title: Changes in plasma free fatty acid levels in septic patients are associated with cardiac damage and reduction in heart rate variability.
abstract: Free fatty acids (FFAs) have been shown to produce alteration of heart rate variability (HRV) in healthy and diabetic individuals. Changes in HRV have been described in septic patients and in those with hyperglycemia and elevated plasma FFA levels. We studied if sepsis-induced heart damage and HRV alteration are associated with plasma FFA levels in patients. Thirty-one patients with sepsis were included. The patients were divided into two groups: survivors(n = 12) and nonsurvivors (n = 19). The following associations were investigated: (a) troponin I elevation and HRV reduction and (b) clinical evolution and HRV index, plasma troponin, and plasma FFA levels. Initial measurements of C-reactive protein and gravity Acute Physiology and Chronic Health Evaluation scores were similar in both groups. Overall, an increase in plasma troponin level was related to increased mortality risk. From the first day of study, the nonsurvivor group presented a reduced left ventricular stroke work systolic index and a reduced low frequency (LF) that is one of HRV indexes. The correlation coefficient for LF values and troponin was r(2) = 0.75 (P < 0.05). All patients presented elevated plasma FFA levels on the first day of the study (5.11 +/- 0.53 mg/mL), and this elevation was even greater in the nonsurvivor group compared with the survivors (6.88 +/- 0.13 vs. 3.85 +/- 0.48 mg/mL, respectively; P < 0.05). Cardiac damage was confirmed by measurement of plasma troponin I and histological analysis. Heart dysfunction was determined by left ventricular stroke work systolic index and HRV index in nonsurvivor patients. A relationship was found between plasma FFA levels, LFnu index, troponin levels, and histological changes. Plasma FFA levels emerged as possible cause of heart damage in sepsis.
authors.affiliation: São Paulo University Hospital, São Paulo, Brazil.
authors.forename: Antonio Carlos
authors.initials: AC
authors.lastname: Nogueira
authors.forename: Victor
authors.initials: V
authors.lastname: Kawabata
authors.forename: Paolo
authors.initials: P
authors.lastname: Biselli
authors.forename: Marcelo Henrique
authors.initials: MH
authors.lastname: Lins
authors.forename: Carla
authors.initials: C
authors.lastname: Valeri
authors.forename: Mauricio
authors.initials: M
authors.lastname: Seckler
authors.forename: Wagner
authors.initials: W
authors.lastname: Hoshino
authors.forename: Luiz Gonzaga
authors.initials: LG
authors.lastname: Júnior
authors.forename: Marcia Martins Silveira
authors.initials: MM
authors.lastname: Bernik
authors.forename: Juliana B
authors.initials: JB
authors.lastname: de Andrade Machado
authors.forename: Marina Baquerizo
authors.initials: MB
authors.lastname: Martinez
authors.forename: Paulo Andrade
authors.initials: PA
authors.lastname: Lotufo
authors.forename: Elia Garcia
authors.initials: EG
authors.lastname: Caldini
authors.forename: Edgair
authors.initials: E
authors.lastname: Martins
authors.forename: Rui
authors.initials: R
authors.lastname: Curi
authors.forename: Francisco Garcia
authors.initials: FG
authors.lastname: Soriano
mesh_terms: D000328:Adult; D001145:Arrhythmias, Cardiac / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D001786:Blood Glucose / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood*; D005260:Female; D006331:Heart Diseases / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D011446:Prospective Studies; D012307:Risk Factors; D018805:Sepsis / Q000097:blood* / Q000150:complications / Q000401:mortality / Q000503:physiopathology; D014280:Triglycerides / Q000097:blood; D019210:Troponin I / Q000097:blood
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D008074:Lipoproteins; D014280:Triglycerides; D019210:Troponin I