Regional left ventricular function in acute myocardial infarction: Evaluation with quantitative radionuclide ventriculography

Regional and global left ventricular performance was noninvasively assessed with quantitative gated equilibrium radionuclide ventriculography in 43 patients an average of 40 hours after the onset of a first acute transmural myocardial infarction. In all 16 patients with anterior infarction, regional ejection fraction, a quantitative measure of regional left ventricular performance, was uniformly depressed in the infarcted zone. In patients with inferior infarction the abnormalities of regional performance were less severe. Fourteen of 20 patients (70 percent) with inferior infarction had depressed performance in the infarcted zone. Function in noninfarcted zones was abnormal in only 6 of the 20 patients (30 percent) with inferior infarction, but it was abnormal in 11 of the 16 patients (69 percent) with anterior infarction, particularly in those with severe pump failure. As a consequence, global left ventricular ejection fraction was significantly lower in patients with anterior than in those with inferior infarction (mean ± standard error of the mean 31 ± 3 percent versus 51 ± 3 percent, p < 0.005). Prognosis and clinical functional class were related to performance not only in infarcted zones, but also in noninfarcted zones as assessed with electrocardiography.It is concluded that depressed function in apparently noninfarcted left ventricular zones contributes significantly to left ventricular dysfunction after acute myocardial infarction, particularly in patients with anterior infarction.     

Tritiated digoxin. XX. Tissue distribution in experimental myocardial infarction

The role and potential hazards of digitalis glycoside administration in acute myocardial infarction remain controversial. We investigated the concentration of tritiated digoxin in normal, ischemic, and infarcted left ventricular myocardium of the dog after ligation of the anterior interventricular coronary artery. The normal homogeneous distribution of tritiated digoxin in the normal canine left ventricle was altered following acute myocardial infarction. The ischemic and infarcted zones exhibited a marked diminution in digoxin concentration. Oxidative phosphorylation determinations confirmed tissue hypoxia in the infarcted zone. The gradient of digoxin concentration between normal, ischemic, and infarcted zones of myocardium may potentiate the development of an arrhythmia in the electrically unstable infarcted myocardium.     

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

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

抗心肌肌凝蛋白抗体亲大鼠梗塞心肌特性的研究

目的　探讨抗心肌肌凝蛋白单克隆抗体 (antimyosinantibody ,AMA)亲梗塞心肌的特点。方法　心肌梗死大鼠静脉注射放射性锝 99m标记的抗心肌肌凝蛋白单克隆抗体 (99mTc AMA) ,观察注射时间 ,梗死时间和梗塞区对梗塞心肌摄取AMA的影响。结果　注射后 2h梗塞心肌开始摄取AMA ,以后摄取逐渐增加 ,2 4h达到高峰。心肌梗死后 2 0d ,梗塞心肌持续摄取AMA ,期间心肌梗死后 1～ 5d摄取最强 ,梗塞中央区以及梗塞区内层摄取强于其他梗塞区域。结论　急性心肌梗死大鼠梗塞心肌特异性地摄取AMA ,注射AMA后摄取迅速、持久 ,受心肌梗死时间影响较小 ,梗塞中央区内层心肌摄取最强 ,AMA具有亲梗塞心肌的特性。     

Expansion and remodelling of the left ventricle after myocardial infarction

The remodelling of the left ventricle after myocardial infarction results from the expansion of the infarcted zone in the acute phase and the dilation of the healthy zone of the left ventricle which complicates the initial expansion. It brings about an increase in the left ventricular volume which is a major pejorative prognosis factor after myocardial infarction. The expansion, defined by the dilation and parietal stricture of the infarcted zone, complicates about 30 p. cent of the infarctions and appears in the first hours of the infarction. It is favoured by the transmural nature of the infarction, by its extent and its previous topography, and by arterial hypertension. It is accompanied by a higher mortality rate, increases the risk of parietal rupture, exposes to post-infarction aneurysm and to intraventricular thrombi, and initializes the ventricular remodelling, factor of secondary cardiac failure. The dilation of the healthy zone of the left ventricle is observed mainly in case of initial expansion. Its importance increases with the size of the infarction. It corresponds to the volume overload secondary to the increase in the telediastolic parietal constraint of the left ventricle. The remodelling of the left ventricle after infarction is limited by captopril, and possibly by the restoration of the blood flow in the artery responsible for the infarction. Captopril, administered in the first weeks following the infarction, limits the dilation of the left ventricle in man as well as in animals. This beneficial effect is due to a decrease in the post-load of the left ventricle. Captopril improves the survival after infarction in animals, but its effect on the post-infarction mortality in man is still under study.     

Myocardial enzyme depletion in infarcted human hearts: infarct size and equivalent tissue mass

Myocardial activities of several enzymes were measured in infarcted and non-infarcted areas of heart sections obtained from eight patients who died after acute myocardial infarction. Similar data were obtained from four patients with cardiovascular disorders who died from causes other than myocardial infarction and from six patients without previously known heart disease. It was found that both non-infarcted and infarcted tissue samples contained considerably altered enzyme activities. This finding explains the low correlations between enzymatic and histological estimates of infarct size previously reported. However, when the residual myocardial activities of different enzymes were compared with each other, a close correlation was found between creatine kinase, alpha-hydroxybutyrate dehydrogenase, and aspartate aminotransferase. It appears that the pathological changes in the myocardial activities of these enzymes may be explained by the phenomenon of diluted myocardium. This indicates that myocardial injury, as estimated from plasma enzyme activities, may still be expressed meaningfully in gram equivalents of healthy myocardium.     

家兔急性心肌梗死后梗死周边区心交感神经受损的研究

目的探讨家兔急性心肌梗死(简称心梗)后梗死周边区心交感神经受损对家兔心电生理的影响。方法20只家兔随机分为两组:假手术组(n=10)和心梗组(n=10)。采用结扎冠状动脉左室支的方法制备心梗模型,假手术组开胸后穿线但不结扎左室支,其他同心梗组。梗死后1 h刺激支配心脏的交感神经,观察刺激前后梗死周边区,内、中、外三层心肌单相动作电位复极90%的时程(MAPD90)的变化,并计算跨室壁复极离散度(TDR)及其变化。测定心室颤动(简称室颤)阈值。免疫组化法研究梗死周边区心肌中酪胺酸羟化酶(TH)阳性纤维的分布和密度。结果假手术组交感神经刺激后三层心肌的MAPD90较基础状态明显缩短(P<0.01),但刺激前后TDR无显著变化(P>0.05);心梗组交感神经刺激后MAPD90缩短(P<0.05),但不如假手术组显著(P<0.01),刺激前后TDR也无显著改变(P>0.05)。两组比较,心梗组刺激后TDR较假手术组增加(P<0.01),室颤阈值显著降低(P<0.05),梗死周边区神经纤维密度较假手术组显著降低(P<0.05)。结论急性心梗后梗死周边区存在心交感神经受损,使心电不稳定性增加。     

Serial changes of complement titers in the acute phase of myocardial infarction

Although some studies suggest the involvement of a complement activation in the development of acute myocardial infarction, there has been little convincing evidence of the change of the complement in patients suffering from myocardial infarction. In 11 patients with acute myocardial infarction the serial changes of the total hemolytic complement titer (CH50), C3, C4, total serum protein and C3 conversion were investigated up to 120 hours after its attack. The level of CH50 and C4 increased consistently in the acute phase of myocardial infarction, but C3 did not show any change and total serum protein declined after 96 hours. Beta 1 A globulin, the split product of C3, could not be detected in the blood stream. These results suggest that the infarcted or ischemic myocardium would activate complements, and C3 might be consumed continuously by the infarcted or ischemic myocardium. Such consumption of complements should stimulate the production of complement and would give rise of an increase in C4 and CH50. It is suggested that activated complement might play a significant role in the development of myocardial infarction.     

The prognostic value of dobutamine echocardiography after an uncomplicated acute myocardial infarct

BACKGROUND AND PURPOSE: The identification of patients at risk for future events after an infarction is mandatory. The aim of this study was to assess the prognostic value of dobutamine stress echocardiography after an uncomplicated myocardial infarction. METHODS: One hundred and twenty five patients (mean age 65 +/- 11 years, males 82%) underwent dobutamine-echo within ten days after an uncomplicated myocardial infarction. Four myocardial responses were identified: a) negative; b) sustained improvement of myocardial contractility; c) initial improvement followed by worsening, and d) worsening at a distance or in the infarcted zone. RESULTS: Mean follow-up was 7.4 +/- 4.6 months. An adverse outcome occurred in 47 patients: non cardiac death in 3, cardiac death in 6, myocardial infarction in 5, angina in 21, congestive heart failure in 2, and in 10 patients revascularization. Cox regression analysis showed that worsening of contractility was the best predictor for adverse events (p < 0.0001, relative risk 2.8; 95% confidence interval: 1.7-4.5). Non-smoking and previous angina were also predictors of adverse events (p = 0.003 and p = 0.04, respectively). Similar results were obtained after excluding the revascularized patients. CONCLUSIONS: Sustained improvement of contractility in the infarcted region is not a predictor of adverse events. Asynergy at a distance or in the infarcted region during dobutamine echocardiography within ten days after an uncomplicated myocardial infarction predicts adverse cardiac events during follow-up. Therefore, dobutamine echocardiography could be used for risk stratification after acute myocardial infarction.     

Detection of local abnormalities in ventricular activation sequence by body surface isochrone mapping in patients with previous myocardial infarction

Body surface isochrone mapping was performed in 36 normal subjects and in 85 patients with previous myocardial infarction. Eighty-seven unipolar electrocardiograms distributed over the anterior chest and the back were recorded simultaneously. For each lead, activation time was measured as the time from the onset of QRS to the peak of the R wave. The lead points where R waves were not observed were designated the "no R wave area" (NR area). Isochrone maps of normal subjects had a consistent pattern, with isochrone lines extending from the right upper anterior chest to the left anterior chest and then to the back. NR area was small and was located only on the right upper chest or the upper back. On the isochrone maps of patients with myocardial infarction, abnormal findings were observed; NR area was found in 26 of 28 patients with anterior infarction on the upper to middle anterior chest, in 13 of 22 patients with inferior infarction on the lower chest, and in 24 of 25 patients with anterior and inferior infarction on the upper to lower anterior chest. Activation time was delayed near the NR area (peri-NR area delay) in 37 patients. In patients with apical infarction, an islandlike zone of delayed activation was typically found on the left precordium. These abnormal patterns are considered to indicate local abnormalities in the activation of infarcted myocardium; the NR area indicates dead unexcitable scar, and the peri-NR area delay and islandlike zone of delayed activation indicate partially infarcted myocardium of slow activation. Patients with NR area had greater degree of left ventricular asynergy and lower ejection fraction than those without.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrical Impedance Properties of Normal and Chronically Infarcted Left Ventricular Myocardium

Background: Previous reports have disclosed that a significant difference exists between the electrical impedance properties of healthy and chronically infarcted ventricular myocardium.Purpose: To assess the potential utility of electrical impedance as the basis for mapping in chronically infarcted left ventricular myocardium. Specifically: (1) to delineate electrical impedance properties of healthy and chronically infarcted ventricular myocardium, with special emphasis on the infarction border zone; (2) to correlate impedance properties with tissue histology; (3) to correlate impedance properties with electrogram amplitude and duration; (4) To demonstrate that endocardial impedance can be measured effectively in vivo using an electrode mounted on a catheter inserted percutaneously.Methods: An ovine model of chronic left ventricular infarction was utilized. Sites of healthy myocardium, densely infarcted myocardium and the infarction border zone were investigated. Bulk impedance was measured in vitro using capacitor cell, four-electrode and unipolar techniques. Epicardial and endocardial impedances were measured in vivo using four-electrode and unipolar techniques. Impedance was measured at multiple frequencies. Electrographic amplitude, duration and amplitude/duration ratio were measured using bipolar electrograms during sinus rhythm. Quantitation of tissue content of myocytes, collagen, elastin and neurovascular elements was performed.Results: Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the border zone transitioning between healthy myocardium and dense infarction. Decreasing impedance correlated with a decrease in tissue myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as the measurement frequency decreased. Healthy myocardium exhibited a marked frequency dependence in its impedance properties; this phenomenon was not observed in densely infarcted myocardium. There was a direct association between impedance and both electrogram amplitude and amplitude/duration ratio. There was an inverse association between impedance and electrogram duration. Endocardial impedance, measured in vivo using a electrode catheter inserted percutaneously, was demonstrated to distinguish between healthy and infarcted myocardium.Conclusions: The electrical impedance properties of healthy and infarcted left ventricular myocardium differ markedly. The properties of the infarction border zone are intermediate between healthy and infarcted myocardium. Impedance may be a useful assay of cardiac tissue content and adaptable for cardiac mapping in vivo.Condensed Abstract. To delineate the electrical impedance properties of healthy and chronically infarcted left ventricular myocardium emphasizing the infarction border zone, impedance was measured in chronically infarcted ovine hearts. Densely infarcted myocardial impedance was significantly lower than healthy myocardium. Impedance gradually decreased in the infarction border zone in transition between healthy myocardium and dense infarction. This correlated with a decreasing myocyte content. The magnitude of the difference in impedance between densely infarcted and healthy myocardium increased as measurement frequency decreased. There was a direct association between impedance and electrogram characteristics. Endocardial impedance, measured in vivo using an electrode catheter inserted percutaneously, distinguished between healthy and infarcted myocardium     

Cellular electrophysiological changes during ischemia in isolated, coronary-perfused cat ventricle with healed myocardial infarction

Cellular electrophysiological consequences of acute ischemia superimposed on healed myocardial infarction were studied in isolated, coronary-perfused cat left ventricles 2-4 months after ligation of multiple distal tributaries of the left anterior descending and circumflex coronary arteries. Oxygenated Tyrode's solution was perfused through the left anterior descending and circumflex coronary arteries, and the preparations were superfused with Tyrode's solution gassed with 95% N2-5% CO2. Transmembrane action potentials were recorded from the endocardial cells in normal and infarcted zones. There were no significant differences in measured action potential variables and refractory periods between cells in the normal and infarcted zones before acute ischemia. When coronary perfusion was discontinued ("ischemia"), resting potential, action potential amplitude, and action potential duration were reduced, and the refractory period was shortened progressively in cells of the normal zone. However, the action potential changes were less prominent, and the refractory period was unchanged in cells in the infarcted zone. As a result, there were significant differences in resting membrane potential, action potential amplitude, action potential duration, and refractory period between cells in the normal and infarcted zones at 10 minutes of ischemia. These differences became larger as the ischemic period was prolonged. Spontaneous rapid ventricular activity was observed during the last 20-30 minutes of ischemia in four of eight preparations with healed myocardial infarction, whereas no spontaneous rapid ventricular activity was recorded in any of six normal heart preparations. Our data suggest that superimposition of acute ischemia on healed myocardial infarction produces electrophysiological inhomogeneities that may enhance arrhythmogenesis.     

黄芪总黄酮对急性心肌梗死心室肌细胞钠电流的作用

目的探讨黄芪总黄酮（TFA）对急性心肌梗死（AMI）后大鼠心室肌细胞钠电流（ⅠNa）的影响。方法大鼠开胸左前降支结扎造成AMI，酶解分离心室肌细胞，采用全细胞膜片钳记录技术记录左前降支供血区心外膜细胞的ⅠNa。结果应用TFA（20mg／kg）后与AMI组比较，ⅠNa峰值从（-4．79±1．88）nA下降到（-2．74±1．67）nA，差异有统计学意义（P〈0．01，n=6）。结论TFA可显著降低AMI大鼠心室肌细胞ⅠNa的幅值。     

Exercise two-dimensional echocardiography in recent myocardial infarction. Is it useful in the detection of multivessel disease?

Exercise two-dimensional echocardiography (2D-ECHO) can be used to detect coronary artery disease in patients (pts) by the development of stress-induced transient asynergy in areas without wall motion abnormalities when at rest. The aim of the study is to verify the accuracy of exercise 2D-ECHO in the identification of high risk pts with multivessel disease after the first acute myocardial infarction (AMI). Technically adequate 2D-ECHO examinations were obtained in 21 of 28 (75%) consecutive patients after acute myocardial infarction. 30-50 days after acute myocardial infarction, these 21 pts (19 males and 2 females, mean age +/- SD = 54.3 +/- 8.7) underwent 2D-ECHO during bicycle exercise in supine position. The marker of multivessel disease was the development, during the stress test, of new areas of asynergy not adjacent to the infarcted area (i.e. transient remote asynergy). Two months after acute myocardial infarction all pts underwent coronary angiography to verify the severity of coronary obstruction (reduction of luminal diameter greater than or equal to 75% in the non infarct related vessel).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravenous administration of molsidomin in the acute period of myocardial infarct

A study of central hemodynamic parameters, ECG charting and the activity of serum CPK and its MB fraction in 58 patients with acute myocardial infarction demonstrated that intravenous administration of 20 mg Corvaton, at the rate of 3 micrograms/kg/min, was effective for both controlling an acute left-ventricular failure, and limiting the infarcted area. A three-day treatment normalized systemic and central hemodynamic parameters in cases of medium-size infarction, and considerably reduced manifestations of acute left-ventricular failure in patients with a large area of necrosis.     

Quantification of myocardium at risk in unstable angina: comparison of patients with and without previous infarction

We studied two subgroups of patients with unstable angina pectoris: 35 without (Group A) and 73 with (Group B) previous myocardial infarction. The severity of coronary artery disease was assessed by means of a previously described scoring system. This scoring system was used to calculate the proportion of left ventricular myocardium fed by significantly (greater than 75% luminal area reduction) stenosed coronary arteries (called percent myocardium threatened). To estimate the amount of myocardium lost by previous infarction we used a four-point wall motion score for each of seven left ventricular wall segments: a value of 2 was given to normokinetic segments, 1 for hypokinetic segments, 0 for akinetic and -1 for dyskinetic segments. The deficit in wall motion score was used to estimate the amount of myocardium infarcted. This was then subtracted from the proportion of myocardium threatened to yield the proportion of myocardium still in jeopardy. We found a different extent and severity of coronary artery disease between the two subgroups. In the group without previous infarction, the numbers of patients with one-, two- and three-vessel disease were 15, 9, and 11, respectively (or 43, 26, and 31%). In those with a previous infarction, the respective numbers were 11, 23, and 39 (or 15, 31.5, and 53.5%). This difference is statistically significant (P less than 0.01). The mean number of stenotic arteries was 1.9 +/- 0.9 in the patients without previous infarction and 2.4 +/- 0.7 in those with an infarction (P less than 0.05). Using the above-mentioned scoring system the score was 3.2 +/- 1.4 in patients without previous infarction and 4.0 +/- 1.6 in those with previous infarction (P less than 0.05). The percent myocardium threatened was 53.6 +/- 24.1 vs. 68.7 +/- 24.7 (P less than 0.01). Wall motion score was 13.8 +/- 0.6 in Group A and 10.6 +/- 3.1 in Group B (P less than 0.01), which gives values for the proportion of myocardium infarcted of 1.6 +/- 4.2 and 24.2 +/- 22.0%, respectively. The percentage still in jeopardy (after subtracting that infarcted from that threatened) was 51.8 +/- 22.7 in those without and 44.2 +/- 31.1 in those with a previous infarction: this difference is not statistically significant. We conclude that patients with unstable angina pectoris who have sustained a previous myocardial infarction have more severe coronary artery disease than similar patients without previous infarction. The amount of left ventricular myocardium still in jeopardy of becoming infarcted is, however, the same.     

Studies on pathophysiological significance of sympathetic activity in myocardial infarction.

In an attempt to elucidate the pathophysiological significance of the sympathetic hyperactivity in the acute stage of myocardial infarction, the author observed changes in the urinary excretion of CA, the CA content in the myocardium and the hemodynamics in both clinical and experimental myocardial infarction, and the following were found: 1) In clinical myocardial infarction, the urinary excretion of CA was markedly increased immediately after an attack, and the assay of myocardial specimens form the autopsied patients of acute myocardial infarction revealed that the CA content in the non-infarcted area was lower than that in the infarcted area. 2) In the experiments on rabbits with ligated coronary artery, the increase in cardiac contractility and rise in blood pressure in response to CA was supressed after the ligation of coronary artery. In the early stage of experimental myocardial infarction, the decrease of myocardial CA content in the non-infarcted area was, as in autopsied patients, predominant over the decrease of that in the infarcted area. In the chronic stage (more than one week after the coronary ligation), the CA content in the infarcted area showed further decrease, but in the non-infarcted area it was recovered to the level in the control animals. The uptake of exogenous NA into the non-infarcted area decreased in the acute stage, and in the infarcted area it showed marked decreased in the chronic stage. The urinary excretion of CA was increased in the acute stage of myocardial infarction. 3) The administration of betamethasone suppressed the decrease in the CA content in the myocardium following the ligation of coronary artery. Based on these findings, the author came to a postulation that the sympathetic hyperactivity which is suggested by increased urinary excretion of CA and decreased CA content in the myocardium results from the reasonable biophylactic reaction so as to supplement the cardiac hypofunction derived from myocardial infarction.     

Basic fibroblast growth factor increases regional myocardial blood flow and salvages myocardium in the infarct border zone in a rabbit model of acute myocardial infarction.

Basic fibroblast growth factor (bFGF) has been shown by some to promote angiogenesis and myocardial salvage in experimentally induced acute myocardial infarction. Although these findings have spurred much clinical interest, they are not universally observed, and the true efficacy of bFGF remains unclear. The authors used a rabbit model of acute myocardial infarction to further elucidate the effects of bFGF on acutely infarcted myocardium containing few collaterals. Myocardial infarction was evoked by ligation of the left coronary artery. Prior to ligation, either 100 microg of bFGF (bFGF group; n = 15) or physiological saline (control group; n = 22) was injected into the myocardium supplied by the ligated artery. With use of nonradioactive colored microspheres, regional blood flow (Qm) was measured before, immediately after, and 4 weeks after coronary artery ligation. Infarct and border zone sizes were measured in cross-sectional slices of the resected hearts, and the amount of viable myocardium (myocardium score) and the extent of fibrosis were histologically determined in each area. Four weeks after ligation, Qm values in the infarcted area did not significantly differ between the bFGF and control groups (0.54 +/- 0.36 vs 0.48 +/- 0.30 mL/min/g); in the border zone, Qm tended to be higher in the bFGF group (3.39 +/- 2.68 vs 1.47 +/- 0.80 mL/min/g), but the difference was not significant; finally in the noninfarcted area, Qm was significantly (p < 0.05) higher in the bFGF group (6.06 +/- 3.85 vs 2.09 +/- 0.82 mL/min/g). There was no significant difference in the amount of viable myocardium or the extent of fibrosis in the infarcted areas of the two groups. In the border zone, however, the amount of viable myocardium was significantly (p < 0.005) larger in the bFGF group (61.8 +/- 8.5% vs 35.8 +/- 20.3% of the visual field). Likewise, as graded on a scale from 0 to 5, the extent of fibrosis was significantly (p < 0.005) less in the bFGF group (2.1 +/- 0.5 vs 3.3 +/- 0.8). In conclusion, injection of bFGF into acutely infarcted myocardium increased blood flow to the noninfarcted area and salvaged the myocardium in the border zone.     

Lack of regeneration of myocardium by autologous intracoronary mononuclear bone marrow cell transplantation in humans with large anterior myocardial infarctions

BACKGROUND: Experimental and preliminary clinical data suggest that transplantation of autologous bone marrow cells (BMC) may contribute to regeneration of the myocardium after acute myocardial infarction. This approach should be tested in patients with large infarctions in whom a positive effect would be most beneficial. METHODS AND RESULTS: After successful recanalization within 5.9 +/- 2.5 h and stent implantation in five patients with a large acute anterior myocardial infarction (AMI), the patients received autologous mononuclear BMCs via a balloon catheter placed into the left anterior descending artery 6.3 +/- 0.4 days after revascularization. At 3-month follow-up, no improvement was observed for left ventricular ejection fraction, regional wall motion in the infarcted zone, contractility index measured via dobutamine stress echocardiography, coronary blood flow reserve and maximal oxygen uptake, respectively. After further follow-up of 12 months, again no change of the left ventricular ejection fraction could be detected. CONCLUSIONS: Intracoronary transplantation of autologous mononuclear BMCs did not improve cardiac function in our patients with large anterior myocardial infarctions after 3 and 12 months.     

Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p less than .01), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p less than .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p less than .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p less than .05) and significant increases in angiographic cardiac index (p less than .01) and LVESV index (p less than .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akinetic-dyskinetic segments and volume-overload hypertrophy of noninfarcted segments.(ABSTRACT TRUNCATED AT 400 WORDS)