Skip to main content
NCBI home page
Heart logoLink to Heart
. 2001 Feb;85(2):208–212. doi: 10.1136/heart.85.2.208

Effects of coronary revascularisation on myocardial blood flow and coronary vasodilator reserve in hibernating myocardium

D Pagano 1, F Fath-Ordoubadi 1, K Beatt 1, J Townend 1, R Bonser 1, P Camici 1
PMCID: PMC1729621  PMID: 11156674

Abstract

OBJECTIVE—Previous studies have suggested that resting myocardial blood flow is within normal limits in most chronically dysfunctional left ventricular segments which improve function after coronary artery revascularisation (hibernating myocardium). The aim of this study was to assess myocardial blood flow and coronary vasodilator reserve in hibernating myocardium before and after coronary revascularisation.
PATIENTS AND METHODS— 30 patients with multivessel coronary disease undergoing coronary revascularisation (21 patients with bypass grafting and nine with coronary angioplasty), and 21 age and sex matched healthy volunteers (controls). Myocardial blood flow (MBF, ml/min/g) was measured by positron emission tomography using oxygen-15 water at rest and after dipyridamole (MBFdip, 0.56 mg/kg in four minutes). Coronary vasodilator reserve was calculated as MBFdip/MBF. Regional wall motion was assessed with echocardiography.
RESULTS—Before revascularisation there were 48 remote and 275 dysfunctional myocardial segments, of which 163 (59%) improved function after revascularisation (hibernating). In hibernating segments coronary vasodilator reserve before revascularisation was significantly lower than in remote segments (1.97 (0.7), p < 0.0001) and controls (3.2 (1.5), p < 0.0001). In hibernating segments, myocardial blood flow remained unchanged after revascularisation (0.94 (0.3) v 0.95 (0.3) ml/min/g, p = 0.3) while coronary vasodilator reserve increased (1.47 (0.7) v 1.98 (1.0), p < 0.0001). Myocardial blood flow was similar in remote, hibernating segments before and after revascularisation and in controls.
CONCLUSIONS—This study confirms that myocardial blood flow at rest in hibernating myocardium is within normal limits in most segments, and that hibernating myocardium is characterised by an impaired coronary vasodilator reserve which improves significantly after coronary revascularisation.


Keywords: hibernating myocardium; myocardial blood flow; heart failure; positron emission tomography

Full Text

The Full Text of this article is available as a PDF (134.8 KB).

Figure 1  .

Figure 1  

Open in a new tab

Perfusion data on 163 hibernating myocardial segments before (baseline) and after coronary revascularisation. MBF, myocardial blood flow; MBFdip, post-dipyridamole myocardial blood flow; CVR, coronary vasodilator reserve.***p < 0.0001. 

Figure 2  .

Figure 2  

Open in a new tab

Comparison of myocardial blood flow between hibernating, remote (before and after revascularisation), and control myocardial segments. HIB, hibernation segments before revascularisation; REM, remote segments; -post refers to post-revascularisation.

Figure 3  .

Figure 3  

Open in a new tab

Scatterplot showing the distribution of myocardial blood flow (uncorrected and corrected for the rate-pressure product) before revascularisation in the hibernating segments. The thresholds of 0.55 and 0.45 ml/min/g represent the mean value minus 2 SDs of myocardial blood flow in control segments (uncorrected and corrected for the rate-pressure product). MBF, myocardial blood flow uncorrected for the rate-pressure product; MBFcorr, myocardial blood flow corrected for the rate-pressure product.

Figure 4  .

Figure 4  

Open in a new tab

Comparison of post-dipyridamole myocardial blood flow between hibernating, remote (before and after revascularisation), and control myocardial segments. See fig 2 for key to abbreviations.

Figure 5  .

Figure 5  

Open in a new tab

Comparison of coronary vasodilator reserve between hibernating, remote (before and after revascularisation), and control myocardial segments. See fig 2 for key to abbreviations. ***p < 0.0001. 

Selected References

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

  1. Ambrosio G., Betocchi S., Pace L., Losi M. A., Perrone-Filardi P., Soricelli A., Piscione F., Taube J., Squame F., Salvatore M. Prolonged impairment of regional contractile function after resolution of exercise-induced angina. Evidence of myocardial stunning in patients with coronary artery disease. Circulation. 1996 Nov 15;94(10):2455–2464. doi: 10.1161/01.cir.94.10.2455. [DOI] [PubMed] [Google Scholar]
  2. Bland J. M., Altman D. G. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet. 1986 Feb 8;1(8476):307–310. [PubMed] [Google Scholar]
  3. Camici P. G., Wijns W., Borgers M., De Silva R., Ferrari R., Knuuti J., Lammertsma A. A., Liedtke A. J., Paternostro G., Vatner S. F. Pathophysiological mechanisms of chronic reversible left ventricular dysfunction due to coronary artery disease (hibernating myocardium). Circulation. 1997 Nov 4;96(9):3205–3214. doi: 10.1161/01.cir.96.9.3205. [DOI] [PubMed] [Google Scholar]
  4. Czernin J., Müller P., Chan S., Brunken R. C., Porenta G., Krivokapich J., Chen K., Chan A., Phelps M. E., Schelbert H. R. Influence of age and hemodynamics on myocardial blood flow and flow reserve. Circulation. 1993 Jul;88(1):62–69. doi: 10.1161/01.cir.88.1.62. [DOI] [PubMed] [Google Scholar]
  5. Deanfield J. E., Maseri A., Selwyn A. P., Ribeiro P., Chierchia S., Krikler S., Morgan M. Myocardial ischaemia during daily life in patients with stable angina: its relation to symptoms and heart rate changes. Lancet. 1983 Oct 1;2(8353):753–758. doi: 10.1016/s0140-6736(83)92295-x. [DOI] [PubMed] [Google Scholar]
  6. Diamond G. A., Forrester J. S., deLuz P. L., Wyatt H. L., Swan H. J. Post-extrasystolic potentiation of ischemic myocardium by atrial stimulation. Am Heart J. 1978 Feb;95(2):204–209. doi: 10.1016/0002-8703(78)90464-7. [DOI] [PubMed] [Google Scholar]
  7. Gerber B. L., Vanoverschelde J. L., Bol A., Michel C., Labar D., Wijns W., Melin J. A. Myocardial blood flow, glucose uptake, and recruitment of inotropic reserve in chronic left ventricular ischemic dysfunction. Implications for the pathophysiology of chronic myocardial hibernation. Circulation. 1996 Aug 15;94(4):651–659. doi: 10.1161/01.cir.94.4.651. [DOI] [PubMed] [Google Scholar]
  8. Grandin C., Wijns W., Melin J. A., Bol A., Robert A. R., Heyndrickx G. R., Michel C., Vanoverschelde J. L. Delineation of myocardial viability with PET. J Nucl Med. 1995 Sep;36(9):1543–1552. [PubMed] [Google Scholar]
  9. Heyndrickx G. R., Millard R. W., McRitchie R. J., Maroko P. R., Vatner S. F. Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs. J Clin Invest. 1975 Oct;56(4):978–985. doi: 10.1172/JCI108178. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Hoffman J. I. Heterogeneity of myocardial blood flow. Basic Res Cardiol. 1995 Mar-Apr;90(2):103–111. doi: 10.1007/BF00789440. [DOI] [PubMed] [Google Scholar]
  11. Homans D. C., Laxson D. D., Sublett E., Lindstrom P., Bache R. J. Cumulative deterioration of myocardial function after repeated episodes of exercise-induced ischemia. Am J Physiol. 1989 May;256(5 Pt 2):H1462–H1471. doi: 10.1152/ajpheart.1989.256.5.H1462. [DOI] [PubMed] [Google Scholar]
  12. Lorenzoni R., Pagano D., Boyd H., Camici P. G. A report system for PET assessment of myocardial viability. Nucl Med Commun. 1999 Oct;20(10):895–899. doi: 10.1097/00006231-199910000-00005. [DOI] [PubMed] [Google Scholar]
  13. Marinho N. V., Keogh B. E., Costa D. C., Lammerstma A. A., Ell P. J., Camici P. G. Pathophysiology of chronic left ventricular dysfunction. New insights from the measurement of absolute myocardial blood flow and glucose utilization. Circulation. 1996 Feb 15;93(4):737–744. doi: 10.1161/01.cir.93.4.737. [DOI] [PubMed] [Google Scholar]
  14. Pagano D., Townend J. N., Parums D. V., Bonser R. S., Camici P. G. Hibernating myocardium: morphological correlates of inotropic stimulation and glucose uptake. Heart. 2000 Apr;83(4):456–461. doi: 10.1136/heart.83.4.456. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Rahimtoola S. H. The hibernating myocardium. Am Heart J. 1989 Jan;117(1):211–221. doi: 10.1016/0002-8703(89)90685-6. [DOI] [PubMed] [Google Scholar]
  16. Rinaldi C. A., Masani N. D., Linka A. Z., Hall R. J. Effect of repetitive episodes of exercise induced myocardial ischaemia on left ventricular function in patients with chronic stable angina: evidence for cumulative stunning or ischaemic preconditioning? Heart. 1999 Apr;81(4):404–411. doi: 10.1136/hrt.81.4.404. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Robertson W. S., Feigenbaum H., Armstrong W. F., Dillon J. C., O'Donnell J., McHenry P. W. Exercise echocardiography: a clinically practical addition in the evaluation of coronary artery disease. J Am Coll Cardiol. 1983 Dec;2(6):1085–1091. doi: 10.1016/s0735-1097(83)80334-9. [DOI] [PubMed] [Google Scholar]
  18. Sambuceti G., Parodi O., Marcassa C., Neglia D., Salvadori P., Giorgetti A., Bellina R. C., Di Sacco S., Nista N., Marzullo P. Alteration in regulation of myocardial blood flow in one-vessel coronary artery disease determined by positron emission tomography. Am J Cardiol. 1993 Sep 1;72(7):538–543. doi: 10.1016/0002-9149(93)90348-g. [DOI] [PubMed] [Google Scholar]
  19. Schneider R. M., Weintraub W. S., Klein L. W., Seelaus P. A., Agarwal J. B., Helfant R. H. Rate of left ventricular functional recovery by radionuclide angiography after exercise in coronary artery disease. Am J Cardiol. 1986 Apr 15;57(11):927–932. doi: 10.1016/0002-9149(86)90732-0. [DOI] [PubMed] [Google Scholar]
  20. Segar D. S., Brown S. E., Sawada S. G., Ryan T., Feigenbaum H. Dobutamine stress echocardiography: correlation with coronary lesion severity as determined by quantitative angiography. J Am Coll Cardiol. 1992 May;19(6):1197–1202. doi: 10.1016/0735-1097(92)90324-g. [DOI] [PubMed] [Google Scholar]
  21. Shen Y. T., Vatner S. F. Mechanism of impaired myocardial function during progressive coronary stenosis in conscious pigs. Hibernation versus stunning? Circ Res. 1995 Mar;76(3):479–488. doi: 10.1161/01.res.76.3.479. [DOI] [PubMed] [Google Scholar]
  22. Uren N. G., Marraccini P., Gistri R., de Silva R., Camici P. G. Altered coronary vasodilator reserve and metabolism in myocardium subtended by normal arteries in patients with coronary artery disease. J Am Coll Cardiol. 1993 Sep;22(3):650–658. doi: 10.1016/0735-1097(93)90172-w. [DOI] [PubMed] [Google Scholar]
  23. Uren N. G., Melin J. A., De Bruyne B., Wijns W., Baudhuin T., Camici P. G. Relation between myocardial blood flow and the severity of coronary-artery stenosis. N Engl J Med. 1994 Jun 23;330(25):1782–1788. doi: 10.1056/NEJM199406233302503. [DOI] [PubMed] [Google Scholar]
  24. Vanoverschelde J. L., Wijns W., Depré C., Essamri B., Heyndrickx G. R., Borgers M., Bol A., Melin J. A. Mechanisms of chronic regional postischemic dysfunction in humans. New insights from the study of noninfarcted collateral-dependent myocardium. Circulation. 1993 May;87(5):1513–1523. doi: 10.1161/01.cir.87.5.1513. [DOI] [PubMed] [Google Scholar]
  25. Zaret B. L., Wackers F. J. Nuclear cardiology (2). N Engl J Med. 1993 Sep 16;329(12):855–863. doi: 10.1056/NEJM199309163291208. [DOI] [PubMed] [Google Scholar]
  26. Zeiher A. M., Drexler H., Wollschläger H., Just H. Modulation of coronary vasomotor tone in humans. Progressive endothelial dysfunction with different early stages of coronary atherosclerosis. Circulation. 1991 Feb;83(2):391–401. doi: 10.1161/01.cir.83.2.391. [DOI] [PubMed] [Google Scholar]

Articles from Heart are provided here courtesy of BMJ Publishing Group

RESOURCES