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Highlights • Mechanistic studies illustrate the effects of PD on systemic inflammation, platelet and endothelial function, and lipoproteins. • Trials of PD treatment have not shown reductions in cardiovascular outcomes therefore a definite causal association is lacking. • The morbidity and impact on quality of life, mutual risk factors and systemic inflammation warrant preventive efforts. • Improved screening, better collaboration, and targeted health policies could greatly improve prevention of PD and its sequelae., Periodontal disease (PD) is common in the US and globally. Evidence suggests that poor oral health is associated with atherosclerotic cardiovascular disease (ASCVD); however, this relationship has not been a major focus in clinical cardiology. This manuscript will review the growing evidence linking PD to ASCVD, including pathophysiologic mechanisms and coexistent risk factors. Public health considerations with a focus on disparities, social determinants, preventive strategies, and a call to action to reduce the burden of coincident ASCVD and PD are also reviewed., Graphical abstract Image, graphical abstract

Graphical abstract, Highlights • Cardiac involvement is common in EPGA. • Multimodality images and endomyocardial biopsy are essential in diagnosing EPGA. • Early treatment of EPGA is essential to prevent progression of the disease.

Introduction: Black men and women are at higher risk for atherosclerotic cardiovascular disease (ASCVD) and when diagnosed, have greater morbidity and mortality as compared to individuals from European ancestry (EA). In patients with familial hypercholesterolemia (FH), it remains unknown whether Black patients have similarly increased risk for ASCVD. Hypothesis: To characterize the prevalence of ASCVD and to determine the strongest predictors of ASCVD in Black FH patients compared to EAs. Methods: The prevalence of ASCVD in 173 Black adult patients with FH followed in US-based lipid clinics was assessed retrospectively through a multicenter. A multivariate logistic regression model was used to determine the strongest predictors of ASCVD. Covariates included age, sex, diabetes mellitus, hypertension, and current smoking. ASCVD was defined as coronary, peripheral, and cerebrovascular events including angina, myocardial infarction, coronary angioplasty, peripheral arterial surgery, claudication, peripheral angioplasty, transient ischemic attack, stroke, and carotid endarterectomy. Results: Baseline characteristics of the 173 Black adult patients compared to EAs are shown in table 1. Black patients with FH were more likely to have higher BMI, hypertension, diabetes and to be current smokers. The prevalence of ASCVD in Black patients with FH was 38% compared to 30% in EAs, an absolute difference of 8% (p=0.047). The strongest predictors of ASCVD in Black patients with FH were hypertension and current smoking (table 2). Conclusions: Black patients with FH have a significantly higher prevalence of ASCVD when compared to EAs with FH. The strongest predictors of ASCVD in Black patients with FH were hypertension and current smoking. Aggressive primary prevention strategies specifically focused on the management of hypertension and smoking cessation should be tested for impact on the cardiovascular risk profile of Black patients with FH.

It is critical that diet quality be assessed and discussed at the point of care with clinicians and other members of the healthcare team to reduce the incidence and improve the management of diet-related chronic disease, especially cardiovascular disease. Dietary screening or counseling is not usually a component of routine medical visits. Moreover, numerous barriers exist to the implementation of screening and counseling, including lack of training and knowledge, lack of time, sense of futility, lack of reimbursement, competing demands during the visit, and absence of validated rapid diet screener tools with coupled clinical decision support to identify actionable modifications for improvement. With more widespread use of electronic health records, there is an enormous unmet opportunity to provide evidence-based clinician-delivered dietary guidance using rapid diet screener tools that must be addressed. In this scientific statement from the American Heart Association, we provide rationale for the widespread adoption of rapid diet screener tools in primary care and relevant specialty care prevention settings, discuss the theory- and practice-based criteria of a rapid diet screener tool that supports valid and feasible diet assessment and counseling in clinical settings, review existing tools, and discuss opportunities and challenges for integrating a rapid diet screener tool into clinician workflows through the electronic health record.

The potential cardiovascular (CV) benefits of many trending foods and dietary patterns are still incompletely understood, and scientific inquiry continues to evolve. In the meantime, howeve...

Background Nutrition is one of the foundations of cardiovascular guidelines for risk reduction and treatment. However, little is known about whether cardiologists, cardiology fellows-in-training, and cardiovascular team members have the nutrition education and knowledge necessary to implement these guidelines. The aim of this study was to describe the educational experiences, attitudes, and practices relating to nutrition among cardiovascular professionals. Methods Surveys completed by cardiologists, fellows-in-training, and cardiovascular team members inquired about their personal dietary habits, history of nutrition education, and attitudes regarding nutrition interventions. Results A total of 930 surveys were completed. Among cardiologists, 90% reported receiving no or minimal nutrition education during fellowship training, 59% reported no nutrition education during internal medicine training, and 31% reported receiving no nutrition education in medical school. Among cardiologists, 8% described themselves as having "expert" nutrition knowledge. Nevertheless, fully 95% of cardiologists believe that their role includes personally providing patients with at least basic nutrition information. The percentage of respondents who ate ≥5 servings of vegetables and fruits per day was: 20% (cardiologists), 21% (fellows-in-training), and 26% (cardiovascular team members). Conclusions A large proportion of cardiovascular specialists have received minimal medical education and training in nutrition, and current trainees continue to experience significant education and training gaps.

Growing scientific evidence of the benefits of heart-healthy dietary patterns and of the massive public health and economic burdens attributed to obesity and poor diet quality have triggered national calls to increase diet counseling in outpatients with atherosclerotic cardiovascular disease or risk factors. However, despite evidence that physicians are willing to undertake this task and are viewed as credible sources of diet information, they engage patients in diet counseling at less than desirable rates and cite insufficient knowledge and training as barriers. These data align with evidence of large and persistent gaps in medical nutrition education and training in the United States. Now, major reforms in undergraduate and graduate medical education designed to incorporate advances in the science of learning and to better prepare physicians for 21st century healthcare delivery are providing a new impetus and novel ways to expand medical nutrition education and training. This science advisory reviews gaps in undergraduate and graduate medical education in nutrition in the United States, summarizes reforms that support and facilitate more robust nutrition education and training, and outlines new opportunities for accomplishing this goal via multidimensional curricula, pedagogies, technologies, and competency-based assessments. Real-world examples of efforts to improve undergraduate and graduate medical education in nutrition by integrating formal learning with practical, experiential, inquiry-driven, interprofessional, and population health management activities are provided. The authors conclude that enhancing physician education and training in nutrition, as well as increasing collaborative nutrition care delivery by 21st century health systems, will reduce the health and economic burdens from atherosclerotic cardiovascular disease to a degree not previously realized.

Historically, low-carbohydrate (CHO) and very-low-CHO diets have been used for weight loss. Recently, these diets have been promoted for type 2 diabetes (T2D) management. This scientific statement provides a comprehensive review of the current evidence base available from recent systematic reviews and meta-analyses on the effects of low-CHO and very-low-CHO diets on body weight, lipoprotein lipids, glycemic control, and other cardiometabolic risk factors. In addition, evidence on emerging risk factors and potential safety concerns of low-CHO and very-low-CHO diets, especially for high-risk individuals, such as those with genetic lipid disorders, was reviewed. Based on the evidence reviewed, low-CHO and very-low-CHO diets are not superior to other dietary approaches for weight loss. These diets may have advantages related to appetite control, triglyceride reduction, and reduction in the use of medication in T2D management. The evidence reviewed showed mixed effects on low-density lipoprotein cholesterol levels with some studies showing an increase. There was no clear evidence for advantages regarding effects on other cardiometabolic risk markers. Minimal data are available regarding long-term (>2 years) efficacy and safety. Clinicians are encouraged to consider the evidence discussed in this scientific statement when counseling patients on the use of low-CHO and very-low-CHO diets.

The effects of glucagon, epinephrine, and vasopressin on phospholipid synthesis and glycogen phosphorylase a activity were investigated in rat hepatocytes. There was a stimulation of [32P]Pi ncorporation into phosphatidylinositol by vasopressin and epinephrine but not by glucagon. A mild degree of calcium depletion abolished the activation of glycogen phosphorylase by vasopressin but the increase in [32P]Pi ncorporation into phosphatidylinositol was still present. However, the activation of glycogen phosphorylase by epinephrine was not abolished by any degree of calcium depletion. The increase in [32P]Pi ncorporation into phosphatidylinositol due to epinephrine was mediated through an amechanism which was very sensitive to inhibition by prazosin, inhibited by phentolamine and yohimbine at fairly high concentrations, and unaffected by propranolol. The uptake of [2-3H]inositol into phosphatidylinositol was accelerated by hormones and correlated poorly with 32P uptake into this phospholipid. Depletion of calcium from or the addition of manganese to the incubation medium markedly enhanced the uptake of labeled inositol into phosphatidylinositol. However, these increases in [2-3H]inositol incorporation did not parallel any changes in basal or hormone stimulated 32P incorporation into phosphatidylinositol. The use of labeled inositol to measure phosphatidylinositol synthesis is unreliable since it appears to reflect the activity of the freely reversible Mn2+-dependent enzyme which catalyzes the reaction of CDP-diacylglycerol with inositol to give cytidine monophosphate and phosphatidylinositol. These data support the hypothesis that vasopressin and catecholamine activation of phosphatidylinositol turnover in hepatocytes is linked in an unknown fashion to the release of bound intracellular calcium and the entry of extracellular calcium.