Current Vascular Pharmacology - Volume 20, Issue 5, 2022

In addition to the association of dietary patterns, specific foods and nutrients with several diseases, including cardiovascular disease and mortality, there is also strong emerging evidence of an association of dietary patterns with the risk of sudden cardiac death (SCD). In this comprehensive review, data are presented and analyzed about foods and diets that mitigate the risk of ventricular arrhythmias (VAs) and SCD, but also about arrhythmogenic nutritional elements and patterns that seem to enhance or facilitate potentially malignant VAs and SCD. The antiarrhythmic or protective group comprises fish, nuts and other foods enriched in omega-3 polyunsaturated fatty acids, the Mediterranean and other healthy diets, vitamins E, A and D and certain minerals (magnesium, potassium, selenium). The arrhythmogenic-food group includes saturated fat, trans fats, ketogenic and liquid protein diets, the Southern and other unhealthy diets, energy drinks and excessive caffeine intake, as well as heavy alcohol drinking. Relevant antiarrhythmic mechanisms include modification of cell membrane structure by n-3 polyunsaturated fatty acids, their direct effect on calcium channels and cardiomyocytes and their important role in eicosanoid metabolism, enhancing myocyte electric stability, reducing vulnerability to VAs, lowering heart rate, and improving heart rate variability, each of which is a risk factor for SCD. Contrarily, saturated fat causes calcium handling abnormalities and calcium overload in cardiomyocytes, while a high-fat diet causes mitochondrial dysfunction that dysregulates a variety of ion channels promoting VAs and SCD. Free fatty acids have been considered proarrhythmic and implicated in facilitating SCD; thus, diets increasing free fatty acids, e.g., ketogenic diets, should be discouraged and replaced with diets enriched with polyunsaturated fatty acids, which can also reduce free fatty acids. All available relevant data on this important topic are herein reviewed, large studies and meta-analyses and pertinent advisories are tabulated, while protective (antiarrhythmic) and arrhythmogenic specific diet constituents are pictorially illustrated.

Ischemic preconditioning (IP) is an innate phenomenon, triggered by brief, non-lethal cycles of ischemia/reperfusion applied to a tissue or organ that confers tolerance to a subsequent more prolonged ischemic event. Once started, it can reduce the severity of myocardial ischemia associated with some clinical situations, such as percutaneous coronary intervention (PCI) and intermittent aortic clamping during coronary artery bypass graft surgery (CABG). Although the mechanisms underlying IP have not been completely elucidated, several studies have shown that this phenomenon involves the participation of cell triggers, intracellular signaling pathways, and end-effectors. Understanding this mechanism enables the development of preconditioning mimetic agents. It is known that a range of medications that activate the signaling cascades at different cellular levels can interfere with both the stimulation and the blockade of IP. Investigations of signaling pathways underlying ischemic conditioning have identified a number of therapeutic targets for pharmacological manipulation. This review aims to present and discuss the effects of several medications on myocardial IP.

Background: The important risk factors for atrial fibrillation (AF) in the general population are not always equally important in specific and relatively prevalent diseases. Objective: The main goal of this narrative review is to focus attention on the presence and the relationship of AF with several important diseases, such as cancer or sepsis, in order to: 1) stimulate further research in the field, and 2) draw attention to this relationship and search for AF in clinical practice. Methods: We searched PubMed, SCOPUS, Elsevier, Wiley, Springer, Oxford Journals, Cambridge, SAGE, and Google Scholar for less-known comorbidities of AF. The search was limited to publications in English. No time limits were applied. Results: AF is widely represented in cardiovascular and other important diseases, even in those in which AF is rarely mentioned. In some specific clinical subsets of AF patients (e.g., patients with sepsis or cancer), the general risk factors for AF may not be so important. Patients with new-onset AF have a several-fold increase in relative risk of cancer, deep vein thrombosis, and pulmonary thromboembolism (PTE) during the follow-up. Conclusion: AF presence, prognosis, and optimal therapeutic approach are insufficiently recognised in several prevalent diseases, including life-threatening ones. There is a need for a better search for AF in PTE, pulmonary oedema, aortic dissection, sepsis, cancer and several gastrointestinal diseases. Improved AF detection would influence treatment and improve outcomes.

Background and Aim: Proton pump inhibitors (PPIs) are among the most widely prescribed agents. Although PPIs are widely regarded as harmlesss, long-term use of PPIs (LTUPPI) can have the potential to increase the risk of developing cardiovascular (CV) disease (CVD). Pulse wave velocity (PWV) is a good indicator of arterial stiffness. Several studies show a relationship between LTUPPI and CVD. However, the association between LTUPPI and PWV or arterial stiffness has not been reported. Patients and Methods: Patients (n=64) with LTUPPI and controls (n=91) were included. PWV, glucose, creatinine, total cholesterol, triglyceride, low-density lipoprotein cholesterol, cholesterol, highdensity lipoprotein cholesterol, and magnesium levels were measured. Results: In the LTUPPI group, PWV was greater than in controls (9.08±2.04 vs. 7.77±1.52 m/s, respectively, p=0.01); 34.4% of patients and 8.8% of controls had PWV levels >10 m/s (p=0.000). Multiple logistic regression analysis showed age (p<0.001) and LTUPPI (p=0.024) as predictors of elevated PWV. Conclusion: PWV values are increased in patients with LTUPPI compared to controls independently of conventional CV risk factors. Measurement of PWV and other arterial stiffness parameters in cases with LTUPPI may be useful to predict possible CVD. Studies involving greater numbers are needed to confirm these findings.

Background: Atrial arrhythmias are associated with an increased risk of stroke and death in the elderly. The risk and predictive factors of recurrent atrial arrhythmias in elderly patients after coronary stenting are not well known. Objective: This research sought to investigate the roles of pro- and anti-inflammatory cytokine imbalances in different types of recurrent atrial arrhythmias in elderly patients defined as individuals aged 65 years or older after sirolimus eluting stent (Cordis, Warren, New Jersey) implantation. Methods: We measured interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-17 (IL-17), interleukin-13 (IL-13) and interleukin- 37 (IL-37) in elderly patients with recurrent atrial arrhythmias and assessed the impact of pro- and antiinflammatory cytokine imbalances on recurrent atrial arrhythmias in elderly patients after coronary stenting. Results: Levels of IL-1 β, IL-6, IL-8, and TNF-α were remarkably increased (p<0.001), and IL-10, IL- 17, IL-13, and IL-37 were remarkably lowered (p<0.001) in elderly patients with recurrent atrial arrhythmias after coronary stent implantation. Imbalance of pro- and anti-inflammatory cytokines induced recurrent atrial arrhythmias after coronary stenting. Pro- and anti-inflammatory cytokine imbalances may be used to identify elderly patients who have an increased risk of developing recurrent atrial arrhythmias after coronary stenting. Conclusion: The imbalance of pro- and anti-inflammatory cytokines was associated with recurrent atrial arrhythmias in elderly patients after coronary stenting. Pro- and anti-inflammatory cytokines may be clinically useful biomarkers for predicting recurrent atrial arrhythmias in elderly patients after coronary stent implantation.