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Nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD) are both manifestations of end-organ damage of the metabolic syndrome. Through multiple pathophysiological mechanisms, CVD and NAFLD are associated with each other. Systemic inflammation, endothelial dysfunction, hepatic insulin resistance, oxidative stress, and altered lipid metabolism are some of the mechanisms by which NAFLD increases the risk of CVD. Patients with NAFLD develop increased atherosclerosis, cardiomyopathy, and arrhythmia, which clinically result in cardiovascular morbidity and mortality. Defining the mechanisms linking these 2 diseases offers the opportunity to further develop targeted therapies. The aim of this comprehensive review is to examine the association between CVD and NAFLD and discuss the overlapping management approaches.

Cardiac rehabilitation is a key component of secondary prevention for patients who have undergone coronary artery bypass graft surgery. Cardiac rehabilitation is a comprehensive, multidisciplinary, long-term provision of medical evaluation, prescriptive exercise, cardiac risk factor modification, and education. Not only does cardiac rehabilitation reduce cardiovascular mortality and hospital readmissions, but it also improves the functional status and quality of life for patients. Despite the strong evidence and recommendation for referral to and utilization of cardiac rehabilitation early in the postoperative period, it remains underutilized, especially in the elderly and women.

Atherosclerotic cardiovascular disease (ASCVD) and its associated economic burden are increasing globally. Although cardiac rehabilitation is a vital component of secondary prevention with proven benefits, it is underutilized due to numerous barriers, especially in resource-limited settings. New care models for delivery of comprehensive prevention programs such as community-based, home-based, and "hybrid" models implementing m-health, e-health, and telemedicine need to be adopted. Such new care models should be offered to all patients with established ASCVD (coronary, cerebral, and peripheral) and additionally to those at high risk of developing ASCVD with multiple risk factors for panvascular prevention.

Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality in women. Historically, medical research has focused on male patients, and subsequently, there has been decreased awareness of the burden of ASCVD in females until recent years. The biological differences between sexes and differences in societal expectations defined by gender roles contribute to gender differences in ASCVD risk factors. With these differing risk profiles, risk assessment, risk stratification, and primary preventive measures of ASCVD are different in women and men. In this review article, clinicians will understand the risk factors unique to women, such as preeclampsia, gestational diabetes, and those that disproportionately affect them such as autoimmune disorders. With these conditions in mind, the approach to ASCVD risk assessment and stratification in women will be discussed. Furthermore, the literature behind the effects of primary preventive measures in women, including lifestyle modifications, aspirin, statins, and anticoagulation, will be reviewed. The aim of this review article was to ultimately improve ASCVD primary prevention by reducing gender disparities through education of physicians.

Coronary microvascular disease in the absence of myocardial diseases has traditionally been diagnosed through coronary reactivity testing in the cardiac catheterization laboratory. Compared with invasive procedures, blood-based biomarkers may have reduced cost, less risk of physical harm and greater accessibility, making them ideal for an outpatient management strategy. There are a variety of biomarkers available with potential utility in the management of microvascular disease; however, none have yet been extensively validated or established in this clinical patient population.

Nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD) are both manifestations of end-organ damage of the metabolic syndrome. Through multiple pathophysiological mechanisms, CVD and NAFLD are associated with each other. Systemic inflammation, endothelial dysfunction, hepatic insulin resistance, oxidative stress, and altered lipid metabolism are some of the mechanisms by which NAFLD increases the risk of CVD. Patients with NAFLD develop increased atherosclerosis, cardiomyopathy, and arrhythmia, which clinically result in cardiovascular morbidity and mortality. Defining the mechanisms linking these 2 diseases offers the opportunity to further develop targeted therapies. The aim of this comprehensive review is to examine the association between CVD and NAFLD and discuss the overlapping management approaches.

It is unknown whether the association of high-sensitivity troponin I (hs-TnI) with adverse cardiovascular outcomes varies by the presence of chronic kidney disease (CKD). We examined the association of hs-TnI with adverse cardiovascular outcomes in those with and without CKD in 4,107 (mean age, 64 years; 63% men; 20% black) patients from the Emory Cardiovascular Biobank who underwent coronary angiography. CKD (n = 1,073) was defined as estimated glomerular filtration rate 30 mg/g at baseline. Cox regression was used to compute hazard ratios (HR) for the association between hs-TnI levels (per doubling of hs-TnI: log2[hs-TnI] + 1) and death, cardiovascular death, and major adverse cardiac events (MACE), separately. Hs-TnI was a stronger predictor of death (CKD: HR 1.23, 95% confidence interval [CI] 1.15 to 1.31; no CKD: HR 1.11, 95% CI 1.05 to 1.17, p-interaction = 0.023), cardiovascular death (CKD: HR 1.24, 95% CI 1.14 to 1.34; no CKD: HR 1.15, 95% CI 1.07 to 1.22, p-interaction = 0.12), and MACE (CKD: HR 1.18, 95% CI 1.11 to 1.25; no CKD: HR 1.11, 95% CI 1.06 to 1.16, p-interaction = 0.095) in CKD compared with non-CKD. The association between hs-TnI and death in patients with CKD was stronger for patients without obstructive coronary artery disease (no obstructive coronary artery disease: HR 1.60, 95% CI 1.27 to 2.01; obstructive coronary artery disease: HR 1.19, 95% CI 1.11 to 1.27, p-interaction = 0.041). In conclusion, hs-TnI is a stronger predictor of adverse cardiovascular events in patients who have CKD than those without, even in the absence of obstructive coronary artery disease. Hs-TnI may identify CKD patients who are high risk for adverse cardiovascular outcomes in whom aggressive risk factor modification strategies are warranted.

Ischemic heart disease (IHD) continues to be a major health threat to women worldwide. Sex-specific differences in IHD presentation, pathophysiology, treatment, and outcomes have increasingly been identified. While IHD care has focused around detection and treatment of obstructive coronary artery disease (CAD), it is clear that symptomatic patients with evidence of ischemia do not always have obstructive CAD. This problem appears to disproportionately impact women; compared to men, women who present with acute coronary syndrome/unstable angina as well as stable angina are more likely to have non-obstructive CAD on coronary angiography, and yet have a high IHD morbidity and mortality. Data indicates that coronary microvascular dysfunction (CMD), due to endothelial and non-endothelial dependent mechanisms, may be an explanation in at least half of these symptomatic women who have evidence of myocardial ischemia. CMD is associated with adverse cardiovascular outcomes, including myocardial infarction, stroke, and heart failure. This chapter focuses on CMD diagnosis and treatment (pharmacological and non-pharmacological approaches) in women with no obstructive CAD.

From the development of open heart surgery in the 1950s, dramatic technological advances have facilitated progressively complex cardiac procedures with approaches ranging from the open or minimally invasive surgical to the percutaneous endovascular. Treatments that involve securing prosthetic material in, or in communication with, the heart are employed in a variety of cardiac pathologies, including valvular heart disease, cardiomyopathy, and undesired communications between cardiac chambers. These devices carry with them the risk of thromboembolic complications that are mitigated by the use of antithrombotic therapies. In this chapter, we review the features of cardiac prosthetic devices associated with thrombosis, the indications for device use, their hematologic complications, and the evidence guiding current recommendations for management of these devices. Cardiac devices discussed include prosthetic heart valves (mechanical, bioprosthetic, and transcatheter aortic valves), valve repair (surgical, MitraClip, and endovascular plugs for prosthetic paravalvular leak), left ventricular assist devices (LVADs), temporary mechanical circulatory support, septal closure devices, and left atrial appendage (LAA) occlusion devices.