Cardiorenal syndrome encompasses a spectrum of disorders involving both the heart and kidneys in which acute or chronic dysfunction in 1 organ may induce acute or chronic dysfunction in the other organ. It represents the confluence of heart-kidney interactions across several interfaces. These include the hemodynamic cross-talk between the failing heart and the response of the kidneys and vice versa, as well as alterations in neurohormonal markers and inflammatory molecular signatures characteristic of its clinical phenotypes. The mission of this scientific statement is to describe the epidemiology and pathogenesis of cardiorenal syndrome in the context of the continuously evolving nature of its clinicopathological description over the past decade. It also describes diagnostic and therapeutic strategies applicable to cardiorenal syndrome, summarizes cardiac-kidney interactions in special populations such as patients with diabetes mellitus and kidney transplant recipients, and emphasizes the role of palliative care in patients with cardiorenal syndrome. Finally, it outlines the need for a cardiorenal education track that will guide future cardiorenal trials and integrate the clinical and research needs of this important field in the future.

SARS-CoV-2, the cause of the COVID-19 pandemic has significantly impacted cardiovascular healthcare. Patients with pre-existing cardiovascular disease are at higher risk of morbidity and mortality. The virus may affect the heart directly and indirectly with clinical syndromes of acute myocardial injury, myocarditis, acute coronary syndromes, heart failure, arrhythmias, and venous thromboembolism. Some therapeutics under investigation for COVID-19 may also have adverse cardiac effects. The involvement of the RAAS system in viral entry makes it pertinent to consider the effects of medications that modulate the system. Comprehensive knowledge of peculiar cardiovascular manifestations of COVID-19 and the role of RAAS in the prognosis of COVID-19 disease is needed for optimal patient management.

Transcatheter aortic valve replacement (TAVR) is a treatment option in high-risk patients with severe aortic stenosis who are not surgical candidates. In light of emerging evidence, it is being increasingly performed even in intermediate-risk patients in recent years. Patients who develop acute kidney injury (AKI) following TAVR are known to have worse outcomes. The objective of this concise review was to identify the prevalence and the impact of AKI following TAVR on patient outcomes by including the most recent literature in our search. After a thorough search on MEDLINE, Google Scholar, and PubMed, we included all literature relevant to AKI following TAVR. We found that AKI was caused by a variety of reasons, such as hemodynamic instability during rapid pacing, blood transfusion, periprocedural embolization, and use of contrast medium, to name a few. In patients who developed AKI following TAVR, 30-day and 1-year mortality were increased. Further, in these patients, length and cost of hospital stay were increased as well. Preventive measures such as optimal periprocedural hydration, careful contrast use, and techniques to prevent embolization during device implantation have been tried with limited success. Given that TAVR is expected to be increasingly performed, this review aimed to summarize the rapidly expanding currently available literature in an effort to reduce procedural complications and thereby improve patient outcomes.

Background: While growing evidence suggests a link between periodontal disease (PD) and cardiovascular disease (CVD), the independence of this association and the pathway remain unclear. Herein, we tested the hypotheses that: (1) inflammation of the periodontium (PD inflammation) predicts future CVD independently of disease risk factors shared between CVD and PD, and (2) the mechanism linking the two diseases involves heightened arterial inflammation. Methods: 18 F-fluorodeoxyglucose positron emission tomography/computed tomography (18 F-FDG-PET/CT) imaging was performed in 304 individuals (median age 54 years; 42.4% male) largely for cancer screening; individuals without active cancer were included. PD inflammation and arterial inflammation were quantified using validated 18 F-FDG-PET/CT methods. Additionally, we evaluated the relationship between PD inflammation and subsequent major adverse cardiovascular events (MACE) using Cox models and log-rank tests. Results: Thirteen individuals developed MACE during follow-up (median 4.1 years). PD inflammation associated with arterial inflammation, remaining significant after adjusting for PD and CVD risk factors (standardized β [95% CI]: 0.30 [0.20-0.40], P < 0.001). PD inflammation predicted subsequent MACE (standardized HR [95% CI]: 2.25 [1.47 to 3.44], P <0.001, remaining significant in multivariable models), while periodontal bone loss did not. Furthermore, mediation analysis suggested that arterial inflammation accounts for 80% of the relationship between PD inflammation and MACE (standardized log odds ratio [95% CI]: 0.438 [0.019-0.880], P = 0.022). Conclusion: PD inflammation is independently associated with MACE via a mechanism that may involve increased arterial inflammation. These findings provide important support for an independent relationship between PD inflammation and CVD.