Forst, B

Preeclampsia (PE) is a multifactorial hypertensive disorder of pregnancy that significantly increases both short- and long-term cardiovascular risk for affected women. PE and cardiovascular disease (CVD) share common risk factors, including endothelial dysfunction, obesity, insulin resistance, and dyslipidemia. Women with a history of PE face a markedly elevated risk of chronic hypertension, heart failure, and adverse cardiac remodeling, with evidence suggestive of persistent vascular and myocardial changes after pregnancy. The complex pathophysiology of PE is multifactorial and is thought to involve a combination of abnormal placentation, immune dysregulation, and anti-angiogenic factors, which may induce permanent cardiovascular alterations. Genetic predispositions may further link PE with cardiomyopathies and peripartum cardiomyopathy. However, despite these well-established risks, standardized long-term surveillance and management strategies for women with prior PE remain lacking. Early identification and targeted intervention in women with a history of PE represent critical opportunities to mitigate future cardiovascular morbidity and mortality. This review highlights the urgent need for comprehensive, evidence-based strategies that incorporate personalized follow-up and risk stratification to improve cardiovascular outcomes in this high-risk population.

Abstract Introduction/Background Transthyretin amyloidosis (ATTR) is a debilitating disease that leads to progressive cardiac dysfunction. Tafamidis is the gold standard therapy for ATTR cardiomyopathy. In recent observational studies, sodium-glucose cotransporter-2 inhibitors (SGLT2-Is) have demonstrated cardiovascular benefits in ATTR cardiomyopathy, but their role in ATTR cardiomyopathy as combination therapy with tafamidis remains unclear. Purpose To investigate the impact of combination therapy with tafamidis and SGLT2-Is versus just tafamidis in patients with known ATTR cardiomyopathy. Methods This retrospective cohort study utilized data from the TriNetX multinational database. Patients diagnosed with ATTR cardiomyopathy who received tafamidis were identified and stratified into two cohorts based on SGLT2-I use. Outcomes were assessed over three years, including all-cause mortality, all-cause hospitalizations, acute myocardial infarction (AMI), acute heart failure (HF) hospitalizations, ischemic stroke, atrial fibrillation/flutter, end-stage renal disease (ESRD) or requirement for renal replacement therapy, and ventricular tachycardia. Propensity score matching was used to balance both cohorts based on clinical comorbidities, medication use, and laboratory data. Adjusted odds ratios (OR) were calculated by logistic regression models. Results After propensity score matching, 409 patients were included in each cohort with a follow-up duration of 722 days (SD 320.87) for the SGLT2-I cohort and and 755.90 days (SD 363.26) for the non-SGLT2-I cohort. SGLT2-Is were associated with significantly lower rates of all-cause hospitalizations (41.1% vs. 50.9%; OR 0.67 [p = 0.005]) and AMI (6.6% vs. 13.9%, OR 0.44 [p = 0.001]), which persisted by three years (all-cause hospitalizations: 52.1% vs. 61.4%, OR 0.67 [p = 0.006] and myocardial infarction: 11.2% vs. 18.3%, OR 0.56 [p = 0.004]). No significant differences among the two cohorts were observed for all-cause mortality, acute HF hospitalizations, ischemic stroke, atrial fibrillation/flutter, ventricular tachycardia, or ESRD/need for renal replacement therapy. Conclusions SGLT2-Is, in combination with tafamidis, are associated with decreased all-cause hospitalizations and AMI in ATTR cardiomyopathy. While a mortality benefit was not demonstrated, these results depict the magnitude of clinical benefit derived from combination therapy with tafamidis and SGLT2-Is as opposed to prior observational studies which investigated SGLT2-I single therapy