Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphic evidence of adjacent posterolateral or inferoseptal involvement.

To investigate the myocardial perfusion correlates of precordial ST segment depression during acute inferior myocardial infarction, a rest thallium-201 scintigram and a closely timed 12 lead electrocardiogram were obtained within 6 hours of the onset of infarction in 44 patients admitted with their first acute inferior myocardial infarction. Thirty-six patients demonstrated precordial ST segment depression (group 1) and eight did not (group 2). A perfusion defect involving the inferior wall was present in all 44 patients. Additional perfusion defects of the adjacent posterolateral wall (n = 20), the ventricular septum (n = 9) or both (n = 6) were present in 35 of 36 patients from group 1 compared with only 1 of 8 patients from group 2 (p less than 0.001). There was no significant difference in the frequency of multivessel coronary artery disease or disease of the left anterior descending artery between group 1 and group 2 or between patients with and those without a thallium-201 perfusion defect involving the ventricular septum. Thus, precordial ST segment depression during an acute inferior myocardial infarction is associated with thallium-201 scintigraphic evidence of more extensive involvement of the adjacent posterolateral or inferoseptal myocardial segments, which probably reflects the extent and pattern of distribution of the artery of infarction, rather than the presence of coexistent multivessel coronary artery disease or disease of the left anterior descending artery.

Reverse redistribution of thallium-201: a sign of nontransmural myocardial infarction with patency of the infarct-related coronary artery.

The pattern of reverse redistribution on the day 10 poststreptokinase resting thallium-201 myocardial scintigrams is a common finding in patients who have undergone streptokinase therapy in evolving myocardial infarction. To investigate this phenomenon, 67 patients who underwent streptokinase therapy were studied pre- and 10 days poststreptokinase therapy resting thallium-201 studies, poststreptokinase therapy resting radionuclide ventriculography and coronary arteriography (60 of the 67 patients). Of the 67 patients, 50 (75%) showed the reverse redistribution pattern on the day 10 thallium-201 study (Group I), 9 (13%) had a nonreversible defect (Group II) and the remaining 8 (12%) had a normal study or showed a reversible defect (Group III). The reverse redistribution pattern was associated with patency of the infarct-related artery (100%), quantitative improvement in resting thallium-201 defect size from day 1 to day 10 study (94%) and normal or near normal wall motion on day 10 radionuclide ventriculography (80% of segments with marked and 54% of those with mild reverse redistribution). In contrast, nonreversible defects were associated with significantly less frequent patency of the infarct-related artery (67%, p = 0.01), improvement in defect size (11%, p less than 0.001) and normal or near normal wall motion (21%, p less than 0.05). Group III patients were similar to Group I with respect to these variables. The quantitated thallium-201 percent washout was higher in the regions with the reverse redistribution pattern (49 +/- 15%) compared with the contralateral normal zone (24 +/- 15%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Transient ischemic dilation of the left ventricle on stress thallium-201 scintigraphy: a marker of severe and extensive coronary artery disease.

On exercise thallium-201 scintigraphy, it has been noted that the size of the left ventricle is sometimes larger on the immediate poststress image than on the 4 hour redistribution image; this phenomenon has been termed transient ischemic dilation of the left ventricle. The angiographic correlates of this finding were assessed in 89 consecutive patients who underwent both stress-redistribution thallium-201 scintigraphy and coronary arteriography. A transient dilation ratio was determined by dividing the computer-derived left ventricular area of the immediate postexercise anterior image by the area of the 4 hour redistribution image. In patients with a normal coronary arteriogram or nonsignificant coronary stenoses (less than 50%), the transient dilation ratio was 1.02 +/- 0.05 and, therefore, an abnormal transient dilation ratio was defined as greater than 1.12 (mean + 2SD). The transient dilation ratio was insignificantly elevated in patients with noncritical coronary artery disease (50 to 89% stenosis) (1.05 +/- 0.05) and in patients with critical stenosis (greater than or equal to 90%) of only one coronary artery (1.05 +/- 0.05). In contrast, in patients with critical stenoses in two or three vessels, the transient dilation ratio was significantly elevated (1.12 +/- 0.08 and 1.17 +/- 0.09, respectively; p less than 0.05 compared with all other patient groups). An abnormal transient dilation ratio had a sensitivity of 60% and a specificity of 95% for identifying patients with multivessel critical stenosis and was more specific (p less than 0.05) than were other known markers of severe and extensive coronary artery disease, such as the presence of multiple perfusion defects or washout abnormalities, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term angiographic follow-up of coronary balloon angioplasty in patients with diabetes mellitus: a clue to the explanation of the results of the BARI study. Balloon Angioplasty Revascularization Investigation.

OBJECTIVES: We sought to compare the angiographic outcome of diabetic patients (treated with insulin or oral hypoglycemic agents) after successful coronary angioplasty with that in nondiabetic patients. The analysis included the outcome of the dilated (restenosis) and nondilated narrowings (disease progression). BACKGROUND: Recent data have confirmed that diabetes mellitus is an important risk factor for long-term adverse events. These adverse events are more common after balloon angioplasty than after bypass surgery (Bypass Angioplasty Revascularization Investigation [BARI]). METHODS: We examined retrospectively 353 coronary angiograms of 248 patients (55 diabetic, 193 nondiabetic) who were referred for diagnostic angiography >1 month after successful angioplasty (1.4 +/- 0.6 [mean +/- SD] repeat angiograms/patient). Restenosis and disease progression/regression were compared between groups by means of quantitative angiography. RESULTS: Baseline clinical and angiographic characteristics were similar in both groups. There was a nonsignificant trend for a higher restenosis rate of dilated narrowings in diabetic patients. There were no significant changes between diabetic and nondiabetic patients in the rates of progression and regression of narrowings that were not dilated during the initial angioplasty. The main difference was in the rate of appearance of new narrowings: There was a 22% increase in the number of narrowings on the follow-up angiogram in diabetic patients (38 new, 174 preexisting narrowings) compared with 12% (86 new, 734 preexisting narrowings) in nondiabetic patients (p < 0.004). Diabetes mellitus and the performance of angioplasty in the artery had an additive risk for development of new narrowings, which were identified in 15 (16.9%) of 89 arteries with and 16 (13.2%) of 121 without angioplasty in diabetic patients and in 42 (12.7%) of 331 arteries with and 38 (7.3%) of 518 without angioplasty in nondiabetic patients (p = 0.009). CONCLUSIONS: The combination of diabetes mellitus and an artery that was instrumented during balloon angioplasty is additive and increases the risk of formation of new narrowing in that artery. This finding may explain the high adverse event rates observed in diabetic patients in the angioplasty arm of the BARI study, most of whom had angioplasty performed in at least two arteries.

Early treatment of acute myocardial infarction with intravenous streptokinase. A high-risk syndrome.

Fifty-one successive patients treated with intravenous streptokinase 1.7 +/- 0.8 (mean +/- SD) hours after onset of symptoms of acute myocardial infarction were evaluated during a three-month posthospital follow-up period. Coronary angiography was performed four to nine days after the initial hospital admission. Twenty-eight patients had a second late angiogram. Forty-one patients had successful reperfusion but only 25% of all patients were without significant clinical cardiovascular manifestations during this period. Postmyocardial infarction angina pectoris occurred in 21 patients, an abnormal stress test result was present in 28 patients, eight patients developed congestive heart failure, and five patients had reinfarction. An intervention with percutaneous transluminal coronary angioplasty or coronary artery bypass graft was performed in 15 (37%) of 41 reperfused patients. A significantly higher intervention rate was present in patients treated with streptokinase within one hour following the onset of symptoms. Early reocclusion (within three months of the infarct) was noted in patients with 60% or more residual stenosis in their infarct-related coronary artery. These patients also had a significantly greater incidence of angina pectoris. Our findings indicate that early thrombolytic therapy of acute myocardial infarction preserves myocardium, and since the infarct-related artery is patent, but narrowed, the jeopardized area is responsible for a high-risk syndrome with an increased likelihood of ischemic symptoms. An early aggressive approach may be indicated, especially for patients with greater than 60% residual stenosis in their infarct-related coronary artery.

Combined isoproterenol and epinephrine for the resuscitation of patients with cardiac asystole secondary to coronary artery disease.

In summary, the use of isoproterenol as an adjuvant to epinephrine in asystolic patients may increase the likelihood of return of spontaneous circulation.

Left ventricular volumes and function during atrial pacing in coronary artery disease: a radionuclide angiographic study.

This study set out to determine the pathophysiologic changes in the left ventricle during atrial pacing in 22 patients with coronary artery disease. Graduated right atrial pacing to a rate of 160 beats/min, or the induction of angina pectoris or significant ST depression was undertaken. Ventricular volumes were measured at rest and at rates of 100, 120, 140 and 160 beats/min using radionuclide angiography. The volumes at a pacing rate of 100 beats/min were used as a reference standard (100%). In the 22 patients with coronary artery disease, left ventricular end-diastolic volume decreased from 118 +/- 3% at rest to 80 +/- 5% at a rate of 160 beats/min; stroke volume from 121 +/- 3% to 54 +/- 5%; and ejection fraction (EF) from 49 +/- 3% to 37 +/- 5%. End-systolic volume decreased from 118 +/- 4% at rest, reached its minimal value of 94 +/- 5% at a rate of 120 beats/min and then increased slightly to 106 +/- 9% at 160 beats/min. Cardiac output and blood pressure did not change significantly. Compared to the control group of 10 normal subjects, the patients had a significantly smaller decrease in end-diastolic volume and end-systolic volume than in normal control subjects. EF in the normal subjects did not change. Blood pressure, cardiac output and stroke volume were similar in both groups. Atrial pacing tachycardia induced reversible ventricular dysfunction with a decrease in EF. Stroke volume was maintained because of relative ventricular dilatation.

Partial resistance to anticoagulation after streptokinase treatment for acute myocardial infarction.

This study examines the response of 3 different groups of patients to anticoagulants: 50 patients previously treated with streptokinase for acute myocardial infarction (AMI) (group 1), 24 patients with AMI who had received anticoagulants without prior thrombolysis (group 2) and 11 subjects who received anticoagulants for noncoronary indications (group 3). No significant differences were detected between groups 2 and 3; therefore, they were combined for analysis. After streptokinase, patients required 37,755 +/- 1,516 (mean +/- standard error of the mean) U of heparin per day to achieve the desired activated partial thromboplastin time (APTT). The dosage was 30,294 +/- 1,089 U/day in patients without antecedent thrombolysis (p less than 0.001). Group 1 patients required 5 +/- 0.4 days until adequate anticoagulation was achieved, compared with 3 +/- 0.2 days in the control group (p = 0.01). Despite higher heparin requirements, group 1 patients had a lower APTT value than the other subjects (87 +/- 5 vs 101 +/- 6 seconds, p = 0.08). Group 1 patients required 5 +/- 0.3 days to reach anticoagulation with warfarin versus 4 +/- 0.2 days in groups 2 + 3 (p = 0.05). Comparison of groups 1 and 2 yielded similar, although smaller, differences. Patients treated with streptokinase for AMI seem to be partially resistant to anticoagulation, which may increase the risk of reocclusion.

Pituitary apoplexy as a first manifestation of pituitary adenomas following intensive thrombolytic and antithrombotic therapy.

Apoplexy of a previously asymptomatic pituitary macroadenoma may occur in the setting of intensive thrombolytic, antithrombotic, or anticoagulant therapy for acute myocardial infarction. Classic clinical findings may initially be nonspecific and a high index of suspicion is therefore required for early diagnosis.

One-stage coronary angiography and angioplasty.

The combination of diagnostic angiography and angioplasty as a single procedure is becoming common practice in many institutions, but the feasibility and safety of this strategy have not been reported. This report describes 2,069 patients who underwent coronary angioplasty over a 3-year period at an institution where combined angiography and angioplasty is the norm. All patients were prepared before angiography for potential immediate angioplasty. In 1,719 patients, angioplasty was performed immediately after the diagnostic angiogram, while separate procedures were performed in 350 patients. Of those 350 patients, 254 were referred for angioplasty after diagnostic angiography at other hospitals. One thousand one hundred ninety-seven patients were admitted electively for treatment of stable angina pectoris, and 872 underwent procedures during hospitalization for unstable angina or acute myocardial infarction. One thousand nine hundred seven patients (92.2%) had successful angioplasties; in 130 patients (6.3%) the lesion could not be dilated, but no complication occurred, and in 32 patients (1.5%) angioplasty ended with a major complication (0.8% death, 1.0% Q-wave myocardial infarction, 0.5% emergency coronary artery bypass surgery). There was no difference between the combined and staged groups with regard to success, major and minor complication rates or in length of hospitalization after angioplasty. We conclude that routine combined strategy for angiography and angioplasty is feasible, safe, easier for the patient, and more cost-effective than 2 separate procedures.

Importance of early initiation of intravenous streptokinase therapy for acute myocardial infarction.

The importance of timing of intravenous streptokinase (SK) administration in patients with acute myocardial infarction (AMI) was evaluated. Intravenous SK, 750,000 U, was administered within 4 hours of the onset of ischemic chest pain to 72 consecutive patients having their first AMI. Six days later, cardiac catheterization was performed to calculate global ejection fraction (EF), and computer-derived infarct-related regional EF and dysfunction index were also determined; electrocardiograms were recorded, from which QRS scores could be calculated to estimate infarct size. Of 19 patients who had an anterior AMI, 12 (63%) who received intravenous SK within 2 hours after onset of pain sustained only minimal damage in terms of global EF, infarct-related EF, dysfunction index and QRS score. All 10 patients who received SK 2 to 4 hours after pain onset had large infarcts (p less than 0.001). Of the former group, 11 of 12 patients (91%) whose pain was relieved within 1.5 hours of intravenous SK administration (presumably due to successful reperfusion) had a good outcome, whereas all 7 whose pain lasted longer did poorly (p less than 0.001). Furthermore, among patients with anterior AMI, 11 of 14 (79%) whose pain was relieved within 3.5 hours of onset had small infarcts, compared with none of the 12 patients whose pain lasted longer (p less than 0.0001). In inferior AMI, the critical time between onset of pain and initiation of intravenous SK was 1.5 hours (p less than 0.05). The timing of initiation of thrombolytic therapy and the total pain duration are critical in determining outcome in AMI, and time intervals vary depending on infarct localization.

Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction.

Sixty-one patients with inferior acute myocardial infarction (AMI) and no evidence of prior AMI were studied to determine which factors influence the magnitude of precordial ST-segment depression. In the total study group, there was a significant but weak correlation between the magnitude of precordial ST-segment depression and the magnitude of inferior ST-segment elevation (r = -0.46, p less than 0.001). In the 29 patients with evidence of concomitant right ventricular (RV) involvement, precordial ST-segment depression was significantly smaller both in absolute terms (-1.3 +/- 1.8 vs -2.8 +/- 1.9 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -0.2 +/- 1.0 vs -1.1 +/- 0.5, p less than 0.01), whereas in the 15 patients with lateral ST-segment elevation (greater than or equal to 1 mm in lead V6), precordial ST-segment depression was significantly greater both in absolute terms (-3.5 +/- 2.3 vs -1.6 +/- 1.7 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -1.1 +/- 0.8 vs -0.5 +/- 0.9, p less than 0.02). Consistent with these findings, the correlation between the magnitudes of precordial and inferior ST-segment deviations was considerably improved when only the 24 patients with neither evidence of RV involvement nor lateral ST-segment elevation were analyzed (r = 0.89, p less than 0.001, n = 24). These data suggest that in patients with inferior AMI, there is a reciprocal relation between precordial and inferior ST-segment deviations, which is distorted by concomitant RV involvement and by concomitant lateral left ventricular wall involvement.

The effect of prolonged hypothermia on cardiac function in a young patient with accidental hypothermia.

A 20-year-old man had accidental, prolonged, and severe hypothermia. Serial radionuclide ventriculography disclosed reduced myocardial contractility during hypothermia that resolved after warming. The effects of hypothermia on cardiac function are discussed.

Scorpion sting-induced pulmonary edema. Scintigraphic evidence of cardiac dysfunction.

We report two cases of pulmonary edema due to scorpion sting. Radionuclide ventriculography (MUGA scan) showed localized cardiac dysfunction. The cardiac injury induced by the scorpion venom persisted for a prolonged period.

Evidence of prolonged myocardial dysfunction in heat stroke.

Heat stroke is a life-threatening syndrome of multi-organ dysfunction caused by elevated body temperature. It may result from failure of the thermoregulatory mechanisms or from inadequate heat dissipation and affects members of several risk groups. A number of authors reported cardiac involvement in heat stroke, but heart failure rarely has been documented. We report the cases of two heat stroke victims, one of whom developed pulmonary edema and the other, peripheral edema. In both, RVG demonstrated dilatation and diffuse hypokinesis of the right ventricle, which persisted for several weeks. We conclude that the heart may be involved in heat stroke and that heart failure is a potential complication of the syndrome that can have a prolonged subclinical course. Fluid replacement in heat stroke should be done under careful observation, which may be facilitated by noninvasive assessment of cardiac function.

Systemic embolization following thrombolytic therapy for acute myocardial infarction.

We describe a patient with acute inferior myocardial infarction who developed a "saddle" aortic embolus during streptokinase infusion. Three months previously, this patient had sustained an anterior infarction, and an apical aneurysm was found. This patient's embolus had most probably originated from a left ventricular mural thrombus that had been dislodged by streptokinase. As fibrinolytic treatment is gaining wide acceptance, physicians should be aware of this rare, but possible, complication.

The use of thallium 201 myocardial imaging to exclude myocardial infarction after dissection in congenital coarctation of the aorta.

The use of a mobile gamma camera with thallium 201 myocardial imaging is described to exclude myocardial infarction in a patient admitted to the coronary care unit in shock and with clinical, enzyme, and ECG changes consistent with infarction. The patient suffered from acute aortic dissection associated with congenital coarctation of the aorta. The myocardial scan excluded transmural myocardial injury.

Diagnosis of coronary artery disease by multigated radionuclide angiography during right atrial pacing.

Right atrial pacing in conjunction with radionuclide angiography was used as a method to augment gradually myocardial oxygen demand in seven normal subjects and 11 patients with angiographically documented coronary artery disease (CAD). In five of the seven normal subjects the ECG during atrial pacing was normal and falsely pathologic in the two others; in all seven the ejection fraction (64 +/- 8 percent) did not change during the pacing. The atrial pacing was positive in seven of the eleven patients with CAD and falsely negative in four. In comparison, nine of these patients had more than 15 percent reduction in ejection fraction, while only two were regarded as negative. A maximal decrease of 31 percent in the average ejection fraction was observed in CAD patients at a pacing rate of 160/min. Wall motion pattern remained normal in all seven normal subjects, while new wall motion abnormalities developed during the atrial pacing in nine of the 11 CAD patients. We concluded that changes in ejection fraction induced by atrial pacing are sensitive indicators of myocardial ischemia. In patients with CAD, ejection fraction falls during pacing compared with normal subjects in whom ejection fraction remains unchanged.

Cardiac rupture and ventricular septal defect in isolated right coronary artery disease.

A patient is described who had both ventricular septal defect and then cardiac rupture with death within 24 hours of the onset of acute posteroinferior myocardial infarction. At autopsy he was found to have single-vessel disease involving the right coronary artery. Isolated disease of the right coronary artery can produce unexpected, fatal mechanical complications.

Prehospital coronary thrombolysis. A new strategy in acute myocardial infarction.

Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of prehospital intravenous streptokinase given by a physician-operated mobile intensive care unit. The 29 prehospital-treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase inhospital. Patients receiving streptokinase in the prehospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase inhospital in terms of peak creatinine phosphokinase, ejection fraction, computer-derived dysfunction index, and electrocardiographic QRS score. The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy. There were no major complications related to prehospital administration of streptokinase.