Unusual Site of Left Ventricular Thrombus after Acute Myocardial Infarction

Left ventricular (LV) thrombus formation is a frequent complication in patients with acute anterior myocardial infarction (MI). Its incidence is lower with inferior wall MI. Risk factors for the development of LV thrombus are consistently irrespective of infarct treatment and include large infarct size, severe apical akinesia or dyskinesia LV aneurysm, and anterior MI.     

Inaccuracy of various proposed electrocardiographic criteria in the diagnosis of apical myocardial infarction--a critical review

The diagnostic accuracy of the standard electrocardiogram (ECG) in apical myocardial infarction (MI) was evaluated in 112 consecutive patients with recent MI and wall-motion abnormalities limited to the left ventricular (LV) apex on two-dimensional echocardiography, performed at rest 21 to 84 days after MI. The following patterns of abnormal (greater than or equal to 30 ms) Q waves were found: anteroseptal (Q V1-V4) in 44 patients (39.3%), anterolateral (Q V1-V6 and/or I, aVL) in 22 (19.6%), inferior (Q III, aVF or II, III, aVF) in five (4.5%), lateral (Q I, aVL and/or V5-V6) in five (4.5%), anteroinferior in six (5.3%); non-Q MI was present in 30 patients (26.8%). By applying various proposed ECG criteria, the presence of apical MI was correctly identified in very few (24, 21%) patients. LV apex was extensively asynergic in 85 patients (76%) and partially asynergic in 27 (24%). All the patients with Q waves in lateral leads and 47% of the patients with non-Q MI had partially asynergic LV apex, while in the other ECG patterns, extensively asynergic LV apex was predominant. The presence of both greater than or equal to 30 ms Q waves and loss of R in left precordial leads and I strongly suggests extensive apical asynergy; normal QRS in the same leads, however, does not exclude extensive apical involvement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlation between ST Elevation and Q Waves on the Predischarge Electrocardiogram and the Extent and Location of MIBI Perfusion Defects in Anterior Myocardial Infarction

Background: The common electrocardiographic subclassification of anterior acute myocardial infarction (AMI) is not reliable in presenting the exact location of the infarct. We investigated the relationship between predischarge electrocardiographic patterns and the extent and location of perfusion defects in 55 patients with first anterior AMI. Methods: Predischarge electrocardiogram was examined for residual ST elevations and Q waves which were correlated with technetium‐99m‐sestamibi function and perfusion scans. Results: Patients with ST elevations in V2–V4 and Q waves in leads V3–V5 had worse global perfusion scores. Perfusion defects in the apex inferior segment were significantly less frequent in patients with Q waves in leads I and aVL (11% vs 54%, P = 0.027; and 22% vs 60%, P = 0.011, respectively). Patients with Q wave in aVF had more frequently involvement of the apex inferior segment (80% vs 40%; P = 0.035). Patients with Q wave in lead II had significantly more frequent perfusion defects in the inferior wall. ST elevation in V3 and V4 was associated with perfusion abnormalities of the infero‐septal segments. ST elevation in V5 and V6 and Q wave in V5 were associated with regional perfusion defects in apical inferior segment (73% vs 30%, P = 0.002), extending into the mid inferior segment (55% vs 18%, P = 0.005 for Q wave in V5). Q wave in lead aVL is associated with less apical and inferior involvement. Q waves in leads II and aVF are a sign of inferior extension of the infarction. Conclusions: Residual ST elevation in leads V3 and V4 are more frequently associated with involvement of the apical‐inferoseptal segment rather than the anterior wall. Residual ST elevation and Q waves in V5 are related to a more inferior rather than a lateral involvement.     

Q-wave prediction of myocardial infarct location, size and transmural extent at magnetic resonance imaging

OBJECTIVE: We investigated how pathologic Q waves or equivalents predict location, size and transmural extent of myocardial infarction (MI). METHODS: MI characteristics, detected by contrast-enhanced magnetic resonance imaging, were compared with 12-lead electrocardiogram in 79 patients with previous first MI. RESULTS: Q waves involved only the anterior leads (V1-V4) in 13 patients: in all patients MI involved the anterior and anteroseptal walls and apex; 81% of scar tissue was within these regions. Q waves involved only the inferior leads (II, III, aVF) in 13 patients: in 12 of these patients MI involved the inferior and inferoseptal walls; however, only 59% of scar occupied these regions. Q waves involved only lateral leads (V5, V6, I, aVL) in 11 patients: in nine of these patients MI involved the lateral wall but only 27% of scar tissue was within this wall. Q waves involved two electrocardiogram locations in 42 patients. In the 79 patients as a whole, the number of anterior Q waves was related to anterior MI size (r=0.70); however, the number of inferior and lateral Q waves was only weakly related to MI size in corresponding territories (r=0.35 and 0.33). A tall and broad R wave in V1-V2 was a more powerful predictor of lateral MI size than Q waves. Finally, the number of Q waves accurately reflected the transmural extent of the infarction (r=0.70) only in anterior infarctions. CONCLUSION: Q waves reliably predict MI location, size and transmural extent only in patients with anterior infarction. A tall and broad R wave in V1-V2 reflects a lateral MI.     

The effect of the localization of Q wave myocardial infarction on ventricular electromechanics

BACKGROUND: The exact location of a Q wave myocardial infarction has an important effect on overall left ventricular function. OBJECTIVES: To assess the effect of localization of Q wave infarction on left ventricular minor and long axis function, with particular reference to electromechanical disturbances. METHODS: We studied 72 patients with Q wave myocardial infarction; 35 anterior, age 61+/-15 years and 37 inferior, age 62+/-12 years. ECG intervals were automatically measured by Hewlett-Packard Pagewriter and LV dimension and filling velocities studied by transthoracic echocardiography and simultaneous phonocardiogram. Findings were compared with 21 controls of similar age. RESULTS: Heart rate and all ECG intervals were similar in the two patient groups and controls. QRS axis was more to the left in patients with inferior MI. Normal septal q wave was absent in lead V5 and V6 in 33/35 (94%) patients with anterior MI and in only 3/37 (8%) with inferior MI, p<0.001. LV minor axis dimensions were enlarged vs. normal (p<0.001) in the two patient groups and to a greater extent in anterior MI compared with inferior MI, p<0.05. Isovolumic relaxation time was prolonged only in-patients with an inferior MI, p<0.01. Long axis amplitude was globally reduced (p<0.001) in the two patient groups as were shortening and lengthening velocities (p<0.001). The onset of septal long axis shortening with respect to the q wave was delayed by 30 and 40 ms in inferior MI and anterior MI and that of lengthening with respect to A2 by 20 and 30 ms, respectively, compared to normal (p<0.001 for both). Post ejection shortening was localized to the septal long axis in 32/35 patients with anterior MI but was generalized involving all three LV long axes in inferior MI, p<0.001. Transmitral Doppler flow velocities and the frequency of mild mitral regurgitation were similar in the two groups. CONCLUSION: These results confirm a close association between anterior Q wave infarction, septal incoordination and absent septal q waves. The global incoordinate long axis behaviour in inferior Q wave MI may be due to significant papillary muscle dysfunction, and results in significant shape change in early diastole. This disturbance in electromechanical behaviour might play an important role in the differing outcomes between the two different sites of myocardial infarction.     

Correlation between non-reversible thallium-201 myocardial perfusion defect and ECG criteria in the diagnosis of apical myocardial infarction

BACKGROUND: ECG identification of apical myocardial infarction (MI) is controversial and lacks of accuracy. Our aim was to investigate the sensitivity of different proposed ECG criteria in the presence of apical perfusion defects assessed with SPECT analysis. METHODS: One hundred twenty-four (98 M, 26 F) out of 1500 patients with suspected coronary artery disease, showed apical perfusion defect not reversible at rest and after reinjection at tomographic SPECT analysis during thallium-201 scintigraphy. RESULTS: In the group of 29 patients presenting wide isolated apical perfusion defect (wAPD) Q waves in anterior segments with definition of antero-septal MI was prevalent (51.7%), while few patients (41.3%) presented the ECG criteria of apical MI as proposed in the literature. In 19 of the 25 patients with partial isolated apical perfusion defect (pAPD), the absence of Q wave was clearly prevalent. Fifty patients had a wAPD partially extended in surrounding regions, as anterior or septal, inferior or lateral myocardial segments, in these patients, the site of Q wave location was more variable, with prevalent Q wave in anterior leads, but with more incidence of Q waves in leads II III aVF, especially in patients with associated perfusion defect in inferior segments. Substantially, the same finding resulted in the 20 patients showing a pAPD extended in surrounding myocardial segments. CONCLUSION: In conclusion, the low diagnostic sensitivity of the ECG criteria of identification of apical MI is clearly demonstrated by our analysis carried out using SPECT perfusion scintigraphy, with ECG findings of anterior/anterior-septal myocardial necrosis in the patients with wAPD.     

Left ventricular wall motion with and without Q-wave disappearance after acute myocardial infarction

Since post-acute myocardial infarction (AMI) Q waves may disappear independent of reinfarction or development of left bundle branch block, the relation between the presence of Q waves and segmental asynergy was assessed in 58 patients with initial Q waves after first AMI. Two-dimensional (2-D) echocardiograms and electrocardiograms were recorded 1 year later. By electrocardiography, 28 had anterior and 25 inferior AMI. At 1 year Q waves had disappeared in 12 of 53 patients (23%): 5 with anterior and 7 with inferior AMI. Segmental asynergy, however, was present in 9 of these 12 patients, although dyskinesia was absent. Presence of Q waves at 1 year (41 patients) was always associated with segmental asynergy. Wall motion score, based on degree of segmental asynergy, was higher in the 41 patients with Q waves compared with patients in whom Q waves disappeared (7.8 +/- 4.4 vs 2.7 +/- 1.9, p less than 0.001). In patients with anterior AMI the number of Q waves at 1 year and the grade of asynergy were correlated. Segmental dyskinesia was rare in patients with inferior AMI (1 of 25) but was common in those with anterior AMI (18 of 28), and was consistently present in patients with more than 2 anterior Q waves.     

Natural history of left ventricular thrombi: their appearance and resolution in the posthospitalization period of acute myocardial infarction

A series of 198 consecutive patients with acute myocardial infarction were prospectively studied before hospital discharge and during 24.0 +/- 8.6 months of follow-up. A predischarge thrombus was found in 38 (31%) of 124 patients with anterior infarction but in none of 74 patients with inferior infarction (p less than 0.001). Early thrombolytic therapy in 34 patients did not decrease the rate of thrombus occurrence. Acute anterior infarction, ejection fraction less than or equal to 35% and apical dyskinesia or aneurysm (but not akinesia) were significantly related to the appearance of thrombus during hospitalization by stepwise logistic regression analysis. Echocardiographic follow-up of 159 patients for at least 6 months (mean 26.6 +/- 8.4) revealed that thrombus disappeared in 14 (48%) of 29. Disappearance of thrombus was related to predischarge apical akinesia (but not dyskinesia) and to warfarin therapy during the follow-up period. A new thrombus first appeared after hospital discharge in 13 of 130 patients, and in 7 of the 13 it resolved during further follow-up. Thus, 30% (13 of 42) of thrombi in these patients appeared after discharge from the hospital. Three factors were related to occurrence of new thrombi during the follow-up period: deterioration in left ventricular ejection fraction, predischarge ejection fraction less than or equal to 35% and ventricular aneurysm or dyskinesia. Systemic embolism occurred in six patients, all with a predischarge thrombus (p less than 0.001). Mobility of the thrombus was the only variable significantly related to subsequent embolic events (p = 0.001) by logistic regression analysis. Thus, the predischarge echocardiogram identifies patients with thrombus and those at highest risk of embolic events. It can indicate patients who are likely to have thrombus resolution and those at risk of developing a new thrombus after hospital discharge. Follow-up echocardiograms may help in guiding the length of long-term anticoagulant therapy. Four additional patients with a predischarge apical mobile thrombus (not part of the consecutive series) received thrombolytic therapy. In two of the four, lysis of thrombus was achieved without complications, but systemic embolism occurred in the other two, and proved fatal in one.     

Left ventricular thrombus formation after first anterior wall acute myocardial infarction

The characteristics of the left ventricle and coronary arteries associated with left ventricular (LV) thrombus in patients with recent anterior acute myocardial infarction were defined. Of 77 patients studied, 35 (46%) had LV thrombi. The presence of LV thrombus was not correlated to the extent of coronary artery disease. The frequency of LV thrombus progressively increased with groups of increasing wall motion abnormality as determined by the extent of akinesia and dyskinesia (%AD) (%AD 0 to 14, thrombus present in 3 of 16 [19%], %AD 15 to 29, thrombus in 8 of 27 [30%]; %AD greater than or equal to 30%, thrombus in 24 of 34 [71%]; p less than 0.001) and with increasingly severe degrees of early ventricular shape change (normal or mildly abnormal contour, 16% with thrombus; moderately abnormal contour, 36% with thrombus; severely abnormal contour, 70% with thrombus; p less than 0.001). Patients with thrombi had higher diastolic (249 +/- 55 vs 225 +/- 48 ml; p less than 0.05) and systolic (158 +/- 48 vs 120 +/- 45 ml; p less than 0.001) volumes than patients without thrombi, respectively. A stepwise discriminant analysis identified ejection fraction, extent of early shape change and LV end-diastolic pressure as independent correlates of LV thrombus after acute myocardial infarction.     

Echocardiographic determinants of left ventricular ejection fraction after acute myocardial infarction

OBJECTIVE: This study was performed to determine if factors other than the size of regional dysfunction influence the global left ventricular ejection fraction after acute myocardial infarction. BACKGROUND: Left ventricular ejection fraction is an important prognostic variable after acute myocardial infarction. Although infarct size is known to affect the subsequent global left ventricular ejection fraction, it remains unclear whether other factors such as site or severity of the wall motion abnormality influence the ejection fraction after acute myocardial infarction. METHODS: Sixty-nine consecutive patients (mean age 61 +/- 14 years, 46 [67%] male) who did not receive thrombolytic therapy or undergo early revascularization were studied by echocardiography 1 week after Q-wave myocardial infarction. The absolute size of the region of abnormal wall motion (AWM) and the percentage of the endocardium involved (%AWM) were quantitated along with the wall motion score. A severity index was then derived as the mean wall motion score within the region of AWM. Site of myocardial infarction was classified as either anterior or inferior from the endocardial map. Left ventricular ejection fraction was measured by Simpson's method with 2 apical views. RESULTS: Twenty-nine (42%) patients had anterior and 40 had inferior myocardial infarction. The mean left ventricular ejection fraction was significantly lower in anterior than in inferior myocardial infarction (44.8% +/- 11.5% vs 53% +/- 8.6%; P =. 001). The mean %AWM was greater in anterior than in inferior myocardial infarction (32.1 +/- 15.5 vs 22.4 +/- 14.1; P =.01). The mean wall motion score was greater in anterior than in inferior myocardial infarction (9.8 +/- 6.4 vs 6.4 +/- 4.4; P =.01). The mean severity index did not differ by site. Multiple regression analysis demonstrated that, in descending order of importance, %AWM, extent of apical involvement, and site of myocardial infarction were independent determinants of global left ventricular ejection fraction. CONCLUSIONS: For myocardial infarctions of similar size, left ventricular ejection fraction is lower when apical involvement is extensive and the site of infarction is anterior. This site-dependent difference may be related to characteristics specific to the apex.     

Diagnostic significance for coronary artery disease of abnormal Q waves in the "lateral" electrocardiographic leads

To determine the diagnostic significance for coronary artery disease of abnormally large Q waves in leads I, aVL, V5 and V6--the "lateral" electrocardiographic leads--the electrocardiograms of 240 patients who had undergone cardiac catheterization were studied. First, the electrocardiograms of 99 subjects proved normal by cardiac catheterization (group 1) were studied to determine the values of the durations of Q waves in leads I, aVL, V5 and V6 that should be exceeded to be considered abnormal. These values were 30, 30, 20 and 25 ms, respectively. Then, 67 patients were identified who had abnormal Q waves in at least 1 of these leads (group 2) and 74 patients with at least 1 angiographic abnormality but without abnormal Q waves in any of these leads (group 3). Group 2 had generally more extensive left ventricular disease and a higher prevalence of anterior, inferior and apical healed myocardial infarction (MI) than group 3. However, compared with group 3, group 2 had lower prevalences of significant narrowing of the coronary arteries that supply the left ventricular lateral wall. Within group 2, abnormal Q waves in leads I and aVL (traditionally designated high lateral MI) were associated with anterior as well as apical MI, and abnormal Q waves in leads V5 and V6 (traditionally designated anterolateral MI) were associated with inferior as well as apical MI. Thus, abnormal Q waves in leads I, aVL, V5 and V6 tend to reflect apical rather than lateral MI and the term anterolateral MI is especially misleading.     

Abnormal Q waves on the admission electrocardiogram of patients with first acute myocardial infarction: Prognostic implications

Background: Q waves developed in the subacute and persisting into the chronic phase of myocardial infarction (MI) usually signify myocardial necrosis. However, the mechanism and significance of Q waves that appear very early in the course of acute MI (<6 h from onset of symptoms), especially if accompanied by ST elevation, are probably different. Hypothesis: This study assesses the prognostic implications of abnormal Q waves on admission in 2,370 patients with first acute MI treated with thrombolytic therapy <6 h of onset of symptoms. Results: Patients with abnormal Q waves in ≥2 leads with ST-segment elevation (n = 923) were older than patients without early Q waves (n = 1,447) (60.6 ±11.9 vs. 58.8 ±11.9 years, respectively; p = 0.0003), and had a greater incidence of hypertension (34.3 vs. 30.5% p = 0.05) and anterior MI (60.6 vs. 41.1 % p<0.0001). Time from onset of symptoms to therapy was longer in patients with Q waves upon admission (208 ± 196 vs. 183 ± 230 min; p = 0.01). Peak serum creatine kinase (2235 ± 1544 vs. 1622 ± 1536 IU; p<0.0001), prevalence of heart failure during hospitalization (13.8 vs. 7.0%, p<0.0002), hospital mortality (8.0 vs. 4.6% p = 0.02), and cardiac mortality (6.6 vs. 4.5%, p = 0.11) were higher in patients with anterior MI and with abnormal Q waves than in those without abnormal Q waves upon admission. There was no difference in peak creatine kinase, prevalence of heart failure, in-hospital mortality, and cardiac mortality between patients with and without abnormal Q waves in inferior MI. Multivariate regression analysis confirmed that mortality is independently associated with presence of Q waves on admission (odds ratio 1.61; 95% CI 1.04–2.49; p = 0.04 for all patients; odds ratio 1.65; 95% CI 0.97–2.83; p=0.09 for anterior wall MI. Conclusion: Abnormal Q waves on the admission electrocardiogram (ECG) are associated with higher peak creatine kinase, higher prevalence of heart failure, and increased mortality in patients with anterior MI. Abnormal Q waves on the admission ECG of patients with inferior MI are not associated with adverse prognosis.     

Reliability of standard electrocardiogram in detecting left ventricular asynergy in 315 patients with recent myocardial infarction

The relationship between asynergy of the left ventricular wall detected by two-dimensional echocardiography and ECG signs of necrosis (number of Q waves greater than or equal to 40 ms, Wagner's score) was evaluated in 315 patients (NYHA I-II) 23-90 days after a first Q-wave myocardial infarction (MI). Poor correlations were found between asynergy and ECG parameters. An ECG anterior MI is an apicoseptal MI by echo (independently of the ECG extent of Q waves) and the ECG is of little or no help in predicting the extent of asynergy to the inferior wall and proximal segments of the septum. An ECG inferior MI is inferoposterior by echo and the ECG has very limited value in predicting the extent of asynergy to the apex and septum. Patients with Q waves in leads II, III, and aVF had more extensive asynergy than those with either 2Q or greater than 3Q. R/S greater than or equal to 1 in V1 and/or V2 was present in 44% of patients with inferior MI while asynergy of at least one segment of the posterior wall was observed in 94%. In conclusion, standard ECG is sensitive in identifying anterior versus inferior infarct but it is unreliable in predicting the real extent of asynergy of the left ventricle, particularly in inferior infarcts.     

ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction

In 5 of 69 patients (7%) undergoing intracoronary or intravenous streptokinase treatment, the ST-segment elevations in leads V₁ to V₅ were caused by occlusion of the right rather than the left anterior descending coronary artery and by myocardial infarction (MI) of the right ventricular (RV) wall rather than the anterior left ventricular (LV) wall or the ventricular septum. RV involvement was documented by technetium pyrophosphate uptake, hypokinesia, dilatation and depressed RV ejection fraction. The left anterior descending artery was patent and the anterior LV wall had normal thallium-201 uptake, no technetium uptake and normal wall motion. ST-segment elevation was highest in lead V₁ or V₂ and decreased toward lead V₅; in patients with anterior LV MI, the ST-segment elevations are usually lowest in lead V₁ and increase toward the V₅ lead. In contrast to anterior LV infarcts, the R waves in leads V₁ to V₅ did not decrease and Q waves did not evolve with progression of the MI.The ST-segment elevations in leads V₁ to V₅ in our patients were associated with small or absent ST-segment elevations in leads, II, III and aVF, suggesting that in other cases of RV infarction, the appearance of ST-segment elevations in leads V₁ to V₅ is blocked by the dominant electrical forces of the LV inferior MI. This suggestion was confirmed in a canine model. Recognition of the presence of RV infarction may be therapeutically important.     

Hemodynamic significance of an anatomo-functional classification of myocardial infarction

Recently we proposed a topographical classification of myocardial infarction (MI) based on the site and extension of left ventricular asynergy (AS) detected by Two-dimensional Echocardiography (2D ECHO) at rest: a) Anterior MI: 1) apical MI with AS of apical segments only, 2) apico-septal MI with AS of apex and septum, 3) apico-septo-lateral MI with involvement of septum, apex and antero-lateral wall. b) Inferior MI: 1) isolated inferior MI with involvement of infero-dorsal wall segments; 2) infero-apical MI with AS of inferior wall and apex, 3) infero-apico-septal MI with kinetic abnormalities of inferior wall, apex and septum and finally c) antero-inferior MI with large AS of septum, apex, antero-lateral and inferior wall. In order to validate the functional significance of this classification, 2D ECHO at rest and symptom limited bicycle ergometric test (E) in supine position with EC-Graphic and hemodynamic monitoring (Swan-Ganz cath.), were performed in the same day within two months after a first transmural MI, in 259 patients, I-II NYHA classes. Among anterior MIs, diastolic pulmonary arterial pressure (PAedP) at rest was normal and similar in apical and apico-septal MIs (11 +/- 3 mmHg). It was significantly (p less than .001) higher 14 +/- 5 mmHg in apico-septo-lateral MIs. Left ventricular stroke work index (LVSWI) was higher in apical MIs (55 +/- 14) than in apico-septal (47 +/- 12, p less than .01) and in apico-septo-lateral MIs (38 +/- 9, p less than .001). Maximal work load during E was 86 +/- 31 watt in apical MIs, 77 +/- 29 watt in apico-septal MIs and 70 +/- 25 in apico-septo-lateral MIs with significant difference (p less than .05) only between the last ones and apical MIs. The PAedP during E was normal (20 +/- 7 mmHg) in apical MI, but increased abnormally in apico-septal (24 +/- 7 mmHg) and in apico-septo-lateral (27 +/- 7 mmHg) with a significant difference (p less than .01) only between apical and apico-septo-lateral MIs. In inferior MIs, hemodynamic data at rest were similar in pts with isolated inferior, infero-apical and infero-apico-septal MIs. Maximal work load, similar in inferior and infero-apical MI (88 +/- 30 W) was higher (p less than .01) than in infero-apico-septal (68 +/- 22W).(ABSTRACT TRUNCATED AT 400 WORDS)     

Post-operative outcome of ventricular reshaping by septal exclusion in patients with severe left ventricular dysfunction

BACKGROUND: Post-myocardial infarction, anteroseptal dysfunction or akinesia is treated by septal reshaping to improve the surgical outcome in patients with severe left ventricular dysfunction. METHODS AND RESULTS: Between February 2003 to December 2003, 30 consecutive patients with previous anterior wall myocardial infarction and severe ventricular dysfunction underwent septal reshaping. All the dyskinetic and akinetic septal areas were excluded using an oval dacron patch which was sutured from the healthy septal area to the anterior wall, resulting in formation of a new apex. There were two mortalities in the group. After a mean follow-up of 4.2 +/- 1.6 months (1-7 months) it was seen that this procedure resulted in significant reduction of ventricular volume, increase in ejection fraction, an improvement in New York Heart Association class from 2.9 +/- 1.1 to 1.7 +/- 0.3, and a better apical geometry. CONCLUSIONS: In selected patients with left anterior descending artery occlusion resulting in anteroseptal dyskinesia or akinesia, septal exclusion technique provides good clinical and morphological results with significant improvement in left ventricular function.     

Myocardial damage and left ventricular dysfunction in patients with and without persistent negative T waves after Q-wave anterior myocardial infarction

Persistent T-wave inversions during the chronic stage of Q-wave myocardial infarction (MI) indicate the presence of a transmural infarction with a fibrotic layer pathologically. The aim of the present study was to examine the relation between left ventricular (LV) damage and changes in polarity of the T waves from the acute to chronic phase in patients with Q-wave anterior wall MI. We studied 140 patients with persistent T-wave inversions in leads with Q waves (negative T-wave group) and 158 patients with positive T waves (positive T-wave group) at 12 months after anterior MI. In the positive T-wave group, the precordial T waves reverted from a negative to a positive morphology < 3 months after MI in 21 patients (3 M-positive T-wave subgroup), 3 to 6 months in 52 patients (6 M-positive T-wave subgroup), and 6 to 12 months in 75 patients (12 M-positive T-wave subgroup). Ten patients had persistent positive T waves without initial T-wave inversion (persistent positive T-wave group). Wall motion index and LV dimension were higher and the wall thickness for the infarct area and LV ejection fraction were lower in the negative T-wave than in the positive T-wave groups, except the persistent positive T-wave group in the chronic stage (p < 0.0001). Wall motion in the infarcted area improved over the course of 1 year in the 3 M-, 6 M-, and 12 M-positive T-wave subgroups (p < 0.0001), but not in the persistent positive T-wave group. Among the patients with T-wave inversions after admission, those who had persistent negative T waves after 12 months had worse LV function. In patients with initial T-wave inversion, earlier normalization of the precordial T waves was associated with greater improvement in LV function. Patients with persistent positive T waves without initial negative T waves had poorer recovery of LV function than patients with persistent negative T waves. We conclude that the presence of inverted T waves in leads with abnormal Q waves 12 months after MI and the time required for T-wave normalization can be used to assess the degree of LV dysfunction.     

The atrioventricular plane displacement as a means of evaluating left ventricular systolic function in acute myocardial infarction.

Displacement of the atrioventricular (AV) plane toward the cardiac apex in systole was studied quantitatively by echocardiography in 37 patients with first-time acute myocardial infarction (MI) in order to evaluate left ventricular systolic function. The amplitude of AV plane displacement was recorded from the apex at four different sites corresponding to the septal, lateral, anterior, and posterior walls of the left ventricle from apical 4- and 2-chamber views. The patients had a decreased displacement of the AV plane compared with controls which was more pronounced at the sites of infarction. The mean value of the AV plane displacement (AV mean) correlated linearly with the left ventricular (LV) ejection fraction calculated by radionuclide angiography (r = 0.87, p less than 0.001, SEE = 6.2). An AV mean of 10 mm or more had a high sensitivity (95%) and specificity (82%) in defining a normal ejection fraction (greater than or equal to 50%). A high correlation coefficient was found between LV wall motion index and the AV plane displacement. Thus, in acute MI the LV function can be assessed noninvasively using AV plane displacement.     

Comparison of single and biplane ventriculography for determination of left ventricular volume and ejection fraction.

This study was done to compare single and biplane left ventriculography in quantitating left ventricular (LV) volumes and ejection fraction. LV volumes and ejection fraction were measured from a 30 degrees right anterior oblique single plane ventriculogram and a 30 degrees right anterior oblique 60 degrees left anterior oblique biplane ventriculogram in 152 men (aged 59 +/- 9 [mean +/- standard deviation] years), of whom 102 had hypokinesia, akinesia, or dyskinesia. There was excellent agreement between the results of single and biplane ventriculography with respect to LV end-diastolic volume (r = 0.96), end-systolic volume (r = 0.98) and ejection fraction (r = 0.97). The end-diastolic and end-systolic volumes measured by biplane ventriculography were consistently slightly larger than those measured by single plane, whereas ejection fractions measured by the 2 techniques were remarkably similar, even for the 46 patients with biplane ejection fractions less than 0.50 and the 102 with hypokinesia, akinesia or dyskinesia. Thus, LV volumes and ejection fractions determined by single plane ventriculography correlate very well with those determined by biplane ventriculography, even in patients with hypokinesia, akinesia, or dyskinesia and depressed LV systolic performance. Biplane ventriculography appears to provide little information that cannot be obtained reliably from single plane.     

Left ventricular dilatation after primary transmural anterior myocardial infarction. Influence of the percentage of akinesia on echocardiography]

The aim of this study was to determine whether the percentage of akinesia on echocardiography during the acute phase of transmural anterior myocardial infarction could predict secondary left ventricular dilatation. The study group comprised 24 patients (18 men and 6 women) with an average age of 59 years. The patients underwent two echocardiographic examinations, the first during the acute (< 72 hours) phase and the second, 6 months later. Ventricular volumes were calculated by the ellipse monoplane method in the apical 4 chamber view. The percentage of akinesia was defined as the ratio between the length of the akinetic segment and the left ventricular end diastolic perimeter in the apical 4 chamber view. An increase in end diastolic volume (83 +/- 25 vs 62 +/- 18 ml/m2; p < 0.01) and in end systolic volume (51 +/- 27 vs 34 +/- 11 ml/m2; p < 0.01) was observed 6 months after infarction without a significant change in ejection fractions (42 +/- 17% vs 44 +/- 10%). The percentage of akinesia in the acute phase was > 30% in 15 patients (Group I) and < 30% in 9 patients (Group II). The increase in ventricular volumes at 6 months after infarction was significant in Group I (p < 0.02) but not in Group II. At 6 months after infarction, the end systolic volumes were greater (60 +/- 27 vs 37 +/- 22 ml/m2, p < 0.5) and the ejection fractions were lower (35 +/- 13% vs 53 +/- 18%, p < 0.01) in Group I than in Group II.(ABSTRACT TRUNCATED AT 250 WORDS)