ST-segment elevation on Q-leads during exercise in patients with ST-segment elevation at rest after myocardial infarction

INTRODUCTION: ST-segment elevation on Q-leads after an acute myocardial infarction is related to a greater infarct size. The meaning of a further exercise-induced ST-segment elevation in these patients has not been analyzed. METHOD: Thirty-six patients with ST-segment elevation on Q-leads were studied after a first acute myocardial infarction. Exercise testing and cardiac catheterization were performed at the first week. Left ventricular volumes (ml/m(2)); the extent of abnormal wall motion (AWM: chords); contractile reserve (AWM improvement with low dose dobutamine) and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 20 patients; systolic recovery (AWM improvement), left ventricular volumes and coronary patency were again evaluated. RESULTS: Patients with exercise-induced ST-segment elevation in two or more Q-leads (n=21) showed lesser contractile reserve (6+/-6 vs. 12+/-7 chords, P=0.01) than patients without exercise-induced ST-segment elevation (n=13). AWM (F=8.1) and absence of exercise-induced ST-segment elevation (F=9.5; positive predictive value: 80%; negative predictive value: 68%) were the only independent predictors of contractile reserve. Nevertheless, this electrocardiographic sign was not related to left ventricular volumes, coronary patency or systolic function and it did not predicted late systolic recovery. CONCLUSIONS: In patients with baseline ST-segment elevation on Q-leads an exercise-induced ST-segment elevation is independently related to a lesser contractile reserve but not to the evolution of volumes or regional dysfunction during the first 6 months post-infarction. Therefore, the clinical value of this sign seems to be limited to the non-invasive detection of myocardial viability during the early post-infarction phase.     

Effects of reperfusion obtained two to six months after acute myocardial infarction on myocardial electrical stabilization in patients with an occluded infarct-related coronary artery

To assess the changes in electrical stability markers in patients with previous myocardial infarction after very late reopening of the infarct-related artery, we studied QT dispersion, corrected-QT dispersion, and late potentials before and 1, 3, and 6 months after an attempt at late percutaneous coronary intervention (PCI) in 31 consecutive patients with single-vessel disease (infarct-related artery occlusion or subocclusion) diagnosed > or = 4 weeks after the ST-elevation myocardial infarction. Patients underwent PCI 3.9 +/- 2 months after ST-elevation myocardial infarction. PCI was successful in 24 patients (group A) and unsuccessful in 7 (group B). The 2 groups were similar in clinical and angiographic characteristics, as well as the prevalence of basal late potentials, average QT dispersion, and corrected-QT dispersion. One month after PCI, the successful reperfusion group had a significant 67% decrease in the prevalence of late potentials and average QT dispersion and corrected QT dispersion (51 +/- 9 vs 72 +/- 11 ms, p <0.00001, and 51 +/- 10 vs 76 +/- 15 ms, p <0.00001, respectively). These benefits remained stable at 3 and 6 months after PCI. Conversely, the unsuccessful group did not show any improvement in electrical stability markers after PCI failed. Thus, reperfusion obtained very late after ST-elevation myocardial infarction confers significant electrical stabilization that may contribute to a better outcome in patients with patent infarct-related arteries.     

Differentiation of myocardial ischemia and left ventricular aneurysm in the genesis of exercise-induced ST-T changes in previous anterior myocardial infarction

We attempted to differentiate between myocardial ischemia and left ventricular asynergy as the underlying mechanisms of exercise-induced ST-segment elevation in patients with previous myocardial infarction (MI). Sixty patients with previous anterior MI, who underwent stress myocardial scintigraphy (SMS) and coronary angiography (CAG), which revealed a single vessel disease of the left anterior descending artery, were entered in this study. SMS and CAG were performed within 3 months of MI onset, and SMS and ECG were quantitatively analyzed. T wave changes to a complete upright position with concomitant ST-segment elevation (T-dominant ST-elevation) was seen in 56% of the patients with post-MI angina pectoris (N = 16) and in 50% of those with significant redistribution in SMS (n = 20). On the other hand, ST-segment elevation without T wave reversion (ST-dominant ST-elevation) was seen in 43% of patients with severe LV asynergy (akinesis and dyskinesis, n = 39) and in 50% of those with severe scintigraphic defect in delayed images (relative thallium uptake less than or equal to 40%, n = 10). When these findings were combined, T-dominant ST-elevation had sensitivity and specificity of 54% and 78%, respectively, for the diagnosis of myocardial ischemia, while the corresponding values for ST-dominant ST-elevation were 44% and 100%, for the diagnosis of severe ventricular asynergy. We conclude that the two underlying mechanisms, ischemia and asynergy, may produce different changes in ST-T shape in patients with previous myocardial infarction.     

Quantitation of infarct size in patients with chronic coronary artery disease using rest-redistribution Tl-201 myocardial perfusion SPECT: correlation with contrast-enhanced cardiac magnetic resonance.

BACKGROUND: Rest and rest-redistribution thallium 201 myocardial perfusion single photon emission computed tomography (SPECT) (MPS) has been incompletely validated in patients for determination of the total amount of scarred myocardium. We sought to determine whether rest or redistribution Tl-201 MPS provides an accurate determination of infarct size as defined by delayed contrast-enhanced cardiac magnetic resonance (CMR). METHODS AND RESULTS: We studied patients (n = 44) with chronic coronary artery disease referred for rest-redistribution Tl-201 MPS, who were also studied by contrast-enhanced CMR within 3 +/- 4 days. Patients were considered retrospectively based on a series of patients referred for clinically indicated MPS. Defect size, as a percent of left ventricular mass (% LV), was determined by quantitative perfusion SPECT (QPS) and compared with the volume of delayed hyperenhancement on contrast-enhanced CMR, normalized to LV mass. Infarct size varied from 0% to 43% LV. Rest QPS defect size correlated with the amount of nonviable myocardium assessed by contrast-enhanced CMR (r = 0.76; mean difference, 4.3% +/- 8.0% LV). When delayed thallium data were considered, redistribution QPS was superior to rest QPS for determination of infarct size (redistribution r = 0.90; mean difference, 2.4% +/- 5.2% LV; P = .03 vs rest). CONCLUSION: Rest-redistribution Tl-201 MPS provides a more accurate measurement of total infarct size than rest-only Tl-201 MPS and correlates with contrast-enhanced CMR.     

Effect of quinapril initiated during progressive remodeling in asymptomatic patients with healed myocardial infarction

Approximately 20% of patients with healed myocardial infarction develop asymptomatic progressive left ventricular (LV) dilation and remodeling and are at increased risk for progression to symptomatic congestive heart failure and premature death. It was the goal of this study to test whether quinapril may interrupt this process and to analyze potential mechanisms. Of 138 patients with an average infarct age of 56 months, 25 had asymptomatic progressive LV dilation and were randomized in a prospective, double-blind study to placebo or quinapril. At baseline (mean +/- SEM) ejection fraction was reduced (35 +/- 3% and 39 +/- 3%) and end-diastolic volume (gated single-photon emission computed tomography) increased (104 +/- 9 and 117 +/- 12 ml/m(2)) with placebo (n = 13) and quinapril (n = 12), respectively. Progressive dilation continued in patients taking placebo (6 months: 9.4 +/- 5.2 ml/m(2), 12 months 24.6 +/- 5. 4 ml/m(2); change from baseline: p <0.05 vs baseline; p <0.05 vs 6 months), but not with quinapril (6 months: -0.9 +/- 4.0 ml/m(2); 12 months: 4.1 +/- 5.2 ml/m(2) [p <0.05] vs placebo). Wedge pressure during bicycle exercise was similar at baseline, but at 12 months tended to be lower with quinapril (17 +/- 1 mm Hg) than with placebo (24 +/- 4 mm Hg, p = 0.1673). Thus, quinapril prevented further progression of asymptomatic LV dilation and remodeling after remote myocardial infarction, possibly due to attenuation of an exercise-induced increase in LV filling pressure.     

Reciprocal ST-segment depression associated with exercise-induced ST-segment elevation indicates residual viability after myocardial infarction

OBJECTIVES: We evaluated the clinical significance of reciprocal ST-segment depression associated with exercise-induced ST-segment elevation for detecting residual viability within the infarcted area. BACKGROUND: Although the relation between residual viability and exercise-induced ST-segment elevation has been described, there are no reports focusing on the relation between myocardial viability and reciprocal ST-segment depression associated with exercise-induced ST-segment elevation. METHODS: We evaluated regional blood flow and glucose utilization using N-13 ammonia (NH3) and F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) in 30 patients with a previous Q-wave myocardial infarction (anterior in 15, inferior in 15). All subjects had single-vessel disease and had exercise-induced ST-segment elevations (> or =1 mm) in electrocardiographic leads. RESULTS: Reciprocal ST-segment depression (> or =1 mm) was present in 16 patients (Group A; anterior in 6, inferior in 10) but not in the remaining 14 patients (Group B). The degree of exercise-induced ST-segment elevation (1.8+/-0.2 vs. 2.0+/-0.2 mm) and the time from the onset of infarction to the study (75+/-49 vs. 74+/-52 days) did not differ between groups. There were no significant differences between groups in the severity of left ventricular dysfunction and the residual luminal narrowing in the infarct-related artery (45+/-21 vs. 48+/-25%). The presence and site of infarction were confirmed by NH3-PET in all patients. FDG-PET demonstrated residual tissue viability within infarct-related area in all patients in Group A and in 3 (21%) of 14 patients in Group B (p < 0.01). The sensitivity, specificity and accuracy of reciprocal ST-segment depression associated with exercise-induced ST-segment elevation for detecting residual viability were 84%, 100% and 90%, respectively. CONCLUSIONS: The occurrence of reciprocal ST-segment depression associated with exercise-induced ST segment elevation in patients with a previous Q-wave infarction who had single-vessel disease indicates residual tissue viability within the infarct-related area.     

Lack of pathologic Q waves: a specific marker of viability in myocardial hibernation

BACKGROUND: The present study evaluates the lack of Q waves on the electrocardiogram (ECG) in the prediction of myocardial viability compared with dobutamine stress echocardiography (DSE) and rest-redistribution thallium-201 (Tl-201) scintigraphy. HYPOTHESIS: The lack of pathologic Q waves (NoQ) may be a readily available and specific marker for the presence of viability. METHODS: Sixty four patients with stable coronary artery disease (CAD) and ventricular dysfunction underwent rest ECG, DSE, and Tl-201 scintigraphy before revascularization, and a repeat rest 2-Dimensional (2-D) echocardiogram more than 3 mo later. RESULTS: Total viability at baseline (% of total segments) was higher in the NoQ group by Tl-201 scintigraphy (87 +/- 19% versus 70 +/- 20%, p = 0.008) and by DSE (81 +/- 20% versus 65 +/- 24%, p = 0.013). As expected, the sensitivity of NoQ waves was low in predicting recovery of function (23%), and inferior to Tl-201 (82%) and DSE (84%) (p<0.08). However, specificity of NoQ waves for predicting recovery of global function was high (72%); higher than Tl-201 (50%) and DSE (45%). Positive predictive values were comparable among all modalities. Results were similar if the data were analyzed regionally for viability. CONCLUSION: Lack of pathologic Q waves is a specific and readily available marker of myocardial viability in patients with chronic CAD, which should alert the clinician for myocardial hibernation. Copyright (c) 2008 Wiley Periodicals, Inc.     

New Q waves on the presenting electrocardiogram independently predict increased cardiac mortality following a first ST-elevation myocardial infarction.

AIMS: The prognostic significance of pathological Q waves appearing in the acute phase of myocardial infarction has not been determined. We investigated whether new Q waves on the presenting electrocardiogram of patients with acute ST-segment elevation were independently associated with a worse outcome after a first myocardial infarction. METHODS AND RESULTS: The presence or absence of new Q waves on the presenting electrocardiogram was assessed in 481 patients who presented within 4 h of symptom onset and were randomized to receive either captopril or placebo within 2 h of streptokinase therapy for myocardial infarction. Ventriculography was performed at 22+/-6 days and mortality status was obtained at a median follow-up of 5.6 years. New Q waves were associated with a lower ejection fraction (51+/-13% vs 61+/-12%, P<0.0001), a larger end-systolic volume index (37 ml vs 28 ml, P<0.001), and increased cardiac mortality at 30 days (7% vs 2%, P=0.01) and at follow-up (17% vs 7%, P=0.002). On multivariate analysis, age (P<0.01), new Q waves at presentation (P<0.01) and a history of angina (P=0.046) were independent predictors of cardiac mortality, whereas randomization to captopril and the time from symptom onset to streptokinase administration were not. CONCLUSION: New Q waves at presentation are independently associated with a worse outcome after a first myocardial infarction. The presence of new Q waves on the presenting electrocardiogram allows very early identification of patients at risk of increased cardiac mortality.     

Effect of eating on thallium-201 myocardial redistribution after myocardial ischemia

To determine whether eating a high-carbohydrate meal between initial and delayed postexercise thallium-201 (Tl-201) imaging affects detection of Tl-201 redistribution during exercise stress testing, 16 patients with stable angina performed 2 Tl-201 treadmill exercise stress tests within a 14-day interval. Immediately after initial postexercise imaging, patients either drank a commercially available instant breakfast preparation for the intervention test or drank an equivalent volume of water for the control test. Comparable exercise workloads were achieved by exercising patients to the same heart rate for both tests. The order of the 2 (intervention and control) tests were randomized. All patients had at least 1 region of Tl-201 myocardial redistribution on either their eating or control test scans, although only 7 of the 16 had positive treadmill exercise test responses. Forty-six regions showing Tl-201 myocardial redistribution were identified in all 144 regions examined. Significantly more of these regions were identified on control test scans than on eating test scans: 11 of 46 on both test scans, 6 of 46 only on eating test scans and 29 of 46 only on control scans (p less than 0.001). Consistent with results of the quantitative regional analysis, the percentage of Tl-201 clearance over 4 hours in the 46 Tl-201 myocardial redistribution regions was 39 +/- 8% for the eating tests and 29 +/- 8% for control tests (mean +/- standard deviation, p less than 0.003). In 4 patients diagnosis of transient ischemia would have been missed because their 14 Tl-201 myocardial redistribution regions were detected only on the control test scans.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hyperoxemic perfusion of the left anterior descending coronary artery after primary angioplasty in anterior ST-elevation myocardial infarction.

OBJECTIVES: To assess left ventricle function recovery, ST-segment changes, and enzyme kinetic in ST-elevation myocardial infarction patients treated with intracoronary hyperoxemic perfusion (IHP) after primary percutaneous coronary intervention and compare them with the results obtained in control patients. BACKGROUND: IHP has been shown to attenuate microvascular reperfusion injury, which may result in poor LV function recovery despite successful primary percutaneous coronary intervention. METHODS: Twenty seven anterior ST-elevation myocardial infarction patients treated < or = 12 hr after symptom onset by primary percutaneous coronary intervention were subjected to selective IHP into the left anterior descending coronary artery for 90 min. They were compared with 24 anterior ST-elevation myocardial infarction control patients matched in clinical and angiographic characteristics and treated with conventional primary percutaneous coronary intervention. Left ventricular function recovery was evaluated by serial 2D contrast echocardiography. RESULTS: Left anterior descending coronary artery recanalization was successful in all patients. After IHP (100% successful, duration 90 +/- 5.4 min), patients showed a 4.8 +/- 2.2 hr shorter time-to-peak creatine kinase release (P = 0.001), a shorter creatine kinase half-life period (23.4 +/- 8.9 hr vs. 30.5 +/- 5.8 hr, P = 0.006), and a higher rate of complete ST-segment resolution (78% vs. 42%, P = 0.01). A significant improvement of mean left ventricular ejection fraction (from (44 +/- 9)% to (55 +/- 11)%, P < 0.001) and wall motion score index (from 1.77 +/- 0.2 to 1.39 +/- 0.4, P < 0.001) was observed at 3 months in IHP patients only. CONCLUSION: After successful primary coronary intervention, IHP is associated with significant left ventricular function recovery when compared to conventional treatment. Enzyme kinetic and ST-segment changes suggest faster and more complete microvascular reperfusion and may explain the salutary effects of this new therapy on left ventricular function.     

Dobutamine- vs exercise-induced ST segment elevation early after Q wave myocardial infarction. Prediction of functional recovery after revascularization.

AIMS: The association between stress-induced ST elevation and functional recovery following revascularization after myocardial infarction remains unclear. We assessed the relative accuracy of dobutamine- and exercise-induced ST elevation in Q wave leads in predicting functional recovery following revascularization, and we investigated the relationship of ST elevation to different wall motion responses to dobutamine. METHODS AND RESULTS: Thirty-nine patients underwent dobutamine stress echo and exercise test 8+/-2 days after Q wave myocardial infarction. All patients underwent angiography and subsequent revascularization. Follow-up echocardiograms were obtained 7+/-4 weeks after revascularization. Functional recovery was assessed by the difference between the baseline and the follow-up asynergy index. Nineteen patients (48%) developed dobutamine- and exercise-induced ST elevation. There was significant agreement between the tests (k=0.58, P<0.001). We found a significant correlation between dobutamine and exercise-induced ST elevation with functional recovery following revascularization (r=0. 45, P<0.005 and r=0.7, P<0.001, respectively). The parameters with the highest predictive value for functional recovery were: (a) the biphasic response during dobutamine infusion, (b) the development of ST elevation in both tests, and (c) the development of exercise-induced ST elevation in more than three leads. CONCLUSION: There is a strong association between dobutamine- and exercise-induced ST elevation with functional recovery following revascularization. Exercise-induced ST elevation in more than three leads and a biphasic response during dobutamine infusion accurately predict functional recovery.     

Exercise training following myocardial infarction improves myocardial perfusion assessed by thallium-201 scintigraphy

AIM: We assessed the effects of a 6-week exercise programme on the thallium-201 myocardial perfusion characteristics of patients following myocardial infarction. METHODS: Twenty-five patients presenting with a first acute myocardial infarction were randomised into two groups: (i) those undergoing a supervised exercise training programme over 6 weeks (n=15) and (ii) a control group who did not attend the exercise programme (n=10). All underwent three sequential stress thallium myocardial perfusion scans at 10 days, 6 weeks and 3 months after infarction. The stress conditions were identical on each occasion. The images were analysed using a polar plot with a computer assisted algorithm comparing stress and redistribution data. Values for extent, severity and percentage redistribution of the thallium images were generated. RESULTS: A total of 29 perfusion defects were identified, 18 in the exercise group and 11 in the control group. Over 3 months in the exercise group the mean extent of the stress image defect fell from 109+/-64 to 95+/-51 pixels (P<0.05) while in the control group there was an increase from 133+/-57 to 144+/-57 pixels (P=ns). Stress defect severity fell in the exercise group from 581+/-417 to 494+/-346 S.D. (P<0.05) but increased in the control group from 765+/-494 to 877+/-543 S.D. (P=ns). On redistribution imaging in the exercise group a significant decrease was observed in both extent (94+/-56 to 76+/-43 pixels (P<0.05)) and severity (541+/-387 to 438+/-291 S.D. (P<0.05)) of the defects. However in the control group no significant change was observed for extent (125+/-54 to 125+/-52 pixels) or severity (745+/-485 to 820+/-503 S.D.) of the redistribution defects (P=ns). Reversibility of the defects increased slightly in both the exercise group (from 14.6+/-17 to 17.5+/-20%) and the control group (5.2+/-5 to 9.6+10%) (P=ns). CONCLUSION: Following myocardial infarction a 6-week exercise programme improves myocardial perfusion characteristics. An exercise programme should be integrated into cardiac rehabilitation protocols for patients after infarction.     

Correlation between ECG and myocardial perfusion after mechanical reperfusion of acute myocardial infarction

The identification of viable myocardium after myocardial infarction (MI) carries major prognostic impact. Due to myocardial stunning early after successful mechanical reperfusion of acute myocardial infarction, analysis of myocardial perfusion but not of contractile function can be used to differentiate between necrotic and viable myocardium. Although being widely regarded as an indicator of infarct transmurality, the relation between post-infarct Q-wave formation and the amount of viable myocardium has not been studied. We hypothesized that there was a correlation between the extent of Q-wave formation and the extent of perfusion abnormalities on myocardial contrast echocardiography early after successful mechanical reperfusion of first acute myocardial infarction and that the extent of post-infarct Q-wave formation might therefore be used as a simple estimate of the amount of viable myocardium. METHODS AND RESULTS: 47 patients with first MI and treated by direct PCI were enrolled. Patients were divided into 3 groups according the presence and number of abnormal Q waves (group A-no abnormal Q wave; group B-< or =2 abnormal Q waves, group C-> or =3 abnormal Q waves). Left ventricular pump function was defined by ejection fraction (EF) on ventriculography and wall motion score index (WMSI) on echocardiography. Myocardial perfusion was defined by perfusion score index (PSI) on myocardial contrast echocardiography. Patients in group A had significantly better LV function than patients in other groups [EF 57+/-5 vs. 48+/-11% (group B) and 47+/-10% (group C); p<0.05], also WMSI was the best in this group [1.34+/-0.22 vs. 1.67+/-0.39 (group B) and 1.68+/-0.31 (group C); p<0.01]. Myocardial perfusion assessed by PSI was best in group A (1.2+/-0.3, p<0.05). With respect to PSI, there was a significant difference between group B and C (1.41+/-0.21 vs. 1.56+/-0.29; p<0.05), even though EF and WMSI did not differ in these groups. The amount of perfused segments with severe wall motion abnormality was higher in group B compared to group C (47% vs. 25%; p<0.05). CONCLUSION: In patients after successful mechanical reperfusion of first MI, the extent of Q-wave formation on ECG may be regarded as a corollary of the amount of myocardial microvascular damage and may, therefore, be used to estimate the amount of viable myocardium post-infarct.     

Predicting cardiac mortality after uncomplicated myocardial infarction by exercise radionuclide ventriculography and exercise-induced ST segment elevation.

In 183 consecutive patients with recent, uncomplicated myocardial infarction, the following variables were associated with 4-year cardiac death: haemodynamic decompensation with exercise (P = 0.01), left ventricular ejection fraction at rest (P = 0.004) and at peak exercise (P = 0.003), persistent ST segment elevation at rest in the area of infarction = (P = 0.004), exercise-induced ST segment elevation (P = 0.02), and late aneurysmal evolution (P = 0.01). Exercise left ventricular ejection fraction was the sole variable selected by Cox regression analysis as an independent predictor of cardiac death. In 40 patients with ST segment elevation at rest, left ventricular ejection fraction was 42 +/- 17% at rest and 40 +/- 18% at peak exercise, versus 52 +/- 12% and 52 +/- 14% in the remaining patients (both P less than 0.01). Among these 40, 16 (all with anterior infarction) also had exercise-induced ST segment elevation; their ejection fraction was 32 +/- 13% at rest, 30 +/- 13% during exercise, versus 53 +/- 15% and 53 +/- 15% in 129 patients with no ST segment elevation either at rest, or during exercise (both P less than 0.01). The 4-year risk of death was 20% in the former 40 patients, 36% in the latter 16, while in the complete absence of ST segment elevation, such risk was 3%. All 14 patients with ST segment elevation only during exercise were alive after 4 years: their left ventricular ejection fraction was 47 +/- 12% at rest, 45 +/- 13% with exercise. ST segment elevation was associated with late aneurysmal evolution but not with exercise-induced ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of exercise training soon after myocardial infarction on regional myocardial perfusion and resting left ventricular function.

There is scant information regarding the effect of exercise training begun soon after hospital discharge for myocardial infarction (MI) with respect to subsequent improvement in exercise tolerance, enhancement of regional myocardial perfusion, or left ventricular function. Accordingly, 19 post-MI patients (mean age 53 +/- 7 years) underwent treadmill exercise quantitative thallium-201 (Tl-201) scintigraphy and rest radionuclide angiography (RNA) prior to and after 12 weeks of thrice-weekly exercise training which was targeted to 70-85% of maximum exercise heart rate achieved. Training was begun at 25 +/- 3 days after hospital discharge. Eight Tl-201 scan segments were each scored from 1-6 points based upon uptake and washout criteria with 6 being the most severe defect (greater than 50% reduction in Tl-201 events with no delayed redistribution). When matched to the pretraining peak workload on exercise testing, 12 weeks of training significantly lessened heart rate (120 +/- 4 to 97 +/- 4, p less than 0.001), peak systolic blood pressure (142 +/- 6 to 129 +/- 5 mmHg, p less than 0.01), and significantly reduced double product [17.2 +/- 10.8 to 12.7 +/- 9 (x10(3), p less than 0.001]. Training was associated with a reduction of exercise-induced ST depression or angina (42 to 16%) which was not statistically significant. The mean resting by RNA ejection fraction was 50 +/- 3% prior to training and 51 +/- 3% after training. There was no significant change in overall Tl-201 defect score or the number of defect regions per patient scan comparing pre- and post-training scintigrams.(ABSTRACT TRUNCATED AT 250 WORDS)     

ST-segment elevation on Q leads at rest and during exercise: relation with myocardial viability and left ventricular remodeling within the first 6 months after infarction.

BACKGROUND: Resting ST-segment elevation on Q leads after an acute myocardial infarction has been related to a greater infarct size. Otherwise, the relation between exercise-induced ST-segment elevation and myocardial viability is controversial. We investigated the relation between ST-segment elevation on Q leads at rest and during exercise and regional dysfunction and its evolution, contractile reserve, left ventricular dilation, and coronary patency. METHODS AND RESULTS: Exercise testing and cardiac catheterization were performed at the first week after infarction in 51 patients. The study group was divided according to the existence (in 2 or more Q leads; n = 36) or not (n = 15) of resting ST-segment elevation and according to the existence (n = 28) or not (n = 23) of exercise-induced ST-segment elevation. Left ventricular end-diastolic and end-systolic volumes (mL/m2), regional wall motion (SD/chord), contractile reserve (wall motion percentage improvement with low-dose dobutamine), and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 35 patients; systolic recovery (wall motion percentage improvement), left ventricular volumes, and coronary patency were again evaluated. Patients with resting ST-segment elevation showed poorer wall motion (2.1 +/- 0.8 SD/chord vs 1.2 +/- 1 SD/chord, P =.002), lesser contractile reserve (17% [0% to 39%] vs 41% [4% to 92%], P =.04), greater end-systolic volume (32 +/- 15 mL/m2 vs 23 +/- 11 mL/m2, P =.04), and higher percentage of occlusion (36% vs 7%, P =.04) than did patients without ST-segment elevation. Likewise, patients with exercise-induced ST-segment elevation showed lesser contractile reserve (8% [0% to 40%] vs 35% [12% to 86%], P =.03) than did patients without exercise-induced ST-segment elevation. The only independent predictors of contractile reserve were wall motion <2 SD/chord (odds ratio [OR] 7.1, confidence interval [CI] 6.3 to 7.9, P =.01) and the absence of exercise-induced ST-segment elevation (OR 5.7, CI 4.9 to 6.5, P =. 02). There were no significant differences between patients with and those without ST-segment elevation (at rest or during exercise) in systolic recovery or left ventricular volumes at the sixth month. CONCLUSIONS: ST-segment elevation on Q leads at rest is related to a poorer systolic function (more severe regional dysfunction, greater end-systolic volume, and less response to dobutamine). ST-segment elevation during exercise is independently related to a lesser contractile reserve. ST-segment elevation (at rest or during exercise) is not related to the evolution of volumes or regional dysfunction during the first 6 months after infarction.     

Coexistence of prothrombic risk factors and its relation to left ventricular thrombus in acute myocardial infarction

OBJECTIVE: Within the last few years a number of thrombophilic mutations have been identified. Pre-symptomatic testing for these established genetic risk factors identifies individuals predisposed to a disease and often allows to select suitable prophylactic interventions in time. We investigated whether or not the prothrombin G20210A allele, the factor V Leiden G1691A, and MTHFR C677T allele are risk factors for left ventricular thrombus (LV) in patients with myocardial infarction (AMI) or not. METHODS AND RESULTS: We analysed clinical, echocardiographic and biochemical data in 183 consecutive patients (aged 58 +/- 12 years; 34 women) with a first anterior acute myocardial infarction. Two-dimensional echocardiographic examination was performed on days 1, 3, 7, 15, and 30. LV thrombi were detected in 42 (23%) of the 183 patients with acute myocardial infarction. We have used multiplex assays based on PCR and DNA hybridization in microtitre plates for the simultaneous analysis of three mutations (FV Leiden G1691A, prothrombin G20210A, and MTHFR C677T). No significant differences in allele frequencies of FV Leiden G1691A (9.5% vs. 8.5%, p = 0.75), prothrombin G20210A (9.5% vs 7.1%, p = 0.74) and MTHFR C677T (47.6% vs. 50.3%, p = 0.74) were found in patients with LV thrombus when compared with those without LV thrombus. No significant differences in haemostatic factor levels were found in patients with LV thrombus when compared with those without LV thrombus. CONCLUSION: FV Leiden, prothrombin 20210 variant, and MTHFR mutation are no risk factors for left ventricular thrombus in patients with myocardial infarction.The presence of multiple mutations did not influence the development and outcome of LV thrombus in patients with myocardial infarction     

Long-term outcome of fetal cell transplantation on postinfarction ventricular remodeling and function

OBJECTIVES: The purpose of this study was to determine the long-term outcome of fetal cell transplantation into myocardial infarction on left ventricular (LV) function and remodeling. BACKGROUND: While neonatal cell transplantation improved function for acute myocardial infarction, long-term data on the effects of cell-transplant therapy using a more primitive cell on ventricular remodeling and function are needed.Methods. - Therefore, we injected 4 x 10(6) Fischer 344 fetal cardiac cells or medium into 1-week old infarcts in adult female Fischer rats to assess long-term outcome. RESULTS: Ten months after transplantation histologic analysis showed that cell implants were readily visible within the infarct scar. Infarct wall thickness was greater in cell-treated at 0.69 +/- 0.05 mm (n = 11) vs. medium-treated hearts at 0.33 +/- 0.01 mm (n = 19; P = 0.0001). Postmortem LV volume was 0.41 +/- 0.04 ml in cell-treated vs. 0.51 +/- 0.03 ml in medium-treated hearts (P < 0.04). Ejection fraction assessed by LV angiography was 0.40 +/- 0.02 in cell-treated (n = 16) vs. 0.33 +/- 0.02 in medium-treated hearts (n = 24; P < 0.03) with trends towards smaller in vivo end-diastolic and end-systolic volumes in cell-treated vs. medium-treated hearts. Polymerase chain reaction analysis of the Sry gene of the Y chromosome was positive in four of five cell-treated and zero of five medium-treated hearts confirming viability of male cells in female donors. CONCLUSION: Over the course of 10 months, fetal cardiac cell transplantation into infarcted hearts increased infarct wall thickness, reduced LV dilatation, and improved LV ejection fraction. Thus, fetal cell-transplant therapy mitigated the longer-term adverse effects of LV remodeling following a myocardial infarction.     

Myocardial viability in patients with Q wave myocardial infarction and no residual ischemia.

BACKGROUND. Coronary revascularization in patients with persistent angina after myocardial infarction reduces the incidence of recurrent angina pectoris and myocardial infarction and improves left ventricular function. The results of revascularization after a Q wave myocardial infarction when there is no residual ischemia may depend on myocardial viability. METHODS AND RESULTS. To determine whether there was viable myocardium in the infarct area in the absence of clinical and scintigraphic evidence of myocardial ischemia, 15 asymptomatic patients with a Q wave myocardial infarction, no redistribution on stress 201Tl test, and single-vessel disease (greater than 70% stenosis) with persistent anterograde blood flow were randomized to percutaneous transluminal coronary artery angioplasty (PTCA) or conservative medical treatment. After 2 months of follow-up, mean coronary blood flow measured by Doppler catheter in the infarct-related artery was higher in the PTCA treatment group (33 +/- 6 ml/min, n = 8) than in the conservative treatment group (16 +/- 4 ml/min, n = 7; p less than 0.05 between groups). The 201Tl pathological-to-normal ratios measured on postexercise images did not change in patients treated conservatively during the follow-up period (delta = +1.1 +/- 2.2%; NS from baseline) but increased significantly in patients treated by PTCA (delta = +8.5 +/- 2.3%; p less than 0.01 from baseline; p less than 0.05 between groups). Segmental wall motion improved on left ventricular angiography 2 months after PTCA (delta = +11.5 +/- 2.2%; p less than 0.001 from baseline) significantly more than in the conservative treatment group (delta = +4.1 +/- 1.4%; p less than 0.05 between both groups). Improvements of 201Tl ratios and segmental wall motion indexes correlated significantly (r = 0.73, p = 0.002). The mild improvement of global left ventricular ejection fraction measured in the PTCA treatment group did not differ significantly from changes in the conservative treatment group. CONCLUSIONS. Successful angioplasty of the stenotic infarct artery in patients with a Q wave myocardial infarction and no residual ischemia improved coronary flow, 201Tl uptake in the infarct area, and regional wall motion. Therefore, myocardial viability may last several weeks, as long as residual blood flow persists in the infarct-related artery. Optimal assessment of viability by imaging techniques should identify patients who are most likely to benefit from revascularization.     

Changes in left ventricular volumes after acute transmural myocardial infarction: clinical, angiographic and prognostic correlations

The relation of left ventricular (LV) volume changes to clinical and angiographic features was assessed in 57 patients with a first transmural myocardial infarction. LV volumes were measured by two-dimensional echocardiography within 72 hours of admission and repeated at one month. The infarct-related artery (IRA) patency and collateral circulation were determined by coronary arteriography performed before discharge. LV end-diastolic and end-systolic volumes increased (155 +/- 44 vs 203 +/- 65 ml; 96 +/- 32 vs 134 +/- 57 ml, all P less than 0.01), and ejection fraction decreased (0.38 +/- 0.06 vs 0.34 +/- 0.09, P less than 0.05) in patients with totally occluded IRA without collaterals. In contrast, LV volumes and systolic function were unchanged in those who had subtotally occluded IRA or with collaterals. LV dilation (greater than or equal to 20% increase in LV end-diastolic volume) occurred more frequently in patients without residual flow to the infarct region (77%) than in those with (9%) (P less than 0.01). Thirteen patients with LV dilation developed congestive heart failure, 3 of whom having cardiac death. However, congestive heart failure was found in only 11 patients without LV dilation and no death occurred. Thus, the cardiac event rate was higher in patients with (65%) than in those without (30%) LV dilation (P less than 0.05). The study indicates that the changes in LV volumes following acute myocardial infarction are largely related to the status of residual flow to the infarct region and affect the clinical outcome of the patients.