The sequential changes in myocardial thickness and thickening which occur during acute transmural infarction, infarct reperfusion and the resultant expression of reperfusion injury.

AIM: Successful primary PTCA (with TIMI 3 reflow) in patients with acute transmural infarction has been observed to result in an immediate abnormal increase in wall thickness associated with persisting abnormal post-systolic thickening. To understand the sequential changes in regional deformation during: (i) the development of acute transmural infarction, (ii) upon TIMI grade 3 infarct reperfusion and (iii) during the subsequent expression of reperfusion injury the following correlative experimental study was performed in a pure animal model in which there was no distal dispersion of thrombotic material causing either no reflow or secondary microvascular obstruction. METHODS: In 10 closed-chest pigs, a 90 min PTCA circumflex occlusion was used to induce a transmural infarction. This was followed by 60 min of TIMI 3 infarct reperfusion. M-mode ultrasound data from the "at risk" posterior wall infarct segment and from a control remote non-ischemic septal segment were acquired at standardized time intervals. Changes in regional deformation (end-diastolic (EDWT), end-systolic (ESWT) and post-systolic (PSWT) wall thickness, end-systolic strain (epsilonES) and post-systolic strain (epsilonps)) were measured. RESULTS: In this pure animal model of acute transmural infarction/infarct reperfusion (with no pre-existing intra-luminal thrombus), the induced changes in wall thickness and thickening were complex. During prolonged occlusion, after an initial acute fall in ESWT, there was no further change in systolic deformation to indicate the progression of ischaemia to infarction. Both transmurally infarcted and reperfused-infarcted myocardium retained post-systolic thickening indicating that this parameter, taken in isolation, is not a consistent marker of segmental viability and, in this regard, should be interpreted only in combination with other indices of segmental function. The most striking abnormality induced by reperfusion was an immediate increase in EDWT which then increased logarithmically over a 60 min period as reperfusion injury was further expressed. PS did not change significantly during reperfusion. Histology confirmed the wall thickness changes on reperfusion to be due to massive extra-cellular oedema. CONCLUSIONS: The identification of an acute increase in regional wall thickness in a reperfused infarct zone by cardiac ultrasound following primary PTCA might be used in patients to both identify successful infarct reperfusion and to monitor the presence, extent and resolution of the oedema associated with reperfusion injury.     

Usefulness of changes in left ventricular wall thickness to predict full or partial pressure reperfusion in ST-elevation acute myocardial infarction

Experimental studies have shown that if an acute transmural myocardial infarction is reperfused at full pressure there is an immediate and persisting increase in end-diastolic wall thickness (EDWT) due to massive intramural edema, with the amount of edema inversely related to the residual stenosis in the infarct-related artery. This study investigated if these findings are paralleled in the clinical setting and whether the resultant myocardial substrate differs after percutaneous coronary intervention (PCI) versus thrombolysis (the latter having a higher incidence of residual flow limiting stenosis in the culprit vessel). Eighty-eight consecutive patients with ST-elevation myocardial infarction were enrolled. Twenty-seven patients underwent primary PCI, 23 had rescue PCI, and 38 had thrombolysis. Standard M-mode and 2-dimensional echocardiographies were performed within 12 hours. Regional EDWT was measured in 904 infarct-related segments after the different reperfusion strategies and compared with 504 remote noninfarcted segments. EDWT of infarct-related segments after primary PCI was significantly increased compared with normal segments. At follow-up, after 6 months, EDWT of these segments was significantly decreased, indicating transmural infarction. EDWT of infarct-related segments after thrombolysis did not differ from that of normal segments. After rescue PCI, EDWT of infarct-related segments was significantly decreased compared with that of normal segments. In conclusion, full-pressure restoration of epicardial blood flow after transmural myocardial infarction causes an immediate increase in EDWT, easily detected by echocardiography. In contrast, pressure-limiting reperfusion (typical for thrombolysis) resultsin normal EDWT. This confirms experimental data that PCI and thrombolysis can differ in their resultant myocardial substrate.     

Effects of early myocardial reperfusion on left ventricular function in patients with acute myocardial infarction

The effect of early myocardial reperfusion (within six hours after the onset of symptoms) on left ventricular (LV) function in 106 patients with acute myocardial infarction was studied. The subjects consisting of 26 with conventional therapy, 19 with percutaneous transluminal coronary recanalization (PTCR), 16 with percutaneous transluminal coronary angioplasty (PTCA) after PTCR, 32 with direct-PTCA and 13 with coronary artery bypass graft (CABG) were randomly observed after 1981. In these patients, left ventricular ejection fraction (LVEF), regional wall motion, end-diastolic pressure and the contractility index were measured as the indices of LV function. 1. Compared to the conventional therapy group, LVEF and regional wall motion improved significantly in all groups with reperfusion therapy except in the PTCR group. This LV function in patients with subtotal obstruction or good initial collaterals significantly improved compared to patients with total obstruction and no collateral circulation. Patients with a 75 percent or more residual stenosis after reperfusion therapy had significantly decreased LV function compared to those with residual stenosis of less than 75 percent. These findings support the potential role for reperfusion therapy in patients with acute myocardial infarction.     

Mechanical left ventricular unloading prior to reperfusion reduces infarct size in a canine infarction model.

We tested the hypothesis that unloading the left ventricle just prior to reperfusion provides infarct size reduction compared with left ventricular (LV) unloading postreperfusion and reperfusion alone. Twenty-four mongrel dogs were subjected to 2 hr of left anterior descending artery occlusion and 4 hr of reperfusion. A transvalvular (TV) left ventricular assist device (LVAD) was inserted just prior to reperfusion and maintained during the rest of the experiment (LV Assist Pre group). In the LV Assist Post group, the TV LVAD was inserted and activated just after reperfusion. A control group was subjected to reperfusion alone with a sham-TV LVAD. At baseline, the hemodynamic data were similar in the three groups. Myocardial infarct size expressed as percentage of area at risk was significantly reduced in the LV Assist Pre group compared to the control group (P = 0.011) and to the LV Assist Post group (P < 0.05). At 4 hr of reperfusion, transmural myocardial blood flow in the ischemic zone was slightly higher in the animals unloaded prior to reperfusion compared to controls and significantly higher than in the LV Assist Post group (P = 0.04). Postreperfusion end-diastolic wall thickness returned to baseline level in the TV LV Assist Pre group compared to both controls and TV LV Assist Post group. In these latter two groups, a significant increase in postreperfusion end-diastolic wall thickness and contraction band necrosis in the central ischemic zone correlated well with the degree of reperfusion injury. LV unloading prior to, but not after, reperfusion reduces the extent of myocardial necrosis in canine hearts subjected to 2 hr of left anterior descending artery occlusion and 4 hr of reperfusion compared to either reperfusion alone or LV unloading after reperfusion.     

Percutaneous transluminal coronary angioplasty in evolving acute myocardial infarction

In 29 patients with evolving acute myocardial infarction, acute reperfusion of the infarct-related coronary artery was attempted using percutaneous transluminal coronary angioplasty (PTCA). Before PTCA, angiography showed 23 totally occluded and 6 severely stenotic infarct-related coronary arteries. PTCA was initially successful in 25 of 29 patients (86%). Reocclusion occurred in 4 patients within 12 hours after successful PTCA and was associated with new electrocardiographic changes or recurrence of symptoms. In 17 patients the infarct-related coronary artery remained patent at early follow-up; late stenosis occurred in 4 patients. Recurrence of stenosis was accompanied by development of angina. No clinical or angiographic features distinguished those with ultimate vessel patency, occlusion or recurrence of stenosis. On follow-up, ventricular function appeared better preserved or improved in those with a patent infarct-related coronary artery than in those with an occluded infarct-related coronary artery. Further studies are warranted to compare PTCA and streptokinase as primary reperfusion modalities in evolving acute myocardial infarction.     

Assessment of residual coronary arterial stenosis after thrombolytic therapy during acute myocardial infarction

Maximal myocardial salvage appears to be related to the severity of residual coronary arterial stenosis after thrombolysis. The degree of residual infarct vessel stenosis was assessed in 119 consecutive patients with patent arteries who received streptokinase during acute myocardial infarction. After administration of streptokinase, 99 of 119 patients (83%) had a residual stenosis 70% or more in diameter. Assuming that a residual diameter stenosis of at least 70% is flow limiting, the feasibility for percutaneous transluminal coronary angioplasty (PTCA) was determined by the following criteria: length less than 10 mm, no significant distal narrowing or left main stenosis, and an adequate-sized distal artery. In 81 of 99 patients (82%), arterial anatomy was suitable for PTCA. Thus, after therapy with streptokinase for acute myocardial infarction, most patients have a significant infarct arterial residual stenosis and are candidates for PTCA.     

Effect of reperfusion therapy for acute myocardial infarction on ventricular function and heart failure

Thrombolytic therapy reduces mortality and improves ventricular function in acute myocardial infarction. We review the short- and long-term effects of reperfusion after acute myocardial infarction on left ventricular function and heart failure. The beneficial effects of reperfusion may be achieved by immediate limitation of infarct size or through delayed improvement in ventricular remodeling. Infarct size is dependent on the area at risk, the time delay to reperfusion, the completeness and persistence of reperfusion, and collateral blood flow. The main prognostic parameters after myocardial infarction are vessel patency, infarct size, and ventricular volume and function. Initial infarct size and patency of the infarct-related artery are independent predictors of ventricular volume and function, as well as of survival in the long-term following acute myocardial infarction. The beneficial effects of a patent infarct-related artery are only evident if normal flow is achieved and maintained, and are dependent on the degrees of the residual stenosis. Thrombolytic therapy reduces the incidence of in-hospital congestive heart failure, and this improvement is sustained for at least 5 years. As only a fraction of patients with acute myocardial infarction currently receive thrombolytic therapy, heart failure after myocardial infarction can be reduced by administering thrombolytic therapy earlier to more patients with evolving acute myocardial infarction.     

Percutaneous transluminal coronary angioplasty for treatment of acute myocardial infarction: comparison with percutaneous transluminal coronary recanalization

Percutaneous transluminal coronary angioplasty (PTCA) was evaluated as a means of reperfusion of the infarct-related coronary artery, and the results were compared with those of percutaneous transluminal coronary recanalization (PTCR). There were no difference in sex, age, infarct location and time from the onset to start of treatment between 135 patients with evolving acute myocardial infarction treated with PTCA (PTCA group) and 113 patients treated with PTCR alone (PTCR group). Fifty-nine patients in the PTCA group underwent PTCA following PTCR; the remaining 76 patients were without prior PTCR. Successful PTCA, defined as a 20% or more reduction in percent luminal stenosis diameter, was achieved in 123 (90%) of the 135 patients in the PTCA group. The reperfusion rate was 93% in the PTCA group and 77% in the PTCR group (p less than 0.01). Residual stenosis immediately after the treatment was 30 +/- 13% in the PTCA group and 70 +/- 16% in the PTCR group (p less than 0.01). In the PTCA group, three cases developed serious complications which were associated with angioplasty: coronary perforation, side branch occlusion resulting in cardiogenic shock and exacerbation of cardiogenic shock. The latter two patients died, however, there was no difference in hospital mortality rate: 6% in the PTCA group versus 11% in the PTCR group. At follow-up angiography performed four weeks after admission, reocclusion of the successfully recanalized arteries was observed in 3% of the PTCA group and in 14% of the PTCR group (p less than 0.01). Regional wall motion was evaluated by left ventriculography using a wall motion score system which consisted of six grades; from normal counted as 0, to dyskinesis counted as 5. There was no difference in the wall motion score between the successful PTCA group and the successful PTCR group (2.6 +/- 1.4 versus 2.8 +/- 1.4), but the scores of both groups were better than those of the non-recanalized group (3.4 +/- 1.0: p less than 0.01). In conclusion, PTCA and PTCR have the same effect on hospital mortality rate and regional wall motion, but PTCA has a higher reperfusion rate and a lower reocclusion rate than does PTCR. Although PTCA has a potential disadvantage inducing serious complications, it appears to be a useful treatment for acute myocardial infarction.     

Characteristics and outcome of patients in whom reperfusion with intravenous tissue-type plasminogen activator fails: results of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I trial

To examine the outcome of patients with persistent coronary artery occlusion despite treatment with intravenous tissue-type plasminogen activator (t-PA), the clinical course of 96 patients with persistent occlusion after 90 min of therapy was evaluated. All patients underwent cardiac catheterization 90 min after initiation of intravenous t-PA. Immediate coronary angioplasty (PTCA) was attempted when the infarct-related artery failed to reperfuse unless the vessel was technically unsuitable or the infarct was thought to be small. No baseline differences could be found between these 96 patients and 288 patients who achieved perfusion with the same protocol. Although patients with and without successful perfusion after t-PA had similar clinical courses before cardiac catheterization, those without perfusion had more complications (ventricular fibrillation, severe bradycardia, hypotension) during catheterization. PTCA achieved reperfusion with less than 50% residual stenosis in 73% of the 86 patients in whom it was attempted, while 16% were left with a high-grade (greater than 50%) residual stenosis and PTCA failed in 11%. Mortality was highest in the nine patients with complete PTCA failure (44%), compared with a 6% mortality in the 63 patients with an insignificant residual stenosis after PTCA and a 14% mortality in the 14 patients with reperfusion, but a greater than 50% residual stenosis after PTCA. In 10 patients with small infarcts (six), unsuitable anatomy (two), or "spontaneous" drug induced (but later) opening before contemplated PTCA (two), PTCA was not attempted and no mortality occurred. The in-hospital reocclusion rate after successful PTCA was 29%, despite the use of heparin and antiplatelet agents.(ABSTRACT TRUNCATED AT 250 WORDS)     

Results of emergency bypass operation following percutaneous transluminal coronary angioplasty

Between 1980 and 1988, percutaneous transluminal coronary angioplasty (PTCA) was performed in 1,514 patients. Fifty-five patients (3.6%) underwent emergency coronary bypass surgery because of an acute occlusion of the vessel or a dissection with sustained angina and signs of ischemia on the electrocardiogram. Twenty-five of these 55 patients had a myocardial infarction and 5 patients died, 3 perioperatively, 2 after hospital discharge. The degree of stenosis of the dilated vessel significantly influenced the incidence of infarction, while left ventricular ejection fraction prior to PTCA significantly influenced mortality. Patients who underwent surgery with an occluded vessel experienced myocardial infarction significantly more often (87%) than patients with a patent vessel (24%). The incidence of infarction was 27% when reperfusion of the vessel occluded during PTCA was achieved with a reperfusion catheter, repeated PTCA or intracoronary lysis. The patients' age, presence of unstable angina, left ventricular ejection fraction prior to PTCA, the dilated vessel, the extent of coronary artery disease, collateralization of the dilated vessel, and the time between the onset of the event necessitating bypass surgery and the beginning of extracorporeal circulation were found to have no influence on the incidence of infarction. Patients who died had a significantly lower ejection fraction before PTCA than survivors and all patients who died had experienced a large perioperative myocardial infarction.     

Myocardial reperfusion in the pig heart model: infarct size and duration of coronary occlusion

The effect of coronary artery reperfusion on infarct size was studied in a pig heart model. Forty four open chest pigs underwent occlusion of the mid-left anterior descending artery. Fifteen minutes after occlusion the animals were randomised to one of five groups: reperfusion at 30, 45, 60, or 90 min after occlusion (groups 1-4) or permanent occlusion (group 5). Twenty four hours after coronary occlusion the pigs were killed. The heart was sectioned in slices, which were incubated in triphenyl-tetrazolium. Mean(SEM) infarct sizes calculated by planimetry were 0.46(0.42), 2.85(1.14), 9.74(1.65), 8.93(1.37), and 13.17(1.17)% of left ventricular mass in the five groups. The transmural extension of the infarct was 14.6(11.4), 42.1(12.9), 87.4(6.6), 96.2(3.2), and 100(0)% and a transmurality index used as an estimate of the mean extension of the infarct relative to wall thickness was calculated to be 0.08(0.06), 0.32(0.10), 0.72(0.06), 0.79(0.04), and 0.92(0.02) respectively. Infarct size was similar in groups 3-5, but significantly smaller in groups 1 and 2 (p less than 0.05). Infarct size and the transmurality index correlated exponentially with the duration of the occlusion (r = 0.80, p less than 0.01; and r = 0.95, p less than 0.001 respectively). These results indicate that in the pig heart model submitted to an acute coronary occlusion cell viability may be less than that suggested by previous canine studies. This observation is probably related to a less well developed collateral blood flow in the pig heart and may provide an experimental model that better resembles certain clinical conditions.     

Management of Patients with Heparin-Induced Thrombocytopenia: Focus on Recombinant Hirudin

It remains controversial whether percutaneous transluminal coronary angioplasty (PTCA) performed 24 hours after the onset of acute myocardial infarction (AMI) in coronary arteries with 99% stenosis is useful in preserving left ventricular function. We investigated the effectiveness of PTCA in preventing left ventricular remodeling when it was performed 24 hours after the onset of AMI in infarct-related coronary arteries (IRCAs) having 99% stenosis and thrombolysis in myocardial infarction (TIMI) grade 3 flow. The subjects were 19 patients with AMI (anterior wall, 9 patients; inferior wall, 7 patients; and non-Q, 3 patients) who, within 24 hours of the onset of AMI, underwent coronary angiography and left ventriculography during the acute and/ or chronic phases. The patients were divided into a PTCA group, comprised of patients in whom PTCA was successfully performed 24 hours after the onset of AMI (n = 10), and a non-PTCA group (n = 9). The non-PCTA group included patients who were successfully reperfused by thrombolysis and did not include patients who had spontaneous reperfusion or reperfusion after PTCA. In the non-PTCA group, the left ventricular end-diastolic volume (mean ± SD) was significantly increased in the chronic phase (86 ± 23 mL/m² as compared with the acute phase (67 ± 13 mL/m², whereas in the PTCA group no significant difference was observed between end-diastolic volumes in the acute and chronic phases (67 ± 26 and 68 ± 13 mL/m², respectively). Left ventricular remodeling is prevented by PTCA when it is performed 24 hours after the onset of AMI in IRCAs with 99% stenosis and TIMI grade 3 flow.     

Initial experience with hyperoxemic reperfusion after primary angioplasty for acute myocardial infarction: results of a pilot study utilizing intracoronary aqueous oxygen therapy

OBJECTIVES: The purpose of this study was to evaluate the feasibility and safety of intracoronary hyperoxemic reperfusion after primary angioplasty for acute myocardial infarction (MI). BACKGROUND: Hyperoxemic therapy with aqueous oxygen (AO) attenuates reperfusion injury and preserves left ventricular (LV) function in experimental models of MI. METHODS: In a multi-center study of patients with acute MI undergoing primary angioplasty (PTCA), hyperoxemic blood (pO(2): 600 to 800 mm Hg) was infused into the infarct-related artery for 60 to 90 min after intervention. The primary end points were clinical, electrical and hemodynamic stability during hyperoxemic reperfusion and in-hospital major adverse cardiac events. Global and regional LV function was evaluated by serial echocardiography after PTCA, after AO infusion, at 24 h and at one and three months. RESULTS: Twenty-nine patients were enrolled (mean age: 58.9+/-12.6 years). Hyperoxemic reperfusion was performed successfully in all cases (mean infusion time: 80.8+/-18.2 min; mean coronary perfusate pO(2): 631+/-235 mm Hg). There were no adverse events during hyperoxemic reperfusion or the in-hospital period. Compared with baseline, a significant improvement in global wall motion score index was observed at 24 h (1.68+/-0.24 vs. 1.48+/-0.24, p < 0.001) with a trend toward an increase in ejection fraction (48.6+/-7.3% vs. 51.8+/-6.8%, p = 0.08). Progressive improvement in LV function was observed at one and three months, primarily due to recovery of infarct zone function. CONCLUSIONS: Intracoronary hyperoxemic reperfusion is safe and well tolerated after primary PTCA. These preliminary data support the need for a randomized controlled trial to determine if hyperoxemic reperfusion enhances myocardial salvage or improves long-term outcome.     

Pathologic implications of restored positive T waves and persistent negative T waves after Q wave myocardial infarction

Objectives. We sought to study the pathologic implications of restored positive T waves and persistent negative T waves in the chronic stage of Q wave myocardial infarction.Background. Some inverted T waves (coronary T waves) become positive after acute myocardial infarction: others retain their negative T wave component for a long time. The pathologic implications of the difference between restored positive T waves and persistent negative T waves in leads with Q waves has not, until now, been given much careful study.Methods. Of 17 patients with anterior or anteroseptal myocardial infarction confirmed by autopsy, 8 (group P) had positive and 9 (group N) had negative T waves in precordial leads with Q waves ≥ 1 year after the onset of myocardial infarction. The appearance and extent of the infarct area and the degree of coronary artery stenosis were evaluated in both groups.Results. At autopsy, seven of eight patients in group P had nontransmural fibrotic changes in the anteroseptal or anterior wall. However, seven of nine patients in group N had a transmural myocardial infarction consisting of only a thin fibrotic layer in the anteroseptal or anterior wall. The left anterior descending coronary artery showed 75% stenosis in 1 patient in each group but >90% stenosis in the remaining 15 patients.Conclusions. Persistent negative T waves in leads with Q waves in the chronic stage of myocardial infarction indicate the presence of a transmural infarction with a thin fibrotic layer, whereas positive T waves indicate a nontransmural infarct containing viable myocardium within the layer.     

Streptokinase improves reperfusion blood flow after coronary artery occlusion

Streptokinase is an effective thrombolytic agent which, with early restoration of coronary blood flow, has the potential for limiting infarct size. Distinct from thrombolysis, we studied the effects of streptokinase on reperfusion coronary blood flow and infarct size. Open-chest anesthetized canines underwent a 90 minute snare occlusion of the left circumflex coronary artery followed by release and reperfusion through a critical stenosis for 6 hours. The animals were assigned randomly to two groups. Intracoronary streptokinase [group 1 (n = 8): 6000 IU/kg in 3 ml of saline] or saline [group 2 (n = 8): 3 ml of saline] was infused at 0.05 ml/min for 60 minutes beginning 30 minutes before reperfusion. Coronary blood flow was stable in group 1 during reperfusion, while in group 2 it fell during 6 hours of reperfusion (30 +/- 4 ml/min to 18 +/- 2 ml/min, P = 0.05). The ST-segment elevation on the limb lead II electrocardiogram 15 minutes after coronary artery occlusion was similar in both groups (group 1: 3.9 +/- 0.6 mV, group 2: 2.3 +/- 0.5 mV), suggesting the extent of myocardial ischemia was also similar in both groups. The infarct sizes were similar when expressed both as a percent of the total left ventricular mass [(IZ/LV) group 1: 17 +/- 2.5%, group 2: 17.5 +/- 2.5%] or as a percent of the area at risk of infarction [(IZ/AR) group 1: 39 +/- 6%, group 2: 39 +/- 5%]. In both groups, the mass of left ventricle dependent on the blood flow distribution of the left circumflex coronary artery was similar when compared to total left ventricular mass [(AR/LV) group 1: 41 +/- 3%, group 2: 44 +/- 4%]. These results demonstrate that streptokinase maintains reperfusion coronary blood flow through a critical stenosis at a rate similar to baseline levels. Despite the fact that coronary blood flow remained stable with streptokinase during reperfusion, infarct size was not limited after 90 minutes of fixed coronary artery occlusion in this canine model of myocardial injury.     

Surgical treatment of acute myocardial infarction

In 1989 the following indications for surgical treatment of acute myocardial infarction are: (1) acute evolving myocardial infarction less than 6 h from onset, in patients in whom percutaneous transluminal coronary angioplasty (PTCA) or streptokinase (SK), depending on the coronary anatomy, has been unsuccessful; if single vessel disease, coronary artery bypass grafting (CABG) is unlikely; if multiple vessel disease, CABG is preferable to SK/PTCA unless a very major 'culprit' lesion can be identified with certainty; (2) postinfarction angina hours to days after a transmural myocardial infarction unyielding to maximal medical therapy and in patients with a coronary artery obstruction not amenable to PTCA; (3) occlusion of a coronary artery during cardiac catheterization that cannot be fixed by PTCA and/or SK; (4) occlusion of a coronary artery during PTCA causing hemodynamic obstruction and a threatened myocardium subtended by the obstructed coronary artery; (5) balloon-dependent patients in cardiogenic shock without mechanical defects who have adequate residual left ventricular function as determined by regional wall motion studies; (6) ventricular septal defect secondary to myocardial infarction unless there is terminal organ damage; (7) mitral valve replacement with coronary bypass for acute papillary muscle rupture; (8) semi-emergency cardiac transplantation, either with or without a mechanical bridge to transplant in young individuals (less than 50 years) who have suffered massive destruction of left ventricular myocardium by an acute coronary occlusion with or without recurring ventricular tachyarrhythmias. Ejection fraction in this clinical category is always under 0.20 and usually under 0.15.     

Early prediction of infarct size by strain Doppler echocardiography after coronary reperfusion.

OBJECTIVES: The objective of this study was to investigate whether strain Doppler echocardiography performed immediately after revascularization by percutaneous coronary intervention could predict the extent of myocardial scar, determined by contrast-enhanced magnetic resonance imaging (MRI). BACKGROUND: There is considerable variability in survival rate after percutaneous coronary intervention, and accurate early risk stratification is therefore of major clinical importance. METHODS: Thirty individuals with acute anterior myocardial infarction were examined with longitudinal strain by Doppler 1.5 h after revascularization. The extent of scarring 9 months later was analyzed by MRI in 16 corresponding myocardial segments. Strain in all left ventricular segments was averaged to obtain a global value. Infarct size was estimated by clinical parameters and cardiac markers. RESULTS: A good correlation was found between the global strain and total infarct size (R = 0.77, p < 0.00001). A multivariate regression analysis showed that global peak strain and serum glutamic oxaloacetic transaminase correlated with the infarct size measured by MRI (p = 0.0001 and p = 0.001, respectively). Furthermore, a clear inverse relationship was found between the segmental strain and the transmural extent of infarction in each segment (R = 0.67, p < 0.0001). CONCLUSIONS: This study demonstrates that assessment of regional and global strain at 1.5 h after reperfusion therapy correlates with size and transmural extent of myocardial infarction as determined by contrast-enhanced MRI. The novel global strain parameter is a valuable predictor of the total extent of myocardial infarction and may therefore be an important clinical tool for risk stratification in the acute phase of myocardial infarction.     

Evaluation of coronary reperfusion for acute myocardial infarction by emission CT using technetium-99m pyrophosphate

Twelve patients with acute transmural myocardial infarction (AMI) were treated with percutaneous transluminal coronary angioplasty (PTCA) following intracoronary thrombolysis using urokinase, and underwent technetium-99m stannous pyrophosphate (Tc-99m-PPi) imaging 9.2 +/- 2.1 hours after the onset of chest pain. The imaging was performed with emission computed tomography (ECT). Compared to planar imaging, this allowed more accurate detection of small myocardial infarcts and accurate measurements of infarcts irrespective of their location was also made. Early Tc-99m-PPi images were obtained to test the hypothesis that an early, abnormal Tc-99m-PPi image suggest successful reperfusion. The results were presented for two groups of patients: three with unsuccessful reperfusion (Group A) and nine with successful reperfusion (Group B). Eight of the nine patients with successful reperfusion had positive acute Tc-99m-PPi images. On the contrary, all the three patients for whom reperfusion failed had negative acute Tc-99m-PPi images. We also examined the feasibility of estimating infarct size using positive Tc-99m-PPi images in patients with successful reperfusion during the early phase of AMI. The Tc-99m-PPi uptake score (Tc-US) was used to measure infarct size in this study. Areas of increased Tc-99m-PPi uptake within myocardial infarcts were threshold at 60% of the peak activity. The Tc-US of each patient was obtained to sum the scores of all myocardial segments using a scoring system with a maximum score of 108. Using this method, Tc-US ranged from 2 to 39. The correlation of Tc-US with the peak serum creatine kinase level was significant (r = 0.91).(ABSTRACT TRUNCATED AT 250 WORDS)     

Randomized trial of late elective angioplasty versus conservative management for patients with residual stenoses after thrombolytic treatment of myocardial infarction. Treatment of Post-Thrombolytic Stenoses (TOPS) Study Group.

BACKGROUND. After thrombolytic therapy for patients with acute myocardial infarction (MI), percutaneous transluminal coronary angioplasty (PTCA) is frequently performed because of the presence of a "significant" infarct vessel stenosis demonstrated at predischarge coronary angiography. Several studies have shown PTCA performed early after thrombolysis to be unnecessary or even harmful. However, PTCA in these trials was generally performed 1-3 days after MI, when the milieu in the infarct artery may be unsuited for PTCA, and the incidence of major ischemic complications was high. To date, no trial has assessed whether delayed PTCA (4-14 days) should be performed in patients without evidence of ischemia on stress testing. METHODS AND RESULTS. To test the hypothesis that delayed PTCA might provide clinical benefit compared with medical therapy alone, 87 patients treated within 6 hours of chest pain onset with thrombolytic therapy and with negative functional test were randomized between PTCA to be performed 4-14 days after MI versus no PTCA. Both groups received medical therapy. Patients with postinfarct angina or prior Q wave infarction in the infarct distribution were excluded. The primary study end point was increase in left ventricular ejection fraction with exercise measured by radionuclide studies 6 weeks after MI, a parameter known from other studies to correlate inversely with future ischemic events. Clinical outcome was also monitored for 12 months. There were no differences between the study groups for any prerandomization variable recorded. Mean age was 57 +/- 10 years, 84% of patients were male, 21% had prior MI, 36% had anterior MI, 7% had multivessel disease, and the infarct stenosis measured 70 +/- 17% before randomization. PTCA was successful in 38 of 42 patients (88%) but resulted in non-Q wave MI due to acute closure of the treated site in three of 42 (9.5%). There was no difference in 6-week resting ejection fraction or increase in ejection fraction with exercise between the two groups (47 +/- 12% and 6 +/- 8%, respectively, in the PTCA group; 49 +/- 10% and 5 +/- 9% in the no-PTCA group; p = NS for both.) There were no deaths in either group. Actuarial 12-month infarct-free survival was 97.8% in the no-PTCA group and 90.5% in the PTCA group (p = 0.07). CONCLUSIONS. There was no functional or clinical benefit from routine late PTCA after MI treated with thrombolytic therapy in this relatively low-risk cohort of patients. These data strongly suggest that patients with an uncomplicated MI after thrombolytic therapy, even if they have a "significant" residual stenosis of the infarct vessel, should be treated medically if they are without evidence of ischemia on stress testing before hospital discharge.     

Myocardial cell hypertrophy after myocardial infarction with reperfusion in dogs.

BACKGROUND. The potential role of myocardial cell hypertrophy in the ischemic zone in the mechanism of late recovery of regional contractile function after myocardial infarction followed by reperfusion has not been examined. METHODS AND RESULTS. Eight chronically instrumented, conscious dogs were subjected to 90-120 minutes of circumflex coronary artery occlusion followed by reperfusion. The thickness and function of the anterior (AT) and posterior (PT) walls was measured by ultrasonic gauges at control, during occlusion, and after reperfusion. After 3 weeks, cross-sectional areas of surviving cells were determined from subepicardial (epi), midwall (mid), and subendocardial (endo) regions in six dogs and compared with those from six animals without infarction, including three sham-operated control dogs. PT systolic wall thickening showed dyskinesia during occlusion but recovered after reperfusion to 48% of control at 1 week and 67% at 3 weeks. End-diastolic thickness of the PT wall increased markedly after reperfusion, but AT and PT walls were only slightly thicker (p = NS) than in control dogs at 3 weeks. Cross-sectional areas of reperfused dogs in the infarct region averaged 279 (PTepi), 291 (PTmid), and 317 microns 2 (PTendo) and were significantly larger than in control animals (237 [PTepi], 241 [PTmid], and 233 microns 2 [PTendo]). PT cell areas were significantly larger than AT cells, ENDO cell areas were larger than EPI cells (both p < 0.05), and ENDO cells of the AT wall were larger than those of noninfarcted dogs (p < 0.05). CONCLUSIONS. In dogs with myocardial infarction followed by reperfusion, the cross-sectional areas of cells in the infarcted PT wall were larger than those in the noninfarcted AT wall, and within both the infarcted and noninfarcted zones, cell areas were larger in the endocardial than the epicardial region. In all regions of the infarcted wall and in the ENDO region of the noninfarcted wall, cell areas were generally larger than those of control dogs without infarction, and the control dogs showed no transmural differences in cell areas. The mechanisms responsible for this significant remodeling of the reperfused infarcted zone, which involves myocardial cellular hypertrophy, are unknown, but it is possible that hypertrophy of surviving regions of the infarcted wall played a role in the late recovery of regional function that accompanied this hypertrophic response.