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Ann Thorac Surg 1995;60:833-838
© 1995 The Society of Thoracic Surgeons

II: Surgical Myocardial Protection

Protection of Evolving Myocardial Infarction and Failed PTCA

Friedhelm Beyersdorf, MD

Department of Cardiovascular Surgery, Albert-Ludwigs-University Freiburg, Freiburg Germany

Abstract

Acute myocardial infarction is caused by acute coronary occlusion and is the major cause of death in Europe and the United States. In-hospital mortality is due principally to cardiogenic shock because of extensive ischemic muscle damage. Previous surgical results of coronary artery bypass grafting for left ventricular power failure have been disappointing because intraoperative ischemic injury is superimposed on severe damage already sustained by the myocardium. Surgical revascularization has, in general, been restricted to patients with acute occlusion after elective percutaneous transluminal coronary angioplasty with or without thrombolytic therapy. During the last years new knowledge has been gained in the pathophysiology of acute coronary occlusion on ischemic and nonischemic (remote) myocardium that has evolved in a new surgical strategy for revascularization of patients with evolving myocardial infarctions and failed percutaneous transluminal coronary angioplasty. Studies of the natural history of acute regional ischemia have shown that acute occlusion of a coronary artery not only affects the ischemic myocardium but causes structural, functional, and metabolic alterations in the remote and adjacent myocardium. These changes in the remote myocardium are even more severe if the remote myocardium is supplied by a stenotic coronary artery. Furthermore, many experimental and clinical studies have shown that normal blood reperfusion of myocardium injured previously by ischemia leads to additional damage (reperfusion injury). This damage can be reduced or even avoided by therapeutic interventions during the initial reperfusion period. These observations on the pathophysiology of ischemic myocardium and myocardium remote from the ischemic zone led to the development of operative strategies intended both to restore early segmental contractility in the previously ischemic area and to restore or maintain hypercontractility in remote myocardium. These strategies involve use of mechanical cardiac decompression on total vented bypass, and use of warm, substrate-enriched blood cardioplegia to resuscitate both acute ischemic muscle and metabolically depleted remote muscle.

Patients with acute coronary occlusions are almost always treated by thrombolysis or percutaneous transluminal coronary angioplasty (PTCA) to avoid or reduce myocardial necrosis. Nevertheless, in-hospital mortality is due principally to cardiogenic shock because of extensive ischemic muscle damage. Previous surgical results of coronary artery bypass grafting for acute myocardial infarction have been disappointing [1, 2], because intraoperative ischemic injury is superimposed on the severe damage already sustained by the myocardium. Therefore, surgical revascularization has, in general, been restricted to patients with acute coronary occlusion after PTCA.

During recent years, new observations have been made on the pathophysiology of ischemic and remote myocardium [3–7] that gave the impetus for the development of new operative strategies for patients with acute myocardial infarction. These strategies are intended to treat the myocardial segments damaged by the preceding ischemic period and involve use of mechanical cardiac decompression on total vented bypass and use of combined antegrade/retrograde warm, substrate-enriched blood cardioplegia to resuscitate both acute ischemic muscle and metabolically depleted remote muscle.

This communication will summarize our current understanding of the pathophysiology of acute coronary occlusion on ischemic and nonischemic (remote) myocardium, the technical details of our current surgical strategy for patients with acute myocardial infarction, and our clinical results with these techniques in patients with acute evolving infarction.

Pathophysiology of Acute Myocardial Infarction

Recent studies of the natural history of acute regional ischemia after coronary occlusion have shown that acute occlusion of a coronary artery not only affects the ischemic myocardium, but causes structural, functional, and metabolic alterations in the remote and adjacent myocardium [5–7].

Ischemic Myocardium and Reperfusion
The regional wall motion abnormalities after acute coronary occlusion (dyskinesia) are accompanied by progressive ultrastructural [8] and biochemical sequences [9–11]. However, the myocardial cell remains intact even after 6 hours of ischemia [4], as long as the damaged tissue is not exposed to a sudden reperfusion with normal blood.

Normal blood reperfusion can reverse successfully the damage imposed by a 15-minute coronary occlusion [9], but cannot prevent massive structural, biochemical, and functional changes (not present before the onset of reflow) after 40 minutes of regional ischemia [12, 13]. Normal blood reperfusion after longer periods of ischemia (6 hours) produce such extensive transmural necrosis that muscle salvage is unlikely [12, 14]. Whether this myocardial reperfusion injury occurs after normal blood reperfusion depends on the severity of ischemia [15]. Short ischemic periods or high collateral blood flow [16] during longer ischemic periods, might preserve cellular regulatory mechanisms and prevent reperfusion injury, whereas normal blood reperfusion after prolonged severe ischemia always produces additional damage.

Our new approach to reduce or avoid this additional injury after reperfusion and thus preserve ventricular function even after prolonged periods of ischemia is based on a treatment of ischemic tissue during the initial reperfusion phase, before normal blood reperfusion is allowed to occur.

Our current strategy for controlled reperfusion incorporates each of the principles of modification of the conditions of reperfusion (total heart decompression, gentle reperfusion pressure, regional cardioplegia, normothermia, prolonged reperfusion duration) and the composition of the reperfusate (oxygenation, cardioplegia [K+], glutamate/aspartate, hypocalcemia, reversal of acidosis, hyperosmolarity, oxygen free radical scavengers, hyperglycemia, leukopenia) that evolved from our previous studies [3, 6, 11, 17–26].

Remote Myocardium
The function of remote muscle is the principal determinant of early survival after an otherwise nonlethal coronary occlusion (ie, 30% of left ventricle at risk) [5]. Survival after acute coronary occlusion is determined by the infarct size [27] and the capacity of remote, nonischemic myocardium to support the systemic circulation [5, 28, 29]. Cardiogenic shock or left ventricular power failure occurs if more than 40% of the left ventricular muscle mass acutely looses its contractile properties [30, 31] or if there is insufficient remote myocardium to compensate for the acute loss of less than 40% of contractile mass (Fig 1Go). Failure of remote muscle to hypercontract may be caused by one or more of the following factors:



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  		Fig 1. . Segmental shortening (SS) (ultrasonic crystals) of remote myocardium during simulated single vessel disease (left anterior descending coronary artery [LAD] occlusion) and multivessel disease (LAD occlusion and circumflex [Cx] stenosis). Note (1) compensatory hypercontractility in isolated LAD occlusion and survival of all 11 animals (open circles) and (2) progressive remote muscle hypocontractility in simulated multivessel disease (solid circles) and high mortality from cardiogenic shock. (Reprinted with permission from Beyersdorf F, Buckberg GD. Myocardial protection in patients with acute myocardial infarction and cardiogenic shock. Semin Thorac Cardiovasc Surg 1993;5:151–61.)

 
  1. Remote muscle hypercontractility, which might be present during the initial few hours after the acute coronary occlusion, may decrease progressively to normokinesis and eventually to hypokinesis (see Fig 1Go) [5, 32]. Our experimental studies have shown that despite maintenance of normal or increased blood flow (ie, open coronary artery), mild energy and substrate depletion and evidence of anaerobic metabolism in the remote muscle occurs several hours after the acute coronary occlusion [5].
  2. Remote myocardium may become relatively ischemic if it is supplied by stenotic coronary arteries when called upon to increase contractile function, and compensatory hypercontractility may not either occur or be sustained and lead to cardiogenic shock or intractable ventricular fibrillation. We found remote muscle to become progressively hypocontractile with resultant reduction in stroke work index when it was supplied by a noncritically stenotic coronary artery (see Fig 1Go) [5]; the functional deterioration was accompanied by moderate substrate and energy depletion and more pronounced evidence of anaerobic metabolism despite normal blood flow.
  3. A previous myocardial infarction can reduce the available muscle mass in the remote myocardium, ie, a patient with an acute left anterior descending coronary artery occlusion and a previous inferior infarction secondary to prior occlusion of the right coronary artery has only a limited capacity to develop hypercontractility in the now ``nonischemic myocardium'' and might develop cardiogenic shock a short time after acute coronary occlusion.

The critical importance of remote muscle in determining the natural history of patients having acute myocardial infarction is reinforced by a recent report by Jaarsma and associates [28] showing a 69% mortality rate (usually from left ventricular power failure) in such patients who did not have remote hypercontractility. Schuster and Bulkley [29] report a 72% late mortality rate in patients with ``ischemia at a distance'' and suggest that prognosis appears related more to ischemic events in remote muscle than to the quantity of myocardium lost during the acute infarction.

These data indicate that unimpaired blood flow to remote muscle should be provided by revascularization in patients with multivessel disease and that active resuscitation of the remote muscle is necessary during surgical revascularization. These observations form the basis for our strategy directed at maximizing myocardial protection of ischemic and remote myocardium during operations for acute coronary occlusion and cardiogenic shock.

Surgical Technique for Patients With Acute Myocardial Infarction

In many centers, surgical interventions are currently considered during or soon after an acute myocardial infarction only for rupture of an area of cardiac necrosis leading to acute mitral incompetence, ventricular septal perforation, or free wall perforation [33].

Surgical revascularization during acute coronary occlusions is only performed after failed elective angioplasty, failed emergency angioplasty, and failed angioplasty in patients with a previous bypass operation. In the future, patients with naturally occuring acute coronary occlusions and especially those with additional coronary stenosis of the remote myocardium may be considered as possible candidates for surgical treatment to avoid a large, transmural myocardial infarction and cardiogenic shock. Surgical treatment for this patient group should include complete myocardial revascularization using controlled reperfusion for myocardial protection.

However, if normal blood reperfusion has been already instituted after a prolonged period of ischemia (eg, by fibrinolysis, perfusion balloons, laser balloons, directional atherectomy, PTCA, stents, or reperfusion catheters) severe reperfusion damage is already present and cannot be reversed by controlled reperfusion [34]. Therefore, if an acute occlusion occurs in the catheterization laboratory and can be quickly traversed with a guidewire, a perfusion catheter or stent can restore flow and reverse ischemia [35]. However, if an occlusion was already present for more than 1 or 2 hours, attemps at dilation may result in reperfusion injury, and valuable time may be wasted [35].

The surgical strategy for acute myocardial infarction can be separated into the phases of total vented bypass, aortic cross-clamping, regional controlled reperfusion, and prolonged beating empty state.

Total Vented Cardiopulmonary Bypass
Extracorporeal circulation is established as quickly as possible by means of single venous and aortic cannulation and connecting the cannulas to a membrane oxygenator, primed with lactated Ringer's solution. The left ventricle is vented routinely by a catheter passed through the right pulmonary vein. For patients who need preoperative cardiopulmonary resuscitation, peripheral cannulation is used for extracorporeal bypass, ie, the femoral vein is cannulated with a catheter passed into the right atrium (femoroatrial cannula), and the femoral artery is cannulated in the usual fashion. For antegrade delivery of blood cardioplegia, a cardioplegic needle is inserted into the ascending aorta.

Period of Aortic Cross-Clamping
The strategies for myocardial protection with blood cardioplegia in patients with acute coronary occlusion during the period of aortic cross-clamping may be separated into the phases of induction, maintenance and distribution, and global reperfusion.

The total blood cardioplegic dose is divided equally between antegrade and retrograde delivery for induction, maintenance and reperfusion. The doses are never given simultaneously by the two roots.

INDUCTION.
Cardioplegia may be induced immediately after extracorporeal circulation has begun and the pulmonary artery is collapsed. Starting the antegrade perfusion before aortic clamping ensures aortic valve competence. The blood cardioplegic solution may be given cold or warm.

MAINTENANCE OF CARDIOPLEGIA.
After each distal anastomosis or not later than every 20 minutes, multidose cold blood cardioplegic solution is delivered antegrade into the aorta and into each graft at 200 mL/min over 1 minute after completion of each distal anastomosis. Thereafter, retrograde delivery through the coronary sinus is done for 1 additional minute. Systemic rewarming is begun after the last distal anastomosis has been started.

GLOBAL REPERFUSION.
After completion of the last distal anastomosis, warm (37°C) substrate-enriched blood cardioplegia containing diltiazem is given into the aorta and all grafts for 2 minutes at 150 mL/min. Thereafter the aortic clamp is removed.

Controlled Regional Reperfusion
After removal of the aortic clamp controlled regional blood cardioplegic solution is given at a flow rate of 50 mL/min (line pressure less than 50 mmHg) only into the graft supplying the region revascularized for acute coronary occlusion for additional 18 minutes. In patients with acute occlusion of the left main coronary artery or with acute occlusion of two coronary arteries, flow is increased to 100 mL/min and given into both vein grafts. Normal blood is delivered into the remainder of the heart via the aortic segment not including in the tangential clamp (Fig 2Go). Cannulation of a side branch of the vein graft allows delivery of the controlled blood cardioplegic reperfusate while the proximal anastomosis is performed so that no additional ischemic time is imposed on the previously ischemic region. The proximal anastomosis of the vein graft supplying the ischemic region is always constructed first. Immediately after this 18-minute period, the tangential clamp is removed and normal blood flow is restored. The cannula is then removed from the vein graft.



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  		Fig 2. . Surgical technique for controlled regional reperfusion. (Reprinted with permission from Beyersdorf F, Buckberg GD. Myocardial protection in patients with acute myocardial infarction and cardiogenic shock. Semin Thorac Cardiovasc Surg 1993;5:151–61.)

 
Beating Empty State
The heart is kept in the beating empty state for 30 more minutes after completion of the controlled regional cardioplegic reperfusion. Recovery of jeopardized myocardium is best achieved by lowering oxygen demands and increasing oxygen delivery. The oxygen requirements of nonischemic muscle can be reduced to 50% by converting a beating working heart (9 mL • 100 g-1 • min-1) into the beating empty state (4.5 mL • 100 g-1 • min-1) [18]. Whereas the oxygen requirements of dyskinetic muscle are almost 55% of beating working needs [18, 36], decompression by total vented bypass abolished systolic bulging immediately and produced an immediate fall in regional oxygen uptake to 1 mL • 100 g-1 • min-1 [18]. The importance of lowering oxygen demands by ventricular decompression during ischemia is established further by the report by Pennock and associates [37], who showed that 95% cardiopulmonary bypass reduced left ventricular oxygen consumption 30% and that total bypass lowered oxygen demands to 50% of the nonischemic, contracting muscle.

A large right atrial drainage cannula or double cannulation with caval tapes will not ensure continuous left heart decompression, which is also known from clinical experience during elective operations. Some coronary sinus return or bronchial flow will enter the left ventricle, distend it, allow wall tension to develop, and result in occasional ejection despite apparent right heart decompression. Therefore, effective left heart decompression requires a ventricular vent, usually placed through the right pulmonary veins.

Extracorporeal circulation is discontinued after 30 minutes of beating empty state; bypass is resumed if cardiac output is not satisfactory.

Results

Until April 1992 a total of 89 patients at the Johann Wolfgang Goethe-University Medical Center in Frankfurt/Main and the University of California Los Angeles Medical Center with acute coronary occlusion underwent emergency surgical revascularization followed by controlled reperfusion. In patients with naturally occurring occlusions, the onset of ischemia was defined as the time of origin of chest pain and was always corroborated by angiographic evidence of coronary occlusion. In elective or emergency PTCA patients (n = 55) with previously patent but stenotic arteries, the onset of acute coronary occlusion was defined as the time of acute vessel closure. In both subsets, electrocardiographic evidence of hyperacute ST elevation with or without Q waves or loss of R-wave progression was present. The duration of ischemia was defined as the period of time until the start of reperfusion, and averaged 4.7 +/- 3.1 hours (range, 1.5 to 23 hours). Cardiogenic shock was present preoperatively in 35 patients. The diagnosis of cardiogenic shock was made according to accepted criteria (hypotension, oliguria, evidence of inadequate peripheral perfusion, elevated left atrial filling pressures, need for inotropes or intraaortic balloon pump). Regional contractility was assessed in all patients during the immediate postoperative period by echocardiography, radionuclide ventriculography, or both. The wall motion score was graded from 0 = normal to 4 = dyskinesia.

Early recovery of substantial regional contractility occurred in 76 of 89 patients treated by controlled reperfusion; 85% of patients showed either normokinesis or only mild to moderate hypokinesis on the seventh postoperative day. Reperfusion arrhythmias were infrequent, hemodynamic instability was present preoperatively in 49 of 89 patients (55%) and was usually reversed in 18 to 24 hours postoperatively, and hospitalization averaged only 9 days despite delay of treatment for up to 23 hours. Hospital mortality was 5.6% (5/89).

These clinical results, together with our recent reports [21, 38–40] comparing controlled reperfusion with standard CABG techniques [40] as well as studies from other authors [41], provide confirmation of our belief that the fate of jeopardized myocardium is determined by how the reperfusion strategy is managed, rather than by how quickly the blood supply is restored. The most recent report of controlled regional blood cardioplegic reperfusion is a multicenter clinical trial applying these concepts to patients with acute evolving infarction [38]. A total of 156 patients with acute coronary occlusions were treated in five different institutions according to the principles of controlled reperfusion. The results of this study showed that despite long ischemic intervals (6.3 hours), high incidence of left anterior descending coronary artery occlusion (61%), multivessel disease (42%), and cardiogenic shock (41%), surgical mortality was only 3.9% and regional wall motion recovered significantly in 140/156 (90%) patients. In contrast, a consecutive series [40] of 126 patients with acute coronary occlusion after PTCA failure who underwent normal blood reperfusion between 1977 and 1989 after only 3.5 hours of ischemia at the University of Frankfurt showed that recovery of regional wall motion was incomplete and hospital mortality was 10.3%. Furthermore, a recent review of PTCA for acute myocardial infarction in five reported series that included a total of 1,203 patients showed overall mortality of 9.2% despite successful PTCA in 93% of patients after only 3.6 hours of ischemia [42–46]. In these PTCA series, subgroup mortality was highest if there was left anterior descending coronary artery occlusion, multivessel disease, age greater than 70 years, cardiogenic shock, or unsuccessful PTCA. Additionally, mortality in the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico trial [47] was 9% in unselected patients treated by thrombolysis within 2 hours of chest pain and increased to 13% in patients treated after a longer time interval. We presume a greater than 70% success rate of reperfusion in these patients. The recent ISIS-3 preliminary results in 44,000 patients presented at the 40th Annual Scientific Session of the American College of Cardiology showed 35-day mortality rates of approximately 10.5% in the groups receiving streptokinase, anistreptase, and duteplase [48]. These clinical results of reperfusion of unmodified blood in beating working or bypassed hearts suggest that the value of these methods of reperfusion must be reassessed, because early return of contractile function is marginal; these clinical findings are consistent with the experimental studies on unmodified reperfusion [12, 14, 49, 50].

Conclusions

Our recent experimental and clinical studies suggest that myocardial salvage with early recovery of contractile function after acute coronary occlusion is possible beyond the generally accepted 2 hours, provided that the initial reperfusion is controlled carefully. Overall in-hospital survival depends on the function of the remote, nonischemic myocardium as failure of remote muscle compensation may cause cardiogenic shock. Surgical revascularization has to restore and maintain significant hypercontractility in the remote area to allow the generation of a sufficient cardiac output in patients with left ventricular power failure. Myocardial protection techniques are described for improving salvage and restoring contractile function in the ischemic area, and for successfully restoring hypercontractility in the remote myocardium. Hopefully, subsequent clinical studies will test these approaches and, if confirmatory, reduce the mortality of acute coronary occlusion.

Footnotes

Presented at the International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, Sep 25–28, 1994.

Address reprint requests to Dr Beyersdorf, Department of Cardiovascular Surgery, Albert-Ludwigs-University Freiburg, Hugstetterstr 55, D-79106 Freiburg, Germany.

References

  1. Berg R Jr, Selinger SL, Leonard JJ, et al. Immediate coronary artery bypass for acute evolving myocardial infarction. J Thorac Cardiovasc Surg 1981;81:493–7.[Abstract]
  2. Phillips SJ, Kongtahworn C, Skinner JR, et al. Emergency coronary artery reperfusion: a choice of therapy for evolving myocardial infarction. Results in 339 patients. J Thorac Cardiovasc Surg 1983;86:679–88.[Abstract]
  3. Buckberg GD. Studies of controlled reperfusion after ischemia. J Thorac Cardiovasc Surg 1986;92:483–648.[Medline]
  4. Beyersdorf F, Allen BS, Buckberg GD, et al. Studies of prolonged acute regional ischemia. I. Evidence of preserved cellular viability after 6 hours of coronary occlusion. J Thorac Cardiovasc Surg 1989;98:112–26.[Abstract]
  5. Beyersdorf F, Acar C, Buckberg GD, et al. Studies of prolonged acute regional ischemia. III. Early natural history of simulated single and multivessel disease with emphasis on remote myocardium. J Thorac Cardiovasc Surg 1989;98: 368–80.[Abstract]
  6. Beyersdorf F, Acar C, Buckberg GD, et al. Studies on prolonged acute regional ischemia. IV. Aggressive surgical treatment for intractable ventricular fibrillation after acute myocardial infarction. J Thorac Cardiovasc Surg 1989;98: 557–66.[Abstract]
  7. Beyersdorf F, Acar C, Buckberg GD, et al. Studies on prolonged acute regional ischemia. V. Metabolic support of remote myocardium during left ventricular power failure. J Thorac Cardiovasc Surg 1989;98:567–79.[Abstract]
  8. Schaper J. Ultrastructure of the myocardium in acute ischemia. In: Schaper W, ed. The pathophysiology of myocardial perfusion. Amsterdam: Elsevier/North-Holland, 1979:581–673.
  9. Jennings RB, Schaper J, Hill ML, et al. Effect of reperfusion late in the phase of reversible ischemic injury. Circ Res 1985;56:262–78.[Abstract/Free Full Text]
  10. Jennings RB, Reimer KA. Lethal myocardial ischemic injury. Am J Pathol 1981;102:241–55.[Medline]
  11. Allen BS, Okamoto F, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. XV. Immediate functional recovery after 6 hours of regional ischemia by careful control of conditions of reperfusion and composition of reperfusate. J Thorac Cardiovasc Surg 1986;92(Suppl):621–35.[Abstract]
  12. Jennings RB, Reimer KA. Factors involved in salvaging ischemic myocardium: effect of reperfusion of arterial blood. Circulation 1983;68(Suppl 1):25–36.
  13. Jennings RB, Ganote CE. Structural changes in myocardium during acute ischemia. Circ Res 1974;35(Suppl 3):156–72.[Medline]
  14. Kloner RA, Ellis SG, Carlson NV, et al. Coronary reperfusion for the treatment of acute myocardial infarction: post-ischemic ventricular dysfunction. Cardiology 1983;70:233–46.[Medline]
  15. Becker LC, Schaper J, Jeremy R, et al. Severity of ischemia determines the occurrence of myocardal reperfusion injury. Circulation 1991;84(Suppl 2):254.[Abstract/Free Full Text]
  16. Schaper W, Pasyk S. Influence of collateral flow on the ischemic tolerance of the heart following acute and subacute coronary occlusion. Circulation 1976;53(Suppl 1):57–62.
  17. Vinten-Johansen J, Buckberg GD, Okamoto F, et al. Studies of controlled reperfusion after ischemia. V. Superiority of surgical versus medical reperfusion after regional ischemia. J Thorac Cardiovasc Surg 1986;92:525–34.[Abstract]
  18. Allen BS, Rosenkranz ER, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. VII. High oxygen requirements of dyskinetic cardiac muscle. J Thorac Cardiovasc Surg 1986;92:543–52.[Abstract]
  19. Allen BS, Okamoto F, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. XII. Effects of ``duration'' of reperfusate administration versus reperfusate ``dose'' on regional functional, biochemical, and histochemical recovery. J Thorac Cardiovasc Surg 1986;92:594–604.[Abstract]
  20. Allen BS, Okamoto F, Buckberg GD, et al: Studies of controlled reperfusion after ischemia. XIII. Reperfusion conditions. Critical importance of total ventricular decompression during regional reperfusion. J Thorac Cardiovasc Surg 1986;92:605–12.[Abstract]
  21. Allen BS, Buckberg GD, Schwaiger M, et al. Studies of controlled reperfusion after ischemia. XVI. Consistent early recovery of regional wall motion following surgical revascularization after eight hours of acute coronary occlusion. J Thorac Cardiovasc Surg 1986;92:636–48.[Abstract]
  22. Okamoto F, Allen BS, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. VIII. Regional blood cardioplegic reperfusion during total vented bypass without thoracotomy. A new concept. J Thorac Cardiovasc Surg 1986;92:553–63.[Abstract]
  23. Okamoto F, Allen BS, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. X. Reperfusate composition: supplemental role of intravenous and intracoronary coenzyme Q10 in avoiding reperfusion damage. J Thorac Cardiovasc Surg 1986;92:573–82.[Abstract]
  24. Okamoto F, Allen BS, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. XI. Reperfusate composition. Interaction of marked hyperglycemia and marked hyperosmolarity in allowing immediate contractile recovery after four hours of regional ischemia. J Thorac Cardiovasc Surg 1986;92:583–93.[Abstract]
  25. Okamoto F, Allen BS, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. XIV. Reperfusion conditions. Importance of ensuring gentle versus sudden reperfusion during relief of coronary occlusion. J Thorac Cardiovasc Surg 1986;92:613–20.[Abstract]
  26. Kofsky ER, Julia PL, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. XXII. Reperfusate composition. Effects of leucocyte depletion of blood and blood cardioplegic reperfusates after acute coronary occlusion. J Thorac Cardiovasc Surg 1991;101:350–9.[Abstract]
  27. Thanavaro S, Kleiger RE, Province MA, et al. Effect of infarct location on the in-hospital prognosis of patients with first transmural myocardial infarction. Circulation 1982;66:742–7.[Abstract/Free Full Text]
  28. Jaarsma W, Visser CA, Van Einige JM, et al. Prognostic implication of regional hyperkinesia and remote asynergy of noninfarcted myocardium. Am J Cardiol 1986;58:394–8.[Medline]
  29. Schuster EH, Bulkley BH. Early post-infarction angina: ischemia at a distance and ischemia in the infarct zone. N Engl J Med 1981;305:1101–5.[Abstract]
  30. Page DL, Caulfield JB, Kastor JA, et al. Myocardial changes associated with cardiogenic shock. N Engl J Med 1971;285:133–7.[Medline]
  31. Alonso DR, Scheidt S, Post M, et al. Pathophysiology of cardiogenic shock. Quantification of myocardial necrosis, clinical, pathologic and electrocardiographic correlations. Circulation 1973;48:588–96.[Abstract/Free Full Text]
  32. Wyatt HL, Forrester JS, da Luz PL, et al. Functional abnormalities in nonoccluded regions of myocardium after experimental coronary occlusion. Am J Cardiol 1976;37:366–72.[Medline]
  33. Kirklin JW, Frye RL, Blackstone EH, et al. Some comments on the indications for the coronary artery bypass graft operation. Int J Cardiol 1991;31:23–30.[Medline]
  34. Quillen J, Kofsky ER, Buckberg GD, et al. Studies of controlled reperfusion after ischemia. XXIII. Deleterious effects of simulated thrombolysis preceeding simulated coronary artery bypass grafting with controlled blood cardioplegic reperfusion. J Thorac Cardiovasc Surg 1991;101:455–64.[Abstract]
  35. Loop FD, Whitlow PL. Coronary angioplasty in patients with previous bypass surgery. J Am Coll Cardiol 1990;16:1348–50.[Medline]
  36. Weiss HR. Effect of coronary artery occlusion on regional arterial and venous O2 saturation, O2 extraction, blood flow, and O2 consumption in the dog heart. Circ Res 1980;47:400–7.[Free Full Text]
  37. Pennock JL, Pierce WS, Waldhausen JA. Quantitative evaluation of left ventricular bypass in reducing myocardial ischemia. Surgery 1976;79:523–33.[Medline]
  38. Allen BS, Buckberg GD, Fontan FM, et al. Superiority of surgical reperfusion versus PTCA in acute coronary occlusion. J Thorac Cardiovasc Surg 1993;105:864–84.[Abstract]
  39. Beyersdorf F, Sarai K, Maul FD, et al. Immediate functional benefits after controlled reperfusion during surgical revascularization for acute coronary occlusion. J Thorac Cardiovasc Surg 1991;102:856–66.[Abstract]
  40. Beyersdorf F, Mitrev, Z, Sarai K, et al. Changing patterns of patients undergoing emergency surgical revascularization for acute coronary occlusion. Importance of myocardial protection techniques. J Thorac Cardiovasc Surg 1993;106:137–48.[Abstract]
  41. Bottner RK, Wallace RB, Visner NS, et al. Reduction of myocardial infarction after emergency coronary artery bypass grafting for failed coronary angioplasty with use of a normothermic reperfusion cardioplegia protocol. J Thorac Cardiovasc Surg 1991;101:1069–75.[Abstract]
  42. O'Keefe JH, Rutherford BD, McConahay DR, et al. Early and late results of coronary angioplasty without antecedent thrombolytic therapy for acute myocardial infarction. Am J Cardiol 1989;64:1221–3.[Medline]
  43. Stack RS, Califf RM, Hinohara T, et al. Survival and cardiac event rates in the first year after emergency coronary angioplasty for acute myocardial infarction. J Am Coll Cardiol 1988;11:1141–9.[Abstract]
  44. Rothbaum DA, Linnemeier T, Landin RJ, et al. Emergency percutaneous transluminal coronary angioplasty in acute myocardial infarction: a 3 year experience. J Am Coll Cardiol 1987;10:264–72.[Abstract]
  45. Miller PF, Brodie BR, Weintraub RA, et al. Emergency coronary angioplasty for acute myocardial infarction. Arch Intern Med 1987;147:1525–7.
  46. Erbel R, Pop T, Henrichs KJ, et al. Percutaneous transluminal coronary angioplasty after thrombolytic therapy: a prospective controlled randomized trial. J Am Coll Cardiol 1986;8:485–95.[Abstract]
  47. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986;1:397–402.[Medline]
  48. Rogers WJ. Update on recent clinical trials of thrombolytic therapy in myocardial infarction. J Invasive Cardiol 1991;3:11A–9A.
  49. Lavallee M, Cox D, Patrick TA, et al. Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs. Circ Res 1983;53:235–47.[Abstract/Free Full Text]
  50. Bush LR, Buja LM, Samowitz W, et al. Recovery of left ventricular segmental function after long term reperfusion following temporary coronary occlusion in conscious dogs: comparison of 2- and 4-hour occlusion. Circ Res 1983;53: 248–63.[Free Full Text]



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