Introduction

Substantial changes in cardiac structure can occur in the months to years following a completed myocardial infarct (MI), particularly if the culprit coronary artery supplied a large territory or flow was not rapidly restored. These changes may be clinically silent as they evolve, but with time can lead to extensive morbidity and mortality, including increased risk of developing heart failure and sudden cardiac death (SCD). Most of the pharmacologic, electrophysiologic, and interventional therapies indicated following MI are targeted toward prevention or amelioration of these complications. Both common and rare long-term complications after MI are summarized in Box. 20.1 . Most of these complications occur more commonly after large transmural infarcts, where revascularization was unsuccessful.

Echocardiography is appropriately used for the initial evaluation of ventricular function following an acute coronary syndrome (ACS), but is also very useful during the recovery phase to guide therapy (see Chapter 47 ). For the chronic care of patients with coronary artery disease, deterioration in clinical status or physical exam (without a clear precipitating change in medication or diet), or intent to initiate or change therapy because of clinical status change is also grounds for a cardiac ultrasound. Echocardiography can also supply much prognostic data with respect to patient trajectory and outcomes.

Left Ventricular Scar and Aneurysm

A transmural infarct will result in a myocardial scar, seen on echocardiography as an akinetic or dyskinetic segment with thinning and increased echoreflectivity. One or more segments may be large and weak enough to form an aneurysm. An aneurysm is a discrete outpouching of the ventricle with preservation of all three heart layers (endocardium, residual myocardium, and epicardium). They tend to develop at either the basal inferior wall or at the left ventricular (LV) apex, and can grow to a size that rivals that of the adjacent chambers ( Fig. 20.1 and ). Because there is no acute mechanical disruption of tissue, the transition from normal myocardium to aneurysm tends to be smooth and gradual, the outpouching may be relatively shallow, and flow by color Doppler tends to be laminar and nonturbulent (in contrast to pseudoaneurysms, as discussed in Chapter 19 ). The presence of the large aneurysmal area alters LV geometry and diminishes cardiac output. Attempts to improve the remodeling by surgically resecting or excluding aneurysmal and marginally viable surrounding areas (i.e., partial left ventriculectomy, or Batista operation) have shown limited benefits and a high overall failure rate, and thus is rarely recommended today. Aneurysms need to be distinguished from pseudoaneurysms, which are confined free wall ruptures, have a much worse prognosis, and represent a surgical emergency (see Chapter 19 ).

Left ventricular aneurysms.

(A) Inferobasal left ventricular aneurysm (arrow) , on apical three-chamber view. Note the thinning, increased reflectivity, and dyskinesis (outward bulge in systole) of the basal inferolateral segment. See also the corresponding Video 20.1 . (B) Giant apical left ventricular aneurysm on apical four-chamber view. An 8-cm true aneurysm (arrow) is noted bulging from the apex and distal lateral wall of the left ventricle. Features typical of such aneurysms include a wide neck, smooth tapering of the walls, which contain all three tissue layers, and spontaneous echo contrast consistent with sluggish blood flow within the aneurysmal pouch. A pacemaker/automatic implantable cardioverter-defibrillator wire is present in the right heart. See also corresponding Video 20.2 . LA , Left atrium; LV , left ventricle.

Flow within an aneurysm is frequently sluggish, as evidenced by spontaneous echo contrast, which can be more prominent and swirl locally (see Video 20.2 ) within the aneurysm. If the patient is not anticoagulated, this will predispose to formation of LV thrombus. The presence of extensive myocardial scarring, which conducts electrical impulses poorly, can also pave the way for reentrant arrhythmias such as ventricular tachycardias (VTs). VTs due to scars tend to be monomorphic, have sudden onset, and can cause symptoms that range from palpitations to sudden loss of consciousness, and even SCD. For this reason, after large MIs, echocardiography is used to evaluate for global depression of left ventricular ejection fraction (LVEF), one of the criteria used for determining the need to implant an automatic implantable cardioverter-defibrillator (AICD) for primary and secondary prevention of SCD (generally indicated if LVEF is ≤35%). In cases where a ventricular tachyarrhythmia has already occurred or recurs post-MI, echocardiography is also useful for gross localization of areas likely to have slow conduction and for ruling out LV thrombi prior to a planned VT ablation. The presence of mobile thrombus is an absolute contraindication to catheter ablation, because it can be dislodged by catheter manipulations, induction of VT, or repeated cardioversions. If a laminated (immobile) mural thrombus is visualized, some electrophysiologists may consider VT ablation after the patient has been anticoagulated at therapeutic levels (conventionally with warfarin for 4 weeks prior to procedure). In high-risk cases, some centers use intracardiac echocardiography (ICE) with electroanatomic mapping systems to avoid inadvertent catheter entry into the thrombus. The ablation procedure itself can induce complications of thromboembolism or cardiac perforation leading to tamponade.

Left Ventricular Thrombus

Formed thrombus may be detected in the left ventricle within 24 hours after MI, and most are formed within the first 1–2 weeks after MI. The incidence is estimated to be 8%–15% in patients with acute anterior MI (treated with percutaneous coronary intervention and dual antiplatelet therapy). Patients with large anterior MIs, LVEF of less than 40%, and severe akinesis or dyskinesis are at high risk of LV thrombus. They most frequently occur in the region with the most severe wall motion abnormality, and hence are most often at the apex. Approximately 11% occur at the septum and 3% at the inferolateral wall.

Thrombi appear as discrete homogeneously echogenic deformable masses abutting the endocardial border, invariably next to an akinetic or dyskinetic segment. They are termed mural thrombi when they are fixed, flattened (i.e., parallel to the endocardial surface), and adhere closely to the endocardium. Other thrombi may protrude more prominently into the LV cavity and be more mobile ( Fig. 20.2 and ). Of note, serial echocardiography on untreated patients has shown that the morphology of LV thrombi can change markedly over the first several months post-infarct.

Left ventricular apical thrombi.

(A) A flat immobile mural thrombus (arrow) is layered within the aneurysmal left ventricular (LV) apex. (B) A 2-cm mobile finger-like thrombus (arrow) is seen protruding from an akinetic LV apex. See also corresponding .

Although the specificity (>90%) of transthoracic echocardiography for detection of thrombus is good, the sensitivity ranges from only 30% to 60% in routine echocardiograms performed without echocardiographic contrast, when compared with delayed enhancement cardiac magnetic resonance imaging (MRI) as a gold standard. However, if performed specifically to evaluate for possible LV thrombus with echo contrast, echocardiography has a good negative predictive value (91%) and positive predictive value is approximately 93%. Accuracy is highly dependent on pretest probability, image quality, and the size and type of thrombus (the mural type being more difficult to detect than smaller protuberant thrombi). For echocardiograms that are inconclusive, the use of intravenous echocardiographic contrast increases sensitivity. In contrast to its primary role in detecting thrombi in the left atrium and appendage, transesophageal echocardiography has less sensitivity in detecting LV thrombus, because the LV apex is in the far field on transesophageal echocardiogram (TEE) windows.

The larger and more mobile thrombi, particularly if they reside near hinge points with hypercontractile myocardium, may be more likely to embolize. Persistent thrombi tend to become more compact, less mobile, and more echodense. Warfarin is currently the recommended treatment of LV thrombus. With anticoagulation, LV thrombi resolve in almost 50% of patients by 1 year and approximately 85% by 2 years of follow-up. The optimal duration of therapy remains unclear: although the risk of embolization decreases over time, as the thrombus resolves or organizes further, there may be residual risk, particularly if large wall motion abnormalities remain.

Left Ventricular Remodeling (Ischemic Cardiomyopathy)

After MI, changes in left ventricular structure may not be limited to the infarcted area. The left ventricle as a whole can begin to expand in size and mass, in a process termed ventricular remodeling. In the broadest context, left ventricular remodeling can be defined as an increase in left ventricular volume in response to a physiologic or pathologic state, such as chronic ischemia or chronic volume overload.

On echocardiography, left ventricular diameters and volumes will increase. If the left ventricular wall thickness remains the same or increases, overall LV mass will increase (i.e., hypertrophy occurs). This pattern of enlargement is known as eccentric hypertrophy ( Fig. 20.3 ). On echocardiography, a ratio termed the relative wall thickness (RWT), in combination with the total LV mass, allows one to characterize the type of hypertrophy (see Chapter 22 ). RWT ( Fig. 20.4 ) is simply the ratio of the summed wall thicknesses of opposing sections (interventricular septum and posterior wall) over the LV end-diastolic diameter.

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