Objective: To test prospectively depolarisation and repolarisation body surface maps (BSMs) for mirror image reversal, which is less susceptible to artefact, in patients with acute ischaemic-type chest pain, and to compare these BSM criteria with previously published 12 lead ECG criteria Methods: An 80 lead portable BSM system was used to map patients presenting with acute ischaemic-type chest pain and a 12 lead ECG with left bundle branch block (LBBB). Acute myocardial infarction (AMI) was defined by serial cardiac enzymes. Each 12 lead ECG was assessed by the criteria of Sgarbossa et al and Hands et al for diagnosis of AMI. Depolarisation and repolarisation BSMs were assessed for loss of mirror image reversal of QRS with ST-T isointegral map patterns and a change in vector angle from QRS to ST-T outside 180±15°-findings typically seen in LBBB with AMI. Results: Of 56 patients with chest pain and LBBB, 18 had enzymatically confirmed AMI. Patients with loss of BSM image reversal were significantly more likely to have AMI (odds ratio 4.9, 95% confidence interval 1.5 to 16.4, p = 0.007). Loss of BSM image reversal was significantly more sensitive (67%) for AMI than either 12 lead ECG method (17%, 33%) albeit with some loss in specificity (BSM 71%, 12 lead ECG 87%, 97%). Patients with AMI compared with those without AMI had a greater mean change in vector angle outside the normal range (180±15°), particularly between QRS isointegral and ST60 isopotential (the potential 60 ms after the J point at each electrode site) BSMs (19°v 9°, p = 0.038). Loss of image reversal and QRS-ST60 vector change outside 180±15°had 61% sensitivity and 82% specificity for AMI (odds ratio 7.0, 95% confidence interval 2.0 to 24.4, p = 0.001). Conclusions: BSM compared with the 12 lead ECG improved the early diagnosis of AMI in the presence of LBBB.
A 45-year-old woman with a 5-year history of treated essential hypertension presented with a 2-month history of exertional dyspnea and a 2-week history of intermittent palpitations. Two weeks earlier, she presented to the emergency department of another hospital with palpitations, but these had terminated on arrival. She was told her ECG displayed "low voltages." During the next 2 weeks, she became increasingly dyspneic, feeling short of breath most of the time. She had a sensation of fullness in the chest, frequent palpitations, and ankle edema, so she was referred to a cardiologist. An echocardiogram revealed the presence of a large blood-filled sac markedly compressing the right heart ( Figure 1A through 1C). A CT scan of the thorax confirmed the presence of this sac, which measured 9.6 cm maximum diameter (Figure 2). A differential diagnosis of a sinus of Valsalva aneurysm, a giant right coronary artery aneurysm, or a pseudoaneurysm of the aortic sinus was made. She was referred for surgery because of the severity of her right heart compression and the possibility of rupture of the blood-filled sac. Surgical exploration confirmed that the sac was a true right coronary artery aneurysm, communicating proximally with the right coronary artery ostium and distally with the distal right coronary artery (Figure 3). The right coronary artery was ligated proximally, the aneurysm was excised, and a saphenous vein conduit grafted to the distal vessel. Postoperatively, the patient complained of excessive fatigue and occasional swelling of the ankles. Echocardiography revealed mildly impaired right ventricular function with moderate tricuspid regurgitation. Cardiac catheterization confirmed these findings, but because the right atrial pressure remained low (V wave is 8 mm Hg), we elected to continue with medical management initially.
The acute coronary syndromes consist of two groups: unstable angina and non-Q wave myocardial infarc-tion, and ST segment elevation myocardial infarction. This article reviews the management only of patients with unstable angina and non-Q wave myocardial infarction. Unstable angina can be defined as ischaemic-type chest pain that is more frequent, severe, or prolonged than the patient's usual angina symptoms, occurs at rest or minimal exertion, or is difficult to control with drugs. 1 Angina of recent onset is also classified as unstable. Non-Q wave myocardial infarction presents similarly to unstable angina but is accompanied by a rise in cardiac enzyme concentration without new Q waves on the electrocardiogram. Acute coronary syndromes are major causes of morbidity and mortality. The burden on the health service will be further clarified by the UK prospective registry of acute ischaemic syndromes (PRAIS-UK), which has studied the prevalence and management of unstable angina in the United Kingdom. 2 The recent growth in treatment options for acute coronary syndromes has followed increased awareness of their pathophysiology. The initial event is erosion or rupture of the fibrous cap of an atherosclerotic plaque leading to intracoronary thrombosis. The thrombosis results from platelet activation mediated by exposure of plaque contents, collagen, and other vessel wall components. 3 Downstream embolisation from friable coronary thrombus may occur, leading to focal cell necrosis and the release of cardiac troponins. 3 Patients with acute coronary syndromes are at high risk of myocardial infarction and death. 4 Optimal treatment of patients with ST segment elevation myocardial infarction is clearly defined. 5 However, the management of patients with unstable angina and non-Q wave myocardial infarction remains controversial because of the heterogeneous nature of these conditions and recent advances in their treatment options. In this article we discuss risk stratification of these patients based on symptoms, the initial electrocardiogram, and serum markers and best use of new treatments. Methods The topics for inclusion in this article were decided by all contributing authors. We obtained further material from recent major cardiology meetings and from searches of the internet and electronic medical databases (search words: unstable angina, acute coronary syndromes). Risk stratification High risk Numerous clinical studies have been carried out to identify factors that place patients at particularly high risk of death or myocardial infarction. The two most important are acute ST segment depression on the initial electrocardiogram and cardiac troponin concentration. Additional risk factors include advanced patient age and pain at rest, with or without haemo-dynamic instability (figure). 1 6 Risk stratification of these patients should start in accident and emergency departments. In a study of 773 consecutive patients presenting within 12 hours of onset of cardiac-type chest pain and without ST segment elevation, Hamm et ...
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