Circulatory support with shock due to acute myocardial infarction

Circulatory Support With Shock Due to Acute Mvocardial Infarction J

Anton Moritz, MD, and Ernst Wolner, MD Second Surgical Department, University of Vienna, Vienna, Austria

Cardiogenic shock after acute myocardial infarction develops according to the amount of lost myocardium, function of remote myocardium, and the phenomenon of infarct expansion. Patients treated with mechanical support alone, without additional measures, have a mortality rate of 80%, the same as patients treated medically. Emergency angioplasty and emergency coronary artery bypass grafting can reduce mortality in certain subsets of patients to 40%. Patients with more severe shock and secondary organ dysfunction may be treated with me-

P

atients in whom cardiogenic shock develops after acute myocardial infarction have a very high inhospital death rate. This dismal prognosis can be only slightly improved by intensive treatment in coronary care units using hemodynamic monitoring, fluid substitution, and inotropic agents. Mechanical circulatory support with the intraaortic balloon pump improves the hemodynamic condition but not the ultimate outcome [I]. Most patients in cardiogenic shock after acute myocardial infarction have lost 40% or more of their myocardium, either acutely or in combination with earlier infarcts [2]. Despite this fact the death rate is not strictly correlated to the mass of necrotic myocardium [3], but also depends on the functional state of remote myocardium [4]. As the amount of myocardium temporarily nonfunctioning is not known in the acute clinical setting, it is difficult to decide which patient will benefit from any type of revascularization. Another option for patients who are transplant candidates is to use mechanical blood pump support to bridge the waiting period until a suitable donor organ is available.

Patient Selection There are several reasons why left ventricular power failure develops in patients with acute myocardial infarction. If the absolute amount of myocardium lost during the acute event or the addition of old and new infarctions adds to more than 40%, development of shock is highly probable [2, 51. In addition, patients dying of cardiogenic shock showed marginal extension of the recent infarct and focal areas of necrosis throughout both ventricles in retrospective pathological studies [2]. Presented at the Circulatory Support 1991 Symposium of The Society of Thoracic Surgeons, San Francisco, CA, Nov 16-17, 1991. Address reprint requests to Dr Wolner, 11. Chir. Univ. Klinik, Spitalgasse 23, 1090 Vienna, Austria.

0 1993 by The Society of

Thoracic Surgeons

chanical bridging to transplantation with survival rates varying between 45% and 76%. Percutaneous support systems may be used to resuscitate a patient or to temporize, allowing time to perform diagnostic studies to determine if the patient is suitable for revascularization or heart transplantation. Intravenous enoximone may improve cardiac function as well and thus allow better decision making for further therapy. (Ann Thorac Surg 1993;55:23844)

Infarcted regions may undergo expansion by stretching of myofibrils during the first days. This increase in ventricular volume is correlated with hemodynamic deterioration and is the substrate for left ventricular aneurysm formation [6-81. Reperfusion appears to limit this phenomenon by development of contraction band necroses, myocardial stiffening, and enhanced reparative processes [9, 101. The development of myocardial infarction is often evolutionary, and infarcts of different age and signs of infarct extension at the margins of vital tissue are observed [2, 71. The function of remote, noninfarcted myocardium determines the degree of compensation for lost contractile force. In general the stress produced by infarction causes deterioration of the metabolic condition of the entire heart [ll, 121. The amount of hypercontractility is inversely related to infarct size [4, 1>15]. In addition, blood flow to viable tissue supported by a stenotic noninfarct-related vessel may be severely impaired by occlusion of the culprit vessel [16,171. As the functional and pathologic changes leading to ventricular power failure are so complex, there must be several therapeutic strategies adapted to the individual circumstances of the patient. Successful percutaneous angioplasty of the infarct-related vessel within 12 hours of the onset of chest pain reduced the in-hospital mortality rate from 60% to 19% in hypotensive patients [18] and from 82% to 33% for patients in cardiogenic shock [19]. Mortality for emergency coronary artery bypass grafting within 18 hours after onset of cardiogenic shock was 7% when protection of the remote myocardium was accomplished with blood cardioplegia [20]. Survival for patients undergoing bypass grafting for shock is reported to be between 66% and 80% [20, 211. Cardiogenic shock was defined differently in these studies, so the hemodynamic condition of the patients cannot be compared. Mechanical assistance with intraaor0003-4975/93/$6.00

CIRCULATORY SUPPORT MORITZ AND WOLNER CIRCULATORY SUPPORT AITER AM1

Ann Thorac Surg 1993:55:238-44

Table I . Results of the Use of Mechanical Assist Devices Without the lntention for Later Heart Transplantation Report

No. of Patients

Noda et a1 [22] Pennington et a1 (231 Zumbro et a1 [24] Total ISHT-ASAIO

2 3 1 6 79

Weaned 1 2 1 4

22 (28%)

Discharged 0 0

1 1 8 (10%)

ISHT-ASAIO = International Society for Heart Tranplantation and the American Society for Artificial Internal Organs.

tic balloon pumps or ventricular assist devices improved heart failure, but in-hospital mortality rate remained at 80% to 90% [l](Table 1). A decision therefore must be made as to whether the patient should undergo any form of revascularization or should be considered a transplant candidate. To buy time to perform the necessary diagnostic studies, Loisance and associates [25] use a pharmacological bridge concept. In 7 of 10 patients in massive cardiogenic shock after acute myocardial infarction the hemodynamic situation improved after administration of a 1.5 to 2 mg/kg bolus of enoximone. A mechanical device had to be implanted on an emergency basis in only 3 patients [26]. Percutaneous assist devices are also able to stabilize patients for further diagnostic studies. Patients not considered transplant candidates may be offered revascularization techniques as an alternative even at high risk or, in the future, may be candidates for totally implantable assist devices.

Percutaneous Devices There are several options for circulatory support by a quick, percutaneous approach. This avoids the need for a thoracotomy for installation and can be done in the catheterization laboratory. This method can be used to resuscitate patients, to perform diagnostic studies or angioplasty, or to buy time until more definitive measures can be taken. In addition there is experimental evidence that ventricular unloading can significantly reduce infarct size [27]. Reduction in infarct size was related to the degree of pressure unloading of the left ventricle, which is usually only achieved by direct ventricular cannulation [28, 291. Adding counterpulsation to a percutaneous extracorporeal membrane oxygenation circuit was similarly effective in reducing myocardial necrosis [30, 311. Mobile extracorporeal circuits mounted on a cart have been made commercially available. In the case of hemodynamic deterioration or during resuscitation one arterial and two venous cannulas are inserted into the femoral vessels using a Seldinger technique. Circulation can be reestablished by this technique as reported by Phillipps [32] and Pennington and associates [33, 341, and survival rates are about 20% after subsequent treatment with angioplasty, bypass grafting, or heart transplantation. The Nimbus Hemopump (Nimbus Medical Inc, Rancho Cordova, CA) can be inserted through a vascular graft sewn to the iliac or femoral vessels under fluoroscopic

239

guidance. It consists of a high-speed rotary pump contained in a perfusion cannula inserted across the aortic valve into the left ventricle. The system is powered and flushed through an axial cable. Insertion can be accomplished within 20 minutes and flow rates up to 3 to 3.5 L/min can be achieved. It definitely adds more circulatory support than does the intraaortic balloon pump, and it is possible to maintain circulation during ventricular fibrillation after sufficient fluid loading [35]. Coronary perfusion is improved, as shown in an experimental model [36]. On the other hand, unloading of a failing left ventricle may diminish its output, with blood flow achieved only by the Hemopump. As its flow maximum is limited, reversal of shock or recovery of organ function is often not achieved. Therefore most successful applications are reported when only short-term support was necessary [37, 381. Deeb and associates [38] reported 3 surviving patients after successful implantation in 5 patients with acute myocardial infarction. In 3 patients the device could not be inserted due to technical reasons (Table 2). Dennis and colleagues [39] designed a specially curved cannula containing an aspiration needle and a retractable knife to perforate the interatrial septum and thus to install left heart bypass. Lefemine and Dunbar [40] used percutaneous biventricular bypass with left ventricular and right atrial withdrawal, without the use of an oxygenator. For both methods only limited clinical experience is reported.

Bridging to Transplantation After Acute Myocardial Infarction Since the first report of a successful bridge to cardiac transplantation for acute myocardial infarction shock [41], the combined registry of the International Society for Heart Transplantation and the American Society for Artificial Internal Organs (ISHT-ASAIO) lists a total of 262 patients treated with mechanical blood pumps to stabilize hemodynamics for cardiogenic shock complicating acute myocardial infarction. The devices used were total artificial hearts and pulsatile and centrifugal ventricular assist devices for either left, right, or biventricular support. Sixty-three of the 262 (24%) survived to hospital discharge. However, the treatment modalities of these patients were quite different. Seventy-nine patients were treated without the intention for later heart transplantation. Twenty-eight percent could be weaned from the

Table 2. Results of Percutaneous Mechanical Suvport ~

Report

~~

Device

Kanter et a1 [MI PCPB Phillips [32] PCPB Deeb et a1 [38] Hemopump

~

No. of Patients Weaned 15 14 5 (8)”

11 9 3

In 3 patients the device could not be inserted. PCPB = percutaneous cardiopulmonary bypass system

Discharged 2 (13%) 4 (29%) 3 (60% [38%])”

240

CIRCULATORY SUPPORT MORITZ AND WOLNER CIRCULATORY SUPPORT AFTER AMI

device, and only 10% were discharged from the hospital. Of the 76 patients who had an artificial blood pump implanted for later heart transplantation, 46 (60.5%)underwent transplantation and 34 (44.7%) could be discharged. Seventy-four percent of transplanted patients were discharged, indicating that mortality after the bridge period is somewhat higher than after conventional heart transplantation in mortally ill patients [42]. For the whole series there was no difference in the survival after support with centrifugal or pneumatic blood pumps. The survival for patients who had a total artificial heart implanted was 15 of 42 (36%).Though not clearly indicated, probably all of them were implanted with the intention of later heart transplantation. Farrar and associates [43] reported 17 patients receiving the Thoratec ventricular assist device system for acute myocardial infarction shock. Thirteen of these underwent transplantation and all of them survived to hospital discharge (76%). This is better than the reported 63% survival rate for the whole series including cardiomyopathies, transplant rejections, and myocarditis and the data for the combined registry (Table 3). This is consistent with the experience that survival rates after the use of ventricular assist devices tend to be better than those after use of total artificial hearts in bridged patients [43, 45-47]. Total artificial hearts have been used mostly before ventricular assist systems became easily available for clinical use, so the better results achieved with assist systems can be explained by the gain in experience. Kormos and associates [45] preferred the use of a total artificial heart over the use of an apicoaortic implantable left ventricular assist device (Novacor, Baxter Healthcare, Oakland, CA) due to the risk of ventricular arrhythmias and dislodgement of the apical cannula. This lethal complication was observed by Lewis and colleagues [26] after implantation of the TCI implantable left ventricular assist device (Thermo Cardiosystems Inc, Woburn, MA) in a patient with acute infarction. Difficulties arise when one reviews the literature for mechanical circulatory support after acute myocardial infarction as some of the patients are operated on for infarct complications. So it is not clear whether these patients should be considered to receive implants for postcardiotomy shock or acute myocardial infarction shock. Survival for postoperative mechanical assistance is 24% (107 of 451 implants) [48] as reported by the ISHTTable 3 . Rate of Transplantation and Hospital Survival After Use of Mechanical Blood Pumps as a Bridge to Transplantation After Acute Myocardial lnfarction Shock Report Farrar et a1 [43] Loisance et al [44] Zumbro et a1 [24] Our results ISHT-ASAIO

No. of Patients 17 3 4 6 76

Transplanted

Discharged

13 (76%)

13 (76%)

2 1

3 46 (60.5%)

2

1 2

34 (45%)

ISHT-ASAIO = International Society for Heart Transplantation and the American Society for Artificial Internal Organs.

Ann Thorac Surg

1993;5523&44

Table 4 . Survival Rates for the Use of Ventricular Assist Devices After Operation for Complications of Acute Myocardial lnfarction Report Noda et a1 [22]

ISHT-ASAIO

No. of Patients

Weaned

8 99

6 (75%) 45 (46%)

Discharged 3 (3%) 20 (20%)

ISHT-ASAIO = International Society for Heart Transplantation and the American Society for Artifiaal Internal Organs.

ASAIO combined registry, although survival rates up to 40% may be achieved in experienced centers [49, 501. Certainly timely implantation of the support device avoiding multiple attempts to wean the patient off extracorporeal circulation is a predictor for outcome [51], and the intention to implant a support device should be part of the surgical strategy in patients with preoperative shock. Noda and colleagues [22] reported a 38% survival rate for patients operated on for shock complicating acute myocardial infarction, whereas Pennington and associates [52] reported a dismal prognosis for patients with perioperative infarction requiring mechanical assistance. Still, in their series perioperative infarction did not preclude myocardial recovery and subsequent weaning from the assist device. The survival rate for patients with mechanical support after operation for acute myocardial infarction shock is reported to be 20% in the combined registry (Table 4).

Our Results Six patients with cardiogenic shock complicating acute myocardial infarction were transferred to the Second Surgical Department of the University of Vienna for mechanical circulatory assistance as a bridge to heart transplantation. The Vienna Heart was designed and is manufactured in cooperation between the Second Surgical Department and the Institute for Biomedical Engineering of the University of Vienna and the Ludwig Boltzmann Institute for Cardiosurgical Research in Vienna. A 65-mL ventricle is vacuum-formed from sheets of thermoplastic polyurethane (Pellethane). The two-layer pump membrane is solution-casted; the second layer also lines the inner surface of the pump housing, guaranteeing a seamless transition between housing and membrane. Flow is directed by a 29-mm (inflow)and a 27-mm (outflow) tiltingdisk valve (Sorin, Italy). A 51F Sams lighthouse cannula, bent to 90 degrees and coated with Pellethane, is used as inflow and a 12-mm expanded polytetrafluoroethylene graft is glued to the outflow cannula (Fig 1). Left heart bypass was always instituted between the right upper pulmonary vein and the ascending aorta. The ventricles are powered by a pneumatic drive unit [53]. Membrane position and motion was estimated by analysis of driveline pressure and gas flow. All patients were transferred in a state of cardiogenic shock (Table 5). They had been treated in coronary care units for several days after first or recurrent (patients 2,4,

241

CIRCULATORYSUPPORT MORITZ AND WOLNER CIRCULATORY SUPPORT AFTER AM1

Ann Thorac Surg 1993;55:23644

Fig 1 . The Vienna Heart left ventricular assist device. The housing is vacuum-formed, and the two-layer membrane is solution-casted. A modified lighthouse cannula is used for inflow and a vascular graft bonded to a cannula is used for outflow.

and 5) acute myocardial infarction. Four had renal failure, 1 of them treated with hemofiltration; 2 had impaired liver function with disorder of the coagulation system. A 65-year-old man had signs of adult respiratory distress syndrome indicated by roentgenogram and blood gas analysis after experiencing a large anterior infarction and cardiogenic shock. He underwent successful transplantation after 5 days of circulatory support (Fig 2). None of the patients had undergone coronary angiography due to their unstable hemodynamic condition. In all patients except patient 1, in whom no adequate pump flow could be achieved, the hemodynamic situation improved and organ function recovered. Recurrent ventricular fibrillation developed in 4 patients while they were supported by left ventricular assist. In 2 patients (patients 5 and 6) prolonged attacks of ventricular fibrillation led to multiorgan failure and neurologic deficit, respectively. Both had recovered initially, and the arrhythmia must be considered the main reason for the fatal outcome. Patient 4 improved hernodynamically and could be extubated 3 days after left ventricular assist device implantation. Urine flow had normalized, although serum creatinine level remained elevated. Severe graft failure developed on the first day after transplantation, with metabolic acidosis lowering pH to 6.9. Despite recovery of cardiac function

Fig 2. The chest roentgenogram of patient 3 shows signs of adult respiratory distress syndrome the first day after left ventricular assist device implantation, despite normal to low left atrial pressures.

he died of multiorgan failure acquired during this period of hypoperfusion. Patient 2 had an elevated white blood cell count of 40 x 1O’/L (40,OOO/pL) but no proven infection other than severe stomatitis. His renal failure necessitated hemofiltration before left ventricular assist device implantation. On the first postoperative day 17 L of fluid was necessary to stabilize his hemodynamics. In the later course multiple blood cultures were positive for Klebsiella, enterococci, and Candida. Under antibiotic treatment his organ functions stabilized, and as the implanted left ventricular assist device or the left ventricular thrombus was considered the septic focus, he underwent successful transplan-

Table 5. Chnrncteristics of the 6 Patients Treated With Left Ventricular Assist Device Support With the lntent of Later Heart Transplantation at O u r Institution Patient No.

Age

(Y)

1 2 3

48 41 65

4

60

5

61 41

6

Creatinine (mg/dL) 2.4 1.7 2.6 4.3 2 0.8

Bilirubin (mg/dL)

Diureses Oliguria Anuria (HF) Oliguria Anuria Oliguria Oliguria

Lungs

... ...

6.6 16 0.9 1.3 0.6 0.6

ARDS

... PE PE

Tx

Survival

Complications

-

-

Leg ischemia, MOF Sepsis ARDS Graft failure Neurologic deficit, VF VF, MOF

+ +

+ +

+

-

-

-

-

~

ARDS = adult respiratory distress syndrome; transplantation,

HF

=

hemofiltration;

MOF

=

rnultiorgan failure;

~~

PE

=

pulmonary edema;

Tx

=

heart

242

CIRCULATORYSUPPORT MORITZ AND WOLNER CIRCULATORY SUPPORT AFTER AM1

tation after 22 days of support. All consecutive blood cultures were negative and he is alive and well 2 years later.

Comment Decision making in the situation of cardiogenic shock complicating acute myocardial infarction is complex as optimal treatment depends on diagnostic information frequently not available in the acute setting. In addition to the amount of myocardium lost by the acute and earlier infarctions, the function of remote myocardium, infarct expansion, and infarct extension lead to left ventricular power failure. This range of causes explains why a variety of treatment modalities are reported to be successful in treatment of cardiogenic shock. The results of studies using different therapies are difficult to compare as the definition of cardiogenic shock varies and patients are treated at different times from onset of chest pain or cardiac failure. Mechanical assistance using intraaortic balloon pumps or mechanical blood pumps was able to relieve cardiogenic shock, but in-hospital mortality and 1-year mortality were not improved significantly compared with medical treatment alone, ranging between 71% and 90% [l, 541 (see Table 1). Restoring adequate blood flow to the myocardium may limit infarct size [55], avoid infarct expansion [lo], or improve the function of remote myocardium [4]. Once cardiogenic shock is established it is usually too late to salvage myocardium in the infarct area. Despite this, angioplasty done within 12 hours of onset of pain improved survival in shock patients from 18%to 67% [19]. It is worth noting that mortality rates for patients with unsuccessful angioplasties parallel those of medically treated patients. Successful relief of cardiogenic shock is reported in 94% when surgical revascularization of the infarcted, as well as remote myocardium is done within a mean of 3.4 days after infarction [20]. In this study cardiac index was 2.1 L/m2and pulmonary capillary wedge pressure was increased to 27 mm Hg preoperatively. Inhospital mortality for the whole series was 18%and 1-year survival was 70%. Most of the late deaths were due to congestive heart failure. Patients operated on later than 18 hours after onset of shock had the worst short-term and long-term prognosis. In a review of 101 patients who underwent emergency coronary artery bypass presented by Bolooki [21], perioperative mortality was 66%. Farrar and associates [43] reported a favorable outcome in patients with cardiogenic shock due to severe acute myocardial infarction (cardiac index, 1.6 Wm2; pulmonary capillary wedge pressure, 27 mm Hg) after mechanical bridging to transplantation. Thirteen of 17 patients could undergo transplantation and were discharged from the hospital (76%). This survival rate is higher than that for their total series of 72 patients (63%)and the survival rate reported by the ISHT-ASAIO registry for this indication (45%).Although not generally achieved, these data indicate that even patients in severe shock can be managed with a very good outcome.

Ann Thorac Surg 1993;55:23&44

At this point there are no clear guidelines as to which devices are optimally used. Myocardial infarctions mostly affect left ventricular output, and so left ventricular assist is frequently sufficient to reestablish sufficient circulation. In all patients in our series we had to treat right ventricular failure with inotropes, but shock could be reversed in all but 1. Four of our patients had episodes of ventricular fibrillation while on the device, and in 2 of them these episodes were clearly related to death. Kormos and colleagues [45] thus suggest use of a total artificial heart preferentially in this setting. Biventricular assist is an adequate alternative as this overcomes problems of circulatory failure due to both arrhythmias and right ventricular failure, especially when the right coronary artery is diseased. In contrast to patients with chronic cardiomyopathy, patients after acute myocardial infarction are not conditioned to hypoperfusion. Thus secondary end-organ dysfunction develops quickly and accounts for the increased mortality after coronary operation for shock [20]. The 2 survivors in our series had organ dysfunction that was considered in the literature to be a contraindication [56]. Still, reestablishing sufficient perfusion allowed for recovery of organ systems. Percutaneous support was used to resuscitate patients in two series with a 20% survival after subsequent definitive treatment [32, 33, 381. In addition, such devices may be used to temporize, allowing performance of diagnostic studies necessary to decide which treatment is optimal for the individual patient. In the state of evolving infarction, infarct size may be limited by these techniques as well [27, 311. New inotropic drugs may be used as well to stabilize patients until the decision for final treatment can be made [44]. Patients with clear contraindications against heart transplantation, which cannot be expected to resolve during mechanical bridging, have the option to undergo revascularization procedures with increased risk or in the future to have one of the permanently implantable assist devices inserted. Patients after acute myocardial infarction are seen in cardiogenic shock at variable intervals after onset of pain and with various reasons for ventricular failure. The value of different treatment strategies for these patients is not yet established, but revascularization techniques as well as mechanical assistance as a bridge to heart transplantation certainly significantly improve survival rates.

References Scheidt S, Wdner G, Mueller H, et al. Intra-aortic balloon counterpulsation in cardiogenic shock: report of a cooperative clinical trial. N Engl J Med 1973;288:979-84. Page DL, Caulfield JB, Kastor JA, DeSanctis RW, Sanders CA. Myocardial changes associated with cardiogenic shock. N Engl J Med 1971;285133-7. Hackel DB, Reimer KA, Ideker RE, et al. Comparison of enzymatic and anatomic estimates of myocardial infarct size in man. Circulation 1984;70824-35. Grines CL, Topol EJ, Califf RM, et al. Prognostic implications and predictors of enhanced regional wall motion of the noninfarcted zone after thrombolysis and angioplasty of acute myocardial infarction. Circulation 1989;80:245-53.

Ann Thorac Surg 1993;55:23844

5. Harnarayan C, Bennett MA, Pentecost BL, Brewer DB. 6. 7. 8.

9.

10. 11. 12. 13.

14.

15.

16.

17. 18.

19.

20.

21. 22. 23. 24.

Quantitative study of infarcted myocardium in cardiogenic shock. Br Heart J 1970;32:72&32. Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Weisfeldt ML. Regional cardiac dilatation after acute myocardial infarction. N Engl J Med 1979;300:57-62. Hutchins GM, Bulkley BH. Infarct expansion versus extension: two different complications of acute myocardial infarction. Am J Cardiol 1978;41:1127-32. Erlebacher JA, Weiss JL, Eaton LW, Kallman C, Weisfeldt ML, Healy-Bulkley B. Late effects of acute infarct dilatation on heart size: a two dimensional echocardiographic study. Am J Cardiol 1982;49:1120-8. Althaus U, Gurtner HP, Baur H, Hamburger S, Roos 8. Consequences of myocardial reperfusion following temporary coronary occlusion in pigs: effects on morphologic, biochemical and hemodynamic findings. Eur J Clin Invest 1977;743743. Hochman JS, Choo H. Limitation of myocardial infarct expansion by reperfusion independent of myocardial salvage. Circulation 1987;75:299-306. Corday E, Kaplan L, Meerbaum S, et al. Consequences of coronary arterial occlusion on remote myocardium: effects of occlusion and reperfusion. Am J Cardiol 1975;36:385-94. Vikhert AM, Cherbachenko NM. Changes in metabolism of undamaged sections of myocardium following infarction. Circ Res 1974;35(Suppl 3):182-91. Lefkowitz CA, Gallagher KP, Pace DP, Wright LA, Krause LC, Buda AJ. Compensatory augmentation of normal regional function following coronary occlusion: relation to myocardial area at risk and extent of ischemic dysfunction [Abstract]. J Am Coll Cardiol 1987;9:92A. Rigaud M, Rocha P, Boschat J, Farcot JC, Bardet J, Bourdarias JP. Regional left ventricular function assessed by contrast angiography in acute myocardial infarction. Circulation 1979; 60:130-9. Marshall RC, Tillisch JH, Phelps ME, et al. Identification and differentiation of resting myocardial ischemia and infarction in man with positron computed tomography, "F-labeled fluorodesoxyglucose and N-13 ammonia. Circulation 1983;67: 766-78. Naccarella FF, Weintraub WS, Agarwal JB, Helfant RH. Evaluation of "ischemia at a distance": effects of coronary occlusion on a remote area of left ventricle. Am J Cardiol 1984;54:869-74. Schwartz GS, Cohn JN, Bache RJ. Effects of coronary occlusion on flow in the distribution of a neighboring stenotic coronary artery in the dog. Am J Cardiol 1983;52:189-95. Ghitis A, Flaker GC, Meinhardt S, Grouws M, Anderson SK, Webel RR. Early angioplasty in patients with acute myocardial infarction complicated by hypotension. Am Heart J 1991;122:38M. Lee L, Bates ER, Pitt B, Walton JA, Laufer N, ONeill WW. Percutaneous transluminal angioplasty improves survival in acute myocardial infarction complicated by cardiogenic shock. Circulation 1988;78:1345-51. Allen BS, Rosenkranz E, Buckberg GD, et al. Studies on prolonged acute regional ischemia 1V. Myocardial infarction with left ventricular power failure: a medical surgical emergency requiring urgent revascularization with maximal protection of remote muscle. J Thorac Cardiovasc Surg 1989;98: 691-703. Bolooki H. Emergency cardiac procedures in patients in cardiogenic shock due to complications of coronary artery disease. Circulation 1989;79(Suppl 1):13748. Noda H, Takano H, Taenaka Y, et al. Treatment of acute myocardial infarction with cardiogenic shock using left ventricular assist device. Int J Artif Organs 1989;12:175-9. Pennington DG, Kanter KR, McBride LR, et al. Seven years experience with the Pierce-Donachy ventricular assist device. J Thorac Cardiovasc Surg 1988;96:901-11. Zumbro GL, Kitchens WR, Shearer G, Harville G, Bailey L, Galloway RF. Mechanical assistance for cardiogenic shock

CIRCULATORY SUPPORT

MORITZ AND WOLNER

CIRCULATORY SUPPORT AFTER AM1

243

following cardiac surgery, myocardial infarction and cardiac transplantation. Ann Thorac Surg 1987;44:11-3. 25. Loisance D, Dubois Rande JL, Deleuze PH, et al. Pharmacological bridge to cardiac transplantation. Eur J Thorac Cardiovasc Surg 1989;3:196-202. 26. Lewis CT, Graham TR, Marrinan MT, Chalmers JAC, Colvin MP, Withington PS.The use of an implantable left ventricular assist device following irreversible ventricular fibrillation secondary to massive myocardial infarction. Eur J Cardiothorac Surg 1990;4:54-6. 27. Catinella FP, Cunningham JN, Glassman E, Laschinger JC, Baumann FG, Spencer FC. Left atrium-to-femoral artery bypass: effectiveness in reduction of acute experimental myocardial infarction. J Thorac Cardiovasc Surg 1983;86: 887-96. 28. Pennock JL, Pae WE, Pierce WS, Waldhausen JA. Reduction of myocardial infarct size: comparison between left atrial and left ventricular bypass. Circulation 1979;59:275-9. 29. Laas J, Campbell CD, Takanashi Y, Pick R, Replogle RL, Sebening F. Critical analysis of intra-aortic balloon counterpulsation and transapical left ventricular bypass in the sufficient and insufficient circulation. Thorac Cardiovasc Surg 1981;29:17-31. 30. Laschinger JC, Cunningham JN, Catinella FP, Knopp EA, Glassman E, Spencer FC. "Pulsatile" left atrial-femoral artery bypass. Arch Surg 1983;118:965-9. 31. Axelrod HI, Galloway AC, Murphy MMS, et al. Percutaneous cardiopulmonary bypass with a synchronous pulsatile pump combines effective unloading with ease of application. J Thorac Cardiovasc Surg 1987;93:358-65. 32. Phillips SJ. Percutaneous cardiopulmonary bypass and innovations in clinical counterpulsation. Crit Care Clin 1986;2: 297-318. 33. Pennington DG, Mejavy JP, Codd JE, Swartz MT, Miller LL, Williams GA. Extracorporeal membrane oxygenation for patients with cardiogenic shock. Circulation 1984;7O(Suppl): 130-5. 34. Kanter KR, Swartz MT, Pennington DG, McBride LR, Miller LW, Ruzewich SA. Emergency extracorporeal membrane oxygenation (ECMO) for cardiopulmonary resuscitation [Abstract]. J Heart Transplant 1988;7:75. 35. Pantalos G, Long J, Kinoshita M, et al. In vivo evaluation of Hemopump function in a large animal model of LV dysfunction and fibrillation. International Workshop on Rotary Blood Pumps, Baden, Austria, 1991:17%. 36. Zelinsky R, Shiiya N, Deleuze P, Geschwind H, Loisance D. Hemopump improves oxygen supply to the failing heart. Proceedings of the International Workshop on Rotary Blood Pumps, Baden, Austria, 1991:184. 37. Phillips SJ, Barker L, Balentine B, et al. Hemopump support for the failing heart. Trans Am Soc Artif Intern Organs 1990;36:M629-32. 38. Deeb GM, Bolling SF, Nicklas J, et al. Clinical experience with the Nimbus pump. Trans Am SOCArtif Intern Organs 1990; 36:M632-6. 39. Dennis C, Carlens E, Senning A, et al. Clinical use of a cannula for left heart bypass without thoracotomy. Ann Surg 1962;156:623-37. 40. Lefemine AA, Dunbar J. Simple alternatives using a single centrifugal pump for biventricular assistance in cardiogenic shock. J Biomater Appl 1990;4:333-61. 41. Hill JD, Farrar DJ, Hershon JJ, et al. Use of a prosthetic ventricle as a bridge to cardiac transplantation for postinfarction cardiogenic shock. N Engl J Med 1986;314:626-8. 42. Hardesty RL, Griffith BP, Trento A, Thompson ME, Ferson PF, Bahnson HT. Mortally ill patients and excellent survival following cardiac transplantation. Ann Thorac Surg 1986;41: 126-9. 43. Farrar DJ, Lawson JH, Litwak P, Cederwall G. Thoratec VAD system as a bridge to heart transplantation. J Heart Transplant 1990;9:415-23. 44. Loisance D, Deleuze P, Hillion ML, et al. The real impact of mechanical bridge strategy in patients with severe acute

244

Ann Thorac S q

CIRCULATORY SUPPORT MORITZ AND WOLNER CIRCULATORY SUPPORT AFTER AMI

infarction. Trans Am SOCArtif Intern Organs 1990;36. M1357. 45. Kormos RL, Borovets HS, Gasior T, et al. Experience with univentricular support in mortally ill cardiac transplant candidates. AM Thorac Surg 1990;49261-72. 46. Joyce LD, Johnson KE, Toninato CJ, et al. Results of the first 100 patients who received Symbion total artificial heart as a bridge to cardiac transplantation. Circulation 1989;8O(Suppl 3):192-201. 47. Griffith BP, Hardesty RL, Kormos RL, et al. Temporary use of the Jarvik-7 total artificial heart before transplantation. N Engl J Med 1987;3161304. 48. Miller CA, Pae WE, Pierce WS. Combined registry for the clinical use of mechanical ventricular assist devices. Postcardiotomy cardiogenic shock. Trans Am SOCArtif Intern Organs 1990;34:43-6. 49. Pennington DG, Samuels LD, Williams G, et al. Experience with the PierceDonachy ventricular assist device in postcardiotomy patients with cardiogenic shock. World J Surg 1985;93746. 50. Gaines WE, Pierce WS, Donachy JH, et al. The Pennsylvania

1993;55:238-44

51. 52.

53. 54.

55.

56.

State University paracorporeal ventricular assist pump: optimal methods of use. World J Surg 1985;9:47-53. Magovem GJ, Park SB, Maher TD. Use of a centrifugal pump without anticoagulants for postoperative left ventricular assist. World J Surg 1985;9:25-36. Pennington DG, McBride LR, Kanter KR, et al. Effect of perioperative myocardial infarction on survival of postcardiotomy patients supported with ventricular-assist devices. Circulation 1988;78(Suppl3):110-5. Thoma H, Schima H. Drive and management of circulatory support systems. In: Unger F, ed. Assisted circulation3. New York Springer, 1989:542-67. Goldberger M, Tabak SW, Shah PK. Clinical experience with intra-aortic balloon counterpulsation in 112 consecutive patients. Am Heart J 1986;111:497-502. Cheung EH, Arcidi JM, Dorsey LM, Vinten-Johansen J, Hatcher CR, Guyton RA. Reperfusion of infarding myocardium: benefit of surgical reperfusion in a chronic model. Ann Thorac Surg 1989;48:331-8. Moritz A, Rokitansky A, Trubel W, et al. Timing for implantation and transplantation in mechanical bridge to transplantation. Int J Artif Organs 1991;14270-5.