ST-Segment Elevation Myocardial Infarction



ST-Segment Elevation Myocardial Infarction


James A. de Lemos

David A. Morrow



Advances in the prevention, diagnosis, and management of patients with acute ST-segment elevation myocardial infarction (STEMI) have led to a reduction in mortality from this condition over the past few decades [1]. Rapid delivery of reperfusion therapy remains the cornerstone of management of STEMI. In recent years, substantial improvements in adjunctive therapies and processes of care delivery have been made, and these are expected to contribute to continued improvement in outcomes following STEMI.


Pathophysiology

The initial pathophysiologic event leading to STEMI is rupture or erosion of a lipid-rich atherosclerotic plaque. The atherosclerotic plaque “vulnerable” to rupture tends to have a dense lipid-rich core and a thin protective fibrous cap, and is often not associated with critical narrowing of the arterial lumen. Molecular factors that regulate synthesis and dissolution of the extracellular matrix appear to modulate integrity of the protective fibrous cap. In unstable atherosclerotic lesions, inflammatory cells accumulate at the “shoulder” region of the plaque and release cytokines that degrade extracellular matrix and weaken the fibrous cap at this critical site [2].

Following plaque rupture, platelets adhere to subendothelial collagen, von Willebrand factor, or fibrinogen, and become activated by various local mediators such as adenosine diphosphate (ADP), collagen, and thrombin. Activated platelets undergo a conformational change and secrete the contents of their α-granules, promoting vasoconstriction and clot retraction. Activated platelets also express glycoprotein (GP) IIb/IIIa receptors in increased number and with greater binding affinity; fibrinogen-mediated cross-linking at this critical receptor leads to platelet aggregation. On the phospholipid surface of
the platelet membrane prothrombin is converted to thrombin, catalyzing the conversion of fibrinogen to fibrin [3].








Table 39.1 Differential Diagnosis of Acute MI








































Condition Characterization of pain Physical findings ECG findings Helpful diagnostic tests
Acute coronary syndrome Pressure-type pain at rest, often radiating to neck or left arm Examination often normal; check for signs of cardiogenic shock or CHF ST-segment elevation, ST-segment depression, T-wave abnormalities, LBBB Measurement of cardiac enzymes
Tako-Tsubo cardiomyopathy Similar to AMI, but commonly precipitated by emotional stress Examination often normal; may have signs of CHF Anteroapical ST-segment elevation commonly with T-wave inversion Cardiac enzymes only minimally elevated; anteroapical akinesis; normal coronary arteries
Aortic dissection “Tearing” pain radiating to back Diminished pulse or blood pressure in left arm Nonspecific changes, LVH; ST-segment elevation if dissection involves coronary ostia Chest x-ray, CT scan, or MRI; transesophageal echocardiography; aortogram
Pulmonary embolism Pleuritic chest pain with dyspnea and cough Tachypnea; tachycardia; pleural rub; right ventricular heave Sinus tachycardia with nonspecific ST and T-wave changes; S1Q3T3 pattern classic, but rarely seen High-resolution chest CT; ventilation-perfusion lung scan; pulmonary angiogram
Pericarditis Positional pain (worse lying flat) Pericardial friction rub Diffuse, concave ST-segment elevation with PR-segment depression Echocardiogram
CT, computed tomography; CHF, congestive heart failure; LBBB, left bundle branch block; MRI, magnetic resonance imaging.

The distinguishing feature of the platelet–fibrin clot in STEMI is that it completely occludes the epicardial coronary artery, leading to transmural myocardial injury, manifested by ST-segment elevation on the electrocardiogram (ECG). Despite similar initial pathophysiologic features, unstable angina and non-STEMI (NSTEMI) are rarely associated with complete occlusion of the culprit coronary artery and do not benefit from fibrinolytic therapy. The distinction between Q-wave and non–Q wave MI can only be made retrospectively, and is not useful for early patient management. Accordingly, this terminology has been superseded by the terms STEMI and NSTEMI. Without reperfusion therapy, most patients with STEMI suffer transmural infarction and evolve Q-waves over the first few days after MI. Successful reperfusion therapy, however, may limit necrosis to the subendocardial regions and prevent development of Q-waves.


Diagnosis and Risk Assessment


History and Physical Examination

The pain of acute MI is qualitatively similar to angina and is classically described as a severe pressure-type pain in the midsternum, often radiating to the left arm, neck, or jaw. Associated symptoms include dyspnea, diaphoresis, nausea, vomiting, and weakness. In the elderly and those with diabetes, pain is often atypical, and may not be present at all [4]. Not uncommonly, inferior STEMI presents with nausea and vagal symptoms rather than chest pain. Silent infarction may occur in 25% or more cases. Characterization of the quality of the pain may help to distinguish MI from other conditions that cause chest discomfort, such as aortic dissection, pulmonary embolism, pericarditis, and gastrointestinal (GI) disorders such as cholecystitis and peptic ulcer (Table 39.1).

Patients with acute MI often appear pale and clammy; in many cases, they are in obvious distress. Elderly patients, in particular, may be agitated and incoherent. In contrast, patients with cardiogenic shock may be confused and listless. The objective of the initial examination should be to rapidly narrow the differential diagnosis and assess the stability of the patient. A focused examination can help to differentiate ischemia from conditions such as pneumothorax, pericarditis, aortic dissection, and cholecystitis (Table 39.1). Concomitant conditions, such as valvular heart disease, peripheral vascular disease, and cerebrovascular disease, may complicate patient management and can be rapidly detected by physical examination. A brief survey for signs of congestive heart failure should be performed. Cool extremities or impaired mental status suggests decreased tissue perfusion, whereas elevated jugular venous pressure and rales suggest elevated cardiac filling pressures. Finally, the hemodynamic and mechanical complications of acute MI can often be detected by careful attention to physical findings.

An increasingly recognized syndrome that may mimic acute MI is Tako-Tsubo cardiomyopathy, or the apical ballooning syndrome. This syndrome, more common among elderly women, is typically precipitated by an acute stress, including severe emotional distress or acute noncardiac medical illness. Chest pain associated with anteroapical ST-segment elevation and T-wave inversions is usually indistinguishable from an evolving anterior infarct. The diagnosis is typically made when normal coronary arteries and the distinctive anteroapical wall motion abnormality (Fig. 39.1) are seen at the time of
emergent cardiac catheterization. In contrast to acute MI, cardiac enzymes usually elevate only modestly and the left ventricular (LV) functional abnormalities tend to be transient. The pathophysiology of this syndrome is thought to be due to catecholamine-mediated myocardial stunning.






Figure 39.1. Representative contrast ventriculogram from a patient with Tako-Tsubo cardiomyopathy, demonstrating an anteroapical wall motion abnormality. The ventriculogram in Panel A was obtained at end diastole and in Panel B at end systole. [From the Libyan J Med, AOP: 070707, published July 19, 2007.]


Electrocardiogram

Performance of the 12-lead ECG in the prehospital setting significantly reduces time to reperfusion and shows a strong trend toward reducing mortality [5]. Because only about 25% of patients with STEMI transported by emergency medical services in the United States receive a prehospital ECG, this represents an important target for improvement [5]. The ability to transmit the 12-lead ECG and activate a STEMI care team prior to hospital arrival has provided an opportunity for a major enhancement in systems for STEMI care.






Figure 39.2. Inferoposterior ST elevation MI complicated by complete heart block.

The ST-segment elevation of acute MI must be distinguished from that due to pericarditis or even the normal early repolarization variant. Ischemic ST-segment elevation typically has a convex configuration, is limited to selected ECG leads, and is often associated with reciprocal ST-segment depression (Fig. 39.2). Pericarditis, on the other hand, is typically associated with diffuse ST-segment elevation and depression of the PR segment (Fig. 39.3). The contour of the elevated ST segment in pericarditis and early repolarization variant is typically concave (upward sloping), in contrast to that seen with myocardial injury. Reversible ischemic ST-segment elevation is also seen with coronary vasospasm (Prinzmetal’s variant angina).

A new (or presumed new) left bundle branch block (LBBB) in a patient with ischemic chest discomfort suggests a large
anterior infarction, and is also an indication for reperfusion therapy. A LBBB of unknown age, however, presents a diagnostic dilemma, because many of these patients do not have ongoing transmural myocardial ischemia. Here, emergent echocardiography (to look for an anterior wall motion abnormality); bedside testing of serum cardiac markers, such as myoglobin, CKMB, or troponin; and even emergent cardiac catheterization should be considered. It should be emphasized that an acute STEMI leading to LBBB requires a very large ischemic territory, and would not be expected to be a subtle clinical event. In patients with a preexisting LBBB, no ECG criteria are sufficiently sensitive and specific to diagnose acute MI [6], so alternative methods are needed to make the diagnosis.






Figure 39.3. ECG changes characteristic of pericarditis. Concave (upsloping) ST-segment elevation is seen diffusely, together with PR-segment depression. Importantly, T-waves are essentially normal, another distinguishing feature from ST elevation MI.


Cardiac Biomarkers and Other Tools for Risk Assessment

Cardiac biomarkers of necrosis are considerably more important in the initial diagnosis of NSTEMI than they are in the diagnosis of STEMI. For patients with STEMI, cardiac marker measurements are used to confirm the diagnosis in patients with equivocal electrocardiographic changes, to help gauge prognosis, and to estimate the likelihood of successful reperfusion therapy. Cardiac markers also provide prognostic information. Patients with an elevated myoglobin, troponin, or B-type natriuretic peptide level prior to initiation of reperfusion therapy are at higher risk for death and congestive heart failure (CHF), even after accounting for baseline variables such as infarct location and time to treatment [7,8,9]. When combined with subsequent measures of the efficacy of reperfusion therapy, such as the degree of ST-segment resolution, an accurate assessment of prognosis can be made [8]. Although the rate of rise of cardiac biomarkers (particularly myoglobin) can be used to help determine which patients have had successful or unsuccessful reperfusion [10], the clinical role of biomarker testing for reperfusion assessment is limited. The peak levels of troponin, CK, or CKMB provide a crude estimation of infarct size. It should be noted that with successful reperfusion, although the total amount of biomarker released is reduced, the peak value may actually increase, with an earlier peak and more rapid fall in biomarker levels.

Information from the patient’s clinical presentation and physical examination are also very valuable for assessing the patient’s prognosis. Evidence for heart failure or hemodynamic stress at the time of presentation is weighted heavily in this assessment. For example, it is possible to use the patient’s age and vital signs at presentation to rapidly and accurately obtain a preliminary estimate of short-term survival [11]. Anterior infarct location, delays to therapy, and information regarding medical comorbidity all offer additional prognostic information [12]. As such, several tools that integrate age, the physical examination, the ECG, and other clinical parameters such as serum creatinine provide very strong discrimination of short- and long-term mortality risk, and may be implemented using either simple bedside calculation [12,13], handheld devices, or web-based tools [14,15] (Fig. 39.4).


Reperfusion Therapy

Rapid provision of reperfusion therapy is the primary treatment objective in patients presenting with STEMI. The managing clinician may choose between two principal reperfusion strategies: pharmacologic reperfusion versus primary percutaneous coronary intervention (PCI). This decision may be based on institutional resources, as well as patient factors as discussed in this section.


The Evolving Definition of “Optimal” Reperfusion

Early successful coronary reperfusion limits infarct size and improves LV dysfunction and survival. These benefits are due at least in part to the early restoration of antegrade flow in the infarct-related artery (IRA). In a retrospective analysis of six angiographic trials of different fibrinolytic regimens, patients who achieved normal (TIMI grade 3) antegrade flow in the IRA had a 30-day mortality rate of 3.6%, versus 6.6% in patients
with slow (TIMI grade 2) antegrade flow, and 9.5% in patients with an occluded artery (TIMI grade 0 or 1 flow) [16].






Figure 39.4. TIMI risk score for STEMI: a simple, bedside, clinical tool for predicting 30-day mortality. At the high end, a score of more than 5 identified 12% of patients with a mortality risk at least twofold higher than the mean for the population. In contrast, the 12% of patients with a risk score of zero had a mortality rate of less than 1%. Discriminating among the lower risk groups, nearly two-thirds of the population had risk scores of 0 to 3 with a 5.3-fold gradient in mortality over this range where smaller differences in absolute risk may have clinical impact. h/o, history of; HTN, hypertension; LBBB, left bundle branch block; STE, ST-segment elevation; TIMI, Thrombosis in Myocardial Infarction. [Adapted from Morrow DA, Antman EM, Charlesworth A, et al: TIMI risk score for ST-elevation myocardial infarction: a convenient, bedside, clinical score for risk assessment at presentation: an intravenous nPA for treatment of infarcting myocardium early II trial substudy. Circulation 102(17):2031–2037, 2000.]

Even among patients who achieve normal (TIMI grade 3) epicardial blood flow in the IRA after reperfusion therapy, however, tissue-level perfusion may be inadequate. Using a number of different diagnostic tools (Table 39.2), investigators have demonstrated that measures of tissue and microvascular perfusion provide prognostic information that is independent of TIMI flow grade [17] (Fig. 39.5). For example, Ito and colleagues, using myocardial contrast echocardiography, found impaired tissue and microvascular perfusion in approximately one-third of patients with TIMI grade 3 blood flow after primary PCI: these patients were at increased risk for the development of CHF and death [18]. Impaired microvascular perfusion assessed with cardiac magnetic resonance imaging also correlates with higher mortality risk. Microvascular dysfunction is thought to occur in the setting of MI as a result of distal embolization of microthrombi, tissue inflammation from myocyte necrosis, and arteriolar spasm caused by tissue injury.








Table 39.2 Diagnostic Tools Used to Evaluate Tissue and Microvascular Perfusion in Patients with St Elevation MIa




























Technique Finding suggestive of microvascular injury
Myocardial contrast echocardiography Absence of microbubble contrast uptake in the infarct zone
Doppler flow wire Abnormal coronary flow reserve; systolic reversal of coronary flow
PET scanning Impaired regional myocardial blood flow as measured with 13NH3
Nuclear SPECT imaging Absence of tracer uptake into infarct zone
Contrast angiography Abnormal myocardial “blush,” with failure to opacify myocardium or prolonged dye washout from myocardium
MRI Hypoenhancement of infarct zone following gadolinium contrast injection
ECG Failure to resolve ST-segment elevation
aAssumes that the epicardial infarct artery is patent. These techniques can be presumed to reflect microvascular and tissue perfusion only when the infarct artery has been successfully recanalized.

Perhaps the most clinically relevant measure of tissue perfusion is a simple bedside assessment of the degree of resolution of ST-segment elevation on the 12-lead ECG. Greater degrees of ST-segment resolution are associated with a higher probability of achieving a patent IRA and TIMI grade 3 flow [19]. Furthermore, patients who have normal epicardial blood flow, but persistence of ST-segment elevation on the 12-lead ECG, have been shown to have abnormal tissue and microvascular perfusion using a variety of specific imaging modalities such as contrast echocardiography and nuclear SPECT perfusion imaging [20,21]. In addition, persistent ST-segment elevation has been shown to predict poor recovery of infarct zone wall motion and the clinical endpoints of death and heart failure [22]. As a result, ST-segment resolution appears to integrate epicardial and myocardial (microvascular) reperfusion, and as such may actually provide a more clinically useful assessment of reperfusion than coronary angiography [23].


Time to Reperfusion

Regardless of the choice of reperfusion strategy, several common themes are evident. First, the benefits of reperfusion therapy are time dependent. Patients who receive fibrinolytic therapy within 1 hour from the onset of chest pain have an approximately 50% reduction in mortality, whereas those presenting more than 12 hours after onset of symptoms derive little, if any, benefit. For each hour earlier that a patient is treated, there is an absolute 1% decrease in mortality [24]. Similarly, for primary PCI, the “door-to-balloon” time has been shown to be directly correlated with clinical benefit [25].


Fibrinolytic Therapy

The use of fibrinolytic therapy worldwide has decreased substantially. Nevertheless, fibrinolytic therapy remains the primary approach to reperfusion therapy in some countries and in some regions in the United States where there is no access to experienced centers for timely primary PCI.







Figure 39.5. Relationship between epicardial perfusion, myocardial perfusion, and mortality after fibrinolytic therapy in the TIMI 10B trial. Myocardial perfusion was assessed using the TIMI Myocardial Perfusion Grade, which assesses the degree of microvascular “blush” seen on the routine coronary angiogram. This study found that myocardial perfusion was significantly associated with mortality independent of epicardial blood flow; using these two measures together provided incremental risk prediction. [Adapted from Gibson CM, Cannon CP, Murphy SA, et al; for the TIMI Study Group: The relationship of the TIMI Myocardial Perfusion Grade to mortality after thrombolytic administration. Circulation 101:125–130, 2000.]

Placebo-controlled trials using streptokinase, anistreplase (APSAC), and tissue plasminogen activator (tPA) established a clear benefit of fibrinolytic therapy for patients with STEMI. The Fibrinolytic Therapy Trialists’ overview of all the large placebo-controlled studies reported a 2.6% absolute reduction in mortality for patients with STEMI treated within the first 12 hours after the onset of symptoms [24]. This benefit has been shown to persist through 10 years of follow-up. Highlights of differences in dosing, pharmacokinetics, recanalization rates, and cost between agents are shown in Table 39.3.

Several mutant forms of tPA have been developed that have a prolonged half-life (to allow bolus administration), as well as increased fibrin specificity and resistance to endogenous inhibitors of plasminogen, such as PAI-1. Bolus administration may minimize the risk for dosing errors, decrease “door to needle” time, and allow for prehospital administration. Reteplase (rPA) is a double-bolus agent that was shown to have similar efficacy and bleeding risk to accelerated tPA in the GUSTO III trial [26]. In the ASSENT II trial, tenecteplase (TNK-tPA)—a single-bolus agent—was shown to be equivalent to tPA in terms of mortality and intracranial hemorrhage (ICH), but was associated with a lower rate of noncerebral bleeding complications [27]. The safety advantage of this agent may be due to its increased fibrin specificity and the fact that the dose is adjusted for body weight.








Table 39.3 Thrombolytic Agents in Current Clinical Use










































































  Alteplase Reteplase Tenecteplase Streptokinase
Fibrin selective +++ ++ ++++
Half-life 5 min 14 min 17 min 20 min
Dose 15 mg bolus; then 0.75 mg/kg over 30 min; then 0.5 mg/kg over 60 min (max 100 mg total dose) Two 10 unit bolus doses given 30 min apart 0.53 mg/kg as a single bolus 1.5 million units over 30–60 min
Weight adjusted Partial No Yes No
Adjunctive heparin Yes Yes Yes Probably
Possible allergy No No No Yes
TIMI grade 2 or 3 flow (90 min) 80% 80% 80% 60%
TIMI grade 3 flow (90 min) 55%–60% 60% 55%–65% 32%
Efficacy vs. tPA NA Similar Equivalent 1% ↑ mortality
Safety NA Similar Similar ICH
↓ non-ICH bleeding
↓ ICH
↓ overall bleeding
Cost +++ +++ +++ +

Although the bolus fibrinolytic agents have not been demonstrated in placebo-controlled trials to reduce mortality or ICH, they are easier to use and have largely replaced tPA for this reason in the United States. Tenecteplase appears to offer a modest advantage in safety over other agents. Readministration of streptokinase or anistreplase should be avoided for at least 4 years (preferably indefinitely) because potentially neutralizing antibodies may develop and because anaphylaxis can occur on reexposure to these drugs.









Table 39.4 Contraindications to Fibrinolytic Therapy




























Absolute contraindications Relative contraindications
Any prior intracranial hemorrhage Blood pressure > 180/110a
Stoke within past year Any prior stroke or TIA
Recent head trauma Known bleeding diathesis
Known brain tumor Proliferative diabetic retinopathy
Active internal bleeding Prolonged CPR
Suspected aortic dissection Pregnancy
Major surgery or trauma within 2 wk  
CPR, cardiopulmonary resuscitation; TIA, transient ischemic attack.
aPrior recommendations have considered only a sustained blood pressure > 180/110 a relative contraindication; however, even a single blood pressure greater than this threshold is associated with an increased risk for intracranial hemorrhage.


Current Guidelines for Fibrinolysis

Fibrinolytic therapy is indicated as an option for reperfusion therapy in patients presenting within 12 hours of symptom onset if they have ST-segment elevation or new LBBB and no contraindications to lytic therapy (Table 39.4). Patients who are older than 75 years of age, those who present more than 12 to 24 hours after the onset of acute MI, and those who are hypertensive but present with high-risk MI have a less favorable balance of risk and potential benefit, but may be considered for treatment with a fibrinolytic therapy when primary PCI is not available. Patients should not be given fibrinolytic therapy if the time to treatment is longer than 24 hours or if they present only with ST-segment depression [28].


Limitations of Fibrinolytic Therapy

Current fibrinolytic regimens achieve patency (TIMI grade 2 or 3 flow) in approximately 80% of patients, but complete reperfusion (TIMI grade 3 flow) in only 50% to 60% of cases. In addition, as noted previously in the chapter, approximately one-third of patients with successful epicardial reperfusion have inadequate myocardial and microvascular reperfusion [18]. Finally, even after successful fibrinolysis, a 10% to 20% risk of reocclusion is present. Reocclusion and reinfarction are associated with a two- to threefold increase in mortality [29,30] (Fig. 39.6).

Bleeding is the most common complication of fibrinolytic therapy. Major hemorrhage occurs in 5% to 15% of patients. ICH is the most devastating of the bleeding complications, causing death in the majority of patients affected and almost universal disability in survivors. In major clinical trials, ICH has occurred in 0.5% to 0.9% of patients, but in clinical practice, where patient selection is less rigorous, rates are higher. Patients at particularly high risk for ICH include the elderly (particularly elderly females), patients with low body weight, and those who receive excessive doses of heparin.


Combination Therapy with a GP IIb/IIIa Inhibitor and Reduced-Dose Fibrinolytic

Standard fibrinolytic therapy is directed at the fibrin-rich “red” portion of the coronary thrombus. Activated platelets are the critical component of the white portion of the arterial thrombus. Paradoxically, fibrinolytic agents directly and indirectly promote platelet activation [31], and activated platelets themselves contribute to fibrinolytic resistance by secreting PAI-1 and promoting clot retraction, thereby limiting penetration of the fibrinolytic agent into the thrombus. As a result of these observations, it was hypothesized that potent platelet inhibition with a GP IIb/IIIa inhibitor might augment the efficacy of fibrinolytic therapy.






Figure 39.6. Limitations of current fibrinolytic regimens. [From Lincoff AM, Topol EJ: Illusion of reperfusion. Does anyone achieve optimal reperfusion during acute myocardial infarction? Circulation 87:1792–1805, 1993.]

Although a series of phase II studies comparing standard fibrinolytic therapy with various combinations of GP IIb/IIIa inhibitors and reduced doses of fibrinolytic agents suggested improved TIMI flow grade and ST-segment resolution with the combination regimens [32,33,34,35], definitive phase III trials revealed no convincing improvement in outcomes and an increase in ICH in the elderly with combination regimens [36,37]. Thus, despite initial promise, data do not support the use of GP IIb/IIIa inhibitor/fibrinolytic combinations as the primary reperfusion strategy for treatment of STEMI.


Rescue Percutaneous Coronary Intervention

Because failure of fibrinolytic therapy is associated with high rates of morbidity and mortality, “rescue” PCI is frequently performed in such patients. Data to support rescue PCI in patients with an occluded infarct artery are limited, as tools to diagnose failed reperfusion are only modestly effective, and clinical trials evaluating rescue PCI have enrolled very slowly. In the MERLIN trial, 307 patients with ECG evidence of failed reperfusion (ST-segment resolution < 50% measured 60 minutes after fibrinolytic therapy) were randomized to rescue PCI or conservative therapy. Rescue PCI was performed an average of approximately 90 minutes after the qualifying ECG and was associated with a 26% reduction in the composite endpoint of death, reinfarction, stroke, heart failure, and revascularization at 30 days. However, mortality was not significantly reduced. The most recent study performed was the REACT trial, in which 427 patients with ECG evidence of failed fibrinolysis at 90 minutes were randomized to repeat fibrinolysis, conservative treatment, or rescue PCI. No benefit was observed for repeat fibrinolysis, but rescue PCI reduced the primary
endpoint of death, reinfarction, stroke, or severe heart failure at 6 months by 53%. Mortality was also reduced from 12.8% in the conservative therapy arm to 6.2% in the rescue PCI arm. We recommend urgent catheterization and PCI for all patients with persistent ST-segment elevation and ongoing chest pain 90 minutes after the administration of reperfusion therapy, unless they are at particularly low risk for complications (i.e., a young patient with an uncomplicated inferior MI). For patients who are pain free, but in whom the ST segments remain elevated, urgent catheterization should also be strongly considered, particularly if the patient has high-risk features, such as older age, anterior location of infarction, diabetes, or prior CAD.


Primary Percutaneous Coronary Intervention

In centers with adequate resources, experienced operators, and an institutional commitment to programmatic excellence, immediate or “primary” PCI has become the preferred reperfusion method for patients with STEMI. Randomized trials performed in both referral centers and experienced community hospitals have shown that primary PCI reduces the likelihood of death or MI when compared to fibrinolytic therapy [38]. Moreover, rates of major bleeding and stroke are also significantly lower with primary PCI than with fibrinolytic therapy (Fig. 39.7). The relative benefits of primary PCI are greatest in patients at highest risk, including those with cardiogenic shock, right ventricular infarction, large anterior MI, and increased age (due partly to an increased ICH rate with fibrinolytic therapy). However, as with fibrinolytic therapy, rapid time to treatment is paramount to success [25]. In addition, while operator and institutional experience are critical to realize the full benefit of primary PCI, excellent results with primary PCI have been demonstrated in well-trained community hospitals without on-site cardiac surgery [39]. Current ACC/AHA guidelines recommend primary PCI over fibrinolytic therapy when it can be performed by experienced operators in experienced centers within 90 minutes of presentation. When the door-to-balloon time is expected to be longer than 90 minutes, fibrinolysis is generally preferred for patients presenting within 12 hours of symptom onset unless contraindications are present [28].






Figure 39.7. Short-term (4- to 6-week) outcomes from a meta-analysis of 23 randomized controlled trials comparing fibrinolytic therapy with primary PCI. [Adapted from Keeley EC, Boura JA, Grines CL: Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet 361(9351):13–20, 2003.]

Advances in PCI technology have been rapidly translated from elective to emergent PCI. Compared with primary PTCA, primary stenting is associated with similar rates of death and reinfarction, but lower subsequent target vessel revascularization rates [40,41]. Initial fears about stent thrombosis when drug-eluting stents (DES) were placed in the setting of STEMI have not been realized, and recent studies demonstrate that the advantages of DES over bare metal stents (BMS) with regard to in-stent restenosis and target vessel revascularization extend to patients with STEMI [42,43]. One logistical issue merits comment regarding stent choice. It may be difficult in the setting of an evolving STEMI to determine whether a patient is a good candidate for at least 1 year of uninterrupted aspirin and thienopyridine therapy; a BMS would be preferred in situations where the clinician cannot make this determination.

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Sep 5, 2016 | Posted by in CRITICAL CARE | Comments Off on ST-Segment Elevation Myocardial Infarction

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