PCI in STEMI, NSTEMI, and shock

Key points

Acute myocardial infarction (AMI) is best treated with timely revascularization using percutaneous coronary intervention (PCI).
ST-segment elevation myocardial infarction (STEMI) systems of care are crucial in allowing patients with AMI to have the opportunity for timely care at a PCI-capable center.
A focused history and electrocardiogram (ECG) interpretation are of great importance to rapidly diagnose STEMI and initiate activation of the cardiac catheterization laboratory.
Nonculprit PCI with the goal of providing complete revascularization should be the goal in the majority of patients. In STEMI without cardiogenic shock, this can occur carefully in the index procedure or in a staged fashion, taking into account patient hemodynamics. In cardiogenic shock, this should occur in a staged fashion.
AMI complicated by cardiogenic shock is a deadly condition associated with significant morbidity and mortality.
Technological advancements will lead to continued development of more mobile, smaller-caliber, and more powerful mechanical circulatory support devices. Understanding the mechanism of action and physiologic effects of these devices is important.
Mechanical circulatory support devices are increasingly used to support and prevent hemodynamic collapse. Intra-aortic balloon pumps (IABPs) have been found to have limited utility in AMI with cardiogenic shock (AMI-CS), whereas more robust support devices, including venoarterial extracorporeal membrane oxygenation (VA-ECMO) and Impella, are currently enrolling in large scale randomized control trials to elicit their use in AMI-CS.
Although these large-scale studies are being conducted, the use of shock protocols and teams has been associated with improved outcomes in AMI-CS.

Incidence

Approximately 1 million Americans have an acute myocardial infarction (AMI) every year, corresponding to one AMI every 40 seconds. An ST-elevation myocardial infarction (STEMI) should be considered in patients who present with ischemic symptoms (angina, chest pressure/pain, heartburn, nausea, indigestion, diaphoresis, shortness of breath) and corresponding electrocardiographic (ECG) ST-elevation ( Table 9.1 ). Prompt recognition of STEMI is crucial to activate the cardiac catheterization laboratory and provide percutaneous coronary intervention (PCI). ECGs also serve as an important tool to localize injury ( Fig. 9.1 ).

Table 9.1

ECG Criteria for STEMI

STEMI Anatomic Location	ECG Leads with ST Elevation	Males <40 years	Males ≥40 years	Females (all Ages)
Anterior	V2–V4	V2, V3 > 2.5 mm, V4 > 1 mm	V2, V3 > 2 mm V4 > 1 mm	V2, V3 > 1.5 mm, V4 > 1 mm
Septal	V1–V2	V1 > 1 mm V2 > 2.5 mm	V1 > 1 mm V2 > 2 mm	V1 > 1mm V2 > 1.5 mm
Inferior	II, III, aVF	> 1 mm	> 1 mm	> 1 mm
Lateral	I, aVL, V5–V6	> 1 mm	> 1 mm	> 1 mm

ECG , Electrocardiogram; STEMI , ST-segment elevation myocardial infarction.

Figure 9.1, (A) Anterior ST-segment elevation myocardial infarction (STEMI) with ST elevation in leads V1 to V4. (B) Inferior STEMI with ST elevation in leads II, III, and aVF. (C) Lateral STEMI with ST elevation in leads I, aVL, V5, and V6. (D) Posterior STEMI with ST depression in leads V1 to V3.

Non-STEMI (NSTEMI) are typically diagnosed in the presence of ischemic symptoms and elevated biomarkers. Ischemic changes on ECG can still be present ( Fig. 9.2 ). High-risk features that should prompt early consideration for revascularization in NSTEMI include ongoing ischemic symptoms despite medical therapy, cardiogenic shock, arrhythmia, or a Global Registry of Acute Coronary Events (GRACE) risk score greater than 140.

Figure 9.2, Electrocardiogram (ECG) showing high-risk non-ST segment elevation myocardial infarction (NSTEMI) with aVR ST elevation and diffuse ST depression and T-wave inversions.

Hospital mortality after AMI has steadily decreased and is currently less than 5%, with most patients now being discharged home within 1 to 3 days. This is largely driven by the ability to provide rapid early revascularization through PCI using current STEMI systems of care.

Pathophysiology

The pathophysiology of an AMI is outlined in Fig. 9.3 . Plaque deposition leads to progressive atherosclerosis. Plaque rupture can result in thrombosis and decreased blood flow, leading to myocardial ischemia and necrosis. This injury can be measured by biomarkers, such as troponin. AMI can result in diastolic dysfunction and an increase in left ventricular (LV) end-diastolic pressure. If not promptly treated, AMI can progress to systolic dysfunction and decreasing stroke volume, which can lead to cardiogenic shock (CS) and death.

Revascularization

Methods of revascularization in patients suffering from AMI have evolved from thrombolytic therapy to mechanical revascularization using coronary artery bypass grafting (CABG) or PCI. Thrombolytics can achieve infarct artery patency in approximately 50% to 70% of patients presenting with an AMI within 90 minutes. Primary percutaneous balloon angioplasty and stenting, however, restores TIMI (thrombolysis in myocardial infarction) grade 3 coronary blood flow in over 95% of patients. Thrombolytic therapy has also been associated with complications, such as bleeding and stroke. PCI is thus the standard mode of revascularization in patients presenting with AMI, with a goal of reducing infarct size, preserving LV function, and improving survival.

STEMI systems of care

To facilitate timely revascularization, an enormous infrastructure has been developed over the past three decades to provide rapid access to the cardiac catheterization laboratory for patients presenting with AMI. The creation of this STEMI system-of-care has allowed more than 80% of Americans access to the cardiac catheterization laboratory for PCI. For those patients who cannot be transferred to a PCI-capable center within 120 minutes, thrombolytics remain a therapeutic option ( Fig. 9.4 ).

Figure 9.4, Emergency Medical Services (EMS) and ST-segment elevation myocardial infarction (STEMI) system of care.

The COVID-19 pandemic has highlighted vulnerabilities in providing such services at certain unforeseen times. Modified actions plans should be in place for the rare event in which either Emergency Medical Services (EMS) or cardiac catheterization laboratory personnel cannot provide such services.

STEMI mimickers

The importance of a detailed history cannot be overemphasized because STEMI mimickers are frequently identified ( Table 9.2 ). These can include the presence of hyperkalemia or left bundle branch blocks and diseases such as LV aneurysm, Brugada syndrome, pericarditis, and pulmonary embolism.

Table 9.2

Pathologies With Similar ECG as STEMI

Pathology	ECG Characteristics	ECG Example
Hyperkalemia	Symmetric, narrow, peaked T waves without ST elevation
Left bundle branch block	QRS > 120 ms, ST elevation is usually < 5 mm. Use Sgarbossa Criteria to determine the presence of true infarct: Concordant ST elevation > 1 mm in leads with a positive QRS complex (score 5) Concordant ST depression > 1 mm in V1-V3 (score 3) Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2). A total score of ≥ 3 = 90% specificity for myocardial infarction.
Left ventricular aneurysm	Persistent ST elevations after a myocardial infarction, associated with Q waves in the location of the infarct
Brugada syndrome	Na+ channel mutation. Type 1 and 2 will have ST elevation in V1–V3.
Acute pericarditis	Diffuse ST elevations along with PR depression. Reciprocal changes are not present.
Acute pulmonary embolism	ST elevation in AVR, associated with sinus tachycardia and incomplete right bundle branch block pattern.

ECG , Electrocardiogram; STEMI , ST-segment elevation myocardial infarction.

Complications of acute myocardial infarction

When timely reperfusion is not provided because of delays in presentation, unrecognized AMI, untimely revascularization, or complicated revascularization, mechanical complications of AMI can occur. Common complications of AMI are listed in Table 9.3 . In the era of primary PCI, the incidence of mechanical complications is 0.3% in patients presenting with STEMI compared with 6.2% of patients in the thrombolytic era. Mechanical complications are more common in STEMI than NSTEMI and are seen more commonly in patients who are older, female, or presenting with their first AMI.

Table 9.3

Complications After a STEMI

	Time of onset	Presentation	Management	Mortality
Mechanical Complications
Papillary muscle rupture and acute mitral regurgitation	Within 7 days post-MI	Acute pulmonary edema, cardiogenic shock	Urgent surgery, inotropes, ECMO, diuretics	10%–30%
Ventricular septal rupture	Within 7 days post-MI	Chest pain, acute heart failure	Urgent surgery, inotropes, ECMO, diuretics	50%–90%
Free wall rupture	Within 7 days post-MI	Cardiogenic shock, tamponade, cardiac arrest	Urgent surgery, pericardiocentesis, ECMO	50%–90%
Nonmechanical Complications
Pericarditis (Dressler syndrome)	10–14 days	Chest pain, persistent ST elevation, fever, friction rub on exam	Aspirin 650 mg TID	Low
Ventricular arrhythmias	0–48 hours	Palpitations, syncope	Beta-blocker, ICD placement	Low
Cardiogenic shock	0–24 hours	Hypotension, altered mental status, acute respiratory failure	Right heart catheterization, mechanical circulatory support, inotropes	50%

ECMO , Extracorporeal membrane oxygenation; ICD , implantable cardioverter-defibrillator; MI , myocardial infarction; STEMI , ST-segment elevation myocardial infarction; TID , thrice daily.

Pharmacotherapy

Dosing for antiplatelet therapy ( Table 9.4A ), anticoagulation (see Table 9.4B ), and important post-PCI medications ( Fig. 9.5 ) are listed. Potent oral antiplatelet therapies have been shown to be superior to clopidogrel in AMI. It is important to consider intravenous (IV) antiplatelet therapies, particularly when PCI is performed using a radial approach, because patients with AMI have significant risk factors for poor absorption of oral medications, including the use of opioids, the presence of nausea and vomiting, mechanical ventilation, and cardiac arrest. Interventional pharmacology is discussed in more detail in Chapter 3 .

Table 9.4A

Antiplatelets Therapies in Acute Coronary Syndrome

Antiplatelets	Target	Loading Dose	Maintenance Dose	Onset of action	Offset of action
Aspirin	COX-1	150–325 mg PO	81–100 mg daily	60 min	7–10 days
Clopidogrel	P2Y12 receptor (I)	600 mg PO	75 mg daily	2 hours	7–10 days
Ticagrelor	P2Y12 receptor (R)	180 mg PO	90 mg twice a day	30 min	3–5 days
Prasugrel	P2Y12 receptor (I)	60 mg PO	10 mg daily	30 min	7–10 days
Cangrelor	P2Y12 receptor (R)	30 mcg/kg IV	Infusion rate: 4 mcg/kg/min IV	2 min	1 hour
Abciximab	GP IIb/IIIa receptor (I)	0.25 mg/kg IV	0.125 μg/kg/min IV for 12 hours	10 min	48–72 hours
Eptifibatide	GP IIb/IIIa receptor (R)	180 μg/kg IV	2 μg/kg/min for 18–24 hours	5–60 min	4 hours
Tirofiban	GP IIb/IIIa receptor (R)	0.4 μg/kg IV bolus	0.1μg/kg/min for 18–24 hours	10 min	4 hours

(I), Irreversible blockade; IV , intravenous; PO , oral; (R), Reversible blockade.

Table 9.4B

Anticoagulation Therapies in Acute Coronary Syndrome

Anticoagulation	Target	Half-life	Monitoring	Use if GFR < 30
Unfractionated heparin	Factor Xa and IIa (thrombin)	1 hour	Anti Xa level, PTT	Yes
Low-molecular-weight heparin	Factor Xa and IIa (thrombin)	3–6 hours	Anti-Xa level 4 hrs post dose	Contraindicated
Bivalirudin	Direct thrombin inhibitor	25 minutes	PTT	Yes (needs dose reduction)
Fondaparinox	Factor Xa	17 – 21 hours	Anti-Xa level 4 hrs post dose	Contraindicated

GFR, Glomerular filtration rate.

Figure 9.5, Routine therapies in acute coronary syndrome.

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