Relationship between angiographic infarct size and left ventricular filling.

Infarct size may influence left ventricular filling after acute myocardial infarction. Pulsed Doppler transmitral flow velocities were compared in 47 patients at 7 +/- 6 days following acute myocardial infarction and 47 age-matched controls. Patients were stratified by angiographic infarct size into Groups I, II, III (corresponding angiographic hypokinetic scores less than 2; 2-2.99; greater than or equal to 3 SD/cord). Early diastolic transmitral Doppler flow velocities did not differ between infarct groups but atrial transmitral Doppler flow measurements did: peak A velocity (p = 0.001), A velocity time integral (p less than 0.001), and total velocity time integral (p = 0.001). Compared to controls atrial transmitral Doppler flow was augmented in Group I, whilst atrial and total transmitral Doppler flow were depressed in Group III. Peak A velocity and A velocity time integral were inversely related to infarct size (R = -0.44 to -0.54) and directly to left ventricular ejection fraction (R = 0.59 to 0.65). Large infarct size following myocardial infarction is associated with lower atrial and total transmitral Doppler flow velocities.     

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.     

Hemodynamic profile of patients with acute myocardial infarction at risk of infarct expansion

To identify patients at risk of cardiac expansion during hospital stay for a first acute myocardial infarction (AMI), 41 patients underwent right-sided cardiac catheterization soon after admission and serial 2-dimensional echocardiography on days 1, 3 or 4 and between days 7 and 10. Infarct expansion was recognized by echocardiography in 11 patients (27%), most often on the second recording (day 3 or 4). Age, sex, time from onset of pain to catheterization, peak levels of creatine kinase and creatine kinase-MB isoenzyme, heart rate, mean pulmonary artery wedge pressure and left ventricular stroke work index were similar in the 2 groups. Patients in whom infarct expansion developed had a higher incidence of previous systemic hypertension (73% vs 27%, p less than 0.01) and anterior AMI (91% vs 30%, p less than 0.001) and a higher mortality rate at 1 year (73 vs 7%, p less than 0.001) than those who did not. They also had higher systolic (139 +/- 24 vs 126 +/- 18 mm Hg, p less than 0.05) and diastolic (91 +/- 14 vs 75 +/- 13 mm Hg, p less than 0.001) arterial pressures, lower stroke volume index (31 +/- 10 vs 40 +/- 10 ml/m2, p less than 0.01) and much higher systemic vascular resistance (SVR) values (1,713 +/- 380 vs 1,253 +/- 264 dynes s cm-5, p less than 0.0001). In the subgroups of patients with anterior AMI, differences were significant for diastolic arterial pressure, stroke volume index, SVR and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early beneficial effect of streptokinase on left ventricular function in acute myocardial infarction

The effect of intravenous streptokinase therapy on the time course of functional recovery was investigated in a controlled study of 64 patients randomized within 3 hours after the onset of acute myocardial infarction (AMI). Contrast ventriculography was performed 1 to 4 days after AMI and repeated 5 weeks later. Wall motion was analyzed by the centerline method in the central infarct, peripheral infarct and noninfarct regions. In patients with ventriculographic data at the early catheterization, streptokinase-treated patients had less severe hypokinesia in the central infarct region than control patients (-2.9 +/- 0.9 [n = 29] vs -3.4 +/- 0.7 standard deviations below normal [n = 21], p less than 0.05). The benefit of streptokinase was more marked in the peripheral infarct region (-1.5 +/- 0.7 vs -2.1 +/- 0.6, p less than 0.001). As a result, the ejection fraction was slightly higher in treated versus control groups (46 +/- 10 vs 43 +/- 7%, respectively; difference not significant). At 5 weeks, function in the streptokinase and control groups had diverged further because of continued improvement in the streptokinase-treated patients. This study shows that streptokinase benefits left ventricular (LV) function by 1 to 4 days after AMI, earlier than previously reported. The benefit was not limited to the peripheral infarct region, where ischemia might have been less severe, but was also seen in the central infarct region. The implication is that thrombolytic therapy can improve LV function during the period of myocardial stunning, while myocardial function is still recovering.     

Association of patency of the infarct-related coronary artery with plasma levels of plasminogen activator inhibitor activity in acute myocardial infarction.

To examine the fibrinolytic capacity in patients with acute myocardial infarction (AMI), baseline levels of plasma plasminogen activator inhibitor (PAI) activity and tissue-type plasminogen activator (t-PA) antigen were measured in 47 patients with Q-wave AMI who underwent emergent coronary angiography 3.0 +/- 0.2 hours after the symptom onset. They received intracoronary injection of urokinase if their infarct-related arteries were occluded. They were classified into 3 groups according to the patency of the infarct-related artery before and after thrombolytic therapy: the patent group (13 patients), the recanalized group (23 patients) and the occluded group (11 patients). The mean level of plasma PAI activity (IU/ml) was higher in patients with AMI as a whole than in the control group (12.8 +/- 1.6 vs 5.4 +/- 0.5, p less than 0.01). The level was lower in the patent group (3.0 +/- 1.1) and higher in the recanalized (18.6 +/- 2.2) and occluded (10.8 +/- 2.5) groups than in the control group (each p less than 0.01). The level was lower in the occluded than in the recanalized group (p less than 0.01) and 62% of the patients in the occluded group had levels within range of the control group. The mean level of plasma t-PA antigen (ng/ml) was higher in patients with AMI as a whole than in the control group (10.3 +/- 0.8 vs 5.8 +/- 0.3, p less than 0.01). There was no difference in the level among the 3 groups with AMI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary venous flow dynamics before and after balloon mitral valvuloplasty as determined by transesophageal Doppler echocardiography.

The pattern of left atrial filling was studied in 14 patients with severe mitral stenosis in sinus rhythm before and immediately after successful balloon mitral valvuloplasty by transesophageal pulsed Doppler echocardiography of the left superior pulmonary vein. Mean mitral valve orifice area increased from 0.8 +/- 0.1 to 2.2 +/- 0.3 cm2 (p less than 0.0001), and left atrial mean pressure decreased from 30 +/- 5 to 12 +/- 4 mm Hg (p less than 0.0001) after the procedure. After balloon mitral valvuloplasty, significant increases in peak systolic pulmonary velocity (35 +/- 16 to 44 +/- 10 cm/s; p less than 0.01), systolic flow velocity time integral (3.3 +/- 1.5 to 5.9 +/- 2.0 cm; p less than 0.001) and the ratio of systolic/diastolic pulmonary venous flow velocity time integrals (0.8 +/- 0.4 to 1.4 +/- 0.5; p less than 0.001) were observed. An acute increase in mitral valve orifice area caused no significant changes in peak diastolic forward flow velocity (40 +/- 7 to 41 +/- 9 cm/s; p = not significant [NS]), diastolic forward flow velocity time integral (4.3 +/- 1.7 to 4.6 +/- 1.8 cm; p = NS) and atrial flow reversal velocity (30 +/- 3 to 35 +/- 3 cm/s; p = NS) compared with at baseline. The results suggest that in patients with severe mitral stenosis and sinus rhythm, left atrial filling is biphasic with a diastolic preponderance, and successful mitral valvuloplasty is associated with an immediate increase in pulmonary venous systolic forward flow.     

Anterolateral ST segment depression in acute inferior myocardial infarction: angiographic and clinical implications

We examined the relationship between coronary anatomy and anterolateral ST segment depression during inferior acute myocardial infarction (AMI) in 84 consecutive survivors of inferior AMI, who underwent prospective coronary angiography a median time of 2 weeks after AMI. Multivessel disease was defined as two or more significantly (greater than 70%) stenosed vessels. A QRS scoring system was used to estimate myocardial infarct size. Patients with ST depression had more multivessel disease compared to patients with no ST depression (53% vs 6%, p less than 0.01), more left anterior descending stenoses (36% vs 10% p less than 0.05), and higher QRS scores (5.8 +/- 3.2 vs 2.6 +/- 1.8, p less than 0.01) indicating larger infarcts. Patients with ST depression and one-vessel disease (47%) still had higher QRS scores compared to patients with no ST depression (4.8 +/- 2.9 vs 2.6 +/- 1.8, p less than 0.001) and had an increased prevalence of infarct-related vessels with a terminal branch supplying the left ventricular lateral wall or apex. We conclude that anterolateral ST depression during inferior AMI may indicate the presence of additionally stenosed vessels or that the infarct-related vessel has a large vascular territory. The absence of ST depression virtually precludes multivessel disease.     

Doppler echocardiographic evaluation of left ventricular diastolic filling in isolated valvular aortic stenosis

Doppler echocardiography was used to study left ventricular (LV) diastolic filling in 49 adults with isolated aortic stenosis (AS), selected from 155 consecutive patients with AS by excluding coexisting mitral disease (n = 41) and/or significant aortic regurgitation (n = 80). There were no differences between patients with AS and age-matched normal subjects for early diastolic filling (E) velocity (68 +/- 17 vs 67 +/- 13 cm/s), late diastolic filling (A) velocity (79 +/- 25 vs 67 +/- 21 cm/s), E/A ratio (1.00 +/- 0.78 vs 1.06 +/- 0.32) or early diastolic deceleration slope (264 +/- 151 vs 319 +/- 137 cm/s2, differences not significant for all). There was no correlation between any LV filling parameter and AS severity, but late diastolic filling velocity was higher in patients with AS who had LV hypertrophy (n = 33) vs those who did not (n = 16) (86 +/- 23 vs 65 +/- 26 cm/s, p less than 0.01). In the patients with AS and systolic dysfunction (LV ejection fraction less than 50%) (n = 6), early diastolic filling velocity was higher (88 +/- 20 vs 65 +/- 15 cm/s, p less than 0.01), late diastolic filling velocity lower (53 +/- 23 vs 83 +/- 23 cm/s, p less than 0.01), E/A ratio higher (2.20 +/- 1.80 vs 0.84 +/- 0.28, p less than 0.01), deceleration slope steeper (439 +/- 230 vs 240 +/- 121 cm/s2, p = 0.02) and LV end-diastolic pressure higher (23 +/- 9 vs 10 +/- 6 mm Hg, p less than 0.01) than in patients with AS and normal systolic function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiographic findings after myocardial infarction in patients with previous bypass surgery: explanations for smaller infarcts in this group compared with control patients

The incidence of previous coronary artery bypass surgery (CABS) in patients with acute myocardial infarction admitted to our hospital has risen from 2.3% to 11.2% in 6 years. We compared infarct size and the angiographically determined cause of infarction in 52 control patients and in 52 consecutive patients with acute myocardial infarction at least 2 months after they had undergone CABS. Baseline characteristics were similar in both groups except for a higher incidence of preexisting Q waves in the post-CABS group (22 vs 10; p less than .05). Indexes of myocardial infarct size were smaller in the post-CABS group compared with those in control patients: peak creatine kinease (CK) level (IU/liter) 1113 +/- 1094 (mean +/- SD) vs 1824 +/- 1932 (p less than .01), peak CK-MB level (IU/liter) 173 +/- 230 vs 272 +/- 332 (p less than .02), peak summed ST segment elevation (mm) 3.5 +/- 4.8 vs 8.2 +/- 9.9 (p less than .005), and QRS score on days 7 to 10, 1.9 +/- 3.0 vs 4.3 +/- 3.4 (p less than .001). Postinfarction left ventricular ejection fraction was higher in the post-CABS group (53 +/- 13%) compared with that in control patients (47 +/- 12%; p less than .05). The incidence of total occlusion of the artery to the infarct zone was similar in the post-CABS and control patients (33 vs 27), as was the incidence of one-, two-, and three-vessel disease (artery plus graft). Collateral blood flow to the infarct zone was found in 27 post-CABS patients and in 23 control patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lengths of stay of patients with uncomplicated acute myocardial infarction at three Boston hospitals

Variability in length of stay (LOS) and its determinants were studied in 60 patients without complications after acute myocardial infarction (AMI) at three teaching hospitals. The patients at the three hospitals had similar clinical presentations and in-hospital courses. However, 81% of patients admitted to the intensive care unit (ICU) at one hospital were transferred to lower levels of care within 48 hours, compared with 40% and 56% at the other two hospitals (p less than 0.05). Patients who underwent pre-discharge exercise tests (ETT) had a longer total LOS than patients who did not (11.9 +/- 4.3 vs 9.2 +/- 2.9 days; p less than 0.01). Similarly, patients who underwent 24-hour ambulatory monitoring (AMB-MON) had a longer total LOS than patients who did not (12.3 +/- 4.3 vs 9.1 +/- 2.8 days; p less than 0.001). No differences in clinical characteristics or in survival at six months were detected between patients who did and did not undergo ETT or AMB-MON. Total LOS correlated with whether patients underwent 0, 1, or both of these tests (p less than 0.0001); each test was associated with a 2.3-day increase in the duration of hospitalization. The authors conclude that such tests may prolong total LOS of patients without complications after AMI.     

Transoesophageal Doppler pulmonary venous flow pattern and left atrial spontaneous contrast in mitral stenosis.

The relationship between transoesophageal Doppler pulmonary venous flow pattern and spontaneous left atrial contrast was studied in 23 patients with isolated severe mitral stenosis (mitral valve area = 0.8 +/- 0.2 cm2). The patients with none or minimal (1+) spontaneous contrast (n = 15, group I) were compared with those with significant spontaneous contrast (grade 2+, n = 8, group II) with regard to peak systolic velocity (33 +/- 14 cm/s vs 28 +/- 12 cm/s, p = NS), peak diastolic velocity (36 +/- 14 cm/s vs 28 +/- 8 cm/s, p = NS) and peak atrial reversal velocity (19 +/- 4 cm/s vs 19 +/- 8 cm/s, p = NS), systolic forward flow velocity time integral (3.37 +/- 1.73 cm vs 2.78 +/- 0.9 cm, p = NS), diastolic forward flow velocity time integral (2.85 +/- 1.2 cm vs 2.65 +/- 1.87 cm, p = NS), ratios of peak systolic and diastolic velocity (0.91 +/- 0.21 vs 0.95 +/- 0.29, p = NS) and duration of diastolic deceleration (117 +/- 59 ms vs 132 +/- 106 ms, p = NS). The results show that the occurrence of spontaneous contrast in the left atrium in patients with mitral stenosis is not related to the Doppler-estimated pulmonary venous flow.     

Clinical and prognostic significance of lung thallium uptake on rest imaging in acute myocardial infarction

Exercise-induced pulmonary uptake of thallium-201 in patients with ischemic heart disease is probably due to transient pulmonary edema and left ventricular failure induced by exercise. The significance of increased lung uptake of thallium-201 at rest after acute myocardial infarction (AMI) has not been described. Ninety-six patients admitted with chest pain for suspected AMI or unstable angina underwent thallium-201 imaging at rest. Using conventional diagnostic criteria, 62 had AMI, 12 had unstable angina and 22 had neither. Increased lung uptake of thallium-201 was present in 24 of the total 96 (25%) patients, 20 of the 62 (32%) patients with AMI and 4 of 34 (13%) patients with no evidence of infarction. In the AMI group, those with increased lung thallium-201 uptake had a higher mean +/- standard deviation segmental thallium-201 defect score (22 +/- 7 vs 12 +/- 8, p less than 0.0001), lower ejection fraction (35 +/- 14 vs 49 +/- 14%, p less than 0.002), higher peak creatine kinase levels (2,410 +/- 1,247 vs 1,496 +/- 1,228 IU/liter, p less than 0.01), higher wall motion abnormality score (25 +/- 13 vs 13 +/- 12, p less than 0.0001), increased incidence of clinical in-hospital heart failure (15 of 20 vs 7 of 42, p less than 0.0001) and higher short-term mortality (4 of 20 vs 1 of 42, p less than 0.02) compared to those without increased lung thallium-201 uptake.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular remodeling in the year after first anterior myocardial infarction: a quantitative analysis of contractile segment lengths and ventricular shape.

Infarct expansion after myocardial infarction results in early ventricular enlargement and distortion of ventricular geometry. To characterize the components of late volume enlargement, biplane left ventriculography was performed in 52 patients 3 weeks and 1 year after a first anterior myocardial infarction. Biplane diastolic circumference and contractile and noncontractile segment lengths were measured. Global geometry was evaluated by using a sphericity index (angiographic volume of the ventricle divided by the volume of a sphere with the same circumference). Regional geometry was assessed by measurement of endocardial curvature, an important determinant of wall tension. End-diastolic volume was enlarged at baseline and increased at 1 year (230 +/- 42 to 244 +/- 55 ml, p = 0.01) as a result of increases in contractile segment length (34 +/- 5 to 37 +/- 5 cm, p less than 0.001) and sphericity index (0.74 +/- 0.07 to 0.76 +/- 0.08, p less than 0.001), whereas the noncontractile segment length decreased (15 +/- 6 to 12 +/- 6 cm, p less than 0.005). Curvature analysis revealed a flattening of presumably high tension concavity at the anterobasal (-6.0 +/- 4.0 to -4.5 +/- 3.7, p less than 0.01) and inferior (-4.5 +/- 2.0 to -3.6 +/- 2.1, p less than 0.005) margins of the infarct and less bulging of the anterior wall (9.4 +/- 2.5 to 8.2 +/- 2.3, p less than 0.001). Patients selected for late enlargement (diastolic volume increase greater than 20 ml, n = 19) had an increase in sphericity (0.75 +/- 0.05 to 0.80 +/- 0.08, p less than 0.005) and in diastolic circumference (54 +/- 3 to 56 +/- 4 cm, p less than 0.001) secondary to elongation of the contractile segment (32 +/- 4 to 36 +/- 4 cm, p = 0.001) at 1 year. Thus, late ventricular enlargement after anterior infarction results from an increase in contractile segment length and a change in ventricular geometry and is not a result of progressive infarct expansion. In the group of patients at high risk for late ventricular enlargement because of persistent occlusion of the infarct-related vessel, captopril therapy attenuated late volume enlargement by preventing these changes in contractile segment length and chamber geometry.     

Early estimation of acute myocardial infarct size soon after coronary reperfusion using emission computed tomography with technetium-99m pyrophosphate

Early appearance of positive findings on a technetium-99m pyrophosphate scan has been shown to be associated with the presence of a reperfused acute myocardial infarction (AMI). Early technetium-99m pyrophosphate imaging was performed by emission computed tomography to evaluate reperfusion and to test the feasibility of estimating infarct size soon after coronary reperfusion based on acute positive tomographic findings. Twenty-seven patients with transmural AMI who were treated with intracoronary urokinase infusion followed by percutaneous transluminal coronary angioplasty underwent pyrophosphate imaging 8.7 +/- 2.1 hours after the onset of AMI. None of the 8 patients in whom reperfusion was unsuccessful had acute positive findings. Of 19 patients in whom reperfusion was successful, 17 had acute positive findings (p less than 0.001). In these 17, tomographic infarct volumes were determined from reconstructed transaxial images. The threshold for areas of increased pyrophosphate uptake within the infarct was set at 60% of peak activity by the computerized edge-detection algorithm. The total number of pixels in all transaxial sections showing increased tracer uptake were added and multiplied by a size factor and 1.05 g/cm3 muscle to determine infarct volume. The correlations of tomographic infarct volumes with peak serum creatine kinase (CK) levels (r = 0.82) and with cumulative release of CK-MB isoenzyme (r = 0.89) were good. Moreover, the time to positive imaging was significantly shorter than that to peak CK level (8.5 +/- 2.3 vs 10.4 +/- 2.2 hours, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional infarct expansion, left ventricular dilation and isovolumic relaxation time after coronary occlusion: a two-dimensional echocardiographic study

Left ventricular dilation and infarct expansion after acute myocardial infarction are associated with an increased morbidity and mortality. The purpose of this study was to determine whether angiotensin-converting enzyme inhibition could reverse left ventricular dilation and improve the diastolic properties of the left ventricle very early after coronary occlusion. The acute time course of left ventricular dilation and infarct expansion (as determined by two-dimensional echocardiography) and early diastolic isovolumic relaxation time were studied in 20 dogs subjected to 3 h of coronary occlusion. End-diastolic area before occlusion was 8.4 +/- 0.5 and 8.9 +/- 0.7 cm2 (p = NS) in the captopril- and the saline-treated group, respectively. At 30 min after occlusion (pretreatment), end-diastolic area increased to 12.6 +/- 0.8 cm2 in the captopril-treated group (p less than 0.01) and 11.3 +/- 0.9 cm2 (p less than 0.05) in the saline-treated group. Three hours after occlusion and after captopril treatment, end-diastolic area decreased to 9.4 +/- 0.6 cm2 (p less than 0.05 versus 30 min after occlusion), whereas it was unchanged in the saline-treated group. Functional infarct expansion (as assessed by end-systolic anterior to posterior endocardial segment length ratio) occurred early after occlusion, and captopril reduced this expansion. Pretreatment values for early diastolic isovolumic relaxation time increased from 29.1 +/- 2.4 to 50.5 +/- 2.9 ms in captopril-treated dogs (p less than 0.01) and from 34.3 +/- 3.4 to 46.9 +/- 2.7 ms in saline-treated dogs (p less than 0.01) after coronary occlusion, implying a worsening of diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pressure-derived fractional collateral blood flow: a primary determinant of left ventricular recovery after reperfused acute myocardial infarction

OBJECTIVES: We evaluated the relation between pressure-derived fractional collateral flow (PDCF) and left ventricular (LV) recovery after reperfused acute myocardial infarction (AMI). BACKGROUND: The functional significance of collateral flow remains uncertain in AMI. METHODS: The PDCF was measured in 70 patients with first AMI (pain onset <12 h) treated with primary angioplasty (PA), being determined by simultaneous measurement of mean aorta pressure (Pa), distal coronary pressure during the balloon occlusion (Poc), and central venous pressure (CVP): (Poc - CVP)/(Pa - CVP)*100. Sufficient collateral (group I) was defined as PDCF index >24% and insufficient collateral (group II) as PDCF index <24%. Echocardiography was performed before, and on day 3, day 7, and day 30 after PA. Wall-motion recovery index (RI) was obtained by dividing the number of improved wall-motion segments (>grade 1) at follow-up by the number of abnormal wall-motion segments within the infarct zone at baseline. RESULTS: Baseline characteristics were similar between both groups. Peak levels of creatine kinase were lower in group I than in group II (2,600+/-1,900 U/liter vs. 4,100+/-3,000, p < 0.05). At one month, infarct zone wall-motion score index (1.65+/-0.54 vs. 2.31+/-0.46, p < 0.01) and LV volume indexes were smaller in group I than in group II, whereas, LV ejection fraction was higher in group I than in group II (52.8+/-8.3 vs. 45.9+/-9.0, p < 0.01). The PDCF index was the strongest predictor of RI at one month (r = 0.61, p < 0.01). Time to reperfusion was not related to RI at one month. However, it was significantly related to RI in group II (r = -0.34, p < 0.05). CONCLUSIONS: The LV recovery after reperfused AMI is primarily determined by PDCF and is less dependent on time to reperfusion in patients with sufficient collaterals.     

Relationship between terminal QRS distortion on the admission electrocardiogram and the time course of left ventricular wall motion in anterior wall acute myocardial infarction

In order to clarify the time course of left ventricular (LV) wall motion in patients with anterior acute myocardial infarction (AMI) showing terminal QRS distortion on the admission electrocardiogram (ECG), the present study examined 106 patients with their first anterior AMI (< or =6 h) who underwent emergency coronary arteriography and cardiac cathetherization at 1 and 6 months after the infarction. The patients were classified into 2 groups according to the presence (group A, n=23) or absence (group B, n=83) of terminal QRS distortion (emergence of the J point at > or =50% of the R-wave amplitude in leads with QR configuration and/or absence of S waves in leads with RS configuration) on the admission ECG. Group A had a lower LV ejection fraction and more reduced regional wall motion (RWM) in the infarct region at both 1 and 6 months after AMI than group B. The degree of improvement in RWM between 1 and 6 months after AMI was less in group A than in group B (-0.1+/-0.5 vs 0.4+/-0.6 SD/chord, p<0.01). This study indicates that patients with anterior AMI showing terminal QRS distortion on the admission ECG have more severely depressed LV wall motion and less improvement in RWM in the infarct region in the healing stage, suggesting that this sign is an indicator of severe myocardial damage.     

Effect of mitral regurgitation on pulmonary venous velocities derived from transesophageal echocardiography color-guided pulsed Doppler imaging

The effect of mitral regurgitation on pulmonary venous flow velocity was studied in 66 patients undergoing transesophageal echocardiography. Nine patients were studied intraoperatively before and after surgery, so that 75 pulmonary venous flow tracings were analyzed. Fifty-four patients had no significant (0 to 1+) mitral regurgitation and 21 had significant (2 to 3+) mitral regurgitation. Comparison of both groups revealed significant differences in the pulmonary venous flow pattern. In patients with no significant mitral regurgitation, the peak systolic velocity was higher (55 +/- 16 vs. -4 +/- 16 cm/s; p less than 0.0001) and the peak diastolic velocity was lower (43 +/- 13 vs. 59 +/- 17 cm/s; p less than 0.01) when compared with values in patients with significant mitral regurgitation. Consequently, the peak systolic/diastolic velocity ratio was significantly higher in the patients without significant mitral regurgitation (1.4 +/- 0.5 vs. 0.4 +/- 1.3; p less than 0.0001). The same trend was noted with respect to the systolic and diastolic velocity integrals. As the degree of mitral regurgitation increased, the peak diastolic velocity and diastolic velocity integral increased, whereas the peak systolic velocity and systolic velocity integral decreased. In patients with severe mitral regurgitation, the systolic flow became reversed (retrograde). The sensitivity of reversed systolic flow for severe mitral regurgitation was 90% (9 of 10), the specificity was 100% (65 of 65), the positive predictive value was 100% (9 of 9), the negative predictive value was 98% (65 of 66) and the predictive accuracy was 99% (74 of 75).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of preload and heart rate manipulation on Doppler transmitral flow velocity pattern: search for load--independent parameters.

Pulsed Doppler transmitral flow-velocity provides a non-invasive method for serial evaluation of diastolic function. However confounding influence of loading conditions and heart rate on transmitral flow makes many conclusions suspect. To study the effect of preload, various parameters of Doppler mitral spectrum were studied in 11 patients with stable effort angina, angiographic coronary artery disease and intact global and segmental systolic function, before and after administration of sublingual isosorbide dinitrate (group 1). Following isosorbide dinitrate administration, there was a significant increase in heart rate (p less than 0.001), decrease in left ventricular end-diastolic volume (p less than 0.01), no change in left ventricular ejection fraction and systolic blood pressure. Peak E velocity, E velocity-time integral, E/A velocity time integrals ratio, acceleration and deceleration rates and diastolic filling period were significantly reduced whereas peak A velocity, A velocity time integral, acceleration and deceleration times and atrial filling period were unchanged. In 10 age-matched patients (group 2), atrial pacing performed to achieve similar degree of increase in heart rate as in group 1 (10 +/- 1 vs 12. +/- 4, p = NS), resulted in a decrease in E velocity time integral, E/A velocity time integrals ratio and diastolic filling period (p less than 0.01) without any significant change in any other parameter. Absolute A velocity time integral, acceleration and deceleration times are the only parameters of transmitral diastolic flow-velocity profile which are relatively independent of preload and heart rate provided the change is small.     

Doppler echocardiographic evaluation of left ventricular diastolic function after percutaneous transluminal coronary angioplasty for unstable angina pectoris or acute myocardial infarction

The effect of percutaneous transluminal coronary angioplasty (PTCA) on left ventricular (LV) diastolic function has not been systematically investigated in patients treated for unstable angina or ischemia after acute myocardial infarction (AMI). To assess the relation between reduction of stenosis severity and improvement in diastolic function in this setting, 42 patients with either unstable angina (n = 22) or post-AMI ischemia (n = 20) were serially monitored by Doppler echocardiography 8 +/- 5 hours before and 2 +/- 1 days after PTCA. Doppler LV filling indexes included isovolumic relaxation time, mitral deceleration time, E/A peak velocity ratio and atrial filling fraction. Eighteen aged-matched control subjects served to establish normal values for comparison. Before PTCA, both groups exhibited abnormal diastolic function demonstrated by prolonged isovolumic relaxation time and mitral deceleration time, decreased E/A ratio and increased atrial filling fraction. After PTCA isovolumic relaxation time and deceleration time decreased 18 +/- 28 (p less than 0.005) and 33 +/- 43 ms (p less than 0.002) in the unstable angina group and 18 +/- 23 (p less than 0.003) and 14 +/- 34 ms (difference not significant), respectively, in the post-AMI ischemia group. An increase in E/A ratio and a decrease in atrial filling fraction occurred in both groups; however, these changes were significant only in patients with post-AMI ischemia (+21%, p less than 0.03 and -11.4%, p less than 0.005, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)