Tired
Answer: B
This woman with incompletely controlled diabetes mellitus (DM) and hypertension most likely suffered an acute myocardial infarction (MI) earlier in the week, as outlined by her prodrome of fatigue and acute, non-provoked anginal equivalents of shortness of breath and extreme fatigue and lethargy. She appeared to have fared relatively (and fortunately) well at home, until she presents to you approximately one week later with complications of her previously undiagnosed MI.
Post-MI complications can be broken down into five main categories: ischemic (angina or equivalent,
reinfarction, extension of original infarction); mechanical (heart failure, cardiogenic shock, mitral valve dysfunction, aneurysm, cardiac rupture); dysrhythmic (atrial or ventricular dysrhythmias, nodal dysfunction); embolic (CNS or peripheral emboli); and inflammatory (pericarditis).
Ischemic complications, including infarct extension, recurrent infarction, and recurrent angina:
Post-infarction angina can occur hours to 30 days post-MI and is highest in non-ST elevation MI patients and those who receive thrombolytic therapy (rather than percutaneous coronary intervention, PCI). Following fibrinolytic therapy, reocclusion of the affected artery can occur in 5 to 30% of patients.
Presentation of suspected post-infarct angina is similar to that patient’s expected presentation for unstable angina, and diagnosis and management should follow suit. However, it is important to remember that those with post-infarction angina have a worse prognosis in terms of a higher incidence of sudden death,
reinfarction, and acute cardiac events.
Mechanical complications, including heart failure, cardiogenic shock, mitral valve dysfunction, aneurysm, cardiac rupture:
An example here is free wall rupture, which occurs in 3% of MI patients and accounts for 10% of post-MI mortality. The first 1-2 weeks are the highest risk: 50% of ruptures occur within 5 days post-MI and 90% occur within the two weeks following. Risk factors include female gender, hypertension, first MI, and poor
coronary collaterals. Cardiac rupture most commonly occurs in the lateral wall.
Symptoms include acute onset of new chest pain (or equivalent symptoms), sudden death, or a more subacute course suggesting some containment of the bleed: jugular venous distention, pulsus paradoxus, diminished heart sounds, or a pericardial rub.
Below is an echocardiogram of a middle-aged man with impending complete rupture of the lateral wall:
This woman with incompletely controlled diabetes mellitus (DM) and hypertension most likely suffered an acute myocardial infarction (MI) earlier in the week, as outlined by her prodrome of fatigue and acute, non-provoked anginal equivalents of shortness of breath and extreme fatigue and lethargy. She appeared to have fared relatively (and fortunately) well at home, until she presents to you approximately one week later with complications of her previously undiagnosed MI.
Post-MI complications can be broken down into five main categories: ischemic (angina or equivalent,
reinfarction, extension of original infarction); mechanical (heart failure, cardiogenic shock, mitral valve dysfunction, aneurysm, cardiac rupture); dysrhythmic (atrial or ventricular dysrhythmias, nodal dysfunction); embolic (CNS or peripheral emboli); and inflammatory (pericarditis).
Ischemic complications, including infarct extension, recurrent infarction, and recurrent angina:
Post-infarction angina can occur hours to 30 days post-MI and is highest in non-ST elevation MI patients and those who receive thrombolytic therapy (rather than percutaneous coronary intervention, PCI). Following fibrinolytic therapy, reocclusion of the affected artery can occur in 5 to 30% of patients.
Presentation of suspected post-infarct angina is similar to that patient’s expected presentation for unstable angina, and diagnosis and management should follow suit. However, it is important to remember that those with post-infarction angina have a worse prognosis in terms of a higher incidence of sudden death,
reinfarction, and acute cardiac events.
Mechanical complications, including heart failure, cardiogenic shock, mitral valve dysfunction, aneurysm, cardiac rupture:
An example here is free wall rupture, which occurs in 3% of MI patients and accounts for 10% of post-MI mortality. The first 1-2 weeks are the highest risk: 50% of ruptures occur within 5 days post-MI and 90% occur within the two weeks following. Risk factors include female gender, hypertension, first MI, and poor
coronary collaterals. Cardiac rupture most commonly occurs in the lateral wall.
Symptoms include acute onset of new chest pain (or equivalent symptoms), sudden death, or a more subacute course suggesting some containment of the bleed: jugular venous distention, pulsus paradoxus, diminished heart sounds, or a pericardial rub.
Below is an echocardiogram of a middle-aged man with impending complete rupture of the lateral wall:
The goal in managing these patients is rapid recognition and early open heart surgery. Temporizing measures such as pericardiocentesis may provide a very brief stop-gap measure as the patient is prepared for surgery, but it may also worsen the situation if, as the pericardial pressure is relieved, the communication between the ventricle and the pericardial sac is reopened. If there is frank rupture of the wall (at times leaking through the wall will
precede this), the outcome is dismal. There are case reports of bedside resuscitative thoracotomy, identifying the rupture, and stabilizing the injury with a Foley catheter or lock stitches. Medical management has no role in patients with wall rupture and the goal in the ED is to support them and expedite rapid deployment of the operating room.
Another example of a mechanical complication that deserves mention: acute papillary rupture after MI resulting in acute mitral regurgitation. Although some mild to moderate MR is found in up to approximately half of those after acute MI, it is often transient and asymptomatic. Papillary wall rupture occurs after inferior MI and presents with a new pansystolic murmur at the apex radiating to the axilla and results in instant pulmonary edema, cardiogenic shock, and/or death. Patients with previously low ejection fraction may not present with
enough contractile force to cause a murmur.
Patients with papillary rupture and acute MR need aggressive medical management with nitroprusside to decrease systemic vascular resistance (SVR); an intra-aortic balloon pump may be used as a temporizing measure to decrease left ventricular afterload, improve coronary perfusion, and increase forward cardiac output. Medical management is temporizing for emergency valve replacement.
Dysrhythmic complications, including atrial or ventricular dysrhythmias and sinus or atrioventricular nodal
dysfunction:
After MI ventricular dysrhythmias are very common, due to the setup of re-entry circuits along the conduction system where the injured and healthy tissues meet. Premature ventricular contractions (PVCs) occur in 90% of post-MI patients; ventricular fibrillation is seen in 2-4%. Amiodarone may be used in post-MI patients with frequent PVCs or non-sustained ventricular tachycardia, at 150 mg IV bolus, then 1 mg/min x 6 hours, then 0.5 mg/min thereafter.
Patients with a poor ejection fraction and history of ventricular fibrillation are at high-risk for subsequent sudden cardiac death. Implantable defibrillators have been shown to decrease mortality in patients with low ejection fraction (30% or lower).
Supraventricular tachycardias, although less common (less than 10% of post-MI patients) portend a poorer prognosis (in contradistinction to SVT in a non-ischemic setting). Bradydysrythmias in turn carry a poor prognosis after MI.
Embolic complications, including CNS or peripheral emboli:
Emboli may occur after the formation of a mural thrombus after MI, especially in large anterior MIs or after the establishment of a post-MI atrial fibrillation. If they occur, systemic emboli may manifest as stroke, limb ischemia, renal failure, and/or mesenteric ischemia. Beware of the vague and varied (read: multisystem) symptoms in the patient post-MI, especially in the 1-2 weeks following.
Inflammatory complications, including pericarditis:
Early pericarditis (within 1-4 days) occurs in 10% of post-MI patients. Dressler’s syndrome, or late pericarditis (1-8 weeks after) is found in 1-3% of post-MI patients. In both cases, the immune system mounts a response to necrotic tissue, triggering a cascade of inflammation which typically presents as constant progressive chest pain that may be worse in the supine position, and may be (rarely unfortunately for diagnosticians) associated with a friction rub. Aspirin is the drug of choice for post-MI pericarditis. In distinction from non-ischemic pericarditis, NSAIDs should be avoided of the first month post MI, as they are thought to interfere with myocardial
healing.
Returning to our patient:
Although acute myocardial infarction (A) is possible her acute change in presentation and previously history are suggestive of something more. Dysrhythmia (C) although a likely complication, should not account for her abrupt change in symptoms and this pulse rate. Peri-myocarditis (early) should be considered, but the abrupt nature and
severity of symptoms argue against this. This woman suffered a mechanical complication of her MI: acute wall rupture with resultant tamponade (B) as evidenced by her abrupt presentation, distended jugular veins, and narrowing pulse pressure.
Bottom Line:
● Patients post-MI are at risk for multiple complications, including ischemic, mechanical, dysrhythmic, embolic,
and inflammatory
● Post-MI angina (even without evidence of the above complications) is high-risk and associated with significant
morbidity and mortality
● Typical presentations such as SVT or pericarditis have vastly different treatments and outcomes depending
on the clinical setting: ischemic or non-ischemic
References
Brener SJ, Tschopp D. Complications of Acute Myocardial Infarction. Cleveland Clinic. Continuing Medical Education. January 2009.
McNeill AJ, Adgey AAJ, O’Kane HO. Cardiogenic shock due to papillary muscle rupture in acute myocardial infarction. Int J Cardiol. 1987; 14(3):376–379.
Reynen K, Strasser RH. Impending Rupture of the Myocardial Wall. N Engl J Med. 2003; 348.
precede this), the outcome is dismal. There are case reports of bedside resuscitative thoracotomy, identifying the rupture, and stabilizing the injury with a Foley catheter or lock stitches. Medical management has no role in patients with wall rupture and the goal in the ED is to support them and expedite rapid deployment of the operating room.
Another example of a mechanical complication that deserves mention: acute papillary rupture after MI resulting in acute mitral regurgitation. Although some mild to moderate MR is found in up to approximately half of those after acute MI, it is often transient and asymptomatic. Papillary wall rupture occurs after inferior MI and presents with a new pansystolic murmur at the apex radiating to the axilla and results in instant pulmonary edema, cardiogenic shock, and/or death. Patients with previously low ejection fraction may not present with
enough contractile force to cause a murmur.
Patients with papillary rupture and acute MR need aggressive medical management with nitroprusside to decrease systemic vascular resistance (SVR); an intra-aortic balloon pump may be used as a temporizing measure to decrease left ventricular afterload, improve coronary perfusion, and increase forward cardiac output. Medical management is temporizing for emergency valve replacement.
Dysrhythmic complications, including atrial or ventricular dysrhythmias and sinus or atrioventricular nodal
dysfunction:
After MI ventricular dysrhythmias are very common, due to the setup of re-entry circuits along the conduction system where the injured and healthy tissues meet. Premature ventricular contractions (PVCs) occur in 90% of post-MI patients; ventricular fibrillation is seen in 2-4%. Amiodarone may be used in post-MI patients with frequent PVCs or non-sustained ventricular tachycardia, at 150 mg IV bolus, then 1 mg/min x 6 hours, then 0.5 mg/min thereafter.
Patients with a poor ejection fraction and history of ventricular fibrillation are at high-risk for subsequent sudden cardiac death. Implantable defibrillators have been shown to decrease mortality in patients with low ejection fraction (30% or lower).
Supraventricular tachycardias, although less common (less than 10% of post-MI patients) portend a poorer prognosis (in contradistinction to SVT in a non-ischemic setting). Bradydysrythmias in turn carry a poor prognosis after MI.
Embolic complications, including CNS or peripheral emboli:
Emboli may occur after the formation of a mural thrombus after MI, especially in large anterior MIs or after the establishment of a post-MI atrial fibrillation. If they occur, systemic emboli may manifest as stroke, limb ischemia, renal failure, and/or mesenteric ischemia. Beware of the vague and varied (read: multisystem) symptoms in the patient post-MI, especially in the 1-2 weeks following.
Inflammatory complications, including pericarditis:
Early pericarditis (within 1-4 days) occurs in 10% of post-MI patients. Dressler’s syndrome, or late pericarditis (1-8 weeks after) is found in 1-3% of post-MI patients. In both cases, the immune system mounts a response to necrotic tissue, triggering a cascade of inflammation which typically presents as constant progressive chest pain that may be worse in the supine position, and may be (rarely unfortunately for diagnosticians) associated with a friction rub. Aspirin is the drug of choice for post-MI pericarditis. In distinction from non-ischemic pericarditis, NSAIDs should be avoided of the first month post MI, as they are thought to interfere with myocardial
healing.
Returning to our patient:
Although acute myocardial infarction (A) is possible her acute change in presentation and previously history are suggestive of something more. Dysrhythmia (C) although a likely complication, should not account for her abrupt change in symptoms and this pulse rate. Peri-myocarditis (early) should be considered, but the abrupt nature and
severity of symptoms argue against this. This woman suffered a mechanical complication of her MI: acute wall rupture with resultant tamponade (B) as evidenced by her abrupt presentation, distended jugular veins, and narrowing pulse pressure.
Bottom Line:
● Patients post-MI are at risk for multiple complications, including ischemic, mechanical, dysrhythmic, embolic,
and inflammatory
● Post-MI angina (even without evidence of the above complications) is high-risk and associated with significant
morbidity and mortality
● Typical presentations such as SVT or pericarditis have vastly different treatments and outcomes depending
on the clinical setting: ischemic or non-ischemic
References
Brener SJ, Tschopp D. Complications of Acute Myocardial Infarction. Cleveland Clinic. Continuing Medical Education. January 2009.
McNeill AJ, Adgey AAJ, O’Kane HO. Cardiogenic shock due to papillary muscle rupture in acute myocardial infarction. Int J Cardiol. 1987; 14(3):376–379.
Reynen K, Strasser RH. Impending Rupture of the Myocardial Wall. N Engl J Med. 2003; 348.