Prognostic significance of location and type of myocardial infarction: independent adverse outcome associated with anterior location.

To determine the relative prognostic significance of location (anterior or inferior) and type (Q wave or non-Q wave) of infarction, the hospital course and follow-up outcome (mean duration 30.8 months) of 471 patients with a first infarction were analyzed. Analyses were performed grouping the patients according to infarct location (anterior, n = 253; inferior, n = 218), infarct type (Q wave, n = 323; non-Q wave, n = 148), and both location and type (inferior non-Q wave, n = 85; inferior Q wave, n = 133; anterior non-Q wave, n = 63; and anterior Q wave, n = 190). Patients with anterior infarction had a substantially worse in-hospital and follow-up clinical course compared with those with inferior infarction, evidenced by a larger infarct size (21.2 versus 14.9 g Eq/m2 creatine kinase, MB fraction [MB CK], p less than 0.001), lower admission left ventricular ejection fraction (38.1 versus 55.3%, p less than 0.001) and higher incidence of heart failure (40.7 versus 14.7%, p less than 0.001), serious ventricular ectopic activity (70.2 versus 58.9%, p less than 0.05), in-hospital death (11.9 versus 2.8%, p less than 0.001) and total cumulative cardiac mortality (27 versus 11%, p less than 0.001). Patients with Q wave infarction similarly experienced a worse in-hospital course compared with patients with non-Q wave infarction, evidenced by a larger infarct size (20.7 versus 12.7 MB CK g Eq/m2, p less than 0.001), lower admission left ventricular ejection fraction (43.7 versus 50.6%, p less than 0.001), and a higher incidence of heart failure (31.9 versus 21.6%, p less than 0.05) and in-hospital death (9.3 versus 4.1% p less than 0.05). However, there was no increased rate of reinfarction or mortality in hospital survivors with non-Q wave infarction compared with those with Q wave infarction, and total cardiac mortality was similar (16 versus 21%, p = NS). To evaluate the role of infarct location and type independent of infarct size, patients were grouped according to quartile of infarct size, and outcome was reanalyzed within each group. Patients with anterior infarction demonstrated a lower left ventricular ejection fraction on admission and after 10 days than did patients with inferior infarction, even after adjustment for infarct size, as well as a higher incidence of congestive heart failure and cumulative cardiac mortality.(ABSTRACT TRUNCATED AT 400 WORDS)

Prognostic significance of the treadmill exercise test performance 6 months after myocardial infarction.

A submaximal treadmill exercise test performed before hospital discharge after an uncomplicated myocardial infarction is often utilized to estimate prognosis and guide management, but there is little experience with a maximal exercise test performed 6 months after infarction to identify prognosis later in the convalescent period. The performance characteristics during an exercise test 6 months after myocardial infarction were related to the development of death, recurrent nonfatal myocardial infarction and coronary artery bypass surgery in the subsequent 12 months (that is, 6 to 18 months after infarction) in 473 patients. Mortality was significantly greater in patients who exhibited any of the following: inability to perform the exercise test because of cardiac limitations, the development of ST segment elevation of 1 mm or greater during the exercise test, an inadequate blood pressure response during exercise, the development of any ventricular premature depolarizations during exercise or the recovery period and inability to exercise beyond stage I of the modified Bruce protocol. By utilizing a combination of four high risk prognostic features from the exercise test, it was possible to stratify patients in terms of risk of mortality, from 1% if none of these features were present to 17% if three or four were present. Recurrent nonfatal myocardial infarction was predicted by an inability to perform the exercise test because of cardiac limitations, but not by any characteristics of exercise test performance. Coronary artery bypass surgery was associated with the development of ST segment depression of 1 mm or greater during the exercise test. Although clinical evidence of angina and heart failure 6 months after infarction was predictive of subsequent mortality among all survivors, among the low risk group without severely limiting cardiac disease, the exercise test provided unique prognostic information not available from clinical assessment alone. Therefore, a maximal exercise test performed 6 months after myocardial infarction is a valuable, noninvasive tool to evaluate prognosis. It provides information that is independent of and additive to clinical evaluation performed at the same time.

Abrupt withdrawal of beta-blockade therapy in patients with myocardial infarction: effects on infarct size, left ventricular function, and hospital course.

The effects of abrupt withdrawal or continuation of beta-blockade therapy during acute myocardial infarction were evaluated in 326 patients participating in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Thirty-nine patients previously receiving a beta-blocker and randomly selected for withdrawal of beta-blockers and placebo treatment during infarction (group 1) were compared with 272 patients previously untreated with beta-blockers who were also randomly assigned to placebo therapy (group 2). There were no significant differences between the two groups in MB creatine kinase isoenzyme (15.8 +/- 10.9 vs 18.2 +/- 14.4 g-eq/m2, respectively) estimates of infarct size, radionuclide-determined left ventricular ejection fractions within 18 hr of infarction (0.44 +/- 0.15 vs 0.47 +/- 0.16) or 10 days later (0.42 +/- 0.14 vs 0.47 +/- 0.16), creatine kinase-determined incidence of infarct extension (13% vs 6%), congestive heart failure (43% vs 37%), nonfatal ventricular fibrillation (5% vs 7%), or in-hospital mortality (13% vs 9%). Patients in group 1 had more recurrent ischemic chest pain (p = .002) within the first 24 hr after infarction, but not thereafter. However, this did not appear to be related to a rebound increase in systolic blood pressure, heart rate, or double product. In a separate analysis, 20 propranolol-eligible group 1 patients randomly selected for withdrawal of beta-blockade (group 3) were compared with 15 patients randomly selected for continuation of prior beta-blockade therapy (group 4). This comparison yielded similar results. These data indicate that the beta-blockade withdrawal phenomenon is not a major clinical problem in patients with acute myocardial infarction. beta-Blockade therapy can be discontinued abruptly during acute myocardial infarction if clinically indicated.

A simplified method to predict occurrence of complete heart block during acute myocardial infarction.

Data were analyzed from 698 patients with proved acute myocardial infarction (AMI) to develop a method to predict the occurrence of complete heart block (CHB). The presence of electrocardiographic abnormalities of atrioventricular or intraventricular conduction during hospitalization was determined for each patient. The electrocardiographic risk factors considered were: first-degree atrioventricular block, Mobitz type I atrioventricular block, Mobitz type II atrioventricular block, left anterior hemiblock, left posterior hemiblock, right bundle branch block and left bundle branch block. A CHB risk score was developed that consisted of the sum of each patient's individual risk factors. CHB risk scores of 0, 1, 2 or 3 or more were associated with incidences of CHB of 1.2, 7.8, 25.0 and 36.4%, respectively. When applied to an independent AMI data base, as well as to the summed results of 6 previously reported series that identified predictors of CHB during AMI, a similar incremental risk of CHB as predicted by the risk score method was demonstrated.

Digoxin therapy and mortality after myocardial infarction. Experience in the MILIS Study.

Recent studies have led to controversy about whether long-term digoxin therapy after confirmed or suspected myocardial infarction increases mortality. We analyzed the mortality experience in 903 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size (MILIS). As in previous studies, the decision to treat or not to treat with digoxin was made by the patient's personal physician on the basis of the usual clinical indications. Cumulative mortality was 28 percent for the 281 digoxin-treated patients as compared with 11 percent for the 622 patients who did not receive digoxin (P less than 0.001; follow-up interval, six days to 36 months; mean, 25.1 months). However, patients treated with digoxin had more base-line characteristics predictive of mortality than did their counterparts. Adjustment for these differences with two separate applications of the Cox method yielded P values of 0.14 and 0.34 for tests of difference in mortality, providing no evidence for a significant excess mortality associated with digoxin. Thus, the findings in the MILIS population do not support the assertion that digoxin therapy is excessively hazardous after infarction, but the existence of an undetected harmful effect can only be excluded with a randomized study. Until the results of such a study are available, we recommend careful consideration of whether any treatment of ventricular dysfunction is actually needed, consideration of alternatives to digoxin therapy, and restriction of digoxin use to the subgroup of patients (with severe chronic congestive failure and a dilated left ventricle) previously shown to have a beneficial clinical response.

Electrocardiographic, enzymatic and scintigraphic criteria of acute myocardial infarction as determined from study of 726 patients (A MILIS Study).

Methods for detecting acute myocardial infarction (AMI) were compared in a prospective study of 726 patients with pain presumed to be caused by ischemia that lasted 30 minutes or longer and was associated with electrocardiographic changes (ST-segment deviation greater than or equal to 0.1 mV and/or new Q waves or left bundle branch block). Using MB-CK values of more than 12 IU/liter as the standard criterion for detection of AMI, 639 patients (88%) were judged to have AMI. Total plasma CK values, technetium-99m stannous pyrophosphate images 48 to 72 hours after admission, and serial 12-lead electrocardiograms over 10 days were analyzed by investigators blinded to other clinical and laboratory data. For detection of AMI, total CK, electrocardiograms (ECGs) and pyrophosphate imaging were all highly accurate and sensitive (total CK accuracy 97%, ECG 92%, pyrophosphate 88%; total CK sensitivity 98%, ECG 96% and pyrophosphate 91%). However, both pyrophosphate and ECG were less specific than total CK (p less than 0.01) (total CK specificity 89%, pyrophosphate 64% and ECG 59%). The sensitivity (p less than 0.05) and accuracy (p less than 0.01) of total CK and pyrophosphate for those patients with Q-wave development were slightly greater than for those in whom Q waves did not evolve. The ECG was less accurate (p less than 0.02) and pyrophosphate was less specific (p less than 0.04) in patients with prior MI compared with those with initial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Risk factors for sudden death after acute myocardial infarction: two-year follow-up.

The risk of sudden coronary death after myocardial infarction (MI) was assessed in 533 patients who survived 10 days after MI and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of multiple clinical and laboratory variables determined before hospital discharge revealed that frequent ventricular premature beats (VPBs) (greater than or equal to 10/hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction less than or equal to 0.40) were independently significant markers of risk for subsequent sudden death believed to be the result of a primary ventricular arrhythmia. The incidence of sudden death was 18% in patients with both LV dysfunction and frequent VPBs (11 times that of patients with neither of these findings). Seventy-nine percent of all sudden deaths occurred within 7 months after the index MI. In 280 survivors reclassified 6 months after MI with regard to the presence or absence of frequent VPBs and LV dysfunction, these risk factors could not be associated with sudden coronary death over a further follow-up period of up to 18 months; the overall incidence of sudden cardiac death was low (1.4%) after 6 months. Thus, the presence of frequent VPBs in association with LV dysfunction early after MI identifies patients at high risk for sudden death over the next 7 months.

Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients.

Over a 34.5-month period, all admissions to 5 university hospital coronary care units were screened for eligibility for the Multicenter Investigation of the Limitation of Infarct Size (MILIS), an ongoing study of the effects of hyaluronidase, propranolol and placebo on myocardial infarct (MI) size. Of 3,697 patients with greater than or equal to 30 minutes of discomfort that was thought to reflect myocardial ischemia who were assessed for the presence or absence of certain electrocardiographic abnormalities at the time of hospital admission, the electrocardiogram was considered predictive of acute MI if greater than or equal to 1 of the following abnormalities was present: new or presumably new Q waves (greater than or equal to 30 ms wide and 0.20 mV deep) in at least 2 of the 3 diaphragmatic leads (II, III, aVF), or in at least 2 of the 6 precordial leads (V1 to V6), or in I and aVL; new or presumably new ST-segment elevation or depression of greater than or equal to 0.10 mV in 1 of the same lead combinations; or complete left bundle branch block. In the screened population, the diagnostic sensitivity of the electrocardiographic criteria was 81%, whereas the overall infarct rate in the total population screened was 49%. The diagnostic specificity of these entry criteria was 69% and the predictive value 72%.(ABSTRACT TRUNCATED AT 250 WORDS)

Prediction of single versus multivessel disease following myocardial infarction using 201thallium scintigraphy and electrocardiographic stress testing.

We evaluated 50 patients who suffered a single myocardial infarction with graded electrocardiographic stress testing, 201thallium myocardial perfusion imaging and coronary angiography to assess the role of noninvasive indices as predictors of single versus multivessel coronary artery disease. Multivessel involvement was defined angiographically as the presence of two or more major coronary arteries with at least a 70% intraluminal diameter narrowing. Multivessel disease was defined scintigraphically as the presence of stress and/or redistribution perfusion defects in the distribution of more than one coronary artery. The results of stress electrocardiography were not useful in differentiating patients with single (9/16 positive) versus multivessel (22/34 positive) disease. The degree of exercise-induced ST-segment depression was also not helpful. Stress 201thallium imaging did offer limited additional information with correct predictions of multivessel disease in 21 of 26 patients. Predictions of single-vessel disease were accurate in 11 of 24 patients. Eleven of these 13 incorrect predictions of single-vessel disease were due to the relative insensitivity of the thallium stress image to perceive defect in the anterior wall when the left anterior descending artery had significant obstruction at catheterization. Further refinements of stress perfusion imaging are needed before this method can be used to reliably separate patients with single and multivessel disease after myocardial infarction.

Anatomic and prognostic significance of new T-wave inversion in unstable angina.

The significance of the development of new T-wave inversion was studied in 118 consecutive patients with unstable angina. The electrocardiograms during hospitalization in the coronary care unit were analyzed for occurrence of new T-wave inversion greater than or equal to 2 mm and correlated with findings at coronary angiography (73 patients) and at follow-up (112 patients). Twenty-nine patients had anterior T-wave inversion. Of these, 25 patients (86%) had greater than or equal to 70% diameter reduction of the left anterior descending (LAD) artery, compared with 11 (26%) of 42 patients without anterior T-wave inversion (p less than 0.001). The sensitivity of T-wave inversion for significant LAD stenosis was 69%, specificity 89%, and positive predictive value 86%. Two patients had T-wave inversion in the inferior leads. Both patients had significant right coronary artery disease, compared with 18 of 55 patients without inferior T-wave inversion (difference not significant [p = NS]. Seventy-one patients who were treated medically had 16 +/- 9 months' follow-up. Of 26 patients who had T-wave inversion, 10 (38%) had cardiac events, compared with 7 (16%) of the remaining 45 patients without T-wave inversion (p less than 0.05). Forty-one patients who had undergone coronary bypass surgery had 19 +/- 9 months' follow-up. Of 22 patients with T-wave inversion, 4 (18%) had cardiac events, compared with 2 (11%) of the remaining 19 patients without T-wave inversion (p = NS). Thus, development of new T-wave inversion greater than or equal to 2 mm in patients with unstable angina (1) is predictive of significant coronary artery stenosis, and (2) identifies a subgroup with poor prognosis when treated medically.

Enzymatic estimation of myocardial infarct size when early creatine kinase values are not available.

Estimates of myocardial infarct (MI) size based on plasma creatine kinase (CK) are used widely for prognosis and in the assessment of therapy designed to salvage ischemic myocardium. However, if the initial plasma CK activity is elevated, MI size will be underestimated. To determine the impact of loss of early CK values on estimates of MI size and to develop a procedure to compensate for it, estimates of MI size based on complete and incomplete MB and total CK time-activity curves from 120 patients (experimental group) were compared. Estimates of MI size based on data inclusion intervals beginning at 24, 12, 8, and 4 hours before peak CK were 11, 14, 23, and 47% smaller than values based on complete CK curves, but the correlation was good between complete and incomplete estimates of MI size at any given interval, with r values ranging from 0.91 to 0.98. The derived correction factors were then prospectively applied to a new population (n = 25) with complete CK curves to compensate for purposely omitted early CK values. The corrected estimates of MI size were within 7% of those based on the complete CK curves. Similar results were obtained for transmural and nontransmural and anterior or inferior MI. Thus, if peak plasma CK is known, underestimation of MI size can be compensated for despite the unavailability of early CK values. Since greater than 90% of patients present before plasma CK has reached its peak (24 hours), MI size can be obtained in nearly all patients. Thus, being able to correct for unavailable early CK values makes MI size a more widely applicable endpoint for use in clinical trials and patient management.

Management of unstable angina pectoris.

The diagnosis of unstable angina may be confirmed if an ECG taken during an episode of pain demonstrates ST-segment changes that resolve when the pain is relieved. An intra-aortic balloon device should be used in the rare patient who has recurrent episodes of ischemia despite maximum drug therapy. Coronary angiography should be performed as soon as possible after the device is inserted.

Diagnostic criteria for acute myocardial infarction in patients undergoing coronary artery bypass surgery.

Current techniques for diagnosing perioperative myocardial infarction were studied in 58 patients who underwent coronary bypass surgery. All patients had preoperative and postoperative ECGs and technetium-99m stannous pyrophosphate myocardial scintigrams; serum CK-MB was measured immediately after surgery and daily for 3 days. Postoperative bypass graft visualization and left ventriculography were performed before hospital discharge in every patient. Nine patients (16%) had new Q waves postoperatively. Five of these nine patients had positive pyrophosphate scintigrams, postive CK-MB and new wall motion abnormalities, and the remaining four had negative CK-MB, negative phyrophosphate scintigrams and no new wall motion abnormalities. Seven patients (12%) had newly positive postoperative pyrophosphate scintigrams, positive CK-MB and new wall motion abnormalities on postoperative ventriculography, but only four had new Q waves postoperatively. Eight patients (14%) had new wall motion abnormalities; seven had positive pyrophosphate scintigrams and all had positive CK-MB, but only five had new Q waves. Sixteen patients (28%) had positive CK-MB, including all patients with either positive pyrophosphate scintigrams or new wall motion abnormalities, Eight patients had positive CK-MB without other evidence of perioperative infarction. A newly positive postoperative pyrophosphate scintigram is more senstive and specific than the development of new postoperative Q waves for the diagnosis of hemodynamically significatn perioperative myocardial in farction. CK-MB is highly sensitive, but too nonspecific to be useful for the diagnosis of perioperative infarction.

Coronary ostial stenosis following aortic valve replacement without continuous coronary perfusion.

The development of coronary ostial stenosis following aortic valve replacement has been attributed to intraoperative trauma to the coronary vessels during continuous coronary perfusion. We describe two patients with this lesion in whom continuous coronary perfusion was not used during aortic valve replacement. Both patients were successfully treated with saphenous vein bypass grafting. Intraoperative observation of the aortic root at the time of the bypass operation in one case revealed the left coronary ostium to be pinpoint in size and involved in a dense fibrous reaction extending up from the sewing ring of the prosthesis. The findings in these cases support the hypothesis that coronary ostial stenosis following aortic valve replacement may be due to a fibrous reaction in the aortic root secondary to turbulent flow through the aortic prosthesis.

Treatment of variant angina pectoris with perhexilene maleate.

Three patients with variant angina pectoris resistant to therapy with nitrates and propranolol were treated with perhexilene maleate. Two patients had normal coronary arteries with documented coronary artery spasm, while the third patient had a fixed coronary artery obstruction. In all three patients, attacks of variant angina pectoris disappeared following institution of therapy with perhexilene maleate. When the dose of this drug was decreased to 100 mg per day or less, symptoms reappeared in all patients. Reinstitution of therapeutic doses of perhexilene maleate once again resulted in complete control of symptoms. Perhexilene maleate is therefore a useful agent for the treatment of variant angina pectoris.

Right ventricular infarction.

Serial hemodynamic measurements were made in a patient with a massive infarction of the right ventricle complicated by cardiogenic shock, right ventricular failure, and tricuspid insufficiency. A favorable hemodynamic response was obtained by reducing afterload with administration of sodium nitroferricyanide (nitroprusside) while maintaining preload with infusion of fluids.

Favorable effects of hyaluronidase on electrocardiographic evidence of necrosis in patients with acute myocardial infarction.

To evaluate hyaluronidase's effect in reducing post-infarction myocardial necrosis, we randomized 91 patients with anterior infarction to control (45) or to hyaluronidase-treatment (46) groups. A 35-lead precordial electrocardiogram was recorded on admission and seven days later. Hyaluronidase was administered intravenously after the first electrocardiogram and every six hours for 48 hours. QRS-complex changes were analyzed to assess the drug's effect. Precordial sites with ST-segment elevation (larger than or equal to 0.15 mV) on the initial electrocardiogram that retained an R wave were considered vulnerable for the development of electrocardiographic signs of necrosis. The sum of R-wave voltages of vulnerable sites fell more in the control group than in the hyaluronidase group (70.9 +/- 3.6 per cent [+/- 1 S.E.M.] vs 54.2 +/- 5.0 per cent P less than 0.01). Q waves appeared in 59.3 +/- 4.9 per cent of the vulnerable sites in control versus 46.4 +/- 4.9 per cent in hyaluronidase-treated patients (P less than 0.05). Thus, hyaluronidase reduced the frequency of electrocardiographic signs of myocardial necrosis.

Cavernous hemangioma of the right atrium: presumptive diagnosis by coronary angiography.

The angiographic findings in a patient with an interesting vascular tumor of the right atrium are described. The tumor was supplied by vessels from both the right and left coronary arteries and consisted of dilated blood spaces in which contrast material persisted for a prolonged period of time.