(first-degree to second-degree then third-degree AV block), and resolve gradually. Complete AV block is seen in ~4-5% of inferior MIs, mostly on the first day.150,151
Complete AV block is associated with a larger MI, more RV MI, and a 2-fold higher in-hospital mortality.150,151 Patients who survive to hospital discharge, however, do not have an increase in long-term mortality in some,152 but not all studies.150
Treatment – AV block that occurs in the first 24 hours responds to atropine, which should be used in case of hemodynamic instability. Since it is not driven by a high vagal tone, later AV block (>24 hours) does not typically respond to atropine but may respond to aminophylline (adenosine-receptor blocker) (ACC); being usually well tolerated with a good escape, complete AV block does not require pacing. It only requires temporary transvenous ventricular pacing in case of shock, HF, or low-output signs.
Symptomatic sinus bradycardia or pauses are initially treated with up to 2 mg of atropine. Transcutaneous or transvenous pacing may be used if symptomatic bradycardia persists.
B. Anterior MI
The bundle branches and fascicles are, at least partially, supplied by the LAD. Anterior MI may lead to bundle branch blocks and AV block. The AV block is Hisian or infra-Hisian and is usually preceded by bundle branch blocks. A high-degree AV block is seen in ~1-2% of anterior MIs and portends a very high mortality related to pump failure (3–4 times increase in mortality; mortality was >50% in the pre-reperfusion era).152,153 The anterior MI’s AV block often resolves but may recur in a minority of patients.153
Transvenous pacing, while indicated for any high-grade second- or third-degree AV block occurring with anterior MI, even if asymp- tomatic, does not improve the grim overall prognosis that is dictated by the pump function. Permanent pacing is indicated for persistent, infranodal second- or third-degree AV block.
C. Bundle branch and fascicular blocks
Approximately 2–8% of STEMI patients develop some form of new intraventricular block, LAFB being the most common block. Note the following arterial supply:154
The right bundle mainly has a single arterial supply from the LAD (first septal branch).
The left anterior fascicle has a single arterial supply from the LAD (first septal branch).
The His bundle, the main left bundle, and the posterior fascicle have a dual supply from the LAD septal branches and the AV nodal artery. Thus, the composite of the anterior and posterior fascicles, the branching left bundle, usually has a dual supply. This explains why it is difficult to infarct the left bundle and why most new LBBBs are non-ischemic in nature.
RBBB or LAFB are most commonly seen in anterior MI,155 but may also be seen in inferior MI if the LAD has severe disease and is dependent on the RCA for collaterals. LBBB may result from either anterior or inferior MI, and is more likely seen when both RCA and LAD are com- promised, with one acutely occluded and the other chronically obstructed (in the GUSTO trial, LBBB was associated with an RCA culprit at least as much as an LAD culprit).10,156
The conduction system is more resistant to ischemia than the myocardium, as the myocardial cells require much more O2 for their continuous mechanical work than the electrical cells, which also frequently receive dual or collateral supply. This explains why conduction blocks are frequently due to edema or ischemia rather than necrosis and are frequently reversible (25-75% of the cases).155,156 If not reversible, and if secondary to MI rather than degenerative disease, the myocardial injury is usually quite extensive (e.g., persistent RBBB or LBBB).
While a chronic bundle branch block (BBB) has a very low risk of progression to complete AV block, 20% of acute BBBs progress to complete AV block, and 25–40% of acute bifascicular blocks progress to complete AV block.
Beside the risk of progressing to complete AV block, a new BBB is independently associated with a two- to threefold increase in in-hospital mortality, HF, and VF, particularly because it correlates with a more extensive infarction (mortality 18% vs. 11% in GUSTO-I trial; 35–50% in the pre-reperfusion era).156 Up to 75% of these blocks are transient, and transient blocks do not portend any increase in mortality.155,156 Old BBBs do not portend any increase in mortality either. Both RBBB and LBBB are associated with the same increase in mortality. 155,156
A standby temporary transcutaneous or transvenous pacemaker is indicated for a new BBB or bifascicular block occurring in anterior MI.
VI. LV aneurysm and LV pseudoaneurysm
A. LV aneurysm
Dyskinesis signifies that a non-contractile myocardial segment moves out during myocardial contraction and moves in during relaxation (paradoxical motion). LV aneurysm is an extreme form of dyskinesis and consists of a thin area of infarcted, dyskinetic myocardium that forms a myocardial pocket. Dyskinesis without an aneurysm implies that the myocardium protrudes only during systole, whereas an aneu- rysm protrudes in both systole and diastole, forming a separate chamber, and always has thin walls. LV aneurysm usually reflects the presence of extensive transmural necrosis; contrarily, dyskinesis may be seen with acute reversible ischemia, post-ischemic stunning, or takotsubo cardiomyopahty without any necrosis, in which case the myocardial wall is not thin (it may appear thin in systole from the lack of thickening, but it is not thin in diastole). Dyskinesis without an aneurysm is much more common than a true aneurysm.
LV aneurysm is a form of adverse LV remodeling and dilatation of the necrotic area. ~50% develop acutely in the first 48 hours, from early dilatation of the necrotic, expansile myocardium, and the remainder usually appear within 2 weeks.157 The mature, thick scar appears several weeks later, followed by calcifications. The early use of ACE-I, β-blocker, and aggressive blood pressure control prevents LV aneurysm from appearing or expanding.
An aneurysm leads to increased preload and afterload, and a double mortality for the same EF.158 LV aneurysm occurs in 5% of STEMI cases, mainly anteroapical STEMI (80% of LV aneurysms are anteroapical; the rest are inferoposterior). LV aneurysm may initiate or worsen: (i) HF, (ii) angina (from the adverse loading conditions), (iii) VT, and (iv) mural thrombosis.
The diagnosis is made by echo. ST elevation that persists >3 weeks suggests LV aneurysm, but may also be seen with a dyskinetic, often non-viable wall.
Treatment consists of standard HF therapy which aims to reverse LV remodeling. Aneurysmectomy is indicated for refractory HF or refractory VT, mainly in conjunction with CABG. Operative mortality is <10%.
B. LV pseudoaneurysm
Pseudoaneurysm is a myocardial rupture that has been sealed by pericardium, organized thrombus and fibrosis. Unlike a true LV aneurysm, the LV pseudoaneurysmal wall does not contain any myocardium. Note that thrombus is layered inside both the LV aneurysm and LV pseudoaneurysm. A pseudoaneurysm may also be seen after trauma or cardiac surgery (especially mitral surgery, at the posterobasal level) (Figure 2.7).
A pseudoaneurysm has a 40–50% risk of progressing to a full rupture, and thus warrants urgent surgical suturing. Rupture often occurs in the first week,159 but rupture
