Document Detail


Relation of left ventricular longitudinal and circumferential shortening to ejection fraction in the presence or in the absence of mild hypertension.
MedLine Citation:
PMID:  9321749     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: To study left ventricular longitudinal shortening in arterial hypertension and the relative contribution of longitudinal and circumferential fiber shortening to ventricular ejection. METHODS: Two-dimensional and M-mode echocardiograms were obtained for 50 normotensive subjects (aged 49 +/- 12 years) and 50 never-treated mild hypertensive patients (aged 49 +/- 11 years), to measure the minor-axis endocardial and midwall shortening, long-axis shortening and ejection fraction. RESULTS: The midwall shortening was lower in hypertensive than it was in normotensive subjects (P < 0.001) and was related inversely to the circumferential wall stress for both groups (P < 0.04 and 0.0001, respectively). The long-axis shortening in hypertensive patients (22.2 +/- 4.2%) and in normotensives (23.6 +/- 5.4%) was not statistically different, and was not related either to the meridional or to the circumferential wall stress. The ejection fraction was also similar for the two groups (68.2 +/- 6.3 versus 68.6 +/- 5.6%). Both for normotensive and for hypertensive subjects, the ejection fraction was influenced mainly by the midwall shortening (61 and 40% of the variance for normal and hypertensive individuals, respectively), with a minor contribution from the long-axis shortening, which was 7% for normotensive subjects and 18% for hypertensive patients, a statistically significant difference (P < 0.001). The combined effect of midwall and longitudinal shortenings on the ejection fraction was regulated by the relative wall thickness, and was maximal for hypertensive patients with an ejection fraction greater than that predicted by the midwall shortening. CONCLUSIONS: Left ventricular ejection is produced principally by circumferential shortening and is related independently to the relative wall thickness. In the presence of arterial hypertension and an altered cardiac load, longitudinal shortening becomes an important mechanism by which to augment ejection, thereby offsetting the reduction in midwall shortening.
Authors:
G de Simone; A Ganau; M J Roman; R B Devereux
Related Documents :
3359589 - Efficiency of energy transfer from pressure-volume area to external mechanical work inc...
16644429 - Effects of radial left ventricular dyssynchrony on cardiac performance using quantitati...
123419 - Dimensional analysis of the left ventricle: effects of acute aortic regurgitation.
3202369 - The effects of controlled oxygen therapy on ventricular function in patients with stabl...
3893739 - Modeling the isovolumic relaxation period.
6831669 - Influence of atrial systole on the frank-starling relation and the end-diastolic pressu...
7508029 - Volume expansion in renal failure patients: a paradigm for a clinically relevant [na,k]...
17324369 - Cerebrovascular disease and the pathophysiology of obstructive sleep apnea.
3983909 - Fibrin degradation products increase lung transvascular fluid filtration after thrombin...
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of hypertension     Volume:  15     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  1997 Sep 
Date Detail:
Created Date:  1998-01-13     Completed Date:  1998-01-13     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1011-7     Citation Subset:  IM    
Affiliation:
Division of Cardiology, New York Hospital-Cornell Medical Center, New York, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adult
Echocardiography
Female
Heart Ventricles / physiopathology*
Humans
Hypertension / physiopathology*
Male
Middle Aged
Stroke Volume*
Ventricular Dysfunction, Left / physiopathology*
Ventricular Function
Ventricular Function, Left / physiology*
Grant Support
ID/Acronym/Agency:
HL-18323/HL/NHLBI NIH HHS; HL-41654/HL/NHLBI NIH HHS

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Angiotensin receptor antagonism and angiotensin converting enzyme inhibition improve diastolic dysfu...
Next Document:  Effects of angiotensin II on myocardial contractility during short-term pressor responses to angiote...