Skip to main content

PTCA acutely expands perfused myocardial mass and increases flow homogeneity

  • Chapter
Myocardial Ischemia and Preconditioning

Summary

In absence of collaterals, coronary stenosis produces a pressure drop in the microcirculation which might compromise capillary pressure and physiological blood—tissue exchanges. The present study tests the hypothesis that a derecruitment of vascular units occurs in the post-stenosis territory to maintain capillary pressure constant and that the restoration of a normal distal coronary pressure by PTCA is able to recruit additional myocardium to perfusion. Nine patients with single left coronary vessel disease, no previous myocardial infarct and normal ventricular function, were studied in a single session, before and after successful PTCA and stenting. Flow entering the stenotic vessel (CBF = ml/min, by Doppler catheter and quantitative angiography), and flow per gram of myocardium downstream the stenosis (MBF = ml/min/g of tissue, by the analysis of radioactive Xenon wash-out curves) were simultaneously measured. Perfused tissue was calculated as CBF/MBF and heterogeneity of flow distribution as the ratio between high and low flow sub-compartments estimated by bi-exponential analysis of Xenon curves. Distal coronary pressure was assessed by pressure wire. Heterogeneity of perfusion was also assessed in the remote region perfused by the angio-graphically normal left coronary branch. Distal coronary pressure during balloon occlusion was 21 ± 10 mmHg. PTCA increased CBF following i.e. adenosine from 19.8 ± 16.1 to 48 ± 27 ml/min, coronary flow reserve from 1.5 ± 0.2 to 2.3 ± 0.8 (p < 0.01) and distal coronary pressure from 68 ± 9 to 99 ± 8 at rest, and from 54 ± 10 to 99 ± 10 mmHg during adenosine. Perfused myocardial volume at rest increased from 27 ± 21 to 39 ± 8 g. A strict correlation was found between the increase in distal coronary pressure and the increase in perfused volume after PTCA (r = 0.79, p < 0.001). Flow homogeneity significantly increased following PTCA to the level of the remote region. In conclusion severe coronary stenosis contracts the amount of normally perfused myocardium likely to preserve capillary pressure and flow reserve in the residual perfused vascular units. PTCA expands perfused volume and decreases flow heterogeneity, according to the increase in distal coronary pressure.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 169.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 219.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 219.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Gould KL, Lipscomb K, Calvert C. 1975. Compensatory changes of the distal coronary vascular bed during progressive coronary vasoconstriction. Circulation 51:1085–1094.

    Article  PubMed  CAS  Google Scholar 

  2. Gould KL. 1978. Pressure-flow characteristics of coronary stenoses in unsedated dogs at rest and during coronary vasodilation. Circ Res 43:242–253.

    Article  PubMed  CAS  Google Scholar 

  3. Landis EM, Pappenheimer JR. Exchange of substances through capillary walls. In: Handbook of Physiology, Hamilton WF, Dow P eds, vol II, section 2 Circulation. American Physiological Society Bethesda MD 1927, Chapter 29, pp. 961–1034.

    Google Scholar 

  4. Austin RE, Aldea GS, Coggins DL, Flynn AE, Hoffman JIE. 1990. Profound spatial heterogeneity of coronary reserve. Circ Res 67:319–331.

    Article  PubMed  Google Scholar 

  5. Steenbergen C, Deleeuw G, Barlow C, Chance B, Williamson JR. 1977. Heterogeneity of the hypoxic state in perfused rat heart. Circ Res 41:606–615.

    Article  PubMed  CAS  Google Scholar 

  6. Miyazaki K, Hori S, Inoue S, Adachi T, Bessho M, Kuwahira I, Mori H, Nakazawa H, Aikawa N, Ogawa S. 1997. Characterization of energy metabolism and blood flow distribution in myocardial ischemia in hemorrhagic shock. Am J Physiol 273:H600–H607.

    PubMed  CAS  Google Scholar 

  7. Sambuceti G, Marzilli M, Mari A, Marini C, Marzullo P, Testa R, Raugei I, Papini M, Schluter M, L’Abbate A. 2000. Clinical evidence for myocardial derecruitment downstream from severe stenosis: pressure-flow control interaction. Am J Physiol 279:H2641–H2648.

    CAS  Google Scholar 

  8. L’Abbate A, Maseri A, Ballestra AM, Michelassi C, Marzilli M, Cemici P, Trivelle MG. 1981. Stochastic and exponential analysis of precardial washout curves for myocardial blood flow measurement. Experimental evoluation. Circ Res 49(1):41–51.

    Article  PubMed  Google Scholar 

  9. Zierler K. 1965. Equations for measuring blood flow by external monitoring of radioisotopes. Circ Res 16:309–321.

    Article  PubMed  CAS  Google Scholar 

  10. L’Abbate A, Marzilli M, Ballestra AM, Camici P, Trivella MG, Pelosi G, Klassen GA. 1980. Opposite transmural gradients of coronary resistance and extravascular pressure in the working dog’s heart. Cardiovasc Res 14:21–29.

    Article  PubMed  Google Scholar 

  11. Kuo L, Davis MJ, Chilian WM. 1995. Longitudinal gradients for endothelium-dependent and independent vascular responses in coronary microcirculation. Circulation 92:518–525.

    Article  PubMed  CAS  Google Scholar 

  12. Klocke FJ. 1976. Coronary blood flow in man. Prog Cardiovasc Dis 19:117–166.

    Article  PubMed  CAS  Google Scholar 

  13. Gerber BL, Melin JA, Bol A, Labar D, Cogneau M, Michel C, Vanoverschelde JL. 1998. Nitrogen-13-ammonia and oxygen-15-water estimates of absolute myocardial perfusion in left ventricular ischemic dysfunction. J Nucl Med 39:1655–1662.

    PubMed  CAS  Google Scholar 

  14. Marinho NV, Keogh BE, Costa DC, Lammerstma AA, Ell PJ, Camici PG. 1996. Pathophysiology of chronic left ventricular dysfunction. New insights from the measurement of absolute myocardial blood flow and glucose utilization. Circulation 93:737–744.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Gianmario Sambuceti MD .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2003 Springer Science+Business Media New York

About this chapter

Cite this chapter

Sambuceti, G. et al. (2003). PTCA acutely expands perfused myocardial mass and increases flow homogeneity. In: Dhalla, N.S., Takeda, N., Singh, M., Lukas, A. (eds) Myocardial Ischemia and Preconditioning. Progress in Experimental Cardiology, vol 6. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0355-2_1

Download citation

  • DOI: https://doi.org/10.1007/978-1-4615-0355-2_1

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-5036-1

  • Online ISBN: 978-1-4615-0355-2

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics