title: Maximal exercise capacity is related to cardiovascular structure in patients with longstanding hypertension. A LIFE substudy. Losartan Intervention For Endpoint-Reduction in Hypertension.
abstract: BACKGROUND
  Cardiovascular hypertrophy and remodeling in patients with never-treated hypertension has been associated with impaired exercise capacity, but whether this relationship remains in patients with longstanding hypertension and target organ damage is less elucidated.
  
  
  METHODS
  In 43 unmedicated patients with essential hypertension and electrocardiographic left ventricular (LV) hypertrophy, we measured maximal workload and oxygen reserve by bicycle test, 24-h ambulatory blood pressure (BP), LV mass index by magnetic resonance imaging (LVMI(MRI), n = 31), LVMI(echo) and systemic vascular compliance by echocardiography, minimal forearm vascular resistance (MFVR) by plethysmography, and intima media thickness and distensibility in the common carotid arteries by ultrasound.
  
  
  RESULTS
  The patients did not achieve the maximal workload as predicted by age, gender and body composition (146[129-163] v 162[146-179] Watt, P = .01). This impaired exercise capacity, calculated as the ratio between achieved and predicted maximal workload, was in simple regression analyses related to lower distensibility of the common carotid artery (r = 0.38, P = .01) and lower oxygen reserve (r = 0.68, P < .001). In multiple regression analyses, lower oxygen reserve was related to higher LVMI(MRI) (beta = -0.44), lower systemic vascular compliance (beta = -0.36), and higher MFVR (beta = -0.52) (adjusted R2 = 0.53, P < .001).
  
  
  CONCLUSIONS
  Patients with longstanding hypertension and target organ damage cannot achieve the predicted maximal workload. This impaired exercise capacity was associated with lower common carotid distensibility and lower oxygen reserve. The latter was independently related to LV hypertrophy, low systemic vascular compliance and peripheral vascular remodeling, suggesting that cardiovascular hypertrophy and remodeling may reduce exercise capacity by itself.
authors.affiliation: Department of Clinical Physiology, Nuclear Medicine Glostrup Hospital, University of Copenhagen, Denmark. mho@dadlnet.dk
authors.forename: M H
authors.initials: MH
authors.lastname: Olsen
authors.forename: K
authors.initials: K
authors.lastname: Wachtell
authors.forename: K L
authors.initials: KL
authors.lastname: Hermann
authors.forename: J N
authors.initials: JN
authors.lastname: Bella
authors.forename: U B
authors.initials: UB
authors.lastname: Andersen
authors.forename: H
authors.initials: H
authors.lastname: Dige-Petersen
authors.forename: J
authors.initials: J
authors.lastname: Rokkedal
authors.forename: H
authors.initials: H
authors.lastname: Ibsen
mesh_terms: D000367:Age Factors; D000368:Aged; D001823:Body Composition; D005080:Exercise Test; D017079:Exercise Tolerance / Q000502:physiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000502:physiology; D011237:Predictive Value of Tests; D012737:Sex Factors