Characterizing the normal heart using quantitative three-dimensional echocardiography.

We present normative data on cardiac volume, geometry and shape derived using three-dimensional echocardiography (3-DE). Three-dimensional reconstructions were created using the piecewise smooth surface subdivision (PSSS) reconstruction technique of the left and right ventricular (LV and RV) endocardium and the mitral and tricuspid annuli (MA and TA) of 67 normal subjects. We derived LV end-diastolic (ED) and end-systolic (ES) volume indices (VI) of 76.5 +/- 16.8 ml m(-2) and 35.3 +/- 14.1 ml m(-2), LV ejection fraction (EF) of 56.1 +/- 9.93%, RV EDVI and ESVI of 93.2 +/- 20.0 ml m(-2) and 49.9 +/- 13.5 ml m(-2) and RVEF of 47.3 +/- 7.69%, along with data on the geometry and shape of the MA, TA, LV and RV. There was no pattern of consistent understatement or overstatement of volumes or dimensions compared with other imaging modalities, and observed variance in data can largely be accounted for through examination of the physics or protocol of each modality.

Physiologic determinants of exercise capacity in patients with different types of right-sided regurgitant lesions: Ebstein's malformation with tricuspid regurgitation and repaired tetralogy of Fallot with pulmonary regurgitation.

BACKGROUND: Exercise capacity relates to right ventricular (RV) volume overload in congenital heart disease and may improve after surgery. We herewith investigate the relation between exercise capacity, cardiac index, and RV volume overload due to tricuspid regurgitation (TR) in Ebstein's malformation and pulmonary regurgitation (PR) after repair of tetralogy of Fallot (rToF). METHODS: We measured cardiac index and tricuspid/pulmonary regurgitant fraction by cardiovascular magnetic resonance in patients with Ebstein's malformation (n = 40) or rTOF (n = 53) with at least moderate TR/PR and 24 healthy controls. Exercise tolerance was determined by peak oxygen consumption (peak VO2) during cardiopulmonary exercise testing. RESULTS: TR and PR fraction were similar in Ebstein and rTOF patients (43 ± 17% versus 39 ± 12%, respectively). Cardiac index was reduced in Ebstein (2.7 ± 0.6L/min/m(2) compared to controls 3.5 ± 0.9L/min/m(2), p < 0.001) but not in rToF patients (3.2 ± 0.5L/min/m(2)). Multiple regression analysis revealed a significant correlation between peak VO2 and cardiac index in Ebstein. Furthermore, peak VO2 correlated with peak heart rate in both groups but not with regurgitation fraction. CONCLUSIONS: Despite comparable amounts of regurgitation from a right sided heart valve in patients with Ebstein and rToF, reduction of cardiac index was observed only in the former group. Greater physiologic complexity and adverse ventricular interaction with chronotropic incompetence in Ebstein's malformation may account for this.

Cardioprotective effects of the Na(+)/H(+) exchange inhibitor cariporide in patients with acute anterior myocardial infarction undergoing direct PTCA.

BACKGROUND: Activation of Na(+)/H(+) exchange in myocardial ischemia and/or reperfusion leads to calcium overload and myocardial injury. Experimental studies have shown that Na(+)/H(+) exchange inhibitors can attenuate Ca(2+) influx into cardiomyocytes. We therefore performed a multicenter, randomized, placebo-controlled clinical trial to test the hypothesis that inhibition of Na(+)/H(+) exchange limits infarct size and improves myocardial function in patients with acute anterior myocardial infarction (MI) treated with direct PTCA. METHODS AND RESULTS: One hundred patients were randomized to receive placebo (n=51) or a 40-mg intravenous bolus of the Na(+)/H(+) exchange inhibitor cariporide (HOE 642) (n=49) before reperfusion. Global and regional left ventricular functions were analyzed by use of paired contrast left ventriculograms performed before and 21 days after PTCA and myocardial enzymes (ie, creatine kinase ¿CK, CK-MB, and LDH) as markers for myocardial tissue injury were evaluated. At follow-up, the ejection fraction was higher (50% versus 40%; P<0.05) and the end-systolic volume was lower (69.0 versus 97.0 mL; P<0.05) in the cariporide group. Significant improvements in some indices of regional wall motion abnormalities were observed, such as the percentage of chords with hypokinesis < -2 SD (P=0.045) and the severity of hypokinesis in the border zone of the infarct region (P=0.052). In addition, CK, CK-MB, or LDH release was significantly reduced in the cariporide patients. CONCLUSIONS: Our findings suggest that inhibition of Na(+)/H(+) exchange by cariporide may attenuate reperfusion injury and thereby improve the recovery from left ventricular dysfunction after MI.

Determinants of improved left ventricular function after thrombolytic therapy in acute myocardial infarction.

Many studies have been performed to evaluate the efficacy of thrombolytic therapy in achieving reperfusion, salvaging myocardium and enhancing survival. This review discusses the concordance between the results of these clinical studies and the observations made in experimental animals of the effect of reperfusion on the recovery of left ventricular function. The evaluation of functional recovery is affected by the timing of the measurement and the sensitivity of the method for detecting regional abnormalities. In addition, the underlying coronary anatomy also determines outcome, so that infarct location, collateral circulation and the degree of coronary obstruction merit consideration. Two factors are of paramount importance in determining the amount of myocardium salvaged, the recovery of left ventricular function and the reduction in mortality. These factors are: the time delay until reperfusion is achieved and the adequacy of the coronary reflow. The close agreement between studies measuring the effect of reperfusion on left ventricular function and studies with mortality as the end point provides indirect evidence that enhancement of survival in patients treated with thrombolytic agents is mediated by recovery of ventricular function.

Quantitative contrast angiography for assessment of ventricular performance in heart disease.

Contrast angiography provides much information about ventricular and valvular size and function. This review describes the calculation of left ventricular chamber volume and wall thickness and the derivation of ejection fraction, cardiac output, mass and wall tension and stress. In patients with valvular regurgitation, valve orifice area can be calculated by using the angiographic output and regurgitant flow determined by comparing the angiographic output with the cardiac output measured using Fick or indicator-dilution techniques. By analyzing ventricular volume in conjunction with pressure, it is possible to assess pressure-volume work, compliance and contractility. Regional wall motion can be measured from the change in ventricular contour with time. When applied clinically, these methods and measurements have been used to determine the hemodynamic characteristics of the compensated and decompensated left ventricle in valvular and coronary heart disease. The information derived from quantifying information in angiographic images contributes to patient diagnosis, assessment of prognosis and evaluation of therapy, and has added to our knowledge concerning the pathophysiology of heart disease.

Measurement of postsystolic shortening to assess viability and predict recovery of left ventricular function after acute myocardial infarction.

OBJECTIVES: We sought to determine whether left ventricular (LV) postsystolic shortening in the region of acute myocardial infarction (MI) predicts functional recovery after primary angioplasty. BACKGROUND: Previous studies in experimental animals have shown that postsystolic shortening during temporary coronary occlusion predicts functional recovery after reperfusion. METHODS: Contrast ventriculography was performed on 35 patients with acute MI before and immediately after angioplasty, and one day, one month, three months and one year later. The centerline method was used to measure regional LV wall motion at end systole from all six ventriculograms as well as motion during isovolumic relaxation (motion(iso)) and postsystolic shortening from end systole until the end of contraction. The ventriculograms of 23 patients with normal anatomy were similarly analyzed. RESULTS: Wall motion at end systole improved significantly from baseline to follow-up in the infarct region. Postsystolic shortening at baseline correlated most closely with the recovery of wall motion at three months in patients with anterior infarction (r = 0.69, n = 25, p = 0.0001) but also with recovery at one month and one year. The correlation was slightly less powerful for motion(iso). Functional recovery could not be predicted from assessment of motion(iso) and postsystolic shortening in patients with inferior infarction. CONCLUSIONS: In patients with acute anterior MI, analysis of postsystolic shortening in the infarct region predicts the recovery of systolic LV function after reperfusion. Postsystolic shortening represents active contraction and indicates viable myocardium.

Effect of thrombolysis on acute mitral regurgitation during evolving myocardial infarction. Experience from the Thrombolysis in Myocardial Infarction (TIMI) Trial.

OBJECTIVES: This study was undertaken to determine whether early successful thrombolysis can reverse infarct-associated mitral valve dysfunction. BACKGROUND: Mitral regurgitation is a common complication of acute myocardial infarction and has been shown to adversely affect both short- and long-term prognosis. Although anecdotal reports have suggested that reperfusion of the infarct-related artery may restore normal function to the mitral valve, this theory has not been subjected to formal investigation. METHODS: Patients with total or partial obstruction of the infarct-related artery received intravenous thrombolytic therapy with either streptokinase or recombinant tissue-type plasminogen activator within 7 h of symptom onset (mean 4.8 h) as part of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial. Repeat coronary angiography assessed arterial patency at 90 min and 10 days after attempted reperfusion. The presence and severity of mitral regurgitation were determined by contrast ventriculography both before thrombolysis and before hospital discharge. RESULTS: Overall, 21 (16%) of the 132 study patients exhibited mitral regurgitation on either their initial or their predischarge ventriculogram. The proportion of infarct-related arteries found to be patent (TIMI flow grade 2 or 3) was statistically similar in patients with and without mitral regurgitation during each angiographic evaluation period (initial, 90 min and 10 days). Although coronary artery perfusion increased overall during sequential measurement (mean TIMI grade was 0.4 +/- 0.6 initially, 1.5 +/- 1.3 at 90 min and 2.2 +/- 1.0 at 10 days), the pattern of reperfusion observed could not predict an increase or decrease in regurgitant severity (p = NS). Early mitral regurgitation resolved in 57% of patients by 10 days, but this resolution appeared independent of the presence or absence of improved coronary perfusion (60% vs. 50%). The development of new regurgitation during the recovery period (6%) was also unrelated to improved perfusion (7% vs. 4%). CONCLUSIONS: Acute mitral regurgitation developing during myocardial infarction shows frequent changes in its presence or severity during the 1st 10 days, appears independent of coronary artery patency both early and late after thrombolysis and cannot be reliably treated by improving arterial perfusion with thrombolytic agents.

Extension of hypokinesia into angiographically perfused myocardium in patients with acute infarction.

OBJECTIVE: This study was performed to determine whether left ventricular hypokinesia due to acute myocardial infarction lies between the site of coronary artery occlusion and the end of the infarct-related artery in patients. BACKGROUND: Normalizing for the size of the risk region reduces variability in measuring infarct size in experimental studies. The ability to gauge the size of the region at risk of becoming dysfunctional may help reduce variability in measuring regional hypokinesia due to acute myocardial infarction. METHODS: Angiograms of 84 patients with acute infarction due to isolated stenosis of the right coronary artery (n = 40) or the left anterior descending coronary artery (n = 44) were analyzed. The location and length of the segment with hypokinesia more severe than -1 or -2 SD below the normal mean were determined by the centerline method. The risk region was defined as the left ventricular contour between the site of the occlusion and the end of the infarct-related artery on the angiogram. RESULTS: The segment with hypokinesia below -1 SD was longer than the risk region in 52% of patients with occlusion of the left anterior descending coronary artery, more frequently (p < 0.01) than in right coronary artery occlusion (22%), owing to extension of hypokinesia beyond the distal end of the artery. Extension of severe hypokinesia (below -2 SD) beyond the risk region occurred in 33% of patients with an anterior infarct and in 9% of patients with an inferior infarct. CONCLUSIONS: The size of the risk region cannot be assessed accurately from coronary angiography.

Time from onset of symptoms to thrombolytic therapy: a major determinant of myocardial salvage in patients with acute transmural infarction.

To determine whether myocardial salvage after successful intracoronary or intravenous thrombolysis is time dependent, the relation between left ventricular wall motion and the time to treatment was studied in 69 patients admitted less than 3 hours after onset of acute transmural myocardial infarction (42 patients with reperfusion by intracoronary streptokinase, 27 by intravenous urokinase). A similar significant relation between the time to treatment and the severity of regional hypokinesia at follow-up was found in the intracoronary and intravenous groups. To better define this relation, particularly during the early phase of infarction, the groups were combined. In patients in whom thrombolytic treatment was initiated within 2 hours after symptom onset, wall motion at follow-up was within 2 standard deviations of the normal mean in 82% (14 of 17 patients). If treatment was started 2 to 5 hours after symptom onset, the probability of improved wall motion decreased to 46% (24 of 52 patients, p less than 0.025). The time/wall motion relation appeared to be independent of infarct location, angiographically visible collateral vessels and the presence of subtotal coronary artery occlusion. The severity of hypokinesia at follow-up study correlated with the magnitude of peak serum creatine kinase (r = -0.71), indicating that thrombolytic therapy initiated within 2 hours after the onset of symptoms improves regional left ventricular function and reduces infarct size more than later therapy does.

Early recovery of left ventricular function after thrombolytic therapy for acute myocardial infarction: an important determinant of survival.

Thrombolytic therapy for acute myocardial infarction reduces early mortality, but full recovery of left ventricular function after reperfusion is delayed. Therefore, the relations among reperfusion, survival and the time course of left ventricular functional recovery were examined in 226 patients treated with intracoronary streptokinase; 77% (134 patients) had sustained reperfusion and 31 patients had no reperfusion or had reocclusion by day 3. Wall motion was measured from contrast ventriculograms performed in the acute period and 3 days later in the central and peripheral infarct regions and the noninfarct region by the centerline method in 165 patients. Patients with reperfusion had better survival (p less than 0.05, mean follow-up 4.5 years) and a higher ejection fraction at 3 days (52 +/- 12 versus 46 +/- 10%, p less than 0.02) attributable to a significantly different change in peripheral infarct region function between the acute and 3 day studies (0.1 +/- 1.0 versus -0.3 +/- 0.9 SD, p less than 0.05). These early functional changes were significant in patients with anterior myocardial infarction and showed similar trends in those with inferior myocardial infarction. On Cox regression analysis, function measured at 3 days was more predictive of survival than was function measured acutely (chi square for acute ejection fraction = 11.48 versus 24.59 at 3 days). Although, as previously reported, greater than 45% of total recovery of left ventricular function occurs later, the ejection fraction achieved by day 3 is already predictive of survival. Thus, the mechanism by which successful thrombolytic therapy enhances survival is improvement of regional and global left ventricular function early after acute myocardial infarction.

Recovery of regional left ventricular dysfunction after coronary revascularization. Impact of myocardial viability assessed by nuclear imaging and vessel patency at follow-up angiography.

OBJECTIVES: This study sought to evaluate an imaging approach using technetium-99m sestamibi scintigraphy and positron emission tomography with fluorine-18 fluorodeoxyglucose for assessment of myocardial viability proved by serial quantitative left ventricular angiography. Furthermore, the influence of successful long-term revascularization on functional recovery was studied. BACKGROUND: Previous studies using positron emission tomography of myocardial perfusion and metabolism have demonstrated accurate identification of myocardial viability. However, most of these studies used a qualitative or semiquantitative wall motion analysis approach. METHODS: Nuclear imaging with semiquantitative analysis of tracer uptake was performed in 193 patients with regional wall motion abnormalities. Regions were categorized as normal, viable with perfusion/metabolism mismatch, viable without mismatch (intermediate) and scar. Seventy-two of 103 patients with subsequent revascularization underwent follow-up angiography. In 52 of 72 patients, changes in regional wall motion were measured by the centerline method from serial angiography. RESULTS: Wall motion improved in mismatch regions from -2.2 +/- 1.0 to -1.1 +/- 1.4 SD (p < 0.001). In contrast, regions with an intermediate pattern and those with scar did not improve. Restenosis or graft occlusion influenced functional outcome because regions with preoperative mismatch and successful long-term revascularization improved at follow-up (from -2.3 +/- 1.0 to -0.8 +/- 1.4 SD, p < 0.001), whereas wall motion did not change with recurrent hypoperfusion. Metabolic imaging added diagnostic information, particularly in regions with mild and moderate perfusion defects. CONCLUSIONS: This imaging approach allows detection of viability in regions with myocardial dysfunction. Wall motion benefits most in myocardium with perfusion/metabolism mismatch and successful long-term revascularization.

Myocyte degeneration and cell death in hibernating human myocardium.

OBJECTIVES: The aim of this study was to analyze the morphologic characteristics of myocyte degeneration leading to replacement fibrosis in hibernating myocardium by use of electron microscopy and immunohistochemical techniques. BACKGROUND: Data on the ultrastructure and the cytoskeleton of cardiomyocytes in myocardial hibernation are scarce. Incomplete or delayed functional recovery might be due to variable degree of cardiomyocyte degeneration in hibernating myocardium. METHODS: In 24 patients, regional wall motion abnormalities were analyzed by use of the centerline method before and 6 +/- 1 months after coronary artery bypass surgery. Preoperative technetium-99m sestamibi uptake was measured by single-photon emission computed tomography for assessing regional perfusion. Fluorine-18 fluorodeoxyglucose uptake was measured by positron emission tomography to assess glucose metabolism. Transmural biopsy specimens were taken during coronary artery bypass surgery from the center of the hypocontractile area of the anterior wall. RESULTS: The myocytes showed varying signs of mild-to-severe degenerative changes and an increased degree of fibrosis. Immunohistochemical analysis demonstrated disruption of the cytoskeletal proteins titin and alpha-actinin. Electron microscopy of the cell organelles and immunohistochemical analysis of the cytoskeleton showed a similarity in the degree of degenerative alterations. Group 1 (n = 11) represented patients with only minor structural alterations, whereas group 2 (n = 13) showed severe morphologic degenerative changes. Wall motion abnormalities showed postoperative improvements, and nuclear imaging revealed a perfusion-metabolism mismatch without significant differences between the groups. CONCLUSIONS: Long-term hypoperfusion causes different degrees of morphologic alterations leading to degeneration. Preoperative analysis of regional contractility and perfusion-metabolism imaging does not distinguish the severity of morphologic alterations nor the functional outcome after revascularization. The insufficient act of self-preservation in hibernating myocardium may lead to a progressive structural degeneration with an incomplete and delayed recovery of function after restoration of blood flow.

Coronary thrombolysis with intravenous urokinase in patients with acute myocardial infarction.

Regional left ventricular wall motion, about two to three weeks after acute myocardial infarction (MI), is perhaps the best clinical measure of myocardial salvage and limitation of infarct size by thrombolytic therapy. Normal or only slightly depressed wall motion at the site of infarction indicates significant limitation of infarct size, whereas markedly abnormal wall motion indicates irreversible myocardial damage. Early studies found significant improvement in regional wall motion in only 40 percent of patients undergoing successful intracoronary thrombolytic therapy after the onset of symptoms of acute MI. Why only 40 percent of these reperfused patients demonstrated salvage of ischemic myocardium could not be answered at that time. Animal experiments show that the duration of coronary occlusion is an important factor in determining myocardial salvage after reperfusion. To study whether this time dependency also exists under clinical circumstances in patients with coronary artery disease, the relationship between regional wall motion (as an index of infarct size) and the time to thrombolytic therapy after the onset of symptoms (as an index of duration of coronary occlusion) was examined. After showing that such time dependency does indeed exist in patients with acute MI, the efficacy and safety of intravenous bolus injections of urokinase were then demonstrated.

Four radionuclide methods for left ventricular volume determination: comparison of a manual and an automated technique.

This study compared the accuracy and reproducibility of three previously described and one new radionuclide method of measuring left ventricular volumes in 19 subjects using contrast ventriculographic volumes (n = 38, mean volume = 126.6 ml) as the gold standard. The four methods were compared using both manual and automated ROIs. For manual ROIs, the Links (189.7 ml, r = 0.85), Starling (183.2 ml, r = 0.77) and the new count ratio method (141.4 ml, r = 0.90) overestimated contrast volumes, while the Massardo method (122.5 ml, r = 0.91) provided accurate volumes. For the automated ROIs, we performed an interpolative background subtraction and used a 50% threshold of the highest count pixel to define the ventricular regions. The automated Massardo method severely underestimated the contrast volume (59.5 ml, r = 0.90), while the other automated methods yielded accurate volumes: Links (122.4 ml, r = 0.89), Starling (118.1 ml, r = 0.81) and the new count ratio method (125.0 ml, r = 0.90). The interobserver reproducibility of the automated methods was excellent (mean difference = 1%-4%) compared to the manual methods (2%-8%). Because no additional images, blood counting, attenuation, or decay correction were necessary, the manual Massardo method and the automated count ratio method are the simplest to perform. We conclude that automated determination of left ventricular volumes using the new count ratio method is rapid, accurate, reproducible and could readily be incorporated into routine clinical use.

Radionuclide cardiac volumes: effects of region of interest selection and correction for Compton scatter using a buildup factor.

The effects of region of interest (ROI) selection and correction for Compton-scattered photons using a buildup factor on radionuclide left ventricular volumes calculated by the Links method were compared in 19 humans with contrast ventriculography and in phantoms. Three different methods of ROI selection were compared: a manual ROI, a second derivative ROI and a 50% count-threshold ROI. In phantoms without Compton scatter correction, volumes were overestimated by 30% (manual ROI), 20% (derivative ROI) and 1% (count threshold ROI). In subjects, results without Compton scatter correction were similar with overestimates of 50% (manual ROI) and 20% (derivative ROI) and an underestimate by 3% (count threshold method). Correction for Compton-scattered photons with the use of a phantom-derived buildup factor resulted in improved accuracy for the manual ROI (+15%) and the derivative ROI (0%). A 50% count threshold ROI following interpolative background subtraction allows the accurate calculation of cardiac volumes without the need for scatter correction, while a second derivative ROI method requires a correction for Compton scatter with the use of a buildup factor.

Effect of myocardial viability assessed by technetium-99m-sestamibi SPECT and fluorine-18-FDG PET on clinical outcome in coronary artery disease.

UNLABELLED: PET imaging of myocardial perfusion and metabolism identifies regional viability as well as patients at high risk for future cardiac events. This study evaluated a combined "hybrid" imaging approach using 99mTc-sestamibi SPECT and [18F]fluoro-2-deoxy-D-glucose (FDG) PET with regard to reversibility of regional dysfunction and to patient clinical outcome during a 2-yr follow-up. METHODS: In this study, 161 consecutive patients underwent baseline viability imaging. All had regional wall motion (RWM) abnormalities and 88% had a history of previous myocardial infarction. Regions were classified by semiquantitative analysis of sestamibi and FDG uptake as normal, mild match, mismatch or scar. For clinical outcome, patients were divided into three groups: predominantly scar tissue (Group A, n = 90), mild match (Group B, n = 26) and mismatch (Group C, n = 45). Treatment was performed with the knowledge of nuclear results. Cardiac events during follow-up were defined as death, myocardial infarction, unstable angina requiring revascularization, heart transplantation and survived resuscitation. RESULTS: Patients were followed for 29 +/- 6 mo. Revascularization rate was 30% in Group A, 81% in Group B and 80% in Group C, whereas the other patients were treated by medication. Only Group C demonstrated a significant reduction of cardiac events after revascularization, whereas, particularly in Group A, revascularization did not influence the frequency of events. Subjective assessment of angina pectoris and heart failure revealed more patients with improvement after revascularization as compared with conservative treatment. Of the 84 revascularized patients, 61 underwent follow-up angiography at 5 +/- 2 mo with RWM analysis using the centerline method. RWM improved only in mismatch regions from -2.2 +/- 1.0 s.d. to -1.0 +/- 1.4 s.d. (p < 0.01), whereas regions with a mild match or scar did not change. CONCLUSION: Nuclear imaging using 99mTc-sestamibi SPECT and [18F]FDG PET allows diagnosis of viability in regions with reduced perfusion and function with prognostic implications for functional outcome as well as for identification of patients who benefit most from revascularization.

Left ventricular dysfunction in acute myocardial infarction due to isolated left circumflex coronary artery stenosis.

The characteristics of regional and global left ventricular dysfunction due to isolated left circumflex (LC) artery stenosis were determined from the contrast ventriculograms of 52 patients studied during acute myocardial infarction. In patients with a left dominant coronary circulation (35%), the severity, circumferential extent and location of hypokinesia resembled those of right coronary artery stenosis. However, in patients with a right dominant or balanced circulation (65%), the location of LC artery-related hypokinesia varied over the entire left ventricular contour, overlapping with the territories of the left anterior descending and right coronary arteries. The method for measuring the severity of hypokinesia was adjusted to take into account the wide territory of the LC artery. This enhanced the sensitivity of the method, particularly in the right anterior oblique view, as indicated by the greater severity of hypokinesia measured (-2.5 +/- 0.9 vs -1.8 +/- 1.1 standard deviations by our previously published method, p less than 0.001). However, the overlap of the artery territories may make it difficult to selectively measure the dysfunction due to stenosis of an artery of interest in patients with multiple infarctions. The circumferential extent of hypokinesia due to LC artery thrombosis was greater in the left than the right anterior oblique view. When averaged over both views, the size of the dysfunctional segment approached that due to left anterior descending coronary artery thrombosis, exceeding the size previously reported. These results suggest that current eligibility criteria for thrombolytic therapy select patients with extensive LC artery beds.

Factors influencing accuracy in left ventricular volume determination.

The accuracy with which left ventricular volume is determined from contrast ventriculograms depends on the care with which the analysis protocol is followed. Therefore, the effect of variations in the method used for calculating the correction factor (CF) that adjusts for magnification and image distortion on volume calculation was measured. The results showed that error in the CF is caused by (in order of decreasing importance): filming the calibration figure at a different magnification mode from that of the ventriculogram, at a different height from the table than the level of the ventricle, or with the image intensifier at a different height than used during ventriculography; use of a calibration figure less than half the size of the ventricle; calculation of the CF from only 1 band pair of a banded catheter; or placement of the calibration figure at the periphery rather than the center of the imaging field. Error in volume determination was proportional to error in the CF. With care, the error in volume can be reduced to that due to interobserver variability in tracing the endocardial contours.

Effect of acute myocardial infarction on the angle between the mitral and aortic valve plane.

The present study shows that acute myocardial infarction affects the left ventricle at the base as well as in the infarct region by widening of the angle between the mitral and aortic valve planes. The valve plane angle did not change over time despite significant recovery of left ventricular function, suggesting that acute myocardial infarction causes irreversible structural changes in the left ventricular myocardium remote from the infarct region.

Influence of coronary arterial thrombus location on left ventricular function in acute myocardial infarction.

In 238 patients with acute myocardial infarction studied during intracoronary streptokinase therapy, the circumferential extent of left ventricular hypokinesis was measured by 5 methods and correlated with the location of the infarct-related coronary artery segment and with 1-year survival. Of the 5 methods, 1 focused only on the infarct region, and 4 varied in the complexity of the noise filter. Hypokinetic segment length measurements by all 5 methods correlated significantly with the location of occlusion along the left anterior descending coronary artery. No method yielded measurements that correlated with occlusion location along the right coronary artery. Measurements by all methods correlated significantly with survival, but the method that focused on the infarct region performed least well. Thus, the circumferential extent of hypokinesis in patients with acute myocardial infarction is greater for proximal than mid- or distal occlusions of the left anterior descending but not the right coronary artery. Survival is influenced by the function of periinfarct and noninfarct regions and by the function of the infarct region. Complex noise filters provide no advantage over simpler filters in measuring the extent of hypokinesis.