. worse clinical outcomes in subjects with ischemic cardiomyopathy after resynchronization treatment. P2446 | BEDSIDE