Myocardial infarction zones

Myocyte replication is the failing heart s attempt to compensate for a limited capacity for hypertrophy. When Urbanek et al. [37] used Ki-67 (a nuclear protein expressed during cell division) to assess the mitotic activity of myocytes, they observed significantly greater mitotic activity at infarct border zones than in distant myocardium or undiseased control hearts. The evidence that cardiac myocytes divide shortly after a myocardial infarction led investigators to search for the origin of the dividing myocytes [82]. This culminated in the description of resident CSCs [35-37]. 

Factor SM, Sonnenblick EH, Kirk ES The histologic border zone of acute myocardial infarction Islands or peninsulas Am J Pathol 1978 92 111-124. 

Urseh PC, Gardner PI, Albala A, Fenoglio JJ, Wit AL Structural and electrophysiological changes in the epicardial border zone of canine myocardial infarcts during infarct healing. Cite Res 1985 56 436-451. 

Several disease states can result from abnormal blood clots. For example, strokes were mentioned previously. However, the most common and deadliest thrombotic disease is myocardial infarction (MI). Atherosclerosis has long been associated with reduced cardiac function and elevated mortality due to rupture of atherosclerotic plaques. The rupture of an atherosclerotic plaque usually results not only in blockage due to the plaque itself but also in the immediate formation of an occlusive blood clot, which results in an MI. Immediately after the initiation of an MI, a zone of necrosis begins to develop around the area as ischemia proceeds. It is during this early phase of ischemia (several hours) that therapeutic intervention not only can be life-saving but also can minimize the amount of necrotic heart tissue formed. 

Myocardial infarction (MI) is caused by the acute thrombotic occlusion of a coronary artery. The myocardial region that has been cut off from its blood supply dies within a short time owing to the lack of 02 and glucose. The loss in functional muscle tissue results in reduced cardiac performance. In the infarct border zone, spontaneous pacemaker potentials may develop, leading to fatal ventricular fibrillation. The patient experiences severe pain, a feeling of annihilation, and fear of dying. 

A 73-year-old man with a history of breathlessness, cough, and weight loss had some ill-defined peripheral shadow in the upper zones of a chest X-ray. He had fiberoptic bronchoscopy with cocaine and lidocaine and 5 minutes later became distressed, with dyspnea, chest pain, and tachycardia. Electrocardiography showed an evolving anterior myocardial infarction. Coronary angiography showed a stenosis of less than 25% in the proximal left anterior descending artery with coronary artery spasm. He made an uneventful recovery. 

Aortic arch dissection can cause profound hypotension, with global, and sometimes boundary zone, cerebral ischemia or focal cerebral ischemia if the dissection spreads up one of the neck arteries. Clues to this diagnosis are anterior chest or interscapular pain, along with diminished, unequal or absent arterial pulses in the arms or neck and a normal electrocardiogram, unlike acute myocardial infarction, acute aortic regurgitation and pericardial effusion. 

Figure 2.2 (A) A patient with myocardial infarction of anteroseptal zone in a subacute phase (1) normal recording that displays extension of Q waves up to V6 (qrs). Small changes in the placement of precordial V3-V6 leads have significantly modified the morphology of QRS, now being qR in a lead V6. Therefore, according to the...

Figure 4.17 Acute myocardial infarction with ST-segment elevation in II, III and VF and ST-segment depression in V1-V3. This pattern corresponds classically to an infarction involving inferior and posterior walls. Nowadays, this is the pattern of STE-ACS of inferolateral zone evolving to inferolateral infarction due to distal occlusion of a dominant RCA (ST-segment depression in I and V1-V3,...

Figure 4.66 Above (A) Acute phase of evolving Q-wave myocardial infarction of anteroseptal zone. There is a huge ST-segment elevation, especially in I, VL and from V2 to V5, QRS >0.12 s and morphology of complete RBBB that was not present in previous ECG. (B) Twenty-four hours later RBBB have disappeared and subacute anterior extensive infarction becomes evident. There is ST-segment elevation from V1 to V4. The transient presence of new...

Figure 5.52 The ECG of a patient with complete LBBB and associated infarction. There are ECG criteria suggestive of extensive anterior myocardial infarction (qR in I, QR in VL and low voltage of S in V3). The CMR images (A-D) demonstrated the presence of an extensive infarction of anteroseptal zone (type A-3) (proximal LAD occlusion). The inferolateral wall is free of necrosis (see (D)), because the...

Figure 8.13 (1) The three types of repolarisation abnormalities that may be seen in an acute phase of myocardial infarction involving the inferolateral zone ...

In addition to simply quantifying the extent of myocardial infarcts, DE-CMR can provide other potentially useful anatomic findings to help risk-stratify patients. Yan et al. (13) evaluated 144 patients with CAD and abnormal DE-CMR findings and determined that the extent of the peri-infarct zone was superior to EF in predicting mortality over a median follow-up period of 2.4 years. Even after adjustment for age and ejection fraction, the size of the peri-infarct zone maintained strong and independent associations with all-cause and cardiovascular-related mortality. 

Yan AT, Shayne AJ, Brown KA, et al. Characterization of the peri-infarct zone by contrast-enhanced cardiac magnetic resonance imaging is a powerful predictor of post-myocardial infarction mortality. Circulation 2006 114(l) 32-9. 

The localization of adducts to the epicardial border zone suggested the possibility that IsoK/LG adducts contribute to cardiac arrhythmias. Ventricular tachycardia/fibrillation following myocardial infarction is a major cause of sudden cardiac death. Arrhythmias in ischemic myocardium arise from sodium channel blockade. Sodium channels are hypothesized to cycle between three conformational states a deactivated closed state, an activated open state, and an inactivated closed state. Upon depolarization, the deactivated state converts to the activated state and sodium current flows for a brief time before the channel enters the inactive state. The channel only converts from the inactive state to the deactivated state when the membrane repolarizes during the falling phase of the action potential. Changes in the ability to convert from the inactive to the deactivated state are critical to the initiation and perpetuation of arrhythmias. 

Kurmukov AG, Ermishina OA (1986) Influence of ecdysterone on the size of the necrotic zone after experimental myocardial infarction. In Otsenka Razmera i Taktika Lecheniya Infarkta Miokarda (Estimation of the size, and methods for treating, myocardial infarction), Tomsk, pp 62-63 (in Russian)... 

Figure 15. Extension and stress distributions in infarcted heart. A. Systolic circumferential extensions in the border zone are larger than normal. B. Circumferential stresses at the edge of the infarct are 3.7 times greater than those at 180°. (Reproduced from Bogen et aL An analysis of the mechanical disdvantage of myocardial infarction in the canine left ventricle, Circ Res 47, 728, 1980 with permission from the American Heart Association.)...

---