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Patients with chronic kidney disease (CKD) have an increased risk of thrombosis and approximately 50% of patients with advanced CKD die because of a cardiovascular disease. In addition to an increased risk of thrombosis, patients with CKD and particularly with advanced CKD, have an increased risk of hemorrhage, which increases parallel to the decline of kidney function. Due to this parallel existence of the prohemorrhagic and prothrombotic phenotype, antiplatelet treatment is difficult in the daily routine and data show that CKD patients with acute coronary syndrome (ACS) are less likely to receive guideline-conform treatment. The underlying mechanisms are currently insufficiently understood and both platelet-dependent mechanisms and also platelet-independent mechanisms are under discussion. Accordingly, there is currently no specific treatment or treatment strategy for patients with CKD. In addition, CKD patients are underrepresented in registration studies on antiplatelet treatment and there are no data from randomized trials for patients with advanced CKD (CKD >= 4). Current guideline recommendations are therefore based on subgroup analyses and observational studies. In addition, questions on the duration of treatment, on risk scores for estimation of the risk of hemorrhage and on potential benefits of escalation and de-escalation strategies remain largely unanswered and should therefore be the focus of future studies.

Objectives: To evaluate the effect of age in an all-comers population undergoing percutaneous coronary intervention (PCI). Background: Age is an important consideration in determining appropriateness for invasive cardiac assessment and perceived clinical outcomes. Methods: We analysed data from 29,012 consecutive patients undergoing PCI in the Melbourne Interventional Group (MIG) registry between 2005 and 2017. 25,730 patients <80 year old (78% male, mean age 62±10 years; non-elderly cohort) were compared to 3,282 patients ≥80 year old (61% male, mean age 84±3 years; elderly cohort). Results: The elderly cohort had greater prevalence of hypertension, diabetes and previous myocardial infarction (all p<0.001). Elderly patients were more likely to present with acute coronary syndromes, left ventricular ejection fraction <45% and chronic kidney disease (p<0.0001). In-hospital, 30-day and long-term all-cause mortality (over a median of 3.6 and 5.1 years for elderly and non-elderly cohorts, respectively) were higher in the elderly cohort (5.2% vs. 1.9%; 6.4% vs. 2.2%; and 43% vs. 14% respectively, all p<0.0001). In multivariate Cox regression analysis, estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2 (HR 3.8, 95% CI: 3.4–4.3), cardiogenic shock (HR 3.0, 95% CI: 2.6–3.4), ejection fraction <30% (HR 2.5, 95% CI: 2.1–2.9); and age ≥80 years (HR 2.8, 95% CI: 2.6–3.1) were independent predictors of long-term all-cause mortality (all p<0.0001). Conclusion: The elderly cohort is a high-risk group of patients with increasing age being associated with poorer long-term mortality. Age, thus, should be an important consideration when individualising treatment in elderly patients.

Transcutaneous aortic valve implantation (TAVI) has led to a paradigm shift in the treatment of severe aortic stenosis (AS) in the elderly and is expanding to still younger and lower-risk patients with severe AS as an alternative to surgical aortic valve replacement (SAVR). While the role of coronary artery bypass grafting with SAVR is well-documented, the analog of percutaneous coronary intervention with TAVI is less so. The aim of this review is to provide an overview of the important challenges in treating severe AS and co-existing coronary artery disease in patients planned for TAVI.

Transcutaneous aortic valve implantation (TAVI) has led to a paradigm shift in the treatment of severe aortic stenosis (AS) in the elderly and is expanding to still younger and lower-risk patients with severe AS as an alternative to surgical aortic valve replacement (SAVR). While the role of coronary artery bypass grafting with SAVR is well-documented, the analog of percutaneous coronary intervention with TAVI is less so. The aim of this review is to provide an overview of the important challenges in treating severe AS and co-existing coronary artery disease in patients planned for TAVI.

Data on anti-platelet therapy (APT) for prevention of atherothrombotic events in thrombocytopaenic cancer patients is lacking. We aimed to identify patient and physician characteristics associated with APT management in thrombocytopaenic patients with haematological malignancy. A clinical vignette-based experiment was designed. Eleven haematologists were interviewed, identifying five variable categories. Next, 18 hypothetical vignettes were generated. Each physician received three vignettes and chose to: hold all APT; continue APT without platelet transfusion support; or continue APT with platelet transfusion support. The survey was distributed to haematologists and thrombosis specialists in three countries. Multivariate cluster robust Poisson regression models were used to calculate relative risks (RRs) of using one management option (over the other) for each variable in comparison to a reference variable. A total of 145 physicians answered 434 cases. Clinicians were more likely to hold APT in case of 20,000/mu L platelets (vs. 40,000/mu L; RR for continuing: 0.82 [95% confidence interval: 0.75-0.91]), recent major gastrointestinal bleeding (vs. none; RR 0.81 [0.72-0.92]) and when the physician worked at a university-affiliated community hospital (vs. non-academic community hospital; RR 0.84 [0.72-0.98]). Clinicians were more likely to continue APT in ST elevation myocardial infarction with dual APT (vs. unstable angina with single APT; RR 1.31 [1.18-1.45]) and when there were institutional protocols guiding management (vs. none; RR 1.15 [1.03-1.27]). When APT was continued, increased platelet transfusion targets were used in 34%. In summary, the decision process is complex and affected by multiple patient and physician characteristics. Platelet transfusions were frequently chosen to support APT, although no evidence supports this practice.

Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.

Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.

Data on anti-platelet therapy (APT) for prevention of atherothrombotic events in thrombocytopaenic cancer patients is lacking. We aimed to identify patient and physician characteristics associated with APT management in thrombocytopaenic patients with haematological malignancy. A clinical vignette-based experiment was designed. Eleven haematologists were interviewed, identifying five variable categories. Next, 18 hypothetical vignettes were generated. Each physician received three vignettes and chose to: hold all APT; continue APT without platelet transfusion support; or continue APT with platelet transfusion support. The survey was distributed to haematologists and thrombosis specialists in three countries. Multivariate cluster robust Poisson regression models were used to calculate relative risks (RRs) of using one management option (over the other) for each variable in comparison to a reference variable. A total of 145 physicians answered 434 cases. Clinicians were more likely to hold APT in case of 20,000/mu L platelets (vs. 40,000/mu L; RR for continuing: 0.82 [95% confidence interval: 0.75-0.91]), recent major gastrointestinal bleeding (vs. none; RR 0.81 [0.72-0.92]) and when the physician worked at a university-affiliated community hospital (vs. non-academic community hospital; RR 0.84 [0.72-0.98]). Clinicians were more likely to continue APT in ST elevation myocardial infarction with dual APT (vs. unstable angina with single APT; RR 1.31 [1.18-1.45]) and when there were institutional protocols guiding management (vs. none; RR 1.15 [1.03-1.27]). When APT was continued, increased platelet transfusion targets were used in 34%. In summary, the decision process is complex and affected by multiple patient and physician characteristics. Platelet transfusions were frequently chosen to support APT, although no evidence supports this practice.

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