Complications of acute mi

Complications of acute mi

1. Complications of Acute M.I Prof. Dr. Tarek Abd ElGhaffar Consultant Cardiologist , NHI Dr. Kareem Mandour Resident of Cardiology , NHI

2. The term myocardial infarction should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischaemia . Under these conditions any one of the following criteria meets the diagnosis for myocardial infarction : • Detection of rise and/or fall of cardiac biomarkers (preferably troponin ) with at least one value above the 99th percentile of the upper reference limit (URL) together with evidence of myocardial ischaemia with at least one of the following: • Symptoms of ischaemia . • ECG changes indicative of new ischaemia (new ST-T changes or new left bundle branch block [LBBB]). • Development of pathological Q waves in the ECG. • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. ( Kristian Thygesen , et al 2007)

3. Complications Electrical Complications Mechanical complications Heart Failure Pericarditis Post Infarction Angina or ReInfarction . Take Home Message

4. Cardiogenic shock and heart failure are the most common causes of death in patients hospitalized with acute myocardial infarction. At least 75% of patients with acute myocardial infarction (MI) have an arrhythmia during the periinfarct period.

5. Electrical Complications : In acute M.I , Arrythmias are mainly due to reentry caused by inhomogenicity of ischaemic myocardium . While Reperfusion Arrythmias are due to washout of the accumlated ions and metabolites . Ventricular Arrythmias Ventricular premature beats ( PVCs ) No correlation to the development of primary vent. Fibrillation . Treated by correction of the electrolyte or metabolic disturbances . If associated with sinus tachycardia , Beta Blockers are used to suppress the sympathetic overdrive.

6. Accelerated idioventricular rhythm : occurs in 20% of patients with STEMI , most often after successful reperfusion . Ventricular Tachycardia : Non-Sustained V.Tach . isn’t associated with increase mortality during hospitalization or one year after . Sustained V.tach with haemodynamic stability should be treated immediately by amiodarone or procainamide , while if it's not aborted or associated with chest pain or haemodynamic deterioration , DC shock should be used for cardioversion .

7. Ventricular fibrillation : Primary V.F Secondary V.F Late V.F - Treatment Consists of: Unsynchronized DC shock with at least 200 – 300 joules monophsic Amiodarone I.V , helps interruption of the attack and prevent recurrence . Treatment of hypokalaemia and magnesium deficits . ( aim K ≥ 4.5 Prophylactic Lidocaine is no longer recommended .

8. Supraventricular Arrythmias Sinus Tachycardia : very common in patients with acute M.I esp. Ant. M.I , it may be caused by other post-infarction causes as anxiety , persistant pain , LV dysfunction , fever , hypotension , hypovolaemia , pericarditis , pulmonary embolism , etc ….. Premature Atrial beats : may be due to atrial ischaemia or pericarditis . No specific therapy is indicated . Paroxysmal SVT : usually transient and needs rate control using carotid massage , adenosine , verapamil , diltiazem or Beta blockers .

9. Atrial Flutter and Fibrillation : both are usually transient and may occur with patients with LV dysfunction , extension of ischaemia or pulmonary embolism . Bradyarrythmias Sinus Bradycardia : it’s common especially in Inferior and posterior Infarctions . If heart rate is below 40-50 , Atropine is administered . First Degree A-V block : it may be caused by the use of Beta blockers or Calcium channel blockers

10. Second degree AV block : Type I: Does not require treatment except if ventricular rate is below 50 bpm , then atropine is indicated. Type II: has a potential to progress to complete heart block so temporary pacing is indicated and set at about 60 bpm . Complete AV block : If associated with Inferior infarctions , 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 infarction , 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 .

11. 5. Intraventricular block : RBBB with ant. MI is associated with increased mortality .

12. Indications of Temporary Pacing in Acute M.I : Asystole Symptomatic bradycardia not responsive to atropine Complete Heart Block Second degree H.B ( Mobitz type II ) New Bifasicular block Bilateral Bundle branch block Sinus pauses > 3 sec. , not resposive to atropine Incessant Vent. Tachycardia ( overdrive pacing )

13. Mechanical complications Acute Mitral Regurge : Papillary muscle dysfunction: Caused by posteromedial papillary ms dysfunction , It’s usually transient during ischaemia . It usually presents with an apical systolic murmur , confirmed by echocardiography . It requires no specific therapy , in intermediate cases it may require antifailure treatment , while in severe cases it requires treatment like that of papiilary ms rupture . Papillary ms Rupture : It occurs with Inferior Infarction 6-12 times more than Anterior infarctions . It may present with acute pulmonary oedema or even sudden cardiac death , it can occur upto 2-7 days post infarction . Intra-Aortic Balloon , vasodilators or inotropic therapy may be required for temporary stabilization before surgery ( CABG + Mitral Valve Repair or Replacement )

14. Papillary muscle rupture complicating acute inferior myocardial infarction; magnified four-chamber view. The ruptured head of the posteromedial papillary muscle ( arrow) prolapses freely into the left atrium; the posterior mitral valve leaflet ( arrowhead) is flail.

15. Ventricular Septal Rupture It occurs within the first week post-Infarction . It occurs equally with Inferior and Anterior infarctions. Rupture with Anterior Infarctions tend to be apical while it’s basal and has a worse prognosis with inferior infarctions . It usually presents with a new onset murmur ( new harsh holosystolic murmur along the left sternal border ) . The patient is usually stable and develops sudden clinical deterioration . Patients with acute VSR usually lie flat , while patients with acute MR develop pulmonary oedema & cann’t Lie flat . Medical therapy is ineffective , Emergency Surgical Intervention is the treatment of choice .

16. Transthoracic sub-costal 4-chamber echocardiographic findings showing a large ventricular septal rupture (VSR)

17. Free wall Rupture : Occurs within 2 weeks , and most common cause of death after cardiogenic shock and arrythmias . Early use of thrombolytic therapy appears to reduce the incidence of cardiac rupture , while late use appears to increase the incidence . It usually presents by sudden Dea th. Few cases can be salvaged by immediate pericardiocentesis , emergency Thoracotomy and surgical repair .

18. Cardiac free wall rupture post myocardial infarction. Pericardial tamponade from left ventricular free wall rupture and hemopericardium .

19. 4. Ventricular Aneurysm : Diff. between True and Pseudo-aneurysm . True Aneurysm Pseudo-Aneurysm

20. Clinically : abnormal precordial impulse in the 3 rd left intercostal space ECG : ST Seg . Elevation persists more than 2 weeks . ( it may indicate a large infarction with RWMA not necessarily Aneurysm ) . Other Mechanical Complications Pulmonary Embolism : Post-infarction patients have greater tendancies for Pulmonary embolism ( P.E ) due to decreased cardiac output and immoblization , Early mobilization and treatment aiming to increase Cardiac output are the most effective prophylactic methods .

21. Systemic embolism : LV thrombi occurs in 20-40 % of ant. Infarction Patients . If LV thrombus is clearly demonstrated in Echocardiography , Systemic anticoagulation should be given for 3-6 months .

22. Heart Failure and Cardiogenic shock: Heart Failure occurs when LV function decrease by 30% of normal function . Killip Class: Clinical Examination I No S3 or rales II Rales in less than half of lung field III Rales in more than half of lung field IV Cardiogenic shock May present acutely after MI ( killip class II or III ) or as a delayed presentation ( NYHA II-IV) .

23. Cardiogenic shock is persistent hypotension with a systolic pressure <80 mm Hg for more than 30 minutes in the absence of hypovolemia . It occurs when ≥ 40 % of myocardium is affected . The most common causes of cardiogenic shock include 1) large left ventricular infarct (usually >40% of left ventricle) seen in about 80% of shock patients 2)right ventricular infarct in 10% of shock patients 3) mechanical complications of myocardial infarction (ventricular septal defect, acute mitral regurgitation, tamponade ) in 10% of shock patients.

24. Pericarditis : Early post-infarction Pericarditis Occurs 2-4 days following acute infarction . Patients who develop this condition usually have larger infarcts , lower EF and higher incidence of CHF . Presented by Fever , Chest pain and friction rub . Pain is aggrevated by movement and inspiration , Radiated to the trapezius . Treated by Aspirin 160 – 325 mg daily ( although higher doses may be required 650 mg / 4-6 hrs ) , Anticoagulants are relatively contraindicated .

25. 2 . Post MI syndrome ( Dressler’s Syndrome ) Fever , chest pain , friction Rub . Occurs after 1 week up to several weeks of MI . Treatment as that of early post-MI pericarditis except that an oral corticosteroid course maybe required . Anti-Coagulants should be stopped . May cause pericardial effusion but rarely tamponading .

26. Take Home Message Cardiac Rehabilitation and extended follow up of the post-Infarction patient clinically and by imaging modalities are as important as the early follow up. Anticipate complications in every patient , so you won’t miss it when it occurs .