Optimal right ventricular filling pressures and the role of pericardial constraint in right ventricular infarction in dogs.

BACKGROUND. Previous studies have reported an important role for right ventricular function in the pathophysiology of the low cardiac output state that can accompany right ventricular infarction. Some studies have suggested that right ventricular distensibility impairs right ventricular filling and stroke output; others have demonstrated that the pericardium can mediate depressed left ventricular filling and stroke output. METHODS AND RESULTS. To determine the role of pericardial constraint and optimal volume loading in an experimental model of right ventricular wall infarction, six mongrel dogs were studied before and after right ventricular wall infarction and after volume loading. The pericardium was then opened in two phases. In the first phase, the pericardium was opened partially to allow the atria to distend freely, and in the second phase, the pericardium was opened completely. The animals were preinstrumented with two sets of piezoelectric crystals attached to the right ventricular free wall, one in the infarct and the other in the noninfarct territory. Left ventricular size was estimated by left ventricular crystals on the anterior wall of the left ventricle. Right ventricular and left ventricular Millar catheters were used to assess intracavitary pressure, and a flat balloon was used to assess intrapericardial pressure. Right ventricular infarction reduced cardiac output by 23% and stroke volume by 30%. End-diastolic segment length and transmural pressure of the left ventricle decreased. Volume loading restored cardiac output to baseline values and was mediated by a significant increase in end-diastolic length in the noninfarct territory. This was achieved by increasing right ventricular end-diastolic pressure from 9 +/- 2 to 16 +/- 3 mm Hg (p less than 0.01). Partial opening of the pericardium mediated significant increases in both end-diastolic segment lengths of the left ventricle and the noninfarct territory. Left ventricular end-diastolic pressure decreased slightly by 3 mm Hg (p = NS). Complete opening of the pericardium increased cardiac output and stroke volume and mediated a significant decrease in right and left ventricular end-diastolic pressures. Left ventricular transmural pressure and end-diastolic segment lengths of the left ventricle and the noninfarct territory increased. Left ventricular diastolic pressure-segment length relations were shifted upward by right ventricular infarction. A partial opening of the pericardium shifted this relation downward in all animals, and complete opening of the pericardium shifted the relation rightward and further downward. CONCLUSIONS. Cardiac output is restored to baseline values by volume loading sufficient to increase the right ventricular diastolic pressure to 16 +/- 3 mm Hg. Evidence of pericardial constraint was observed and appears to be mediated by an atrioventricular interaction in addition to the direct ventricular interaction.     

Aneurysm of the interatrial septum and right-to-left shunt during biventricular infarction. Diagnosis by transesophageal echocardiography

A right-to-left shunt during infarction with right ventricular extension is a rare and recently described complication. It results from opening of a foramen ovale due to increased right heart pressures. The authors describe another case occurring in a patient with an interatrial septal aneurysm, the diagnosis of which was made by transoesophageal echocardiography.     

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.     

Global and regional right ventricular function after acute myocardial infarction: dependence upon site of left ventricular infarction

The relation of global and regional right and left ventricular function during the acute phase after a first myocardial infarction was assessed by first pass radionuclide angiography in 20 patients (10 after anterior and 10 after inferior myocardial infarction). The right ventricular ejection fraction did not differ significantly between the groups, but left ventricular ejection fraction was significantly depressed after anterior myocardial infarction. There was evidence of right ventricular dilatation and impaired transit in the group with inferior infarction. Five patients with anterior infarction and six with inferior infarction had abnormal right ventricular ejection fractions. Right ventricular wall motion abnormalities affected the septal wall in the group with anterior infarction and the free wall in the group with inferior infarction. The relation between right and left ventricular ejection fractions was markedly different in the two groups. In the group with anterior infarction there was a significant linear relation between right and left ventricular ejection fraction, whereas in the group with inferior infarction there was not. Thus right ventricular dysfunction commonly occurs after both anterior and inferior myocardial infarction. Right and left ventricular impairment are related after anterior myocardial infarction, but are independent after inferior myocardial infarction. Finally, the different effects of anterior and inferior myocardial infarction on right ventricular function may be explained by differences in septal and free wall involvement.     

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.     

Global and regional right ventricular function after acute myocardial infarction: dependence upon site of left ventricular infarction.

The relation of global and regional right and left ventricular function during the acute phase after a first myocardial infarction was assessed by first pass radionuclide angiography in 20 patients (10 after anterior and 10 after inferior myocardial infarction). The right ventricular ejection fraction did not differ significantly between the groups, but left ventricular ejection fraction was significantly depressed after anterior myocardial infarction. There was evidence of right ventricular dilatation and impaired transit in the group with inferior infarction. Five patients with anterior infarction and six with inferior infarction had abnormal right ventricular ejection fractions. Right ventricular wall motion abnormalities affected the septal wall in the group with anterior infarction and the free wall in the group with inferior infarction. The relation between right and left ventricular ejection fractions was markedly different in the two groups. In the group with anterior infarction there was a significant linear relation between right and left ventricular ejection fraction, whereas in the group with inferior infarction there was not. Thus right ventricular dysfunction commonly occurs after both anterior and inferior myocardial infarction. Right and left ventricular impairment are related after anterior myocardial infarction, but are independent after inferior myocardial infarction. Finally, the different effects of anterior and inferior myocardial infarction on right ventricular function may be explained by differences in septal and free wall involvement.     

Two dimensional echocardiography and Doppler in the right ventricular infarction

Two dimensional and Doppler echocardiography provide reliable and valuable information in order to evaluate right ventricular function and associated complications in patients with right ventricular infarction. Right ventricular function in right ventricular infarction. There are a number of indirect findings that may support the noninvasive diagnosis of ischemic right ventricular dysfunction and right ventricular infarction: 1. Right ventricular dilatation: A right ventricular diastolic dimension greater than 8 mm/m2 is highly indicative of ischemic right ventricular dysfunction, provided that other causes of right ventricular dilatation, but the sensitivity of this findings is low (50%), the same is true for a RVDD/LVDD ratio greater than 0.63. 2. Right ventricular contraction abnormalities: Wall motion abnormalities constitute the most sensitive and specific echocardiographic findings in the right ventricular infarction. The most common site of involvement is the posterior wall, over 32 patients with right ventricular infarction, 60% present abnormalities confined to the posterior segment; in 30% there is also abnormal contraction of the lateral wall and 10% of the cases present asyneresys of the anterior, lateral and posterior segments. Those patients with the most severe right ventricular dysfunction presented a higher number of right ventricular wall segments with abnormal wall motion. Abnormalities in right ventricular contraction may still be present after evolution and normalization of the hemodynamic data of right ventricular infarction. These findings suggest that wall motion abnormalities can be more sensitive than the hemodynamic in detecting right ventricular infarction. 3. Paradoxical septal motion: Is a common findings after right ventricular infarction and has been attributed to volume overload and alterations in right ventricular compliance, near of 50% present abnormalities of septal motion and those patients with most severe ventricular dysfunction presented most frequently abnormal septal motion. Right ventricular infarction complications. Right ventricular aneurysm: In a series of 50 consecutive patients surviving an episode of right ventricular infarction, we could only find five (10%) with a true ventricular aneurysm. The segments included always the apex and in two cases a thrombus was identified inside its cavity. Functional right ventricular aneurysm may be found in a high percentage (10/50.20%) of patients with right ventricular infarction. Right ventricular thrombi: The identification of thrombi in the right heart is more difficult than in the left ventricle, due to the trabeculation of the right ventricular wall. We could only find 6 cases, in a series of 50 patients studied by two dimensional echocardiography. In all of the cases the ventricular wall adjacent to the thrombus presents contraction abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)     

Right ventricular infarction: identification by hemodynamic measurements before and after volume loading and correlation with noninvasive techniques

To evaluate the potential occurrence of right ventricular infarction, 53 patients with acute inferior transmural myocardial infarction were studied within 36 hours of symptoms by right heart catheterization, equilibrium radionuclide angiography and two-dimensional echocardiography. Technetium-99m pyrophosphate myocardial scintigraphy was performed 3 days after the onset of symptoms. The hemodynamic standard for right ventricular infarction was defined as both a right atrial pressure of 10 mm Hg or more and a right atrial/pulmonary artery wedge pressure ratio of 0.8 or more. Eight (15%) of the 53 patients had hemodynamic measurements at rest characteristic of right ventricular infarction, and 6 (11%) additional patients met these criteria after volume loading (p less than 0.05). Nineteen (37%) of the 51 patients who had radionuclide angiography had right ventricular dysfunction manifested by both a reduced right ventricular ejection fraction (less than 40%) and right ventricular regional wall motion abnormalities (akinesia or dyskinesia). An abnormal radionuclide angiogram was observed in 12 of 13 patients with hemodynamic measurements indicating right ventricular infarction. In 12 patients with an abnormal radionuclide angiographic study, right ventricular ejection fraction improved 6 to 12 weeks after infarction (27 +/- 7 to 36 +/- 9%, p less than 0.01). Twenty-two (49%) of the 45 patients with adequate two-dimensional echocardiograms had a right ventricular regional wall motion abnormality. An abnormal two-dimensional echocardiogram was seen in 9 of 11 patients with hemodynamic measurements characteristic of right ventricular infarction. Technetium-99m pyrophosphate scintigraphy was positive for right ventricular infarction in 3 of 12 patients who had hemodynamic measurements indicating right ventricular infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性右心室心肌梗死的临床特点及预后分析

目的 对急性下壁心肌梗死住院患者的临床资料进行分析,观察合并右心室梗死对病情和转归的影响,并探讨早期再灌注治疗对预后的作用.方法 急性下壁心肌梗死患者304例,其中单纯下壁心肌梗死232例,合并右心室梗死72例,记录一般资料、并发症、实验室检查和治疗情况.结果 右心室梗死组心源性休克、机械并发症、完全性房室传导阻滞、心室颤动、持续性室速和再梗死均明显增高.单纯下壁心肌梗死组病死率为8.6%,右心室梗死组病死率为34.7%.右心室梗死组进行再灌注治疗者病死率为27.8%,保守治疗者病死率为55.6%.结论 右心室梗死作为急性心肌梗死的高危亚组,其严重并发症和病死率显著增加.通过早期再灌注治疗能显著降低右心室梗死的住院期病死率,改善预后.     

Isolated Right Ventricular Myocardial Infarction

Abstract Isolated right ventricular infarction is uncommon. A 73-year-old man without previous cardial complaints was admitted pulseless to hospital. An infarct of the left ventricle was suspected. Autopsy showed a fresh thrombus located in a small branch artery of the right coronary artery accompanied by a fresh infarction of the anterior free wall of the right ventricle. Only 8 cases of isolated right ventricular infarction located in the anterior free wall were found in a review of the literature of right ventricular infarction. The diagnosis, treatment and prognosis of right ventricular infarction are discussed.     

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.     

Assessment of right ventricular infarction with contrast-enhanced magnetic resonance imaging

OBJECTIVE: Evaluation of contrast-enhanced magnetic resonance imaging to assess right ventricular infarction in patients with acute inferior myocardial infarction. BACKGROUND: Contrast-enhanced magnetic resonance imaging has been used for assessing scar tissue after left ventricular infarction. The value of contrast-enhanced magnetic resonance imaging to assess right ventricular infarction is unknown and was evaluated. METHODS: Consecutive patients (n=18) with first acute inferior infarction were included. Resting electrocardiogram and right-sided electrocardiogram were acquired to assess right ventricular involvement. Resting cine magnetic resonance imaging was performed to evaluate right ventricular function and volumes, whereas the extent of right ventricular scar tissue was assessed by contrast-enhanced magnetic resonance imaging. Cine magnetic resonance imaging was repeated at 6-months follow-up to re-assess right ventricular function and volumes. RESULTS: Sensitivity and specificity of magnetic resonance imaging were 100 and 78%, respectively, to detect right ventricular infarction (using the right-sided electrocardiogram as the gold standard). At 6 months follow-up, patients with scar tissue on contrast-enhanced magnetic resonance imaging showed right ventricular dilatation. Moreover, the extent of right ventricular scar tissue was linearly related to the severity of right ventricular dilatation. CONCLUSIONS: Contrast-enhanced magnetic resonance imaging permits accurate assessment of right ventricular scar tissue. Patients with extensive right ventricular infarction demonstrate right ventricular dilatation at 6 months follow-up.     

ST segment elevation in anterior precordial leads and right ventricular infarction. Apropos of 6 cases]

ST segment elevation in the anterior precordial chest leads may be observed in some cases of right ventricular infarction alone or associated with left ventricular inferior wall infarction. Six out of 700 patients admitted to our Coronary Care Unit over a 2 year period had right ventricular infarction with these electrocardiographic changes. In three cases, isolated right ventricular infarction was due to occlusion of a right marginal artery (N = 2) or of a small right coronary artery (N = 1) which only vascularised the right ventricle. In 2 cases, right ventricular infarction was associated with a recent or chronic left ventricular inferior wall infarct. This type of ST segment elevation may suggest a left ventricular anterior wall infarct especially when there are no changes in the inferior leads, as was the case in our first patient. However, the dome-like appearance of the ST segment, the reduction in amplitude of ST elevation from V2 to V5, the progressive regression of the ST changes without the appearance of Q waves, are more suggestive of the diagnosis of right ventricular infarction. In addition, normal left ventricular dilatation on echocardiographic examination rapidly confirms the diagnosis.     

Rechtsventrikuläre Beteiligung beim akuten Myokardinfarkt

Within the course of an acute posterior wall myocardial infarction there may be involvement of the right ventricle leading to right ventricular infarction. The long-term prognosis of patients with right ventricular infarction is not meaningfully compromised provided that the left ventricular function is preserved. However, in the acute phase, there may be a threefold increase in mortality if the right ventricular infarction leads to substantial right ventricular dysfunction. Consequently, right ventricular involvement should be detected as early as possible. In addition to the clinical presentation, the ECG and echocardiogram can provide decisive information. In addition to reperfusion, specific measures are employed to address the hemodynamic derangement of right ventricular dysfunction. These include administration of fluids for volume expansion to increase filling pressure and avoidance of vasodilators and diuretics.     

Right ventricular infarction with shock but without significant left ventricular infarction: a new clinical syndrome

Right ventricular infarction has been described as concurrent with infarction involving the inferior (posterior) aspect of the left ventricular free wall and adjacent interventricular septum. Patients with right ventricular infarction typically show the ECG changes of inferior infarction in leads II, III, and aVF. This report describes two patients with right ventricular infarction but without changes in the QRS complex of the ECG, indicating an inferior infarct of the left ventricle. An autopsy-proven infarct of the right ventricular free wall with neither QRS nor other clinical evidence of left ventricular involvement was responsible for cardiogenic shock and death in one patient. This observation led to a review of a computerized data bank containing records of patients who had undergone cardiac catheterization to determine if there were other patients with clinical criteria suggesting right ventricular infarction without QRS changes of left ventricular infarction. One of the 167 patients with a history of a myocardial infarction also met the following clinical criteria: (1) transiently elevated total creatine kinase and creatine kinase myocardial band; (2) diffuse ST segment elevation without QRS changes indicative of left ventricular infarction on the ECG; (3) normal left ventricular function; (4) hemodynamic evidence of right ventricular dysfunction; and (5) cardiogenic shock.     

Right ventricular filling abnormalities in acute inferior wall myocardial infarction--a pulsed Doppler study

Pulsed Doppler derived velocity profile of right ventricular filling was used to assess right ventricular diastolic function in 29 patients with acute inferior wall myocardial infarction. The peak velocities of the early filling wave 'E' and the atrial wave 'A' were measured. Diastolic dysfunction, defined as E/A ratio less than 1.0, was seen in 15 patients. Of these 15 patients, 9 had electrocardiographic evidence of right ventricular infarction and only 6 had clinical evidence of right ventricular failure. None of the 14 patients without right ventricular diastolic dysfunction (E/A ratio more than 1.0) had electrocardiographic evidence of right ventricular infarction or clinical evidence of right ventricular failure. Pulsed Doppler appears to be a sensitive technique in identifying hemodynamic derangements induced by right ventricular infarction.     

Volume loading improves low cardiac output in experimental right ventricular infarction

To evaluate the effect of volume loading in the low output state associated with right ventricular infarction, isolated right ventricular infarction was produced in seven dogs with the pericardium intact. Volume loading and pericardiotomy were then sequentially performed. After the production of right ventricular infarction, right ventricular systolic pressure decreased by 25%, aortic pressure by 36% and cardiac output by 32%. Right ventricular ejection fraction decreased by 57%, but left ventricular ejection fraction did not change significantly. Left ventricular transmural pressure and diastolic size decreased, and right ventricular diastolic size increased. Intrapericardial pressure increased and equalization of diastolic pressures was noted. Volume loading resulted in increased right ventricular systolic pressure and stroke work, increased aortic pressure and cardiac output and increased transmural pressure and diastolic size in both ventricles. Pericardiotomy resulted in further increases in right and left ventricular filling, stroke work and cardiac output, as well as resolution of equalized diastolic pressures. These results indicate that cardiac output in experimental right ventricular infarction increases with volume loading, which enhances left ventricular preload by augmenting right ventricular output. Elevated intrapericardial pressure affects filling of both ventricles and may play a role in the pathophysiology of low cardiac output in right ventricular infarction.     

Right ventricular hypertrophy is an important determinant of right ventricular infarction complicating acute inferior left ventricular infarction

To explore the role of right ventricular hypertrophy and chronic obstructive pulmonary disease in the pathogenesis of right ventricular infarction, 27 consecutive patients with a first inferior left ventricular infarction were prospectively studied. Right ventricular infarction was diagnosed using established hemodynamic criteria. Right ventricular hypertrophy was defined as right ventricular free wall thickness greater than or equal to 5 mm. Patients were classified into two groups: Group I patients with right ventricular infarction (n = 15), and Group II patients without right ventricular infarction (n = 12). The ratio of forced expiratory volume over forced vital capacity (FEV1/FVC) and forced expiratory flow between 25 and 75% expired volume (FEF) as a percent of predicted values were significantly reduced in Group I versus Group II (90 +/- 5 versus 105 +/- 6% and 63 +/- 13 versus 103 +/- 15%, respectively; p less than 0.05). This was associated with increased right ventricular wall thickness (Group I 5.5 +/- 0.3 mm versus Group II 3.9 +/- 0.2 mm, p less than 0.001). Multiple logistic regression analysis demonstrated that right ventricular wall thickness was the strongest predictor of right ventricular infarction (p less than 0.0005). No significant difference was found in the site of right coronary occlusion, collateral blood supply or extent of coronary artery disease between the two groups. These findings suggest that right ventricular hypertrophy predisposes patients with acute inferior myocardial infarction to right ventricular infarction independent of the site or extent of coronary artery disease.     

Bedside recognition,incidence and clinical course of right ventricular infarction

To evaluate the incidence, clinical characteristics and course of right ventricular infarction, 96 patients with an established diagnosis of acute myocardial infarction were evaluated during a 10 month study period. Of the 44 patients with acute inferior wall myocardial infarction, 16 had bedside evidence of right ventricular dysfunction. All had a positive Kussmaul's sign, and 12 had either a right ventricular third or fourth heart sound. Inspiratory elevation of right atrial and right ventricular end-diastolic pressures was documented in nine patients. Ventricular fibrillation developed in one patient and advanced atrioventricular block in three. All 16 patients survived and were alive 3 months after infarction. The hospital course and 3 month survival rate were not different from those of the usual patient with inferior wall infarction. Approximately one third of the patients with inferior wall myocardial infarction have bedside evidence of right ventricular infarction, which usually does not alter short-term prognosis.     

Right ventricular ejection fraction in patients with acute anterior and inferior myocardial infarction assessed by radionuclide angiography

We measured right and left ventricular ejection fracttion (EF) from high frequency time-activity curves obtained during the initial passage of an intravenous bolus of 99mTc (Sn) pyrophosphate. In 22 normal controls right ventricular EF averaged 0.52 +/- 0.04 (SD). In 24 acute anterior or lateral infarction patients right ventricular EF was normal (0.56 +/- 0.10), while left ventricular EF was reduced (0.45 +/- 0.10, P less than 0.001 vs controls). In 19 acute inferior infarction patients left ventricular EF also was depressed (0.51 +/- 0.09, P less than 0.001 vs controls). Among 7 of 19 inferior infarction patients with right ventricular by scintigraphy, right ventricular EF was reduced (0.39 +/- 0.05; P less than 0.001 vs normals; P less than 0.01 vs inferior infarction patients without right ventricular involvement). In the latter group right ventricular EF averaged 0.51 +/- 0.10 (NS vs normals). We conclude 1) a single injection of 99mTc (Sn) pyrophosphate can identify right and left ventricular dysfunction and infarct location in acute myocardial infarction, 2) right ventricular EF is well-preserved except when inferior infarction involves the right ventricle.