Coronary Angioplasty: A Controlled Model for Ischemia, Softcover reprint of the original 1st ed. 1986 Developments in Cardiovascular Medicine Series, Vol. 58

Since the introduction of coronary angioplasty in 1977, this procedure has gained a steadily increasing position in the treatment of coronary artery obstmction. From the available evidence it can be estimated, that this thera­ peutic tool will get even more additional momentum of many ten-thousands of patients to be treated in the next few years, due to a growing fraction of patients who are candidates for this intervention. Information about the indications, benefits and risks of coronary angioplasty is accumulating rapidly in addition to publications about refinements of the technique itself. Recently, a number of investigators have realized that coronary angioplasty is not only a therapeutic tool, but can, during the procedure, be used as a source of diagnostic information. When the catheter is placed in a coronary artery obstruction, inflation of the balloon produces transient myocardial ischemia. Before, during, and after this period of severe ischemia, studies of the perfor­ mance of the myocardium at risk can be carried out. The fact that therapeutic coronary angioplasty is carried out in a cardiac catheterization laboratory which is by definition optimally equipped for the measurement of hemodynamic parameters, has probably also contributed to the effectuation of these investigations. The combination of hemodynamic and biochemical parameters with morphological information from the coronary angiogram can be utilized for the quantification of myocardial involvement and the success of coronary dilatation with angioplasty. Studies of interactions with pharmacological substances are also feasible and informative.

1. Effects of acute myocardial ischemia and reperfusion in conscious animals.- Instrumentation techniques for measurements of regional myocardial function in conscious animals.- Relationship between reduction in regional blood flow and myocardial function.- Adjustment to global LV ischemia.- Adjustment to regional myocardial ischemia.- Effects of reperfusion.- Enzyme leakage from ischemic myocardium.- Summary.- References.- 2. Early changes in wall thickness and epicardial wall motion during coronary angioplasty in man. Similarities with in vitro and in vivo model.- Echocardiographic changes in wall thickness.- Changes in epicardial wall motion.- Regional marker motion.- Analysis of pressure-derived indexes during systole and diastole.- Results.- Changes in regional epicardial wall motion.- Changes in global left ventricular function.- Discussion.- Early wall motion changes during acute ischemia.- Wall motion abnormalities in chronic ischemia.- References.- 3. Intracoronary electrocardiogram during transluminal coronary angioplasty.- and methods.- Results.- Discussion.- References.- 4. Clinical, electrocardiographic and hemodynamic changes during coronary angioplasty. Influence of nitroglycerine and nifedipine.- Methods.- Results.- Ischemic tolerance.- Ventricular function.- Discussion.- Summary.- References.- 5. Wall thickening and motion in transient myocardial ischemia: Similarities and discrepancies between different models of ischemia in man (Prinzmetal’s angina, coronary angioplasty, Dipyridamole test).- Echocardiographic markers of ischemia.- The clinical model of transmural vasospastic ischemia and coronary angioplasty.- Evaluating the site of myocardial ischemia before coronary angioplasty: a role for the Dipyridamole-echocardiography test.- References.- 6. Effect of prolonged balloon inflations on hemodynamics and coronary flow with respect to balloon position in patients undergoing coronary angioplasty.- Methods.- Results.- Coronary sinus flow.- Coronary sinus flow and hemodynamics.- Collateral flow.- Discussion.- Flow during occlusion.- Reactive hyperemia.- Coronary sinus flow and hemodynamics.- Implications.- References.- 7. Myocardial release of hypoxanthine and lactate during coronary angioplasty: A quickly reversible phenomenon, but for how long?.- Patients and methods.- PTCA technique.- Lactate measurements.- Hypoxanthine determination.- Flow measurements.- Statistical analysis.- Results.- Coronary hemodynamic measurements.- Lactate and hypoxanthine metabolism.- Discussion.- Use of purine release as a marker for ischemia during transluminal occlusion in man.- Metabolism during reperfusion.- Summary.- References.- 8. Role of potassium in the genesis of arrhythmias during ischemia. Evidence from coronary angioplasty.- Electrolytes in the ischemic myocardium.- Calcium.- Sodium.- Hydrogen ion.- Potassium.- Shortening of the action potential during myocardial ischemia.- Changes in the plasma potassium during myocardial ischemia.- Conclusion.- References.- 9 “Collateralpressure” (occlusion pressure) during coronary angioplasty in coronary artery disease.- Methods.- Results.- The relation between the collateral pressure (OP) and the amount of visible collaterals (study 1).- The influence of Nifedipine on the collateral pressure (study 2).- The relation between the collateral pressure and the occurrence of restenosis (study 3).- Discussion.- Summary.- References.- 10. Assessment of the dynamic and functional characteristics of collateral flow observed during sudden controlled coronary artery occlusion.- Methods.- Study patients.- Cardiac catheterization and angioplasty protocol.- Study protocol.- Results.- Changes in collateral filling during coronary occlusion (Fig. 5).- Hemodynamics.- Indices of myocardial ischemia with reference to collateral flow.- Discussion.- The coronary collateral circulation is a dynamic circulation.- Can collateral circulation limit ischemia?.- Present study.- Clinical implications.- Summary.- References.- 11. Left ventricular cineangiography during coronary angioplasty.- Selection of the patients.- Left ventricular cineangiography procedure during PTCA.- Results.- Left ventricular pressures.- Left ventricular volumes and ejection fraction.- Left ventricular diastolic function.- Segmental wall motion.- Reversibility of the ischemic changes.- Comments.- References.- 12. Left ventricular filling during acute ischemia.- Methods.- Results.- Left ventricular relaxation.- Left ventricular stiffness.- Left atrial contraction.- Discussion and conclusions.- References.- 13. Ejection filling diastasis during transluminal occlusion in man. Consideration on global and regional left ventricular function..- Study population and protocol.- Methods.- Analysis of pressure derived indices during systole and diastole.- Analysis of regional and global left ventricular function.- Ejecting dynamics.- Filling dynamics.- Diastasis.- Statistical analysis.- Results.- Global left ventricular function during systole and diastole.- Regional indexes of left ventricular ejection and filling and regional pressure-radius length relations.- Regional pressure-radius length relation.- Discussion.- Myocardial ischemia, transient asynergy and altered relaxation.- Uncoordinated segmental contraction as a cause of impaired filling dynamics.- Determinants of filling dynamics.- Role of the asynchronous contraction.- Effect of coronary occlusion on left ventricular chamber stiffness and regional diastolic pressure-radius relations.- Significance of the upward shift in pressure-volume and pressure-radius relations.- Comparison with animal models of acute low-flow ischemia.- Mechanism of increased myocardial stiffness.- Conclusion: PTCA as an ischemic model?.- Early wall motion during acute ischemia: how to interpret?.- Are there clinical implications in chronic ischemia?.- Are there clinical implications for the PTCA procedure?.- References.