Abstract 4369800: Association of Inflammatory Hypertension with Left Ventricular Hypertrophy in Black Adults from the Genetic Epidemiology Network of Arteriopathy Study
Background: Hypertension and systemic inflammation are independently associated with adverse cardiovascular outcomes. While hypertension is a known risk factor for left ventricular (LV) hypertrophy, the role of inflammation in LV structural changes remains unclear. It is also uncertain whether concomitant inflammation and hypertension ("inflammatory hypertension") exacerbate LV hypertrophy. Research Question: Is inflammatory hypertension associated with increased LV mass index (LVMI) compared to hypertension without inflammation? Methods: We analyzed baseline data from Black adults enrolled in the Genetic Epidemiology Network of Arteriopathy (GENOA) cohort in Jackson, Mississippi. Inflammation was defined by high sensitivity C-reactive protein (hsCRP) >3 mg/L, and hypertension as systolic blood pressure (SBP) >130 mmHg. Participants were classified into four groups: noninflammatory-normotensive (reference group), noninflammatory-hypertensive, inflammatory-normotensive, and inflammatory-hypertensive. The primary outcome was LVMI, assessed by echocardiography. Associations between groups and LVMI were evaluated using generalized estimating equations to account for familial clustering and adjusted for covariates including age, sex, education, smoking status, body mass index, number of antihypertensive medications, statin use, cholesterol, and diabetes. Results: Among 1,027 participants (mean age 64 ± 8.5 years; 71% women), baseline LVMI differed by inflammation-hypertension status. Compared with the LVMI in noninflammatory-normotensive cohort (n=108; 74.5 g/m 2 [70.4–78.6]), significantly higher LVMI was observed in noninflammatory-hypertensive (n=343; 83.6 g/m 2 [81.3–85.9], p<0.001) and inflammatory-hypertensive groups (n=497; 84.7 g/m 2 [82.8–86.7], p<0.001). There was no statistically significant difference between inflammatory-hypertensive and noninflammatory-hypertensive groups (84.7 vs 83.6 g/m 2 )(p=0.460). The inflammatory-normotensive cohort also did not differ from the reference group (74.9 g/m 2 [70.2–79.5], p=0.901). Secondary analyses using elevated IL-6 to define inflammation yielded similar findings ( Figure 1 ). Conclusion: In individuals with inflammatory hypertension, hypertension appears to be the primary driver of LV hypertrophy. Further studies in larger, diverse populations are needed to definitively evaluate the potential additive effect of inflammatory hypertension on LV remodeling.
Management of Acute Decompensated Valvular Heart Disease
Abstract Worldwide, valvular heart disease (VHD) is a common cause of hospitalization for acute heart failure. In acute heart failure caused by VHD, symptoms result from rapid haemodynamic changes and subsequent decline in cardiac function, and if left untreated, leads to acute decompensation and cardiogenic shock. Current evidence remains scarce and recommendations regarding the management of acute heart failure caused by VHD are lacking in most recent international guidelines. Herein, we review the management of acute heart failure caused by VHD with a focus on transcatheter therapies and describe currently available evidence based on a systematic literature search on the following valve pathologies: (i) aortic stenosis, (ii) aortic regurgitation, (iii) mitral regurgitation, and (iv) mitral stenosis. Articles reporting outcomes following urgent or emergent valve intervention in the setting of cardiogenic shock or acute heart failure were considered. After screening a total of 2234 articles, 76 published between 1994 and 2023 were included in subsequent analysis. Based on available evidence, proposed treatment algorithms to guide optimal management of acute heart failure caused by VHD were created. As the number of patients presenting with acute heart failure caused by VHD continues to rise and outcomes following transcatheter valve interventions continue to improve, it is inevitable that minimally invasive options will play an increasingly important role in the acute setting, especially given these patients are at an increased operative risk. This review aims to present an organized approach to the complex management and interventional treatment of patients with acute heart failure caused by VHD.