Oral anticoagulation for stroke prevention in atrial fibrillation and advanced kidney disease

Figures

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  Figure 1. Study population flowchart. eGFR, estimated glomerular filtration rate.

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  Figure 2. Oral anticoagulation treatment strategy and associated age and sex-adjusted standardized risk of (A) thromboembolic event, (B) major bleeding, and (C) death during the first year after index date. Standardized risks were obtained from G-computation standardized to the distribution of risk factors in the sample based on Cox regression models adjusted for age and sex.

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  Figure 3. Alluvial diagram visualizing outcomes during first year after index in patients treated with or without oral anticoagulation.

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  Figure 4. Hazard ratios and 1-year standardized risks of (A) thromboembolic events, (B) major bleeding, and (C) death in prespecified subgroups, including P for interaction. (A–C) Standardized risks were obtained from G-computation standardized to the distribution of risk factors in the sample based on Cox regression models adjusted for age and sex. CHA2DS2-VASc score calculated as: congestive heart failure (1 point), hypertension (1 point), age ≥75 years (2 points), diabetes (1 point), previous stroke/transient ischemic attack/thromboembolism (2 points), vascular disease (1 point), age 65-74 years (1 point), and female sex (1 point).

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  Figure 5. Standardized age and sex-adjusted risk of (A) a thromboembolic event, (B) major bleeding, and (C) death in event-free 1-year survivors stratified by no anticoagulation, nonsufficient VKA, sufficient VKA, and DOAC. (A–C) Treatment was defined by the latest prescription refill in the 6 to 12 months after index date. VKA-treated patients had to have at least 1 international normalized ratio measurement >1.3 to be included. Sufficient VKA was defined as ≥70% of international normalized ratio measurements between 2.0 and 3.0. DOAC, direct oral anticoagulant; TTR, time in therapeutic range; VKA, vitamin K antagonist.