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. 2016 May 12;59:1573–1574. doi: 10.1007/s00125-016-3987-3

Erratum to: SGLT2 Inhibition and cardiovascular events: why did EMPA-REG Outcomes surprise and what were the likely mechanisms?

Naveed Sattar 1,, James McLaren 1, Søren L Kristensen 2, David Preiss 3, John J McMurray 1
PMCID: PMC4969788  PMID: 27174369

Erratum to: Diabetologia

DOI 10.1007/s00125-016-3956-x

Unfortunately an error occurred during the typesetting of Fig. 1 which meant that the arrow in the ‘KIDNEY: SGLT2 inhibition’ text box was incorrectly orientated. The arrow is corrected in the version of the figure shown overleaf.

Fig. 1.

Fig. 1

Potential pathway linking empagliflozin (and possibly other SGLT2 inhibitors) with lower risks for HFH (and, linked to this, death due to cardiovascular disease). By increasing fluid losses via urinary glucose and sodium losses (1), intravascular volumes and systolic blood pressure are reduced and there is a significant rise in haematocrit (2). These latter effects may also be, to a small extent, assisted by weight loss. These changes in turn lessen cardiac stressors (pre- and afterload) and may also help improve myocardial oxygen supply (3). The net result is a likely improvement in cardiac systolic and diastolic function, lessening chances of pulmonary congestion, thus lowering risks of HFH and fatal arrhythmias. These cardiac function benefits will, in turn, feed back to improve renal blood flow and function (4). In this way, the cardio-renal axis is improved at a number of levels with SGLT2 inhibitor therapy

Footnotes

The online version of the original article can be found at 10.1007/s00125-016-3956-x.


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