Left ventricular end-systolic wall stress during antihypertensive treatment

Czech version

Authors: J. Bulas ¹; J. Murín ¹; I. Janiga ²; K. Kozlíková ³
Authors‘ workplace: I. interná klinika Lekárskej fakulty UK a UN Bratislava, Slovenská republika, prednostka doc. MUDr. Soňa Kiňová, PhD. ¹; Slovenská technická univerzita Bratislava, Slovenská republika, dekan prof. Ing. Ľubomír Šóoš, PhD. ²; Ústav lekárskej fyziky, biofyziky, informatiky a telemedicíny Lekárskej fakulty UK Bratislava, Slovenská republika, prednostka prof. MUDr. Elena Kukurová, CSc. ³
Published in: Vnitř Lék 2011; 57(3): 243-247
Category: 60th birthday of prof. Mudr. Jiřího Vítovce, CSc, FESC

Overview

Introduction:
The mechanical load of left the ventricular wall by blood pressure generated during systole causes a strain associated with the impedance to ventricular emptying. Among several indices, the circumferential systolic wall stress is used to describe this load. The calculated stress depends on systolic blood pressure, wall thickness and ventricular cavity dimension. Methods enabling non-invasive quantification of those indices are based on echocardiographic examinations and blood pressure measurements. Left ventricular hypertrophy in hypertension is considered as a compensatory mechanism allowing the heart to withstand the hemodynamic strain associated with increased arterial pressure.

Subjects and methods:
In the group of 25 female patients with treated arterial hypertension with suboptimal blood pressure levels in the initial evaluation, we realized echocardiographic examination and calculated left ventricular mean circumferential systolic wall stress. The re-evaluation was done after achieving the target blood pressure levels (below 140/90 mm Hg) in the time interval of 6 month to 2 years.

Results:
The statistically significant decrease of systolic wall stress was mainly due to lowering of blood pressure. The next favourable factor was diminishing of the left ventricular end-diastolic diameter, though the difference was not statically significant. By the multiple regression analysis we found that the final significant lowering of systolic wall stress was influenced also by favourable geometrical remodelling of the left ventricle by the tendency of diminishing of left ventricular diastolic diameter and the increase of relative wall thickness.

Conclusion:
We considered repeated echocardiographic examination and the systolic wall stress calculation (which integrates the ventricular geometry with the blood pressure values achieved) as an appropriate parameter for evaluation of the effect of antihypertensive therapy in the long-term management of hypertensive patients.

Key words:
systolic wall stress – arterial hypertension – echocardiography

Sources

1. Kaplan NM. Kaplan’s Clinical Hypertension. 8th ed. Philadelphia: Lippincott Williams and Wilkins 2002.

2. Devereux RB, Alderman MH. Role of Preclinical Cardiovascular Disease in the Evolution From Risk Factor Exposure to Development of Morbid Events. Circulation 1993; 88: 1444–1455.

3. Mancia G, Backer G, Domincziak A et al. 2007 Guidelines for the Management of Arterial Hypertension. The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2007; 25: 1105–1187.

4. Berk BG, Fujiwara K, Lehgoux S. ECM remodeling in hypertensive heart disease. J Clin Invest 2007; 117: 568–575.

5. Ganau A, Devereux RB, Roman MJ et al. Patterns of left ventricular hypertrophy and remodeling in essential hypertension. J Am Coll Cardiol 1992; 19: 1550–1558.

6. Prisant M. Hypertensive heart disease. J Clin Hypertens 2005; 7: 231–238.

7. Rysä J, Aro J, Ruskoaho H. Early left ventricular gene expression profile in response to increase in blood pressure. Blood Press 2006; 15: 375–383.

8. Sugishita Y, Iida K, Ohtsuka O et al. Ventricular Wall stress revisted. A keystone of Cardiology. Jpn Hear J 1994; 35: 577–587.

9. Hurlburt HM, Aurigema GP, Hill JC et al. Direct ultrasound measurement of longitudinal, circumferential and radial strain using 2-dimensional strain imaging in normal adults. Echocardiography 2007; 24: 723–731.

10. Blake J, Devereux RB, Herrold EM et al. Relation of concentric left ventricular Hypertrophy and extracardiac target organ damage to supranormal left ventricular performance in estabilished hypertension. Am J Cardiol 1988; 62: 246–252.

11. Lee R, Kamm RD. Vascular mechanics for the cardiologist. JACC 1994; 23: 1289–1295.

12. White E. Mechanosensitive channels: Therapeutic targets in the myocardium? Curr Pharmacol Design 2006; 12: 3645–3663.

13. Celentano A, Pietropaolo I, Plamieri Vet al. Inappropriate left ventricular mass and angiotensin converting enzyme gene polymorphism. J Human Hypertens 2001; 15: 811–813.

14. Devereux RB, Alonso RD, Lutas EM et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy finding. Am J Cardiol 1986; 57: 450–458.

15. Quinones M, Mokotoff DM, Nouri S et al. Noninvasive quantification of left ventricular wall stress. Validation of method and application to assessment of chronic pressure overload. Am J Cardiol 1980; 45: 782–790.

16. Statgraphics® PLUS, version 3 for Windows. User manual. Rockville: Manugistics, Inc., 1997. 738 p.

17. Schmieder RE, Messerli F, Sturgill D et al. Cardiac performance after reduction of myocardial hypertrophy. Am J Med 1989; 87: 22–27.

18. Opie HL, Commerford PJ, Gersh BJ et al. Controversies in ventricular remodelling. Lancet 2006; 367: 356–367.

19. Niederle P, Cífková R, Widimský J et al. Echokardiografické sledování regrese zbytnění srdeční svaloviny během účinné a dlouhodobé antihypertenzní léčby. Vnitř Lék 1985; 31: 1050–1057.

20. Perlini S, Muiesan ML, Cuspidi C et al. Midwall mechanics are improved after regression of hypertensive left ventricular hypertrophy and normalization of chamber geometry. Circulation 2001; 103: 678–683.

21. Moyssakis I, Moschos N, Triposkiadis F et al. Left ventricular end-systolic stress/diameter relation as a contractility index and as a predictor of survival. Independence of preload after normalisation for end-diastolic diameter. Heart Vessels 2005; 20: 191–198.

22. de Gregorio C, Micari A, Di Bella G et al. Systolic wall stress may affect the intramural coronary blood flow velocity in myocardial hypertrophy, independently on the left ventricular mass. Echocardiography 2006; 22: 642–648.

23. Schussheim A, Diamond J, Philips RA. Left ventricular midwall function improves with antihypertensive therapy and regression of left ventricular hypertrophy in patients with asymptomatic hypertension. Amer J Cardiol 2001; 87: 61–65.

24. Diamond JA, Phillips RA. Hypertensive heart disease. Hypertens Res 2005; 28: 191–202.