Myocardial infarction evolving

E. Therapeutic response Activase, and other thrombolytic agents, used in a timely manner during an evolving myocardial infarction, decrease mortality and improve left ventricular function. Resolution of chest pain, resolution of baseline EKG changes, reduced total creatine phospho-kinase (CPK) release, and preserved left ventricular function are evidence of cardiac reperfusion. Activase, administered within the first 3 hours of ischemic stroke onset, has been shown to improve recovery. 

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. 

The acute coronary syndromes (ACS) are now classified on the basis of the ECG and plasma troponin measurements into (1) patients with ST elevation myocardial infarction (STEMI), (2) non-ST elevation myocardial infarction (non-STEMI, by ECG and a positive troponin test) and (3) unstable angina (by ECG and negative troponin test). The present account recognises that this is a rapidly evolving field, but therapeutic strategies are likely to evolve according to these forms of ACS. 

Generally, the clinical presentation of myocardial ischaemia is the characteristic pain known as angina pectoris or some equivalents (e.g. dyspnoea), although sometimes ischaemia may be silent (see Silent ischaemia , p. 302). If the anginal pain is new or if it has increased with respect to previous discomfort (crescendo angina), this constitutes the clinical condition called acute coronary syndrome (ACS), which may evolve into myocardial infarction (MI) (see Section Acute coronary syndrome , p. 209). If the angina pain appears with exercise... 

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...

In ACS the clinical situation can be controlled and the ACS might not evolve, whereby it is unstable angina (UA) or may well progress towards an acute myocardial infarction that may or may not... 

ECG in mechanical complications of an ACS evolving to myocardial infarction (Figures 8.27-8.29)... 

This term is applied to ACS evolving towards a large (Q-wave or non-Q-wave) myocardial infarction. Currently, the 30-day mortality rate is greater than 20-30%. 

On some occasions patients with ACS and wide QRS present ST-segment elevation evolving to a Q-wave myocardial infarction. The ECG criteria to diagnose Q-wave infarction in presence of ACS with wide QRS have been explained in the first part (see p. 170). 

Table 6.1, p. 274). Rarely, ST-segment elevation may occur, which is probably explained by multiple mi-crocirculatory spasms. The prognosis is generally good and, in general, does not evolve to myocardial infarction. 

Fiol M, Cygankiewicz I, Bayes-Genis A et al. The value of ECG algorithm based on ups and downs of ST in assessment of a culprit artery in evolving inferior myocardial infarction. Am J Cardiol 2004b 94 709. 

Lew AS, Laramee P, Shah PK, Maddahi J, Peter T, Ganz W. Ratio of ST-segment depression in lead V2 to ST-segment elevation in lead aVF in evolving inferior acute myocardial infarction an aid to the early recognition of right ventricular ischemia. Am J Cardiol 1986 57 1047. 

Acute evolving transmural myocardial infarction, pulmonary embolism, deep vein thrombosis, arterial thrombosis or embolism, and occlusion of arteriovenous cannulae... 

Acute infarct artery PCI was demonstrated initially to be feasible in conjunction with intracoronary thrombolysis in a small registry study reported in 1982 (43). The approach evolved quickly to one in which the intracoronary thrombolysis component was abandoned. The separation of mechanical and pharmacological approaches was reinforced by results in a small (56-patient), but very influential, randomized trial comparing primary PCI with administration of intracoronary streptokinase in 1986 (44). Primary PCI led to greater recovery of left ventricular function. Results from another relatively small, randomized trial (n = 142) were concordant. They demonstrated greater recovery of left ventricular function with primary PCI compared with intravenous streptokinase (45). The Primary Angioplasty in Myocardial Infarction... 

Van de Werf F, Ludbrook PA, Bergmann SR, Tiefenbrunn AJ, Fox KAA, de Geest H, Verstraete M, Collen D, Sobel BE. Coronary thrombolysis with tissue-type plasminogen activator in patients with evolving myocardial infarction. N Engl J Med 1984 310 609-613. 

Many factors have contributed to the decline in cardiovascular-related mortality over the past quarter century, including lifestyle modifications, the development of multiple new drug categories, the introduction and subsequent dramatic improvements in percutaneous coronary intervention (PCI), cardiac transplantation, and advances in electrophysiology and implantable devices. One of the more important new treatments is reperfusion therapy for patients with evolving acute myocardial infarction (AMI), which has now become the standard of care for these individuals. This chapter will review selected major developments in historical perspective that led to the widespread application of pharmacological reperfusion therapy for the treatment of AMI (Fig. 2.1). 

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