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Complications of Myocardial Infarction (MI)

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Complications of Myocardial Infarction (MI)

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Complications of Myocardial Infarction (MI)

  1. 1. Complications of AcuteComplications of Acute Myocardial InfarctionMyocardial Infarction
  2. 2. OverviewOverview  Recurrent Ischemia/InfarctionRecurrent Ischemia/Infarction  Congestive Heart Failure/LV FailureCongestive Heart Failure/LV Failure  Cardiogenic ShockCardiogenic Shock  Interventricular Septal RuptureInterventricular Septal Rupture  Free Wall RuptureFree Wall Rupture  Acute Mitral RegurgitationAcute Mitral Regurgitation  Right Ventricular InfarctionRight Ventricular Infarction  ArrhythmiasArrhythmias  Pericardial Effusion and PericarditisPericardial Effusion and Pericarditis
  3. 3. Recurrent Ischemia andRecurrent Ischemia and InfarctionInfarction  Incidence of postinfarction angina withoutIncidence of postinfarction angina without reinfarction is 20-30%reinfarction is 20-30%  Reduced incidence with primary PTCAReduced incidence with primary PTCA  May be due to occlusion of an initiallyMay be due to occlusion of an initially patent vessel, reocclusion of an initiallypatent vessel, reocclusion of an initially recanalized vessel, or coronary spasm.recanalized vessel, or coronary spasm.
  4. 4. Ischemic complications These can include infarct extension, recurrent infarction, and recurrent angina. Prevalence Infarct extension is a progressive increase in the amount of myocardial necrosis within the infarct zone of the original MI. This may manifest as an infarction that extends and involves the adjacent myocardium or as a subendocardial infarction that becomes transmural. Reocclusion of an infarct-related artery (IRA) occurs in 5% to 30% of patients following fibrinolytic therapy. These patients also tend to have a poorer outcome.1 Reinfarction is more common in patients with diabetes mellitus or prior MI.
  5. 5. SponsoredSponsored Medical Lecture Notes –Medical Lecture Notes – All SubjectsAll Subjects USMLE Exam (America) –USMLE Exam (America) – PracticePractice
  6. 6. Infarction in a separate territory (recurrent infarction) may be difficult to diagnose within the first 24 to 48 hours after the initial event. Multivessel coronary artery disease is common in patients with acute myocardial infarction. In fact, angiographic evidence of complex or ulcerated plaques in noninfarct-related arteries is present in up to 40% of patients with acute MI. Angina, which occurs from a few hours to 30 days after acute MI, is defined as postinfarction angina. The incidence of postinfarction angina is highest in patients with non–ST-elevation MI (approximately 25%) and those treated with fibrinolytics compared with mechanical revascularization (percutaneous coronary intervention [PCI]).
  7. 7. Pathophysiology Reinfarction occurs more frequently when the IRA reoccludes than when it remains patent; however, reocclusion of the IRA does not always cause reinfarction because of abundant collateral circulation. After fibrinolytic therapy, reocclusion is found on angiograms of 5% to 30% of patients and is associated with a worse outcome. The pathophysiologic mechanism of postinfarction angina is similar to that of unstable angina and should be managed in a similar manner. Patients with postinfarction angina have a worse prognosis with regard to sudden death, reinfarction, and acute cardiac events.
  8. 8. Signs and Symptoms Patients with infarct extension or postinfarction angina usually have continuous or recurrent chest pain, with protracted elevation in the creatine kinase (CK) level and, occasionally, new electrocardiographic changes.
  9. 9. Diagnostic Testing The diagnosis of infarct expansion, reinfarction, or postinfarction ischemia can be made with echocardiography or nuclear imaging. A new wall motion abnormality, larger infarct size, new area of infarction, or persistent reversible ischemic changes help substantiate the diagnosis. CK-MB is a more useful marker for tracking ongoing infarction than troponin, given its shorter half-life. Re-elevation and subsequent decline in CK-MB levels suggest infarct expansion or recurrent infarction. Elevations in the CK-MB level of more than 50% over a previous nadir are diagnostic for reinfarction.
  10. 10. Treatment Medical therapy with aspirin, heparin, nitrates, and beta blockers is indicated in patients who have had a myocardial infarction and have ongoing ischemic symptoms. An intra- aortic balloon pump (IABP) should be inserted promptly in patients with hemodynamic instability or severe LV systolic dysfunction. Coronary angiography should be performed in patients who are stabilized with medical therapy, but emergency angiography may be undertaken in unstable patients. Revascularization, percutaneous or surgical, is associated with improved prognosis.
  11. 11. Left Ventricular FailureLeft Ventricular Failure  THE single most important predictor of mortalityTHE single most important predictor of mortality after AMIafter AMI  Characterized by either systolic dysfunction aloneCharacterized by either systolic dysfunction alone or both systolic and diastolic dysfunctionor both systolic and diastolic dysfunction  Increased clinical manifestations as the extent ofIncreased clinical manifestations as the extent of the injury to the LV increasesthe injury to the LV increases  Other predictors of development of symptomaticOther predictors of development of symptomatic LV dysfunction include advanced age and diabetesLV dysfunction include advanced age and diabetes  Mortality increases with the severity of theMortality increases with the severity of the hemodynamic deficithemodynamic deficit
  12. 12. Left Ventricular FailureLeft Ventricular Failure  LV failure – Congestive Heart FailureLV failure – Congestive Heart Failure  Characteristically develop hypoxemia dueCharacteristically develop hypoxemia due to pulmonary vascular engorgementto pulmonary vascular engorgement  Managed most effectively first by reductionManaged most effectively first by reduction of ventricular preload and then, if possible,of ventricular preload and then, if possible, by lowering afterloadby lowering afterload
  13. 13. Left Ventricular FailureLeft Ventricular Failure  Treatment:Treatment: – DiureticsDiuretics – NitroglycerinNitroglycerin – VasodilatorsVasodilators – DigitalisDigitalis – Beta-adrenoceptor agonistsBeta-adrenoceptor agonists – Other positive inotropic agentsOther positive inotropic agents
  14. 14. Incidence of Heart Failure in Acute Myocardial Infarction Killip Class Characteristics I No evidence of congestive heart failure II Rales, ↑ jugular venous distention, or S3 III Pulmonary edema IV Cardiogenic shock
  15. 15. Class of CHF - KillipClass of CHF - Killip  Derived retrospectively in the 60’s, post-MI ptsDerived retrospectively in the 60’s, post-MI pts I - No CHF - 5% mortalityI - No CHF - 5% mortality II - Mild CHF (bibasilar rales and S3) - 15-25%II - Mild CHF (bibasilar rales and S3) - 15-25% mortalitymortality III - Frank pulmonary edema - 40% mortalityIII - Frank pulmonary edema - 40% mortality IV - Cardiogenic shock - 80% mortalityIV - Cardiogenic shock - 80% mortality Killip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A twoKillip T 3rd, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol. 1967 Oct;20(4):457-64.year experience with 250 patients. Am J Cardiol. 1967 Oct;20(4):457-64.
  16. 16. NYHA ClassificationNYHA Classification  Class IClass I: No limitation of physical activity: No limitation of physical activity  Class IIClass II: Slight limitation of activity. Dyspnea: Slight limitation of activity. Dyspnea and fatigue with moderate activity (>2flights ofand fatigue with moderate activity (>2flights of stairs)stairs)  Class IIIClass III: Marked limitation of activity. Dyspnea: Marked limitation of activity. Dyspnea and fatigue with minimal activity (i.e. < 2 flightsand fatigue with minimal activity (i.e. < 2 flights of stairsof stairs  Class IVClass IV: Severe limitation of activity. Sx are: Severe limitation of activity. Sx are present at restpresent at rest
  17. 17. Cardiogenic ShockCardiogenic Shock  Most severe clinical expression of leftMost severe clinical expression of left ventricular failureventricular failure  Occurs in up to 7% of patients with AMIOccurs in up to 7% of patients with AMI  Low output state characterized by elevatedLow output state characterized by elevated ventricular filling pressures, low cardiacventricular filling pressures, low cardiac output, systemic hypotension, and evidenceoutput, systemic hypotension, and evidence of vital organ hypoperfusionof vital organ hypoperfusion
  18. 18. Cardiogenic ShockCardiogenic Shock  At autopsy, more than 2/3 of patients withAt autopsy, more than 2/3 of patients with cardiogenic shock demonstrate stenosis ofcardiogenic shock demonstrate stenosis of 75 percent or more of the luminal diameter75 percent or more of the luminal diameter of all 3 major coronary vessels and loss ofof all 3 major coronary vessels and loss of about 40 percent of LV massabout 40 percent of LV mass
  19. 19. Cardiogenic ShockCardiogenic Shock  Medical ManagementMedical Management – Same as tx for LV failureSame as tx for LV failure – Intraaortic balloon counterpulsationIntraaortic balloon counterpulsation – RevascularizationRevascularization
  20. 20. Mechanical complications Mechanical complications of acute MI include ventricular septal rupture, papillary muscle rupture or dysfunction, cardiac free wall rupture, ventricular aneurysm, LV failure with cardiogenic shock, dynamic left ventricular outflow tract obstruction, and right ventricular failure.
  21. 21. Ventricular Septal Rupture Independent predictors of ventricular septal rupture (VSR) are shown in Older age Female gender Nonsmoker Anterior infarct Worse Killip class on admission Increasing heart rate on admission
  22. 22. Prevalence VSR formerly occurred in 1% to 2% of patients after acute MI in the prethrombolytic era . The incidence has dramatically decreased with reperfusion therapy.2 The GUSTO- I trial has demonstrated an incidence of VSR of approximately 0.2%.3,4 VSR may develop as early as 24 hours after MI but was commonly seen 3 to 7 days after MI in the prefibrinolytic era and 2 to 5 days currently. Fibrinolytic therapy is not associated with an increased risk of VSR.2,5
  23. 23. Pathophysiology The defect usually occurs at the junction of preserved and infarcted myocardium in the apical septum with anterior MI and in the basal posterior septum with inferior MI. VSR almost always occurs in the setting of a transmural MI and is more frequently seen in anterolateral MIs. The defect may not always be a single large defect; it can be a meshwork of serpiginous channels that can be identified in 30% to 40% of patients.
  24. 24. Signs and Symptoms Early in the disease process, patients with VSR may appear relatively comfortable, with no clinically significant cardiopulmonary symptoms. Rapid recurrence of angina, hypotension, shock, or pulmonary edema may develop later in the course.
  25. 25. Diagnosis Rupture of the ventricular septum is often accompanied by a new harsh holosystolic murmur best heard at the left lower sternal border. The murmur is accompanied by a thrill in 50% of cases. This sign is generally accompanied by a worsening hemodynamic profile and biventricular failure. Therefore, it is important that all patients with MI have a well- documented cardiac examination at presentation and daily thereafter daily thereafter.
  26. 26. An electrocardiogram (ECG) may show atrioventricular (AV) nodal or infranodal conduction delay abnormalities in approximately 40% of patients. Echocardiography with color flow imaging is the best method for diagnosing VSR. There are two types of VSR, which can best be visualized in different echocardiographic planes. A basal VSR is best visualized in the parasternal long axis with medial angulation, apical long axis, and subcostal long axis. An apical VSR is best visualized in the apical four-chamber view. Echocardiography can define LV and right ventricular (RV) function—important determinants of mortality—as well as the size of defect and degree of left-to-right shunt by assessing flow through the pulmonary and aortic valves. In some cases, it may be necessary to use transesophageal echocardiography to assess the ventricular septal defect.
  27. 27. Treatment Early surgical closure is the treatment of choice, even if the patient's condition is stable. Initial reports have suggested that delaying surgery is likely to result in improved surgical mortality.6 These benefits were probably the result of selection bias,7 because the mortality rate in patients with VSD treated medically is 24% at 72 hours and 75% at 3 weeks. Therefore, patients should be considered for urgent surgical repair. There is a high surgical mortality associated with cardiogenic shock and multisystem failure. This further supports earlier operation before complications develop.8 Mortality is highest in patients with basal septal rupture associated with inferior MI (70%, compared with 30% in patients with anterior infarcts). The mortality rate is higher because of increased technical difficulty and the frequent need for mitral valve repair or replacement in the patients with mitral regurgutation.9 Regardless of the location and hemodynamic condition of the patient, surgery should always be considered, because it is associated with a lower mortality rate than conservative management.10
  28. 28. Intensive medical management should be started to support the patient before surgery. Unless there is significant aortic regurgitation, an IABP should be inserted urgently as a bridge to a surgical procedure. The IABP will decrease the systemic vascular resistance (SVR) and shunt fraction while increasing coronary perfusion and maintaining blood pressure. After insertion of the IABP, vasodilators can be used, with close hemodynamic monitoring. Vasodilators can also reduce left-to-right shunting and increase systemic flow by reducing SVR. Nevertheless, caution should be exercised to avoid a greater decrease in pulmonary vascular resistance than in SVR and a consequent increase in shunting. The vasodilator of choice is intravenous (IV) nitroprusside, which is started at 0.5 to 1.0 μg/kg/min and titrated to a mean arterial pressure (MAP) of 60 to 75 mm Hg.
  29. 29. Interventricular Septal RuptureInterventricular Septal Rupture  Occurs in 0.2 percent of patients with AMIOccurs in 0.2 percent of patients with AMI  Clinical features associated with increased risk ofClinical features associated with increased risk of rupture:rupture: – Lack of development of collateral networkLack of development of collateral network – Advanced ageAdvanced age – HypertensionHypertension – Anterior location of infarctionAnterior location of infarction – thombolysisthombolysis  Higher 30-day mortality (74%) compared to thoseHigher 30-day mortality (74%) compared to those patients who do not develop this complicationpatients who do not develop this complication (7%)(7%)
  30. 30. Interventricular Septal RuptureInterventricular Septal Rupture  The size of the defect determines:The size of the defect determines: – The magnitude of the left-to-right shuntThe magnitude of the left-to-right shunt – Extent of hemodynamic deteriorationExtent of hemodynamic deterioration – Likelihood of survivalLikelihood of survival  Associated with complete heart block, rightAssociated with complete heart block, right bundle branch block, and atrial fibrillationbundle branch block, and atrial fibrillation in 20-30 percent of casesin 20-30 percent of cases
  31. 31. Interventricular Septal RuptureInterventricular Septal Rupture  Characterized by the appearance of a newCharacterized by the appearance of a new harsh, loud holosystolic murmurharsh, loud holosystolic murmur  Best heard at the lower left sternal borderBest heard at the lower left sternal border  Usually accompanied by a thrillUsually accompanied by a thrill  Can be recognized by 2-DCan be recognized by 2-D echocardiographyechocardiography  Catheter placement of an umbrella-shapedCatheter placement of an umbrella-shaped device within the ruptured septumdevice within the ruptured septum
  32. 32. Free Wall Rupture Prevalence Free wall rupture occurs in 3% of MI patients and accounts for approximately 10% of mortality after MI . The timing of cardiac rupture is within 5 days in 50% of patients and within 2 weeks of MI in 90% of patients. Free wall rupture occurs only among patients with transmural MI. Risk factors include advanced age, female gender, hypertension, first MI, and poor coronary collateral vessels.
  33. 33. Pathophysiology Free wall rupture accounts for part of the early hazard in patients treated with fibrinolytic agents. Nevertheless, the overall incidence of free wall rupture is not higher in patients treated with fibrinolytics.21–23 Although any wall can be involved, cardiac rupture most commonly occurs at the lateral wall. Free wall rupture occurs at three distinct intervals, with three distinct pathologic subsets. Type I increases with the use of fibrinolytics. It occurs early (within the first 24 hours) and is a full-thickness rupture. Type II rupture occurs 1 to 3 days post-MI and is a result of erosion of the myocardium at the site of infarction. Type III rupture occurs late and is located at the border zone of the infarction and normal myocardium. The reduction in type III ruptures as a result of the advent of fibrinolytics has resulted in no change in the overall free wall rupture rate. It has been postulated that type III ruptures can occur as a result of dynamic left ventricular outflow tract obstruction and the resultant increased wall stress.24
  34. 34. Signs and Symptoms Sudden onset of chest pain with straining or coughing may suggest the onset of myocardial rupture. Acute rupture patients often have electromechanical dissociation and sudden death. Other patients may have a more subacute course as a result of a contained rupture. They might complain of pain consistent with pericarditis, nausea, and hypotension. In a study evaluating 1457 patients with acute MI, 6.2% of patients had free wall rupture. Approximately one third of these patients presented with a subacute course.22 Jugular venous distention, pulsus paradoxus, diminished heart sounds, and a pericardial rub suggest subacute rupture. New to-and- fro murmurs may be heard in patients with subacute rupture or pseudoaneurysm. A junctional or idioventricular rhythm, low-voltage complexes, and tall precordial T waves may be evident on the ECG. Additionally, a large number of patients have transient bradycardia just before rupture, as well as other manifestations of increased vagal tone.
  35. 35. Diagnostic Testing Although often there is not enough time for diagnostic testing in the management of patients with acute rupture, echocardiography is the test of choice. Echocardiography will demonstrate a pericar-dial effusion with findings of cardiac tamponade. These findings include right atrium and RV diastolic collapse, dilated inferior vena cava, and marked respiratory variations in mitral and tricuspid inflow. Additionally, a Swan-Ganz pulmonary catheter may reveal hemodynamic signs of tamponade, with equalization of the right atrium, RV diastolic, and pulmonary capillary wedge pressures.
  36. 36. Treatment The goal of therapy is to diagnose the problem and perform early emergency open heart surgery to correct the rupture. Emergency pericardiocentesis may be performed immediately on patients with tamponade and severe hemodynamic compromise while arrangements are being made for transport to the hospital. The procedure may be dangerous because of reopening of communication with the pericardium as the intrapericardial pressure is relieved. Medical management has no role in the treatment of these patients, except for the use of vasopressors to maintain blood pressure temporarily as the patient is rushed to the operating room.
  37. 37. Free Wall RuptureFree Wall Rupture  Usually leads to hemopericardium andUsually leads to hemopericardium and death from cardiac tamponadedeath from cardiac tamponade  Occasionally, rupture of the free wall of theOccasionally, rupture of the free wall of the ventricle occurs as the first clinicalventricle occurs as the first clinical manifestation in patients with undetected ormanifestation in patients with undetected or silent MI, and then it may be considered asilent MI, and then it may be considered a form of “sudden cardiac death”form of “sudden cardiac death”
  38. 38. Free Wall RuptureFree Wall Rupture  The coarse of rupture can vary fromThe coarse of rupture can vary from catastrophic, with an acute tear leading tocatastrophic, with an acute tear leading to immediate death, to subacute, with nausea,immediate death, to subacute, with nausea, hypotension, and pericardial type ofhypotension, and pericardial type of discomfortdiscomfort  Survival depends on the recognition of thisSurvival depends on the recognition of this complication, on hemodynamic stabilizationcomplication, on hemodynamic stabilization of the patient, and most importantly, onof the patient, and most importantly, on prompt surgical repairprompt surgical repair
  39. 39. PseudoaneurysmPseudoaneurysm  Incomplete rupture of the heart, withIncomplete rupture of the heart, with organizing thrombus and hematoma,organizing thrombus and hematoma, together with pericardium, seal a rupture oftogether with pericardium, seal a rupture of the left ventriclethe left ventricle  With time this area of organized thrombusWith time this area of organized thrombus and pericardium can become aand pericardium can become a pseudoaneurysm that maintainspseudoaneurysm that maintains communication with the cavity of the leftcommunication with the cavity of the left ventricle.ventricle.
  40. 40. PseudoaneurysmPseudoaneurysm  Can become quite large, even equaling theCan become quite large, even equaling the true ventricular cavity in size, and theytrue ventricular cavity in size, and they communicate with the LV cavity through acommunicate with the LV cavity through a narrow necknarrow neck  Diagnosis: 2-D echocardiography andDiagnosis: 2-D echocardiography and contrast angiographycontrast angiography
  41. 41. Mitral Regurgitation Prevalence Mitral regurgitation (MR) after acute MI predicts poor prognosis, as demonstrated in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial. Nevertheless, MR of mild to moderate severity is found in 13% to 45% patients following acute MI.11–14 Whereas most MR is transient in duration and asymptomatic, MR caused by papillary muscle rupture (Fig. 3) is a life-threatening complication of acute MI. Fibrinolytic agents decrease the incidence of rupture; however, when present, rupture may occur earlier in the post-MI period than in the absence of reperfusion. Although papillary muscle rupture was reported to occur between days 2 and 7 in the prefibrinolytic era, the SHOCK Trial Registry demonstrated a median time to papillary muscle rupture of 13 hours.15 Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes to 5% of the mortality after acute MI.16,17
  42. 42. Pathophysiology Mitral regurgitation can occur as a result of a number of mechanisms, including the following: (1) mitral valve annular dilation secondary to LV dilation; (2) papillary muscle dysfunction with associated ischemic regional wall motion abnormality in close proximity to the insertion of the posterior papillary muscle; and (3) partial or complete rupture of the chordae or papillary muscle.16 Papillary muscle rupture is most common with an inferior MI. The posteromedial papillary muscle is most frequently involved because of its single blood supply through the posterior descending coronary artery.18 The anterolateral papillary muscle has dual blood supply, being perfused by the left anterior descending (LAD) and left circumflex coronary arteries. In 50% of patients with papillary muscle rupture, the infarct is relatively small
  43. 43. Signs and Symptoms Complete transection of the papillary muscles is rare and usually results in immediate pulmonary edema, cardiogenic shock, and death. Physical examination demonstrates a new pansystolic murmur, which is audible at the cardiac apex and radiates to the axilla or the base of the heart. If there is a posterior papillary muscle rupture, the murmur radiates to the left sternal border and may be confused with the murmur of VSD or aortic stenosis (intensity of the murmur does not always predict the severity of MR). In patients with severe heart failure, poor cardiac output or with elevated left atrial pressures, the murmur may be soft or absent.
  44. 44. Diagnostic Testing The ECG usually shows evidence of a recent inferior or posterior MI. The chest radiograph shows evidence of pulmonary edema. Focal pulmonary edema can occur in the right upper lobe when flow is directed at the right pulmonary veins. The diagnostic test of choice is two-dimensional echocardiography with Doppler and color flow imaging. In severe MR, the mitral valve leaflet is usually flail. Color flow imaging can be useful in distinguishing papillary muscle rupture with severe MR from VSR. Transthoracic echocardiography may not fully appreciate the amount of MR in some patients with posteriorly directed jets. In these patients, transesophageal echocardiography (TEE) may be particularly useful. Hemodynamic monitoring with a PA catheter may reveal large V (more than 50 mm Hg) waves in the pulmonary capillary wedge pressure (PCWP). Nevertheless, patients with VSR can also have
  45. 45. Treatment Patients with papillary muscle rupture should be rapidly identified and receive aggressive medical treatment while being considered for surgery. Medical therapy includes vasodilator therapy. Nitroprusside is useful in the treatment of patients with acute MR. Nitroprusside directly decreases SVR, thereby reducing the regurgitant fraction and increasing the forward stroke volume and cardiac output. Nitroprusside can be started at 0.5 to 1.0 μ/kg/min and titrated to a MAP of 60 to 75 mm Hg. An IABP should be inserted to decrease LV afterload, improve coronary perfusion, and increase forward cardiac output. Patients with hypotension may tolerate vasodilators after the insertion of an IABP.
  46. 46. Patients with papillary muscle rupture should be considered for emergency surgery, because the prognosis is dismal in medically treated patients. Coronary angiography should be performed before surgical repair, because revascularization during MVR is associated with improved short-term and long-term mortality.17,20 Additional surgical candidates include patients with moderate MR who do not improve with afterload reduction Treatment
  47. 47. Right Ventricular InfarctionRight Ventricular Infarction  Frequently accompanies inferior LVFrequently accompanies inferior LV infarction or rarely occurs in isolated forminfarction or rarely occurs in isolated form  Right-sided filling pressures are elevated,Right-sided filling pressures are elevated, whereas left ventricular filling pressure iswhereas left ventricular filling pressure is normal or only slighty raisednormal or only slighty raised  Cardiac output is often markedly depressedCardiac output is often markedly depressed
  48. 48. Right Ventricular InfarctionRight Ventricular Infarction  Common among patients with inferior LVCommon among patients with inferior LV infarctioninfarction  Unexplained systemic arterial hypotensionUnexplained systemic arterial hypotension or diminished cardiac output or markedor diminished cardiac output or marked hypotension in response to small doses ofhypotension in response to small doses of nitroglycerine in patients with inferiornitroglycerine in patients with inferior infarction should lead to the promptinfarction should lead to the prompt consideration of this diagnosisconsideration of this diagnosis
  49. 49. Right Ventricular InfarctionRight Ventricular Infarction  Most patients with RV infarction have STMost patients with RV infarction have ST segment elevation in lead V4R (rightsegment elevation in lead V4R (right precordial lead in V4 position)precordial lead in V4 position)  2-D echocardiography : abnormal wall2-D echocardiography : abnormal wall motion of the right ventricle as well as rightmotion of the right ventricle as well as right ventricular dilitation and depressed RVventricular dilitation and depressed RV ejection fractionejection fraction
  50. 50. Right Ventricular InfarctionRight Ventricular Infarction  Medications routinely prescribed for LVMedications routinely prescribed for LV infarction may produce profoundinfarction may produce profound hypotension in patients with RV infarctionhypotension in patients with RV infarction (especially nitroglycerine)(especially nitroglycerine)  Initial treatment of hypotension in patientsInitial treatment of hypotension in patients with RV infarction include volumewith RV infarction include volume expansionexpansion
  51. 51. Embolic Complications Prevalence The incidence of clinically evident systemic embolism after MI is lower than 2%. The incidence increases in patients with anterior wall MI. The overall incidence of mural thrombus after MI is approximately 20%. Large anterior MI may be associated with mural thrombus in as many as 60% of patients.47,48 Pathophysiology Most emboli arise from the left ventricle as a result of wall motion abnormalities or aneurysms. Atrial fibrillation in the setting of is- chemia may also contribute to systemic embolization.
  52. 52. Signs and Symptoms The most common clinical manifestation of embolic complications is stroke, although patients may have limb ischemia, renal infarction, or intestinal ischemia. Most episodes of systemic emboli occur in the first 10 days after acute MI. Physical findings vary with the site of the embolism. Focal neurologic deficits occur in patients with central nervous system emboli. Limb ischemia manifests with limb pain in a cold pulseless extremity. Renal infarction manifests with flank pain and hematuria. Mesenteric ischemia manifests with abdominal pain out of proportion to physical findings and bloody diarrhea.
  53. 53. Treatment IV heparin should be started immediately with a target PTT of 50 to 70 seconds and continued until the INR is in therapeutic range. Warfarin sodium therapy should also be started immediately, with a goal INR of 2 to 3, and continued for at least 3 to 6 months for patients with mural thrombi and for those with large akinetic areas detected by echocardiography.
  54. 54. Post Cardiac Injury Syndrome (Dressler’s Syndrome) Definition: Dressler’s Syndrome occurs in 5%-6% of patients with acute myocardial infarction4. It characteristically presents with fever, malaise and pleuropericardial chest pain, the onset of whichnis 2-3 weeks after the acute event7. About 28% develop pleural or pericardial effusion2,6. The acute event can also be anything causing inflammation or penetration of the pericardium, cardiac operation, a stab wound, a non- penetrating blow to the chest, or perforation of the heart with a heart catheter, or post-operative cytomegalovirus (CMV) infection. In these cases it is called post- pericardotomy5 or post cardiac injury syndrome1.
  55. 55. Dressler’s syndrome: In Dressler’s syndrome, the pericarditis develops after a myocardial infarction. The theory is that the infarction can cause a pericardial injury that in turn causes a pericardial effusion. This is sometimes a sub- clinical effusion. This is supported by the fact that serial ECHO’s done on post-MI patients show pericardial effusions in 28% of patients which sometimes go undetected7.
  56. 56. Clinical Features: Fever with pericarditis, pleuritis, and/or pneumonitis are the main features of PCIS. The illness usually lasts for one to two weeks. The pericarditis can be fibrinous or serosanguineous, rarely causes tamponade, and can be associated with arthralgias. Some clinical features to look for are: • Prior injury of the pericardium, myocardium, or both. • Latent period between the injury and the development of pericarditis or pericardial effusion. • Tendency for recurrence. • Stabbing chest pain pleuritic in nature • Responsiveness to nonsteroidal antiinflammatory drugs and corticosteroids. • Fever (as high as 104 degrees), leukocytosis, and elevated erythrocyte sedimentation rate. C-reactive protein and other markers of inflammation. • Pericardial and sometimes pleural effusion, with or without a pulmonary infiltrate • Pericardial friction rub. • Alteration in the populations of lymphocytes in peripheral blood.
  57. 57. Treatment: Most cases of PCIS can be adequately treated with non-steroidal anti- inflammatory drugs. For refractory cases, corticosteroids can be used, but they can slow the healing of the already injured myocardium so they should be avoided if possible. Lastly, in patients with frequent recurrences, colchicine has been shown to be effective in some case studies (3).
  58. 58. Early Pericarditis: • Epidemiology: occurs in 10% of patients with acute MI. • Risk factors: transmural MI. • Timing: usually occurs 1-4 days after MI. • Symptoms: worse pain while supine, radiation of pain to the trapezius ridge. • Physical exam: pericardial friction rub. • Diagnosis: ECG may show evidence of pericarditis; echo may show pericardial effusion. • Treatment: aspirin. Avoid NSAIDs and corticosteroids (may interfere with healing of infarcted myocardium)
  59. 59. Prevalence The incidence of early pericarditis after acute MI is approximately 10%. The inflammation usually develops between 24 and 96 hours after MI.49,50 Dressler's syndrome, or late pericarditis, occurs with an incidence between 1% and 3%, 1 to 8 weeks after MI. Pathophysiology The pathogenesis of acute pericarditis is an inflammatory reaction in response to necrotic tissue. As such, acute pericarditis develops more often in patients with transmural MI. The pathogenesis of Dressler's syndrome is unknown, but an autoimmune mechanism has been suggested.
  60. 60. Signs and Symptoms Most patients with early pericarditis report no symptoms. Patients with symptoms from early or late pericarditis describe progressive, severe chest pain that lasts for hours. The symptoms are postural—worse in the supine position—and are alleviated by sitting up and leaning forward. The pain tends to be pleuritic in nature and is therefore exacerbated with deep inspiration, coughing, and swallowing. Radiation of pain to the trapezius ridge is almost pathognomonic for acute pericarditis. The pain also may radiate to the neck and, less frequently, to the arm or back. A pericardial friction rub on examination is pathognomonic for acute pericarditis; however, it can be ephemeral. The rub is best heard at the left lower sternal edge with the diaphragm of the stethoscope.
  61. 61. Signs and Symptoms The rub has three components—atrial systole, ventricular systole, and ventricular diastole. In about 30% of patients, the rub is biphasic and in 10%, it is uniphasic. A pericardial effusion may cause fluctuation in the intensity of the rub. Evolving MI changes may mask the diagnosis of pericarditis. Pericarditis produces generalized ST-segment elevation, which is concave or saddle-shaped. As pericarditis evolves, T waves become inverted after the ST segment becomes isoelectric. Conversely, in acute MI, T waves may become inverted when the ST segment is still elevated. Four phases of electrocardiographic abnormalities have been described in association with pericarditis.
  62. 62. Electrocardiographic Changes of Pericarditis Stage Electrocardiographic Change I ST elevation, upright T waves II ST elevation resolves, upright to flat T waves III ST isoelectric, inverted T waves IV ST isoelectric, upright T waves A pericardial effusion on echocardiography is strongly suggestive of pericarditis. Nevertheless, the lack of an effusion does not rule out pericarditis.
  63. 63. Treatment Aspirin is the therapy of choice for post-MI pericarditis, 650 mg every 4 to 6 hours. NSAIDs and corticosteroids should be avoided less than 4 weeks after the acute event. These agents may interfere with myocardial healing and contribute to infarct expansion. In late pericarditis, NSAIDs and even corticosteroids may be indicated if severe symptoms persist beyond 4 weeks after MI. Colchicine may be beneficial for patients with recurrent pericarditis.
  64. 64. ArrhythmiasArrhythmias  Ventricular arrhythmiasVentricular arrhythmias – Ventricular Premature BeatsVentricular Premature Beats – Accelerated Idioventricular RhythmAccelerated Idioventricular Rhythm – Ventricular TachycardiaVentricular Tachycardia – Ventricular FibrillationVentricular Fibrillation  BradyarrhythmiasBradyarrhythmias – Sinus BradycardiaSinus Bradycardia
  65. 65. ArrhythmiasArrhythmias  Atrioventricular and Intraventricular BlockAtrioventricular and Intraventricular Block – First-Degree AV blockFirst-Degree AV block – Second-Degree AV Block (Mobitz I / II)Second-Degree AV Block (Mobitz I / II) – Third degree (Complete) AV blockThird degree (Complete) AV block – Intraventricular BlockIntraventricular Block – AsystoleAsystole  Supraventricular TachyarrhythmiasSupraventricular Tachyarrhythmias – Sinus TachycardiaSinus Tachycardia – Atrial Premature ContractionsAtrial Premature Contractions – Atrial FlutterAtrial Flutter – Atrial FibrillationAtrial Fibrillation – Paroxysmal Supraventricular TachycardiaParoxysmal Supraventricular Tachycardia
  66. 66. Ventricular ArrhythmiasVentricular Arrhythmias  Ventricular Premature Beats (PVCs)Ventricular Premature Beats (PVCs)  Commonly seen in patients with acute MICommonly seen in patients with acute MI  Usually pursue a conservative approach andUsually pursue a conservative approach and do not routinely prescribe antiarrhythmicdo not routinely prescribe antiarrhythmic drugs but instead determine whetherdrugs but instead determine whether recurrent ischemia or electrolyte/metabolicrecurrent ischemia or electrolyte/metabolic disturbances are presentdisturbances are present
  67. 67. Ventricular ArrhythmiasVentricular Arrhythmias  Accelerated Idioventricular RhythmAccelerated Idioventricular Rhythm  Defined as a ventricular rhythm with a rate of 60-Defined as a ventricular rhythm with a rate of 60- 125 beats/min125 beats/min  Frequently called “slow v. tach”Frequently called “slow v. tach”  Seen in up to 20% of patients with AMISeen in up to 20% of patients with AMI  Occurs frequently during the first 2 daysOccurs frequently during the first 2 days  Probably results from enhanced automaticity ofProbably results from enhanced automaticity of the Purkinje fibersthe Purkinje fibers  Often observed shortly after successfulOften observed shortly after successful reperfusionreperfusion
  68. 68. Ventricular ArrhythmiasVentricular Arrhythmias  Ventricular TachycardiaVentricular Tachycardia  When continuous ECG recordings duringWhen continuous ECG recordings during the first 12 hours of AMI are analyzed,the first 12 hours of AMI are analyzed, nonsustained paroxysms of VT may be seennonsustained paroxysms of VT may be seen in up to 67% of patientsin up to 67% of patients  Hypokalemia and hypomagnesemia mayHypokalemia and hypomagnesemia may increase the risk of developing VTincrease the risk of developing VT  Treatment may include: lidocaine,Treatment may include: lidocaine, procainamide, amiodaroneprocainamide, amiodarone
  69. 69. Ventricular ArrhythmiasVentricular Arrhythmias  Ventricular FibrillationVentricular Fibrillation  Ventricular fibrillation occuring inVentricular fibrillation occuring in association with marked LV failure orassociation with marked LV failure or cardiogenic shock entails a poor prognosis,cardiogenic shock entails a poor prognosis, with an in-hospital mortality rate of 40-60%with an in-hospital mortality rate of 40-60%  Tx : defibrillatorTx : defibrillator  Management : lidocaine, amiodarone,Management : lidocaine, amiodarone, bretyliumbretylium
  70. 70. BradyarrhythmiasBradyarrhythmias  Sinus BradycardiaSinus Bradycardia  Common arrhythmia occuring during the earlyCommon arrhythmia occuring during the early phases of AMIphases of AMI  Particularly frequent in patients with inferior andParticularly frequent in patients with inferior and posterior infarctionposterior infarction  Isolated sinus bradycardia, unaccompanied byIsolated sinus bradycardia, unaccompanied by hypotension or ventricular ectopy, should behypotension or ventricular ectopy, should be observed rather than treated initiallyobserved rather than treated initially  Atropine should be utilized if hypotensionAtropine should be utilized if hypotension accompanies any degree of sinus bradycardiaaccompanies any degree of sinus bradycardia
  71. 71. Atrioventricular andAtrioventricular and Intraventricular BlockIntraventricular Block  First Degree AV BlockFirst Degree AV Block  Occurs in less than 15% of patients withOccurs in less than 15% of patients with AMI admitted to CCUsAMI admitted to CCUs  Generally does not require specificGenerally does not require specific treatmenttreatment  (Digitalis, B-blockers, Calcium antagonists)(Digitalis, B-blockers, Calcium antagonists)
  72. 72. Atrioventricular andAtrioventricular and Intraventricular BlockIntraventricular Block  Second-Degree AV blockSecond-Degree AV block – Mobitz Type I or WenckebachMobitz Type I or Wenckebach  Usually transient and does not persist moreUsually transient and does not persist more than 72 hours after infarctionthan 72 hours after infarction  Rarely progresses to complete AV blockRarely progresses to complete AV block  Do not appear to affect survivalDo not appear to affect survival  Caused by ischemia of the AV nodeCaused by ischemia of the AV node  Specific therapy not requiredSpecific therapy not required
  73. 73. Atrioventricular andAtrioventricular and Intraventricular BlockIntraventricular Block  Second Degree AV blockSecond Degree AV block – Mobitz Type IIMobitz Type II  Rare conduction defect after AMIRare conduction defect after AMI  Often progresses suddenly to complete AVOften progresses suddenly to complete AV blockblock  Treated with a temporary external orTreated with a temporary external or transvenous demand pacemakertransvenous demand pacemaker
  74. 74. Atrioventricular andAtrioventricular and Intraventricular BlockIntraventricular Block  Complete (Third Degree) AV blockComplete (Third Degree) AV block  Often develops gradually, progressing fromOften develops gradually, progressing from first-degree or type II second-degree blockfirst-degree or type II second-degree block  Treat with temporary external orTreat with temporary external or transvenous demand pacemakertransvenous demand pacemaker
  75. 75. Atrioventricular andAtrioventricular and Intraventricular BlockIntraventricular Block  Intraventricular BlockIntraventricular Block – Isolated fasicular blocksIsolated fasicular blocks » LAFBLAFB » LPFBLPFB – Right bundle branch blockRight bundle branch block – Bifasicular blockBifasicular block
  76. 76. SupraventricularSupraventricular TachyarrhythmiasTachyarrhythmias  Sinus TachycardiaSinus Tachycardia  Typically associated with augmentedTypically associated with augmented sympathetic activity (anxiety, persistentsympathetic activity (anxiety, persistent pain, LV failure, hypovolemia, epinephrine,pain, LV failure, hypovolemia, epinephrine, atropine, etc.)atropine, etc.)  Beta-adrenoceptor blocking agentsBeta-adrenoceptor blocking agents frequently utilizedfrequently utilized
  77. 77. SupraventricularSupraventricular TachyarrhythmiasTachyarrhythmias  Paroxysmal Supraventricular TachycardiaParoxysmal Supraventricular Tachycardia  Requires aggressive management becauseRequires aggressive management because of the rapid ventricular rateof the rapid ventricular rate  Augmentation of vagal tone – manualAugmentation of vagal tone – manual carotid massagecarotid massage  Drug of choice – adenosine (in non-AMIDrug of choice – adenosine (in non-AMI patients)patients)  Alternatives: IV verapamil, diltiazem,Alternatives: IV verapamil, diltiazem, metoprololmetoprolol
  78. 78. SupraventricularSupraventricular TachyarrhythmiasTachyarrhythmias  Atrial Flutter and FibrillationAtrial Flutter and Fibrillation  Atrial flutter – usually transientAtrial flutter – usually transient  Atrial Fibrillation occurs in 10-20% ofAtrial Fibrillation occurs in 10-20% of patients with AMIpatients with AMI  The increased ventricular rate and the lossThe increased ventricular rate and the loss of atrial contribution to LV filling result in aof atrial contribution to LV filling result in a significant reduction in cardiac outputsignificant reduction in cardiac output  Atrial fibrillation in AMI is associated withAtrial fibrillation in AMI is associated with increased mortality and strokeincreased mortality and stroke
  79. 79. Pericardial EffusionPericardial Effusion  Generally detected by 2-DGenerally detected by 2-D echocardiographyechocardiography  More common in patients with anterior MIMore common in patients with anterior MI and with larger infarcts and whenand with larger infarcts and when congestive heart failure is presentcongestive heart failure is present  Majority do not cause hemodynamicMajority do not cause hemodynamic compromise; when tamponade occurs, it iscompromise; when tamponade occurs, it is usually due to ventricular rupture orusually due to ventricular rupture or hemorrhagic pericarditishemorrhagic pericarditis
  80. 80. PericarditisPericarditis  When secondary to transmural MI,When secondary to transmural MI, pericarditis may produce pain as early aspericarditis may produce pain as early as the first day and as late as 6 weeks after MIthe first day and as late as 6 weeks after MI  Treatment of pericardial discomfort consistsTreatment of pericardial discomfort consists of aspirin at does as high as 650mg every 4-of aspirin at does as high as 650mg every 4- 6 hours. (corticosteroids should be avoided6 hours. (corticosteroids should be avoided because they may interfere with myocardialbecause they may interfere with myocardial scar formation)scar formation)  Dressler SyndromeDressler Syndrome
  81. 81. Dressler SyndromeDressler Syndrome  Post-myocardial infarction syndromePost-myocardial infarction syndrome  Usually occurs 1 to 8 weeks after infarctionUsually occurs 1 to 8 weeks after infarction  Patients present with malaise, fever,Patients present with malaise, fever, pericardial discomfort, leukocytosis,pericardial discomfort, leukocytosis, elevated ESR,and a pericardial effusionelevated ESR,and a pericardial effusion  Cause of this syndrome not clearlyCause of this syndrome not clearly established (? Immunopathological process)established (? Immunopathological process)  Treatment : ASA 650mg Q4hrsTreatment : ASA 650mg Q4hrs
  82. 82. SummarySummary  Be aware of all the potential complicationsBe aware of all the potential complications that can arise from myocardial infarction,that can arise from myocardial infarction, diagnose these complications when theydiagnose these complications when they occur, and treat the patient appropriately inoccur, and treat the patient appropriately in a timely manner to reduce morbidity anda timely manner to reduce morbidity and mortality.mortality.
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Complications of Myocardial Infarction (MI)


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