Septal infarction

Figure 5.38 ECG with SAH and mild ST/T abnormalities. The patient presented different myocardial infarctions - septal, anterior and lateral detected by CE-CMR that masked each other. This figure can be seen in colour, Plate 4.

Structural abnormalities such as atrial-septal aneurysm Myocardial infarction... 

Post-surgical and post-myocardial infarction ventricular septal defect... 

The vast majority of ventricular septal defects (VSD) are congenital. Acquired VSDs are almost always a consequence of septal rupture following myocardial infarction, traumatic VSDs as a consequence of sharp or blunt chest trauma are exceptionally rare. Typically the post myocardial infarction ventricular septal defect (PMIVSD) occurs within the first week after the event (41). In the current era of thrombolysis about 0.2% of patients develop a VSD as a result of septal necrosis. Medical management of these patients is limited and carries a 30-day mortality of 94% compared with 47% who were treated surgically (42). 

Topaz O, Taylor AL, Interventricular septal rupture complicating acute myocardial infarction from pathophysiologic features to the role of invasive and noninvasive diagnostic modalities in current management. Am J Med 1992 93(6) 683-688. Review. 

Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-1 (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation 2000 101(1 ) 27—32. 

Following septal ablation, patients should be monitored in a coronary care unit for 24 to 48 hours and the temporary pacing wire should be removed at the end of this period in the absence of atrioventricular block. Patients may then be transferred to a telemetry unit for monitoring of arrhythmias. Total hospitalization is usually for three to five days to monitor for occurrence of complete heart block that would require a permanent pacemaker. A sizeable infarction is induced with alcohol ablation and causes creatinine phosphokinase to peak at 1000 to 1500 one day after the ablation. Patients should be maintained on aspirin indefinitely. 

Boekstegers B Steinbigler P Molnar A, et al. Pressure-guided nonsurgical myocardial reduction induced by small septal infarctions in hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001 38 846-853. 

I Veselka J, Prochazkova S, Duchonova R et al. Alcohol septal ablation for hypertrophic obstructive cardiomyopathy Lower alcohol dose reduces size of infarction and has comparable hemodynamic and clinical outcome. Catheter Cardiovasc Interv 2004 63 231-235. 

Toyoda Y, Shida T, Wakita N, Ozaki N, Takahashi R, Okada M. Evidence of apoptosis induced by myocardial ischemia A case of ventricular septal rupture following acute myocardial infarction. Cardiology 1998 90 149-151. 

Figure 1.11 Magnetic resonance imaging. (A) Thoracic horizontal axial plane at the level of the xy line of the drawing on the right side of the figure. The four walls can be adequately observed anterior (A), septal (S), lateral (L) and inferior (I), represented by the inferobasal portion of the wall (segment 4 of Cerqueira statement) that bends upwards in this case (B). The infarction vector generated principally in segments 4 and 10 in case of very lean individuals (Figure 1.13C) it faces lead V3 and not V1 (line CD). On the contrary, the vector of infarction that arises...

Occlusion proximal to the SI branch but distal the D1 branch (Figure 4.25 and Table 4.1A(4)) When the occlusion is located above, the SI but not the D1 (Figure 4.25), which rarely occurs (<15% of the STE-ACS), the area at risk could lead to a relatively extensive anterior infarction when the D1 branch is quite small and the D2 branch is large. However, usually more septal and anterior than lateral involvement is seen (Figure 4.25B,C). Currently, with the new treatments employed in the acute phase, most of these cases end up being just an apical infarction... 

Figure 5.10 Example of small septal Ml (type A1). ECG (Q in V1-V2). Most probable place of occlusion, CE-CMR images and VCG loops (see Figure 5.6). The infarct...

A1). Q waves in V1-V2 (Figures 5.10-5.12). This corresponds to septal infarction. 

It is called septal infarction because it corresponds to infarcted area that involves more or less extensive part of septal wall (especially segments 8, 9 and 14) (Figures 5.10 and 5.11). The midinferior segments (especially segments 8 and 9)... 

The infarction is generally a consequence of non-complete LAD occlusion,which has partly or totally involved the septal branches, but not the diagonal branches, or due to complete distal occlusion of LAD after all the diagonal branches take off. Otherwise, the infarction would be of the A-2 type (apical-anterior). On some rare occasions it maybe secondary to the exclusive occlusion of one septal branch (Figure 4.29). This may occur spontaneously or during the course... 

Since the high-septal area is depolarised after the first 40 milliseconds, the infarction of this area does not generate vector of infarction that can originate Q waves. In these cases, changes the final portions of the QRS complex may be present. For the typical pattern of this type of infarction to appear, it is required, then, that the infarction involves the middle-low portion of the septum. The other parts may or may not be involved. 

The QS pattern in V1-V2 and sometimes in huge septal infarction small r in V3 (rS pattern) (see Figures 5.10 and 5.11) is due to infarction vector that is directed posteriorly and generates changes in the first part of QRS loop, which is also directed posteriorly or, in small infarctions, is very slightly anterior. An example of the ECG-VCG correlation in the acute phase of a septal infarction is shown in Figure 5.12. Therefore, the QRS loop is normal, except for the first few milliseconds, where it is usually not directed anteriorly in the HP (see Figure 5.9A(1) and 5.12). 

It is called extensive anterior infarction because it corresponds to large areas of not only the anterior and septal walls, but also the low- and... 

---