Journal List > J Korean Soc Echocardiogr > v.2(1) > 1075183

Son, Lee, Kang, Choue, Kim, Kim, Song, and Bae: Assessment of Left Ventricular Mass and Diastolic Function in Patients with Essential Hypertension after One Year Antihypertensive Therapy

Abstract

Background

Left ventriculuar hypertrophy(LVH) detected by echocadiography has long been recognized as a consequence of hypertension as well as independent predictor of subsequent cardiovascular morbidity and mortality. Numerous studies have shown left ventricular hypertrophy regression in response to antihypertensive drug therapy. The advent of echocardiography has made possible the noninvasive estimation of left ventricular mass. In this study, we analysed hypertensive patients with LVH and without LVH by echocardiography to assees the changes of the left ventricular mass(LVM) and diastolic function after one year antihypertensive therapy.

Methods

Twenty patients with established hypertension were studied. No patients had a previos history of antihypertensive therapy. Patients were divided two group; patients with LVH(Group I), patients without LVH(Group II). We obtained the basal echocardiography at the diagnosis and follow-up echocardiography after 6months and 12months antihypertensive therapy with angiotensin converting enzyme inhibitor.

Results

1) Group I; Baseline blood pressure was 155/104mmHg and fell to 129/86mmHg (p<0.05) after 12 months antihypertensive therapy. There was no significant reduction in heart rate. Group II; Baseline blood pressure was 149/102mmHg and fell to 123/83mmHg (p<0.05) after 12 months antihypertensive therapy. There was no significant reduction in heart rate.
2) Group I; LVM was reduced significantly from 160g/m2 to 132g/m2 after 12months antihypertensive therapy. Group II; LVM was not significantly reduced after 12 months antihypertensive therapy.
3) Group I; Time velocity intergral dimension E(Ei) was increased from 9.1cm to 12.5cm significantly(p<0.05). and Ei/Ai was significantly increased from 1.7 to 2.1 (p<0.05) after 12 months antihypertensive therapy. Group II; There were no significantly interval changes in time velocity intergral dimension E(Ei), time velocity intergral dimension A (Ai) and Ei/Ai after 12 months antihypertensive therapy.

Conclusions

We concluded that antihypertensive therapy with ACE inhibitor reduced significantly the left ventricular mass and increased left ventricular diastolic function in hypertensive patients with LVH. We demonstrate the useful role that echocardiographic evaluation of left ventricular structure and function may play in hypertension research.

References

1). Levy D, Anderson KM, Savage D, Kannel WB, Christiansen JC, Castelli WP. Echocardiophically detected left ventricular hypertrophy. Am J Cardiol. 67:295–9. 1991.
2). Dianzumba SB, Pette DJ, Corman C, Weber E, Joyner CE. Left ventricular filling characteristics in mild untreated hypertension. Hypertension. 8(suppl 2):1156–1160. 1986.
3). Pearson AC, Labovitz AJ, Mrasek D, Willians GA, Kennedg HL. Assessment of diastolic function in normal and hypertrophies hearts: comparison of Doppler echocardiography and M-mode echocardiography. Am Heart J. 113:1417–1425. 1987.
4). Snider AR, Gidding SS, Rocchini AP. Doppler evaluation of Left ventricular diastolic filling in normal subjects. Am J Cardiol. 59:971–4. 1987.
5). Devereux RB, Alonso DR, Lutas EM. Echocardiography versus Electrocardiography in detecting left ventricular hypertrophy: comparison with postmortem mass measurements. J Am Coll Cardiol. 2:305–311. 1983.
6). Reichek N, Devereux RB. Left ventricular hypertrophy: relationship of anatomic, echocardiographic and electrocardiographic findings. Circulation. 63:1391–8. 1981.
crossref
7). Woythaler JN, Singer SL, Kwan OL, et al. Accuracy of echocardiography in detecting left ventricular hypertrophy: comparison with postmortem mass measurements. J Am Coll Cardiol. 2:305–311. 1983.
8). Hypertension Decetion And Follow-up Program Cooperative Group. Five year findings of the Hypertension detection and Follow – up Program: I. Reduction of mortality of persons with high blood pressure, including mild hypertension. JAMA. 242:2562–71. 1979.
9). Hammond IW, DEvereux RB, Alderman MH, et al. The prevalence and correlates of echocardiographic left ventricular hypertrophy among employed patients with uncomplicated hypertension. J Am Coll Cardiol. 7:639–50. 1986.
crossref
10). Savage DD, Drayer JIM, Henry WL, et al. Echocardiographic assessment of cardiac anatomy and function in hypertensive patients. Circulation. 59:623–32. 1979.
11). Devereux RB, Alonso DR, Lutas EM, Picering TG, Harshfield GA, Laragh JH. Sensitivity of echocardiography for detection of left ventricular hypertrophy. Ter Keurs HEDJ, Schipperheyn JJ, editors. Cardiac Left Ventricular Hypertrophy. The Hague: Martinus Nijhoff;p. 16–37. 1983.
crossref
12). Nakashima Y, Fouad FM, Tarazi RC. Regression of left ventricular hypertrophy from systemic hypertension by enalapril. Am J Cardiol. 53:1044–49. 1984.
crossref
13). Dunn FG, Oigman W, Ventura HO, Messerli FH, Kobrin I, Frohlich ED. Enalapril improves systematic and renal hemodynamics and allow regression of left ventricular mass in essential hypertension. Am J Cardiol. 53:105–8. 1984.
14). Mujais SK, Fouad FM, Tarazi RC. REversal ofleft ventricular hypertrophy with captopril. Clin Cardiol. 1:595–602. 1983.
15). Levy D, Anderson KM, Savage D, Kannel WB, Christiansen JC, Castelli WP. Echocardiographically detected left ventricular hypertrophy: prevalnce and risk factorsAnn Intern Med. 108:7–13. 1988.
16). The Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure. The 1988 Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Detailed recommendations for the diagnosis and Pharmacologic and non-pharmacologic treatment of systemic hypertension. Arch Intrn Med. 148:1023. 1988.
17). Sahn DJ, de Maria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: Result of a survey of echocardiographic measurements Circulation. 58:1072. 1978.
18). Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the method. Circulation. 55:613–8. 1977.
crossref
19). Levy D, Sanage DD, Garrison RJ, Anderson KM, Kannel WB, Castelli WP. Echocardiographic criteria for left ventricular hypertrophy the Framingham Heart Study. Am J Cardiol. 59:956–60. 1987.
crossref
20). Hanrath P, Mathey DG, Siegert R, Bleifeld W. Left venricular relaxation and filling pattern in different forms of left ventricular hypertrophy: An echocardiographic study. Am J Cardiol. 45:15. 1980.
21). Smith V-E, Schulman P, Karimeddini MK, White MB, Meeran MK, Katz AM. Rapid ventricullar filling in left ventricular hypertrophy. II. Pathologic hypertrophy. J Am Coll Cardiol. 5:869. 1985.
22). Inouye I, Massie B, Loge D, Topic N, Silverstein D, Simpson P, Tubau J. Abnormal left ventricular filling: An early finding in mild to moderate systemic hypertension. Am J Cardiol. 53:120. 1979.
crossref
23). Gibson DG, Traill TA, Hall RJC, Brown DJ. Echocardiographic features of secondary left ventricular hypertrophy. Br Heart J. 41:54. 1979.
crossref
24). Topol EJ, Traill TA, Fortuin NJ. Hypertensive cardiomyopathy of the elderly. N Engl J J Med. 312:227. 1985.
25). Folkow B. Cardiovascular structural adaptation: its role in the initiation and maintenance of primary hypertension. Clin sci [suppl]. 55:3–22. 1978.
crossref
26). Shkhvatsabaya IK, usubaliyer NN, Yurenev AP, Panfilow VV. The interrelation of cardiac and vascular wall hypertrophy in arterial hypertension. Cardiovasc Rev Rep. 2:1145–49. 1981.
27). Devereux RB, Savage DD, Sachs I, Laragh JH. Relation of hemodynamic load to left ventricular hypertrophy and performance in hypertension. Am J Cardiol. 51:171–76. 1983.
crossref
28). Devereux RB, Pickering TG, Alderman MH, Chien S, Borer JS, Laragh JH. Left ventricular hypertrophy in hypertension prevalance and relation to pathophysioligic variables. Hypertension. 9(suppl 2):II 53–Ii 60. 1987.
crossref
29). Narayan S, Devereux RB, Lutas EM, et al. Supernormal left ventricular function in essential hypertension: evidence of increased contractility (Abstract). J AM Coll Cardiol. 3:516. 1984.
30). Messerli Fh, Schlant RC. Left ventricular hypertrophy in essential hypertension. Am J Med(suppl 3A). 75:1–120. 1983.
31). Frohlich ED, Tarazi RC. Is arterial pressure the sole factor responsible for hypertensive cardiac hypertrophy 왔 Am J Cardiol. 44:959–62. 1979.
32). Yamori Y, Tarazi RC, Doshima A. Effect of beta-receptor blocking agents on cardiovascular structural changes in spontaneous and noradrenaline-induced hypertension in rats. Clin Sci. 59:457S–460SS. 1980.
33). Starsken NF, Simpsonj PC, Bishopric N, Coughlin SR, Lee WMF, Escabedo JA, Williams LT. Cardiac myocyte hypertrophy is associated c-myc protooncogene expression. Proc Natl Aca Sci. 83:8343–8450. 1986.
34). Robertson AL, Khairallah PH. Angiotensin II, rapid localizations in nuclei of smooth and cardiac muscle. Science. 172:1138–39. 1971.
35). Khairallah PA, Robertson AL, Darila D. Effect of angiotensin on DNA, RNA, and protein synthesis. Hypertension. Genest J, Koiw E, editors. New York: Springer-Verlag;p. 212–20. 1971.
36). Zimmerman BG, Sybertz EJ, Wong PC. Interaction btween sympathetic and renin-angiotensin system. J Hypertens. 9:722–33. 1984.
37). Reid IA, Brooks VL, Rudolph CD, Keil LC. Analysis of the actions of angiotensin on the central nervous system of conscious dogs. Am j Physiol. 243:R82–R91. 1982.
crossref
38). Ferrario CM, Gildenberg PL, McCubbin JW. Cardiovascular effect of angiotensin mediated by the central nervous system. Circ Res. 30:257–69. 1972.
39). Badder EM, Duarte B, Seaton JF, Hamaji M, Harrison TS. Angiotensin restoration of reflex adrenal medullary secretion to anephric dogs is physiologically dose-dependent. Endocrinology. 117:1920–29. 1985.
40). Osthman-Smith I. Cardiac sympathetic nerves as the final common pathway in the inductor of adaptive cardiac hypertrophy. Clin Sci. 61:265–72. 1981.
41). Laks MM, Morody F, Swan HJC. Myocardial hypertrophy produced by chronic infusion of subhypertensive doses of norepinephrine in the dog. Chest. 64:75–78. 1973.
crossref
42). Sen S, Tarazi RC, Bumpus FH. Cardiac hypertrophy in spontaneously hypertensive rats. Circ Res. 35:775–781. 1974.
crossref
43). Sen S, Tarazi RC, Bumpus FH. Cardiac hypertrophy and antihypertensive therapy. Cardiovasc. 11:427–33. 1977.
crossref
44). 최태열 • 김재필 • 강흥선 • 조정휘 • 김권삼 • 김 명식 • 송정상 • 배종화. 고혈압치료에 따른 좌심 실 질량의 퇴행에 관한 연구. 순환기. 25(6):1933.
45). Bryz RJ, William GA, Labouit AJ. Effect of aging on left ventricular diastolic filling in normal subject. Am j Cardiol. 59:971–4. 1987.
46). Smith VE, Schulman P, Karameddini MF, White WB, Meeram MK, Katz AM. Rapid ventricular filling in left ventricular hypertrophy. II. Pathologic hypertrophy. J Am Coll Cardiol. 5:869–74. 1985.
crossref
47). Hanrath P, Mathey DG, Siegert R, Bleifeld W. Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: an echocardiographic study. Am J Cardiol. 45:15–23. 1980.
crossref
48). Pearson AC, Labobitz AJ, Mrosek D, Williams GA, Kennedy HL. Assessment of diastolic function in normal and hypertrophied hearts: comparision of Doppler Echocardiography and M-mode echocardiography. Am Heart J. 113:1417–25. 1987.
49). Inouye I, Massie DG, Loge D, Topic N, Silverstein D, Simpson P, Tubau JF. Abnormal left ventricular filling: an early finding in mild to moderate systemic hypertension. Am J Cardiol. 53:120–6. 1984.
crossref
50). Sartori MP, Quinones MA, Kuo LC. Relation of Doppler derived left ventricular filling parameters to age and radius thickness ratio in normal and pathologic states. Am J Cardiol. 59:1179–82. 1987.
51). Szlachcic J, Tubau JF, O'Kelly B, Massie BM. Correlate of diastolic filling abnormalities in hypertension: A doppler rchocardiographic study. Am Heart J. 38–91:1990.
52). Grossman W, McLaurin LP. Diastoloic properties of the left ventricle. Ann Intern Med. 84:316–26. 1976.
53). Kitakabe A, Inoue M, Asao M, Tanouchi J, Masyama T, Abe H, Morita H, Senda S, Matsuo H. Transmitral blood flow reflecting diastolic behabior of the left ventricle in health and disease: A study by pulsed Doppler technique. Jpn Circ J. 46:92–102. 1982.
54). Glantz SA, Parmley WW. Factor which affect the diastolic pressure-volume curve. Circ Res. 42:171–7. 1978.
55). Peterson KL, Ricci D, Tsuji T, Sasayama S Ross J Jr. Evaluation of camber and myocadial compliance in patients with pressure overload hypertrophy. Eur J Cardiol. 7(suppl 6):195–9. 1978.
56). Pasierski T, Miskiewicz ZC, Perarson AC. Factor influencing trans-mitral flow velocity in normal and hypertensive subject. Am Heart J. 122:1101. 1991.

Table 1.
고혈압 치료전고} 후의 혈압 및 심박수의변화 (Group I)
  치료전 치료6개월 치료12개월
수축기 혈압 (mmHg) 155.4 ± 18.7 129.1 ± 15.6 138.3 ± 15.3∗∗
확장기 혈압 (mmHg) 103.9 ± 5.0 86.3 ± 7.1 90.3 ± 6.7∗∗
심박수 (회/분) 61.0 ± 19.1 64.7 ± 11.3 65.1 ± 7.0

p<0.05 vs. 치료전

∗∗ p<0.05 vs. 치료전

Table 2.
고혈압 치료 전고- 후의 혈압 및 심박수의변화 (Group II)
  치료전 치료6개월 치료12개월
수축기혈압 (mmHg) 149.0 ± 2.5 123.3 ± 10.3 131.4 ± 11.3
확장기혈압 (mmHg) 102.3 ± 6.1 83.7 ± 4.3 84.3 ± 6.9∗∗
섬박수 (회/분) 68.7 ± 4.8 72.0 ± 6.6 65.0 ± 8.0

p<0.05 vs. 치료전-

∗∗ p<0.005 vs. 치료전

Table 3.
고혈압 치료 전괴 후의 좌심실 형태학적변화 (Group I)
  치료잔 치료6개월 치료12개월
LVIDd(mm) 48.9 ± 5.3 50.3 ± 3.2 49.6 ± 4.0
LVIDs(mm) 30.5 ± 4.1 32.2 ± 3.7 30.5 ± 4.0
IVSTd(mm) 14.0 ± 1.8 11.4 ± 2.0 10.8 ± 1.1∗∗
PWTd(mm) 9.4 ± 1.4 9.1 ± 1.2 9.5 ± 1.3
LVM(g) 262.1 ± 78.5 212.5 ± 26.0 221.7 ± 36.0
LVMI(g/m2) 160.0 ± 54.1 126.7 ± 26.0 132.8 ± 18.4∗∗
EF(%) 67.2 ± 6.3 64.6 ± 7.5 67.6 ± 9.2
Vcf(%) 37.6 ± 4.7 36.2 ± 6.0 38.4 ± 6.9

LVIDs: left ventricular end-diastolic internal dimension

LVIDs: left ventricular end-systolic internal dimension

IVSTd: end-diastolic interventricular septal thickness

PWTd: end-diastolic posterior wall thickness

LVM: left ventricular wall mass

LVMI: left ventricular wall mass index

EF: ejection fraction

Vcf: meancircumferential fiber shortening

p<0.05 vs. 치료전

∗∗ p<0.05 vs. 치료전

Table 4.
고혈압 치료 전과 후의 좌심실 형태학적변화 (Group II)
  치료잔 치료6개월 치료12개월
LVIDd(mm) 53.6 ± 4.2 53.7 ± 4.3 53.4 ± 5.9
LVTDs(mm) 33.9 ± 5.4 34.9 ± 5.5 35.8 ± 6.6
IVST(mm) 9.9 ± 1.2 10.2 ± 2.2 9.5 ± 1.2
PWT(mm) 8.2 ± 0.4 7.5 ± 1.6 9.3 ± 1.4
LVM(g) 201.1 ± 27.2 187.3 ± 47.1 195.5 ± 44.4
LVMI(g/m2) 124.9 ± 22.4 118.8 ± 25.4 121.4 ± 19.7
EF(%) 66.1 ± 7.8 63.4 ± 8.9 61.7 ± 8.7
Vcf(%) 37.1 ± 6.1 35.2 ± 6.8 33.8 ± 6.2

약자는 전도표와 동일함

p<0.05 vs. 치료전.

∗∗ p<0.05 vs. 치료전

Table 5.
고혈압 치료 전 과 후의 헐역학적 변화 (Group I)
  치료전 치료6개월 치료12개월
Peak E (cm/sec) 74.5 ± 13.0 73.8 ± 13.2 80.8 ± 15.6
Peak A (cm/sec) 75.9 ± 16.0 62.4 ± 13.2s 68.5 ± 13.0
E/A 1.0 ± 0.2 1.2 ± 0.4 1.2 ± 0.3
Integral E (cm) 9.1 ± 2.4 10.8 ± 2.3 12.5 ± 2.5∗∗
Integral A (cm) 5.7 ± 1.6 5.5 ± 1.6 6.1 ± 1.6
Ei/Ai 1.7 ± 0.5 2.1 ± 0.7 2.1 ± 0.5∗∗

p<0.05 vs. 치 료전.

∗∗ p<0.05 vs. 치 료전

Table 6.
고혈압 치료 전과 후의 혈역학적 변화 (Group II)
  치료전 치료6개월 치료12개월
Peak E(cm/sec) 87.3 ± 11.0 64.0 ± 16.2 90.0 ± 20.6
Peak A(cm/sec) 72.0 ± 14.1 63.5 ± 16.2 70.0 ± 17.5
E/A 1.2 ± 0.2 1.3 ± 0.3 1.3 ± 0.4
Integral E(cm) 12.0 ± 1.3 10.8 ± 1.5 11.8 ± 2.6
Integral A (cm) 5.3 ± 1.0 5.2 ± 1.6 5.6 ± 1.1
Ei/Ai 2.3 ± 0.4 2.3 ± 0.7 2.1 ± 0.3

p<0.05 vs. 치료전.

∗∗ p<0.05 vs. 치료전

TOOLS
Similar articles