Left Ventricular Hemodynamics, Regional Blood Flow, and Lactate Metabolism During Balloon Occlusion: Can we Alter the Sequence of Ischemic Events?

  • P. W. Serruys
  • M. van den Brand
  • R. W. Brower
  • P. G. Hugenhoĺtz
Conference paper


Shortly after the introduction of percutaneous transluminal coronary angioplasty (PTCA) in 1977 [1], the indications for the procedure were viewed conservatively: disease limited to a proximal stenotic lesion in a single vessel, stable angina pectoris, and normal ventricular function. This resulted in relatively short episodes of occlusion during the procedure in relatively healthy hearts. Today, after 5 years of experience with PTCA, these indications have been extended to include distal stenotic lesions in up to three vessels requiring multiple dilatations. Patients with unstable angina and impaired ventricular function have been included. Furthermore, PTCA is performed in stenotic bypass grafts and for residual stenosis after fibrinolytic recanalization during acute or impending myocardial infarction. As a result, the total duration of occlusive episodes during PTCA has increased (Fig. 1): the median is now 4 min and a few cases exceed 10 min in our laboratory.


Lactate Measurement Great Cardiac Vein Coronary Sinus Blood Flow Coronary Sinus Flow Impaired Ventricular Function 
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  1. [1]
    Grlintzig AR (1978) Transluminal dilatation of coronary artery stenosis. Lancet 1: 263CrossRefGoogle Scholar
  2. [2]
    Griintzig AR, Senning A, Siegenthaler WE (1979) Nonoperative dilatation of coronary artery stenosis. Percutaneous transluminal coronary angioplasty. N Engl J Med 301: 61–68Google Scholar
  3. [3]
    Meester GT, Bernard N, Zeelenberg C, Brower RW, Hugenholtz PG (1975) A computer system for real time analysis of cardiac catheterization data. Cathet Cardiovasc Diagn 1: 113–132PubMedCrossRefGoogle Scholar
  4. [4]
    Baim DS, Rothman MT, Harrison DC (1980) Improved catheter for regional sinus flow and metabolic studies. Am J Cardiol 46: 997–1000PubMedCrossRefGoogle Scholar
  5. [5]
    Rothman MT, Baim DS, Simpson JB, Harrison DC (1982) Coronary hemodynamics during percutaneous transluminal coronary angioplasty. Am J Cardiol 49: 1616CrossRefGoogle Scholar
  6. [6]
    Apstein C S, Puchner E, Brachfeld N (1970) Improved automated lactate determination. Ann Biochem 38: 20–34CrossRefGoogle Scholar
  7. [7]
    Verdouw PD, Stam H, Remme WJ (1980) Fundamental validity and clinical usefulness of myocardial lactate balance during ischemia. A comparison with other biochemical markers. In: Moret PR, Weber J, Haissly JC, Denolin H (eds) Lactate. Physiologic, methodologic and pathologic approach. Springer, Berlin Heidelberg New York, pp 207–223Google Scholar
  8. [8]
    Liedtke A J, Hughes HC, Neely JR (1975) Metabolic responses to varying restrictions of coronary blood flow in swine. Am J Physiol 228: 655–662PubMedGoogle Scholar
  9. [9]
    Liedtke A J, Hughes HC, Neely JR (1976) Effects of coronary perfusion during myocardial hypoxia: comparison of metabolic and hemodynamic events with global ischemia and hypoxemia. J Thorac Cardiovasc Surg 71: 726–735PubMedGoogle Scholar
  10. [10]
    Opie LH (1975) Metabolism of free fatty acids, glucose and catecholamines in acute myocardial infarction: relation to myocardial ischemia and infarct size. Am J Cardiol 35: 938–953CrossRefGoogle Scholar
  11. [11]
    Brachfeld N (1976) Characterization of the ischemic process by regional metabolism. Am J Cardiol 37: 467–473PubMedCrossRefGoogle Scholar
  12. [12]
    De Jong J W, Verdouw PD, Remme WJ (1977) Myocardial nucleoside and carbohydrate metabolism and hemodynamics during partial occlusion and reperfusion of pig coronary artery. J Mol Cell Cardiol 9: 297–312PubMedCrossRefGoogle Scholar
  13. [13]
    Verdouw PD, Remme WJ, De Jong JW, Breeman WAP (1979) Myocardial substrate utilization and hemodynamics following repeated coronary flow reduction in pigs. Basic Res Cardiol 74: 477–793PubMedCrossRefGoogle Scholar
  14. [14]
    Fabiato A, Fabiato F (1979) Calcium and cardiac excitation-contraction coupling. Ann Rev Physiol 41: 473–484CrossRefGoogle Scholar
  15. [15]
    Verdouw PD, Ten Cate FJ, Schamhardt HC, Bastiaans OL, Van der Hoek TM (1980) Segmental myocardial function during progressive coronary flow reductions and its modification by pharmacological interventions. In: Kreuzer H, Parmley WW, Rentrop P, Weiss HW (eds) Advances in clinical cardiology, vol 1: Quantification of myocardial ischemia. Witzstrock, New York, pp 270–284Google Scholar
  16. [16]
    Nayler WG (1983) Calcium and cell death. Eur Heart J [Suppl C] 4: 33–41Google Scholar
  17. [17]
    Henry PD (1980) Comparative pharmacology of calcium antagonists: nifedipine, verapamil and diltiazem. Am J Cardiol 46: 1047–1058PubMedCrossRefGoogle Scholar
  18. [18]
    Opie LH (1980) Drugs and the heart. III. Calcium antagonists. Lancet 1: 806–810PubMedCrossRefGoogle Scholar
  19. [19]
    Fleckenstein A, Fleckenstein–Gruen G (1980) Cardiovascular protection by Ca-antago-nists. Eur Heart J [Suppl B] 1: 15–21Google Scholar
  20. [20]
    Serruys, PW, Brower RW, Ten Katen HJ, Bom AH, Hugenholtz PG (1981) Regional wall motion from radiopaque markers after intravenous and intracoronary injections of nifedipine. Circulation 63: 584–591PubMedCrossRefGoogle Scholar
  21. [21]
    Serruys PW, Hooghoudt TEH, van den Brand M, Hugenholtz PG (1981) Influence of intracoronary nifedipine on left ventricular performance and myocardial oxygen consumption in human subjects. Eur Heart J [Suppl A] 2: 51Google Scholar

Copyright information

© Springer-Verlag Berlin, Heidelberg 1984

Authors and Affiliations

  • P. W. Serruys
  • M. van den Brand
  • R. W. Brower
  • P. G. Hugenhoĺtz

There are no affiliations available

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