Complications
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Behandeling acuut coronair syndroom in een urgente situatie (in afwachting van hospitalisatie)Published by: Werkgroep Ontwikkeling Richtlijnen Eerste Lijn (Worel)Last published: 2022La prise en charge du syndrome coronarien aigu (SCA) en situation d'urgence (en attente d'hospilatisation)Published by: Groupe de Travail Développement de recommmandations de première ligneLast published: 2022Usually develop with occlusion of the right coronary artery, and are caused by infarction of the atrioventricular node and the conduction system above the His bundle or by increased vagal tone.
These arrhythmias are usually benign and transient and do not require any treatment. If the heart rate goes below 50 bpm and the patient is symptomatic, give intravenous atropine.
Temporary pacing may be required if heart failure, syncope or angina develop.
Can develop acutely in patients with anterior infarcts and may lead to ventricular asystole.
Complete heart block in anterior infarcts occurs because of infarction and necrosis of the bundle branches in the septum.
Transcutaneous or, preferably, transvenous pacing should be carried out in these patients immediately after conduction defects are noticed. Permanent pacing is usually required.
Usually occurs from a defect in the conduction system below the His bundle and can rapidly progress into complete heart block in patients with anterior MI.
Transcutaneous or more preferably transvenous cardiac pacing should be carried out in these patients immediately after conduction defects are noted.
Can develop in patients with inferior infarcts caused by vagal stimulation.
Usually transient or resolved with atropine.
Temporary pacing may be required if heart failure, syncope, or angina develop. Permanent pacing is rarely required.
Acute mitral regurgitation from papillary muscle rupture is a rare but serious complication of acute MI, with in-hospital mortality rates of 10% to 40%.[176] Inferior MI can cause rupture of the posteromedial papillary muscle, while anterolateral infarctions can cause rupture of the anterolateral papillary muscle.[176]
Right ventricular papillary muscle rupture is rare and can cause life-threatening tricuspid regurgitation.
Complete papillary muscle rupture causes wide-open mitral regurgitation and is usually fatal.
Risk factors for papillary muscle rupture include older age, female sex, history of heart failure, chronic kidney disease and delayed presentation with a first acute MI.[176]
Patients typically present 3-5 days after a transmural infarct, with acute pulmonary oedema and cardiogenic shock.[176][177] Diagnosis is made on echocardiogram, which shows severe mitral regurgitation, often with an eccentric jet and a mobile mass, sometimes prolapsing into the left atrium.[176]
Inotropic support, mechanical ventilation and an intra-aortic balloon pump should be considered for transient stabilisation before emergency surgery.[176]
Interventricular septal rupture causing a VSD can occur, though is rare, occurring in about 0.3% of acute MI.[176] Risk factors include older age, female sex and delayed reperfusion following acute MI.[176] Patients typically present 3-5 days after an acute MI with symptoms such as dyspnoea and orthopnoea, hypotension, peripheral vasoconstriction and oliguria.[176] Examination reveals a new pansystolic murmur with signs of pulmonary venous congestion.[176] Diagnosis is made on echocardiogram and cardiac catheterisation.[176]
Treatment depends on the severity at presentation, though is primarily emergency cardiac surgery.[176] Stabilisation with extracorporeal membrane oxygenation (ECMO) or Impella devices may be indicated.[176]
Mortality of an uncorrected VSD is around 80% at 30 days.[176]
Survival depends on early recognition, defect size, and degree of impairment of ventricular function.
The exact incidence of ventricular free wall rupture causing acute pericardial tamponade is unknown, because it most often presents with out-of-hospital sudden cardiac death.[176]
Free wall rupture should be suspected in any patient that presents with cardiovascular collapse or haemodynamic instability after acute MI, particularly following delayed presentation/revascularisation.[176] Patients present with clinical signs of cardiac tamponade; muffled heart sounds, raised jugular venous pressure, pulsus paradoxus and/or frank electromechanical dissociation.[176]
There is an increased risk of ventricular wall rupture involving anterior and lateral walls after anterior MI. Incomplete rupture can result in the development of a pseudoaneurysm.
Free wall rupture is rapidly fatal; however, diagnosis can be confirmed on echocardiogram, and should precipitate immediate surgical correction of the necrotic myocardium, and primary reconstruction of necrotic myocardium and primary reconstruction.
Inotropic support and intra-aortic balloon counterpulsation or ECMO for transient stabilisation should be considered before surgery. Even with surgical correction, the in-hospital mortality is ~35%.[176]
Develops in 4.5% of acute myocardial infarction.[178] NSTEMI accounts for approximately 20% of cardiogenic shock complicating myocardial infarction.[1] Typically, it occurs after a massive myocardial infarction or repeated ischaemic events, and it is predominantly caused by left ventricular failure.[179] Risk increases in time without treatment. Associated mortality is 70% to 80%, with an in-hospital mortality of up to 60%.[1][177][179][180]
Cardiogenic shock requires urgent percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) surgery if not already carried out.[1][72] The patient needs intensive care and pressor support and may need intra-aortic balloon pump counterpulsation or other circulatory assist devices as a bridge towards definitive therapy.
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Dressler syndrome is mediated by inflammatory byproducts and the formation of ischaemic myocardium. Occurs in about 5% of patients with MI.[181] Inflammation involves the pericardium and is treated with non-steroidal anti-inflammatory drugs (NSAIDs) or colchicine (preferably colchicine as it may reduce the risk of recurrence). If haemodynamic compromise is present, pericardiocentesis or surgical intervention is required.
Acute coronary syndrome has been associated with an increased risk of VTE, particularly for pulmonary embolism.[184]
Congestive heart failure caused by decreased LV function occurs frequently after MI because of myocardial damage, infarct progression, and LV remodelling after the acute episode. Heart failure post MI may be more common in females than males.[166]
Appropriate use of drugs, including beta-blockers, ACE inhibitors, angiotensin-II receptor antagonists, and diuretics, when appropriate, decreases the incidence and progression of congestive heart failure.
Biventricular pacing with or without an implantable cardioverter defibrillator should be considered if appropriate criteria are met.
Ventricular tachycardia (VT) and ventricular fibrillation (VF) can occur during ischaemia and reperfusion and can be lethal. They can also occur at any stage following a myocardial infarction (MI) because of re-entry circuits at the border of myocardial scar and normal myocardium, and are commonly seen in patients with decreased ejection fraction. The incidence of VF is <2%. The majority of VT/VF occurs within the first 48 hours after admission.[169]
Electrolytes should be optimised, especially potassium and magnesium, as electrolyte imbalance increases the risk of ventricular arrhythmias. Potassium should be maintained at >4 mmol/L (4 mEq/L) and magnesium at >1 mmol/L (2 mEq/L).
Appropriate therapy should be initiated with direct current cardioversion and anti-arrhythmic therapy.
Optimal medical management (in particular, beta-blockers) decreases incidence of ventricular arrhythmias.
Implantable cardioverter defibrillator should be considered for all patients with persistently decreased left ventricular (LV) ejection fraction (<35%) if there has been no response to 3 months of intensive medical therapy after MI.[170]
Patients with acute MI can have recurrent ischaemia or infarction caused by further plaque rupture and progression of atherosclerosis.
Recurrence should be treated in the same manner as the initial presentation.
Aggressive risk factor modification after the initial presentation decreases incidence of recurrences.
Depression is a risk factor for cardiovascular disease and for adverse outcomes following acute coronary syndrome (ACS).[56] ACS can also precipitate depression in people without prior psychiatric conditions.[56][171][172] Patients should routinely be screened for depression following a MI.[171] Data suggest that a combined psychosocial approach to the treatment of depression improves outcome in patients. Exercise combined with pharmacotherapy may be the most efficacious approach.[55] Pharmacotherapy may be associated with excess risk in patients with residual cardiac dysfunction; cognitive behavioural therapy or exercise therapy may be more appropriate in this patient group.[173]
Dual antiplatelet therapy is recommended for at least 12 months in all patients whether they have been stented or not. In-stent thrombosis is often precipitated by premature cessation of dual antiplatelet therapy, but can also be caused by technical factors and other comorbidities such as diabetes mellitus. Patients and their family should be strongly cautioned in hospital and in follow-up appointments about the importance of dual antiplatelet therapy for 12 months.[182]
LV thrombus can be seen in the early days of acute MI, especially large anterior MI with dyskinesia of the apex.[183] The reported incidence of LV thrombus after anterior ST-segment elevation MI (STEMI) varies widely in the literature, ranging from 4% to 39%.[183] Echocardiography studies conducted before revascularisation became routine practice suggested LV thrombus was present in about one third of patients with large anterior MI; more recent estimates are lower, likely relating to improved reperfusion interventions.[183] Formation of LV thrombus after acute MI is associated with a 5.5-fold increased risk of embolic events compared with no thrombus. Anticoagulation with a vitamin K antagonist (e.g., warfarin) or a direct oral anticoagulant is recommended for patients with LV thrombus.[183]
The incidence of LV aneurysm formation after acute MI is low (<5%) in the era of reperfusion therapy, and it is seen more frequently in large anterior MI, with total occlusion of the left anterior descending artery.[176] The presence of LV aneurysm may increase the risk for angina pectoris, thromboembolic complications and arrhythmia, although surgery is rarely needed to correct the aneurysm.[175][176]
In comparison to true aneurysms, pseudoaneurysms more often occur in the inferior or lateral wall.[176] LV pseudoaneurysms present in a very diverse way, weeks to years after an acute MI.[176] Patients may be asymptomatic, though the majority present with shortness of breath, chest pain or signs and symptoms of congestive cardiac failure.[176] LV pseudoaneurysm requires urgent surgical repair because of the risk of progression to LV rupture.[176]
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