Complications IM Flashcards
0–24 hours post-infarction
✔Sudden cardiac death (SCD)
Definition: A sudden death presumably caused by cardiac arrhythmia or hemodynamic catastrophe, which occurs either within an hour of symptom onset in patients with cardiovascular symptoms, or within 24 hours of being asymptomatic in patients with no cardiovascular symptoms.
Pathophysiology: Fatal ventricular arrhythmia is considered to be the underlying mechanism of SCD.
Underlying conditions
Coronary artery disease: present in ∼ 70% of cases in adults over 35 years
Dilated/hypertrophic cardiomyopathy
Hereditary ion channelopathies (e.g., long QT syndrome, Brugada syndrome)
Prevention: installation of the implantable cardioverter-defibrillator device 💥
✔Arrhythmias (a common cause of death in MI patients in the first 24 hours) Ventricular tachyarrhythmias AV block Asystole Atrial fibrillation
✔Acute left heart failure: death of affected myocardium → absence of myocardial contraction → pulmonary edema
✔Cardiogenic shock (prima causa morte post IM ospedaliera)
1–3 days post-infarction
✔Early infarct-associated pericarditis
Typically occurs within the first week of a large infarct close to the pericardium
Clinical features of acute pericarditis: pleuritic chest pain , dry cough , friction rub, diffuse ST elevations on ECG
Treatment: supportive care
Complications (rare): hemopericardium, pericardial tamponade
NB NSAIDs (except for aspirin) should be avoided 7–10 days after an acute MI.💥
3–14 days post-infarction
NB Il soffio da rottura muscolo papillare è auscultabile sulla linea emiclaveare mentre quello generato dalla rottura del setto è auscultabile over the left sternal border. La rottura del muscolo papillare si manifesta con insufficienza mitralica acuta (ipotensione e dispnea) mentre la rottura del setto con insufficienza acuta del cuore destro (distensione giugulari)
✔Papillary muscle rupture
Usually occurs 2–7 days after myocardial infarction
Can lead to acute mitral regurgitation
Rupture of the posteromedial papillary muscle due to occlusion of the posterior descending artery is most common.
Clinical features
👓New holosystolic, blowing murmur over the 5th ICS on the midclavicular line
Signs of acute mitral regurgitation: dyspnea, cough, bilateral crackles, hypotension
✔Ventricular septal rupture
Usually occurs 3–5 days after myocardial infarction
Pathophysiology: macrophagic degradation of the septum → ventricular septal defect → blood flow from LV to RV following the pressure gradient (left-to-right shunt) → increased pressure in RV and increased O2 content in the venous blood
Most commonly due to LAD infarction (septal arteries arise from LAD)!💥
Clinical features
👓New holosystolic murmur over the left sternal border
Acute-onset right heart failure (jugular venous distention, peripheral edema)
Can progress to cardiogenic shock: tachycardia, hypotension, cool extremities, altered mental status
Treatment: emergency surgery and revascularization (often via CABG)
✔Left ventricular free wall rupture
Usually occurs 5–14 days after myocardial infarction
Greatest risk during macrophage-mediated removal of necrotic tissue
LV hypertrophy and tissue fibrosis from previous MI decrease the risk of free wall rupture.
Clinical features: chest pain, dyspnea, signs of cardiac tamponade (e.g., Beck triad) 💥
Complications: cardiac tamponade , sudden cardiac death (if the rupture occurs acutely)
✔Left ventricular pseudoaneurysm
Usually occurs 3–14 days after myocardial infarction
Refers to the outpouching of the ventricular wall rupture that is contained by either the pericardium, a thrombus, or scar tissue
Associated with mural thromboembolism, decreased cardiac output, and increased risk of arrhythmia
2 weeks to months post-infarction
L’aneurisma ventricolare a dofferenza delle altre complicanze è generalmente asintomatico.
✔Atrial and ventricular aneurysms
Clinical features
Persistent (> 3 weeks post-MI) ST elevation and T-wave inversions💥
Systolic murmur, S3 and/or S4
Diagnosis: echocardiography👓
Visualization of the pathological myocardial wall protrusion
Detection of dyskinetic movements of the thinned aneurysmal wall (uncoordinated contraction occurs due to fibrotic changes of the myocardium)
Complications
Cardiac arrhythmias (risk of ventricular fibrillation)
Rupture → cardiac tamponade
Mural thrombus formation → thromboembolism (stroke, mesenteric ischemia, renal infarction , acute obstruction of peripheral arteries)
Treatment: anticoagulation, possibly surgery
✔Postmyocardial infarction syndrome (Dressler syndrome): pericarditis occurring 2–10 weeks post-MI without an infective cause
Thought to be due to circulating antibodies against cardiac muscle cells (autoimmune etiology)
Clinical features
Signs of acute pericarditis: pleuritic chest pain , dry cough , friction rub
Fever
Laboratory findings: leukocytosis, ↑ serum troponin levels
ECG: diffuse ST elevations
Treatment: NSAIDs (e.g., aspirin), colchicine
Complications (rare): hemopericardium, pericardial tamponade
SCENARIO Un paziente iperteso ed ipercolesterolemico di 63 anni giunge in pronto soccorso con dolore precordiale ad insorgenza acuta, irradiato all’arto superiore sinistro. L’ECG e gli enzimi miocardici indicano la presenza di un infarto STEMI. DOMANDA Indica la complicanza meccanica più frequente dell’infarto miocardico acuto:
Rottura di un muscolo papillare Infarto del ventricolo destro ✔Rottura della parete libera del ventricolo sinistro Rottura del setto interventricolare Tamponamento cardiaco
La complicanza meccanica più frequente e la seconda causa di mortalità intraospedaliera è la rottura della parete libera del ventricolo sinistro. E’ più comune nel sesso femminile, età avanzata, ipertensione pregressa, basso peso, quando la riperfusione è avvenuta con tenecteplase (fibrinolitico) e nella fase subacuta (appare, quindi, verso il 10º-12º giorno dall’infarto). La rottura causa un tamponamento cardiaco che provoca il collasso immediato delle cavità destre e la morte. A volte l’evento può essere meno violento e presentarsi con ipotensione, turgore giugulare e segni di tamponamento cardiaco all’ecocardiografia, in questi casi si deve eseguire una pericardiocentesi
