Skip to main content
NCBI home page
British Heart Journal logoLink to British Heart Journal
. 1989 Mar;61(3):248–257. doi: 10.1136/hrt.61.3.248

Left ventricular filling and early diastolic function at rest and during angina in patients with coronary artery disease.

J R Dawson 1, D G Gibson 1
PMCID: PMC1216653  PMID: 2930663

Abstract

Left ventricular diastolic function was studied in 11 patients with coronary artery disease. Single plane ventriculography (30 degrees right anterior oblique projection) was performed at rest and during an episode of angina immediately after a period of rapid atrial pacing. Left ventricular pressure was recorded simultaneously by a micromanometer tipped catheter. The ventriculograms were digitised frame by frame to derive continuous plots of left ventricular shape, volume, and rate of change of volume. The time constant (tau) of the fall in left ventricular pressure was determined from the exponential portion of pressure decay during isovolumic relaxation. Ventricular pressure-volume loops were constructed to study the left ventricular diastolic pressure-volume relation. The time of minimum left ventricular pressure was used to divide diastole into an early phase and a late phase. Angina was associated with an increase in end systolic volume and a fall in ejection fraction with no significant change in end diastolic volume. Peak left ventricular pressure was unchanged but left ventricular minimum and end diastolic pressures were both increased and the diastolic pressure-volume relation was moved upwards. The time constant of left ventricular pressure fall was prolonged. At rest more than 50% of the stroke volume entered the left ventricle during the period of early diastole. This proportion was significantly reduced during angina and as a consequence a significantly greater proportion of the stroke volume entered the ventricle during late diastole. Despite this, and although the left ventricular diastolic pressure-volume relation was moved upwards with angina, the mean slope of the relation during late diastole--that is, chamber stiffness--was not significantly altered. The upward shift of the left ventricular diastolic pressure-volume relation seen during angina is thus already apparent in early diastole, and its extent does not change during the later phase of diastole, which alone shows the property of passive stiffness. A primary increase in the passive stiffness of the ventricle cannot therefore be the cause of the upward shift of the diastolic pressure-volume relation, and events occurring in early diastole have to be looked to for an explanation. The study findings show that left ventricular function in early diastole is profoundly disturbed during angina pectoris and it is suggested that loss of elastic recoil and dissipation of this restoring force by asynchronous onset of relaxation and abnormal changes in shape are important factors contributing to this disturbance of function.

Full text

PDF
248

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Alderman E. L., Glantz S. A. Acute hemodynamic interventions shift the diastolic pressure-volume curve in man. Circulation. 1976 Oct;54(4):662–671. doi: 10.1161/01.cir.54.4.662. [DOI] [PubMed] [Google Scholar]
  2. Bourdillon P. D., Lorell B. H., Mirsky I., Paulus W. J., Wynne J., Grossman W. Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man. Circulation. 1983 Feb;67(2):316–323. doi: 10.1161/01.cir.67.2.316. [DOI] [PubMed] [Google Scholar]
  3. Brutsaert D. L., Rademakers F. E., Sys S. U. Triple control of relaxation: implications in cardiac disease. Circulation. 1984 Jan;69(1):190–196. doi: 10.1161/01.cir.69.1.190. [DOI] [PubMed] [Google Scholar]
  4. Caillet D., Crozatier B. Role of myocardial restoring forces in the determination of early diastolic peak velocity of fibre lengthening in the conscious dog. Cardiovasc Res. 1982 Feb;16(2):107–112. doi: 10.1093/cvr/16.2.107. [DOI] [PubMed] [Google Scholar]
  5. Carroll J. D., Hess O. M., Hirzel H. O., Krayenbuehl H. P. Exercise-induced ischemia: the influence of altered relaxation on early diastolic pressures. Circulation. 1983 Mar;67(3):521–528. doi: 10.1161/01.cir.67.3.521. [DOI] [PubMed] [Google Scholar]
  6. Chaitman B. R., Bristow J. D., Rahimtoola S. H. Left ventricular wall motion assessed by using fixed external reference systems. Circulation. 1973 Nov;48(5):1043–1054. doi: 10.1161/01.cir.48.5.1043. [DOI] [PubMed] [Google Scholar]
  7. Dawson J. R., Gibson D. G. Regional left ventricular wall motion in pacing induced angina. Br Heart J. 1988 Mar;59(3):309–318. doi: 10.1136/hrt.59.3.309. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Dodge H. T., Sandler H., Baxley W. A., Hawley R. R. Usefulness and limitations of radiographic methods for determining left ventricular volume. Am J Cardiol. 1966 Jul;18(1):10–24. doi: 10.1016/0002-9149(66)90191-3. [DOI] [PubMed] [Google Scholar]
  9. Fioretti P., Brower R. W., Meester G. T., Serruys P. W. Interaction of left ventricular relaxation and filling during early diastole in human subjects. Am J Cardiol. 1980 Aug;46(2):197–203. doi: 10.1016/0002-9149(80)90058-2. [DOI] [PubMed] [Google Scholar]
  10. Gibson D. G., Brown D. J. Continuous assessment of left ventricular shape in man. Br Heart J. 1975 Sep;37(9):904–910. doi: 10.1136/hrt.37.9.904. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Gibson D. G., Brown D. J. Relation between diastolic left ventricular wall stress and strain in man. Br Heart J. 1974 Nov;36(11):1066–1077. doi: 10.1136/hrt.36.11.1066. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Gibson D. G., Prewitt T. A., Brown D. J. Analysis of left ventricular wall movement during isovolumic relaxation and its relation to coronary artery disease. Br Heart J. 1976 Oct;38(10):1010–1019. doi: 10.1136/hrt.38.10.1010. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Glantz S. A., Parmley W. W. Factors which affect the diastolic pressure-volume curve. Circ Res. 1978 Feb;42(2):171–180. doi: 10.1161/01.res.42.2.171. [DOI] [PubMed] [Google Scholar]
  14. Greenbaum R. A., Ho S. Y., Gibson D. G., Becker A. E., Anderson R. H. Left ventricular fibre architecture in man. Br Heart J. 1981 Mar;45(3):248–263. doi: 10.1136/hrt.45.3.248. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Grossman W., Barry W. H. Diastolic pressure-volume relations in the diseased heart. Fed Proc. 1980 Feb;39(2):148–155. [PubMed] [Google Scholar]
  16. Ishida Y., Meisner J. S., Tsujioka K., Gallo J. I., Yoran C., Frater R. W., Yellin E. L. Left ventricular filling dynamics: influence of left ventricular relaxation and left atrial pressure. Circulation. 1986 Jul;74(1):187–196. doi: 10.1161/01.cir.74.1.187. [DOI] [PubMed] [Google Scholar]
  17. Kumada T., Karliner J. S., Pouleur H., Gallagher K. P., Shirato K., Ross J., Jr Effects of coronary occlusion on early ventricular diastolic events in conscious dogs. Am J Physiol. 1979 Nov;237(5):H542–H549. doi: 10.1152/ajpheart.1979.237.5.H542. [DOI] [PubMed] [Google Scholar]
  18. Mann T., Goldberg S., Mudge G. H., Jr, Grossman W. Factors contributing to altered left ventricular diastolic properties during angina pectoris. Circulation. 1979 Jan;59(1):14–20. doi: 10.1161/01.cir.59.1.14. [DOI] [PubMed] [Google Scholar]
  19. Mattheos M., Shapiro E., Oldershaw P. J., Sacchetti R., Gibson D. G. Non-invasive assessment of changes in left ventricular relaxation by combined phono-, echo-, and mechanocardiography. Br Heart J. 1982 Mar;47(3):253–260. doi: 10.1136/hrt.47.3.253. [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Rackley C. E. Quantitative evaluation of left ventricular function by radiographic techniques. Circulation. 1976 Dec;54(6):862–879. doi: 10.1161/01.cir.54.6.862. [DOI] [PubMed] [Google Scholar]
  21. Rickards A. F., Seabra-Gomes R. Observations on the effect of angina on the left ventricle, with special reference to diastolic behavior. Eur J Cardiol. 1978 Jun;7 (Suppl):213–238. [PubMed] [Google Scholar]
  22. SALISBURY P. F., CROSS C. E., RIEBEN P. A. Influence of coronary artery pressure upon myocardial elasticity. Circ Res. 1960 Jul;8:794–800. doi: 10.1161/01.res.8.4.794. [DOI] [PubMed] [Google Scholar]
  23. Sallin E. A. Fiber orientation and ejection fraction in the human left ventricle. Biophys J. 1969 Jul;9(7):954–964. doi: 10.1016/S0006-3495(69)86429-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Sonnenblick E. H. The structural basis and importance of restoring forces and elastic recoil for the filling of the heart. Eur Heart J. 1980;Suppl A:107–110. doi: 10.1093/eurheartj/1.suppl_1.107. [DOI] [PubMed] [Google Scholar]
  25. Waters D. D., Da Luz P., Wyatt H. L., Swan H. J., Forrester J. S. Early changes in regional and global left ventricular function induced by graded reductions in regional coronary perfusion. Am J Cardiol. 1977 Apr;39(4):537–543. doi: 10.1016/s0002-9149(77)80163-x. [DOI] [PubMed] [Google Scholar]
  26. Weisfeldt M. L., Armstrong P., Scully H. E., Sanders C. A., Daggett W. M. Incomplete relaxation between beats after myocardial hypoxia and ischemia. J Clin Invest. 1974 Jun;53(6):1626–1636. doi: 10.1172/JCI107713. [DOI] [PMC free article] [PubMed] [Google Scholar]
  27. Weiss J. L., Frederiksen J. W., Weisfeldt M. L. Hemodynamic determinants of the time-course of fall in canine left ventricular pressure. J Clin Invest. 1976 Sep;58(3):751–760. doi: 10.1172/JCI108522. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from British Heart Journal are provided here courtesy of BMJ Publishing Group

RESOURCES