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Published on: September 17, 2015
Maximal exercise capacity is related to cardiovascular structure in patients with longstanding hypertension. A LIFE
M H Olsen1, K Wachtell, K L Hermann
1Department of Clinical Physiology, Nuclear Medicine Glostrup Hospital, University of Copenhagen, Denmark. mho@dadlnet.dk
Insights
Patients with longstanding hypertension experience reduced exercise capacity due to cardiovascular changes. This impaired ability is linked to stiff arteries and lower oxygen reserves, indicating that heart and blood vessel remodeling directly impacts physical function.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Exercise Science
Background:
- Cardiovascular hypertrophy and remodeling are linked to reduced exercise capacity in never-treated hypertension.
- The relationship between these factors in longstanding hypertension with target organ damage is less understood.
Purpose of the Study:
- To investigate the association between cardiovascular remodeling and impaired exercise capacity in patients with longstanding hypertension and target organ damage.
Main Methods:
- 43 unmedicated patients with essential hypertension and left ventricular (LV) hypertrophy underwent maximal workload and oxygen reserve testing.
- Measurements included 24-h ambulatory blood pressure, LV mass index (MRI and echocardiography), systemic vascular compliance, forearm vascular resistance, and carotid artery intima media thickness and distensibility.
Main Results:
- Patients achieved lower maximal workload than predicted (P = .01).
- Impaired exercise capacity correlated with lower common carotid artery distensibility (r = 0.38, P = .01) and lower oxygen reserve (r = 0.68, P < .001).
- Lower oxygen reserve was independently associated with higher LV mass index, lower systemic vascular compliance, and higher minimal forearm vascular resistance (adjusted R2 = 0.53, P < .001).
Conclusions:
- Patients with longstanding hypertension and target organ damage exhibit reduced maximal workload achievement.
- This impairment is associated with decreased common carotid artery distensibility and lower oxygen reserve.
- Cardiovascular hypertrophy and remodeling appear to independently reduce exercise capacity by affecting vascular compliance and peripheral resistance.
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.
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