Cardiology

Packer, M. (2018). “Contrasting effects on the risk of macrovascular and microvascular events of antihyperglycemic drugs that enhance sodium excretion and lower blood pressure.” Diabet Med 35(6): 707-713.

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Three classes of anti-hyperglycaemic medications are distinguished by their urinary sodium excretion-enhancing and blood pressure-lowering actions: long-acting glucagon-like peptide-1 receptor agonists, dipeptidyl peptidase-4 inhibitors and sodium-glucose co-transporter-2 inhibitors. Yet, these drugs exert different effects on macrovascular risk. Glucagon-like peptide-1 receptor agonists reduce atherosclerotic thromboembolic events, but have little effect on heart failure; sodium-glucose co-transporter-2 inhibitors decrease the occurrence of heart failure, but have minimal effect on myocardial infarction and stroke; and dipeptidyl peptidase-4 inhibitors do not ameliorate either atherosclerotic thromboembolic events or heart failure. Similarly, the three classes of drugs differ in their early effects on renal function. Dipeptidyl peptidase-4 inhibitors produce a small decrease in renal function that persists for the duration of treatment, and they do not prevent serious adverse renal events. For glucagon-like peptide-1 receptor agonists, a small early decrease in renal function persists for 2 years and is superseded by a small improvement in renal function, with no effect on renal outcomes. In contrast, an initial decrease in glomerular filtration with sodium-glucose co-transporter-2 inhibitors persists for only 1 year and is superseded by a durable improvement in renal function and a reduced risk of serious adverse renal events. These differences may be related to different actions on the proximal tubular reabsorption of sodium, and thereby, on glomerular hyperfiltration. Anti-hyperglycaemic drugs that have natriuretic actions differ markedly in their ability to modulate macrovascular and microvascular risk. These contrasting profiles cannot be predicted by their effects on blood glucose or blood pressure.

Lima, B., A. Bansal, J. Abraham, J. D. Rich, S. S. Lee, B. Soleimani, J. N. Katz, A. Kilic, J. S. Young, C. B. Patel and S. M. Joseph (2018). “Controversies and Challenges of Ventricular Assist Device Therapy.” Am J Cardiol 121(10): 1219-1224.

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Left ventricular assist device (LVAD) therapy has emerged as an increasingly vital facet of the treatment algorithm for advanced heart failure. Growing experience with LVAD support has led to substantial improvements in outcomes, with 1-year survival rates approaching that of cardiac transplantation. These therapeutic refinements have engendered growing interests in the potential for expanding the clinical indications for LVAD therapy to patients with less advanced heart failure. The primary obstacles to this evolution of care center largely on the prevention and/or management of the adverse events associated with LVAD therapy along with patient preference. Many programs also face the mounting difficulty of balancing quality outcomes with the increased volume of implants. During the recently assembled Users Meeting organized by St. Jude Medical, heart failure clinicians from nearly 50 LVAD implanting centers discussed these and other challenges and controversies impacting the field. The present review summarizes the key insights gleaned from this meeting.

Lansky, A. J., S. R. Messe, A. M. Brickman, M. Dwyer, H. Bart van der Worp, R. M. Lazar, C. G. Pietras, K. J. Abrams, E. McFadden, N. H. Petersen, J. Browndyke, B. Prendergast, V. G. Ng, D. E. Cutlip, S. Kapadia, M. W. Krucoff, A. Linke, C. Scala Moy, J. Schofer, G. A. van Es, R. Virmani, J. Popma, M. K. Parides, S. Kodali, M. Bilello, R. Zivadinov, J. Akar, K. L. Furie, D. Gress, S. Voros, J. Moses, D. Greer, J. K. Forrest, D. Holmes, A. P. Kappetein, M. Mack and A. Baumbach (2018). “Proposed Standardized Neurological Endpoints for Cardiovascular Clinical Trials: An Academic Research Consortium Initiative.” Eur Heart J 39(19): 1687-1697.

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Surgical and catheter-based cardiovascular procedures and adjunctive pharmacology have an inherent risk of neurological complications. The current diversity of neurological endpoint definitions and ascertainment methods in clinical trials has led to uncertainties in the neurological risk attributable to cardiovascular procedures and inconsistent evaluation of therapies intended to prevent or mitigate neurological injury. Benefit-risk assessment of such procedures should be on the basis of an evaluation of well-defined neurological outcomes that are ascertained with consistent methods and capture the full spectrum of neurovascular injury and its clinical effect. The Neurologic Academic Research Consortium is an international collaboration intended to establish consensus on the definition, classification, and assessment of neurological endpoints applicable to clinical trials of a broad range of cardiovascular interventions. Systematic application of the proposed definitions and assessments will improve our ability to evaluate the risks of cardiovascular procedures and the safety and effectiveness of preventive therapies.

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.)