1. Management of Acute Myocardial Infarction
Sivanandam Vasudevan

2. Management of Acute Myocardial Infarction
Pre Hospital Phase ER
CCU
Step-down - Telemetry
Post Hospital Phase

3. Complications of Acute Myocardial Infarction
Arrhythmic Complications
Mechanical Complications
Ischemic Complications
Miscellaneous Complications
[DVT, PE, Pericarditits, TPA complications, Pneumonia]

4. Arrhythmic Complications [Early < 24 hrs & late >24 hrs]
Ventricular – PVC, V tach/V Fib
Atrial – PAC, SVT, A Fib
Bradycardia – Sinus
AV block – Complete Heart Block
LAFB, LPHB, LBBB & RBBB

5. Mechanical Complications of Acute Myocardial Infarction
Papillary Muscle Rupture – Acute MR
Ventricular Septal Defect
Right Ventricular MI
Free Wall Rupture
Cardiogenic shock
Cardiac Tamponade

6. Hemodynamic findings in complications causing cardiogenic shock with acute MI (a)
Ac Pul edema
Shock MR
Figure Important hemodynamic findings in different complications causing cardiogenic shock with acute MI [24], [25]. A, In acute mitral regurgitation (MR), a v wave is typically present in the pulmonary capillary wedge pressure (PCWP) tracing. In severe acute MR, the v wave may also be reflected in the pulmonary artery (PA) pressure (PAP) tracing, whereas in the more chronic form with a dilated left atrium (LA), an exaggerated v wave may not be present.B, In ventricular septal defect (VSD), the major finding on right heart catheterization is an increase in oxygen saturation between the right atrium (RA) and the right ventricle (RV), which reflects shunting of oxygenated blood from the left ventricle (LV) to the RV. In acute VSD, right heart pressures are often elevated out of proportion to left heart pressures owing to markedly increased pulmonary blood flow. A normal or low PAP may indicate RV failure and is a poor prognostic sign.C, Characteristic findings in RV infarction include Kussmaul´s sign, ie, an elevation in RA pressure (RAP) during inspiration, and a dip-plateau configuration on the RV pressure (RVP) tracing [24]. Typically, RAP and RVP are elevated but PCWP is normal. PCWP may be low in patients with hypovolemia, and RAP may be low in patients with RV infarction and hypotension due to hypovolemia and/or venodilation. Fluid therapy will increase RAP and, in the majority of cases, correct the hypotension. If the hypotension does not resolve, the patient is in true RV shock. If extensive LV infarction/ischemia is also present, the PCWP may also be elevated.D, One of the classic findings in cardiac tamponade is pulsus paradoxus, which is a fall in systemic arterial pressure greater than 15 to 20 mm Hg on inspiration [24], [25]. This is due to the increase in RV filling at the expense of LV filling in the heart compressed by fluid. A deep x descent and a blunted y descent can be seen in the RAP tracing. Intrapericardial pressure rises in conjunction with RA and RV diastolic pressures, reaching levels equal to LV diastolic pressure and creating the classic equalization of diastolic pressures.E, In LV shock, the hemodynamic findings include decreases in aortic pressure (AoP) and cardiac index with a rise in PCWP. The latter may be revealed only after a fluid challenge. Often, right heart pressures also rise due to elevated PCWP and/or RV involvement.
References:
[24]. Lorell B, Leinbach R, Ponot G, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol
[25]. Grossman W, In Cardiac Catheterization and Angiography, edn 2 Philadelphia: Lea and Febiger;

7. Mechanisms causing MR during an acute MI and their treatment modalities
Figure Various mechanisms causing mitral regurgitation (MR) during an acute MI and their treatment modalities. Infarction or ischemia of the posteromedial papillary muscle is far more common than that of the anterolateral papillary muscle. This is explained by the fact that the former receives most of its blood supply from the posterior descending artery, whereas the latter receives a dual blood supply from the left anterior descending artery or its diagonal branches and the marginal branches of the circumflex artery [56].Acute MR during an infarction may be either reversible or nonreversible. Reversible MR can result from ischemia that causes transient papillary muscle dysfunction and may respond to treatment with anti-ischemic agents or may resolve after reperfusion or revascularization. Another possible mechanism for partially reversible MR involves infarct expansion and left ventricular (LV) dilatation that causes mitral annular dilatation and papillary muscle dysfunction. Treatment with diuretics and afterload reduction can improve the initial LV dilatation and decrease MR. However, without further interventions, LV dilatation can progress, particularly in patients with anterior infarcts. Mitral valve (MV) repair or replacement is necessary with or without revascularization in patients with severe MR and cardiogenic shock.Extensive papillary muscle infarction may occur with acute MI and result in severe papillary muscle dysfunction and failure of coaptation of the mitral leaflets, leading to MR. The posteromedial papillary muscle is much more likely to be involved, and fibrosis and contracture of the papillary muscle may follow. Treatment with diuretics and afterload reduction should be instituted. Depending on the patient´s hemodynamic status, intra-aortic balloon pump (IABP) insertion and MV replacement or repair, with or without revascularization, may be necessary.Rupture of the head of a papillary muscle or chord(s) is a severe complication of acute MI. Nonreversible MR includes some papillary muscle infarcts and chordal and papillary muscle rupture. The degree of LV infarction varies and may involve a relatively small amount of myocardium. Pulmonary edema and frequently cardiogenic shock develop suddenly. Treatment includes immediate insertion of an IABP, as well as inotropic agents and vasodilators if tolerated. Immediate cardiac catheterization and MV repair or replacement, with or without coronary bypass surgery, is indicated.
References:
[56]. Cercek B, Shah K, Complicated acute myocardial infarction, heart failure, shock, mechanical complications. Cardiol Clin

8. Rupture of papillary muscle, a rare complication of acute MI (a)
Rupture of papillary muscle, a rare complication of acute MI (b)
Figure Rupture of the papillary muscle is a rare complication of acute myocardial infarction. In the absence of surgical intervention, this type of rupture is associated with a 95% 2-month mortality. Rupture of the papillary muscle is associated most commonly with inferior infarctions and often causes only a relatively small amount of damage to the myocardium. The posteromedial papillary muscle is more frequently affected than the anterolateral muscle because it has only one blood supply (from the posterior descending artery). An echocardiogram can display the mobile portion of the papillary muscle attached to the mitral valve. The portion of the mitral valve supported by this papillary muscle is usually flail. Color-flow mapping confirms the presence of severe mitral regurgitation (MR). The flail leaflet often serves as a deflector of the MR jet, and the color-flow map may demonstrate an eccentric direction of the jet. This unusual direction of the MR jet can lead to an underestimation of its severity if simple Doppler methods, such as measurement of jet area, are used to assess its severity.A, Parasternal long-axis view demonstrating prolapse of the tip of a ruptured papillary muscle (arrow) into the left atrium (LA) and a flail anterior mitral leaflet. B, Apical four-chamber view (left) and Doppler color-flow map (right) from the same patient demonstrating ruptured papillary muscle (arrow) and severe MR. C, Transesophageal echocardiographic view of the LA displaying a portion of another ruptured papillary muscle (arrow) as it swings into the LA during systole. LV-left ventricle.

9. Transesophageal echocardiogram in the four-chamber view

10. Hemodynamic findings in complications causing cardiogenic shock with acute MI (b)
Ac Pul edema
Shock
Systolic murmur
Figure Important hemodynamic findings in different complications causing cardiogenic shock with acute MI [24], [25]. A, In acute mitral regurgitation (MR), a v wave is typically present in the pulmonary capillary wedge pressure (PCWP) tracing. In severe acute MR, the v wave may also be reflected in the pulmonary artery (PA) pressure (PAP) tracing, whereas in the more chronic form with a dilated left atrium (LA), an exaggerated v wave may not be present.B, In ventricular septal defect (VSD), the major finding on right heart catheterization is an increase in oxygen saturation between the right atrium (RA) and the right ventricle (RV), which reflects shunting of oxygenated blood from the left ventricle (LV) to the RV. In acute VSD, right heart pressures are often elevated out of proportion to left heart pressures owing to markedly increased pulmonary blood flow. A normal or low PAP may indicate RV failure and is a poor prognostic sign.C, Characteristic findings in RV infarction include Kussmaul´s sign, ie, an elevation in RA pressure (RAP) during inspiration, and a dip-plateau configuration on the RV pressure (RVP) tracing [24]. Typically, RAP and RVP are elevated but PCWP is normal. PCWP may be low in patients with hypovolemia, and RAP may be low in patients with RV infarction and hypotension due to hypovolemia and/or venodilation. Fluid therapy will increase RAP and, in the majority of cases, correct the hypotension. If the hypotension does not resolve, the patient is in true RV shock. If extensive LV infarction/ischemia is also present, the PCWP may also be elevated.D, One of the classic findings in cardiac tamponade is pulsus paradoxus, which is a fall in systemic arterial pressure greater than 15 to 20 mm Hg on inspiration [24], [25]. This is due to the increase in RV filling at the expense of LV filling in the heart compressed by fluid. A deep x descent and a blunted y descent can be seen in the RAP tracing. Intrapericardial pressure rises in conjunction with RA and RV diastolic pressures, reaching levels equal to LV diastolic pressure and creating the classic equalization of diastolic pressures.E, In LV shock, the hemodynamic findings include decreases in aortic pressure (AoP) and cardiac index with a rise in PCWP. The latter may be revealed only after a fluid challenge. Often, right heart pressures also rise due to elevated PCWP and/or RV involvement.
References:
[24]. Lorell B, Leinbach R, Ponot G, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol
[25]. Grossman W, In Cardiac Catheterization and Angiography, edn 2 Philadelphia: Lea and Febiger;

11. Ventricular Rupture [VSR]
Ventricular septal rupture (a)
Figure Ventricular septal rupture is a rare complication of acute myocardial infarction that, if left untreated, is associated with a grave prognosis. Ventricular septal rupture is more common with a first infarct and in women. Anterior myocardial infarction accounts for 60% of cases of this type of rupture. Echocardiography has improved early detection of the complication and can assist in differentiating septal rupture from severe acute mitral regurgitation. Echocardiographically, septal rupture is detected primarily by delineation of the defect in the septum. Pulsed-wave or color-flow Doppler can confirm the presence of left-to-right shunting across the perforation. A, Transthoracic echocardiography.Modified apical four-chamber view (left) and color-flow Doppler map (right) displaying rupture of the inferior septum (arrow) and left-to-right shunting after inferior myocardial infarction.B, Transesophageal echocardiography. Modified four-chamber view (left) and color-flow Doppler map (right) in a different patient delineate a rupture of the anteroapical septum (arrow) and left-to-right shunting after anterior myocardial infarction. LA-left atrium; LV-left ventricle; RV-right ventricle.
Ventricular septal rupture (b)

12. Hemodynamic findings in complications causing cardiogenic shock with acute MI (c)
CHF
Clear lungs
Hypotension
Systolic murmur
Inf. MI
ECG V4 R
Figure Important hemodynamic findings in different complications causing cardiogenic shock with acute MI [24], [25]. A, In acute mitral regurgitation (MR), a v wave is typically present in the pulmonary capillary wedge pressure (PCWP) tracing. In severe acute MR, the v wave may also be reflected in the pulmonary artery (PA) pressure (PAP) tracing, whereas in the more chronic form with a dilated left atrium (LA), an exaggerated v wave may not be present.B, In ventricular septal defect (VSD), the major finding on right heart catheterization is an increase in oxygen saturation between the right atrium (RA) and the right ventricle (RV), which reflects shunting of oxygenated blood from the left ventricle (LV) to the RV. In acute VSD, right heart pressures are often elevated out of proportion to left heart pressures owing to markedly increased pulmonary blood flow. A normal or low PAP may indicate RV failure and is a poor prognostic sign.C, Characteristic findings in RV infarction include Kussmaul´s sign, ie, an elevation in RA pressure (RAP) during inspiration, and a dip-plateau configuration on the RV pressure (RVP) tracing [24]. Typically, RAP and RVP are elevated but PCWP is normal. PCWP may be low in patients with hypovolemia, and RAP may be low in patients with RV infarction and hypotension due to hypovolemia and/or venodilation. Fluid therapy will increase RAP and, in the majority of cases, correct the hypotension. If the hypotension does not resolve, the patient is in true RV shock. If extensive LV infarction/ischemia is also present, the PCWP may also be elevated.D, One of the classic findings in cardiac tamponade is pulsus paradoxus, which is a fall in systemic arterial pressure greater than 15 to 20 mm Hg on inspiration [24], [25]. This is due to the increase in RV filling at the expense of LV filling in the heart compressed by fluid. A deep x descent and a blunted y descent can be seen in the RAP tracing. Intrapericardial pressure rises in conjunction with RA and RV diastolic pressures, reaching levels equal to LV diastolic pressure and creating the classic equalization of diastolic pressures.E, In LV shock, the hemodynamic findings include decreases in aortic pressure (AoP) and cardiac index with a rise in PCWP. The latter may be revealed only after a fluid challenge. Often, right heart pressures also rise due to elevated PCWP and/or RV involvement.
References:
[24]. Lorell B, Leinbach R, Ponot G, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol
[25]. Grossman W, In Cardiac Catheterization and Angiography, edn 2 Philadelphia: Lea and Febiger;

13. Hemodynamic findings in complications causing cardiogenic shock with acute MI (d)
Figure Important hemodynamic findings in different complications causing cardiogenic shock with acute MI [24], [25]. A, In acute mitral regurgitation (MR), a v wave is typically present in the pulmonary capillary wedge pressure (PCWP) tracing. In severe acute MR, the v wave may also be reflected in the pulmonary artery (PA) pressure (PAP) tracing, whereas in the more chronic form with a dilated left atrium (LA), an exaggerated v wave may not be present.B, In ventricular septal defect (VSD), the major finding on right heart catheterization is an increase in oxygen saturation between the right atrium (RA) and the right ventricle (RV), which reflects shunting of oxygenated blood from the left ventricle (LV) to the RV. In acute VSD, right heart pressures are often elevated out of proportion to left heart pressures owing to markedly increased pulmonary blood flow. A normal or low PAP may indicate RV failure and is a poor prognostic sign.C, Characteristic findings in RV infarction include Kussmaul´s sign, ie, an elevation in RA pressure (RAP) during inspiration, and a dip-plateau configuration on the RV pressure (RVP) tracing [24]. Typically, RAP and RVP are elevated but PCWP is normal. PCWP may be low in patients with hypovolemia, and RAP may be low in patients with RV infarction and hypotension due to hypovolemia and/or venodilation. Fluid therapy will increase RAP and, in the majority of cases, correct the hypotension. If the hypotension does not resolve, the patient is in true RV shock. If extensive LV infarction/ischemia is also present, the PCWP may also be elevated.D, One of the classic findings in cardiac tamponade is pulsus paradoxus, which is a fall in systemic arterial pressure greater than 15 to 20 mm Hg on inspiration [24], [25]. This is due to the increase in RV filling at the expense of LV filling in the heart compressed by fluid. A deep x descent and a blunted y descent can be seen in the RAP tracing. Intrapericardial pressure rises in conjunction with RA and RV diastolic pressures, reaching levels equal to LV diastolic pressure and creating the classic equalization of diastolic pressures.E, In LV shock, the hemodynamic findings include decreases in aortic pressure (AoP) and cardiac index with a rise in PCWP. The latter may be revealed only after a fluid challenge. Often, right heart pressures also rise due to elevated PCWP and/or RV involvement.
References:
[24]. Lorell B, Leinbach R, Ponot G, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol
[25]. Grossman W, In Cardiac Catheterization and Angiography, edn 2 Philadelphia: Lea and Febiger;

14. Hemodynamic findings in complications causing cardiogenic shock with acute MI (e)
BP < 90
Tachycardia
Pul edema
Confused
Skin cold clammy
Ant. MI
Mortality 80%
Figure Important hemodynamic findings in different complications causing cardiogenic shock with acute MI [24], [25]. A, In acute mitral regurgitation (MR), a v wave is typically present in the pulmonary capillary wedge pressure (PCWP) tracing. In severe acute MR, the v wave may also be reflected in the pulmonary artery (PA) pressure (PAP) tracing, whereas in the more chronic form with a dilated left atrium (LA), an exaggerated v wave may not be present.B, In ventricular septal defect (VSD), the major finding on right heart catheterization is an increase in oxygen saturation between the right atrium (RA) and the right ventricle (RV), which reflects shunting of oxygenated blood from the left ventricle (LV) to the RV. In acute VSD, right heart pressures are often elevated out of proportion to left heart pressures owing to markedly increased pulmonary blood flow. A normal or low PAP may indicate RV failure and is a poor prognostic sign.C, Characteristic findings in RV infarction include Kussmaul´s sign, ie, an elevation in RA pressure (RAP) during inspiration, and a dip-plateau configuration on the RV pressure (RVP) tracing [24]. Typically, RAP and RVP are elevated but PCWP is normal. PCWP may be low in patients with hypovolemia, and RAP may be low in patients with RV infarction and hypotension due to hypovolemia and/or venodilation. Fluid therapy will increase RAP and, in the majority of cases, correct the hypotension. If the hypotension does not resolve, the patient is in true RV shock. If extensive LV infarction/ischemia is also present, the PCWP may also be elevated.D, One of the classic findings in cardiac tamponade is pulsus paradoxus, which is a fall in systemic arterial pressure greater than 15 to 20 mm Hg on inspiration [24], [25]. This is due to the increase in RV filling at the expense of LV filling in the heart compressed by fluid. A deep x descent and a blunted y descent can be seen in the RAP tracing. Intrapericardial pressure rises in conjunction with RA and RV diastolic pressures, reaching levels equal to LV diastolic pressure and creating the classic equalization of diastolic pressures.E, In LV shock, the hemodynamic findings include decreases in aortic pressure (AoP) and cardiac index with a rise in PCWP. The latter may be revealed only after a fluid challenge. Often, right heart pressures also rise due to elevated PCWP and/or RV involvement.
References:
[24]. Lorell B, Leinbach R, Ponot G, et al. Right ventricular infarction: clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol
[25]. Grossman W, In Cardiac Catheterization and Angiography, edn 2 Philadelphia: Lea and Febiger;

15. Regional acute MI, infarct expansion, chamber thrombosis and aneurysm formation (a)
Figure Regional acute myocardial infarction (MI), infarct expansion, chamber thrombosis, and aneurysm formation. A and B, Occlusion of the proximal right coronary artery caused posterior/inferior MI, probably 10 days old. In addition to transmural left ventricular (LV) necrosis, the infarct involves the right ventricular (RV) posterolateral wall, complicated by RV chamber thrombosis (T). Curved arrows show the extent of infarction. C, Occlusion of the proximal left anterior descending artery (LAD) with transmural anteroseptal infarction (about 1 week old), infarct expansion, and extensive thrombosis in the LV chamber. D, Old occlusion in the proximal LAD with healed transmural anteroseptal infarct, LV dilatation, endocardial thickening, and myocardial thinning and expansion with external bulging (aneurysm formation). (Panels A, B, and D: nitro blue tetrazolium test, staining viable myocardium blue; necrotic muscle remains pale owing to loss of enzyme.) (Panels B and D adapted from Andersen and coworkers [50]; with permission from the American College of Cardiologists.)
References:
[50]. Andersen HR, Falk E, Nielsen D, Right ventricular infarction: frequency, size and topography in coronary heart disease. A prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol

16. Regional acute MI, infarct expansion, chamber thrombosis and aneurysm formation (b)
Figure Regional acute myocardial infarction (MI), infarct expansion, chamber thrombosis, and aneurysm formation. A and B, Occlusion of the proximal right coronary artery caused posterior/inferior MI, probably 10 days old. In addition to transmural left ventricular (LV) necrosis, the infarct involves the right ventricular (RV) posterolateral wall, complicated by RV chamber thrombosis (T). Curved arrows show the extent of infarction. C, Occlusion of the proximal left anterior descending artery (LAD) with transmural anteroseptal infarction (about 1 week old), infarct expansion, and extensive thrombosis in the LV chamber. D, Old occlusion in the proximal LAD with healed transmural anteroseptal infarct, LV dilatation, endocardial thickening, and myocardial thinning and expansion with external bulging (aneurysm formation). (Panels A, B, and D: nitro blue tetrazolium test, staining viable myocardium blue; necrotic muscle remains pale owing to loss of enzyme.) (Panels B and D adapted from Andersen and coworkers [50]; with permission from the American College of Cardiologists.)
References:
[50]. Andersen HR, Falk E, Nielsen D, Right ventricular infarction: frequency, size and topography in coronary heart disease. A prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol

17. Regional acute MI, infarct expansion, chamber thrombosis and aneurysm formation (c)
Figure Regional acute myocardial infarction (MI), infarct expansion, chamber thrombosis, and aneurysm formation. A and B, Occlusion of the proximal right coronary artery caused posterior/inferior MI, probably 10 days old. In addition to transmural left ventricular (LV) necrosis, the infarct involves the right ventricular (RV) posterolateral wall, complicated by RV chamber thrombosis (T). Curved arrows show the extent of infarction. C, Occlusion of the proximal left anterior descending artery (LAD) with transmural anteroseptal infarction (about 1 week old), infarct expansion, and extensive thrombosis in the LV chamber. D, Old occlusion in the proximal LAD with healed transmural anteroseptal infarct, LV dilatation, endocardial thickening, and myocardial thinning and expansion with external bulging (aneurysm formation). (Panels A, B, and D: nitro blue tetrazolium test, staining viable myocardium blue; necrotic muscle remains pale owing to loss of enzyme.) (Panels B and D adapted from Andersen and coworkers [50]; with permission from the American College of Cardiologists.)
References:
[50]. Andersen HR, Falk E, Nielsen D, Right ventricular infarction: frequency, size and topography in coronary heart disease. A prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol

18. Regional acute MI, infarct expansion, chamber thrombosis and aneurysm formation (d)
Figure Regional acute myocardial infarction (MI), infarct expansion, chamber thrombosis, and aneurysm formation. A and B, Occlusion of the proximal right coronary artery caused posterior/inferior MI, probably 10 days old. In addition to transmural left ventricular (LV) necrosis, the infarct involves the right ventricular (RV) posterolateral wall, complicated by RV chamber thrombosis (T). Curved arrows show the extent of infarction. C, Occlusion of the proximal left anterior descending artery (LAD) with transmural anteroseptal infarction (about 1 week old), infarct expansion, and extensive thrombosis in the LV chamber. D, Old occlusion in the proximal LAD with healed transmural anteroseptal infarct, LV dilatation, endocardial thickening, and myocardial thinning and expansion with external bulging (aneurysm formation). (Panels A, B, and D: nitro blue tetrazolium test, staining viable myocardium blue; necrotic muscle remains pale owing to loss of enzyme.) (Panels B and D adapted from Andersen and coworkers [50]; with permission from the American College of Cardiologists.)
References:
[50]. Andersen HR, Falk E, Nielsen D, Right ventricular infarction: frequency, size and topography in coronary heart disease. A prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol

19. B
Figure Rupture of the papillary muscle is a rare complication of acute myocardial infarction. In the absence of surgical intervention, this type of rupture is associated with a 95% 2-month mortality. Rupture of the papillary muscle is associated most commonly with inferior infarctions and often causes only a relatively small amount of damage to the myocardium. The posteromedial papillary muscle is more frequently affected than the anterolateral muscle because it has only one blood supply (from the posterior descending artery). An echocardiogram can display the mobile portion of the papillary muscle attached to the mitral valve. The portion of the mitral valve supported by this papillary muscle is usually flail. Color-flow mapping confirms the presence of severe mitral regurgitation (MR). The flail leaflet often serves as a deflector of the MR jet, and the color-flow map may demonstrate an eccentric direction of the jet. This unusual direction of the MR jet can lead to an underestimation of its severity if simple Doppler methods, such as measurement of jet area, are used to assess its severity.A, Parasternal long-axis view demonstrating prolapse of the tip of a ruptured papillary muscle (arrow) into the left atrium (LA) and a flail anterior mitral leaflet. B, Apical four-chamber view (left) and Doppler color-flow map (right) from the same patient demonstrating ruptured papillary muscle (arrow) and severe MR. C, Transesophageal echocardiographic view of the LA displaying a portion of another ruptured papillary muscle (arrow) as it swings into the LA during systole. LV-left ventricle.

20. Incidence of cardiogenic shock complicating acute MI
Figure Incidence of cardiogenic shock complicating acute MI in several large, multicenter trials. Early reports by Scheidt et al. [4] and Killip and Kimball [6] cited a higher incidence of cardiogenic shock than has been reported more recently. A retrospective review of cardiogenic shock by Goldberg et al. [5] in the community of Worcester, Massachusetts, over a 12-year period ( ) provides a historical perspective and shows that the incidence of this complication has been constant. Both this study and the Multicenter Investigation for the Limitation of Infarct Size (MILIS) [3] largely reflect treatment before the thrombolytic era. The incidence of cardiogenic shock reported by Hands et al. in MILIS (7.1%) was similar to that in the Worcester study. However, this reported incidence may underestimate the occurrence of cardiogenic shock in this population, since MILIS excluded patients over 75 years of age as well as those who arrived at the hospital already in shock.Three multicenter studies provide information about the incidence of cardiogenic shock during the thrombolytic era [17], [18], [19]. The Third International Study of Infarct Survival (ISIS-3) [17] in 1990 involved 41,299 patients and reported an incidence of shock similar to that in earlier studies. Data from the Second Thrombolysis in Myocardial Infarction (TIMI-II) [18] and the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO) trials [19], however, suggest a trend toward a lower incidence of cardiogenic shock with thrombolysis. Only a minority of patients who ultimately develop cardiogenic shock have it on presentation, as noted in the first Gruppo Italiano per lo Studio della Streptochinasi nell´Infarto Miocardico (GISSI-1) [20], TIMI-II, and GUSTO trials. The pathophysiology in delayed shock is complex and is discussed in detail in Fig and Fig The incidence of several mechanical causes of cardiogenic shock is also shown. Left ventricular (LV) free wall rupture was reported in 1.3% of the patients in ISIS-3 [17]. In the Late Assessment of Thrombolytic Efficacy (LATE) study [21] the incidence of rupture was reported to be 3.4%; however, this included both confirmed and suspected cases of rupture. In the GUSTO population of 41,000 patients, the incidence of acute ventricular septal rupture (VSR) was 0.5% and the incidence of acute mitral regurgitation (MR) was 1.7%[19]. Whether these lower rupture rates represent a less accurate diagnosis or a true change in incidence is not known.
References:
[3]. Hands ME, Rutherford JD, Muller JE, et al. The in hospital development of cardiogenic shock after myocardial infarction: incidence, predictors of occurrence, outcome and prognostic factors. J Am Coll Cardiol
[4]. Scheidt S, Ascheim R, Killip T III, Shock after acute myocardial infarction: a clinical and hemodynamic profile. Am J Cardiol
[5]. Goldberg RJ, Gore JM, Alpert JS, et al. Cardiogenic shock after acute myocardial infarction: incidence and mortality from a community-wide perspective, 1975 to N Engl J Med
[6]. Killip T, Kimball JT, Treatment of myocardial infarction in a coronary care unit: a two-year experience with 250 patients. Am J Cardiol
[17].ISIS-3 (Third International Study of Infarct Survival) Collaborative Group,
ISIS-3: A randomized comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin alone among 41,299 cases of suspected acute myocardial infarction. Lancet
[18].The TIMI Study Group,
Comparison of invasive and conservative strategies after treatment with intravenous tissue plasminogen activator in acute myocardial infarction: results of the thrombolysis in myocardial infarction (TIMI) Phase II Trial. N Engl J Med
[19].The GUSTO Investigators,
An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. N Engl J Med
[20].Gruppo Italiano per lo Studio della Streptochinasi nell´Infarto Miocardico (GISSI),
Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet
[21]. Becker R, Charlesworth A, Wilcox R, et al. Cardiac rupture associated with thrombolytic therapy: impact of time to treatment in the Late Assessment of Thrombolytic Efficacy (LATE) Study. J Am Coll Cardiol

21. Rupture of the heart complicates acute MI in about 10% of cases
Figure Rupture of the heart complicates acute myocardial infarction in about 10% of autopsied cases. Typically, it occurs during the first week after a first infarct and is more common in elderly women. The pathoanatomic substrate for postinfarction rupture of the left ventricular free wall or the interventricular septum includes total occlusion of a functional end artery (poor collateral circulation) causing transmural infarction in a perfusion area that was previously healthy (ie, no myocardial fibrosis). Usually, heart weight is normal. A, Rupture of the anterior wall of the left ventricle (LV; between arrows), parallel to the left anterior descending artery (LAD). B, Perforation of the free wall in this 11-hour-old infarct can be seen clearly on the transventricular myocardial slice (short-axis view). Thrombolytic therapy was not given. C, Postmortem angiogram of a similar case (28-hour-old infarct) showing LAD occlusion (arrowhead). The right coronary (black arrow) and left circumflex (white arrow) arteries appear almost normal (single-vessel disease). The LAD is occluded just distal to the first septal branch, with no distal collateral filling.D, Angiographic short-axis view of transventricular myocardial slice reveals no vascular filling in the area normally perfused by the LAD. Note the treelike coronary branching pattern with well-defined perfusion areas, in contrast to the enlarged anastomotic network frequently seen with subendocardial infarction (see Fig. 3-33B) and, in particular, with diffuse subendocardial necrosis. RV-right ventricle.

22. Ischemic Complications Post Myocardial Infarction Chest pain Post MI
Recurrent angina
Recurrent MI
Pericarditis[ Acute & Dressler’s ]
Pneumonia
Pulmonary Embolism
Shoulder hand syndrome

23. Management of Acute Myocardial Infarction
CT of patients with stroke as a complication of MI (a)
Management of Acute Myocardial Infarction
Pre discharge work up
Secondary prevention – Diet, Exercise, Weight control, Smoking cessation
Lipid control
B Blockers, ACE Inhibitors, ASA, Statins
Cardiac Rehabilitation
Discharge planning
Pre discharge ECHO, Stress test
Figure Computed tomography (CT) of patients with stroke as a complication of MI treated with thrombolytic therapy: intra-cerebral hemorrhage (ICH), subdural hematoma, and infarct. Besides death, stroke is the most feared complication of both MI and thrombolytic therapy. The clinical occurrence of a stroke may correspond pathophysiologically to one or more processes, including non-hemorrhagic cerebral infarct, cerebral infarct with a subsequent hemorrhage into the infarcted brain, primary ICH, subdural hematoma, and subarachnoid hemorrhage. Although the various types of stroke may be difficult to distinguish based on clinical manifestations, their definition and classification based on the process leading to the stroke has important implications for both management as well as understanding the etiology to develop strategies of prevention.Shown are five CT scans from patients suffering stroke in the GUSTO trial. Each is typical of one of the five major types of stroke. A, Primary intracerebral hemorrhage (left parieto-occipital, with compression of the left ventricle and midline shift). B, Subdural hematoma (left-sided with compression of the left ventricle and midline shift). C, Cerebral infarct (acute right parietofrontal with obliteration of sulci). D and E, Cerebral infarct with hemorrhagic conversion (with the acute CT scan showing a large parieto-occipital infarct [D]) and follow-up scan showing secondary hemorrhage into the parietal region [E].)

24. Management of Acute Myocardial Infarction
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