Andres Schuster

Usefulness of cardiac magnetic resonance-guided management in patients with recurrent pericarditis

Recurrent pericarditis (RP) affects 10% to 50% of patients with acute pericarditis. The use of steroids has been associated with increased recurrence rate of pericarditis, along with known major side effects. Cardiac magnetic resonance imaging (CMR) is more frequently used to assess pericardial inflammation and less commonly to guide therapy. The aim of this study was to assess the utility of CMR in the management of RP compared with standard therapy. A total of 507 consecutive patients with RP after the first attack, all of whom were treated with colchicine and nonsteroidal anti-inflammatory drugs as first-line therapy, were retrospectively evaluated. There were 257 patients who were treated with medications and received CMR-guided therapy (group 1) and 250 patients who were treated with medications without CMR (group 2). The 2 groups had similar baseline characteristics and follow-up periods (17 ± 7.9 vs 16.3 ± 16.2 months, respectively, p = 0.97). CMR was used to assess the presence of pericardial inflammation, and on the basis of the results, the clinician made changes to the steroid dose dictated by the severity of inflammation. There was no significant difference in the incidence of constrictive pericarditis, pericardial window, or pericardiectomy between groups during the follow-up. However, group 2 patients had a larger number of steroid pulse therapies (defined as prednisone 50 mg/day orally for 10 days and tapering to none over 4 weeks), and higher overall total milligrams of steroid administered compared with the CMR group (p = 0.003 and p = 0.001, respectively). Recurrence and pericardiocentesis rates were lower in group 1 (p <0.0001). In conclusion, CMR-guided therapy modulates the management of RP. This approach decreased pericarditis recurrence and exposure to steroids.

Quantitative assessment of pericardial delayed hyperenhancement predicts clinical improvement in patients with constrictive pericarditis treated with anti-inflammatory therapy.

Background—Delayed hyperenhancement (DHE) of the pericardium usually represents ongoing inflammation and may identify patients with constrictive pericarditis that will improve with anti-inflammatory therapy. However, a quantitative assessment of pericardial DHE has not been performed, and the hierarchical relationship among clinical factors, inflammatory markers, and pericardial DHE is unknown. Methods and Results—We identified 41 consecutive patients with constrictive pericarditis who had a cardiovascular magnetic resonance study with DHE prior to the initiation of anti-inflammatory medications. Pericardial inflammation was quantified on short-axis DHE sequences by contouring the pericardium, selecting normal septal myocardium as a reference region, and then quantifying the pericardial signal that was >6 SD above the reference. Our primary outcome was clinical improvement with anti-inflammatory therapy. The mean age of our patients was 58 years, most patients were male (83%) with New York Heart Association Class II or III (59%) heart failure, and the median follow-up was 1 year. Chest pain, lower New York Heart Association class, higher Westergren sedimentation rates, and increased pericardial DHE were all significantly associated with clinical improvement (P<0.01 for all). When quantitative pericardial DHE was added to a model that included age, chest pain, New York Heart Association class, and Westergren sedimentation rates, the global &khgr;2 improved significantly (P=0.04 for DHE), and the area under the receiver operating characteristic curve was 0.96. Conclusions—In patients with constrictive pericarditis treated with anti-inflammatory therapy, a quantitative assessment of pericardial DHE can provide incremental information to predict clinical improvement when added to clinical factors and Westergren sedimentation rates.

Impact and persistence of cirrhotic cardiomyopathy after liver transplantation.

Cirrhotic cardiomyopathy causes variable degree of systolic and diastolic dysfunction (DD) and conduction abnormalities. The primary aim of our study was to determine whether pre‐transplant DD and prolonged corrected QT (QTc) predict a composite of mortality, graft failure, and major cardiovascular events after liver transplantation. We also evaluated the reversibility of cirrhotic cardiomyopathy after transplantation. Adult patients who underwent liver transplantation at our institution from January 2007 to March 2009 were included. Data were obtained from institutional registry, medical record review, and evaluation of echocardiographic images. Among 243 patients, 113 (46.5%) had grade 1 DD, 16 (6.6%) had grade 2 DD, and none had grade 3 DD. The mean pre‐transplant QTc was 453 milliseconds. After a mean post‐transplant follow‐up of 5.2 years, 75 (31%) patients satisfied the primary composite outcome. Cox regression analysis did not show any significant association between DD and the composite outcome (P=.17). However, longer QTc was independently associated with the composite outcome (HR: 1.01, 95% confidence interval: 1.00–1.02, P=.05). DD (P<.001) and left ventricular mass index (P=.001) worsened after transplantation. In conclusion, QTc prolongation appears to be associated with worse outcomes. Although DD did not impact outcomes, it significantly worsened after transplantation.

Ivabradine in heart failure: to SHIFT or not to SHIFT.

Despite advances in treatment during the past two decades, long-term prognosis of heart failure (HF) still is poor in patients at advanced stages. Antiadrenergic therapy has demonstrated consistent morbidity and mortality benefits, which often are linked to its ability to facilitate reversal in cardiac remodeling. Although a direct association between heart rate (HR) and cardiovascular (CV) outcomes in patients with HF has been observed [1, 2], there is debate regarding the importance of HR reduction as a contributor to the beneficial effects of antiadrenergic therapy [3–6]. A recent meta-analysis found a significant association between the degrees of HR reduction and the impact of antiadrenergic therapy in survival of patients with HF, whereas the dose of antiadrenergic therapy achieved was not correlated [7]. However, in the real world, β-blocker uptitration in response to persistently elevated HR can be associated with increased risk of adverse reactions [8, 9], and such limitations of antiadrenergic therapy have prompted the interest of looking into alternative treatment strategies to lower HR. Ivabradine is a selective inhibitor of the pacemaker I “funny” (If) channel, which is responsible for the autonomic capacity of the sinoatrial node. If channels are upregulated in atrial tissue of patients with atrial fibrillation or atrial flutter and they also are present in ventricular myocytes of patients with HF [10]. Ivabradine works by reducing its diastolic depolarization slope, thereby decreasing HR via direct sinus node inhibition without direct effects on myocardial contractility and intracardiac conduction. In the BEAUTIFUL (Morbidity–Mortality Evaluation of the If Inhibitor Ivabradine in Patients with Coronary Artery Disease and Left Ventricular Systolic Dysfunction) study, patients with high baseline HR had an increase in serious CV events including death (34%), hospital admission secondary to congestive HF (53%), acute myocardial infarction (46%), or revascularization procedure (38%) [11]. In a subset of patients with baseline HR of 70 bpm and left ventricular ejection fraction (LVEF) less than 40%, ivabradine was associated with a 36% decrease in hospital admissions secondary to fatal and nonfatal myocardial infarction and a 30% decrease in coronary revascularization [11].

Usefulness of Elevated Urine Neopterin Levels in Assessing Cardiac Dysfunction and Exercise Ventilation Inefficiency in Patients With Chronic Systolic Heart Failure

Neopterin is synthesized by macrophages upon stimulation with gamma-interferon, and high neopterin production is associated with cellular immune activation and increased production of reactive oxygen species (oxidant stress), but the clinical utility of urine neopterin levels in patients with heart failure (HF) has not been explored. Fifty-three ambulatory patients with chronic systolic HF (left ventricular [LV] ejection fraction ≤40%) underwent comprehensive echocardiographic evaluation and cardiopulmonary exercise testing. Urine neopterin levels were quantified by liquid chromatography with tandem mass spectrometric analyses and corrected to urine creatinine (Cr) levels. In our study cohort, median urine neopterin level was 60 μmol/mol Cr (interquartile range 40 to 86). There were modest correlations between urine neopterin levels and abnormalities in cardiac structure and function by echocardiography: LV ejection fraction (r = -0.33, p = 0.017), indexed LV end-diastolic volume (r = 0.31, p = 0.029), indexed LV end-systolic volume (r = 0.32, p = 0.024), and E/septal Ea (r = 0.28, p = 0.041). Although there was no significant correlation between urine neopterin and maximal oxygen uptake (peak VO2: r = -0.25, p = 0.07), there was a modest correlation between urine neopterin and maximal ventilation/carbon dioxide production ratio (VE/VCO2 max: r = 0.38, p = 0.005). In conclusion, increase in urine neopterin levels tracks with disease severity in patients with chronic systolic HF.