Myocardial infarction with Q wave

We will now deal with the importance of ECG, especially from a clinical and prognostic standpoint, in patients with Q-wave myocardial infarction. 

Myocardial infarctions with and without Q waves new concepts 

Classically, the electrocardiographic pattern of the established transmural infarction was associated with the presence of a pathological Q wave, 

Moon et al. (2004) showed in a correlation study with CE-CMR that infarctions with predominantly 

Very recently Kwong et al. (2006) in a group of patients with clinical suspicion of CHD but without history of MI demonstrated that the presence of areas of the LV with gadolinium enhancement carries a high cardiac risk. In addition, the presence of gadolinium enhancement areas has prognostic implications beyond the common clinical, angiographic and functional predictors. 

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Myocardial infarction with Q wave or equivalents and normal intraventricular conduction... 

The patient, a 63-year-old Caucasian female, was hospitalized on 4 April 2002 though 10 April 2002 for a non-ST segment elevation myocardial infarction (non-Q-wave MI per chart documentation). She had a negative adenosine stress test after the initial event. Her serum cardiac-specific troponin I (cTnl) concentration 24 hours after her onset of chest pain was 1.4 pg/L (upper limit of normal is 0.3 ng/mL), and her creatine kinase (CK) MB level was 12.5 pg/L (upper limit of normal 6.0 ng/mL). Three days post-event her cTnl level was 0.5 pg/L and her CK-MB level was 4.5 pg/L (Fig. 5-1). MB refers to one of the isoenzyme forms of CK found in serum. The form of the enzyme that occurs in brain (BB) does not usually get past the blood-brain barrier and therefore is not normally present in the serum. The MM and MB forms account for almost all of the CK in serum. Skeletal muscle contains mainly MM, with less than 2% of its CK in the MB form. MM is also the predominant myocardial creatine kinase and MB accounts for 10%-20% of creatine kinase in heart muscle. 

A retrospective chart review was conducted to explore metamfetamine-associated acute coronary syndromes in patients who presented to the emergency room at a University Center between 1994 and 1996 (1). There were 36 admissions, three of which were repeat patients. Nine of these patients had acute coronary syndrome. Of these, one had an acute anterior Q wave myocardial infarction with cardiac arrest, seven had non-Q wave myocardial infarctions, and one had unstable angina. There were potentially life-threatening cardiac complications in three subjects (8%). The authors suggested that acute coronary syndromes and life-threatening complications associated with the use of metamfetamine are not uncommon, as evidenced by their experience in this study. 

A 46-year-old man developed a Q-wave inferior and a right ventricular myocardial infarct with postinfarction angina after the third cycle of vincristine -I- doxorubicin for multiple myeloma. The patient had no risk factors for ischemic heart disease, except for a positive smoking history, nor for hyperviscosity (24). 

Wong CK, French JK, Krucoff MW, Gao W, Aylward PE, White HD. Slowed ST segment recovery despite early infarct artery patency in patients with Q waves at presentation with a first acute myocardial infarction implications of initial Q waves on myocyte reperfusion. Eur Heart J 2002b 23(18) 1449. 

Boden WE, O Rourke RA, Crawford MH, et al. Outcomes in patients with acute non-Q wave myocardial infarction randomly assigned to an invasive as compared with a conservative management strategy (VANQUISH). N Engl J Med 1998 338 1785-1792. 

Tirofiban is a synthetic, nonpeptide inhibitor of glycoprotein-(GP)-receptors. Tirofiban has a rapid onset and short duration of action after intravenous administration. Coagulation parameters turn to normal 4-8 hours after the drug is withdrawn. Tirofiban in combination with heparin and aspirin is indicated in the management of patients with unstable angina or non-Q-wave myocardial infarction. 

In patients with unstable angina, immediate-release short-acting calcium channel blockers can increase the risk of adverse cardiac events and therefore are contraindicated (see Toxicity, above). However, in patients with non-Q-wave myocardial infarction, diltiazem can decrease the frequency of postinfarction angina and may be used. 

Patients The selection of patients for thrombolytic therapy is critical. The diagnosis of acute myocardial infarction is made clinically and is confirmed by electrocardiography. Patients with ST segment elevation and bundle branch block on electrocardiography do best those with ST segment depression or a normal ECG do less well and those with non-Q-wave acute myocardial infarction may even be harmed. All trials to date show the greatest benefit for thrombolytic therapy when it is given early, within 6 hours after symptomatic onset of acute myocardial infarction. 

The PRISM-PLUS Investigators. Inhibition of the platelet glycoprotein llb/llla receptor with tirofiban in unstable angina and non-Q-wave myocardial infarction. N Engl J Med 1998 338 1488-1497. 

The FFtAXIS Study Group. Comparison of two treatment durations (6 days and 14 days) of a low molecular weight heparin with a 6-day treatment of unfractionated heparin in the initial management of unstable angina or non-Q-wave myocardial infarction FRAXIS (fraxiparine in acute ischaemic syndrome). Eur Heart J 1999 20 1553-1562. 

Hussain TF, Heidenreich PA, Benowitz N. Recurrent non-Q-wave myocardial infarction associated with toluene abuse. Am Heart J 1996 131(3) 615-6. 

Gibson RS, Boden WE, Theroux P, Strauss HD, Pratt CM, Gheorghiade M, Capone RJ, Crawford MH, Schlant RC, Kleiger RE, et al Diltiazem and reinfarction in patients with non-Q-wave myocardial infarction. Results of a doubleblind, randomized, multicenter trial. N Engl J Med 1986 315(7) 423-9. 

Schwarzer S, Eber B, Greinix H, Lind P. Non-Q-wave myocardial infarction associated with bleomycin and eto-poside chemotherapy. Eur Heart J 1991 12(6) 748-50. 

Figure 44-4 Electrocardiogram, serial tracing of a patient with an acute myocardial infarction. The sequence is (A) normal, (B) hours after infarction, the ST segment becomes elevated, (C) hours to days later, the T wave inverts and the Q wave becomes larger, (D) days to weeks later, the ST segment returns to near normal, and (E) weeks to months later, the T wave becomes upright again, but the large Q wave may remain.

The coronary angiography (Figure 1.1) is especially important in the acute phase for diagnosing the disease and correlating the place of occlusion with the ST-segment deviations. It is also useful in the chronic phase of the disease. However, in the chronic phase of Q-wave myocardial infarction (MI) the ECG does not usually predict the... 

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