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Obstructive Lung Diseases |

Left Ventricular Hypertrophy as a Predictor of B-Type Natriuretic Peptide Levels and In-Hospital Outcomes in Acute Exacerbation of Chronic Obstructive Pulmonary Disease: A Five-Year Retrospective Analysis FREE TO VIEW

Saraschandra Vallabhajosyula, MBBS; Arun Kanmanthareddy, MD; Pranathi Sundaragiri, MBBS; Anas Ahmed, MBBS; Toufik Mahfood Haddad, MD; Hamza Rayes, MBBCh; Anila Khan, BS; Haitam Buaisha, MBBCh; Gene Pershwitz, MD; Muhammad Sarfraz Nawaz, MBBS; Dustin McCann, DO; Christopher Wichman, PhD; Mark Holmberg, MD; Lee Morrow, MD
Author and Funding Information

Mayo Clinic College of Medicine, Rochester, MN


Chest. 2015;148(4_MeetingAbstracts):677A. doi:10.1378/chest.2260308
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Abstract

SESSION TITLE: COPD and the Heart

SESSION TYPE: Original Investigation Slide

PRESENTED ON: Monday, October 26, 2015 at 01:30 PM - 02:30 PM

PURPOSE: Left ventricular hypertrophy (LVH) due to chronic systemic inflammation in chronic obstructive pulmonary disease (COPD) is well documented. However, its influence on the outcomes of acute exacerbation of COPD (AECOPD) is less understood.

METHODS: This is a 5-year retrospective study on patients admitted with AECOPD. LVH was defined as left ventricular mass index (LVMI) >95 g/m2 (females) and >115 g/m2 (males). Patients with LVH secondary to aortic valve pathology were excluded from the study. Outcomes included need and duration of non-invasive ventilation (NIV) & mechanical ventilation (MV), intensive care unit (ICU) length of stay (LOS), total LOS (days) and in-hospital mortality. Two-tailed p-value <0.05 was considered statistically significant.

RESULTS: A total of 615 patients who met our inclusion criteria were included in our study. LVH was noted in 264 of 615 (42.9%) patients (males 139/309, females 125/306). Comorbidities such as hypertension (80.3% vs 72.1%), diabetes (42.0% vs 29.3%), hyperlipidemia (50.4% vs 33.9%), coronary artery disease (44.7% vs 32.2%), chronic kidney disease (25.8% vs 15.7%) and hemodialysis (4.9% vs 0.6%) were higher in the group with LVH (all p≤0.02). Patients with LVH also had higher baseline creatinine (1.3±1.1 vs 1.0±1.0 mg/dL, p=0.002), B-type natriuretic peptide (BNP) (607±912 vs 299±499 pg/mL, p<0.0001) and lower LV ejection fraction (44.5±21.9% vs 50.0±21.6%, p=0.002). Clinical outcomes of in-hospital mortality (2.7% vs 4.3%), ICU LOS (1.5±3.5 vs 1.3±2.8) and total LOS (5.4±4.9 vs 5.5±5.4) were not significantly different between the two groups (all p>0.05). LVH was not a risk factor for increase in use or duration of NIV (36.3% vs 33.0%; 0.9±1.8 vs 0.8±1.8) or MV (11.4% vs 9.7%; 0.8±2.8 vs 0.6±2.2) (all p>0.05). In patients with BNP >100 pg/mL (upper limit of normal laboratory value) and >500 pg/mL (heart failure range), LVH was noted to increase MV duration by 4.6±0.4 vs 2.3±0.5 days (p=0.001) and 5.0±0.5 vs 3.4±0.3 days (p=0.008) respectively. Additionally, ICU LOS in BNP >100 pg/mL (4.6±0.3 vs 2.3±0.3, p<0.0001) and >500 pg/mL (5.2±0.4 vs 3.3±0.2, p=0.0002) was longer in duration.

CONCLUSIONS: In patients with AECOPD, LVH does not appear to increase in-hospital mortality, LOS or need for supportive ventilation. However, elevated BNP level in patients with LVH is associated with longer MV duration and ICU LOS.

CLINICAL IMPLICATIONS: AECOPD patients with LVH form a higher risk cohort in this hypothesis-generating study and merit further research in prospective trials.

DISCLOSURE: The following authors have nothing to disclose: Saraschandra Vallabhajosyula, Arun Kanmanthareddy, Pranathi Sundaragiri, Anas Ahmed, Toufik Mahfood Haddad, Hamza Rayes, Anila Khan, Haitam Buaisha, Gene Pershwitz, Muhammad Sarfraz Nawaz, Dustin McCann, Christopher Wichman, Mark Holmberg, Lee Morrow

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