Combining whey protein supplementation with exercise is biologically plausible because exercise enhances glucose transport, muscle oxidative capacity, and skeletal muscle remodeling, whereas whey protein provides essential amino acids that support muscle protein synthesis and may acutely stimulate insulin and incretin responses. Despite this potential complementarity, the added clinical value of whey protein in adults with type 2 diabetes mellitus (T2DM) remains uncertain. This review evaluated whether whey protein supplementation combined with structured exercise provides additional benefits for glycemic control, insulin-related outcomes, body composition, functional performance, and cardiovascular markers beyond those achieved with exercise alone. Four randomized trials involving 197 participants met the eligibility criteria. The included studies compared whey protein supplementation, generally administered around exercise sessions or incorporated into broader lifestyle interventions, with placebo or carbohydrate control in adults with T2DM. Across the available evidence, whey protein did not demonstrate a consistent additional benefit over exercise-based control conditions for blood glucose, HbA1c, insulin-related outcomes, or body composition. Substantial clinical and methodological heterogeneity was observed across studies, particularly regarding participant characteristics, exercise protocols, whey protein formulations, supplementation strategies, and outcome assessments. These differences precluded meaningful quantitative pooling, and the findings were therefore synthesized narratively. Individual trials showed that exercise or lifestyle interventions improved several outcomes over time in both groups, whereas the incremental contribution of whey protein remained inconsistent. Although the combination of whey protein and exercise has a plausible anabolic and metabolic rationale, current evidence does not demonstrate a consistent additional benefit of whey protein supplementation beyond structured exercise in adults with T2DM. The certainty of evidence was very low because of small sample sizes, short intervention durations, methodological limitations, clinical heterogeneity, variation in exercise protocols, and differences in whey protein formulations. Whey protein may still be appropriate for selected individuals with inadequate protein intake, sarcopenia risk, or nutritional vulnerability, but the available evidence does not support its routine use as an adjunct to exercise for all adults with T2DM. Larger, longer-term randomized trials using more standardized exercise and supplementation protocols are needed to identify whether specific patient subgroups may benefit.
In this review, we examine racial and ethnic sudden cardiac arrest (SCA) disparities in competitive athletes. We explore disparities across the continuum of care, including preparticipation cardiovascular screening, diagnostic evaluation, emergency response, and post-arrest management. Finally, we highlight opportunities to promote equitable and evidence-based prevention, evaluation, and treatment strategies in sports cardiology. SCA in young competitive athletes occurs disproportionately among Black athletes. Despite improvements in emergency preparedness, post-arrest survival remains disproportionately lower among Black and other non-White athletes. Available evidence does not support an inherited biologic explanation for these disparities. Inequities in structural and socioeconomic determinants of health, access to expert cardiovascular evaluations, emergency preparedness, as well as underrepresentation of minority athletes in registries and research cohorts may contribute to disparate SCA outcomes as a function of race and ethnicity and represent critical points of emphasis in future research efforts. Racial and ethnic SCA disparities among athletes are best understood by appreciating race as a sociopolitical instead of biological construct and considering the entire continuum of care for competitive athletes. Mitigating disparities requires a shift in approach to individualized risk assessments, equitable access to cardiovascular care, comprehensive emergency preparedness, and diversification of research cohorts.
Heart failure with preserved ejection fraction (HFpEF) is the most prevalent heart failure phenotype and carries substantial morbidity and mortality, yet effective device-based therapies are lacking. Sinus node dysfunction and atrioventricular block are common in this population and contribute to impaired cardiac reserve and exercise intolerance, providing a pathophysiologic rationale for cardiac pacing as a therapeutic strategy. This review examines the physiologic rationale, current evidence, and clinical decision-making for contemporary and emerging pacing strategies in HFpEF. A range of contemporary pacing approaches — including personalized accelerated pacing and conduction system pacing — is under investigation, each aiming to optimize cardiac output and loading conditions while avoiding the adverse effects of non-physiologic pacing. Conventional right ventricular pacing is independently associated with worse outcomes in HFpEF, reinforcing the rationale for physiologic alternatives. Contemporary and emerging pacing strategies show promise for HFpEF, but prospective randomized clinical trials are needed to define their role.
Thoracic aortic disease is a notable contributor to maternal morbidity, in which nearly half of affected women are unaware of their diagnosis until acute complication occurs. To frame the discussion of recommendations and evidence specific to common types of thoracic aortic disease, this review compares the 2022 American College of Cardiology (ACC)/American Heart Association (AHA) and 2025 European Society of Cardiology (ESC) guidelines for managing aortopathy across different periods of pregnancy. Both guidelines emphasize preconception counseling, multidisciplinary care, imaging surveillance, and consideration of prophylactic surgery, which is determined by degree of risk based on pathology and aortic measurement. Surgical intervention is generally recommended for aortic diameters > 45 mm, though thresholds differ if there are additional factors that confer risk (i.e. higher-risk genetic mutations, prior history of dissection, or growth rate). With blood pressure control, beta-blocker use (excluding atenolol) is recommended to mitigate risk, though recent registry data and meta-analysis have not shown clear reductions in dissection. Vaginal delivery is often preferred when appropriate, though cesarean delivery is considered in high-risk conditions due to intra-abdominal pressures. Preconception risk stratification, multidisciplinary ‘pregnancy heart teams’, and structured imaging surveillance remain essential to reducing maternal and fetal morbidity in aortopathy. Gaps currently exist in protocolized postpartum follow-up, outcome data surrounding delivery method and beta blocker use, and long-term data on assisted reproductive technology in these high-risk populations. Beyond further outcomes research, continued efforts to broaden access to multidisciplinary cardio-obstetric care teams should remain a priority to improve maternal health.
Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndrome, particularly in younger women without traditional cardiovascular risk factors. This review summarizes recent advances in SCAD pathophysiology, diagnosis, and management, highlighting evolving clinical concepts and areas of uncertainty. SCAD is a non-atherosclerotic cause of myocardial infarction driven by intramural hematoma formation or intimal tear, both resulting in subsequent luminal compression. Advances in coronary imaging have improved recognition of diverse angiographic patterns. Selective use of intracoronary imaging and emerging noninvasive modalities is further refining diagnosis and surveillance. Observational data support a conservative management strategy in hemodynamically stable patients, given high rates of spontaneous healing. Emerging evidence supports beta-blockers for recurrence prevention while questioning the use of routine dual antiplatelet therapy. Long-term morbidity, including recurrent symptoms, coronary microvascular dysfunction, and psychosocial burden, is increasingly recognized. SCAD is a distinct clinical entity with diagnostic and management considerations that differ from atherosclerotic disease. Despite improved recognition, key gaps remain in risk stratification, recurrence prediction, and optimal therapy. Ongoing international registries and emerging clinical trials are expected to address these gaps and inform a more individualized, mechanism-based approach to care.
