title: Recovery kinetics of oxygen uptake after cardiopulmonary exercise test and prognosis in patients with left ventricular dysfunction.
abstract: BACKGROUND
  The prognostic value of peak oxygen uptake (peak VO2) in patients with left ventricular systolic dysfunction is currently recognized and accepted. Some studies have shown that other cardiopulmonary exercise test (CPET) parameters have additional value.
  
  
  OBJECTIVE
  To evaluate whether our population of patients with left ventricular dysfunction had similar results to those found by other investigators who showed that a slow normalization of oxygen uptake (VO2) during the recovery period of a CPET has prognostic value, and whether the recovery phase parameters have additional prognostic value to peak VO2 in these patients.
  
  
  METHODS
  We studied 292 consecutive adult patients (81.5% male; mean age 52.4 +/- 10.6 years) with an ejection fraction below 40% (mean 23.6 +/- 8.8%) given their first symptom-limited CPET between 03/1993 and 08/2000. The etiology was ischemic heart disease in 154, idiopathic cardiomyopathy in 130 and other in 8 patients. NYHA class was I in 7%, II in 50.6% and III in 42.4% of the patients. Two years was defined as the maximum follow-up time; it was 551.5 +/- 242.2 days on average, and 62 events (death or cardiac transplantation) occurred. The following parameters were analyzed: peak VO2 (l/min and ml/kg/min), percent predicted peak VO2 (pred VO2) (l/min and ml/kg/min), VO2 every 15 seconds (sec) of the first 3 minutes of recovery (the difference between peak VO2/kg and VO2/kg every 15 sec in the recovery period (dif VO2), expressed in ml/kg/min, and also the time (sec) to reach 50% of peak VO2 (T1/2). It was considered that a combined end-point was reached if patients died or underwent cardiac transplantation.
  
  
  RESULTS
  ROC curves of these parameters showed the following as cut-off values (area under the curve > 0.7) for the occurrence of events: peak VO2 < 60% of pred VO2, dif VO2 at 60 sec (< 3 ml/kg/min), 90 sec (< 5), 120 sec (< 8), 150 sec (< 8.6) and 180 sec (< 10.5) of the recovery and T1/2 > 115 sec. Survival analysis was performed considering pred VO2 < 60%, dif VO2 at 150 sec (the largest area under the curve) and T1/2 > 115 sec. In the survival analysis, when the decrease in VO2 at 150 sec was less than 8.6 ml/kg/min the number of patients with events increased from 9.2% to 43.5% (p < 0.001; log-rank), and when T1/2 was less than 115 sec the number of events increased from 12.3 to 34.2% (p < 0.001; log-rank). When the criteria of T1/2 and dif VO2 at 150 sec were considered together with pred VO2 < 60%, mortality increased from 31 to 54% and from 33 to 51%, respectively (p < 0.001, for both parameters; chi-square).
  
  
  CONCLUSIONS
  A slow VO2 kinetics in the recovery period of the CPET by itself identified groups of patients with poor prognosis. The association of these parameters with peak VO2 enhanced the identification of groups at greater risk for events. A global evaluation of the CPET should be performed, considering other parameters besides peak VO2, particularly those related to VO2 kinetics in recovery (T1/2 and dif VO2 at 150 sec) as identified in this study.
authors.affiliation: Serviço de Cardiologia-Hospital de Santa Cruz, Carnaxide. superpluto@clix.pt
authors.forename: Maria Conceição
authors.initials: MC
authors.lastname: Queirós
authors.forename: Duarte Espregueira
authors.initials: DE
authors.lastname: Mendes
authors.forename: Miguel Almeida
authors.initials: MA
authors.lastname: Ribeiro
authors.forename: Miguel
authors.initials: M
authors.lastname: Mendes
authors.forename: Maria José
authors.initials: MJ
authors.lastname: Rebocho
authors.forename: Ricardo
authors.initials: R
authors.lastname: Seabra-Gomes
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D005080:Exercise Test; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption; D011379:Prognosis; D012189:Retrospective Studies; D018487:Ventricular Dysfunction, Left / Q000378:metabolism* / Q000503:physiopathology*