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Albert A Hagege

Publications and source records attributed to Albert A Hagege.

4 recordsLinked to original sources
PubMed2006

Chordal cutting does not adversely affect left ventricle contractile function.

BACKGROUND: Severing a limited number of second-order chordae to the anterior leaflet can improve ischemic mitral regurgitation (MR). Some concerns have been raised regarding possible influence on regional and global left ventricle (LV) function. We evaluated changes in cardiac function in 5 normal sheep with cutting of pre-instrumented chords in the beating heart to maintain constant load. METHODS AND RESULTS: Under cardiopulmonary bypass, wires were placed around the 2 central basal chordae and brought outside the heart, which was restarted. Hemodynamic and imaging data were collected before and after chordal cutting by radiofrequency ablation using those wires. Segmental contractility was assessed invasively using sonomicrometers and noninvasively using Doppler tissue velocity and strain rate (with strain rate viewed as less load-dependent than ejection fraction) at 6 sites: base, mid-ventricle, and apex along the anteroseptal and posterolateral walls. We found no changes from before to after chordal cutting in LV end-diastolic volume (47.2+/-3.3 after cutting versus 48.4+/-4.6 mL before cutting, P=0.66), end-systolic volume (21.5+/-1.2 versus 22.3+/-2.8 mL, P=0.68), ejection fraction (54.2+/-1.8 versus 54.2+/-2.7%, P=0.96), systolic ventricular elastance (7.28+/-1.68 versus 7.66+/-2.11 mm Hg/mL, P=0.64), preload-recruitable stroke work (46.6+/-7.7 versus 50.2+/-10.7 mm Hg, P=0.76), and LVdP/dt (1480+/-238 versus 1392+/-250 mm Hg/s, P=0.45). Doppler tissue velocities and longitudinal strain rates surrounding the papillary muscles were unchanged, as were sonomicrometer longitudinal and mediolateral absolute strains. No wall motion abnormalities were visible around the papillary muscles, and no MR developed. CONCLUSIONS: We find no evidence for acutely decreased global or segmental LV contractility with chordal cutting. This absence of adverse effects is consistent with long-term clinical experience with cutting these chords in valve repair.

Animals↗
PubMed2004

Serial left ventricular adaptations in world-class professional cyclists: implications for disease screening and follow-up.

OBJECTIVES: The purpose of this research was to study long-term left ventricular (LV) adaptations in very-high-level endurance athletes. BACKGROUND: Knowledge of cardiac changes in athletes, who are at particularly high risk of sudden cardiac death, is mandatory to detect hypertrophic cardiomyopathy (HCM) or dilated (DCM) cardiomyopathy. METHODS: We carried out echocardiographic examinations on 286 cyclists (group A) and 52 matched sedentary volunteers (group C); 148 cyclists participated in the 1995 "Tour de France" race (group A1), 138 in the 1998 race (group A2), and 37 in both (group B). RESULTS: In groups A, A1, A2, and C, respectively, diastolic left ventricular diameter (LVID) was 60.1 +/- 3.9 mm, 59.2 +/- 3.8 mm, 61.0 +/- 3.9 mm, and 49.0 +/- 4.3 mm (A vs. C and A1 vs. A2, p < 0.0001), and maximal wall thickness (WT) was 11.1 +/- 1.3 mm, 11.6 +/- 1.3 mm, 10.6 +/- 1.1 mm, and 8.6 +/- 1.0 mm (A vs. C and A1 vs. A2, p < 0.0001). Among group A, 147 (51.4%) had LVID >60 mm; 17 of them had also a below normal (<52%) left ventricular ejection fraction (LVEF). Wall thickness exceeded 13 mm in 25 athletes (8.7%) (always <15 mm), 23 with LVID >55 mm. In group B, LVID increased (58.3 +/- 4.8 mm to 60.3 +/- 4.2 mm, p < 0.001) and WT decreased (11.8 +/- 1.2 mm to 10.8 +/- 1.2 mm, p < 0.001) with time. CONCLUSIONS: Over one-half of these athletes exhibited unusual LV dilation, along with a reduced LVEF in 11.6% (17 of 147), compatible with the diagnosis of DCM. Increased WT was less common (always <15 mm) and scarce without LV dilation (<1%), eliminating the diagnosis of HCM. Serial examinations showed evidence of further LV dilation along with wall thinning. These results might have important implications for screening in athletes.

Adult↗
PubMed2002

Cardiovascular phenotypes of kinin B2 receptor- and tissue kallikrein-deficient mice.

To clarify the role of the kallikrein-kinin system in cardiovascular homeostasis, the systemic and regional hemodynamics of kinin B2 receptor-deficient (B2-/-) and tissue kallikrein-deficient (TK-/-) mice were compared with their wild-type (WT) littermates on a pure C57BL/6 genetic background. B2-/-, TK-/-, and WT adult mice were normotensive and displayed normal hemodynamic (left ventricular [LV] pressure, cardiac output, total peripheral resistance, dP/dt(max)) and echocardiographic (septum and LV posterior wall thickness, LV diameter, LV mass, and LV fractional shortening) parameters. However, heart rate was lower in B2-/- mice compared with TK-/- and WT mice. In addition, B2-/- mice, but not TK-/- mice, exhibited lower coronary and renal blood flows and greater corresponding vascular resistances than did WT mice, indicating a tonic physiological vasodilating effect of bradykinin in these vascular beds. However, maximal coronary vasodilatation capacity, estimated after dipyridamole infusion, was similar in the 3 groups of mice. B2-/- mice were significantly more sensitive than were TK-/- mice to the vasoconstrictor effects of angiotensin II and norepinephrine. Finally, renin mRNA levels were significantly greater in B2-/- mice and smaller in TK-/- mice compared with WT mice. Taken together, these results indicate that under basal conditions, the kinin B2 receptor is not an important determinant of blood pressure in mice but is involved in the control of regional vascular tone in the coronaries and the kidneys. The phenotypic differences observed between TK-/- and B2-/- mice could be underlain by tissue kallikrein kinin-independent effect and/or kinin B1 receptor activation.

Angiotensin II↗