Hypertension in pregnancy contributes substantially to maternal morbidity and mortality, persistent hypertension, and rehospitalization. Hypertensive disorders of pregnancy are also associated with a heightened risk of cardiovascular disease, and timely recognition and modification of associated risk factors is crucial in optimizing long-term maternal health. During pregnancy, there are expected physiologic alterations in blood pressure (BP); however, pathophysiologic alterations may also occur, leading to preeclampsia and gestational hypertension. The diagnosis and effective management of hypertension during pregnancy is essential to mitigate maternal risks, such as acute kidney injury, stroke, and heart failure, while balancing potential fetal risks, such as growth restriction and preterm birth due to altered uteroplacental perfusion. In the postpartum period, innovative and multidisciplinary care solutions that include postpartum maternal health clinics can help optimize short- and long-term care through enhanced BP management, screening of cardiovascular risk factors, and discussion of lifestyle modifications for cardiovascular disease prevention. As an adjunct to or distinct from postpartum clinics, home BP monitoring programs have been shown to improve BP ascertainment across diverse populations and to lower BP in the months after delivery. Because of concerns about pregnant patients being a vulnerable population for research, there is little evidence from trials examining the diagnosis and treatment of hypertension in pregnant and postpartum individuals. As a result, national and international guidelines differ in their recommendations, and more studies are needed to bolster future guidelines and establish best practices to achieve optimal cardiovascular health during and after pregnancy. Future research should focus on refining treatment thresholds and optimal BP range peripartum and postpartum and evaluating interventions to improve postpartum and long-term maternal cardiovascular outcomes that would advance evidence-based care and improve outcomes worldwide for people with hypertensive disorders of pregnancy.

Globally significant variation in treatment and course of heart valve disease (HVD) exists, and outcome measurement is procedure focused instead of patient focused. This article describes the development of a patient-related (International Consortium for Health Outcomes Measurement) standard set of outcomes and case mix to be measured in patients with HVD.

Chest radiotherapy (XRT) plays a crucial role in the treatment of a multitude of cancers including breast, lung, esophageal, and lymphoma. Although XRT enhances cancer survival rates, it may also expose healthy bystander tissues to radiation, potentially leading to severe complications. Initially considered relatively resistant to radiation damage, the heart has been shown over the past 4 decades to be susceptible to radiation-induced cardiovascular toxicity and despite advances in XRT which can minimize radiation exposure to heart tissue, no cardiac radiation dose is entirely safe. The clinical spectrum of radiation-induced cardiovascular toxicity is broad, encompassing coronary artery disease, myocardial dysfunction, valvular abnormalities, and pericardial disorders. Radiation-induced cardiovascular toxicity may manifest acutely or many years after XRT, with each condition more likely to present at certain time points post-XRT. Cardiac imaging is a crucial tool in both the screening and diagnosis of radiation-induced cardiovascular toxicity with an understanding of its pathophysiology, incidence, and progression required to implement a comprehensive, multimodality imaging approach to detect and manage these complications effectively.

Critical care cardiology refers to the practice focus of and subspecialty training for the comprehensive management of life-threatening cardiovascular diseases and comorbid conditions that require advanced critical care in an intensive care unit. The development of coronary care units is often credited for a dramatic decline in mortality rates after acute myocardial infarction throughout the 1960s. As the underlying patient population became progressively sicker, changes in organizational structure, staffing, care delivery, and training paradigms lagged. The coronary care unit gradually evolved from a focus on rapid resuscitation from ventricular arrhythmias in acute myocardial infarction into a comprehensive cardiac intensive care unit designed to care for the sickest patients with cardiovascular disease. Over the past decade, the cardiac intensive care unit has continued to transform with an aging population, increased clinical acuity, burgeoning cardiac and noncardiac comorbidities, technologic advances in cardiovascular interventions, and increased use of temporary mechanical circulatory support devices. Herein, we provide an update and contemporary expert perspective on the organizational structure, staffing, and care delivery in the cardiac intensive care unit; examine the challenges and opportunities present in the education and training of the next generation of physicians for critical care cardiology; and explore quality improvement initiatives and scientific investigation, including multicenter registry initiatives and randomized clinical trials, that may change clinical practice, care delivery, and the research landscape in this rapidly evolving discipline.

It remains challenging to determine which hypertrophic cardiomyopathy (HCM) family members will subsequently develop HCM. Standard 2-dimensional and conventional Doppler echocardiography have been unable to reliably distinguish HCM genotype-positive and phenotype-negative (G+P-) from genotype-negative and phenotype-negative (G-P-) family members. We aimed to determine if advanced echocardiographic modalities can discriminate HCM G+P- from G-P- individuals.

TTN (titin) is the third myofilament type of the cardiac sarcomere and performs important functions that include generating passive tension. Changes in TTN expression are associated with cardiac dysfunction, and TTN is one of the main genes linked to dilated cardiomyopathy (DCM). DCM is frequently associated with changes in the expression of N2BA (compliant cardiac TTN isoform), 1 of the 2 major TTN isoforms found in the heart (the other isoform being the N2B [stiff cardiac TTN isoform]). Whether altered expression of N2BA TTN causes DCM or is a secondary change remains unclear.

Hypertensive disorders of pregnancy (HDP) are a major cause of maternal morbidity and mortality and are associated with acute cardiac events in the peripartum period, as well as cardiovascular disease later in life. Despite the robust association between hypertension and atrial fibrillation (AFib), comparatively little is known about HDP and its subtypes as sex-specific risk factors for AFib.

Atherosclerotic cardiovascular disease is a major health concern worldwide and requires effective preventive measures. Lp(a) (lipoprotein [a]) has recently garnered attention as an independent risk factor for astherosclerotic cardiovascular disease, with proinflammatory and prothrombotic mechanisms contributing to its atherogenicity. On an equimolar basis, Lp(a) is ~5 to 6 times more atherogenic than particles that have been widely associated with adverse cardiovascular outcomes, such as LDL (low-density lipoprotein). Lp(a) can enter the vessel wall, leading to the accumulation of oxidized phospholipids in the arterial intima, which are crucial for initiating plaque inflammation and triggering vascular disease progression. In addition, Lp(a) may cause atherothrombosis through interactions between apoA (apolipoprotein A) and the platelet PAR-1 (protease-activated receptor 1) receptor, as well as competitive inhibition of plasminogen. Because Lp(a) is mostly determined on genetic bases, a 1-time assessment in a lifetime can suffice to identify patients with elevated levels. Mendelian randomization studies and post hoc analyses of randomized trials of LDL cholesterol-lowering drugs showed a causal link between Lp(a) concentrations and cardiovascular outcomes, with therapeutic reduction of Lp(a) expected to contribute to estimated cardiovascular risk mitigation. Many Lp(a)-lowering drugs, including monoclonal antibodies, small interfering ribonucleic acids, antisense oligonucleotides, small molecules, and gene editing compounds, are at different stages of clinical investigation and show promise for clinical use. In particular, increased Lp(a) testing and treatment are expected to have a substantial impact at the population level, enabling the identification of high-risk individuals and the subsequent prevention of a large number of cardiovascular events. Ongoing phase 3 trials will further elucidate the cardiovascular benefits of Lp(a) reduction over the long term, offering potential avenues for targeted interventions and improved cardiovascular outcomes.

Peripheral artery disease (PAD) is an atherosclerotic condition that affects a growing number of individuals worldwide, with estimates exceeding 220 million. One of the central hallmarks of PAD is lower extremity pain, which may present as intermittent claudication and atypical leg pain, and, in more severe cases, ischemic rest pain, neuropathic pain, or phantom limb pain in those who underwent amputation. Although the majority of individuals with PAD may experience pain that is chronic in nature, the pathogenesis and phenomenology of pain may differ. Nociceptive, inflammatory, and neuropathic mechanisms all play a role in the generation of pain. Pain in PAD results in severe disability and can copresent with distress, sickness behaviors such as avoidance and further deconditioning, and concomitant depression, anxiety, and addiction secondary to opioid use. These factors potentially lead to chronic pain interacting with a multitude of domains of functioning, including physical, emotional, and behavioral. Whereas pain is a normal adaptive response, self-defeating behaviors and cognitions contribute to the persistence or worsening of the chronic pain experience, disability, and distress. Much remains unknown about the phenomenology of pain in PAD and its clinical subgroups and how it affects outcomes. Borrowing from other chronic pain syndromes, multimodal pain management strategies that emphasize a biopsychosocial model have generated a solid evidence base for the use of cognitive behavioral approaches to manage pain. Multimodal pain management in PAD is not the norm, but theoretical pathways and road maps for further research, assessment, and clinical implementation are presented in this scientific statement.

It is difficult to identify patients with atrial fibrillation (AF) most likely to respond to ablation. While any arrhythmia patient may recur after acutely successful ablation, AF is unusual in that patients may have long-term arrhythmia freedom despite a lack of acute success. We hypothesized that acute and chronic AF ablation outcomes may reflect distinct physiology and used machine learning of multimodal data to identify their phenotypes.

The activation and polarization of T cells play a crucial role in atherosclerosis and dictate athero-inflammation. The epigenetic enzyme EZH2 (enhancer of zeste homolog 2) mediates the H3K27me3 (trimethylation of histone H3 lysine 27) and is pivotal in controlling T cell responses.

Cytokinesis is the last step in the eukaryotic cell cycle, which physically separates a mitotic cell into 2 daughter cells. A few days after birth in mouse cardiomyocytes, DNA synthesis occurs without cytokinesis, leading to the majority of cardiomyocytes becoming binucleated instead of generating 2 daughter cells with 1 nucleus each. This results in cell cycle arrest of cardiomyocytes, and the mouse heart is no longer able to regenerate. A longstanding unanswered question is whether binucleation of cardiomyocytes is a result of cytokinesis failure.

Immune checkpoint inhibitors (ICIs), though revolutionary in cancer treatment, may accelerate atherosclerosis by inducing arterial inflammation. Due to a lack of controlled studies, the capacity of arterial 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) uptake in patients with cancer to detect this arterial inflammation remains unclear.

The PRECISE (Prospective Randomized Trial of the Optimal Evaluation of Cardiac Symptoms and Revascularization) demonstrated that a precision diagnostic strategy reduced the primary composite of death, nonfatal myocardial infarction, or catheterization without obstructive coronary artery disease by 65% in patients with nonacute chest pain compared with usual testing. Medical cost was a prespecified secondary end point.

The PRECISE (Prospective Randomized Trial of the Optimal Evaluation of Cardiac Symptoms and Revascularization) trial compared an investigational precision diagnostic testing strategy (n=1057) with usual testing (n=1046) in patients with stable chest pain and suspected coronary artery disease. Quality of life (QOL) outcomes were a prespecified secondary end point.

Dilated cardiomyopathy (DCM) appears to be diagnosed twice as often in male than in female patients. This could be attributed to underdiagnosis in female patients or sex differences in susceptibility. Up to 30% of cases have an autosomal dominant monogenic cause, where equal sex prevalence would be expected. The aim of this systematic review, meta-analysis, and population study was to assess the sex ratio in patients with DCM, stratified by genetic status, and evaluate whether this is influenced by diagnostic bias.

Over the past decades, hypertrophic cardiomyopathy has become a contemporary treatable disease. However, limited data exist on the global trends of implantable cardioverter defibrillator (ICD) utilization and its impact on mortality/morbidity burden reduction.