Research Spotlight

Gollub, M. J., S. Arya, R. G. Beets-Tan, G. De Prisco, M. Gonen, K. Jhaveri, Z. Kassam, H. Kaur, D. Kim, A. Knezevic, E. Korngold, C. Lall, N. Lalwani, D. Blair Macdonald, C. Moreno, S. Nougaret, P. Pickhardt, S. Sheedy and M. Harisinghani (2018). “Use of magnetic resonance imaging in rectal cancer patients: Society of Abdominal Radiology (SAR) rectal cancer disease-focused panel (DFP) recommendations 2017.” Abdom Radiol (NY). May 21. [Epub ahead of print].

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PURPOSE: To propose guidelines based on an expert-panel-derived unified approach to the technical performance, interpretation, and reporting of MRI for baseline and post-treatment staging of rectal carcinoma. METHODS: A consensus-based questionnaire adopted with permission and modified from the European Society of Gastrointestinal and Abdominal Radiologists was sent to a 17-member expert panel from the Rectal Cancer Disease-Focused Panel of the Society of Abdominal Radiology containing 268 question parts. Consensus on an answer was defined as >/= 70% agreement. Answers not reaching consensus (< 70%) were noted. RESULTS: Consensus was reached for 87% of items from which recommendations regarding patient preparation, technical performance, pulse sequence acquisition, and criteria for MRI assessment at initial staging and restaging exams and for MRI reporting were constructed. CONCLUSION: These expert consensus recommendations can be used as guidelines for primary and post-treatment staging of rectal cancer using MRI.

Filardo, G., R. J. Damiano, Jr., G. Ailawadi, V. H. Thourani, B. D. Pollock, D. M. Sass, T. K. Phan, H. Nguyen and B. da Graca (2018). “Epidemiology of new-onset atrial fibrillation following coronary artery bypass graft surgery.” Heart 104(12): 985-992.

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OBJECTIVES: Postoperative atrial fibrillation (AF) following coronary artery bypass graft surgery (CABG) is significantly associated with reduced survival, but poor characterisation and inconsistent definitions present barriers to developing effective prophylaxis and management. We sought to address this knowledge gap. METHODS: From 2002 to 2010, 11 239 consecutive patients without AF underwent isolated CABG at five sites. Clinical data collected for the Society of Thoracic Surgeons (STS) Database were augmented with details on AF detected via continuous in-hospital ECG/telemetry monitoring to assess new-onset post-CABG AF (adjusted for STS risk of mortality); time to first AF; durations of first and longest AF episodes; total in-hospital time in AF; number of in-hospital AF episodes; operative mortality; stroke; discharge in AF; and length of stay (LOS). RESULTS: Unadjusted incidence of new-onset post-CABG AF was 29.5%. Risk-adjusted incidence was 33.1% and varied little over time (P=0.139). Among 3312 patients with post-CABG AF, adjusted median time to first AF was 52 (IQR: 48-55) hours; mean (SD) duration of first and longest events were 7.2 (5.3,9.1) and 13.1 (10.4,15.9) hours, respectively, and adjusted median total time in AF was 22 (IQR: 18-26) hours. Adjusted rates of operative mortality, stroke and discharge in AF did not vary significantly over time (P=0.156, P=0.965 and P=0.347, respectively). LOS varied (P=0.035), but in no discernible pattern. CONCLUSIONS: Each year, ~800 000 people undergo CABG worldwide; >264 000 will develop post-CABG AF. Onset is typically 2-3 days post-CABG and episodes last, on average, several hours. Effective prophylaxis and management is urgently needed to reduce associated risks of adverse outcomes.

Erwin, J. P., 3rd and B. Iung (2018). “Current recommendations for anticoagulant therapy in patients with valvular heart disease and atrial fibrillation: the ACC/AHA and ESC/EACTS Guidelines in Harmony…but not Lockstep!” Heart 104(12): 968-970.

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The term non-valvular atrial fibrillation (NVAF) has become popular with the development of non-vitamin K antagonists (VKA) novel oral anticoagulants (NOAC), or direct oral anticoagulants (DOAC). Randomised trials evaluating NOACs in atrial fibrillation (AF) targeted NVAF since thromboembolic risk was presumed to be higher, and possibly to involve different mechanisms, in patients with valvular heart disease (VHD). However, it is acknowledged that the definition of NVAF is not uniform. Exclusion criteria for valvular AF differed between trials on NOACs with regard to the type and severity of native VHD and the type of valve prostheses (table 1). The availability of subgroup analyses now allows for a better risk assessment and ascertainment of indications of NOACs in patients with VHD. With increasing life expectancy, the epidemic of VHD is becoming more prevalent. Simultaneously, transcatheter aortic valve implantation (TAVI) has emerged as an alternative therapy for patients with significant VHD and the ideal antithrombotic regimen for these patients has not yet been firmly established. We review here the issues of anticoagulation in VHD, focusing on patients with AF, in the light of recent 2017 American Heart Association (AHA)/American College of Cardiology (ACC) and European Society of Cardiology (ESC)/European Association of Cardio-Thoracic Surgery (EACTS) guidelines on VHD. (Excerpt from text of this editorial, p. 968; no abstract available.)

Damman, K., M. Gori, B. Claggett, P. S. Jhund, M. Senni, M. P. Lefkowitz, M. F. Prescott, V. C. Shi, J. L. Rouleau, K. Swedberg, M. R. Zile, M. Packer, A. S. Desai, S. D. Solomon and J. J. V. McMurray (2018). “Renal Effects and Associated Outcomes During Angiotensin-Neprilysin Inhibition in Heart Failure.” JACC Heart Fail 6(6): 489-498.

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OBJECTIVES: The purpose of this study was to evaluate the renal effects of sacubitril/valsartan in patients with heart failure and reduced ejection fraction. BACKGROUND: Renal function is frequently impaired in patients with heart failure with reduced ejection fraction and may deteriorate further after blockade of the renin-angiotensin system. METHODS: In the PARADIGM-HF (Prospective Comparison of ARNI with ACE inhibition to Determine Impact on Global Mortality and Morbidity in Heart Failure) trial, 8,399 patients with heart failure with reduced ejection fraction were randomized to treatment with sacubitril/valsartan or enalapril. The estimated glomerular filtration rate (eGFR) was available for all patients, and the urinary albumin/creatinine ratio (UACR) was available in 1872 patients, at screening, randomization, and at fixed time intervals during follow-up. We evaluated the effect of study treatment on change in eGFR and UACR, and on renal and cardiovascular outcomes, according to eGFR and UACR. RESULTS: At screening, the eGFR was 70 +/- 20 ml/min/1.73 m(2) and 2,745 patients (33%) had chronic kidney disease; the median UACR was 1.0 mg/mmol (interquartile range [IQR]: 0.4 to 3.2 mg/mmol) and 24% had an increased UACR. The decrease in eGFR during follow-up was less with sacubitril/valsartan compared with enalapril (-1.61 ml/min/1.73 m(2)/year; [95% confidence interval: -1.77 to -1.44 ml/min/1.73 m(2)/year] vs. -2.04 ml/min/1.73 m(2)/year [95% CI: -2.21 to -1.88 ml/min/1.73 m(2)/year ]; p < 0.001) despite a greater increase in UACR with sacubitril/valsartan than with enalapril (1.20 mg/mmol [95% CI: 1.04 to 1.36 mg/mmol] vs. 0.90 mg/mmol [95% CI: 0.77 to 1.03 mg/mmol]; p < 0.001). The effect of sacubitril/valsartan on cardiovascular death or heart failure hospitalization was not modified by eGFR, UACR (p interaction = 0.70 and 0.34, respectively), or by change in UACR (p interaction = 0.38). CONCLUSIONS: Compared with enalapril, sacubitril/valsartan led to a slower rate of decrease in the eGFR and improved cardiovascular outcomes, even in patients with chronic kidney disease, despite causing a modest increase in UACR.

Cherney, D. Z. I., Y. Lytvyn and P. A. McCullough (2018). “Cardiovascular Risk Reduction in Patients With Chronic Kidney Disease: Potential for Targeting Inflammation With Canakinumab.” J Am Coll Cardiol 71(21): 2415-2418. May 29 [epub ahead of print].

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Ridker et al., in a post hoc analysis of CANTOS, report that in patients with moderate CKD (estimated GFR <60 ml/min/1.73 m2), and a high overall rate of CV events, canakinumab reduced the risk of major adverse cardiovascular events. In addition to demonstrating CV benefit, this analysis is of interest because canakinumab was safe and well tolerated in patients with CKD. Although the precise mechanisms responsible for CV protection with canakinumab are not yet clear, the largest benefit was observed in patients with a robust anti-inflammatory response to the first dose, a finding strongly suggesting that reducing inflammation played a role in CV protection. Comparable effects were also observed in patients with baseline albuminuria and in those with diabetes. Thus, the CV benefit observed with IL-1β inhibition in this cohort of patients with earlier stages of CKD may also set the stage for future research in patients with diabetes or more advanced renal disease including stages 3B and 4, who tend to exhibit exaggerated proinflammatory states . . . This post hoc analysis of CANTOS provides strong evidence for CV—but not renal—protection in response to suppressing inflammatory pathways in patients with moderate CKD. To elucidate fully the potential for renal protection with canakinumab, enriched CKD cohorts including patients with significant renal function impairment and proteinuria will likely be required. The lack of any signal, either positive or negative, in CANTOS around renal endpoints suggests that although this agent is generally safe, studies with canakinumab that specifically target CKD risk factors should not yet be prioritized. Nevertheless, dedicated studies are needed to determine whether canakinumab is protective in other high-risk groups and to explore the role of other novel anti-inflammatory agents on markers of CKD progression. (Excerpt from text of this commentary, p. 2416, 2418; no abstract available.)