| Adverse influence of systemic vascular stiffening on cardiac dysfunction and adaptation to acute coronary occlusion. | |
| | |
MedLine Citation:
|
PMID: 8608622 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
BACKGROUND: [corrected] Age is an independent risk factor for increased mortality from ischemic heart disease. Arterial stiffening with widening of the pulse pressure may contribute to this risk by exacerbating cardiac dysfunction after total coronary artery occlusion. METHODS AND RESULTS: To test the above hypothesis, 14 open-chest dogs underwent surgery in which the intrathoracic aorta was bypassed with a stiff plastic tube. Directing ventricular outflow through the bypass widened the arterial pulse pressure from 41 to 115 mm Hg at similar mean pressure and flow. Hearts ejecting into the native aorta (NA) exhibited only modest dysfunction after two minutes of mid-left anterior descending coronary artery occlusion. However, the same occlusion applied during ejection into the bypass tube (BT) induced far more severe cardiodepression (ie, systolic pressure fell by -41+/-10 mm Hg for BT versus -15+/-3 mm Hg for NA, and end-systolic volume rose by 15+/-3 versus 6+/-2 mL), with a threefold greater decline in ejection fraction. This disparity was not due to higher baseline work loads because total pressure-volume area was similar in both cases. Furthermore, marked increases in basal work load and wall stress induced by angiotensin II infusion (in four additional studies) did not reproduce this behavior. Although peak systolic chamber stress was greater with the BT, this did not increase systolic dyskinesis as measured in the central ischemic zone. However, the total mass of myocardium that was rendered severely ischemic (ie, flow reduced by > or = 80%) was twice as large with BT ejection, likely expanding the region of dyskinesis. This disparity may relate to altered phasic coronary flow during BT ejection, which displays marked enhancement of systolic flow and renders the heart more vulnerable to diminished mean and systolic perfusion pressures. CONCLUSIONS: Cardiac ejection into a stiff systemic vasculature augments cardiac dysfunction and ischemia due to coronary occlusion by tightening the link between cardiac systolic performance and myocardial perfusion. This may contribute to the higher mortality risk from ischemic heart disease due to age. |
| | |
Authors:
|
D A Kass; A Saeki; R S Tunin; F A Recchia |
Publication Detail:
|
Type: Journal Article |
Journal Detail:
|
Title: Circulation Volume: 93 ISSN: 0009-7322 ISO Abbreviation: Circulation Publication Date: 1996 Apr |
Date Detail:
|
Created Date: 1996-05-30 Completed Date: 1996-05-30 Revised Date: 2008-07-11 |
Medline Journal Info:
|
Nlm Unique ID: 0147763 Medline TA: Circulation Country: UNITED STATES |
Other Details:
|
Languages: eng Pagination: 1533-41 Citation Subset: AIM; IM |
Affiliation:
|
Division of Cardiology, Department of Internal Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland, 21287, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Acute Disease Angiotensin II / pharmacology Animals Blood Vessels / physiology* Cardiac Output Compliance Coronary Circulation / drug effects Disease Models, Animal Dogs Female Hemodynamics / drug effects Hypertension / physiopathology Male Myocardial Infarction / physiopathology Myocardial Ischemia / physiopathology* Vascular Resistance* |
| Chemical | |
Reg. No./Substance:
|
11128-99-7/Angiotensin II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Fundamental relations between short-term RR interval and arterial pressure oscillations in humans.
Next Document: Neointimal thickening after severe coronary artery injury is limited by a short-term administration ...