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OBJECTIVE: To determine the safety and prognostic value of dipyridamole thallium-201 scintigraphy performed in patients within three to five days of acute myocardial infarction, including those receiving thrombolytic treatment. DESIGN: A prospective study of dipyridamole thallium-201 scintigraphy in patients early after acute myocardial infarction. SETTING: University hospital. PATIENTS: 200 patients who were clinically uncomplicated at day 3 after infarction, 92 (46%) of whom had received thrombolysis. MAIN OUTCOME MEASURES: Incidence of cardiac death, non-fatal reinfarction, readmission to hospital for unstable angina, or non-elective revascularisation procedure within six months' follow up. RESULTS: No patient had a serious complication from the dipyridamole study. At six month follow up, 55 patients (28%) had suffered a defined cardiac event. Patients who received thrombolysis had the same extent of thallium-201 redistribution and the same occurrence of subsequent cardiac events as those not receiving thrombolysis. Patients who subsequently had an event had more myocardial segments showing thallium-201 redistribution than event free patients: 2.7 (SD 1.9) v 1.2 (1.4), respectively (p < 0.001). Among all clinical and scintigraphic variables, multivariate analysis identified the extent of thallium-201 redistribution as the only independent predictor of outcome (p < 0.001). Among 63 patients (32%) of the study cohort who showed more than two myocardial segments with thallium-201 redistribution, the adjusted risk ratio for a cardiac event was 7.5 (95% confidence interval 2.9 to 19.1) compared with patients without any redistribution. CONCLUSIONS: Dipyridamole thallium-201 scintigraphy can be performed safely within a few days of the event in patients with uncomplicated myocardial infarction, including those who received thrombolysis, and can identify a subgroup of patients at high risk of future ischaemic events.

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Myocardial infarction (MI) occurring during pregnancy is a rare but potentially lethal event for both mother and fetus, particularly when it occurs in the third trimester or peripartum period. The authors report two cases of MI occurring in the third trimester of pregnancy and review the literature. Management of the acute infarct and the medical, obstetric, and anesthetic considerations in such patients during labor and delivery are discussed. Successful use of percutaneous transluminal coronary angioplasty is described in a patient with evolving MI and ongoing pain. The preferred method of delivery in the pregnant MI patient is addressed, with emphasis on the need for individualization of care and coordination between the cardiac, obstetric, and anesthetic teams. Finally, the authors review the risks of subsequent pregnancy in this patient population.

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The incidence, outcome and predictors of the in-hospital development of cardiogenic shock and its prognostic significance were analyzed in 845 patients presenting with acute myocardial infarction. Cardiogenic shock developed after hospitalization in 60 patients (7.1%). In half of these patients, cardiogenic shock developed at least 24 h after hospital admission. The in-hospital mortality rate was greater than 15 times higher for patients with cardiogenic shock than for patients without shock (65.0% versus 4.3%, respectively, p less than 0.001). Enzymatic evidence of infarct extension occurred in 23.3% of the patients with shock compared with 7.4% of those without shock (p less than 0.0001). Multivariate analysis indicated that independent predictors for the in-hospital development of cardiogenic shock were age greater than 65 years (p = 0.007), left ventricular ejection fraction on hospital admission less than 35% (p = 0.007), large infarct as estimated from serial enzyme determinations (that is, peak creatine kinase-MB isoenzyme greater than 160 IU/liter (p = 0.008), history of diabetes mellitus (p = 0.011) and previous myocardial infarction (p = 0.012). Patients with three, four or five of these risk factors had a 17.9%, 33.7% or 54.4% probability, respectively, of developing cardiogenic shock after hospital admission. Left ventricular function, as reflected by left ventricular ejection fraction (p = 0.04) and severity of left ventricular wall motion abnormality (p = 0.04), was the most important determinant of in-hospital mortality in the patients with cardiogenic shock.

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Although silent myocardial ischemia (SI) occurs frequently in patients with angina and is of prognostic significance, little is known of its occurrence in other subgroups. We assessed the incidence of SI in offspring of Framingham Heart Study (FHS) patients following unrecognized myocardial infarction (UMI) and in controls without MI but who were matched for age, sex, hypertension, diabetes, smoking, and total cholesterol at entry into the FHS. Of the 20 UMI patients, six had died and one with left bundle branch block was excluded. The remaining 13 UMI patients and 26 control patients underwent 24-hour ambulatory electrocardiographic monitoring (AECG) for SI. Two patients (one from each group) with angina were excluded from the AECG analysis. Only two (15.4%) of the UMI patients and two (7.7%) of the control patients had any AECG evidence of SI. These preliminary results suggest that routine monitoring for SI is not indicated in asymptomatic long-term survivors of UMI or in asymptomatic patients without prior MI but with otherwise similar risk profiles.

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Whether myocardial infarction (MI) can be diagnosed electrocardiographically in the presence of left bundle branch block (LBBB) is controversial. Our study sought to test the reliability of ECG criteria for diagnosing MI in patients with LBBB. Among 985 patients presenting within 18 hours of the onset of ischemic chest pain, 35 had complete LBBB. Acute MI was identified by serial MB-creatine kinase (CK) elevations and prior MI was determined by previously documented ECG and/or enzyme changes. Among those with LBBB, 24 patients had acute and/or prior MI, while 11 had neither. Eleven ECG criteria previously proposed for detecting MI in the presence of LBBB were evaluated. In patients presenting with ischemic chest pain and complete LBBB, presence of any one of the following ECG criteria was highly specific (90% to 100%) and predictive (85% to 100%) for acute or prior MI: Q waves in at least two of leads I, aVL, V5, or V6; R wave regression from V1 to V4; notching of the upstroke of the S wave in at least two of leads V3, V4, or V5, and primary ST-T wave changes in two or more adjacent leads.

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The reasons for the poorer prognosis of anterior versus inferior myocardial infarction of equivalent enzymatic size remain uncertain. We investigated whether there are differences in left ventricular function between patients with anterior and inferior infarctions of equivalent enzymatic size to account for their differing outcomes. Clinical, serum enzyme, and electrocardiographic data were prospectively recorded in a consecutive series of patients less than 70 years of age with their first myocardial infarction. At 29 +/- 6 days following infarction, ejection fraction and left ventricular wall motion were assessed by gated heart scintigraphy and functional capacity by treadmill exercise testing in 19 patients with anterior and in 23 patients with inferior myocardial infarction. Peak creatine kinase and QRS scores were used to estimate total infarct size and left ventricular infarct size respectively. The anterior infarcts were of similar size to the inferior infarcts as determined by peak creatine kinase (1444 [mean] +/- 1161 [SD] U/L versus 1484 [mean] +/- 1182 [SD] U/L, respectively, P = 0.91) and peak aspartate transaminases (174 +/- 112 U/L versus 164 +/- 102 U/L, P = 0.78). The anterior myocardial infarct group had a greater percentage of the left ventricle infarcted on QRS scoring than the inferior infarct group (25.9 +/- 14.4% versus 11.1 +/- 6.0% respectively, P = 0.0004), lower global left ventricular ejection fraction (45.8 +/- 16% versus 54.6 +/- 9.2%, P = 0.04) and greater left ventricular regional wall abnormality. A significant negative correlation existed between left ventricular ejection fraction and peak creatine kinase for both groups, but was more marked with anterior infarction (r = -0.78, P less than 0.01) compared with inferior infarction (r = -0.49, P less than 0.05). Exercise-induced ST segment elevation was more frequent in the anterior than the inferior infarct group (59% versus 18%, P less than 0.02). However, both infarct locations had similar exercise tolerance, exercise-induced angina and ST segment depression. Despite equivalence of infarct size of the two infarct locations on enzyme testing, anterior infarction was associated with greater abnormality of left ventricular function with lower resting global left ventricular ejection fraction; greater resting left ventricular regional wall abnormality and greater exercise-induced ST segment elevation. These differences probably contribute to the poorer prognosis of patients with anterior infarction compared to those with inferior infarction of equivalent enzymatic size, given the previously well-documented prognostic importance of left ventricular function.

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To assess whether the site of myocardial infarction is an independent prognostic indicator, the outcome of patients with anterior myocardial infarction was compared with that of patients with inferior infarction. A consecutive series of patients who had suffered their first myocardial infarction was analyzed (398 with anterior and 391 with inferior infarction). Patients with anterior myocardial infarction had a higher 1 year mortality than those with inferior infarction (18.3% vs 10.5%, p = .002). When patients were matched for infarct size determined by peak creatine kinase (CK) level expressed as a multiple of the upper limit of normal, those with anterior myocardial infarction tended to have a higher 1 year mortality than those with inferior infarction for all subgroups of peak CK. Early mortality (day 1 to 28 after myocardial infarction) was greater in the anterior than in the inferior myocardial infarction group (10% vs 6.4%, p = .03); this was most significant when peak CK was greater than four times normal (12.4% vs 7.0%, p = .04). Late mortality was also higher in the anterior (8.4% vs 4.1%, p = .04) than the inferior infarction group and this was most significant when peak CK was less than two times normal (15.2% vs 0%, p = .02) or greater than eight times normal (10.6% vs 4.1%, p = .04). Multivariate analysis with proportional-hazards regression confirmed the prognostic significance of location of infarction independent of peak CK level. Thus, infarct location was found to be a predictor of prognosis that is independent of infarct size based on peak CK levels.

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We report a case of secondary deposition of carcinoma of the uterine cervix in the myocardium with development of ischaemic cardiac pain, ST segment elevation and asystolic cardiac arrest. The coronary arteries were free of obstruction. To the best of our knowledge, this is a unique presentation of a rare myocardial metastasis.

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Metastatic involvement of the myocardium is a rare premorbid diagnosis. Multiple examinations were performed on a 43-year-old woman who presented with ischemic chest pain, palpitations, and nausea. Twelve months previously, a poorly differentiated squamous cell carcinoma of the uterine cervix was removed with no evidence of metastases or residual tumor. Following numerous investigations, a provisional diagnosis of cardiac tumor was made. At operation, involvement of the septum, inferior wall, and apex with some extension into the distal anterior wall was noted. Histology confirmed nonkeratinizing cell carcinoma in keeping with metastases from the uterine cervix.

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We present a case of an unruptured right coronary sinus of Valsalva aneurysm with dissection into the interventricular septum diagnosed pre-operatively by cross-sectional echocardiography. The unique echocardiographic features of this rare, although potentially fatal congenital lesion, are described.

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