(tissue plasminogen activator [t-PA], anti-thrombin III, heparin sulfate, protein C, thrombomodulin, and prostacyclin). Rare causes of MI are inflammatory vascular diseases, embolism (endocarditis; valve prosthesis), severe coronary spasm (e.g., after taking cocaine), increased blood viscosity as well as a markedly raised O2 demand at rest (e.g., in aortic stenosis).

ECG (^ F). A prominent characteristic of transmural infarction (tml) is an abnormal Q wave (^ F1) of >0.04 seconds and a voltage that is >25% of overall QRS voltage. It occurs n within one day and is due to the necrotic myo-■2 cardium not providing any electrical signal, so ula that when this myocardial segment should be ^ depolarized (within the first 0.04 s), the excita-U tion vector of the opposite, normal portion of "c the heart dominates the summated vector. ™ This "0.04 vector" therefore "points away" is from the site of infarction so that, for example, X in anterior-wall infarction, it is registered par-r^ ticularly in leads V5, V6, I, and aVL as a large Q wave (and small R). (In a transmural infarction of the posterior wall such Q wave changes cannot be registered with the conventional leads). Abnormal Q waves will still be present years later (^ F2,3), i.e., they are not diagnostic of an acute infarction. An infarction that is not transmural usually causes no Qchanges.

ST segment elevation in the ECG is a sign of ischemic but not (yet) dead myocardial tissue. It occurs

- during an anginal attack (see above)

- in nontransmural infarction

- at the very beginning of transmural infarction

- at the margin of a transmural infarction that occurred hours to days before (^ F4)

The ST segment returns to normal one to two days after an MI, but for the next few weeks the Twave will be inverted (^F5,F2).

If sizeable portions of the myocardium die, enzymes are released from the myocardial cells into the bloodstream. It is not so much the level of enzyme concentrations as the temporal course of their maxima that is important in the diagnosis of MI. Myocardial creatine kinase (CK-MB [MB = muscle, brain]) reaches its peak on day 1, aspartate aminotransferase (ASAT) on day 2, and myocardial lactate dehy-drogenase (LDH1) on days three to five (^ C, bottom).

Possible consequences ofMI depend on site, extent, and scarring of the infarct. In addition to various arrhythmias, among them acutely life-threatening ventricular fibrillation (^ p. 186 ff.), there is a risk of a number of morphological/mechanical complications (^ G):

♦ Tearing of the chordae tendineae resulting in acute mitral regurgitation (^G1 and p. 196);

♦ Perforation of the interventricular septum with left-to-right shunting (^ G2 and p. 204);

♦ Fall in cardiac output (^ G,a) that, together with

♦ stiffened parts of the ventricular wall (akinesia) due to scarring (^ G, b),

♦ will result in a high end-diastolic pressure (^ G3 and p. 224). Still more harmful than a stiff infarct scar is

♦ a stretchable infarct area, because it will bulge outward during systole (dyskinesia; ^G4), which will therefore-at comparably large scar area—be more likely to reduce cardiac output to dangerous levels (cardiogenic shock) than a stiff scar will (^ G5);

♦ Finally, the ventricular wall at the site of the infarct can rupture to the outside so that acutely life-threatening pericardial tamponade occurs (^G6 and p. 228).

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