Cardiac Magnetic Resonance Imaging Versus Transthoracic Echocardiography for Prediction of Outcomes in Chronic Aortic or Mitral Regurgitation.

In subjects with aortic regurgitation (AR) or mitral regurgitation (MR), transthoracic echocardiography (TTE) is recommended for surveillance. Few prospective studies have directly compared the ability of TTE and cardiac magnetic resonance (CMR) to predict clinical outcomes in AR and MR. We hypothesized that, given its higher reproducibility, CMR would predict the need for valve surgery or heart failure (HF) hospitalization better than TTE. Quantitative TTE and CMR were performed on the same day for 51 subjects: 29 with chronic AR and 22 with chronic, primary MR for quantification of valve regurgitation. Baseline measurements of valve regurgitation were compared to the combined primary end point of new HF and valve surgery using receiver operating characteristics, simple logistic regression, and Kaplan-Meier survival analyses. The primary end point occurred in 5 AR subjects (all surgery) and 8 MR subjects (7 surgery, 1 HF) after a mean follow-up of 4.4 ± 1.5 years. For AR, CMR-derived regurgitant volume >50 ml identified those at high risk with 50% undergoing valve surgery versus 0% for those with regurgitant volume ≤50 ml and was more strongly associated with outcomes than regurgitant volume by TTE (p <0.05). For MR, 6.8% of those with regurgitant volume by TTE ≤30 ml developed the primary end point versus 70% in those with regurgitant volume >30 ml. Regurgitant volume by CMR showed no significant separation of survival curves for MR. In conclusion, regurgitant volume by CMR was more predictive of outcomes than by TTE in subjects with AR. In MR, the 2 methods performed similarly.

Quantitating aortic regurgitation by cardiovascular magnetic resonance: significant variations due to slice location and breath holding.

OBJECTIVES: Compare variability in flow measurements by phase contrast MRI, performed at different locations in the aorta and pulmonary artery (PA) using breath-held (BH) and free-breathing (FB) sequences. METHODS: Fifty-seven patients with valvular heart disease, confirmed by echocardiography, were scanned using BH technique at 3 locations in the ascending aorta (SOV = sinus of Valsalva, STJ = sinotubular junction, ASC = ascending aorta at level of right pulmonary artery) and 2 locations in PA. Single FB measurement was obtained at STJ for aorta. Obtained metrics (SV = stroke volume, FV = forward volume, BV = backward volume, RF = regurgitant fraction) were evaluated separately for patients with aortic regurgitation (AR, n = 31) and mitral regurgitation (n = 26). RESULTS: No difference was noted between the two measurements in the PA. Significant differences were noted in measured SV at different aortic locations. SV measurements obtained at ASC correlated best with the measurements obtained in the PA. Strongest correlation of AR was measured at the STJ. CONCLUSION: Measurements of flow volumes by phase contrast MRI differ depending on slice location. When using stroke volumes to calculate pulmonary to systemic blood flow ratio (Qp/Qs), ASC should be used. For quantifying aortic regurgitation, measurement should be obtained at STJ. KEY POINTS: • Aortic regurgitation can be accurately measured by MRI. • Aortic regurgitation measurement by MRI varies according to the location where measured. • Aortic regurgitation can also be measured by MRI without breath hold.

Prospective comparison of valve regurgitation quantitation by cardiac magnetic resonance imaging and transthoracic echocardiography.

BACKGROUND: Both transthoracic echocardiography (TTE) and cardiac magnetic resonance (CMR) imaging allow quantification of chronic aortic regurgitation (AR) and mitral regurgitation (MR). We hypothesized that CMR measurement of regurgitant volume (RVol) is more reproducible than TTE. METHODS AND RESULTS: TTE and CMR performed on the same day in 57 prospectively enrolled adults (31 with AR, 26 with MR) were measured by 2 independent physicians. TTE RVol(AR) was calculated as Doppler left ventricular outflow minus inflow stroke volume. RVol(MR) was calculated by both the proximal isovelocity surface area method and Doppler volume flow at 2 sites. CMR RVol(AR) was calculated by phase-contrast velocity mapping at the aortic sinuses and RVol(MR) as total left ventricular minus forward stroke volume. Intraobserver and interobserver variabilities were similar. For AR, the Bland-Altman mean interobserver difference in RVol was -0.7 mL (95% confidence interval [CI], -5 to 4) for CMR and -9 mL (95% CI, -53 to -36) for TTE. The Pearson correlation was higher (P=0.001) between CMR (0.99) than TTE readers (0.89). For MR, the Bland-Altman mean difference in RVol between observers was -4 mL (95% CI, -21 to 13) for CMR compared with 0.7 mL (95% CI, -30 to 32) for the proximal isovelocity surface area and -10 mL (95% CI, -76 to 56) for TTE volume flow at 2 sites. Correlation was similar for CMR (0.94) versus TTE readers (0.90 for the proximal isovelocity surface area). CONCLUSIONS: Compared with TTE, CMR has lower intraobserver and interobserver variabilities for RVol(AR), suggesting CMR may be superior for serial measurements. Although RVol(MR) is similar by TTE and CMR, variability in measured RVol by both approaches suggests that caution is needed in clinical practice.

The aorta wall of patients presenting to the emergency department with acute myocardial infarction by cardiac magnetic resonance.

BACKGROUND: Inflammation has been shown to be a major component in the pathophysiology of acute coronary syndrome (ACS). In patients presenting with acute myocardial infarction (AMI), a critical component of the ACS spectrum, multiple coronary arteries are involved during this inflammatory process. In addition to the coronary vasculature, the inflammatory cascade has also been shown to affect the carotid arteries and possibly the aorta. PURPOSE: To assess the involvement of the aorta during AMI by cardiac magnetic resonance (CMR). METHODS: We prospectively evaluated the aortic wall by CMR in 123 patients. 78 patients were enrolled from the emergency department (ED), who presented with chest pain and were classified as either: (1) AMI: elevated troponin levels and typical chest pain or (2) non-cardiac chest pain (CP): negative troponins and a normal stress test or normal cardiac catheterization. We compared these 2 groups to a group of 45 asymptomatic diabetic patients. The descending thoracic aortic wall area (AWA) and maximal aortic wall thickness (AWT) were measured using a double inversion recovery T-2 weighted, ECG-gated, spin echo sequence by CMR. RESULTS: Patients with AMI were older, more likely to smoke, had a higher incidence of claudication, and had higher CRP levels. The AWA and maximal AWT were greater in patients who presented to the ED with ACS (2.11+/-0.17 mm(2), and 3.17+/-0.19 mm, respectively) than both patients presenting with non-cardiac CP (1.52+/-0.58 mm(2), p<0.001; and 2.57+/-0.10 mm, p<0.001) and the diabetic patients (1.38+/-0.58 mm(2), p<0.001; and 2.30+/-0.131 mm, p<0.001). The difference in the aortic wall characteristics remained significant after correcting for body mass index, hyperlipidemia, statins and C-reactive protein. There was no difference in maximal AWT or AWA between patients with non-cardiac CP and patients with diabetes. CONCLUSION: Patients with AMI have a significantly greater maximal aortic wall thickness and area compared to patients with non-cardiac CP. Longitudinal studies are needed to assess whether this increase is due to inflammation or a higher atherosclerotic burden.

Detection of myocardial damage in patients with sarcoidosis.

BACKGROUND: In patients with sarcoidosis, sudden death is a leading cause of mortality, which may represent unrecognized cardiac involvement. Delayed-enhancement cardiovascular magnetic resonance (DE-CMR) can detect minute amounts of myocardial damage. We sought to compare DE-CMR with standard clinical evaluation for the identification of cardiac involvement. METHODS AND RESULTS: Eighty-one consecutive patients with biopsy-proven extracardiac sarcoidosis were prospectively recruited for a parallel and masked comparison of cardiac involvement between (1) DE-CMR and (2) standard clinical evaluation with the use of consensus criteria (modified Japanese Ministry of Health [JMH] guidelines). Standard evaluation included 12-lead ECG and at least 1 dedicated non-CMR cardiac study (echocardiography, radionuclide scintigraphy, or cardiac catheterization). Patients were followed for 21+/-8 months for major adverse events (death, defibrillator shock, or pacemaker requirement). Patients were predominantly middle-aged (46+/-11 years), female (62%), and black (73%) and had chronic sarcoidosis (median, 7 years) and preserved left ventricular ejection fraction (median, 56%). DE-CMR identified cardiac involvement in 21 patients (26%) and JMH criteria in 10 (12%, 8 overlapping), a >2-fold higher rate for DE-CMR (P=0.005). All patients with myocardial damage on DE-CMR had coronary disease excluded by x-ray angiography. Pathology evaluation in 15 patients (19%) identified 4 with cardiac sarcoidosis; all 4 were positive by DE-CMR, whereas 2 were JMH positive. On follow-up, 8 had adverse events, including 5 cardiac deaths. Patients with myocardial damage on DE-CMR had a 9-fold higher rate of adverse events and an 11.5-fold higher rate of cardiac death than patients without damage. CONCLUSIONS: In patients with sarcoidosis, DE-CMR is more than twice as sensitive for cardiac involvement as current consensus criteria. Myocardial damage detected by DE-CMR appears to be associated with future adverse events including cardiac death, but events were few, and this needs confirmation in a larger cohort.

Prevention of calcific aortic valve stenosis-fact or fiction?

Valve replacement is the only long-term effective treatment for calcific aortic valve stenosis. However, this treatment is aimed only at patients with advanced leaflet disease and symptoms of left ventricular obstruction. Over the past 15 years, our understanding of the pathogenesis of calcific aortic stenosis has changed significantly: away from a passive degenerative disease to an active process involving endothelial dysfunction, lipid accumulation, an inflammatory infiltrate, and a regulated process of calcification. Since many of the same processes are characteristic of atherosclerosis, trials have been undertaken to test whether medical therapy (statins, renin-angiotensin inhibition) can prevent or alter the disease course. Although retrospective and non-randomized studies suggested a positive effect with statins, benefit has not been seen in perspective randomized controlled trials, although two major studies are still in progress. Inhibition of renin-angiotensin has shown discordant results in retrospective studies with no randomized controlled data published. In the future, we need to consider other medical therapies that might target different pathways in this disease process. In addition, we need to define the optimal timing and duration of therapy for this chronic slowly progressive disease; treatments aimed at the early disease process may be ineffective with end-stage tissue changes.

Not the usual cardiac rhythm device infection: a fastidious pathogen with several teaching points.

Because cardiac device infections may include fastidious pathogens, extended incubation of blood cultures is suggested. A patient with an infection of a right ventricular lead implantable cardioverter defibrillator (ICD) system is described. The device was implanted 6 months earlier. The pathogen was identified as Haemophilus parainfluenzae, which was cultured within 72 hours and was presumably from a respiratory tract infection. Extended incubation was not necessary to culture this fastidious pathogen. Two large retrospective studies suggest that prolonged incubation for fastidious organisms is generally not necessary because of advances in culture media and automated blood culture systems.

Successful percutaneous closure of an aortic graft pseudo-aneurysm with a patent foramen ovale occluder device.

Endovascular stent grafts, prosthetic grafts placed over expandable stents, are an alternative therapy for the treatment of arterial aneurysms, pseudo-aneurysms, dissections, penetrating ulcers and coarctations. However, there are limitations to their applicability. This case describes a patient with Takayasu's arteritis, an inflammatory disease of medium- to large-sized vessels, who developed an aneurysm in an open surgically placed aortic graft. The patient had previously undergone two separate surgeries for the treatment of thoracic aortic aneurysms. Due to the potential for reduced morbidity and mortality, endovascular stenting was a rational approach for a focal graft defect. Endovascular stent graft repair could not be performed because the ratio of the required vascular sheath to peripheral vessel size was prohibitive in this patient. Instead, endovascular therapy using an Amplatzer patent foramen ovale occluder device was delivered within the pseudo-aneurysm to seal the connection to the aortic lumen. At 9-month follow up, the patient has done well clinically and has not required any additional procedures.

Direct en face imaging of secundum atrial septal defects by velocity-encoded cardiovascular magnetic resonance in patients evaluated for possible transcatheter closure.

BACKGROUND: Atrial septal defect (ASD) flow can be measured indirectly by velocity-encoded cardiovascular magnetic resonance (veCMR) of the pulmonary artery and aorta. Imaging the secundum ASD en face could potentially enable direct flow measurement and provide valuable information about ASD size, shape, location, and proximity to other structures. METHODS AND RESULTS: Forty-four patients referred for possible transcatheter ASD closure underwent a comprehensive standard evaluation, including transesophageal and/or intracardiac echocardiography and invasive oximetry. CMR was performed in parallel and included direct en face veCMR after an optimal double-oblique imaging plane was determined that accounted for ASD flow direction and cardiac-cycle interatrial septal motion. ASD flow measured by direct en face veCMR correlated better with invasive oximetry than indirect (pulmonary artery and aorta) veCMR (r=0.80 versus r=0.66). Additionally, 95% limits of agreement were narrower (+/-3.9 versus +/-5.1 L/min). En face veCMR determined that defects usually were eccentrically shaped (major/minor axis length >1.5) rather than circular, with 16% having extreme eccentricity (major/minor >2.0). Overall, ASD size by both veCMR and intracardiac echocardiography correlated with final device size; however, in small to medium defects (<3 cm(2)) and extremely eccentric defects, veCMR correlated better with final device size than did intracardiac echocardiography. Importantly, CMR identified additional information in 9 patients (20%) that altered clinical management. Specifically, en face veCMR detected additional defects (n=3), large ASD with insufficient rim tissue (n=2), and sinus venosus defect with anomalous pulmonary vein (n=1). Cine and/or morphological imaging detected interrupted inferior vena cava (n=2) and sinus of Valsalva aneurysm (n=1). CONCLUSIONS: En face veCMR with an optimized imaging plane can determine ASD flow, size, and morphology. CMR provided information incremental to comprehensive standard evaluation that altered clinical management in 20% of patients.