Cardiac remodeling following percutaneous mitral valve repair - initial results assessed by cardiovascular magnetic resonance imaging.

PURPOSE: Percutaneous mitral valve repair with the MitraClip device (Abbott Vascular, Redwood City, California, USA) is a novel therapeutic option in patients with mitral regurgitation. This study evaluated the feasibility of cardiac volume measurements by cardiovascular magnetic resonance imaging (CMR) to assess reverse myocardial remodeling in patients after MitraClip implantation. MATERIALS AND METHODS: 12 patients underwent CMR at baseline (BL) before and at 6 months follow-up (FU) after MitraClip implantation. Cine-CMR was performed in short- and long-axes for the assessment of left ventricular (LV), right ventricular (RV) and left atrial (LA) volumes. RESULTS: Assessment of endocardial contours was not compromised by the device-related artifact. No significant differences in observer variances were observed for LV, RV and LA volume measurements between BL and FU. LV end-diastolic (median 127 [IQR 96 - 150] vs. 112 [86 - 150] ml/m(2); p = 0.03) and LV end-systolic (82 [54 - 91] vs. 69 [48 - 99] ml/m(2); p = 0.03) volume indices decreased significantly from BL to FU. No significant differences were found for RV end-diastolic (94 [75 - 103] vs. 99 [77 - 123] ml/m(2); p = 0.91), RV end-systolic (48 [42 - 80] vs. 51 [40 - 81] ml/m(2); p = 0.48), and LA (87 [55 - 124] vs. 92 [48 - 137] ml/m(2); p = 0.20) volume indices between BL and FU. CONCLUSION: CMR enables the assessment of cardiac volumes in patients after MitraClip implantation. Our CMR findings indicate that percutaneous mitral valve repair results in reverse LV but not in RV or LA remodeling. KEY POINTS: • Volume measurements by cardiovascular magnetic resonance imaging are feasible following percutaneous mitral valve repair despite device-related artifacts.• A significant reduction of left ventricular volume was found in terms of beneficial, reverse left ventricular remodeling after 6-month follow-up.• No significant reduction was found in right ventricular or left atrial volumes after percutaneous mitral valve repair after 6-month follow-up.

Quantification of mechanical ventricular dyssynchrony: direct comparison of velocity-encoded and cine magnetic resonance imaging.

PURPOSE: The preoperative assessment of mechanical dyssynchrony can help to improve patient selection in candidates for cardiac resynchronization therapy (CRT). The present study compared the performance of velocity-encoded (VENC) MRI to cine-magnetic resonance imaging (MRI) for quantifying mechanical ventricular dyssynchrony. MATERIALS AND METHODS: VENC-MRI and cine-MRI were performed in 20 patients with heart failure NYHA class III and reduced ejection fraction (median: 24 %, interquartile range: 18 - 28 %) before CRT device implantation. The interventricular mechanical delay (IVMD) was assessed by VENC-MRI as the temporal difference between the onset of aortic and pulmonary flow. Intraventricular dyssynchrony was quantified by cine-MRI, using the standard deviation of time to maximal wall thickening in sixteen left ventricular segments (SDt-16). The response to CRT was assessed in a six-month follow-up. RESULTS: 14 patients (70 %) clinically responded to CRT. A similar accuracy was found to predict the response to CRT by measurements of the IVMD and SDt-16 (75 vs. 70 %; p = ns). The time needed for data analysis was significantly shorter for the IVMD at 1.69 min (interquartile range: 1.66 - 1.88 min) compared to 9.63 min (interquartile range: 8.92 - 11.63 min) for the SDt-16 (p < 0.0001). CONCLUSION: Measurements of the IVMD by VENC-MRI and the SDt-16 by cine-MRI provide a similar accuracy to identify clinical responders to CRT. However, data analysis of the IVMD is significantly less time-consuming compared to data analysis of the SDt-16.

Delayed-enhancement magnetic resonance imaging in patients with clinically suspected stress cardiomyopathy (Tako-tsubo).

PURPOSE: To compare the ability of delayed-enhancement magnetic resonance imaging (DE-MRI) and other MRI and clinical parameters to identify diseases mimicking stress cardiomyopathy (SCM). MATERIALS AND METHODS: The study included 14 consecutive patients fulfilling the American Heart Association (AHA) criteria for SCM with acute left ventricular dysfunction in the absence of coronary artery disease, triggered by psychological stress. The MRI protocol consisted of cine, T 2-weighted, first-pass-perfusion (FPP) and DE-MRI. RESULTS: Six patients with DE were classified as mimicking SCM (non-SCM) and 8 patients without DE as SCM. FPP defects were found in 4 patients with non-SCM and in none with SCM (p < 0.05). Myocardial edema was found in 5 patients with non-SCM and in 2 patients with SCM (p = ns). No significant differences in clinical findings such as ECG, cardiac markers and echocardiographic recovery of left ventricular function were found between patients with non-SCM and SCM. CONCLUSION: Non-SCM defined by DE-MRI is a frequent finding in patients fulfilling the AHA criteria for SCM. Clinical findings seem to be of limited value to differentiate between non-SCM and SCM.

Diastolic dysfunction in exercise and its role for exercise capacity.

Diastolic dysfunction is frequent in elderly subjects and in patients with left ventricular hypertrophy, vascular disease and diabetes mellitus. Patients with diastolic dysfunction demonstrate a reduced exercise capacity and might suffer from congestive heart failure (CHF). Presence of symptoms of CHF in the setting of a normal systolic function is referred to as heart failure with normal ejection fraction (HFNEF) or, if evidence of an impaired diastolic function is observed, as diastolic heart failure (DHF). Reduced exercise capacity in diastolic dysfunction results from a number of pathophysiological alterations such as slowed myocardial relaxation, reduced myocardial distensibility, elevated filling pressures, and reduced ventricular suction forces. These alterations limit the increase of ventricular diastolic filling and cardiac output during exercise and lead to pulmonary congestion. In healthy subjects, exercise training can enhance diastolic function and exercise capacity and prevent deterioration of diastolic function in the course of aging. In patients with diastolic dysfunction, exercise capacity can be enhanced by exercise training and pharmacological treatment, whereas improvement of diastolic function can only be observed in few patients.

Assessment of myocardial viability in ischemic heart disease by cardiac magnetic resonance imaging.

Assessment of myocardial viability aims at differentiating between viable and non-viable myocardium. The proof of dysfunctional but viable myocardium is crucial to predict outcome of revascularization after acute (AMI) and chronic myocardial infarction (CMI). Cardiac magnetic resonance imaging (CMRI) offers different options to detect viable myocardium: Measurements of end-diastolic wall thickness by cine-CMRI can be used to depict chronically scarred myocardium, but fails to detect acute myocardial necrosis. Low-dose dobutamine stimulation (LDDS) cine-CMRI analyses the contractile reserve of dysfunctional but viable myocardium under pharmacologic stimulus to identify viable myocardium in AMI and CMI with high specificity. Sensitivity of LDDS cine-CMRI is superior to LDDS echocardiography but reduced in patients with severely impaired left ventricular (LV) function. The delayed-enhancement (DE) technique directly visualises non-viable myocardium due to an altered contrast-media distribution in necrotic and fibrotic tissue. DE-CMRI identifies non-viable myocardium with high spatial resolution independently from LV function. The transmural extent of contrast enhancement in DE-CMRI is used to predict functional recovery after revascularization in AMI and CMI. Furthermore, the amount and pattern of contrast enhancement in DE-CMRI provide important prognostic information in both entities. Recent studies demonstrated the superiority of DE-CMRI compared to single photon emission tomography (SPECT) and positron emission tomography (PET) to assess myocardial viability. Therefore, DE-CMRI is currently recognised as the standard of reference for assessment of myocardial viability. The technical background, clinical application and accuracy of the different CMRI techniques to assess myocardial viability in AMI and CMI are discussed in this work.

Anaerobic threshold and maximal oxygen uptake in patients with coronary artery disease and stable angina before and after percutaneous transluminal coronary angioplasty.

In this study, we investigated the effect of percutaneous transluminal coronary angioplasty (PTCA) on functional exercise capacity, oxygen uptake at anaerobic threshold (VO(2 AT)) and maximal oxygen uptake (VO(2 max)) in patients with coronary artery disease (CAD). Twenty-five patients with CAD and stable angina pectoris underwent spiroergometry before and after PTCA. All patients had reduced functional capacity with Weber class B in 5, class C in 16 and class D in 4 patients with mean VO(2 AT) of 9.4 +/- 1.5 ml.kg(-1).min(-1) and mean VO(2 max) of 13.3 +/- 3.3 ml. kg(-1).min(-1). After PTCA, VO(2 max) (15.8 +/- 3.1 ml.kg(-1). min(-1)) increased significantly (p < 0.001) compared to before PTCA. Subgroup analysis revealed that patients with low functional capacity before PTCA (VO(2 max) <15 ml x kg(-1) x min(-1)) had the most benefit from PTCA with an increase in VO(2 AT) from 8.7 +/- 1.0 to 9.6 +/- 1.4 ml x kg(-1) x min(-1) (p < 0.05) and of VO(2 max) from 11.3 +/- 2.2 to 14.8 +/- 3.5 ml x kg(-1) x min(-1) (p < 0.001) whereas in patients with VO(2 max) >15 ml x kg(-1) x min(-1), VO(2 AT) (p = 0.9) and VO(2 max) (p = 0.2) did not improve significantly. In conclusion, there is reduced functional capacity and VO(2 max) which improved after PTCA in CAD patients. In patients with low VO(2 max) before PTCA, functional capacity, VO(2 AT) and VO(2 max) significantly improved after PTCA, suggesting reversible myocardial impairment induced by intermittent myocardial ischemia. Patients with higher VO(2 max) had no significant benefit from PTCA with respect to functional capacity, VO(2 max) and VO(2 AT).