Previous Inferior Myocardial Infarction Research Articles

Body surface mapping of high-frequency components in the terminal portion during QRS complex for the prediction of ventricular tachycardia in patients with previous myocardial infarction.

To study the clinical significance of terminal QRS high-frequency components for the prediction of ventricular tachycardia, an 87-lead body surface signal-averaged mapping was performed in 21 healthy subjects (control) and in 41 patients with previous myocardial infarction (anterior, 20; inferior, 21). Mapping data were analyzed and averaged (129.7 +/- 26.5 beats) for 160 seconds, and the signal-averaged beat was filtered with a bidirectional bandwidth (80-250 Hz) digital filter. J-point was determined from the 87-lead RMS voltage of nonfiltered QRS. For each lead, we calculated the sum of the absolute value of filtered QRS from 20 msec ahead of the J-point to the J-point (A-20). The body surface distribution of A-20 was expressed as A-20 map. The maxima in A-20 maps were mainly located on the upper sternal region in healthy subjects, on the left anterior chest in patients with previous anterior myocardial infarction, and on the central anterior chest in patients with previous inferior myocardial infarction. In the patients in both the group with anterior myocardial infarction and the group with inferior myocardial infarction, the value of maximum was significantly greater than in the subjects in the control group (0.181 +/- 0.086 and 0.138 +/- 0.048, respectively, vs. 0.075 +/- 0.031 mV.msec; p less than 0.01). In patients with myocardial infarction (n = 41), the value of maximum was significantly greater with ventricular tachycardia (n = 11) than without ventricular tachycardia (n = 30) (0.240 +/- 0.076 vs. 0.130 +/- 0.043 mV.msec; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical significance of exercise-induced ST segment changes in patients with previous inferior myocardial infarction

To investigate the clinical significance of exercise-induced ST changes, we performed exercise body surface mapping (87 leads) in 52 patients (one-vessel disease [1 VD] n = 12, multivessel disease [MVD] n = 40) with previous inferior myocardial infarction (MI). ST isointegral maps were constructed and the locations of ST changes were compared with the findings of exercise thallium-201 (TI-201) myocardial scanning. Exercise-induced ST elevation was observed in 14 patients (27%) on the lower chest and on the back, corresponding to the infarcted area. Exercise-induced ST depression was observed more frequently in the MVD group ( n = 30, 75%) than in the 1VD group ( n = 2, 17%). Seventeen (77%) of 22 patients with ST depression had thallium-201 redistribution. There was a significant association between ST depression and TI-201 redistribution ( χ 2 = 13.1, p < 0.001), but no association between ST depression and ST elevation. The body surface distribution of ST depression was shifted upward and rightward compared with its appearance in angina pectoris without MI. These findings suggest that exercise-induced ST depression reflects myocardial ischemia in patients with previous inferior MI.

The significance of bundle branch block in the immediate postoperative electrocardiograms of patients undergoing coronary artery bypass

Three hundred sixteen consecutive patients undergoing coronary artery bypass were studied for postoperative electrocardiographic conduction disturbances. Fifty-five of these 316 patients had postoperative bundle branch block (Group 1). This group had a higher incidence of left main coronary stenosis, together with previous inferior myocardial infarction, than patients without postoperative conduction disturbances (Group 2). Perioperative myocardial infarction, low cardiac output, and death were significantly more common in Group 1 than in Group 2: 7.3% versus 1.9% for perioperative myocardial infarction, 16.4% versus 2.7% for low cardiac output, and 5.5% versus 0.8% for death. Analysis of the type of conduction disturbances indicates that the presence of a new complete left bundle branch block postoperatively in a patient undergoing coronary artery bypass is a sign of intraoperative myocardial damage. This damage is potentially lethal, especially in a patient with left main coronary stenosis and previous inferior myocardial infarction.

Relationships between single-vessel coronary artery obstructions and wall motion dysfunction analyzed by four computer-based methods

We analyzed regional wall motion in 238 patients by using cineangiograms recorded in the 30° right anterior oblique projection. The sample was divided into three groups: a normal group ( n = 71), a group with isolated obstruction of the left anterior descending coronary artery and previous anterior myocardial infarction ( n = 85), and a group with isolated obstruction of the right coronary artery and previous inferior myocardial infarction ( n = 82). Both anterior and inferior groups also had motion abnormality within the corresponding anterior or inferior wall as judged by the qualitative analysis of cineangiograms. Four quantitative methods were compared: a long axis method and a center of mass method using internal reference systems, a method derived from the Stanford model and an area-based method using external reference systems. Normal regional values were determined from the normal group to evaluate the specificity and sensitivity of the methods. The area-based method was the most sensitive in the anterior infarction group, whereas the center of mass method was the most sensitive in the inferior infarction group. We conclude that there is no evidence that any method, among those tested, is superior to others for every expected location of wall motion abnormality.

Surgical management of refractory ventricular arrhythmias in patients with prior inferior myocardial infarction: A preliminary report

Most reports of operations for ventricular arrhythmia have dealt with patients with anterior myocardial infarction. Patients with previous remote inferior myocardial infarction and recurrent ventricular tachycardia or fibrillation are a difficult subset of patients to treat with surgical ablative procedures. Over a 2 year period, 11 patients with prior inferior myocardial infarction and drug-refractory ventricular tachycardia or fibrillation underwent elective operation to control the arrhythmia. Five patients had monomorphic ventricular tachycardia. Three of these five patients had localized endocardial resection and/or cryoablative procedures when the ventricular tachycardia was well localized intraoperatively. In the remaining two patients, ventricular tachycardia was noninducible intraoperatively, and the patients underwent extensive endocardial resection and mitral valve replacement because of sites suspected near the posterior papillary muscle from preoperative catheter mapping. None of these five patients had inducible ventricular tachycardia postoperatively, and all are clinically free of the arrhythmia over a 24 month follow-up period. One patient with two morphologies of ventricular tachycardia previously had an unsuccessful blind endocardial resection. She underwent map-directed cryoablation of both sites of ventricular tachycardia. Postoperatively, the patient was free of inducible arrhythmia and has been asymptomatic over 8 months. Five patients had pleomorphic ventricular tachycardia or fibrillation that could not be electrically localized. One patient with ventricular fibrillation underwent extensive endocardial resection, but the posterior papillary muscle was spared. Postoperative electrophysiological study was positive. The patient has had no clinical ventricular arrhythmias on a regimen of amiodarone, however. Two patients had extensive endocardial resection and mitral valve replacement. One died early in the postoperative course and the other is clinically well. The remaining two patients had an encircling endocardial ventriculotomy. Both are clinically stable although one had inducible ventricular fibrillation postoperatively. We conclude that well-defined monomorphic ventricular tachycardia in patients with a previous inferior myocardial infarction can be successfully treated with localized endocardial resection and/or cryoablation. However, patients with poorly localized monomorphic ventricular tachycardia or pleomorphic ventricular tachycardia or fibrillation may require more extensive procedures. The role of posterior papillary muscle sacrifice with mitral valve replacement remains undefined.(ABSTRACT TRUNCATED AT 400 WORDS)

Chronic effects of myocardial infarction on right ventricular function: A noninvasive assessment

To assess the chronic effects of myocardial infarction on right ventricular function, 48 subjects were studied utilizing radionuclide angiography and two-dimensional echocardiography. Ten were normal subjects (group I), 11 had previous inferior wall myocardial infarction (group II), 10 had previous anteroseptal infarction (group III), 11 had combined anteroseptal and inferior infarction (group IV) and 6 had extensive anterolateral infarction (group V). The mean (+/- standard deviation) left ventricular ejection fraction was 0.66 +/- 0.03 in group I, 0.58 +/- 0.02 in group II, 0.52 +/- 0.02 in group III, 0.33 +/- 0.03 in group IV and 0.33 +/- 0.01 in group V. No systematic correlation between left and right ventricular ejection fraction was observed among the groups. The mean right ventricular ejection fraction was significantly reduced in the presence of inferior myocardial infarction (0.30 +/- 0.03 in group II and 0.29 +/- 0.03 in group IV compared with 0.43 +/- 0.02 in group I [p less than 0.001]). The group II and IV patients also had increased (p less than 0.001) right ventricular end-diastolic area and decreased (p less than 0.001) right ventricular free wall motion by two-dimensional echocardiography. In the presence of anteroseptal infarction (group III), right ventricular free wall motion was increased (p less than 0.05) compared with normal subjects (group I). Thus, the effects of prior myocardial infarction on right ventricular function depend more on the location of infarction than on the extent of left ventricular dysfunction. Inferior infarction was commonly associated with reduced right ventricular ejection fraction and increased right ventricular end-diastolic area. The right ventricular free wall excursion was increased in the presence of anteroseptal infarction, suggested loss of contribution of interventricular septal contraction to right ventricular ejection.

Right ventricular ejection fraction: An indicator of increased mortality in patients with congestive heart failure associated with coronary artery disease

The predictive value of radionuclide ventriculography was studied in 34 patients with depressed left ventricular ejection fraction (less than 40%) and clinically evident congestive heart failure secondary to atherosclerotic coronary artery disease. In addition to left ventricular ejection fraction, right ventricular ejection fraction and extent of left ventricular paradox were obtained in an attempt to identify a subgroup at increased risk of mortality during the ensuing months. The 16 patients who were alive after a 2 year follow-up period had a higher right ventricular ejection fraction and less extensive left ventricular dyskinesia. When a right ventricular ejection fraction of less than 35% was used as a discriminant, mortality was significantly greater among the 21 patients with a depressed right ventricular ejection fraction (71 versus 23%), a finding confirmed by a life table analysis. Depressed right ventricular function was further linked to more severely compromised left ventricular function, as confirmed by a greater reduction in left ventricular ejection fraction and by an increased extent of left ventricular dyskinesia. These patients had a greater prevalence of chronic obstructive pulmonary disease and previous inferior myocardial infarction but the differences between groups were not statistically significant. It appears that the multiple factors contributing to the reduction in right ventricular ejection fraction make it a useful index not only for assessing biventricular function, but also for predicting patient outcome.

Thallium-201 Scintigraphy for Detection of Multivessel Disease in Patients with Prior Inferior Myocardial Infarction

In order to compare the effectiveness of thallium-201 (201Tl) myocardial perfusion scintigraphy and the exercise electrocardiogram for identifying patients with multivessel coronary artery disease, these noninvasive tests and coronary arteriography were performed in 89 patients with prior inferior wall myocardial infarction. Eighty patients performed an adequate exercise test (angina, ST-segment depression or achievement of 85 percent maximum age-predicted heart rate). Of these 80 patients, coronary angiography documented multivessel disease in 57 and single-vessel disease in the remaining 23. Of the 57 patients with multivessel disease, 203Tl correctly predicted multivessel disease in 58 percent and the exercise ECG was positive in 63 percent. Of the 23 patients with single vessel disease 201Tl was negative for multivessel disease in 91 percent, while the exercise ECG was negative in only 52 percent For detecting multivessel disease, combining the two tests increased the sensitivity to 82 percent, but decreased the specificity to 48 percent. The predictive value of positive 201Tl for multivessel disease was 94 percent as compared to 76 percent for the exercise ECG. Thallium-201 identified disease of the left anterior descending vessel in only 33 percent of 42 patients with disease in this vessel. These data suggest that in patients with previous inferior myocardial infarction, both 201Tl and exercise ECG have limited clinical value for predicting multivessel disease. However, unlike exercise ECG, 201Tl is highly specific and, when positive (perfusion defects in more than one vascular segment), highly predictive for multivessel disease. In order to compare the effectiveness of thallium-201 (201Tl) myocardial perfusion scintigraphy and the exercise electrocardiogram for identifying patients with multivessel coronary artery disease, these noninvasive tests and coronary arteriography were performed in 89 patients with prior inferior wall myocardial infarction. Eighty patients performed an adequate exercise test (angina, ST-segment depression or achievement of 85 percent maximum age-predicted heart rate). Of these 80 patients, coronary angiography documented multivessel disease in 57 and single-vessel disease in the remaining 23. Of the 57 patients with multivessel disease, 203Tl correctly predicted multivessel disease in 58 percent and the exercise ECG was positive in 63 percent. Of the 23 patients with single vessel disease 201Tl was negative for multivessel disease in 91 percent, while the exercise ECG was negative in only 52 percent For detecting multivessel disease, combining the two tests increased the sensitivity to 82 percent, but decreased the specificity to 48 percent. The predictive value of positive 201Tl for multivessel disease was 94 percent as compared to 76 percent for the exercise ECG. Thallium-201 identified disease of the left anterior descending vessel in only 33 percent of 42 patients with disease in this vessel. These data suggest that in patients with previous inferior myocardial infarction, both 201Tl and exercise ECG have limited clinical value for predicting multivessel disease. However, unlike exercise ECG, 201Tl is highly specific and, when positive (perfusion defects in more than one vascular segment), highly predictive for multivessel disease.

Acute coronary occlusion with impending infarction as an angiographic complication relieved by a guide‐wire recanalization

In a 45 year old male patient with a history of previous inferior myocardial infarction and unstable angina pectoris, coronary angiography revealed two-vessel disease: a 60-70% lesion in the middle third of the LAD, and a 90% lesion in the middle third of the very large RCA. There was only a small akinetic segment in the posterobasal region of the left ventricle. During angiography total occlusion of the RCA occurred followed the clinical and electrocardiographic signs of impending inferior reinfarction. Recanalization of the occluded vessel was accomplished by using a guide-wire, which was passed through a Sones catheter, placed in the RCA. The patient's symptoms subsided and the electrocardiographic signs of acute ischemia reverted within eight minutes. Aortocoronary bypass surgery with revascularization of the LAD and RCA was performed within 3 hours after recanalization. Postoperatively there was no evidence of major tissue loss by enzyme or electrocardiographic criteria. Control angiography, performed on the ninth day postoperatively, revealed the graft to the RCA to be widely patent. Left ventricular function was unchanged. It is concluded, that the combined approach of early transluminal recanalization of the acutely occluded RCA followed by successful construction of a graft to this vessel, has averted necrosis of a major portion of the left ventricle. However, general use of this technique does not seem advisable at the present time.

Incidence of right ventricular asynergy in patients with coronary artery disease

The effects of coronary artery disease on patterns of left ventricular contractility have been thoroughly investigated. In contrast, little is known about the incidence of right ventricular dysfunction induced by this disease. To evaluate the frequency of right ventricular asynergy, biplane right ventricular cineangiograms were obtained in 26 patients. Seven segmental axes of shortening were analyzed in each end-systolic and end-diastolic frame and normalized as percent decrease (or increase) in axis from end-diastolic length. Of 26 patients, 8 (Group I) served as normal (control) subjects. The remaining 18 patients had significant coronary artery disease; 6 of these (Group II) had no significant disease of the right coronary artery, whereas 12 (Group III) had significant obstruction of this artery. Four patients in Group II had a previous anteroseptal myocardial infarction, and six in Group III had a previous inferior myocardial infarction. There was a progressive decrease in segmental axes of shortening from Group I to II and from Group II to II, but the decrease was not significant at the level P less than 0.01. Only one patient in Group II had frank dyskinetic segmental motion of the interventricular septum (this patient had had a previous anteroseptal myocardial infarction), whereas two patients in Group III had dyskinetic segmental motion of the free right ventricular wall (both had previous inferior myocardial infarction). Therefore, coronary artery disease seldom produces significant right ventricular asynergy. Abnormal septal motion is associated with previous anteroseptal myocardial infarction; however, dyskinetic motion of the free right ventricular wall occurs only in patients with a right coronary arterial lesion and previous inferior myocardial infarction.