Heart failure is a major contributor to maternal morbidity and mortality. Pregnancy is a state of hemodynamic stress, and normal physiologic changes of pregnancy may mimic signs of heart failure. Prepregnancy counseling, multidisciplinary care, and referral to a center with expertise in managing pregnant patients with heart failure can help optimize outcomes. The option for abortion care should be available to all patients with heart failure, regardless of the severity of the disease, and is an essential component of individualized counseling. In this Consult, we provide guidance for managing patients with heart failure with reduced ejection fraction who are continuing pregnancy. The following are Society for Maternal-Fetal Medicine (SMFM) recommendations: (1) we recommend that all patients with right heart failure due to pulmonary arterial hypertension receive counseling about high rates of maternal morbidity and mortality; if pregnancy is pursued, the patient should be referred to a center with expertise in this condition to guide management during pregnancy and postpartum (GRADE 1C); (2) we recommend considering referral to a genetics provider with expertise in heritable cardiac disease for people with peripartum cardiomyopathy (PPCM), particularly when the index of suspicion is high and no other contributing factors are identified (GRADE 1C); (3) we recommend that other causes of heart failure be ruled out before making a diagnosis of PPCM (Best Practice); (4) for acute left ventricular heart failure during pregnancy, we recommend hydralazine or isosorbide dinitrate for afterload reduction and furosemide for diuresis. For acute left ventricular failure postpartum, we recommend afterload reduction with angiotensin-converting enzyme inhibitor (ACEi), angiotensin receptor blocker (ARB), or angiotensin receptor/neprilysin inhibitor (ARNi) unless contraindicated (e.g., renal failure) (GRADE 1B); (5) we recommend against inotropic blockade (i.e., beta-blockers) in the setting of acute decompensated left ventricular heart failure (GRADE 1B); (6) we recommend prophylactic anticoagulation administration in hospitalized pregnant patients with acute left ventricular heart failure (GRADE 1C); (7) in patients who are pursuing pregnancy or pregnant, we recommend discontinuing spironolactone, ACEi, ARB, and ARNi and continuing beta-blockers (metoprolol, carvedilol, bisoprolol) (GRADE 1C); (8) for pregnant patients with left ventricular failure and ejection fraction < 35%, we recommend pharmacologic thromboprophylaxis during pregnancy and for six weeks postpartum (GRADE 1C); (9) for patients with chronic left ventricular failure, we recommend starting or continuing guideline-directed medical therapy when medically able, in consultation with experts in cardiology (GRADE 1C); (10) we recommend fetal echocardiography when maternal heart failure is a result of an underlying congenital cardiac defect (GRADE 1C); (11) we recommend serial growth ultrasounds in pregnancies complicated by maternal heart failure (GRADE 1C); (12) we recommend continuous fetal heart rate monitoring during anesthesia administration, labor, and delivery for pregnant patients with heart failure (GRADE 1B); (13) in the case of maternal cardiovascular changes prompting inpatient assessment or treatment, we recommend continuous or intermittent fetal heart rate monitoring, taking into consideration the gestational age and any relevant maternal or fetal factors that may impact fetal viability or the maternal clinical status (GRADE 1C); (14) we recommend planned vaginal delivery at term in patients with heart failure in the absence of hemodynamic compromise or obstetric indications for cesarean (GRADE 1C); (15) we recommend the use of neuraxial anesthesia in most patients with heart failure to provide appropriate analgesia and to limit the effects of labor on cardiac parameters (GRADE 1C); (16) we recommend considering a limited or assisted second stage for some patients after input from cardiology about each individual patient's cardiac risk (GRADE 1C); (17) we recommend that postpartum patients with heart failure undergo routine counseling regarding infant feeding. We recommend reviewing all medications for compatibility with breastfeeding and using shared decision-making in the absence of robust data (GRADE 1B).

Background Heart failure significantly contributes to the global increase in morbidity and mortality. In managing such chronic conditions, medication adherence plays a critical role in patient outcomes. Given the extensive consequences associated with non-adherence in heart failure, it is crucial to implement focused interventions that support and enhance compliance of patients in taking their prescribed medications. Therefore, this study aims to determine the effect of medication adherence tools (MAT) as an intervention to improve medication adherence and functional capacity in patients with heart failure. Methods In a prospective, open-label, randomized controlled study, 200 patients with heart failure were recruited, with 100 in the control group who received the standard prescribed drugs and 100 in the intervention group who received the intervention in addition to the standard prescribed drugs. A multidrug ABCD drug regimen was used for better understanding and distribution of medicines The four classes of drugs included (A) angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers/angiotensin receptor neprilysin inhibitor, (B) beta-blockers/funny channel blocker (ivabradine), (C) companion drugs (digoxin, hydralazine+isosorbide dinitrate, intravenous iron, statins, oral anticoagulants/antiplatelets, antiarrhythmics, etc.), and (D) diuretics/mineralocorticoid receptor antagonists. The intervention included the ABCD drug regimen as a pharmacological approach, health education, and MAT, such as the Hriday Card, Dhadkan 2 mobile application, and labeled separate zip locks for dispensing the drugs separately as per the ABCD drug regimen. Medication adherence was assessed through the Morisky-Green-Levine (MGL) adherence scale, and quality of life assessment was done using a Likert scale. Further, physical ability was assessed by the capacity to climb floors, ability to do routine household work, and capability to walk 500 m without taking a rest. Results Based on the MGL adherence scale, 42 (21%) patients showed high, 132 (66%) showed medium, and 26 (13%) showed low adherence at baseline, including both the study groups. The reasons for non-adherence were found to be poor memory in 48 (24%), travelling outstation in 42 (21%), ran out of medicines in 32 (16%), adverse effects of medicines in 26 (13%), felt worse while taking medicine in 14 (7%), felt better so stopped taking medicine in 14 (7%), less affordability in six (3%), and other than these reasons in 18 (9%) of the patients. Only 40 (20%) patients demonstrated non-adherence to at least one specific class of medication, with non-adherence being maximum with diuretics. Significant improvement in medication adherence was observed in the intervention group in terms of improvement in the MGL score. There was also a significant improvement in the quality of life and the physical ability in the patients of the intervention group. Conclusion The findings indicate a significant occurrence of medication non-adherence among patients with heart failure within the studied population. Implementing a comprehensive, integrated intervention strategy that includes MAT led to enhanced adherence to the prescribed medications, along with notable improvements in patients' quality of life and physical functioning. Consequently, incorporating MAT as an adjunctive measure could be recommended as an additional step toward improved outcomes in the management of patients with heart failure.

The study examines how African American-led organizations leveraged BiDil (hydralazine-isosorbide dinitrate, HYD/ISDN)'s promotional messaging to highlight broader structural barriers in healthcare following the FDA's approval of the drug as the first race-based heart failure treatment for African Americans. Using a textual analysis guided by the culture-centered approach (CCA), this study analyzes advocacy narratives from organizations such as the National Association for the Advancement of Colored People (NAACP) and the Association of Black Cardiologists (ABC) to explore how promotional messaging extends beyond HYD/ISDN to expose deeper economic, systemic, and ethical challenges in US healthcare. The findings reveal three major themes: (1) Framing HYD/ISDN as a Milestone in Racial Health Equity, (2) Addressing Historical Mistrust Through Advocacy and Medical-Cultural Innovation, and (3) Structural and Economic Barriers in Healthcare Access. These themes illustrate how HYD/ISDN's approval was both a symbol of racial progress and a point of contention, reinforcing debates about racialized medicine, affordability, and systemic bias in clinical research. The study concludes that while HYD/ISDN's promotional messaging helped raise awareness of racial health disparities, true health equity requires structural reforms in drug accessibility, research participation, and culturally centered care.

Racial classifications have a complex and troubled past in the social and scientific history of humankind. They are the result of racism and have been used to devalue and degrade non-White people. Although the concept of race has acquired a social component and the genetic similarity of people based on race has been proven, the category is increasingly used in pharmacogenetic studies to create biased study populations under the guise of personalized medicine. The heart failure drug BiDil, which was only approved for Black people in 2005, gained particular notoriety. Its race-specific approval reignited the debate about the assumption that there are genetic differences between people of different races and led to a further biopolitical instrumentalization of the term 'race'. Despite the expiry of the race-specific patent, race-specific labeling continues to take place in research. In this paper, these racializations of pharmacogenetics are examined, explaining how they arise and how they are kept alive. Finally, this paper argues for better moderation of race in pharmacogenetic studies.

In the last decade, the U.S. Food and Drug Administration has approved 6 drugs to reduce morbidity or mortality and improve functional capacity in patients with heart failure with reduced ejection fraction (HFrEF) and 3 drugs to reduce morbidity or mortality in patients with heart failure with preserved ejection fraction (HFpEF). Of the drugs approved for HFrEF, only 2 reduced mortality (sacubitril/valsartan in the PARADIGM-HF trial and dapagliflozin in the DAPA-HF trial). None of the drugs approved for HFpEF reduced mortality. Four trials, 1 with finerenone (FINEARTS-HF trial), 2 with semaglutide (STEP-HFpEF/DM trial), and 1 with tirzepatide (SUMMIT trial) met their primary endpoint in patients with HFpEF and are currently under review for approval. In contrast, before 2015, the U.S. Food and Drug Administration approved 11 drugs (captopril, enalapril, valsartan, candesartan, long-acting metoprolol succinate, bisoprolol, carvedilol, digoxin, isosorbide dinitrate-hydralazine, spironolactone, and epleronone) for patients with chronic stable HFrEF but none for HFpEF. All 11 drugs reduced mortality and morbidity except for digoxin, which only reduced hospitalization for heart failure. This state-of-the-art review examines the evidentiary support for regulatory actions and incorporation into guidelines of heart therapies approved since 2015.

The management of heart failure with reduced ejection fraction (HFrEF) has advanced in recent decades, and patients are surviving longer. The goals of HFrEF treatment are to reduce mortality, hospitalizations, and the severity of symptoms while improving functional status and quality of life. Treatments shown to reduce morbidity and mortality in patients with HFrEF, known as guideline-directed medical therapy, include renin-angiotensin system/neprilysin inhibitors, beta blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors. Guidelines recommend initiation with target dose titration within 6 to 12 weeks of diagnosis. Secondary therapies such as digoxin, hydralazine and isosorbide dinitrate, ivabradine, and vericiguat are indicated in certain patients with persistent or worsening symptoms. Guideline-directed medical therapy may require dosage adjustment due to adverse effects such as hypotension, hyperkalemia, and worsening kidney function. Intravenous iron replacement is recommended in patients with iron deficiency to improve functional status and quality of life. Device and interventional therapies may be indicated in those with prolonged QRS duration to decrease the risk of sudden cardiac death. Point-of-care ultrasonography can help diagnose heart failure and assess effectiveness of diuretic therapy.

Background Chronic kidney disease (CKD) is an emerging public health problem in India. Pulmonary hypertension (PH) is an overlooked cardiovascular complication of CKD. This study aimed to estimate the burden of PH among CKD patients undergoing hemodialysis in a selected tertiary care hospital. In addition, it aimed to determine the various factors associated with PH and response to various treatment modalities. Methodology This hospital-based, analytical, cross-sectional study was conducted in the nephrology department of a medical college hospital in Tamil Nadu from March 2023 to March 2024. The study included 150 adults diagnosed with stage 5 CKD and registered for hemodialysis. Results Of the 150 participants, 96 (64%) had PH. Of these, 81 (84%) were males and 15 (16%) were females. In the PH group, 58 (60.4%) had type 2 diabetes mellitus, 52 (54%) had been on dialysis for 6-12 months, 67 (69.8%) had chronic glomerulonephritis, 25 (26.04%) had chronic tubular interstitial nephritis, and 72 (75%) had microcytic anemia. PH patients had significantly higher rates of protein-energy malnutrition (26 (48.2%) vs. 67 (80.7%), p < 0.009) and more frequent hospitalizations (19 (35%) vs. 69 (71.9%)) compared to those without PH. Additionally, PH patients exhibited higher incidences of left ventricular hypertrophy (72% vs. 92%), pericardial effusion (0% vs. 65%), and tricuspid regurgitation (16% vs. 100%). Patients treated with a combination of isosorbide dinitrate (ISDN) and hydralazine; extended hemodialysis; and ISDN, hydralazine, and sildenafil showed significant improvement compared to other treatment modalities. Conclusions The high prevalence of PH among CKD patients undergoing hemodialysis underscores the importance of vigilant monitoring and targeted interventions.