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Extreme-Dipper Profile, Increased Aortic Stiffness, and Impaired Subendocardial Viability in Hypertension
Guy Amah1, Rahma Ouardani1, Adrien Pasteur-Rousseau1,2
1AP-HP, Hôpital Lariboisière, Physiologie Clinique-Explorations Fonctionnelles, Paris, France.
Insights
Extreme-dippers with hypertension show increased aortic stiffness and impaired subendocardial viability compared to dippers. This suggests a higher risk of silent myocardial ischemia, especially in women, warranting further screening.
Area of Science:
- Cardiology
- Hypertension Research
- Vascular Physiology
Background:
- Extreme-dippers with hypertension and stable coronary artery disease (CAD) experience more severe nighttime cardiac ischemia than dippers.
- This study investigates subendocardial viability in extreme-dippers versus dippers, excluding confounding factors like diabetes, CAD, or chronic kidney disease (CKD).
Purpose of the Study:
- To assess subendocardial viability in treated hypertensive patients who are extreme-dippers compared to dippers.
- To determine if extreme-dippers exhibit more impaired subendocardial viability, independent of other comorbidities.
Main Methods:
- Included 213 treated hypertensives (156 dippers, 57 extreme-dippers) undergoing 24-hour ambulatory blood pressure (BP) monitoring.
- Utilized radial applanation tonometry for subendocardial viability ratio (SEVR), augmentation index (AIx), and pulse pressure amplification (PPamp).
- Measured carotid-femoral pulse wave velocity (cfPWV) and performed cycle ergometer stress testing.
Main Results:
- Extreme-dippers had higher cfPWV and AIx, but lower PPamp and SEVR than dippers.
- Lower nighttime diastolic BP (DBP) was observed in extreme-dippers.
- Women extreme-dippers showed significantly lower SEVR, PPamp, and nighttime DBP compared to men extreme-dippers.
Conclusions:
- Treated hypertensive extreme-dippers without CAD, diabetes, or CKD exhibit increased aortic stiffness and low PPamp.
- This study demonstrates a higher likelihood of impaired subendocardial viability in extreme-dippers compared to dippers.
- Extreme-dipper hypertensive patients, particularly women, may face a significantly higher risk of silent myocardial ischemia, necessitating systematic screening.
Background:
In treated hypertensives, extreme-dippers with stable coronary artery disease (CAD) exhibit more severe nighttime cardiac ischemia than dippers. After excluding confounding factors such as diabetes, CAD or chronic kidney disease (CKD), we assessed whether subendocardial viability, determined by the Buckberg index, was more significantly impaired in extreme-dippers than in dippers.
Methods:
Two hundred thirteen consecutive treated hypertensives (156 dippers, 57 extreme-dippers), were included. After 24-hour ambulatory blood pressure (BP) monitoring, patients underwent radial applanation tonometry (with determination of: subendocardial viability ratio [SEVR], central augmentation index [AIx], and pulse pressure amplification [PPamp]), carotid-femoral pulse wave velocity (cfPWV) measurement, and cycle ergometer stress testing.
Results:
Extreme-dippers showed higher cfPWV (8.99 ± 2.16 vs. 8.29 ± 1.69 m/s, P = 0.014), higher AIx (29.7 ± 9.4 vs. 26.4 ± 10.4%, P = 0.042), lower PPamp (1.22 ± 0.14 vs. 1.30 ± 0.15, P < 0.001), lower SEVR (146 ± 23% vs. 157 ± 26%, P = 0.007), and lower nighttime diastolic BP (DBP) (70 ± 9 vs. 75 ± 9 mm Hg, P < 0.001) than dippers. SEVR and cfPWV were inversely correlated. Among extreme-dippers, women exhibited lower SEVR (138 ± 21% vs. 161 ± 23%, P = 0.004), PPamp (1.16 ± 0.10 vs. 1.31 ± 0.15, P < 0.001), and nighttime DBP (67 ± 8 mm Hg vs. 72 ± 8 mm Hg, P = 0.017) than men.
Conclusions:
Extreme-dipper treated hypertensives with no history of CAD, diabetes or CKD, present increased aortic stiffness and low PPamp. Furthermore, this is the first demonstration of the greater likelihood of these patients to exhibit impaired subendocardial viability compared to dippers. Extreme-dipper hypertensive patients, women in particular, may have a significantly higher risk of silent myocardial ischemia, thus justifying systematic screening.
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