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PubMed2000

[Clinical significance of pressure measurement in the infarct-related coronary artery in acute myocardial infarction: evaluation of variables predicting recovery of left ventricular function in the convalescent stage].

Early reperfusion and good antegrade flow are essential in restoring better regional left ventricular function in acute myocardial infarction, but they do not always correlate with the extent of recovery. This study evaluated coronary circulation using the new "pressure wire" technique to measure the direct pressure of the coronary circulation including antegrade and collateral flow before and after reperfusion in patients with acute myocardial infarction, and to clarify the influence of these variables on recovery of left ventricular function in the convalescent stage. Fifty six consecutive patients with first acute myocardial infarction underwent percutaneous transluminal coronary angioplasty(PTCA) for totally occluded or severely narrowed infarct-related lesion and evaluation of coronary circulation using pressure wire. Left ventriculography was analyzed at 1 month after the onset in 41 patients. Treatment variables including reperfusion time, reperfusion modality, Thrombolysis in Myocardial Infarction(TIMI) grade after PTCA, and pressure wire variables were compared with parameters of left ventricular function. Reperfusion time was not related to regional wall motion evaluated by the SD chord of left ventriculography in the infarcted zone. Pressure wire measurements showed a correlation between fractional flow reserve measured after PTCA and infarcted regional wall motion(r = 0.558, p < 0.01). Patients with infarct-related lesion in the right coronary artery showed the magnitude of left ventricular regional wall motion was related to fractional collateral flow reserve(maxQc/Qn) during PTCA(r = 0.768, p < 0.05), but no such relationship was observed in patients with infarct-related lesion in the left anterior descending artery. Fractional flow reserve measured after PTCA varied widely in patients with the same TIMI flow grade, so did not vary with it. The pressure wire technique enables assessment of the collateral circulation distal to infarct-related lesion quantitatively before reperfusion in patients with acute myocardial infarction. The fractional flow reserve derived by coronary pressure after reperfusion was significantly related to the recovery of regional wall motion in the infarcted area in the convalescent stage. The fractional flow reserve after reperfusion with PTCA is a better parameter than TIMI flow grade for predicting recovery of regional left ventricular function after myocardial infarction.

Angioplasty, Balloon, Coronary↗
PubMed1989

Myocardial infarct expansion during indomethacin or ibuprofen therapy for symptomatic post infarction pericarditis. Influence of other pharmacologic agents during early remodelling.

Evidence of acute infarct expansion and the frequency of the acute infarct expansion syndrome (acute infarct dilatation and thinning associated with hypotension and left ventricular failure but no evidence of new necrosis) occurring at two days or more after a first acute Q-wave myocardial infarction were studied using serial two-dimensional echocardiography in 221 consecutive patients (100 anterior, 121 inferior). Patients with symptomatic pericarditis were treated with indomethacin (group 1, n = 73) or ibuprofen (group 2, n = 49) and those without symptomatic pericarditis received neither drug (group 3, n = 99). The overall frequency of the acute infarct expansion syndrome was 13% and 69% of these were among the pericarditis groups. The syndrome was significantly more frequent in group 1 (22%) than group 2 (8%) (P less than 0.05) or group 3 (9%) (P less than 0.025). Serial echocardiograms revealed more expansion with greater percentage increase in the infarct containing segment length in group 1 than group 2 or group 3 (18% versus 9% versus 9%, P less than 0.005). However, the decreases in infarct segment thickness were similar in groups 1 (24%) and 2 (25%) but greater (P less than 0.001) than in group 3 (7%). Despite similar infarct size and infarct thinning in groups 1 and 2, the degree of infarct expansion was greater and the infarct expansion syndrome more frequent in group 1. However, when allowance was made for the potential protective effect of prior use of intravenous nitroglycerin and concomitant use of nifedipine, indomethacin and ibuprofen had similar effects on expansion. Thus, indomethacin or ibuprofen should be used with caution after Q-wave infarction so as to avoid further expansion. The fact that short term use of other drugs might modify infarct remodelling should be considered in studies attempting to assess efficacy of one particular drug.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1989

Non-Q-wave myocardial infarction: incidence, pathophysiology, and clinical course compared with Q-wave infarction.

Acute myocardial infarction can be stratified into electrocardiographic subsets based on the presence or absence of new Q waves. This stratification has important clinical and prognostic utility. Coronary angiography during acute non-Q-wave compared with Q-wave infarction shows much higher infarct-related artery patency rates (about 75 vs. 10%) and increased coronary collateralization. Culprit legion morphology in non-Q-wave infarction commonly is complex. The frequent demonstration of recurrent clinical ischemia, or residual thallium-201 uptake abnormalities, and metabolic activity on persistent emission tomography suggest the presence of viable myocardium in the distribution of the non-Q-wave infarction usually represents 20-25% of acute myocardial infarctions. The University of California San Diego Collaborative Postinfarction Database and other large studies have found non-Q-wave infarctions to be more common in patients with a history of previous infarction and congestive heart failure, although their mortality during acute hospitalization is lower. However, in long-term followup to one year and beyond, non-Q-wave infarct mortality rates equal those of Q-wave infarction. Patients at low early and late risk of mortality include those with a first infarction who are under age 70, whereas patients with evidence of residual ischemia postinfarction are at increased risk of events. It is interesting to speculate that the settings of unstable angina pectoris, non-Q-wave infarction, and perhaps the picture after thrombolysis for acute myocardial infarction, have pathophysiologic similarities which may carry implications for future research and therapy.

Electrocardiography↗
PubMed1997

[Acute myocardial infarction and cerebral infarction at Kusatsu-spa].

From January 1989 to June 1995, 31 patients were admitted to our hospital with acute myocardial infarction (15 were tourists and 16 were Kusatsu residents) and 40 were admitted with cerebral infarction (15 tourists and 25 Kusatsu residents). We examined the possibility that hot hot-spring bathing was related to the occurrence of their illness. Fifteen patients with acute myocardial infarction (9 tourists and 6 Kusatsu residents) and 27 patients with cerebral infarction (11 tourists and 16 Kusatsu residents) had a hot hot-spring bath within 24 hours before the onset of symptoms. In 12 of the 15 with acute myocardial infarction (6 tourists and 6 Kusatsu residents) and in 15 of the 27 with cerebral infarction (9 tourists and 6 Kusatsu residents), symptoms began within 3 hours after they began bathing. In 2 of the remaining 3 patients with acute myocardial infarction and in 8 of the remaining 12 patients with cerebral infarction, bathing at night was followed by the onset of symptoms the next morning (more than 3 hour later). Acute myocardial infarction and cerebral infarction within 3 hours after hot hot-spring bathing may be attributable to transient change in blood pressure, heart rate, blood viscosity, fibrinolytic activity, and platelet function. We described previously that hot hot-spring bathing at night can accentuate the nocturnal decrease in blood pressure and can make the early morning increase in blood viscosity more abrupt. These phenomena may account for the occurrence of acute myocardial infarction and cerebral infarction early in the morning.

Aged↗
PubMed2000

Expression of perlecan proteoglycan in the infarct zone of mouse myocardial infarction.

Perlecan, a basal lamina proteoglycan, has been shown to interact with other extracellular matrix (ECM) components, especially type IV collagen, and is thus involved in ECM formation. Perlecan has also been postulated to promote growth factor-receptor interactions, including the binding of basic fibroblast growth factor (bFGF) to its receptor, and to enhance mitogenesis and angiogenesis. To test our hypothesis that perlecan is increased in the myocardial infarct zone, we examined perlecan expression after experimentally induced myocardial infarction in BALb/c mice by the methods of in situ hybridization, Northern blotting, and immunohistochemistry. In situ hybridization revealed mRNA signals for perlecan in the infarct marginal zone on day 2 and in the infarct interior zone around infarct granulation tissue on day 7. On day 14 the signals were observed at the center point of the infarct. The signals were detected in spindle-shaped mesenchymal cells (fibroblasts and myofibroblasts). Some surviving myocytes in the infarct marginal zone also showed positive signals. The sequential changes in the perlecan mRNA signal distribution paralleled those for type IV collagen mRNA. Northern blotting demonstrated increased expression of perlecan consistent with the observations of in situ hybridization. Immunopositive staining for perlecan was observed in the infarct zone around granulation tissue on day 7 and in the entire infarct zone on days 14-28. Immunostaining for bFGF was localized surrounding the infarct granulation tissue on day 7 and overlapped with perlecan immunostaining. The present results demonstrated the expression of perlecan by spindle-shaped mesenchymal cells (fibroblasts and myofibroblasts) and some surviving myocytes in the myocardial infarct, indicating the contribution of perlecan to the pathological course of myocardial infarction.

Animals↗
PubMed1987

Right ventricular myocardial infarction with anterior wall left ventricular infarction: an autopsy study.

Right ventricular myocardial infarction has been reported to occur exclusively in association with inferior left ventricular infarction. To determine the frequency of right ventricular myocardial infarction in association with anterior left ventricular myocardial infarction, all hearts with anterior myocardial infarction studied over a 3-year period were examined for evidence of right ventricular necrosis or scar. Of 97 hearts with anterior myocardial infarction, 13 (13%) had anterior right ventricular myocardial infarction. The right ventricular infarcts involved from 10% to 50% (mean 28%) of the circumference of the right ventricular free wall from base to apex. The associated left ventricular infarcts were all anteroseptal and large and involved from 36% to 67% (mean 50%) of the total area of the left ventricular free wall and septum. Nine of the 13 patients underwent equilibrium radionuclide angiography and six had demonstrable right ventricular regional and global dysfunction. Thus, right ventricular myocardial infarction does occur with anterior wall left ventricular infarction, and right ventricular dysfunction may be demonstrable by radionuclide angiography. Further investigation is needed to define the hemodynamic characteristics, clinical importance, and therapeutic implications of anterior right ventricular myocardial infarction.

Adult↗
PubMed1990

Relation of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction.

This study explores the relation of the presence of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction (MI). The hypothesis was that both the gross peri-infarction block pattern and subtle low-level ventricular late potentials are expressions of conduction abnormality associated with infarction. The consequent question arose whether peri-infarction block may have the same association with sustained ventricular arrhythmias that has been demonstrated in postinfarction patients with ventricular late potentials. Seventy patients with documented Q-wave MI were divided into those with (23) and those without (47) peri-infarction block. Signal-averaged electrocardiograms were obtained. Analysis of the vectormagnitude complex revealed that the total duration of that complex and the duration of terminal potential under 40 microV in the peri-infarction group exceeded that in the group without peri-infarction block (p less than 0.0001). The voltage in the last 40 ms of the vectormagnitude complex was also significantly less in the peri-infarction group (p less than 0.0005). There were 13 instances of sustained ventricular tachycardia, ventricular fibrillation or sudden death occurring subsequent to infarction not associated with the acute ischemic event, 11 of which occurred in the peri-infarction group. The significantly higher incidence of late potentials along with the significantly higher incidence of sustained ventricular arrhythmias in the peri-infarction block on the surface electrocardiogram may provide another marker for identifying persons at increased risk for these arrhythmias subsequent to MI.

Adult↗
PubMed1988

Increased afterload aggravates infarct expansion after acute myocardial infarction.

After acute transmural myocardial infarction, the heart may undergo major remodeling characterized by thinning and dilation of the infarct zone and overall enlargement of the heart. The effect of increased left ventricular pressure on infarct expansion and the extent to which it alters postinfarction remodeling were studied in a rat model. Rats with either aortic banding or a sham operation and a survival period of 3 weeks were further randomized to sham thoracotomy or left coronary ligation. Surviving rats were killed 7 days later and the hearts were fixed in diastole for morphologic analysis. Hearts with aortic banding had a mean peak to peak gradient of 20.7 +/- 4.9 mm Hg across the aortic band at death and a significantly thicker heart than that of the comparison group without an aortic band. Infarct size, as a percent of total left ventricular mass, at the time of death was less in the group with aortic banding, yet infarct expansion was more marked. However, when original infarct size was estimated taking into account the effects of aortic banding, scar formation, infarct expansion and infarct-induced hypertrophy, it was found to be similar in both infarct groups (45.50 +/- 4.2 versus 47.90 +/- 3.1%). Infarct expansion, as measured by cavity dilation and infarct thinning, occurred in both infarct groups but was greater in the group with aortic banding.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Precordial ST segment depression predicts a worse prognosis in inferior infarction despite reperfusion therapy. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group.

The impact of associated precordial ST segment depression in inferior myocardial infarction on angiographic and clinical outcomes after thrombolytic therapy and selective coronary angioplasty was studied in 583 patients with acute myocardial infarction. Anterior infarction (Group I), inferior infarction with precordial ST segment depression (Group II) and inferior infarction without precordial ST segment depression (Group III) were present in 289, 135 and 159 patients, respectively. Precordial ST segment depression was more frequent in circumflex than right coronary infarct-related arteries (44 [71%] of 62 versus 91 [40%] of 230; p = 0.000). Although acute patency rates were not statistically different, there was a trend toward different patency rates at day 7 (Group I 88%, Group II 84%, Group III 80%; p = 0.089) partly because of insignificantly higher reocclusion rates in inferior infarction without precordial ST segment depression (Group I 11%, Group II 10%, Group III 18%, p = 0.104). Infarct zone regional wall motion (standard deviations/chord) in inferior infarction was lower with precordial ST segment depression, both acutely (Group I -2.8 +/- 0.9, Group II -2.5 +/- 1.2, Group III 2.0 +/- 1.1; p = 0.000) and at day 7 (Group I -2.2 +/- 1.1, Group II -2.3 +/- 1.1, Group III -1.9 +/- 1.3; p = 0.011). Precordial ST segment depression was associated with a lower ejection fraction in inferior infarction both acutely (Group I 47 +/- 11%, Group II 53 +/- 11%, Group III 58 +/- 9%; p = 0.000) and at day 7 (Group I 49 +/- 12%, Group II 53 +/- 10%, Group III 58 +/- 8%; p = 0.000). Complication rates tended to be higher in inferior infarction when precordial ST segment depression was present. Mortality rates for Groups I, II and III were 8%, 6% and 5%, respectively. These results suggest that precordial ST segment depression in inferior infarction predicts a worse ventriculographic and clinical outcome despite reperfusion therapy.

Angioplasty, Balloon, Coronary↗
PubMed1994

Eligibility for and benefit of thrombolytic therapy in inferior myocardial infarction: focus on the prognostic importance of right ventricular infarction.

OBJECTIVES: This study was undertaken to determine eligibility for and benefit of thrombolytic therapy in patients with acute inferior myocardial infarction with or without right ventricular involvement. BACKGROUND: Right ventricular involvement commonly complicates acute inferior myocardial infarction and is considered to have prognostic relevance. We hypothesized that the presence of right ventricular infarction, diagnosed early by ST segment elevation in the right precordial lead (V4R), may be of clinical importance in identifying patients who will benefit most from thrombolytic therapy. METHODS: We studied 200 consecutive patients with acute inferior myocardial infarction to assess the prognostic impact of right ventricular infarction in those considered eligible or ineligible for reperfusion therapy. Prognostic analyses were based on the in-hospital period and a 1- to 6-year follow-up (mean [+/- SD] 37 +/- 12 months). RESULTS: ST segment elevation in lead V4R was a reliable marker of right ventricular infarction (sensitivity 88%, specificity 78%, diagnostic efficiency 83%) in 107 patients (54%) with inferior myocardial infarction. Seventy-one eligible patients (36%) received thrombolytic therapy and had a lower mortality (8% [6 of 71]) and complication (31% [22 of 71]) rate than ineligible patients (mortality rate 25% [32 of 129], p < 0.01; complication rate 56% [72 of 129], p < 0.01). However, the overall benefit of thrombolysis was restricted to patients with right ventricular infarction complicating acute inferior myocardial infarction (with vs. without thrombolysis, respectively: mortality rate 10% vs. 42%, p < 0.005; complication rate 34% vs. 54%, p < 0.05). In the absence of right ventricular infarction, no difference was observed in the mortality (7% vs. 6%, p = NS) and major in-hospital complication (27% vs. 29%, p = NS) rates, whether or not the patient underwent thrombolytic therapy. Posthospital course over 37 +/- 12 months was not different in patients with and without right ventricular infarction but was best in all patients considered for reperfusion therapy. CONCLUSIONS: During acute inferior myocardial infarction, the right precordial electrocardiogram is a simple but promising variable to identify a subgroup of patients with an unfavorable course who will benefit most from thrombolytic therapy.

Aged↗
PubMed1996

Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: a multivariate analysis.

OBJECTIVES: This study sought to determine whether the reopening of the infarct-related vessel is related to clinical characteristics or cardiovascular risk factors, or both. BACKGROUND: In acute myocardial infarction, thrombolytic therapy reduces mortality by restoring the patency of the infarct-related vessel. However, despite the use of thrombolytic agents, the infarct-related vessel remains occluded in up to 40% of patients. METHODS: We studied 295 consecutive patients with an acute myocardial infarction who underwent coronary angiography within 15 days (mean [+/- SD] 6.7 +/- 3.2 days) of the onset of symptoms. Infarct-related artery patency was defined by Thrombolysis in Myocardial Infarction trial flow grade > or = 2. Four cardiovascular risk factors--smoking, hypertension, hypercholesterolemia and diabetes mellitus--and eight different variables-age, gender, in-hospital death, history of previous myocardial infarction, location of current myocardial infarction, use of thrombolytic agents, time interval between onset of symptoms, thrombolytic therapy and coronary angiography--were recorded in all patients. RESULTS: Thrombolysis in current smokers and anterior infard location on admission were the three independent factors highly correlated with the patency of the infarct-related vessel (odds ratios 3.2, 3.0 and 1.9, respectively). In smokers, thrombolytic therapy was associated with a higher reopening rate of the infard vessel, from 35% to 77% (p < 0.001). Nonsmokers did not benefit from thrombolytic therapy, regardless of infarct location. CONCLUSIONS: These observational data, if replicated, suggest that in patients with acute myocardial infarction, thrombolytic therapy may be most effective in current smokers, whereas nonsmokers and ex-smokers may require other management strategies, such as emergency percutaneous transluminal coronary angioplasty.

Aged↗
PubMed2004

Infarct resorption, compensatory hypertrophy, and differing patterns of ventricular remodeling following myocardial infarctions of varying size.

OBJECTIVES: We sought to identify advantages of contrast-enhanced magnetic resonance imaging (MRI) in studying postinfarction ventricular remodeling. BACKGROUND: Although sequential measurements of ventricular volumes, internal dimensions, and total ventricular mass have provided important insights into postinfarction left ventricular remodeling, it has not been possible to define serial, directionally opposite changes in resorption of infarcted tissue and hypertrophy of viable myocardium and effects of these changes on commonly used indices of remodeling. METHODS: Using gadolinium-enhanced MRI, the time course and geometry of changes in infarcted and noninfarcted regions were assessed serially in dogs subjected to coronary occlusion for 45 min, 90 min, or permanently. RESULTS: Infarct mass decreased progressively between three days and four to eight weeks following coronary occlusion; terminal values averaged 24 +/- 3% of those at three days. Radial infarct thickness also decreased progressively, whereas changes in circumferential and longitudinal extent of infarction were variable. The ability to define the circumferential endocardial and epicardial extents of infarction allowed radial thinning without epicardial expansion to be distinguished from true infarct expansion. The mass of noninfarcted myocardium increased by 15 +/- 2% following 90-min or permanent occlusion. However, the time course of growth of noninfarcted myocardium differed systematically from that of infarct resorption. Measurements of total ventricular mass frequently failed to reflect concurrent changes in infarcted and noninfarcted regions. Reperfusion accelerated infarct resorption. Histologic reductions in nucleus-to-cytoplasm ratios corresponded with increases in noninfarcted ventricular mass. CONCLUSIONS: Concurrent directionally opposite changes in infarcted and noninfarcted myocardium can be defined serially, noninvasively, and with high spatial resolution and full ventricular coverage following myocardial infarction.

Animals↗
PubMed1986

Infarct expansion: pathologic analysis of 204 patients with a single myocardial infarct.

The reasons for the marked variability in expansion of myocardial infarcts are unknown. To examine this question, the hearts in 204 patients with a single myocardial infarct, autopsied at The Johns Hopkins Hospital and studied after coronary arteriography and fixation in distension, were reviewed. There were 58 (28%) hearts with marked infarct expansion, 34 (17%) with moderate expansion and 112 (55%) with no or minimal expansion. The degree of expansion was greater in larger, more transmural infarcts (p less than 0.001). Infarcts with greater expansion had significantly more endocardial thrombus (p less than 0.001) and endocardial fibroelastosis (p less than 0.01). Larger heart weight and degree of left ventricular hypertrophy had a significant negative correlation with infarct expansion (p less than 0.05). A markedly greater degree of expansion was noted in the 101 infarcts (50%) caused by lesions in the distribution of the left anterior descending coronary artery as compared with the 57 infarcts (28%) secondary to right coronary lesions and the 46 infarcts (23%) in the distribution of the left circumflex coronary artery (p less than 0.001). The results show that expansion is associated with large infarcts but is less marked in hearts with ventricular hypertrophy. Expansion occurs predominantly in infarcts in the left anterior descending coronary artery distribution, that is, regions of the left ventricular myocardium with the greatest curvature. These results suggest that the degree to which an infarct expands may be influenced by the preinfarction thickness of the ventricular wall.

Adult↗
PubMed1998

Long-term effects of beta-adrenergic blocking agent treatment on hemodynamic function and left ventricular remodeling in rats with experimental myocardial infarction: importance of timing of treatment and infarct size.

OBJECTIVES: This study was designed to assess the long-term effects of a beta1-selective beta-adrenergic blocking agent on mortality, in vivo hemodynamic function, left ventricular volume and wall stress in post-myocardial infarction (MI) rats. BACKGROUND: Beta-blockers have shown beneficial results in clinical studies after MI. However, the underlying mechanism is not yet understood, and experimental studies have shown conflicting results. METHODS: Bisoprolol (60 mg/kg body weight per day) was given 30 min or 14 days after MI or sham operation. RESULTS: The mortality rate was reduced only in early bisoprolol-treated rats (29% vs. 46% in untreated rats, p < 0.05). Heart rate was equally reduced in all treatment groups, and the maximal rate of rise of left ventricular systolic pressure (dP/dt(max)) decreased in sham rats and in rats with a small to moderate infarct size. Stroke volume index was unchanged in sham rats and in rats with a small to moderate infarct with early or late bisoprolol treatment and increased in rats with a large infarct in the late bisoprolol group. Left ventricular volume was increased by bisoprolol in sham rats and rats with a small infarct but not in rats with a large infarct. CONCLUSIONS: Treatments starting early (30 min) or late (14 days) after coronary artery ligation with bisoprolol increased left ventricular volume in sham rats and in rats with a small infarct but not in rats with a large infarct. Late bisoprolol treatment improved stroke volume index, and early bisoprolol treatment reduced diastolic wall stress, in rats with a large myocardial infarct. Thus, bisoprolol effects on remodeling and cardiac performance after myocardial infarction strongly depend on infarct size and timing of treatment. This finding may explain previous controversial results that did not consider infarct size and timing of treatment.

Adrenergic beta-Antagonists↗
PubMed1977

Infarct sizing with technetium-99m stannous pyrophosphate scintigraphy in dogs and man; relationship between scintigraphic and praecordial mapping estimates of infarct size in patients.

The present study was performed in order to evaluate the ability of technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigrams to size infarcts in experimental animals and man. In 10 dogs with proximal left anterior descending coronary artery occlusion and acute anterior myocardial infarcts, there was a significant correlation between scintigraphic infarct size and histological infarct weight (P less than 0.01). In 25 patients with acute anterior or anterolateral myocardial infarcts, there was a significant correlation between relatively large infarct size determined scintigraphically and the acute development of left ventricular failure. There was some overlap, however, in 99mTc-PYP scintigraphic infarct size between patients who did and did not develop left ventricular failure with infarction. Presumably this is explained by some patients having had earlier myocardial damage and thus developing left ventricular failure with relatively small new infarcts. There was also a statistically significant, but weak, correlation in patients between scintigraphic infarct size and precordial ST segment mapping including peak ST segment elevation (P less than 0.05) and the number of praecordial sites with ST segment elevation equal to or greater than 2 mm (P less than 0.01). The data suggest that 99mTc-PYP scintigrams and praecordial mapping measure some similar but some dissimilar aspects of infarct size in patients, and that 99mTc-PYP scintigraphy does size acute anterior and anterolateral infarcts in experimental animals and patients.

Animals↗