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Lee DC, Ting W, Oz MC. Myocardial Revascularization after Acute Myocardial Infarction.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:639658.

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Chapter 24

Myocardial Revascularization after Acute Myocardial Infarction

Daniel C. Lee/ Windsor Ting/ Mehmet C. Oz

PATHOGENESIS OF ACUTE OCCLUSION
CARDIOGENIC SHOCK
????Definition
????Prevalence
????Infarct Size and Shock
MEDICAL MANAGEMENT OF MYOCARDIAL INFARCTION
STATES OF IMPAIRED MYOCARDIUM
????Hibernating Myocardium
????Stunned Myocardium
????Diagnosis of Viable Myocardium
????Treatment of Stunned Myocardium
????Summary
RATIONALE FOR AGGRESSIVE MANAGEMENT OF MYOCARDIAL INFARCTION
REPERFUSION
????Methods of Reperfusion
????????ROLE OF THROMBOLYTIC THERAPY
????????CARDIOGENIC SHOCK
????????SUMMARY
????Role of PTCA
????????CARDIOGENIC SHOCK
????????SUMMARY
????????INTRACORONARY STENTS
????Role of Coronary Artery Bypass Grafting (CABG)
????????TIMING AFTER INFARCTION
????????RISK FACTORS
????????CARDIOGENIC SHOCK
????????ADVANTAGES OF CABG
????????DISADVANTAGES OF CABG
????????SUMMARY
USE OF THE INTRA-AORTIC BALLOON PUMP
ROLE OF CIRCULATORY ASSIST
????Weaning of Circulatory Support
????Ethical Considerations
SURGICAL MANAGEMENT
????New York Presbyterian (Columbia Center) Approach
????Operative Techniques for Acute Myocardial Infarction
????????ANESTHESIA
????????BLEEDING
????????CHOICE OF CONDUITS
????????INTRAOPERATIVE CONSIDERATIONS
????????POSTOPERATIVE CARE
CONCLUSION
REFERENCES

?? INTRODUCTION
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The ability of surgical interventions to minimize myocardial loss following myocardial infarction has advanced dramatically over the past two decades. Acute myocardial infarctions still afflict approximately 1.1 million individuals each year in the United States.1 About 250,000 Americans a year die before reaching the hospital.1 Prompt medical attention, including transport to the hospital, diagnosis, and treatment of the myocardial infarction, is critical to patient survival. Since 1989, the death rate due to acute myocardial infarctions has declined 24%, while the actual number of deaths declined only 7%.1 Over the last 40 years, especially during the 1980s, new pharmacologic agents, interventional cardiology procedures, and coronary artery bypass surgical techniques have advanced and have led to a decrease in the overall morbidity and mortality associated with acute myocardial infarction.2,3 Despite this overall improvement, mechanical and electrical complications such as cardiogenic shock, rupture of the ventricular septum or free wall, acute mitral regurgitation, pericarditis, tamponade, and arrhythmias challenge the medical community caring for patients presenting with acute myocardial infarction on a daily basis.2,3 Of these complications, cardiogenic shock complicating acute myocardial infarctions has the most significant impact on in-hospital mortality and long-term survival. Loss of more than 40% of functioning left ventricular mass is the major cause of cardiogenic shock and is determined by both the degree of preinfarction ventricular dysfunction and the size of the infarcted vessel.4,5 Restoration of blood flow to the threatened myocardium offers the best chance of survival following acute coronary occlusion, but the means and timing of revascularization continue to be a highly debated and studied topic. Thrombolytics, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery have decreased the mortality associated with acute myocardial infarctions. Advances in myocardial preservation and mechanical support lead the surgical armamentarium in the treatment of acute myocardial infarctions.


?? PATHOGENESIS OF ACUTE OCCLUSION
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Myocardial ischemia due to coronary occlusion for as little as 60 seconds causes ischemic zone changes from a state of active systolic shortening to one of passive systolic lengthening.6 Occlusions for less than 20 minutes usually cause reversible cellular damage and depressed function with subsequent myocardial stunning. Furthermore, reperfusion of the infarct leads to variable amounts of salvageable myocardium. After 40 minutes of ischemia followed by reperfusion, 60% to 70% of the ultimate infarct is salvageable, but this decreases dramatically to 10% after 3 hours of ischemia.7,8 Animal model evidence has also demonstrated that 6 hours of regional ischemia produces extensive transmural necrosis.9 The exact timing in humans is even more difficult to analyze because of collateral flow, which is a major determinant of myocardial necrosis in the area at risk in humans.8 The collateral blood supply is extremely variable, especially in patients with long-standing coronary disease. However, collateral flow is jeopardized with arrhythmias, hypotension, or the rise of left ventricular end-diastolic pressure above tissue capillary pressure.7 Thus loss of collateral flow to the infarct area may lead to the cellular death of salvageable myocardium. Control of blood pressure and prevention of arrhythmias are vital during this immediate time after infarction.

Many clinical trials have shown the beneficial effects of early reperfusion within 24 hours after acute myocardial infarction.10 Although benefits of late reperfusion beyond 24 hours, particularly in asymptomatic patients, have yet to be shown in large clinical studies, advocates for aggressive management believe that reperfusion is warranted to preserve the border areas that may be underperfused during the early days after an infarction. While some of these patients may develop objective evidence of ischemia, the clinical assumption that a hypotensive patient with a suddenly dilated and pressure-overloaded ventricle is prone to losing more muscle mass in border zones of the infarct is reasonable. This is true even in patients who have had complete revascularization. Conservative measures, such as nitroglycerin and intra-aortic balloon pumps, have demonstrated their efficacy in this population of patients without clearly salvageable myocardium by improving coronary blood supply and reducing the work demand of the left ventricle. More radical approaches such as insertion of a left ventricular assist device (LVAD) have been advocated as well. At our center, placement of long-term assist devices into this group of patients has sometimes resulted in significantly improved ventricular function at the time of device explantation months later.11,12

Table 24-1 outlines the effects of anatomical, physiological, and therapeutic variables on the evolution of final infarct size. Anatomically, the location of the coronary obstructive lesion and additional diseased vessels and the presence of collateral flow will determine the extent of early injury, especially for borderline areas. However, ventricular remodeling of the infarct has important consequences influencing ventricular function after myocardial infarction.13 Thus appropriate and aggressive invasive therapies such as PTCA, IABP, CABG, controlled reperfusion, and LVAD insertion can mitigate myocardial injury and salvage borderline areas even if the interventions occur many hours or days after the initial infarction, particularly in patients with ongoing ischemia.


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TABLE 24-1 Factors that influence the evolution and severity of acute myocardial infarction

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Reperfusion injury also contributes to myocardial damage as free oxygen radicals are released and destroy endothelial cells and produce interstitial edema. The timing and management of reperfusion effects on myocardial damage may have an impact on both survival and functional recovery of individuals following acute myocardial infarction.14 Some centers have argued convincingly that controlled reperfusion with specially designed perfusate and a decompressed, energy-conserving ventricle resting on cardiopulmonary bypass is the best means to preserve muscle mass.15


?? CARDIOGENIC SHOCK
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Definition

Cardiogenic shock is defined clinically as a systolic blood pressure below 80 mm Hg in the absence of hypovolemia, peripheral vasoconstriction with cold extremities, changes in mental status, and urine output of less than 20 mL/h. Hemodynamic parameters for cardiogenic shock include cardiac index less than 1.8 L/min/m2, stroke volume index less than 20 mL/m2, mean pulmonary capillary wedge pressure greater than 18 mm Hg, tachycardia, and a systemic vascular resistance of over 2400 dyn?sec/cm5. These patients are defined as type IV by the Killip classification, a widely used system to classify myocardial infarctions.16

Prevalence

Shock is the most common cause of in-hospital mortality following myocardial infarction.17 The in-hospital mortality associated with cardiogenic shock has remained unchanged at approximately 80% despite the development of new treatment modalities.17 Cardiogenic shock occurs in 2.4% to 12.0% of patients with acute myocardial infarction.18 Since 1975, the incidence of cardiogenic shock complicating acute myocardial infarctions has remained constant at 7.5%, ranging between 5% and 15% (Table 24-2).17 One reason these figures may have remained constant is the increasing efficiency of emergency medical systems in resuscitating patients in the community and bringing them to the hospital. Previously, these patients would have died before reaching the hospital. Similarly, there has been a decrease in the incidence of out-of-hospital deaths due to coronary disease between 1975 and 1988.17 The key to success in patients in shock is early intervention and revascularization. In a prospective randomized study, Hochman et al showed that revascularization within 6 hours of diagnosis of cardiogenic shock confers survival benefits, particularly in those patients under 75 years of age.19,20 Use of mechanical circulatory support also may play a role by resting stunned myocardium to allow its recovery and to prevent the irreversible end-organ injury that may result from prolonged shock.11,12


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TABLE 24-2 Crude incidence rates and adjusted risk estimates for cardiogenic shock resulting from acute myocardial infarction

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Infarct Size and Shock

Shock is directly related to the extent of the myocardium involved. Myocardial infarctions resulting in loss of at least 40% of the left ventricle have been shown to result in cardiogenic shock.4,5,21 Autopsy findings also revealed marginal extension of the recent infarct and focal areas of necrosis in patients with cardiogenic shock.4 Extensive three-vessel disease is usually found in individuals with cardiogenic shock, and extension of the infarct is an important determinant in those individuals.4,5,21 Limiting the size of the infarct and its extension is the key to therapeutic interventions in patients with myocardial infarction. By following creatinine phosphate kinase (CPK) levels, Gutovitz et al22 showed that the progression/extension of myocardial damage results in cardiogenic shock. Patients who develop shock have higher peak values.


?? MEDICAL MANAGEMENT OF MYOCARDIAL INFARCTION
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The management of patients with acute myocardial infarctions demands expeditious treatment and decision making. With the ultimate goal of reperfusing the ischemic myocardium, treatment strategies should be directed toward reducing myocardial oxygen demand, maintaining circulatory support, and protecting the threatened myocardium before irreversible damage and expansion of the infarct occur.

Both clinical and basic science research have demonstrated that reperfusion is the main treatment option for acute myocardial infarction. Unfortunately, the majority of patients with myocardial infarction receive only conservative medical management; only 40% of patients having an acute myocardial infarction receive thrombolytic therapy, the most common means of reperfusion.23

A major tenet of medical management is the provision of adequate arterial oxygenation, defined as greater than 90% saturation. Supplemental oxygen and mechanical ventilation, including positive end-expiratory pressure and endotracheal intubation, aid in the management of pulmonary edema.

Nitroglycerin dilates epicardial arteries, increases collateral flow, and decreases ventricular preload. Although clearly beneficial in the treatment of myocardial infarction, nitrates may increase ventilation-perfusion mismatch and cause hypotension due to preload reduction.

Adequate analgesia is also beneficial. Morphine sulfate, the most commonly used analgesic, reduces preload and afterload, myocardial oxygen demand, anxiety, and circulating catecholamines. Side effects include hypotension and respiratory depression, each of which is treatable with basic resuscitative efforts.

Antiarrhythmic therapy, including lidocaine, is indicated under certain guidelines, along with atropine and countershock therapy when arrhythmias occur. Since arrhythmias are one of the most common complications after myocardial infarction, electrocardiographic (ECG) monitoring is recommended for the first 48 to 72 hours.

Arterial monitoring and the balloon flotation catheter aid in the management of patients who are hemodynamically unstable, developing congestive heart failure, or developing mechanical complications of a myocardial infarction. Long-term therapy for uncomplicated myocardial infarction includes the use of beta blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors.

Medical management includes the use of vasopressors and inotropic agents as first-line treatment strategies for cardiogenic shock. Optimizing filling pressure by balancing fluid management and diuretics is essential. Pulmonary capillary wedge pressures should be kept in the 16- to 22-mm Hg range.2

The use of dobutamine and dopamine is part of the pharmacologic armamentarium. These agents affect adrenergic receptors in different ways. Dopamine at doses of 5 to 8 ?/kg/min stimulates beta-adrenergic receptors; at higher doses, alpha-adrenergic receptors are activated. At rates of more than 10 ?/kg/min, left ventricular filling pressures rise and increase myocardial oxygen consumption. Dobutamine affects beta-adrenergic receptors and thus decreases afterload while stimulating the myocardium. Although vasopressors are necessary to maintain adequate perfusion pressures, they also increase afterload of the heart and increase myocardial oxygen demand, potentially worsening ischemia and extending the area of infarction.

While medical management of cardiogenic shock complicating acute myocardial infarctions is associated with high mortality, early revascularization will reduce mortality. As will be discussed later, early revascularization with PTCA or CABG has been shown to be the treatment of choice in this cohort.

In contrast to using inotropic agents to improve circulation, beta blockers have been used successfully to reduce death after infarction, probably due to their ability to reduce myocardial oxygen demand and arrhythmias. In hypotensive patients or individuals suffering bradycardia after infarctions involving the right coronary artery, beta blockade is contraindicated. Other mainstay therapies mentioned earlierheparin, nitrates, and morphinealso comprise the traditional medical management of these critically ill patients.


?? STATES OF IMPAIRED MYOCARDIUM
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Coronary insufficiency can result in three states of impaired myocardium: infarcted, hibernating, and stunned. Each state requires separate clinical interventions and carries different prognostic implications. Infarcted myocardium is irreversible myocardial cell death due to prolonged ischemia. Hibernating myocardium is a state of impaired myocardial and left ventricular function at rest due to reduced coronary blood flow that can be restored to normal if a normal myocardial oxygen supply-demand relationship is reestablished.24,25 Hibernating myocardium is defined as contractility-depressed myocardial function secondary to severe chronic ischemia that improves clinically immediately following myocardial revascularization. Stunned myocardium is left ventricular dysfunction without cell death that occurs following restoration of blood flow after an ischemic episode. If a patient survives the insult resulting from a temporary period of ischemia followed by reperfusion, the previously ischemic areas of cardiac muscle eventually demonstrate improved contractility (Table 24-3).


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TABLE 24-3 States of myocardial cells after periods of ischemia

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Hibernating Myocardium

Hibernation may be acute or chronic. Carlson et al26 showed that hibernating myocardium was present in up to 75% of patients with unstable angina and 28% with stable angina. The entity also occurs after myocardial infarction. Angina after myocardial infarction commonly occurs at a distance from the area of infarction.27 In fact, mortality is significantly higher in patients with ischemia at a distance (72%) compared with ischemia adjacent to the infarct zone (33%).27 It is the hibernating myocardium that may be in jeopardy and salvageable, although its presence is usually incidental to the occurrence of the acute infarction. By distinguishing between hibernating myocardium and irreversibly injured myocardium, a more aggressive approach to restoring or improving blood flow to the area at risk is reasonable. Function often improves immediately after revascularization of appropriately selected regions.

Stunned Myocardium

In the 1970s it was observed that after brief episodes of severe ischemia, prolonged dysfunction with gradual return of contractile activity occurred. In 1982 Braunwald and Kloner28 coined the phrase stunned myocardium. Stunning is a fully reversible process despite the severity and duration of the insult if the cells remain viable. However, myocardial dysfunction, biochemical alterations, and ultrastructural abnormalities continue to persist after return of blood flow. Within 60 seconds of coronary occlusion, the ischemic zone changes from a state of active shortening to one of passive shortening.6 Coronary occlusion lasting less than 20 minutes is the classic model reproducing the stunning phenomenon.2830

The most likely mechanisms of myocardial stunning are calcium overload, generation of oxygen-derived free radicals, excitation-contraction uncoupling due to sarcoplasmic reticulum dysfunction, or a combination thereof. Other mechanisms that may contribute to the stunning phenomenon include insufficient energy production, impaired energy use by myofibrils, impaired sympathetic neural responsiveness, impaired myocardial perfusion, damaged extracellular collagen matrix, and decreased sensitivity of myofilaments to calcium (Table 24-4).29,31,32


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TABLE 24-4 Mechanisms of contractile dysfunction after myocardial stunning

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Stunned myocardium can occur adjacent to necrotic tissue after prolonged coronary occlusion and can be associated with demand-induced ischemia, coronary spasm, and cardioplegia-induced cardiac arrest during cardiopulmonary bypass. Clinically these regions are edematous and even hemorrhagic. They also have a propensity for arrhythmias, which can lead to more extensive ventricular stunning and hypotension with subsequent infarction of these regions.

In summary, infarcted myocardium is nonviable myocardium, while hibernating myocardium is viable myocardium that is chronically dysfunctional due to impaired blood supply. Stunned myocardium is viable myocardium that is acutely dysfunctional after adequate blood supply has been restored.

Diagnosis of Viable Myocardium

Mechanisms to identify patients with myocardial stunning and hibernation include ECG findings, radionuclide imaging, positron emission tomography (PET), dobutamine echocardiography, and more recently MRI. Thallium identifies perfusion-related defects of the myocardium and can distinguish between viable and scarred myocardium as well. However, early redistribution of thallium does not distinguish between hibernating and scarred myocardium since many segments with irreversible defects by thallium improve after reperfusion.33 Redistribution imaging and reinjection imaging improve the predictive value of thallium imaging in distinguishing hibernating myocardium.

PET measures the metabolic activity of myocardial cells. It has high positive and negative predictive values.34 Many studies have suggested that PET is perhaps the best diagnostic tool to assess myocardial viability.35

Dobutamine echocardiography identifies hibernating and stunned myocardium by monitoring changes in segmental wall motion while the heart is stressed inotropically and chronotropically by dobutamine infusion. It has comparable specificity, sensitivity, and, more importantly, positive predictive value.36

MRI, a recently emerging technique, also has demonstrated effectiveness in distinguishing hibernating myocardium.37 To date, it has not been proved to be sensitive and specific enough for routine use.

Treatment of Stunned Myocardium

Several approaches to management of this critically ill group should be taken. Blocking the production of oxygen free radicals will reduce both additional cell death and edema in stunned myocardium. By reducing inflammation, the prothrombotic effects on injured endothelial cells also can be reduced and thus enhance ventricular recovery. Several techniques attack the production or effects of these oxygen free radicals. Allopurinol blocks the xanthine oxidase-hypoxanthine pathway and decreases superoxide anion radicals; however, clinical trials have yielded conflicting results.3840

Iloprost, an analogue of prostacyclin, has demonstrated some effectiveness in reducing stunning in animals. The proposed mechanism is inhibition of neutrophil and platelet function and reduction in the production of oxygen free radicals. In the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) trial, iloprost did not show improved ventricular function after reperfusion with tissue plasminogen activator (t-PA).41

Recombinant superoxide dismutase (SOD), an oxygen free radical scavenger, is a hydrophilic enzyme that does not cross the cell membrane. Additionally, SOD works most effectively if it is in tissue prior to reperfusion injury and oxygen free radical production.42,43 Perhaps because of these two limitations, the use of SOD has not yet shown clinical effectiveness.44

Other pharmacologic agents, including calcium antagonists, nitrates, beta-blocking agents, and angiotensin-converting enzyme inhibitors, also have been studied with some beneficial results.4549 Recent clinical studies have shown that patients receiving calcium channel blockers had improved recovery from stunning over nitrate therapy.50,51 Intracellular adhesion molecule blockers and p-selectin blockers also may prove beneficial in the coming years.

The use of inotropic agents can overcome stunning in both animal experiments and human observation. It is recognized that contractility of reversibly injured myocardium can be enhanced by catecholamines. Thus inotropic agents may have a role in supporting the patient with borderline function until the stunned myocardium can recover.43

Hemodynamic stability must be maintained while stunned myocardium is recovering or being treated by one of the above-mentioned means. Short-term mechanical circulatory devices can aid in the support of patients until the myocardium has sufficiently recovered.

Summary

Differentiation between infarcted, hibernating, and stunned myocardium guides therapeutic options in patients with poor ventricular function. If adequate regions of hibernating myocardium are present as documented by PET, thallium scanning, or dobutamine echocardiography, revascularization may allow ventricular recovery. In patients without evidence of hibernating or stunned myocardium, medical management or transplantation is a better option.

Further distinction is required between stunned and hibernating myocardium. Hibernating myocardium requires revascularization to restore blood supply to this area. Stunned myocardium requires only support, which may take the form of pharmacologic manipulations, including addition of epinephrine, dobutamine, and/or amrinone. If conservative measures fail, the intra-aortic balloon pump (IABP) or short-term LVAD support becomes necessary.


?? RATIONALE FOR AGGRESSIVE MANAGEMENT OF MYOCARDIAL INFARCTION
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Randomized trials have shown beneficial effects of early reperfusion within 12 hours and possibly up to 24 hours after acute myocardial infarction.10 Early reperfusion clearly reduces infarct size in the major areas at risk. Controlled reperfusion may be even superior. The arguments are more difficult to make for patients outside the 24-hour window; however, patients with ongoing ischemia often have ischemic border regions that are prone to arrhythmias and necrosis. In addition, these patients are at risk for prolonged periods of hypotension with resulting end-organ injury and further left ventricular dysfunction. Even if revascularization does not appear critical, ventricular unloading with IABP or LVAD may provide the bridge to recovery needed in patients dying after myocardial infarction. The major limiting factors to aggressive surgical management are major comorbidities, which make continuation of life undesirable or unlikely, and an unclear neurologic status, especially after a period of cardiopulmonary arrest.


?? REPERFUSION
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Although restoration of blood flow to ischemic regions is essential, the accompanying reperfusion injury initially can worsen rather than improve myocardial dysfunction. The area at risk is affected not only by reperfusion but also by the conditions of reperfusion and the composition of the reperfusate.14 Thus controlling reperfusion itself may aid in reducing myocardial infarct size and ventricular injury.

At the cellular level, myocardial ischemia results in a change in energy production from aerobic to anaerobic metabolism. The consequences of ischemia vary from decreased adenosine triphosphate production and increased intracellular calcium to decreased amino acid precursors such as aspartate and glutamate. These changes can be reversed only by reperfusion.

However, as oxygen is reintroduced into a region, oxygen free radical generation ensues with resulting cellular damage. Cellular swelling and/or contracture leads to a "no-reflow phenomenon" that limits the recovery of some myocytes and possibly adds to irreversible injury of others. The production of oxygen free radicals during ischemia and at the time of reperfusion is the leading mechanism proposed to explain cellular injury. Four basic types of reperfusion injury have been described: lethal cell death, microvascular injury, stunned myocardium, and reperfusion arrhythmias (Table 24-5).


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TABLE 24-5 Potential types of reperfusion injury

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Buckberg et al14,15,5268 conducted studies of controlled reperfusion after ischemia and produced a clinical application for controlled reperfusion. The conditions of reperfusion and the composition of the reperfusate allowed more muscle salvage, less postischemic edema, and greater immediate recovery of systolic shortening than uncontrolled reperfusion.52 The composition of the reperfusate was designed to provide oxygen, reduce calcium influx, reverse acidosis, mobilize edema, and replenish substrates. To accomplish this, the cardioplegic solution was hyperosmolar and basic and contained blood, a chelating agent, aspartate, and glutamate (Table 24-6).53 The duration of reperfusion, 20 minutes, as well as the dose, was critical.60


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TABLE 24-6 Buckberg cardioplegic solution to decrease reperfusion injury

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The surgical strategy of controlled reperfusion, especially as espoused by Buckberg et al, includes several elements. First, extracorporeal circulation is established as expeditiously as possible with venting of the left ventricle as required. Initially, antegrade cardioplegia is delivered using either a warm Buckberg solution to rebuild ATP stores or cold, high-potassium cardioplegia to achieve rapid diastolic arrest. We routinely add retrograde cardioplegia to ensure global cooling, even in areas of active ischemia. The temperatures of the anterior and inferior walls of the ventricle are measured to ensure adequate cooling. After each distal anastomosis, cold cardioplegia is infused into each graft and the aorta at 200 mL/min over 1 minute. This is followed by retrograde infusion through the coronary sinus for 1 minute. After completion of the final distal anastomosis, warm substrate-enriched blood cardioplegia is given at 150 mL/min for 2 minutes into each anastomosis and the aorta. After removal of the aortic cross-clamp, regional blood cardioplegia is given at 50 mL/min into the graft supplying the region at risk for 18 minutes. The proximal vein grafts are then completed, followed by reestablishment of normal blood flow. To decrease oxygen demand, the heart is allowed to beat in the empty state for 30 minutes. After this time, the patient is weaned off bypass.

Application of the Buckberg solution and technique has been shown to be effective in improving mortality rates and myocardial function after acute coronary occlusion. With ischemic times averaging 6 hours, a prevalence of multivessel disease, and cardiogenic shock, the overall mortality in patients with acute coronary arterial occlusions who underwent surgical revascularization applying this method of reperfusion was 3.9%. Postoperative ejection fractions averaged 50%.15 Surgical revascularization in this series using controlled reperfusion compared favorably with percutaneous transluminal coronary angioplasty (PTCA) in several large series.15 The superior results of this method for the treatment of cardiogenic shock, a 9% mortality, have brought this method to the forefront in the treatment of cardiogenic shock (Table 24-7).15


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TABLE 24-7 Reperfusion with Buckberg cardioplegic solution in patients with acute myocardial infarction

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Methods of Reperfusion

ROLE OF THROMBOLYTIC THERAPY

Since myocardial salvage depends on reperfusion of occluded coronary arteries, rapid dissolution of an occluding thrombus with thrombolytic therapy is an appealing intervention. Intracoronary streptokinase in patients with acute myocardial infarction demonstrates that thrombolytic therapy is a safe and efficient way to achieve the desired early reperfusion.69 Following this study, a number of multi-institutional megatrials showed the effectiveness of thrombolytic therapy in treating acute myocardial infarctions.

The trial of the Italian Group for the Study of Streptokinase in Myocardial Infarction (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardio, GISSI)70 and the Second International Study of Infarct Survival (ISIS-2)71 found a reduced hospital mortality in patients treated with streptokinase. The effectiveness of tissue-type plasminogen activator (t-PA) also has been evaluated in randomized studies. The Thrombolysis in Myocardial Infarction (TIMI) study72 and the European Cooperative Study Group (ECSG)73 demonstrated the effectiveness of t-PA for the treatment of acute myocardial infarction.

When streptokinase and t-PA were compared, two studies failed to demonstrate any difference in mortality.74,75 A third study, however, the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) trial, supported the use of t-PA by demonstrating a more rapid and complete restoration of coronary flow that resulted in improved ventricular performance and reduced mortality.76,77 After 90 minutes, 54% of the group receiving t-PA and heparin had normal flow, compared with less than 40% in the other groups. While patency rates were similar after 3 hours, 30-day mortality was lowest in patients whose flow was normal at 90 minutes (4.4%).76,77 This supports the importance of rapid restoration of flow. Although the actual difference in patient survival between the two groups was small (6% vs. 7% mortality), the number of lives saved each year may justify the added expense of t-PA.76,77 The mode of delivery of t-PA has been credited for the differences in the outcomes in these trials. Differences in methods of delivery between t-PA and streptokinase and adjuvant therapy with aspirin and heparin, along with cost factors of each agent, have stimulated a continuing debate over these two drugs.23 Table 24-8 summarizes some of the previously mentioned trials.


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TABLE 24-8 Trials comparing thrombolytic therapy with conventional therapy

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While thrombolyis improves survival and ventricular function, the patency of infarct-related arteries is reported to be between 50% and 85%.7077 Normal flow should be achieved in 60% of patients by today's standards. Thrombolytic therapy works well but is not without complications, including bleeding and intracranial hemorrhage.78 Bleeding is usually minor and occurs mostly at the sites of vascular puncture. Intracranial hemorrhage and stroke rates are around 1% and are an "acceptable" risk.

CARDIOGENIC SHOCK

Thrombolytic therapy for patients presenting in cardiogenic shock or heart failure does not appear to improve survival in this population but may decrease the incidence of patients developing heart failure after myocardial infarction.79 However, a recent randomized SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) trial found clear survival benefits for early revascularization by PTCA or CABG over initial medical stablization by thrombolytic therapy.18,19

SUMMARY

Thrombolytic agents for the treatment of myocardial infarction have demonstrated several important points. Survival is improved by decreasing time to reperfusion. The GUSTO trial showed that patients treated within the first hour had the greatest improvement in survival, with a 1% reduction in mortality for each hour of time saved.76,77 Thrombolytic therapy is easy to administer in the community by trained personnel. Since the time to reperfusion is a critical element in preserving myocardium, thrombolytic therapy is ideal for most communities. One study evaluated the use of prehospital-administered thrombolytics and found a trend toward improved survival.80 Further large-scale trials must be initiated before recommendations are made. However, in communities, thrombolytics should be used for treatment of patients with acute myocardial infarction.

Role of PTCA

Since the first reported use of percutaneous transluminal coronary angioplasty (PTCA) by Gruntzig et al81 in 1979, the efficacy of this procedure in the treatment of coronary artery disease has been well recognized. A number of studies have evaluated the efficacy of primary PTCA in the treatment of acute myocardial infarction. Overall, PTCA hospital mortality rates range from 6% to 9%.8287

Several different strategies employing PTCA for acute myocardial infarction have been developed and examined through clinical trials. Primary, rescue, immediate, delayed, and elective PTCA are options for the treatment of acute myocardial infarction. Primary PTCA uses angioplasty as the method of reperfusion in patients presenting with acute myocardial infarction. Rescue, immediate, delayed, and elective PTCA all are done in conjunction with or following thrombolytic therapy. Rescue PTCA is done following recurrent angina or hemodynamic instability following thrombolytic therapy. Immediate PTCA is performed in conjunction with thrombolytic therapy, and delayed PTCA occurs during the intervening hospitalization. Finally, elective PTCA is done following thrombolytic therapy and medical management when a positive stress test is obtained during the same hospitalization or soon thereafter.

Primary PTCA functions in several roles for the treatment of acute myocardial infarctions. Since there are some absolute and relative contraindications to thrombolytics, PTCA is the best method of reperfusion in patients with acute myocardial infarction, according to studies that evaluated PTCA as first-line therapy. Several studies evaluated the role of PTCA compared with thrombolytic therapy. The Primary Angioplasty in Myocardial Infarction Study Group trial concluded that immediate PTCA without thrombolytics reduced occurrence of reinfarction and death and was associated with a lower rate of intracranial hemorrhage. The trial did not show any differences in left ventricular systolic function.83 Myocardial salvage is similar for PTCA and thrombolytic therapy84; however, primary PTCA may be slightly less costly than thrombolytic therapy.85

There are limits to the use of primary PTCA. Logistic and economic constraints apply to invasive modes of therapy. Catheterization laboratories and personnel must be ready at all times. This is not practical in most communities, and transportation to tertiary care centers raises costs considerably.

Immediate PTCA following thrombolytic therapy does not improve clinical outcome and is associated with increased complication rates. The ECSG,73 the TAMI trial,86 and the TIMI-IIA trial87 demonstrated that immediate angioplasty does not improve clinical outcome or left ventricular function compared with delayed angioplasty.73,86,87 Immediate angioplasty is also associated with a higher risk of bleeding and emergent bypass. The ECSG trial demonstrated a lower incidence of bleeding, hypotension, and ventricular fibrillation as well as lower mortality with delayed PTCA.73 The TAMI trial, which compared immediate versus delayed PTCA after thrombolysis, showed no difference in global ventricular function at 1 week between the two groups in patients with angiographically patent infarct arteries.86 Overall, immediate angioplasty does not lead to better ventricular function or clinical outcome compared with elective PTCA. Finally, TIMI-IIA concluded that immediate PTCA after thrombolytic therapy for acute myocardial infarction does not improve survival or ventricular function87 and is associated with increased bleeding, reinfarction, and emergency coronary artery bypass grafting (CABG) (Table 24-9).


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TABLE 24-9 Comparison of percutaneous transluminal coronary angioplasty and thrombolytic therapy

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Delayed PTCA does not improve clinical outcome either. The Treatment of Post-Thrombolytic Stenoses (TOPS) study group concluded that there is no functional or clinical benefit from routine late PTCA after acute myocardial infarction treated with thrombolytic therapy in patients who did not have ischemia on stress testing before hospital discharge.88 However, the TIMI-IIB trial indicated that thrombolytic therapy followed by angioplasty in individuals with symptomatic or provokable ischemia is appropriate.87

CARDIOGENIC SHOCK

Primary PTCA may play a greater role in patients presenting in cardiogenic shock. The GISSI I and II trials demonstrated no benefit from intravenous thrombolysis, with mortality rates of 70%.70,74 In patients presenting in or developing cardiogenic shock after acute myocardial infarction, PTCA improved survival to 40% and 60%.89,90 This improvement was even greater when angioplasty was successful; in-hospital survival rates increased to 70%. In most of these series an IABP was used in conjunction with PTCA. The SHOCK trial showed that revascularization by PTCA or CABG within 6 hours of the onset of cardiogenic shock results in improved 1-year survival (46.7% versus 33.6% for initial medical stablization followed by revascularization) in this high-risk group, particularly for those under the age of 75 years.19,20

SUMMARY

Primary PTCA should be performed in patients with acute myocardial infarction and contraindications to thrombolytic therapy. Patients with established or developing cardiogenic shock should be revascularized early by PTCA rather than initial medical stablization by thrombolytic therapy. Specialized centers that have 24-hour catheterization facilities can provide primary PTCA as a first-line therapy. Rescue PTCA after failed thrombolytic therapy for patients with ongoing ischemia or clinical compromise is also recommended. Finally, elective PTCA should be performed on patients who have recurrent or provokable angina prior to hospital discharge.

INTRACORONARY STENTS

Intracoronary stents may be useful for acute coronary arterial dissections and have proven benefits in lowered rates of restenosis, abrupt closure, and emergent CABG following PTCA. However, critics have argued that stent trials often involved selection bias leading to better outcomes.91 At this time, identification of patients who may or may not require stents and the optimal rate of stent use remains unclear.

Role of Coronary Artery Bypass Grafting (CABG)

The role of surgical revascularization in the treatment acute myocardial infarction has changed considerably over the past 30 years. Improvements in intraoperative management and myocardial preservation techniques have strengthened the surgeon's armamentarium. However, the development and use of thrombolytic therapy and PTCA offer alternatives to surgery.

Early studies reported increased morbidity and mortality for patients undergoing surgical revascularization within 30 days of the infarct.92 A concern arose over a high risk of extension and hemorrhage into infarction after surgical revascularization of acute myocardial infarction.93 Medical management was believed the more prudent therapy. The only absolute indications for emergent operative intervention treatment of acute myocardial infarctions during this era were papillary muscle rupture, ventricular septal defect, and left ventricular rupture. For these entities, surgery was the only hopeful option.

During the 1980s, reports appeared recommending surgical revascularization in preference to medical therapy for acute myocardial infarction.94100 Mortality rates under 5% were reported. Critics argued that these studies lacked randomization or consecutive entry of patients, that preoperative stratification was absent, and that enzyme levels were not included. Inherent bias that favored surgery in low-risk patients was believed to be the reason for the excellent outcomes.101

At the time these reports surfaced, thrombolytic therapy and interventional cardiology were emerging as alternative options for acute infarction. With the availability of thrombolytics and PTCA, large multicenter trials began looking at the efficacy and usefulness of these two techniques. Randomized trials using CABG were not done, and thus this option was never established as an option for acute myocardial infarction.

However, several centers continued to use surgical revascularization to treat acute myocardial infarction. Excellent results were achieved by coordinated community and hospital systems. However, practical, logistic, and economic constraints relegate surgical revascularization to a third option behind thrombolytics and PTCA for the primary treatment of acute myocardial infarction.

There continue to be several scenarios that require emergent or urgent surgical revascularization. Failure of thrombolytics and PTCA with acute occlusion may require surgical intervention. Additionally, CABG for postinfarction angina has became a critical step in the pathway of treating acute myocardial infarction.

TIMING AFTER INFARCTION

If surgical revascularization within 6 hours after the onset of symptoms is feasible, the mortality rate is improved over that of medically treated, nonrevascularized patients.9497 While these early studies were not controlled and were criticized for selection bias, they did demonstrate that surgical revascularization may be performed with an acceptable mortality in the presence of acute myocardial infarction with improved myocardial protection, anesthesia, and surgical techniques. However, with the advent of thrombolytic therapy, PTCA, and an aging population, the surgical patient we encounter today bears little resemblance to the patient population represented in these early data.

Recent analyses of the New York State Cardiac Surgery Registry, which included every patient undergoing a cardiac operation in the last decade in the state of New York, had resulted in valuable information regarding the optimal timing of CABG in acute myocardial infarction. In this large and contemporary patient population, there is a significant correlation between hospital mortality and time interval from acute myocardial infarction to time of operation, particularly if CABG was performed within one week of acute myocardial infarction. In addition, patients with transmural and nontransmural acute myocardial infarction have different trends in mortality when the time course is taken into consideration. Mortality for the nontransmural group peaked if the operation was performed within 6 hours of acute myocardial infarction, then decreased precipitously (Table 24-10).102 On the other hand, mortality for the transmural group remained high during the first 3 days before returning to baseline (Fig. 24-1). 103 Multivariable analyses confirmed that CABG within 6 hours for the nontransmural group and 3 days for the transmural group were independently associated with in-hospital mortality.102,103 Optimal timing of CABG in patients with acute myocardial infarction is a controversial subject. Early surgical intervention has the advantage of limiting the infarct expansion and ventricular remodeling that may result in possible ventricular aneurysm and rupture.104 However, there is the theoretical risk of reperfusion injury, which may lead to hemorrhagic infarction resulting in extension of infarct size, poor infarct healing, and scar development.105 The data from these studies caution against early revascularization, particularly among patients with transmural acute myocardial infarction within 3 days of onset. Some have advocated the use of mechanical support to stabilize and allow elective rather than emergent surgery.106 Utilizing mechanical support "prophylactically" instead of CABG to improve outcome, however, would require placement of such support in many unnecessary cases. If revascularization cannot be delayed, aggressive mechanical support such as a left ventricular assist device (LVAD) must be available since mortality is most likely due to pump failure. Furthermore, mechanical circulatory support has been shown to be efficacious as a bridge to ventricular recovery or transplantation for this patient cohort.12 While emergent cases such as structure complications and ongoing ischemia clearly cannot be delayed, nonemergent cases, particularly patients with transmural acute myocardial infarction, may benefit from delay of surgery. Early surgery after transmural acute myocardial infarction has a significantly higher risk and surgeons should be prepared to provide aggressive cardiac support including LVADs in this ailing population. Waiting in some may be warranted.


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TABLE 24-10 Comparison of hospital mortality with respect to time of surgerytransmural vs. nontransmural myocardial infarction

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FIGURE 24-1 Hospital mortality versus timing of CABG after transmural MI. Among patients who underwent CABG after transmural MI in New York State, mortality was more than doubled that of the baseline value when surgery was performed within 3 days of transmural MI.

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RISK FACTORS

In addition to timing of surgery as discussed above, risk factors include urgency of the operation, increasing patient age, renal insufficiency, number of previous myocardial infarctions, hypertension,107 reoperation, cardiogenic shock, depressed left ventricular function and the need for cardiopulmonary resuscitation,108 left main disease, female sex, left ventricular wall motion score,109 IABP, and transmural infarction.110 Characteristics associated with better outcome early after myocardial infarction include preservation of left ventricular ejection fraction, male gender, left main disease, younger patients, and subendocardial versus transmural myocardial infarction.

CARDIOGENIC SHOCK

Surgical revascularization in acute myocardial infarction complicated by cardiogenic shock has been shown to improve survival. Cardiogenic shock, as discussed earlier, is accompanied by 80% to 90% mortality rates. DeWood et al111 were the first to demonstrate improved results with revascularization in patients in cardiogenic shock complicating acute myocardial infarction. Patients who were stabilized with an IABP and underwent emergent surgical revascularization had survival rates of 75%. Early surgical revascularization is associated with survival rates of 40% to 88% in patients in cardiogenic shock due to nonmechanical causes. Guyton et al112 reported an 88% in-hospital survival and a 3-year survival of 88%, with no late deaths reported. Furthermore, the SHOCK trial demonstrated survival benefit in early revascularization by CABG or PTCA within 6 hours of the diagnosis of cardiogenic shock for those under 75 years of age.19,20 Thus, for patients in cardiogenic shock, surgical revascularization is a viable option.

ADVANTAGES OF CABG

Reported survival rates are similar for CABG and PTCA in the treatment of acute myocardial infarction. To date there have been no large randomized clinical trials comparing CABG with PTCA and thrombolytics. Due to the lack of prospective, randomized trials, recommendations must be based on retrospective and observational studies. CABG offers several potential advantages. First, surgical revascularization is the most definite form of treatment of the occlusion. CABG offers the longest patency of revascularized stenotic and occluded arteries in elective cases; 90% of internal mammary arteries are patent at 10 years. Second, CABG also offers more complete revascularization, since all the vessels are treated. Third, difficult distal obstructions can be reached. Fourth, there is controlled reperfusion to reverse ischemic injury and reduce reperfusion injury. Fifth, as with other forms of reperfusion, CABG interrupts the progression of ischemia and necrosis and limits infarct size.

DISADVANTAGES OF CABG

Disadvantages of immediate surgical revascularization include the high mortality associated with early CABG. Rapid availability of catheterization and operating room personnel for emergency procedures imposes logistic and economic constraints. Thus CABG is not readily applicable to the vast majority of patients in the community, and to provide this would strain health care resources. Second, it is difficult to analyze published results of CABG for acute myocardial infarction because randomized trials have not been done. Comparisons thus far have used medically treated patients as controls. Patients in the surgical group may be at lower risk; this might explain their progression to operation rather than continuing medical treatment. Crossover of patients from medical to surgical treatment also may have skewed the data.

SUMMARY

Surgical revascularization following acute myocardial infarction can be performed with excellent results when the timing and patient cohort are appropriate. Most patients do not need such measures and would not benefit from this aggressive form of therapy. However, patients with mechanical complications, those in cardiogenic shock, and those with postinfarction angina are likely to benefit from early CABG.


?? USE OF THE INTRA-AORTIC BALLOON PUMP
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The early use of aortic counterpulsation with an intra-aortic balloon pump (IABP) demonstrated the safety but not efficacy of this device for patients in cardiogenic shock following acute myocardial infarction.113 While survival was not improved, aortic counterpulsation did improve the myocardial oxygen requirements and myocardial energetics were reduced in patients in shock.113 As revascularization techniques for the repair of occluded coronary arteries of patients in cardiogenic shock have improved, use of aortic counterpulsation has found a role as an adjuvant to treatment protocols.

IABP counterpulsation in combination with early reperfusion is effective in the treatment of acute myocardial infarction complicated by cardiogenic shock.111,114 While the major improvement in survival is due to early reperfusion, patients who had combined reperfusion and IABP additionally have improved long-term survival. IABP improves circulatory physiology and decreases end-organ damage in the early shock period before the myocardium is reperfused and recovers function.

Aortic counterpulsation decreases the reocclusion rate, recurrent ischemia, and need for emergency PTCA in patients who have coronary artery patency established by emergency cardiac catheterization following acute myocardial infarction.115 Prophylactic counterpulsation for 48 hours sustains patency in coronary arteries after patency is reestablished following myocardial infarction. No increase in vascular or hemorrhagic complications is observed as compared with controls.115

Weaning from the IABP should take place only after there is clear evidence of myocardial and end-organ recovery. In general, inotropic requirements should be reduced first in order to minimize myocardial stress. The one exception is the development of limb ischemia due to the IABP catheter.


?? ROLE OF CIRCULATORY ASSIST
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Circulatory support devices are reserved for patients who are hemodynamically unstable; however, intervention should not be delayed until after irreversible end-organ injury occurs. This group of shock patients has a mortality rate of 80%, and survival data with the use of assist devices reflect the critical condition of patients treated. Mortality rates have changed very little in the last 20 years despite improvements in medical and surgical therapy.

Patients in cardiogenic shock who are candidates for circulatory assist devices may be divided into two groups: individuals who have stunned myocardium and need a bridge to recovery, and those who have irreversible myocardial damage and need a bridge to cardiac transplantation. For example, if a patient with a previously normal ventricle develops a large myocardial infarction, we prefer short-term support, since enough recovery may occur to allow a fruitful existence with the native heart. However, if a patient with preexisting heart failure has another infarction, the need to definitively bridge the patient to transplant with a long-term implantable device is apparent. Difficulty arises in assessing the results of mechanical assistance for patients following acute myocardial infarction and cardiogenic shock because of these different objectives.

Mechanical assist devices augment systemic perfusion and prevent end-organ damage while resting the stunned ventricle.116 Early studies on implantable LVADs have shown that end-organ function is an early predictor of mortality. Treatment of patients prior to end-organ deterioration is essential for improving the odds for long-term survival. In addition to affecting end-organ function, assist devices also may improve myocardial contractility of postischemic hearts.116 Recent studies have shown that circulatory support early after myocardial infarction improved survival and offered a feasible bridge to recovery or transplantation.11,12

Decisions regarding specific device use depend on the degree of circulatory support needed and many other factors. Selection criteria for device placement include:

  1. Potential reversibility of cardiac dysfunction
  2. Cause of the cardiac dysfunction
  3. Degree of right and left ventricular dysfunction
  4. Amount of circulatory support needed
  5. Importance of the device for myocardial functional recovery
  6. Patient size
  7. Anatomic location of collapse or deterioration
  8. Whether the patient is a candidate for cardiac transplantation
  9. Whether the patient can be anticoagulated
  10. Expected duration of support
  11. Patient's age and severity of comorbid conditions117

At New York Presbyterian Hospital (Columbia Center), several circulatory assist devices are available to aid treatment of each group. Short-term devices that can be placed percutaneously include the IABP and extracorporeal membrane oxygenation. Devices that require sternotomy and are beneficial for short-term use include the ABIOMED and Thoratec pumps. Both these devices primarily treat stunned myocardium, but they are capable of bridging to transplant. These devices are easy to insert, do not require excision of ventricular muscle, and do not compromise ventricular function following device removal. These devices can be removed without the need to reinstitute cardiopulmonary bypass. These devices are effective in patients who require emergency support secondary to cardiogenic shock.

Another device that requires thoracotomy is a direct mechanical ventricular actuation device. This elliptically shaped cup that fits over both ventricles compresses and relaxes the ventricles, simulating directed cardiac actuation. Reports document improved cardiac outputs using this device and survival of several patients over prolonged periods of support.118 (A complete discussion of temporary and long-term ventricular assist devices is found in Chs. 17 and 62.)

The Heartmate (Thoratec, Pleasanton, CA) and Novacor (Ottawa Heart, Ottawa, Canada) LVADs are long-term implantable assist devices that we use for bridging to transplantation. Initial reports of increased mortality in this high-risk patient population have been refuted by studies reporting higher than usual survival in acute MI patients who received VAD support. At our facility, over 80% of this patient cohort have survived until transplantation, a result 3-fold better than databases of extracorporeal systems.

Weaning of Circulatory Support

Cardiac enzyme levels at the time of infarction, ECG changes, and the preinfarction condition of the ventricle help determine the likelihood of LV recovery. If the ventricle is considered not likely to recover, early use of a long-term device is rational. On the other hand, if recovery is possible, the heart should be rested for 3 to 5 days, loaded with the institution's choice of inotropic support, including a phosphodiesterase inhibitor, and allowed to beat and eject. If a transesophageal echocardiogram demonstrates recovery, the short-term support device should be removed in the operating room and kept available for 1 hour while the patient is observed for signs of decompensation. If the device cannot be removed within a week, the heart is not likely to recover. In this event, either a longer-term device is placed or patient support is discontinued.

We have reported a baseline LV recovery in more than half of patients supported for a prolonged period with implantable devices. Upon removal of the device, most of these patients have redeveloped CHF in our experience12 although other centers have reported high success rates.119,120 As our understanding of the underlying causes of LV failure improve, we will be able to design targeted therapies that can be used with temporary device support to facilitate sustainable recovery.

Ethical Considerations

Programs that aggressively pursue surgical approaches to high-risk patients also must aggressively seek termination of care in futile cases. A liaison should be developed with a medical ethics individual or group to provide support for primary caregivers; however, the burden of medical decisions must rest with the attending physician. The family should not be forced to sign declarations withdrawing care unless significant controversy and/or the potential of legal action encumbers the decision. In the case of mechanical circulatory support, each pump of the device can be interpreted as a new intervention and therefore can be terminated if necessary. A precedent for this course of action has been set with mechanical ventilation. If significant neurologic or other end-organ dysfunction has developed and cardiac function has not returned, termination of support is reasonable and appropriate.

The Ethics Committee of the Columbia Presbyterian Center of The New York Presbyterian Hospital has drafted a statement that patients and physicians must review together prior to placement of a ventricular assist device (VAD), or, when circumstances do not permit, immediately thereafter. The statement asserts that VAD restoration of hemodynamic stability in a patient with critical myocardial dysfunction may, for various reasons, not reach the goal of enabling the patient to receive a heart transplant or achieve adequate stability to be discharged home on the device.

The statement reads as follows:

Every effort will be made to help our patients on ventricular assist devices (VAD) to improve to the point where they meet the criteria to receive a heart transplant, or stabilize enough to be discharged from the hospital on the VAD. However, if despite all our efforts, a patient has no reasonable chance of achieving either of these goals, we will discontinue the VAD, as it will, under these circumstances, no longer be serving the purpose for which it was originally used. When this occurs, the VAD will be discontinued only after the physicians caring for the patient are in agreement that the goals for VAD use cannot be met, and have consulted with the patient, or, when the patient is too ill, with the family or friends of the patient.

We believe such a document is needed at the beginning of the patient's care to make clear to the family the goals of VAD use. Specifically, a VAD should not be used solely to prolong a patient's dying. Once a medical determination has been made by both the attending cardiac surgeon and the attending cardiologist that the patient cannot survive to leave the hospital, continued use of the VAD is inappropriate.

If the patient or his health care proxy or surrogates disagree with the decision to discontinue the VAD, the case is submitted to the ethics committee for arbitration.


?? SURGICAL MANAGEMENT
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New York Presbyterian (Columbia Center) Approach

Patients who are potential transplant candidates and who are dying of cardiogenic shock after myocardial infarction are all candidates for placement of a long-term implantable left ventricular assist device (LVAD). If at all possible, a coronary angiogram is obtained to allow revascularization with or without LVAD insertion. Surgery is delayed if the culprit vessel can be opened with angioplasty and the patient stabilized in the catheterization laboratory. If hemodynamics continue to deteriorate, the patient is taken directly to the operating suite, even if infarction occurred earlier than 6 hours before the planned procedure. Hemodynamic observations that favor early CABG are pulmonary artery pressures of less than 60/30 mm Hg and cardiac output of more than 3 L/min. If the hemodynamics are worse, early implantation of a long-term implantable LVAD may be needed, especially if the mixed venous oxygen saturation is less than 50%. The decision to place a long-term LVAD is influenced by the patient score on a screening scale designed for this purpose (Table 24-11). These scores were selected to identify end-organ dysfunction (lung, liver, kidney) and operative constraints (right-sided heart failure and bleeding). We have nearly a 90% survival if the summed scores are less than 5 points versus 30% survival with summed scores of greater than 5 points.121 For this reason, if the total score is greater than 5 points, an attempt is made to stabilize the patient prior to beginning long-term LVAD insertion. Patients with lower scores are offered temporary LVAD.


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TABLE 24-11 Preoperative risk scale for left ventricular assist device placement*

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If a patient is not a potential transplant candidate, our approach is more conservative, since we do not have a safety net if coronary revascularization fails and a temporary support device is inserted. An angiogram must be obtained; if hemodynamics are not favorable and no acute ischemia is present, we delay surgery until pulmonary arterial pressures fall. If the patient is ischemic, we proceed with CABG as described below. If the patient cannot be separated from bypass without high-dose inotropic support including alpha agonists, if the cardiac index is less than 2 L/min/m2, and if left-sided filling pressures remain high with mixed venous oxygen saturations of less than 50%, short-term LVAD support with the ABIOMED system is instituted (Fig. 24-2). IABP alone in this patient population often does not prevent death and almost always results in significant renal, hepatic, and pulmonary dysfunction that significantly complicates patient recovery even if adequate cardiac function returns. Most important, stressing the heart with high-dose inotropic agents and high filling pressures when it is weakest during the early reperfusion period after acute infarction may compromise border zone regions. This concern is especially true of patients with older infarctions (more than 6 hours). We err on the side of implanting this short-term device early, since the survival rate is only 7% if the device is inserted after a cardiac arrest in the recovery room.



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FIGURE 24-2 The inflow cannula for short-term left ventricular assist device support can be placed through the right superior pulmonary vein, the dome of the left atrium, or the left atrial appendage. Lighthouse tip cannulas allow improved venous return.

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Operative Techniques for Acute Myocardial Infarction

ANESTHESIA

Anesthesia is provided by a rapid narcotics-based regimen with perfusion and surgical teams prepared to respond to catastrophic hypotension or cardiac arrest. Transesophageal probes are always placed in these patients if possible. As the patient is prepped, a test dose followed by a loading dose of aprotinin is given.

BLEEDING

Bleeding is a significant complication of emergency CABG and often results in further myocardial depression and pulmonary hypertension. Cytokine release induced by infusion of blood products and thromboxane A2 released by cardiopulmonary bypass stimulate pulmonary hypertension, which can be catastrophic in the setting of right ventricular ischemia. Use of aprotinin decreases bleeding during CABG122,123 and reduces right-sided heart failure and death after LVAD insertion.124 There are reported cases of aprotinin use following thrombolytic therapy for acute myocardial infarction.125 Successful use of aprotinin for reoperative, emergency, or high-risk CABG is common in many institutions.

CHOICE OF CONDUITS

For emergency cases, the choice of conduit should not differ from elective cases in most circumstances. The internal mammary artery is not associated with a higher number of complications compared with saphenous vein grafting in emergent situations and can be used in most circumstances.126,127 There is one reported case of successful use of polytetrafluoroethylene for coronary revascularization in a patient in shock.128

INTRAOPERATIVE CONSIDERATIONS

Decompression of the ventricle during revascularization after acute coronary occlusion decreases muscle damage and improves functional outcome by decreasing wall tension and reducing oxygen consumption (Figs. 24-3 and 24-4).62 Indeed, ventricular decompression reduces metabolic energy consumption by 60%. Diastolic basal arrest, by avoiding the energy of contraction, is the second most important means of minimizing oxygen consumption and further reduces metabolic energy consumption by 30%. Cooling of the patient and heart has an impact only on the final 10% of basal energy requirements.



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FIGURE 24-3 Myocardial oxygen uptake (measured in cc/100 g/min) in beating and working, beating and empty, and arrested hearts. Values after cardioplegia were determined both during cardiopulmonary bypass (cardioplegia) and during regional cardioplegic reperfusion in the working heart (paradoxing muscle). Note (1) marked fall in Mvo2 with cardioplegia in the decompressed heart and (2) O2 requirements of dyskinetic muscle increase 5-fold over cardioplegia alone and equal almost 55% of beating, working needs. (Reproduced with permission from 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.)

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FIGURE 24-4 Regional oxygen uptake during selective cardioplegic reperfusion in dyskinetic and vented cardiac muscle. Stippled areas show requirements in working heart (8.5 to 10.5 cc/100 g/min). Note (1) high O2 demands of dykinetic muscle and (2) marked reduction in demands when noncontracting muscle is decompressed by venting. (Reproduced with permission from 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.)

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Reduction of myocardial energy consumption is best achieved by early institution of cardiopulmonary bypass to maintain a high perfusion pressure. If a coronary salvage catheter has been placed across a tight coronary lesion, the catheter is left in place until just before cross-clamping. Antegrade and retrograde catheters are placed prior to cross-clamping to allow quick instillation of retrograde cardioplegia and protection of the territory supplied by the occluded or compromised vessel. The standard Buckberg protocol is followed, including warm induction to allow regeneration of depleted ATP (adenosine triphosphate) stores.

If the territory at risk is grafted by saphenous vein, this anastamosis is performed first to allow direct instillation of cardioplegia into the territory at risk. The proximal anastomoses should be performed prior to removal of the cross-clamp to allow complete perfusion of the entire heart upon removal of the cross-clamp. The role of off-pump CABG in this setting is appealing, but remains unproven.

While large ventricular aneurysms are treated by resection and patch, debate surrounds smaller aneurysms. Our group does not resect small aneurysms, but some groups are more aggressive. If an aneurysm is resected, the defect is repaired with a patch of bovine pericardium sewn to the fibrotic rim of the endoaneurysm surface. The native left ventricular wall is closed over the patch.

Utilization of the Dor procedure (endoventricular circular patch plasty repair) in the post MI setting is a controversial subject. Recent data have shown surgical remodeling may improve systolic pump function.129 However, a large clinical trial is needed to definitively answer this question.

POSTOPERATIVE CARE

A higher incidence of complications in shock patients compared with nonshock emergencies has been reported. Guyton et al112 report a 47% complication rate associated with cardiogenic shock compared with 13% for patients with nonshock emergencies. This increase in complications probably reflects the preoperative condition of the patients rather than the treatment itself. Long-term follow-up in patients following emergency surgical revascularization shows that survival rates are closely correlated with postoperative ejection fraction and left ventricular size.130,131


?? CONCLUSION
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The treatment of acute myocardial infarction should be divided into two approaches (Fig. 24-5). Uncomplicated acute myocardial infarction can be treated in most community hospitals. In most areas of the country, these patients are treated effectively with thrombolytic therapy and medical management. For communities and facilities that have catheterization laboratories, primary angioplasty may be more cost-effective and produce similar results. At this time, emergency coronary artery bypass surgery is not the most cost-effective approach; randomized, controlled studies to demonstrate advantages of emergency CABG have not yet been performed.



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FIGURE 24-5 Acute myocardial infarction algorithm.

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The approach to acute myocardial infarctions complicated by cardiogenic shock presents a more difficult problem. Mortality rates are high with medical management. Reperfusion therapy is the only real hope for improved survival in this group of patients. Thrombolytic therapy is associated with poor outcomes. Early PTCA and CABG are the primary options in patients under the age of 75. Mechanical circulatory assistance has an important role for supporting patients until the myocardium recovers. Use of pharmacologic agents and means to control reperfusion are important areas of current research and development. Assist devices and artificial heart programs offer indispensible options and must be considered in this patient population, especially since all therapies offer suboptimal results.


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