The aim of this article is to review the literature regarding the relationship between vitamin D deficiency and cardiovascular disease (CVD) and its modification in the presence of obesity. Despite the strong association between vitamin D status and cardiovascular outcomes, vitamin D supplementation trials in the general population have failed to decrease the incidence of cardiovascular events and mortality. A comprehensive study of the published literature and a comparison with experimental data lead to the conclusion that obesity, due to its high prevalence and strong association with both vitamin D deficiency and CVD, may act as a critical confounder, which is responsible for the different results on this association. Adoption of a vitamin D preventive supplementation strategy for CVD is unlikely to yield any benefit to the general population. However, it might be particularly useful in obese adults with increased risk for CVD.

Molecules that govern bone metabolism, such as osteoprotegerin (OPG) and osteopontin (OPN), have been isolated from other tissues, including blood vessels. Atherosclerosis and coronary artery disease (CAD) are leading causes of mortality worldwide. Despite novel biochemical and imaging techniques, early detection of CAD is still unsatisfactory. Experimental data indicate that bone turnover markers (BTMs) contribute to the development of atherosclerosis. This finding has sparked interest in their clinical use. This narrative review analyzed information from >50 human studies, which strongly suggest that OPG, OPN, and alkaline phosphatase (ALP) serum concentrations are altered in patients with CAD. Osteoprotegerin seems to be more useful for the detection of early disease, while OPN and ALP are recruited in vessels after the establishment of disease. Osteocalcin may be used as a flow cytometry marker for endothelial progenitor cells and can constitute a marker to monitor response to interventional treatments and risk of restenosis. However, most data derive from observational studies. Incorporation of BTMs in multifactorial computational algorithms could further determine their role in CAD diagnosis and prognosis together with other imaging techniques and biochemical markers.

Background: There is considerable debate about the hemodynamic effects of veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO).Aims: To evaluate the changes in left ventricular (LV) function, volumes, and work in patients treated with VA‐ECMO using invasive LV catheterization and three‐dimensional echocardiographic volumes.Methods: Patients on VA‐ECMO underwent invasive hemodynamic evaluation due to concerns regarding candidacy for decannulation. Hemodynamic parameters were reported as means±standard deviations or medians (interquartile ranges) after evaluating for normality. Paired comparisons were done to evaluate hemodynamics at the baseline (highest) and lowest tolerated levels of VA‐ECMO support.Results: Twenty patients aged 52.3 ± 15.8 years were included. All patients received VA‐ECMO for refractory cardiogenic shock (5/20 SCAI stage D, 15/20 SCAI stage E). At 3.0 (2.0, 4.0) days after VA‐ECMO cannulation, the baseline LV ejection fraction was 20% (15%, 27%). The baseline and lowest VA‐ECMO flows were 4.0 ± 0.6 and 1.5 ± 0.6 L/min, respectively. Compared to the lowest flow, full VA‐ECMO support reduced LV end‐diastolic volume [109 ± 81 versus 134 ± 93 mL, p = 0.001], LV end‐diastolic pressure (14 ± 9 vs. 19 ± 9 mmHg, p < 0.001), LV stroke work (1858 ± 1413 vs. 2550 ± 1486 mL*mmHg, p = 0.002), and LV pressure‐volume area (PVA) (4507 ± 1910 vs. 5193 ± 2388, p = 0.03) respectively. Mean arterial pressure was stable at the highest and lowest flows (80 ± 16 vs. 75 ± 14, respectively; p = 0.08) but arterial elastance was higher at the highest VA‐ECMO flow (4.9 ± 2.2 vs lowest flow 2.7 ± 1.6; p < 0.001).Conclusions: High flow VA‐ECMO support significantly reduced LV end‐diastolic pressure, end‐diastolic volume, stroke work, and PVA compared to minimal support. The Ea was higher and MAP was stable or minimally elevated on high flow.

We evaluated the feasibility of optimising coronary perfusion pressure (CPP) during cardiopulmonary resuscitation (CPR) with a closed-loop, machine-controlled CPR system (MC-CPR) that sends real-time haemodynamic feedback to a set of machine learning and control algorithms which determine compression/decompression characteristics over time. American Heart Association CPR guidelines (AHA-CPR) and standard mechanical devices employ a “one-size-fits-all” approach to CPR that fails to adjust compressions over time or individualise therapy, thus leading to deterioration of CPR effectiveness as duration exceeds 15–20 ​min. CPR was administered for 30 ​min in a validated porcine model of cardiac arrest. Intubated anaesthetised pigs were randomly assigned to receive MC-CPR (6), mechanical CPR conducted according to AHA-CPR (6), or human-controlled CPR (HC-CPR) (10). MC-CPR directly controlled the CPR piston’s amplitude of compression and decompression to maximise CPP over time. In HC-CPR a physician controlled the piston amplitudes to maximise CPP without any algorithmic feedback, while AHA-CPR had one compression depth without adaptation. MC-CPR significantly improved CPP throughout the 30-min resuscitation period compared to both AHA-CPR and HC-CPR. CPP and carotid blood flow (CBF) remained stable or improved with MC-CPR but deteriorated with AHA-CPR. HC-CPR showed initial but transient improvement that dissipated over time. Machine learning implemented in a closed-loop system successfully controlled CPR for 30 ​min in our preclinical model. MC-CPR significantly improved CPP and CBF compared to AHA-CPR and ameliorated the temporal haemodynamic deterioration that occurs with standard approaches.

Background: The incidence and mortality of out‐of‐hospital cardiac arrest (OHCA) remains high, but predicting outcomes is challenging. Being able to better assess prognosis of hospitalized patients after return of spontaneous circulation would enable improved management of survival expectations. In this study, we assessed the predictive value of ECG indexes in hospitalized patients with OHCA. Methods and Results: PR interval and QT interval corrected by the Bazett formula (QTc) for all leads were calculated from standard 12‐lead ECGs 24 hours after return of spontaneous circulation in 93 patients who were hospitalized following OHCA. PR interval and QT and QTc duration did not differentiate OHCA survivors and nonsurvivors. However, QT and QTc dispersion was significantly increased in patients who died during hospitalization compared with survivors discharged from the hospital ( P <0.01). Logistic regression indicated a strong association between increased QT dispersion and in‐hospital mortality ( P <0.0001; area under the curve, 0.8918 for QT dispersion and 0.8673 for QTc dispersion). Multinomial logistic regression indicated that the increase of QTc dispersion correlated with worse Cerebral Performance Category scores at discharge ( P <0.001; likelihood ratio, 51.42). There was also significant correlation between dispersion measures and serum potassium at the time of measurement and between dispersion measures and cumulative epinephrine administration. No difference existed regarding the number of measurable leads. Conclusions: Lesser QT and QTc dispersion at 24 hours after return of spontaneous circulation was significantly associated with survival and neurologic status at discharge. Routine evaluation of QT and QTc dispersion during hospitalization following return of spontaneous circulation might improve outcome prognostication for patients hospitalized for OHCA.