ST-elevation myocardial Infarction(STEMI) is ... ischemic chest pain after 24 hours of MI. .... including rupture of the left ventricular free wall (0.52%), papillary.
Complications of ST-Elevation Myocardial Infarction Chandra Mani Adhikari MD (China) Cardiologist Shahid Gangalal National Heart Centre Associate Professor National Academy of Medical Scieinces(NAMS)
ST-elevation myocardial Infarction(STEMI) is • a life-threatening cardiac emergency. • occurs when thrombus formation results in complete occlusion of coronary artery. • ECG will show significant ST segment elevation. • must be diagnosed and treated promptly.
STEMI
• is a leading cause of death in the world. • Most of these deaths are the direct result of pathophysiologic changes which occur as a result of the AMI. • Many dies from complications of AMI. • Coronary care units and early reperfusion therapy has decreased complication and in-hospital mortality rates.
Complications of STEMI can be classified • Ischemic • Arrhythmic • Mechanical • Inflammatory • Embolic
Ischemic complications Post MI Angina • ischemic chest pain after 24 hours of MI. • develops in approximately 10 to 15% of patients and have a worse prognosis.
Reinfarction • MI that occurs within 28 days of previous MI.
• With fibrinolytic therapy, reinfarction occurs in approximately 5% to 10% of patients by the • incidence is higher in patients treated with time of discharge, and in 25% to 30% of patients at 1 year. fibrinolytics than with primary PCI. • result from ischemia either within the same • Following primary PCI reinfarction rate 3% during the first 90 days after MI. Infarct artery or stenosis of another artery. • acute stent thrombosis, usually within the first few hours after primary PCI in ~1% of patients.
Management of Ischemic Complication • Coronary Angiogram followed by coronary revascularization by coronary angioplasty or bypass operation.
Arrhythmic complications • The incidence of arrhythmias is higher in patients the earlier they are seen after the onset of symptoms. • All type of arrhythmias can occur in Acute STEMI • Sinus Tacycardia • Sinus Bradycardia • Supraventricular arrhythmias • Ventricular arrhythmias
Accelerated idioventricular rhythm (AIVR) • common post-STEMI rhythm • also termed “slow VT. • occurs in upto 20% of MI patients • often observed shortly after successful reperfusion • is a benign, hemodynamically stable rhythm and no treatment is necessary.
Non sustained VT (NSVT) • VT which lasts < 30 s. • NSVT may be seen in up to 67% of patients • not associated with an increased mortality risk. • Hypokalemia and hypomagnesemia should be treated.
Sustained Ventricular Tachycardia • More than 30 seconds or causes hemodynamic instability • Hypokalemia and hypomagnesemia may increase the risk of VT. • Sustained VT with hemodynamic stability should be treated with drugs. • If it's not aborted or associated with chest pain or hemodynamic deterioration, DC cardioversion should be done.
Ventricular fibrillation (VF) • most common cause of pre-hospital death in STEMI • VF can occur in 3 settings in hospitalized patients with AMI. • Primary VF occurs suddenly and unexpectedly in patients with no signs or symptoms of LVF. • Secondary VF often the final event of a progressive downhill course with LV Failure and cardiogenic shock. • Late VF develops more than 48 hours after AMI and mostly occurs in patients with large infarcts and LV dysfunction. • VF in association with marked LV failure or cardiogenic shock entails a poor prognosis, with an in-hospital mortality rate of 40-60%. Unsynchronized DC shock ,Amiodarone I.V to prevent recurrence . Treatment of hypokalaemia and magnesium deficits . ( aim K ≥ 4.5
Atrial fibrillation (AF) • AF occurs in 10-20% of MI patients. • associated with increased mortality and stroke. • If the patient is hemodynamically unstable, presents with HF and chest pain immediate cardioversion is needed. • If the AF has been present for more than 48 hours or if the duration is unclear, cardioversion ideally should be preceeded by TEE to rule out a LA thrombus or anticogulate for 3 month before the cardioversion. • If the patient is hemodynamically stable, cardioversion can be done pharmacologically
First degree AV block
Mobitz type 1
Does not require any treatment
Mobitz type 2 AV block • May progress to complete heart block so temporary pacemaker is indicated.
Complete AV block • If associated with Inferior MI, it’s usually transient and resolves within 72 hrs . Pacing is indicated if Ventricular rate is less than 40- 50 bpm. • If associated with with anterior MI, it usually occurs suddenly after 12-24 hrs , they have unstable escape rhythm and a wide complexes at a rate ≤ 40 bpm. • They are associated with an extensive septal necrosis and may need permenant pacing .
Inferior wall MI arrhythmic complication • SA Nodal artery occlusion
• Sinus bradycardia
• Variable degree of AV block
• A-V nodal artery
• Atrial fibrillation
• L.A. stretch, LA Infarction
• VT/VF
• “re-entry” or increased automaticity
Anterior wall MI arrhythmic complication • Sinus Tachycardia
• Decrease LVEF, decrease stroke volume
• Heart Block. • Septal necrosis Left or Right Bundle branch block,Complete Heart Block
• VT/VF
• re-entry” or increased automaticity
Mechanical complication • mechanical complications are serious events with worse prognosis. • Each of these complications can result in cardiogenic shock. • associated with reduced short-term and long-term survival • surgical therapy is mandatory for mechanical complication in order to decrease the high mortality in this group of patients.
But after the introduction of PPCI • mechanical complications has reduced significantly to less than 1%, including rupture of the left ventricular free wall (0.52%), papillary muscle (0.26%), and ventricular septum (0.17%).
Mechanical • Ventricular septal rupture • free wall rupture • Acute mitral regurgitation • Left ventricular aneurysm • Left ventricular dysfunction and heart failure
VENTRICULAR SEPTAL RUPTURE (VSR) • Defect in the interventricular septum caused by ischemic necrosis • Accounts for 5% of deaths after MIs • Despite optimal medical and surgical treatment, patients have a high in-hospital mortality rate.
Cardiol Clin 31 (2013) 519–531
Natural history for post MI VSR • Only about 75% survived the first 24 hour • 50% the first week
• bimodal distribution: high incidence in the first 24 hours, with another peak on days 3-5 and rarely more than 2 weeks after AMI.
• Less than 30% in 2 week • Only 10-20% more than 4 week
• Risk factors: Advanced age (>65 y), female sex, single-vessel disease, extensive MI, and poor septal collateral circulation. 22
VSD in association with the MI Anterior Wall MI
Inferior wall MI
• Located more towards the apical • patients with inferior MI occur septum. relatively infrequently. • These ruptures involve the basal inferoposterior septum.
Clinical presentation of VSR • chest pain, shortness of breath, hypotension, biventricular failure, and shock within hours to days. • new, loud, and harsh holosystolic murmur. • echocardiography, VSR with left to right shunt.
Management of VSR • Medical therapy is for temporary • In the GUSTO-I trial, the 30-day stabilization before surgery. mortality rate surgical repair vs medical managemnt (47% vs 94%), as was the 1-year mortality • CABG with surgical repair. rate (53% vs 97%).
• Percutaneous closure of septal rupture is a relatively new approach
Left ventricular free wall rupture • is the most serious complication of AMI. • Most common, least recognized complication • third leading cause of death, surpassed only by cardiogenic shock and the ventricular arrhythmias.
• Occurs in 3% of patients with acute MI. • It occurs in about 10-24% of patients who die due to AMI. • 50% in First 5 days post-MI • 90% occur within 2 weeks
• Risk factors: transmural MI, first MI, single vessel disease, lack of collaterals, and female gender. NSAID or corticosteroid use.
• Echocardiography is the diagnostic tool of choice. • key diagnostic finding is a moderate-to-large pericardial effusion with clinical and echocardiographic signs of impending pericardial tamponade.
Acute Left ventricular free wall rupture • Acute rupture is fatal. • With acute rupture, patients have electromechanical dissociation, shock and sudden death. • There may be no time for diagnostic testing. • Not amenable to management
Sub acute Rupture • Some patients have a subacute course as a result of contained rupture. • Smaller tear, temporarily sealed by clot of fibrinous pericardial adhesions • Subacute free wall rupture (30%).
Papillary muscle rupture • Least common mechanical complication 1% of patients with MI. • but often fatal complication of transmural MI • is found in 7% of patients in cardiogenic shock and contributes 5% of the mortality after acute MI. • occurs mainly in patients with inferior MI. • Causes severe Mitral valve regurgitation
Papillary muscle rupture • frequently affected the posteromedial papillary muscle since it has a single blood supply versus the dual supply to the lateral papillary muscle. • typically occurs in the first two weeks after AMI, with bimodal incidence, especially in the first 24 hours of AMI and after 3-5 days of its inception
Papillary muscle rupture: • Epidemiology: Risk factors: inferior MI. • Timing: usually occurs 2-7 days after MI. • Physical exam: holosystolic murmur, loudest at the apex, radiates to the axilla. Intensity of the murmur does not correlate to severity of mitral regurgitation. • Diagnosis: echocardiography, right heart catheterization.
Management • should be considered for emergency surgery, because the prognosis is dismal in medically treated patients.
• When complete papillary muscle rupture happens, even with surgical intervention, the mortality rate is high (30-70%).
Left ventricular aneurysm (LVA) • are discrete, dyskinetic areas of the LV wall with a broad neck. • develop in less than 5% of all patients with STEMI. • 80% of LVAs affect the anterolateral wall • associated with complete occlusion of the LAD
Left ventricular aneurysm • mortality aneurysms is up to 6 times higher than in patients without aneurysms. • Death is often sudden. • Due to high incidence of ventricular tachyarrhythmias associated with LV aneurysms
How to diagnose Left Ventricular Aneurysm ECG
Echocardiography
• ST elevation that persists several weeks after AMI and that appears in the same leads as those showing the acute infarct.
• discrete, dyskinetic areas of the LV wall with a broad neck.
Management of Left ventricular aneurysm • Patients with small or clinically insignificant aneurysms can be treated conservatively with close follow-up. • Anticoagulation is required when patients have severe LV dysfunction and/or thrombus in the LV or aneurysm. • Surgical resection of the LVA is indicated if severe heart failure, ventricular tachyarrhythmias refractory to medical treatment, or recurrent thromboembolism is present.
Cardiogenic Shock • defined as a systolic blood pressure of less than 90 mmHg for at least 30 minutes, which is secondary to myocardial dysfunction. • It is associated with clinical signs of hypoperfusion, which include decreased urine output, altered mental status and peripheral vasoconstriction.
Cardiogenic Shock • Cardiogenic shock continues to be the most common cause of death in patients hospitalized with acute MI. • developed in 7.5% of patients with STEMI • The 30-day mortality rate for patients with cardiogenic shock in GUSTO I trial was 58%.
Etiology of cardiogenic shock • LV dysfunction • acute mitral regurgitation • ventricular septal rupture • isolated right ventricular shock • tamponade or cardiac rupture
• 74.5% • 8.3% • 4.6% • 3.4% • 1.7%
Management • Revascularization by PCI or CABG is recommended in this setting. • Hemodynamic support may be needed using intraaortic balloon counterpulsation (IABP or balloon pump) and when severe left ventricular assist device insertion (LVAD).
Inflammatory ( Pericarditis) • Pericarditis after MI is classified as early pericarditis or late pericarditis. • The frequency of both early and late pericarditis has reduced with early reperfusion therapy. • Has become rare in the primary PCI era. • Often related to late reperfusion or failed coronary reperfusion, as well as to larger infarct size.
Early
• incidence approximately 10%, • usually develops within 24-96h • inflammation of pericardial tissue overlying infarcted myocardium
Late
• incidence between 1% and 3%, • typically 2 to 8 weeks after MI. • exact mechanism not known,? autoimmune process. • Clinical features include fever, chest pain, and other signs and symptoms of pericarditis
Diagnostic criteria • do not differ from those for acute pericarditis • two of the following criteria are fulfilled • (i) pleuritic chest pain • (ii) pericardial friction rub • (iii) new widespread ST-segment elevation • (iv) pericardial effusion
ESC 2017
Early
Late
• The mainstay of therapy usually includes aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). Colchicine may be beneficial in patients with recurrent pericarditis.
• Initial treatment is with NSAID • Steroids are indicated if symptoms are severe or when repeated drainage of a pericardial effusion is necessary.
Embolic complication • LV mural thrombosis • Systemic embolism • DVT • Pulmonary embolism
LV mural thrombus =Thrombus in LV cavity. LV mural thrombus
LV thrombus in ECHO
LV thrombus formation in due to LV regional-wall akinesia or dyskinesia with blood stasis, injury to and inflammation of the endocardial tissue that provides a thrombogenic surface, and a hypercoagulable state.
LV mural thrombus • overall incidence of mural thrombus after MI is approximately 20%. • Up to 60% of those after a large anterior infarction.# • thrombus formation is similar for patients treated with PPCI, thrombolysed and conservatively treated.* • Is associated with a high risk of systemic embolization. • Most common clinical presentation of is stroke. • Most episodes occur within the first 10 days after AMI.
# Curr Treat Options Cardiovasc Med 2001 3:515–521.
Treatment of LV mural thrombus • LV mural thrombus has not been shown to be related to increased intermediate-term mortality when patients are treated with warfarin.* • Anticoagulant therapy substantially decrease the rate of embolic events by 33% compared with no anticoagulation. • Management of LV mural thrombus includes Heparin followed by oral warfarin for 3-6 months. • In patients with LV anerysm, lifelong anticoagulation may be appropriate if a mural clot persists.
Systemic embolism • The incidence of clinically evident systemic embolism after MI is less than 2%.* • The most common clinical manifestation of embolic complications is stroke. • Patients may have limb ischemia, renal infarction, or mesenteric ischemia. • Most episodes of systemic emboli occur within the first 10 days after acute MI.
* Curr Treat Options Cardiovasc Med 2001; 3:515–521.
Systemic embolism Embolism
• central nervous system emboli. • Limb ischemia • Renal infarction • Mesenteric ischemia
Presentation
• Focal neurologic deficits • limb pain in a cold, pulseless extremity. • flank pain, hematuria,acute renal failure. • abdominal pain,anorexia and bloody diarrhea.
DVT and PE • Deep vein thrombosis and pulmonary embolism are now relatively uncommon. • • except in patients kept in bed because of heart failure. • Prophylactic doses of heparin and compression stockings for prevention. • Treatment include heparin, followed by oral anticoagulation for 3-6 months.
Conclusions • STEMI is associated with many complication. • Complications of STEMI are life threatening. • Patients early presentation, early appropriate management of STEMI can prevent development of complications. • Early and appropriate management of complications can improve outcome.
•
Thank you
