Transmural Inferior Infarction Research Articles

P262 Left ventricular pseudoaneurism due to a non-reperfused myocardial infarction: multi-modality cardiac imaging approach

Abstract Introduction Cardiac rupture has been one of the most frequent fatal complications of acute myocardial infarction in cases series reported since 1977. However, in exceptional cases, the rupture of the left ventricle is contained by the pericardium and by fibrous tissue, forming a pseudoaneurysm, which is characterized by the absence of myocardial tissue in its wall and a relatively narrow neck between the ventricle and the ventricular chamber. Although there is no estimated time for rupture, it is well established that the risk of rupture is 30 to 40% and mortality up to 10%. Pseudoaneurysm is a rarer entity than rupture and is usually diagnosed incidentally by imaging methods in up to 48% of cases. The most frequent imaging method for their diagnosis is 2D echocardiography, followed by cardiac catheterization and finally cardiac magnetic resonance. The most frequent location of the pseudoaneurysm secondary to acute myocardial infarction is the inferior wall and the posterolateral wall of the left ventricle. Case Report We present 72-year-old male patient with a history of type 2 diabetes and smoking, who started symptoms with sudden onset of oppressive chest pain of 20 minutes duration, he did not attend medical attention. A month later, he went for a valuation with a first-contact physician, who referred him to our institution with a diagnosis of acute myocardial infarction without reperfusion therapy. At the initial assessment, it was found asymptomatic, in the resting ECG was found QS pattern with reversal of the T wave in leads DII, DIII and AVF. Cardiac SPECT was performed and showed an inferior transmural infarction, which extended as non-transmural to the inferolateral and inferoseptal walls, without ischemia. (Img. 1 and 2). A 2D and 3D transthoracic echocardiogram was performed, in which akinesia of the inferoseptal and apical walls was documented, as well as a saccular pseudoaneurysm of 5.6 X 4.7 cm in the basal and middle segment of the inferior and inferolateral walls, with an entrance orifice. 2.6 X 2.4 cm, as well as pericardial effusion. (Fig. 3 and 4). Coronary angiography was performed, demonstrating chronic total occlusion of the right coronary in its proximal segment and ostial obstruction of the left anterior descending. Cardiac magnetic resonance revealed inferior infarction and the presence of a pseudoaneurysm with lamellar thrombus was corroborated. (Img. 5). The patient was taken to surgical treatment, by reconstruction of the left ventricle with the Dor technique and CABG of the right coronary artery and the anterior descending artery. Receives medical treatment and a 1-month follow-up is in class I of the NYHA. Conclusion It is a clinical case about a potentially fatal complication of acute myocardial infarction, which in our case was detected incidentally since the patient had remained asymptomatic, there lies the importance of obtaining an accurate diagnosis in order to impact on the patient survival. Abstract P262 Figure. Pseudoaneurysm multi-modality images

Simultaneous ST-segment elevation in lead V 1 and depression in lead V 2: A discordant ECG pattern indicating right ventricular infarction

The major electrocardiographic change in right ventricular infarction (RVI) is ST-segment elevation in leads V 4R–V 6R. The authors describe a discordant electrocardiographic pattern of ST-segment elevation in lead V 1 and ST-segment depression in lead V 2 in five patients presenting with acute transmural (Q wave) inferior infarction and RVI. There were 51 patients with transmural inferior infarction from a thrombolytic trial. In 25 patients, the ST-segment in the right-sided precordial leads was elevated by ≥1 mm indicating the presence of RVI. In 5 of these 25 patients, simultaneous ST-segment elevation of 1.0–8.0 mm (mean, 2.8 ± 2.9 mm) in lead V 1 and ST-segment depression of 2.5 to 4.0 mm (mean, 3.3 ± 0.6 mm) in lead V 2 were also present. The discordant pattern of the ST-segments in leads V 1 and V 2 is an important and specific sign for RVI.

Evaluation of biventricular involvement in hypotensive patients with transmural inferior infarction by two-dimensional echocardiography

Hypotension in inferior myocardial infarction (IMI) may be due to extensive involvement of the right ventricle (RV), left ventricle (LV), or both. We verified this hypothesis in 24 patients with IMI and hypotension (systolic blood pressure < 100 mm Hg), within 48 hours of admission, by means of two-dimensional echocardiography (2DE). We measured the extent of regional RV and LV asynergy (akinesis and/or dyskinesis) in parasternal short-axis sections at mitral, chordal, midpapillary muscle, and low papillary muscle levels. Initial right heart catheterization revealed predominant RV dysfunction in 16 patients (group 1) and predominant LV dysfunction in eight patients (group 2). For all patients, the initial 2DE revealed: (1) biventricular asynergy involving the posterior RV, posterior LV, and posterior interventricular septum; (2) a wide range of values for the extent of asynergy (RV 21% to 90%; LV 19% to 48%); and (3) a direct correlation between peak creatine kinase levels and percentage of LV asynergy ( r = 0.80, p < 0.001) or percentage of RV plus LV asynergy ( r = 0.72, p < 0.001). Although the extent of LV asynergy was similar in the two groups (34% vs 34%, NS), the extent of RV asynergy was greater in group 1 than in group 2 (57% vs 30%, p < 0.001). More important, the ratio of RV LV asynergy was greater for group 1 than group 2 (1.75 vs 0.89, p < 0.001), and this difference in ratios between the two groups was also found in 2DE studies at 10 days and 6 months. A RV LV asynergy ratio value of 1.1 provided clear separation between the groups. Thus, the RV LV asynergy ratio on an initial 2DE can clarify the clinical syndrome of hypotension in patients with IMI. An increased asynergy ratio might identify those patients with predominant RV involvement.

First transit and equilibrium radionuclide angiography in patients with inferior transmural myocardial infarction: Criteria for the diagnosis of associated hemodynamically significant right ventricular infarction

To define radionuclide criteria for identifying hemodynamically significant right ventricular infarction, 33 consecutive men with inferior transmural infarction were evaluated prospectively by right heart catheterization and first transit and equilibrium radionuclide angiography within 36 hours of the onset of symptoms. Hemodynamically significant right ventricular infarction was present in 6 of the 33 patients (Group I); the remaining 27 patients did not demonstrate the hemodynamics characteristic of right ventricular infarction (Group II). A right ventricular ejection fraction of less than 40% separated Group I and Group II patients by equilibrium (p = 0.003) but not by first transit (p = NS) radionuclide angiography. However, a right ventricular ejection fraction of less than 35% separated Group I and II patients by both techniques (p = 0.02 and p = 0.005, respectively). The presence of a right ventricular regional wall motion abnormality on either first transit or equilibrium radionuclide angiograms separated Group I and II patients (p less than 0.001). The combination of both a right ventricular ejection fraction of less than 40% and a regional wall motion abnormality separated Group I and II patients using either equilibrium (p less than 0.001) or first transit (p = 0.02) radionuclide angiography. It is concluded that in patients with acute inferior transmural myocardial infarction, a right ventricular regional wall motion abnormality alone or in combination with a right ventricular ejection fraction of less than 40% by either first transit or equilibrium radionuclide angiography is a useful criterion for establishing the presence of hemodynamically significant right ventricular infarction, while its absence argues against the diagnosis of right ventricular infarction.

Ventricular performance and prognosis after primary ventricular fibrillation complicating acute myocardial infarction.

To examine the relationship between early arrhythmias, infarct size and prognosis, we compared 22 consecutive patients surviving acute myocardial infarction (AMI) and primary ventricular fibrillation (VF) with a control population after AMI uncomplicated by primary VF. Left ventricular ejection fraction (EF) was measured by radionuclide ventriculography before discharge from hospital. Mean EF was significantly reduced below normal following AMI with or without primary VF (normal 0.57 +/- 0.05, mean +/- SD; P less than 0.01). Mean EF was lower among patients who survived primary VF than among those with infarction uncomplicated by primary arrhythmia (0.33 +/- 0.12 v. 0.46 +/- 0.07; P less than 0.01). There were striking differences in EF between those patients with anterior and those with inferior infarction. Mean EF for those surviving primary VF after transmural anterior infarction (0.23 +/- 0.06) was lower than those who had primary VF after transmural inferior infarction (0.43 +/- 0.06; P less than 0.01). Normal left ventricular function was seen in four individuals who developed no further complications. Recurrent primary ventricular arrhythmia was seen only in those individuals subsequently shown to have reduced EF. Low EF (less than 0.35) was seen in 12 patients with primary VF in the context of anterior infarction, five developed breakthrough ventricular arrhythmias despite therapy and in a limited follow-up period, three have died.

Speckles in ultrasound: Model-based analysis and clinical relevance: I. Zuna, D. Schlaps, J. Volk, U. Raeth, A. Lorenz, W.J. Lorenz and G. van Kaick, Institut fur Nuklearmedizin, DKFZ, Heidelberg, FRG

Submaximal exercise testing with radionuclide ventriculography was performed in 117 patients prior to hospital discharge 16.7 ± 6.7 days (SD) following acute myocardial infarction. The hypothesis tested in this study was that patients with different locations and types of infarction have different functional responses to submaximal exercise prior to discharge. The distribution of the myocardial infarctions were anterior transmural in 33, Inferior transmural in 39, anterior nontransmural in 23, inferior nontransmural in 19, and indeterminant in three. Patients with transmural infarction generally had significantly larger resting left ventricular volumes at enddiastole and end-systole and lower ejection fractions and systolic blood pressure/end-systolic volume Indexes than patients with nontransmural infarctions (p < 0.05). During submaximal exercise, the change in end-systolic volume was significantly different in these two groups. When patients were separated further into anterior and inferior transmural subgroups, the patients with anterior transmural infarction had significantly lower left ventricular ejection fractions and higher right ventricular ejection fractions than the group with inferior transmural Infarction (p < 0.05). In response to exercise, the group with anterior transmural infarction had a significant decrease in left ventricular ejection fraction and a blunted systolic blood pressure/left ventricular end-systolic volume index, in comparison to patients with inferior myocardial infarction (p < 0.05); this was the only group to have a significant increase in end-systolic volume. The group variance for the parameters studied was large, particularly during exercise when the individual responses were frequently directionally opposite from the group means. The group with anterior transmural infarction was the most homogenous, with 26 of 33 having a directionally abnormal response to submaximal exercise. It was concluded that the group with anterior transmural infarction generally displayed the most abnormal left ventricular function. However, despite significant group differences in resting ventricular function with different infarcts, the intragroup variability at rest and in response to exercise was too great to permit an accurate prediction of the subject's resting ventricular performance or to permit a prediction of exercise response based solely on location of the infarct.

Left ventricular functional alterations at rest and during submaximal exercise in patients with recent myocardial infarction

Submaximal exercise testing with radionuclide ventriculography was performed in 117 patients prior to hospital discharge 16.7 ± 6.7 days (SD) following acute myocardial infarction. The hypothesis tested in this study was that patients with different locations and types of infarction have different functional responses to submaximal exercise prior to discharge. The distribution of the myocardial infarctions were anterior transmural in 33, Inferior transmural in 39, anterior nontransmural in 23, inferior nontransmural in 19, and indeterminant in three. Patients with transmural infarction generally had significantly larger resting left ventricular volumes at enddiastole and end-systole and lower ejection fractions and systolic blood pressure/end-systolic volume Indexes than patients with nontransmural infarctions (p < 0.05). During submaximal exercise, the change in end-systolic volume was significantly different in these two groups. When patients were separated further into anterior and inferior transmural subgroups, the patients with anterior transmural infarction had significantly lower left ventricular ejection fractions and higher right ventricular ejection fractions than the group with inferior transmural Infarction (p < 0.05). In response to exercise, the group with anterior transmural infarction had a significant decrease in left ventricular ejection fraction and a blunted systolic blood pressure/left ventricular end-systolic volume index, in comparison to patients with inferior myocardial infarction (p < 0.05); this was the only group to have a significant increase in end-systolic volume. The group variance for the parameters studied was large, particularly during exercise when the individual responses were frequently directionally opposite from the group means. The group with anterior transmural infarction was the most homogenous, with 26 of 33 having a directionally abnormal response to submaximal exercise. It was concluded that the group with anterior transmural infarction generally displayed the most abnormal left ventricular function. However, despite significant group differences in resting ventricular function with different infarcts, the intragroup variability at rest and in response to exercise was too great to permit an accurate prediction of the subject's resting ventricular performance or to permit a prediction of exercise response based solely on location of the infarct.

Comparative diagnostic performance of the telemed computer ECG program

One thousand consecutive ECG's from an ambulatory population of patients with suspected or proven cardiac disease were evaluated using two versions of the Telemed computerized ECG system. Only minor differences were found between the two programs. In version 6 vs. version 5, 87% vs. 90% of 287 normal ECG's were correctly classified and 93% vs. 96% of abnormal ECG's were correctly classified; the percent of acceptable diagnostic agreement was 86.2% and 87.4% respectively (NS). The sensitivity for arrhythmia detection, transmural inferior infarction and ST-T wave abnormalities was slightly greater in version 6. The increased sensitivity was not accompanied by decreased specificity. The sensitivity for left ventricular hypertrophy decreased from 95.2% to 91.4% in version 6 with a slight increase in specificity (95.2% to 97.0%). In conclusion, criteria changes in the most recent version of the Telemed program have not resulted in a major change in diagnostic performance. Arrhythmia detection is slightly but not significantly improved.

Significance of precordial ST‐segment depression in acute transmural inferior infarction: Coronary angiographic findings

Coronary arteriographic findings in patients with acute transmural inferior infarction were studied from 57 patients (51 men and 6 women). Their ages ranged from 28 to 72 years with a mean of 50 years. Twenty-six patients (Group A) had minimal (less than 0.1 mV) or no precordial ST-segment depression. Thirty-one patients (Group B) had precordial ST-segment depression of 0.1 mV or more. The two groups showed consistent differences in frequency of the left anterior descending artery (LAD) stenosis, multivessel disease, mean peak plasma creatinine phosphokinase (CPK, IU/L), and mean ejection fraction. For Group A vs B, these differences were: LAD stenosis, 31% vs 68%, multivessel disease, 35% vs 81%, mean peak plasma CPK, 1283 versus 1904, and mean ejection fraction, 60.5% vs 45.3%. The incidence of abnormal anterolateral and posterobasal wall motion in Group B was more (p less than 0.01 and p less than 0.05 respectively) than in Group A. All patients in Group B who had precordial ST-segment depression of 0.3 mV or greater, had LAD stenosis. There was no relation between the duration of ST-segment depression and the presence of LAD stenosis. Also, there was no correlation between the presence of collateral circulation and the development of ST-segment depression. The Group B patients tended to have more complications in the acute phase and in the follow up period (p less than 0.05) than did those in Group A. It is concluded that precordial ST-segment depression in acute inferior wall infarction is probably related to anterior injury due to LAD stenosis and these patients were shown to have more severe coronary artery disease, more depression of their ejection fractions, and more myocardial damage than patients without this finding. The earliest recorded ECG is most valuable in identifying the high risk patients. The presence of LAD stenosis in patients with inferior wall infarction who have precordial ST-segment depression of 0.3 mV or more are likely.

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 (V 4R to V 6R) 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 V 4R to V 6R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.

Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction

To assess various factors associated with anterior S-T segment depression during acute inferior myocardial infarction, 47 consecutive patients with electrocardiographic evidence of a first transmural inferior infarction were studied prospectively with radionuclide ventriculography an average of 7.3 hours (range 2.9 to 15.3) after the onset of symptoms. Thirty-nine patients (Group I) had anterior S-T depression in the initial electrocardiogram and 8 (Group II) did not have such “reciprocal” changes. There was no difference between the two groups in left ventricular end-diastolic or end-systolic volume index or left ventricular ejection fraction. Stroke volume index was greater in Group I than in Group II. There were no group differences in left ventricular total or regional wall motion scores. A weak correlation existed between the quantities (mV) of inferior S-T segment elevation and reciprocal S-T depression. No relation between anterior S-T segment depression and the left ventricular end-diastolic volume index could be demonstrated; the extent of left ventricular apical and right ventricular wall motion abnormalities, both frequently associated with inferior infarction, did not correlate with the quantity of anterior S-T depression. These data show that anterior S-T segment depression occurs commonly during the early evolution of transmural inferior infarction, is not generally a marker of functionally significant anterior ischemia and cannot be used to predict left ventricular function in individual patients. Anterior S-T segment depression may be determined by reciprocal mechanisms.

Nontransmural myocardial infarction: A comparison of hospital and late clinical course of patients with that of matched patients with transmural anterior and transmural inferior myocardial infarction

The hospital and long-term course of 67 patients with nontransmural myocardial infarction was compared with that of 66 patients with transmural anterior and 63 patients with transmural inferior infarction matched for age, sex, previous infarction and prior congestive heart failure. During their hospital stay, patients with nontransmural infarction had significantly less congestive heart failure and fewer intraventricular conduction defects than did patients with transmural anterior infarction; fewer atrial tachyarrhythmias and less sinus bradycardia and atrioventricular block than did patients with transmural inferior infarction; and an incidence of hypotension, pericarditis and ventricular irritability similar to that of patients in the other two groups. Patients with nontransmural infarction had a significantly lower coronary care unit mortality rate (9 percent) than that of patients with transmural anterior or transmural inferior infarction (20 and 19 percent, respectively). By 3 months, the mortality rate had risen to 14 percent in patients with nontransmural infarction, but was significantly higher (29 and 27 percent, respectively) in patients with transmural anterior or transmural inferior infarction. Angina was common in all three groups, occurring in more than 50 percent of patients during a mean follow-up period of 28.6 months after hospital discharge. In contrast, the incidence of subsequent myocardial infarction was significantly greater in patients with nontransmural myocardial infarction, occurring in 21 percent at 9 months compared with only 3 percent of patients with transmural anterior (p <0.01) and 2 percent of patients with transmural inferior (p <0.05) infarction. By 54 months, 57 percent of patients with nontransmural infarction had sustained a new infarction contrasted with only 12 percent of patients with transmural anterior (/p <0.001) and 22 percent of patients with transmural inferior (p <0.01) infarction. Late mortality increased in patients with nontransmural myocardial infarction and, although this group had a significantly better survival rate at 3 months, the overall late mortality of the three groups was comparable. The study suggests that nontransmural myocardial infarction is an unstable ischemic event associated with a great risk of later myocardial infarction and high late mortality rate. A more aggressive diagnostic and therapeutic approach may be warranted in patients with nontransmural myocardial infarction.

EARLY ANGIOGRAPHY DURING INFARCTION: A SEARCH FOR SPASM

ABSTRACTThe predominant cause of continuing injury during transmural myocardial infarction is intracoronary thrombosis linked to plaque rupture or plaque hemorrhage. The initiating events, however, remain unknown primarily because angiography is performed late. Postmortem analysis of patients dying suddenly may not be relevant since it is not known whether a transmural myocardial infarction would have followed. Therefore, we must make conclusions from early therapeutic responses and from angiography performed always with some delay.Sixty patients were studied. Twenty‐five showed anterior transmural infarction and were evaluated by systemic nitroglycerin response, followed by coronary angiography after six hours to seven days. Only three of twenty‐five showed greater than 50 % reduction in precordial ST segment elevation during the thirty‐minute postnitroglycerin observation period. Angiography showed left anterior descending occlusion in thirteen and high grade stenosis in twelve. Nitroglycerin response was seen only in patients with left anterior descending stenosis. The mechanism of nitroglycerin response, however, was not observed.Thirty‐five patients with either anterior or inferior transmural infarction received sublingual and intravenous nitroglycerin on admission and coronary angiography within six hours, during which intracoronary nitroglycerin was infused into the obstructed coronary artery. Only two patients responded to systemic nitroglycerin with a greater than 50 % fall in ST segment elevation. At angiography the offending vessel was stenotic and not further dilatable with intracoronary nitroglycerin. Thirty‐two patients receiving intracoronary nitroglycerin showed no reduction in coronary stenosis and no reversal of obstruction. Three patients with coronary occlusion (two with inferior infarction, one with anterior infarction) responded to intracoronary nitroglycerin with slow antegrade flow. This restored flow was adequate to outline intracoronary filling defects but inadequate to reduce injury or to induce ventricular irritability. In these patients streptokinase infusions cleared the defects and augmented antegrade flow.In conclusion, neither responsivity to nitroglycerin nor early coronary angiography demonstrate that coronary spasm is pronounced after onset of transmural myocardial infarction.

Application of radionuclide imaging in the detection of acute myocardial infarction.

Radionuclide imaging was useful for noninvasively visualizing a location and size of infarction in two patients with acute myocardial infarction. In one patient, inferior subendocardial myocardial infarction was detected by 99mTc-PYP myocardial scintigraphy and then inferior transmural infarction was observed as more intense radioactivity with a larger size. In the other patient with acute extensive anterior myocardial infarction, akinesis of the left ventricular wall and left ventricular aneurysm were confirmed by first-pass radionuclide angiocardiography and multigated equilibrium cardiac pool scan.

Noninvasive identification of a high risk subset of patients with acute inferior myocardial infarction

Although S-T segment depression of various degrees is known to occur in the precordial electrocardiogram of patients with acute inferior myocardial infarction its prognostic significance is unknown. Left ventricular ejection fraction and regional wall motion were therefore measured noninvaslvely with radionucilde ventriculography and related to the electrocardiographic changes within 48 hours of the onset of acute transmural inferior infarction in 44 patients who had had no previous infarction. The mean ejection fraction of 0.45 ± 0.13 (standard deviation) in Group A (24 patients with greater than 1 mm S-T segment depression in at least two of six precordial leads) was lower (p < 0.001) than that (0.63 ± 0.08) in Group B (20 patients with no or less than 1 mm S-T depression in these leads). A depressed ejection fraction (less than 0.54) was present in 76 percent of patients in Group A and in 10 percent of patients in Group B (p < 0.01). Total wall motion score, a semiquantitative index of regional wall motion abnormality, was lower in Group A (42 ± 6) than in Group B (54 ± 4) (p < 0.001). Severe wall motion abnormalities of remote anteroseptal left ventricular segments were observed in 50 percent of patients in Group A and 15 percent of patients in Group B (p < 0.05). The peak serum MB creatine kinase levels were higher in Group A than in Group B (167 ± 92 versus 84 ± 56, p < 0.001). Left ventricular failure developed in 50 percent of patients in Group A but did not develop in Group B (p < 0.001). Five (19 percent) of 24 patients in Group A died in the hospital (3 from pump failure, 1 from arrhythmia and another from electromechanical dissociation). There were no deaths in Group B. The overall data indicate that patients with inferior wall infarction who have associated precordial S-T segment depression have greater global and regional left ventricular dysfunction presumably due to associated ischemia or infarction in areas remote from the inferior wall and they have relatively high in-hospital mortality and morbidity rates. Early noninvasive detection of this high risk subset may permit the testing of aggresive modes of therapy designed to limit the extent of myocardial ischemic damage with resultant decrease in mortality and morbidity.

Long term course of subendocardial myocardial infarction compared to that of anterior and inferior transmural infarction. A controlled study

Long term course of subendocardial myocardial infarction compared to that of anterior and inferior transmural infarction. A controlled study

Inferior myocardial infarction and right coronary artery occlusive disease. A correlative study.

The present study represents an attempt to correlate the electrocardiogram and coronary arteriogram in patients with an inferior transmural infarct - or total occlusion of the right coronary artery. The influence of the collateral circulation on these findings was also evaluated. Fifty patients with a total occlusion of the right coronary artery had characteristic electrocardiographic changes of an inferior infarct in 44 per cent, very suspicious changes in 32 per cent, and no changes suggesting an inferior infarct in 24 per cent. However, in this latter group who had no evidence of an inferior infarct, we were able to recognize a small number who showed an anterior wall infarct. Collateral circulation was more frequently present and more extensive in those patients whose electrocardiograms did not show changes typical of inferior transmural infarction. This suggested that collateral circulation might minimize some of the electrocardiographic abnormalities which would normally result from occlusive disease of the right coronary artery. Another 50 patients, selected because of definite electrocardiographic evidence of typical inferior transmural infarction, were evaluated by coronary arteriography. Severe obstructive disease of the right coronary artery was present in 86 per cent of the group. In the remaining 7 patients (14 per cent) minimal or no disease was found. Infarction of the inferior wall may have resulted from occlusive disease of the anterior descending artery or have been the result of a right coronary artery occlusion with subsequent recanalization. We conclude from our study that a careful analysis of electrocardiographic abnormalities in theinferior leads will, with certain limitations, permit us to estimate the likelihood of a severe lesion in the right coronary artery, and, in the face of definite electrocardiographic evidence of an inferior infarct, to predict the diseased artery.

Regional myocardial blood flow in patients with residual anterior and inferior transmural infarction.

Regional myocardial perfusion rates were estimated in ten patients with a residual transmural anterior wall infarction and ten patients with a residual transmural inferior infarction. The results in these two groups of patients were compared to the regional myocardial perfusion patterns obtained in 25 patients with normal coronary arteriograms who failed to demonstrate any electrocardiographic evidence of a myocardial infarction. Clearance rates of xenon-133 from multiple areas of the heart were monitored externally with a multiple-crystal scintillation camera following selective injection of the isotope into either coronary artery. Local myocardial blood flow rates were calculated by the Kety formula. In patients with normal coronary arteriograms, mean myocardial perfusion rates in the left ventricle (62 ml/l00g/min) exceeded flow rates in the right ventricle and atrium. There was slight inhomogeneity of local perfusion rates but no significant differences among major subregions (anterior descending, diagonal, or circumflex) within the left ventricle. In the group with an anterior transmural infarction, myocardial blood flow rates were significantly depressed (44 ml/l00g/min) and asynergy was present in the region of the left ventricle supplied by the anterior descending artery, which was &gt;80% narrowed. Diminished capillary blood flow was found in the right ventricular region in the patients with an inferior transmural infarction and right coronary artery narrowing of &gt;80%. There was no evidence of nutrient flow to the inferior surface of the left ventricle after right coronary 133 Xe injection. The data indicate that myocardial perfusion was reduced in regions of the heart which correspond to the electrocardiographic and angiographic location of residual transmural infarction. The perfusion rates observed in areas showing electrocardiographic evidence of transmural infarction and regional ventricular asynergy, although subnormal, were surprisingly high and suggested the presence of residual viable myocardial cells.

Left ventricular hemodynamics in anterior and inferior myocardial infarction

Initial hemodynamics were studied in 50 patients with acute myocardial infarction classified according to anterior or inferior location. Twenty-two had anterior transmural infarction (indicated by Q wave changes), 12 had anterior necrosis (S-T and T wave changes plus increases in serum enzymes), 11 had inferior transmural infarction and 5 inferior necrosis. When initial left ventricular filling pressure, stroke index, heart rate and stroke work index were considered together in all patients, there was a significant difference (P < 0.05) between patients with anterior infarction and those with inferior infarction. Left ventricular filling pressure and heart rate were higher and stroke index and stroke work index lower in patients with anterior infarction. These hemodynamic abnormalities in patients with anterior infarction were reflected clinically by more frequent ventricular gallops and a higher hospital mortality rate. In clinically uncomplicated acute myocardial infarction, pulmonary arterial end-diastolic pressure ranged from 8 to 27 mm Hg. Stroke index and stroke work index correlated best with bedside classification and were lower in patients with a poorer clinical condition. Initial hemodynamics were studied in 50 patients with acute myocardial infarction classified according to anterior or inferior location. Twenty-two had anterior transmural infarction (indicated by Q wave changes), 12 had anterior necrosis (S-T and T wave changes plus increases in serum enzymes), 11 had inferior transmural infarction and 5 inferior necrosis. When initial left ventricular filling pressure, stroke index, heart rate and stroke work index were considered together in all patients, there was a significant difference (P < 0.05) between patients with anterior infarction and those with inferior infarction. Left ventricular filling pressure and heart rate were higher and stroke index and stroke work index lower in patients with anterior infarction. These hemodynamic abnormalities in patients with anterior infarction were reflected clinically by more frequent ventricular gallops and a higher hospital mortality rate. In clinically uncomplicated acute myocardial infarction, pulmonary arterial end-diastolic pressure ranged from 8 to 27 mm Hg. Stroke index and stroke work index correlated best with bedside classification and were lower in patients with a poorer clinical condition.