Average life expectancy is increasing in the western world resulting in a growing number of frail individuals with coronary heart disease, often associated with comorbidities. Decisions to proceed to invasive interventions in elderly frail patients is challenging because they may gain benefit, but are also at risk of procedure-related complications. Current risk scores designed to predict mortality in cardiac procedures are mainly based on clinical and angiographic factors, with limitations in the elderly because they are mainly derived from a middle-aged population, do not account for frailty and do not predict the impact of the procedure on quality of life which often matters more to elderly patients than mortality. Frailty assessment has emerged as a measure of biological age that correlates well with quality of life, hospital admissions and mortality. Potentially, the incorporation of frailty into current risk assessment models will cause a shift towards more appropriate care. The need for a more accurate method of risk stratification incorporating frailty, particularly for elderly patients is pressing. This article reviews the association between frailty and cardiovascular disease, the impact of frailty on outcomes of cardiac interventions and suggests ways in which frailty assessment could be incorporated into cardiology clinical practice.

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The increasing use of antiplatelet therapy, particularly aspirin and oral P2Y inhibitors, in the prevention and management of arterial thrombosis, has stimulated extensive pharmacodynamic studies and research into tailored antiplatelet regimens. Many different methodologies have been studied for monitoring antiplatelet drugs and some are now well validated and used in clinical practice. However, clinical studies of tailored antiplatelet therapy have not convincingly demonstrated a benefit of this approach in patients treated with aspirin and clopidogrel, coupled with the fact that more potent antiplatelet therapies have more consistent effects compared with clopidogrel and so may reduce the rationale for monitoring. On the other hand, the optimum timing of urgent surgery after cession of oral antiplatelet therapy may be informed by platelet function testing. This review discusses the different methodologies that have been used to monitor the effects of antiplatelet therapy and highlights the current position of platelet function testing in clinical practice.

Higher aspirin doses may be inferior in ticagrelor-treated acute coronary syndrome (ACS) patients and reducing bleeding risk whilst maintaining antithrombotic benefits could improve outcomes. We characterized the pharmacodynamics of a novel dual-antiplatelet-therapy regimen consisting of verylow-dose twice-daily (BD) aspirin with standard-dose ticagrelor. A total of 20 ticagrelor-treated ACS patients entered a randomized crossover to take aspirin 20 mg BD (12-hourly) during one 14-day period and 75 mg once-daily (OD) in the other. After 14 days of treatment, serum thromboxane (TX)B 2 and light-transmittance aggregometry were assessed pre-and 2 h post-morning-dose, bleeding time was measured post-dose, and TXA 2 and prostacyclin stable metabolites were measured in urine collected 2 h post-morning-dose. Data are expressed as mean ± SD. After 14 days treatment, serum TXB 2 levels were significantly greater 2 h post-dosing with aspirin 20 mg BD vs. 75 mg OD (3.0 ± 3.6 ng/mL vs. 0.8 ± 1.9 ng/mL; p = 0.018) whereas pre-dosing levels were not significantly different (3.5 ± 4.1 ng/mL vs. 2.5 ± 3.1 ng/mL, p = 0.23). 1-mmol/L arachidonic acid-induced platelet aggregation was similarly inhibited by both regimens pre-dose (8.5 ± 14.3% vs. 5.1 ± 3.6%, p = 0.24) and post-dose (8.7 ± 14.2% vs. 6.6 ± 5.3%; p = 0.41). Post-dose bleeding time was shorter with 20 mg BD (680 ± 306 s vs. 834 ± 386 s, p = 0.02). Urinary prostacyclin and TX metabolite excretion were not significantly different. In conclusion, compared to aspirin 75 mg OD, aspirin 20 mg BD provided consistent inhibition of platelet TXA 2 release and aggregation, and improved post-dose hemostasis, in ticagrelor-treated ACS patients. Further studies are warranted to assess whether this regimen improves the balance of clinical efficacy and safety.