ST elevation myocardial infarction natural history and complications

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Without treatment, ST elevation myocardial infarction can prove fatal. Complications of ST elevation MI are divided into the following categories: ischemic, mechanical, arrythmic, embolic, and pericarditis. The prognosis for patients with myocardial infarction varies greatly depending upon simple demographic variables like age, infarct artery location, the presence of signs and symptoms of heart failure on presentation, the symptom to door time, and comorbidities that are present. Several risk stratification tools have been developed to predict a patient's mortality. Most of these risk scores are based upon clinical data obtained at the time of admission rather than at the time of discharge.

Complications

Ischemic Complications

Reinfarction or reocclusion of the infarct vessel is associated with a doubling of mortality. Unfortunately, it is difficult to predict who will reinfarct following fibrinolytic therapy. Among patients undergoing primary PCI, bivalirudin monotherapy has been associated with stent thrombosis in the HORIZONS AMI and EUROMAX trials. Aggressive antiplatelet and antithrombotic therapy minimizes the risk of reinfarction.

Mechanical Complications

A new murmur in patients with ST elevation myocardial infarction should raise an immediate concern of mechanical complicaitons such as papillary muscle rupture, septal rupture, and free-wall rupture which portend a dismal prognosis and may be differentiated on the basis of physical and echocardiographic findings or hemodynamic profiles. Other mechanical sequelae include true or false ventricular aneurysm, dynamic left ventricular outflow tract obstruction, cardiogenic shock, and heart failure.

Left ventricular aneurysm

• A true left ventricular aneurysm is an outpouching formed by a stretched, thinned-out myocardial scar. Patients with transmural infarction and patients who do not receive reperfusion therapy are at increased risk. LV aneurysm may manifest acutely as low-output cardiogenic shock or chronically as heart failure or thromboembolism in the presence of mural thrombus. A large, diffuse point of maximal impulse and S₃ gallops may be evident on physical examination. A chest radiograph may demonstrate a localized bulging segment in the cardiac silhouette. Dyskinetic or paradoxical motions of the aneurysmal segment may be detected by echocardiography or ventriculography. True aneurysm connects with the LV cavity by a wide neck and is less susceptible to rupture than a false aneurysm. ACE inhibitor and vasodilator are used in the mangement of chronic heart failure associated with ventricular aneurysm. Anticoagulant is indicated in the presence of mural thrombus. Sustained ventricular arrhythmia from an aneurysm may require defibrillator placement. Surgical resection may be considered in selected cases with refractory symptoms.

Pseudoaneurysm

• In contrast to the true aneurysm which contains viable myocardium in its wall, pseudoaneurysm lacks the myocardial elements and is formed by adherent pericardium and organized hematoma. Unlike true ventricular aneurysm, pseudoaneurysm communicates with the cavity of the left ventricle through a narrow neck and is more prone to rupture. Pseudoaneurysm may partially reduce stroke volume similar to a true aneurysm. Surgery is recommended for all patients regardless of symptoms or the size of pseudoaneurysm in light of a high risk for spontaneous rupture and sudden death.

Rupture of the papillary muscle

• Papillary muscle rupture is characterized by symptoms of acute severe mitral regurgitation and pulmonary edema and should be suspected in STEMI patients with a new soft holosystolic murmur at the apex. Posterior papillary muscle rupture, as occurs in inferior MI, is more common than anterior papillary muscle rupture which may be a complication of anterior or lateral MI. Posterior papillary muscle is considered more susceptible to ischemic rupture due to its singular blood supply from the posterior descending artery. In contradistinction to the posterior papillary muscle, the anterior papillary muscle receives a dual blood supply from the left anterior descending artery and the circumflex artery. Urgent transthoracic echocardiography should be obtained to establish a definite diagnosis. Nitroglycerin or nitroprusside may be used to temporize the patient if systolic blood pressure is above 90 mm Hg. If the patient cannot tolerate vasodilator due to rapid hemodynamic deterioration, intra-aortic balloon counterpulsation should be instituted as a bridging therapy until emergency mitral valve replacement can be performed.

Rupture of the interventricular septum

• Patients with septal rupture frequently report chest pain, shortness of breath, and symptoms of low-output cardiogenic shock. Key physical findings include a harsh, loud holosystolic murmur best heard at the lower left sternal border, palpable thrill at the right precordium, S₃ gallops, and accentuation of pulmonic component of the second heart sound. Color Doppler echocardiography is useful for determining the location and size of the defect and detecting left-to-right shunt and right ventricular overload. Septal rupture should be managed by temporary stabilization with intra-aortic balloon counterpulsation followed by intravenous vasodilator and early surgical closure.

Rupture of the LV free wall

• Free-wall rupture usually leads to hemopericardium and abrupt circulatory collapse. Clinical manifestations range from anginal, pleuritic, or pericardial chest discomfort to catastrophic symptoms of cardiogenic shock, cardiac tamponade, and sudden death. Echocardiography is useful for the diagnosis and emergency pericardiocentesis may be indicated for cardiac tamponade. Survival depends primarily on early recognition and prompt surgical repair.

Features of mechanical complications in ST elevation MI

Feature	Mechanical Complication of ST Elevation Myocardial Infarction
	Papillary Muscle Rupture	Ventricular Septal Rupture	Free-Wall Rupture
Physical Findings	Soft pansystolic murmur best audible at the apex with radiation to the axilla, ⊖ precordial thrill, variable signs of RV overload	Harsh pansystolic murmur best audible at the lower left sternal border with radiation to the right parastenal area, ⊕ precordial thrill, S3, accentuated second heart sound	Diminished heart sounds, pericardial rub, to-and-fro murmur, jugular venous distention, pulsus paradoxus
Echocardiographic Findings	Hypercontractile LV, torn papillary muscle or chordae tendineae, flail leaflet, severe mitral regurgitation	Left-to-right shunt at the ventricular level, pattern of RV overload	Layered high-acoustic echoes within the pericardium, pericardial effusion, RA and RV diastolic collapse, dilated inferior vena cava, marked respiratory variations in mitral and tricuspid inflow
Hemodynamic Profiles	No oxygen saturation gradient from the RA to RV, large V waves in pulmonary artery and capillary wedge tracings, high pulmonary-capillary wedge pressure	Equalization of diastolic pressures among the cardiac chambers	Step-up in oxygen saturation between the RA and RV (or PA), large V waves

Conduction Abnormalities

• Atrial flutter
• Postinfarction conduction abnormalities

Arrhythmic Complications

• Sudden cardiac death

Embolic Complications

• Stroke
• DVT

Pericarditis

• Post myocardial infarction pericarditis
• Dressler's syndrome

Prognosis

Factors Associated with a Poor Prognosis in STEMI

While we as physicians often labor under the impression that we can dramatically change a patient's prognosis, it is noteworthy that 90% of the predictive information regarding 30 day mortality is contained in the following 5 baseline variables that can be modified to only a limited degree:

1. Advanced age
2. Sinus tachycardia
3. Reduced systolic blood pressure
4. Heart failure or Killip class of two or greater
5. Anterior myocardial infarction location

Sinus tachycardia, hypotension, Killip class, and anterior MI are all essentially markers of poor pump function on admission. These risk factors for 30 day mortality have been well validated in a multivariate analysis of 41,020 patients in the GUSTO-I trial. Advanced age was the most significant factor associated with higher 30-day mortality. The rate was only 1.1% in the youngest decile (< 45 years) and climbed to 20.5% in patients > 75 (adjusted chi 2 = 717, P < .0001). Other variables most closely associated with an increased risk of mortality were lower systolic blood pressure at randomization (chi 2 = 550, P < .0001), higher Killip class (chi 2 = 350, P < .0001), elevated heart rate (chi 2 = 275, P < .0001), and the presence of an anterior infarction (chi 2 = 143, P < .0001). When taken together, these five baseline characteristics contained 90% of the prognostic information. Other significant though less important factors included previous myocardial infarction, height, time to treatment, diabetes, weight, smoking status, type of thrombolytic, previous bypass surgery, hypertension, and prior cerebrovascular disease. When these variables were combined, a validated model was created which stratified patients according to their mortality risk and accurately estimated the likelihood of death.

Other Prognostic Variables not Identified in GUSTO I

Other risk factors include, serum creatinine concentration , and peripheral vascular disease.

Left Ventricular Function as a Risk Stratifier

Assessment of left ventricular ejection fraction may increase the predictive power of some risk stratification models. The prognostic importance of Q-waves is debated. Prognosis is significantly worsened if a mechanical complication (papillary muscle rupture, myocardial free wall rupture, and so on) were to occur.

There is evidence that case fatality of myocardial infarction has been improving over the years in all ethnicities.

STEMI Risk Scores

The Thrombolysis in Myocardial Infarction TIMI Risk Score and TIMI Risk Index are two prognostic indices that have been validated in clinical trials and epidemiologic studies to predict 30-day mortality among patients with STEMI.

The TIMI Risk Score incorporates eight clinical variables (age, systolic blood pressure [SBP], heart rate [HR], Killip class, anterior ST elevation or left bundle branch block on electrocardiogram, diabetes mellitus, history of hypertension or angina, low weight and time to treatment >4 hours) and assigns them a point value based on their odds ratio for mortality.

The TIMI Risk Score was developed and validated in clinical trials of fibrinolytic therapy, but it has also been reported to be prognostic in community-based real-world registries as well as elderly patients .

The TIMI Risk Index incorporates age, HR and SBP (HR x [age/10] x 2/SBP), and has been validated in unselected patients , registries and population-based cohorts

Other risk tools such as the GRACE risk score have also been developed to risk stratify patients.

Interestingly, although tobacco abuse is a risk factor for CAD and STEMI, smoking is associated with a lower risk of mortality among patients who present with STEMI This is due, at least in part, to the finding that smokers who present with STEMI are, on average, at least a decade younger than non-smokers. Smokers more often have involvement of the right coronary artery rather than the left anterior descending artery as well. Smokers paradoxically have better myocardial perfusion following reperfusion therapy than non smokers .

2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)

Assessment of Left Ventricular Function (DO NOT EDIT)

Class I

"1. LV ejection fraction should be measured in all patients with STEMI. (Level of Evidence: C)"

Sources

• 2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction