Measurement of myocardial infarction fraction using single photon emission computed tomography

Although infarct size correlates generally with prognosis after acute myocardial infarction, an absolute measure of infarct size may have differing prognostic significance depending on absolute left ventricular mass. To test the hypothesis that single photon emission computed tomography can accurately measure myocardial infarct size as a percent of total left ventricular mass ("infarction fraction"), thallium-201 and technetium-99m pyrophosphate tomograms were acquired in 21 dogs 24 to 48 hours after fixed occlusion of the left anterior descending or circumflex coronary artery. Pathologic infarct weight was measured as the myocardial mass that showed no staining with triphenyltetrazolium chloride. Scintigraphic infarct mass by technetium-99m pyrophosphate was calculated from the total number of left ventricular volume elements (voxels) demonstrating technetium-99m pyrophosphate uptake X voxel dimension [( 0.476 cm]3) X specific gravity of myocardium (1.05 g/cm3). Scintigraphic left ventricular mass was calculated in a similar fashion using an overlay of the thallium-201 and technetium-99m pyrophosphate scans. The "infarction fraction" was calculated as: infarction fraction = infarct mass/left ventricular mass. There was good correlation between single photon emission computed tomography and pathologic measurements of infarct mass (technetium-99m pyrophosphate mass = 1.01 X pathologic infarct mass + 0.96; r = 0.98), left ventricular mass (single photon emission computed tomographic left ventricular mass = 0.60 X pathologic left ventricular mass + 37.4; r = 0.86) and "infarction fraction" (single photon emission computed tomographic infarction fraction = 1.09 X pathologic infarction fraction - 1.7; r = 0.94).(ABSTRACT TRUNCATED AT 250 WORDS)     

Early estimation of acute myocardial infarct size soon after coronary reperfusion using emission computed tomography with technetium-99m pyrophosphate

Early appearance of positive findings on a technetium-99m pyrophosphate scan has been shown to be associated with the presence of a reperfused acute myocardial infarction (AMI). Early technetium-99m pyrophosphate imaging was performed by emission computed tomography to evaluate reperfusion and to test the feasibility of estimating infarct size soon after coronary reperfusion based on acute positive tomographic findings. Twenty-seven patients with transmural AMI who were treated with intracoronary urokinase infusion followed by percutaneous transluminal coronary angioplasty underwent pyrophosphate imaging 8.7 +/- 2.1 hours after the onset of AMI. None of the 8 patients in whom reperfusion was unsuccessful had acute positive findings. Of 19 patients in whom reperfusion was successful, 17 had acute positive findings (p less than 0.001). In these 17, tomographic infarct volumes were determined from reconstructed transaxial images. The threshold for areas of increased pyrophosphate uptake within the infarct was set at 60% of peak activity by the computerized edge-detection algorithm. The total number of pixels in all transaxial sections showing increased tracer uptake were added and multiplied by a size factor and 1.05 g/cm3 muscle to determine infarct volume. The correlations of tomographic infarct volumes with peak serum creatine kinase (CK) levels (r = 0.82) and with cumulative release of CK-MB isoenzyme (r = 0.89) were good. Moreover, the time to positive imaging was significantly shorter than that to peak CK level (8.5 +/- 2.3 vs 10.4 +/- 2.2 hours, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Emission computed tomography with technetium-99m pyrophosphate for delineating location and size of acute myocardial infarction in man.

Emission computed tomography with technetium-99m pyrophosphate was used to delineate the location and estimate the size of myocardial infarcts in 20 patients with documented acute myocardial infarction. Tomography was performed after planar imaging within 2-5 days after the onset of infarction. A series of transaxial, frontal, and sagittal tomograms were reconstructed from 32 views imaged from the left side of the patient's chest with a rotating gammacamera. Infarct volume was measured from the tomographic images by computerised planimetry and was compared with the cumulative release of creatine kinase MB isoenzyme. The planar images showed discrete myocardial uptake in 13 of the 20 patients and diffuse uptake throughout the cardiac region in the remaining seven. In contrast, the tomographic images clearly delineated discrete myocardial uptake by avoiding confusion of myocardial activity with that of surrounding structures, particularly bones, in all patients. For the 10 patients whose infarct size was assessed by analysis of the creatine kinase MB curve there was a close correlation between infarct volume estimated by tomography and by cumulative creatine kinase MB release. Thus emission computed tomography can provide a three dimensional map of technetium-99m pyrophosphate distribution within the heart and is thus able accurately to localise and estimate the size of myocardial infarcts in man.     

Prevalence of right ventricular involvement in inferior wall infarction assessed with myocardial imaging with thallium-201 and technetium-99m pyrophosphate.

To assess the prevalence and clinical relevance of right ventricular involvement in acute inferior wall infarction, 78 consecutive patients with the latter condition were studied with thallium-201 and technethium-99m pyrophosphate myocardial imaging. Right ventricular involvement was determined from superimposition of the 45 degree left anterior oblique thallium-201 and technetium-99m pyrophosphate images. All 78 patients shoed thallium-201 defects. Sixty-four patients had positive pyrophosphate scans, and 24 of these (37.5 percent) showed right ventricular involvement. None of the patients with right ventricular involvement in this consecutive series showed the classic signs of severe right ventricular failure, although subclinicalright ventricular dysfunction may have been present. There was no significant difference in the incidence of cardiogenic shock between the groups with and without right ventricular involvement. It is concluded that right ventricular involvement in acute inferior wall infarction is relatively frequent but not necessarily associated with severe right-sided pump failure. In patients with acute inferior wall infarction and severe pump failure, dual imaging provides a simple nonivasive method of identifying the subgroup of patients with right ventricular involvement who may benefit from volume loading.     

Measurement of myocardial infarct size by technetium pyrophosphate single-photon tomography

The primary determinant of prognosis after acute myocardial infarction (AMI) is the size of the acute infarct. The present study evaluates 46 patients with different infarct distributions and sizes to test the hypothesis that single photon emission computed tomography with technetium-99m pyrophosphate (Tc-99m-PPi) and blood pool overlay allows measurements of AMI size that provide insight into prognosis irrespective of infarct location. Identical Tc-99m-PPi and ungated blood pool projections were acquired over 180 degrees with a rotating gamma camera. Reconstructed sections were color-coded and superimposed for purposes of infarct localization. Areas of increased pyrophosphate uptake within myocardial infarcts were thresholded at 65% of peak activity. The blood pool was thresholded at 50% and subtracted so as to determine an endocardial border for the left ventricle. Using this method, myocardial infarcts weighed 2.5 to 81.2 g. The correlation of infarct mass with prognosis showed that patients without previous AMI and with acute infarcts that weighed more than 40 g had an increased frequency of death and congestive heart failure (p less than 0.001). The correlation of measured infarct mass with peak serum creatine kinase level was significant (r = 0.83, p less than 0.001; y = 0.015x + 13.20). The correlation coefficients for anterior, inferior and nontransmural AMI were not significantly different from those for the entire group. In conclusion, tomographically determined infarct mass data correlate with subsequent clinical prognosis, and Tc-99m-PPi tomography with blood pool overlay is a safe and effective means of sizing infarcts in patients with AMI.     

Myocardial scintigraphy with technetrium-99m pyrophosphate during the early phase of acute infarction.

To determine the sensitivity of myocardial scintigraphy with technetium-99m pyrophosphate during the early phase of acute myocardial infarction, 31 patients admitted to the coronary care unit with prolonged ischemic pain underwent imaging within 4 to 8 hours and again at 24 hours after the onset of symptoms. In 11 of 15 patients with documented acute myocardial infarction, increased focal myocardial uptake was demonstrated on early myocardial scintigraphy. Focal uptake was observed in only 2 of 16 patients with unstable angina pectoris. Three or four patients with normal early scintigrams had massive transmural myocardial infarction. Normal early scintigrams in these three patients may have reflected poor perfusion because the images were abnormal at 24 hours. In four patients the extent of technetium-99m pyrophosphate uptake increased more than 20 percent at 24 hours without other evidence of infarct extension. In the other seven patients, there was no significant change in the area of the abnormal radioactive uptake between early and delayed scintiscans. This study suggests that technetium-99m pyrophosphate scintigraphy can defect acute myocardial infarction as early as 4 hours after the onset of symptoms although the sensitivity rate (73 percent) is less than that at 24 hours.     

Early noninvasive detection of reperfusion and infarct by intravenous technetium 99m pyrophosphate scintigraphy following thrombolysis

To determine whether technetium-99-pyrophosphate accumulation immediately after intravenous thrombolysis can serve as a marker of reperfusion and infarct size, 17 patients with acute myocardial infarction were studied. Immediately after thrombolysis 10 mCi of technetium-99m pyrophosphate were injected intravenously. Coronary and left ventricular angiography were then performed in all patients, revealing patent coronary arteries in 13 patients. In all patients, 0.3 and 0.5 mCi of thallium-201 were injected into the right and left coronary artery, respectively, followed by planar scintigraphy. 6 patients with patent coronary arteries and a large thallium-201 defect had massive (more than one third of the cardiac silhouette) pyrophosphate accumulation (group A), whereas 7 patients with a small or no thallium-201 defect in the presence of a patent infarct artery had either focal or no pyrophosphate accumulation (group B). In contrast, 4 patients with an occluded infarct artery showed no acute pyrophosphate uptake despite a large thallium-201 defect (group C). Emission computed tomography confirmed the planar scintigraphic data in group A patients and revealed small thallium-201 defects and focal pyrophosphate accumulation in group B patients with negative planar scintigrams. Global and regional ejection fractions in the infarct area, measured from the acute and follow-up left ventricular angiograms, were higher in group A than in group B and C patients. It is concluded that early intravenous technetium-99m pyrophosphate scintigraphy in patients with acute myocardial infarction undergoing intravenous thrombolysis may serve as an indicator of reperfusion and infarct size.     

Doughnut pattern of technetium-99m pyrophosphate myocardial uptake in patients with acute myocardial infarction: a sign of poor long-term prognosis.

Thirty survivors of acute myocardial infarction with 3+ or 4+ positive technetium-99m pyrophosphate myocardial scintigrams were followed up for 28 +/- 3.1 months (mean +/- standard deviation). Three patient groups were identified from the pattern of radioactive uptake in the scintigram: Group I, 16 patients with focal uptake (anterior in 7, lateral in 2, posterior in 3 and inferior in 4); Group II, 6 patients with anterior myocardial infarction and a doughnut pattern of uptake; Group III, 8 patients with nontransmural myocardial infarction and a diffuse pattern of uptake. Late complications developed in all patients with the doughnut pattern of uptake compared with 43 percent of patients with the focal pattern and 12 percent of patients with the diffuse pattern. After discharge from the hospital, five of six patients with a doughnut pattern of uptake died (mean survival time 9.8 months after the initial myocardial infarction). This mortality rate (83 percent) was significantly greater than that of patients with a focal (mortality rate 6 percent) or diffuse (no mortality) pattern of uptake. The doughnut pattern of technetium-99m pyrophosphate myocardial uptake in patients with acute myocardial infarction appears to identify a subgroup of patients with a very poor long-term prognosis.     

Detection of acute right ventricular infarction by right precordial electrocardiography

The value of 0.1 mV or greater of S-T segment elevation in at least one right precordial lead (V₄R to V₆R) in defining right ventricular myocardial infarction was assessed prospectively in 43 subjects (33 consecutive patients with enzymatically confirmed infarction of varying type and location, 4 patients with unstable angina and 6 healthy volunteers). Patients with acute myocardial infarction were studied with radionuclide ventriculography and technetium-99m stannous pyrophosphate myocardial scintigraphy 18.2 ± 14.3 (mean ± standard deviation) and 85.1 ± 18.0 hours after the onset of symptoms, respectively. Eleven patients (Group A: 9 patients with transmural inferior infarction, 1 with transmural inferolateral infarction and 1 with transmural anteroseptal infarction) demonstrated right precordial S-T segment elevation and 22 patients (Group B: 6 patients with transmural inferior infarction, 2 with transmural posterior infarction, 3 with transmural inferolateral infarction, 3 with transmural anteroseptal infarction, 3 with transmural extensive anterior infarction, 4 with subendocardial anterior infarction and 1 with unclassified infarction) did not. Right ventricular ejection fraction was significantly lower in Group A (0.47 ± 0.11) than in Group B (0.60 ± 0.12) (p < 0.01). Right ventricular total wall motion score was 63.8 ± 15.6 percent of normal in Group A versus 94.3 ± 8.5 percent in Group B (p < 0.001). Technetium-99m pyrophosphate uptake (2+ or greater) over the right ventricle occurred in nine patients (81.8 percent) in Group A and in one patient (4.5 percent) in Group B (p < 0.001). No patient with unstable angina and no healthy volunteer had S-T segment elevation in a right precordial lead. S-T segment elevation of 0.1 mV or greater in one or more of leads V₄R to V₆R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.     

Dual myocardial imaging with technetium-99m pyrophosphate and thallium-201 for detecting, localizing and sizing acute myocardial infarction.

In order to assess and compare the sensitivity and accuracy of technetium (Tc)-99m pyrophosphate and thallium-201 (Tl-201) in detecting, locating and sizing acute myocardial infarction with respect to the biochemically measured extent of infarction, myocardial imaging with both agents using a gamma scintillation camera was performed in 35 patients with documented acute myocardial infarction within 1 to 5 days after the onset of acute symptoms. Tc-99m pyrophosphate scintigrams were abnormal in 30 patients (86 percent) and the location of uptake corresponded to the electrocardiographic site of the infarct in 23 of the 30 patients (77 percent). The five negative Tc-99m pyrophosphate scintigrams included two from patients with a subendocardial infarction. By contrast, all 35 TI-201 myocardial images showed areas of decreased uptake and 33 (94 percent) corresponded to the electrocardiographic location of the infarct. In three patients with a prior myocardial infarction, separate defects were noted in addition to areas of decreased TI-201 uptake corresponding to new Q waves and ST-T wave changes. Additional abnormal areas in the scintigrams not suggested by the electrocardiogram were noted with Tc-99m pyrophosphate in 9 patients and with TI-201 in 16 patients; in 6 of these patients these areas were identical in extent and location in both radionuclide studies. In patients with negative Tc-99m pyrophosphate scintigrams, the average infarct size obtained from completed creatine kinase (CK) curves using serial serum CK values was smaller at 3.2 ± 0.5 (standard error) IU/literhour than in those with positive images (26.9 ± 4.1 IU/literhour; P <0.02). The planimetered area of Tc-99m pyrophosphate uptake that projected largest in one of the three views averaged 33.2 ± 4.6 cm² in patients with anterior or lateral infarction but only 18.9 ± 2.5 cm² (P <0.03) in patients with inferior infarction, whereas mean infarct size as assessed with CK values was not different in both groups. Correlation between infarct size as assessed with CK curve and area as assessed with Tc-99m pyrophosphate uptake was good (r = 0.90) in anterior infarctions but only fair (r = 0.64) in inferior infarctions.     

Abnormal technetium-99m pyrophosphate images in unstable angina: Ischemia versus infarction?

There is controversy concerning the specificity of myocardial infarct imaging with technetium-99m pyrophosphate due to the high frequency of false positive images, especially in patients with unstable angina. In this study technetium-99m pyrophosphate images were compared with frequent determinations of plasma creatine kinase, MB isoenzyme (MB CK) activity in 116 patients admitted with the diagnosis of unstable angina. It was hypothesized that frequent measurement of MB CK activity, a sensitive and specific marker for myocardial necrosis, using sensitive assay techniques would detect small amounts of myocardial necrosis which might have been unrecognized by conventional clinical methods. The scintigraphic results and isoenzyme determinations agreed in 88 percent of patients; both tests were normal in 69 percent and both were abnormal, indicating acute myocardial infarcation, in 19 percent of patients. In the remaining 14 patients (12 percent), the scans were abnormal, but MB CK activity was normal. In five of these patients (4 percent), abnormal scintigrams presumably reflected persistent scan positivity after previous myocardial infarction. Only the remaining nine patients (8 percent) could be classified as having unexplained false positive scans, a frequency substantially less than that reported by other investigators who based the diagnosis of myocardial infarction on conventional clinical criteria. These results suggest that abnormal technetium-99m pyrophosphate images in patients with unstable angina generally indicate myocardial necrosis.     

Predictors of infarct size after primary coronary angioplasty in acute myocardial infarction from pooled analysis from four contemporary trials

Determinates of infarct size in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) have been incompletely characterized, in part because of the limited sample size of previous studies. Databases therefore were pooled from 4 contemporary trials of primary or rescue PCI (EMERALD, COOL-MI, AMIHOT, and ICE-IT), in which the primary end point was infarct size assessed using technetium-99m sestamibi single-photon emission computed tomographic imaging, measured at the same core laboratory. Of 1,355 patients, infarct size was determined using technetium-99m sestamibi imaging in 1,199 patients (88.5%), at a mean time of 23 +/- 15 days. Median infarct size of the study population was 10% (interquartile range 0% to 23%; mean 14.9 +/- 16.1%). Using multiple linear regression analysis of 18 variables, left anterior descending infarct artery, baseline Thrombolysis In Myocardial Infarction grade 0/1 flow, male gender, and prolonged door-to-balloon time were powerful independent predictors of infarct size (all p <0.0001). Other independent correlates of infarct size were final Thrombolysis In Myocardial Infarction grade <3 flow (p = 0.0001), previous AMI (p = 0.005), symptom-onset-to-door time (p = 0.021), and rescue angioplasty (p = 0.026). In conclusion, anterior infarction, time to reperfusion, epicardial infarct artery patency before and after reperfusion, male gender, previous AMI, and failed thrombolytic therapy were important predictors of infarct size after angioplasty in patients with AMI assessed using technetium-99m sestamibi imaging and should be considered when planning future trials of investigational drugs or devices designed to enhance myocardial recovery.     

Quantitative estimation of infarct size by simultaneous dual radionuclide single photon emission computed tomography: comparison with peak serum creatine kinase activity.

To test the hypothesis that simultaneous dual energy single photon emission computed tomography (SPECT) with technetium-99m (99mTc) pyrophosphate and thallium-201 (201TI) can provide an accurate estimate of the size of myocardial infarction and to assess the correlation between infarct size and peak serum creatine kinase activity, 165 patients with acute myocardial infarction underwent SPECT 3.2 +/- 1.3 (SD) days after the onset of acute myocardial infarction. In the present study, the difference in the intensity of 99mTc-pyrophosphate accumulation was assumed to be attributable to difference in the volume of infarcted myocardium, and the infarct volume was corrected by the ratio of the myocardial activity to the osseous activity to quantify the intensity of 99mTc-pyrophosphate accumulation. The correlation of measured infarct volume with peak serum creatine kinase activity was significant (r = 0.60, p less than 0.01). There was also a significant linear correlation between the corrected infarct volume and peak serum creatine kinase activity (r = 0.71, p less than 0.01). Subgroup analysis showed a high correlation between corrected volume and peak creatine kinase activity in patients with anterior infarctions (r = 0.75, p less than 0.01) but a poor correlation in patients with inferior or posterior infarctions (r = 0.50, p less than 0.01). In both the early reperfusion and the no reperfusion groups, a good correlation was found between corrected infarct volume and peak serum creatine kinase activity (r = 0.76 and r = 0.76, respectively; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic value of a persistently positive technetium-99m stannous pyrophosphate myocardial scintigram after myocardial infarction.

Technetium-99m stannous pyrophosphate myocardial scintigrams were obtained in 138 clinically stable patients 32.7 +/- 47.3 weeks (range 6 to 260) after acute myocardial infarction. Of the 138 patients, 74 (54 percent) had a persistently positive scintigram. Patients with such a scintigram were more likely to have severe angina pectoris, compensated congestive heart failure, anterior location of acute myocardial infarction, Q waves and S-T segment elevation in the electrocardiograms, cardiomegaly, left ventricular dyssynergy (dyskinesia or global dyssynergy), and an ejection fraction of less than 50 percent. During a follow-up period of 11.6 +/- 6.9 months after scintigraphy, 42 percent of the patients with a persistently positive scintigram had either a cardiac death, a nonfatal myocardial infarction, unstable angina pectoris or decompensated congestive heart failure compared with 13 percent of the patients with a negative scintigram (P less than 0.001). Of the 14 patients with cardiac death, 13 (93 percent) had a persistently positive scintigram. A persistently positive scintigram not only was the best single predictor of cardiac death and combined end points, but also added significantly to the predictive ability of the other clinical variables, including age, location of acute myocardial infarct, clinical status, electrocardiographic findings, and chest X-ray findings. It is concluded that technetium-99m stannous pyrophosphate myocardial scintigraphy has prognostic value in patients after acute myocardial infarction.     

Measurement of myocardium at risk by technetium-99m sestamibi: correlation with coronary angiography.

Previous studies have shown that tomographic perfusion imaging with technetium-99m sestamibi (RP-30A) can accurately measure the myocardium at risk during acute myocardial infarction. The ability of coronary angiography to predict the wide variability in myocardium at risk was studied in 21 patients with their first acute myocardial infarction. In blinded fashion, two experienced angiographers provided an overall "best estimate" of the percent of left ventricular myocardium at risk considering multiple angiographic variables--infarct-related artery, location of stenosis (proximal or nonproximal), vessel diameter, length, territory and the number and size of proximal branches and collateral vessels. Many of these individual variables showed a significant association with myocardium at risk. The most important angiographic variable was the mean best estimate of the two angiographers (r = 0.89, p less than 0.0001). However, the SEE was large (8.6% of the left ventricle) and angiography significantly (p less than 0.002) overestimated myocardium at risk. When patients with an anterior or an inferior infarct were considered separately, the angiographic best estimate had a weaker correlation with myocardium at risk measured by technetium-99m sestamibi in patients in both groups (anterior infarction r = 0.65, p = 0.04; inferior infarction r = 0.65, p = 0.04. Seven patients with an inferior infarct and myocardium at risk ranging from 7% to 32% of the left ventricle had identical angiographic best estimates. Although angiographic estimates correlate closely with measurements of myocardium at risk in groups of patients, their ability to predict the myocardium at risk in individual patients is limited.     

Evaluation of a QRS scoring system for estimating myocardial infarct size. II. Correlation with quantitative anatomic findings for anterior infarcts

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricle was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices.The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V₂. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r = 0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.     

Right ventricular infarction: frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit

During a 14 month period autopsies were performed on 107 patients with coronary heart disease and the results were evaluated prospectively with special reference to right ventricular infarction. A total of 214 regional infarcts were found, 107 (50%) of which involved the right ventricle. Right ventricular infarction was found in 90 hearts (84%), but only three isolated right ventricular infarcts were seen. Right ventricular involvement was found with equal frequency in anterior and posterior infarction (64 versus 66%), but posterior right ventricular infarcts were much larger (15% of the right ventricle was infarcted versus 1%). Proximal right coronary artery occlusion caused larger right ventricular infarction than did distal occlusion (15 versus 5 g). Right ventricular infarct size was not influenced by coronary artery disease (evaluated angiographically) in noninfarct-related vessels. Anterior right ventricular infarcts were predominantly located near the apex of the heart (to the left of the sternum), whereas posterior right ventricular infarcts were located near the atrioventricular groove (along the right sternal border). Infarct size was equal in patients who died from a first acute anterior or posterior infarct. However, posterior infarcts had more right ventricular involvement (28% of total infarct size versus 7% in anterior infarcts) leaving more of the left ventricular myocardium intact (79 versus 64%). These differences in infarct topography may explain why right ventricular involvement seldom is diagnosed clinically in patients with anterior infarction, and why left ventricular function and prognosis usually are better after posterior compared with anterior infarcts of enzymatically equal size.     

New method of estimating myocardial infarct size using technetium-99m pyrophosphate and thallium-201 dual single photon emission computed tomography imaging

A new method was devised to estimate infarct size using dual single photon emission computed tomography with thallium-201 and technetium-99m pyrophosphate. Designating the ratio of infarct area to whole myocardial volume as %MI, the correlation of %MI with other markers of left ventricular dysfunction was examined: peak creatine kinase, ejection fraction and left ventricular asynergy. As %MI correlated well with these markers, it is considered that %MI will be useful for estimating infarct size and predicting the severity of left ventricular dysfunction in the early stage of acute myocardial infarction.     

Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease: Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction

Right ventricular infarction associated with left ventricular infarction was identified by gross examination at necropsy in 33 (14 percent) of 236 patients with transmural myocardial infarction. Right ventricular infarction occurred exclusively as a complication of posterior left ventricular infarction. Associated right ventricular infarction occurred in none of the 97 patients with isolated anterior wall infarction of the left ventricle, but in 33 (24 percent) of the 139 patients with posterior left ventricular infarction. Transmural infarction of the posterior ventricular septum was an additional prerequisite for right ventricular infarction. Of the 139 patients with infarction of the posterior left ventricular wall, 74 had no transmural infarction of the ventricular septum and none of these 74 had associated right ventricular infarction. In contrast, of the 65 patients with infarction of the posterior left ventricular wall and transmural infarction of the ventricular septum, 33 (50 percent) had associated right ventricular infarction.

Among the 33 patients with right ventricular infarction, the infarct was limited to the posterior right ventricular free wall in 27 (82 percent); in the other 6 patients (18 percent) it extended to involve the anterolateral right ventricular free wall. Among patients with a posterior left ventricular infarct, those with a right ventricular infarct had right ventricular dilatation nearly three times (P < 0.05) more frequently than the patients without a right ventricular infarct. Comparison of the same two groups disclosed no differences in the patients' age, sex, extent of coronary arterial luminal narrowing, right ventricular hypertrophy, right ventricular thrombi or duration of symptoms of myocardial ischemia.

Hemodynamic data in four patients with a right ventricular infarct disclosed previously reported characteristic hemodynamics of right ventricular infarction in only one patient. Recognition of right ventricular infarction is important because it implies specific therapy, namely, aggressive volume administration. Clinical evidence of posterior left ventricular infarction and right ventricular dilatation should arouse strong suspicion of associated right ventricular infarction.