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Left Ventricular Performance in Patients with Left Ventricular Hypertrophy Caused by Systemic Arterial Hypertension

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Journal Br Heart J
Date 1977 Nov 1
PMID 145228
Citations 8
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Abstract

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.

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References
1.
Popp R, Filly K, Brown O, Harrison D . Effect of transducer placement on echocardiographic measurement of left ventricular dimensions. Am J Cardiol. 1975; 35(4):537-40. DOI: 10.1016/0002-9149(75)90837-1. View

2.
Dodek A, Burg J, Kloster F . Systolic time intervals in chronic hypertension: Alterations and response to treatment. Chest. 1975; 68(1):51-5. DOI: 10.1378/chest.68.1.51. View

3.
Hirshleifer J, Crawford M, ORourke R, Karliner J . Influence of acute alterations in heart rate and systemic arterial pressure on echocardiographic measures of left ventricular perfornmance in normal human subjects. Circulation. 1975; 52(5):835-41. DOI: 10.1161/01.cir.52.5.835. View

4.
Grossman W, Jones D, McLaurin L . Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest. 1975; 56(1):56-64. PMC: 436555. DOI: 10.1172/JCI108079. View

5.
Toshima H, Koga Y, Yoshioka H, Akiyoshi T, Kimura N . Echocardiographic classification of hypertensive heart disease. A correlative study with clinical features. Jpn Heart J. 1975; 16(4):377-93. DOI: 10.1536/ihj.16.377. View