Left ventricular end-diastolic pressure

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1 ID:6624 O R I G I N A L P A P E R Left Ventricular End-Diastolic Pressure and Risk of Subsequent Heart Failure in Patients Following an Acute Myocardial Infarction Left ventricular end-diastolic pressure (LVEDP) is a reflection of ventricular compliance and intravascular volume and pressure; it relates both acutely and chronically to clinical conditions that affect ventricular performance. Following acute myocardial infarction (AMI), LVEDP may be elevated in association with larger infarct size and increased circulatory volume; it may also reflect underlying comorbid cardiac diseases. 1 Acutely, elevations in LVEDP may result in the clinical manifestations of heart failure (HF); however, it is possible that increased LVEDP may be a surrogate of early abnormal ventricular pressure-volume relationships predisposing to the development of recurrent HF events. In asymptomatic survivors with a left ventricular ejection fraction (LVEF) <40%, higher LVEDP may identify patients at increased risk for developing clinical symptoms of HF. Therefore, the objectives of this investigation were to identify the hemodynamic and clinical factors associated with increased LVEDP following AMI and to examine the relationship between elevated LVEDP and the development of subsequent clinical HF morbidity and mortality. Methods This prospective cohort analysis is based on previously obtained clinical and echocardiographic data from the Survival and Ventricular Enlargement (SAVE) trial. 2 Briefly, the SAVE trial was a multicenter, randomized, double-blind placebo-controlled trial that Left ventricular end-diastolic pressure (LVEDP) is an important measure of ventricular performance and may identify patients at increased risk for developing late clinical symptoms of heart failure (HF). The primary outcome in this analysis of 744 patients from the Survival and Ventricular Enlargement (SAVE) trial was the development of death or HF over a mean time of 36 months. The mean LVEDP for all patients was 23±9 mm Hg, and 75% of participants (n=558) had an LVEDP >15 mm Hg. Patients with an LVEDP >30 mm Hg (n=187) had the highest risk of death or HF (unadjusted hazard ratio, 1.40; 95% confidence interval [CI], ) when compared with the other 2 cohorts combined (n=603). After adjustment for other known predictors of cardiac risk, LVEDP no longer remained significant (adjusted hazard ratio, 1.12; 95% CI, ). Elevated LVEDP is common following myocardial infarction; however, it is not an independent predictor of subsequent HF risk. The variability in LVEDP is not fully explained by infarct size and atherosclerotic burden. (CHF. 2007;13: ) 2007 Le Jacq Lisa M. Mielniczuk, MD; 1 Gervasio A. Lamas, MD; 2 Greg C. Flaker, MD; 3 Gary Mitchell, MD; 4 Sidney C. Smith, MD; 5 Bernard J. Gersh, MD; 6 Scott D. Solomon, MD; 7 Lemuel A. Moyé, MD; 8 Jean L. Rouleau, MD; 9 John D. Rutherford, MD; 10 Marc A. Pfeffer, MD 7 From the Cardiology Division, University of Ottawa Heart Institute, Ottawa, Ontario, Canada; 1 Mount Sinai Medical Center, Miami Beach, FL; 2 the Department of Medicine, Division of Cardiology, University of Missouri, Columbia, MO; 3 Cardiovascular Engineering Inc, Waltham, MA; 4 the Center for Cardiovascular Science and Medicine, University of North Carolina, Chapel Hill, NC; 5 Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, MN; 6 the Department of Medicine, Division of Cardiology, Brigham and Women s Hospital, Boston, MA; 7 University of Texas School of Public Health, Health Sciences Center at Houston, Houston, TX; 8 the Department of Medicine, University of Montreal, Montreal, Quebec, Canada; 9 and the Division of Cardiology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 10 Address for correspondence: Lisa M. Mielniczuk, MD, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario K1Y 4W7, Canada lmielniczuk@ottawaheart.ca Manuscript received February 7, 2007; revised May 7, 2007; accepted May 7, 2007 demonstrated the efficacy of captopril on clinical outcomes in 2231 participants with left ventricular systolic dysfunction (LVEF <40%) and absence of clinical HF following AMI. Patients were randomized 3 to 16 days after AMI and followed up an average of 3.5 years (range, 2 5 years). All patients consented to SAVE trial randomization and all follow-up evaluations. By LVEDP and HF post-mi july. august Congestive Heart Failure (ISSN ) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT Copyright 2007 by Le Jacq. All rights reserved. No part of

2 Table I. Baseline Characteristics of the LVEDP Cohort Compared With the General SAVE Trial Population VARIABLE SAVE (N=1472) LVEDP, MM HG (N=744) P VALUE Mean age, y 60.5± ±10.9 <.001 Men 1220 (83) 605 (82).48 White 1319 (89) 674 (90).90 Anterolateral wall MI 945 (64) 467 (62).23 Previous MI 545 (37) 246 (33).18 Previous cardiac surgery 177 (12) 82 (11).44 HR, beats per minute 77.3± ±13.16 Diabetes 335 (23) 153 (21).28 Family history of heart disease 680 (46) 342 (46).75 Hypertension 636 (43) 320 (43).89 History of CHF 97 (6.6) 33 (4.4).04 History of significant valve disease 68 (4.6) 24 (3.2).14 Previous cardiac surgery 177 (11.8) 82 (10.7).48 SBP, mm Hg 113.4± ± DBP, mm Hg 70.2± ± HF between MI and randomization 648 (44) 275 (37).003 Killip class (58) 489 (66) (42) 255 (34) Peak creatinine kinase level, mg/dl 2541± ± Serum creatinine level, mg/dl 1.19± ± LVEF, % 30.6± ±6.5 <.001 Values are expressed as No. (%) unless otherwise indicated. Abbreviations: CHF, congestive heart failure; DBP, diastolic blood pressure; HF, heart failure; HR, heart rate; LVEDP, left ventricular end-diastolic pressure; LVEF, left ventricular ejection fraction; MI, myocardial infarction; SAVE, Survival and Ventricular Enlargement; SBP, systolic blood pressure. protocol, patients were excluded if their baseline serum creatinine level was >2.5 mg/dl (221 μmol/l), and the average serum creatinine level in the SAVE study was 1.1±0.2 mg/dl. LVEDP Measurement. Of the total randomized SAVE trial population of 2231 patients, 1301 had cardiac catheterization between the qualifying AMI and randomization. From this cohort of 1301 patients, 946 had coronary angiograms that could be evaluated, 727 had contrast left ventriculography, and 744 had a measurement of LVEDP reported. These 744 patients were the participants for this present analysis. 3 The decision to perform right and left hemodynamic studies and left ventriculography was based on clinical indications and local practice in each catheterization laboratory and was not mandated by the SAVE trial protocol. The SAVE trial did not restrict or mandate specific aspects of clinical management before the qualifying AMI and randomization; however, in patients with overt ischemia, cardiac catheterization was required before randomization. This included any patient who had recurrent ischemic discomfort 72 hours after the index AMI or a positive exercise test. If catheterization identified a need for revascularization therapy, the study required that revascularization be completed before randomization. 3 All participants in this study were divided into prespecified clinical groups based on their LVEDP measurement: normal or mildly elevated pressures (<15 mm Hg), moderately abnormal (15 30 mm Hg), and markedly elevated (>30 mm Hg) for all clinical end points. 4 Ventricular Analysis. The left ventriculograms at end diastole and at end systole were traced and digitized. Computer-assisted analysis of the traced left ventriculograms provided (1) left ventricular volumes calculated by the area-length method 5 ; (2) determination of left ventricular shape by use of the sphericity index, 6 an index of overall left ventricular shape based on calculating ventricular volume and dividing it by a hypothetical spherical volume generated by using the longest axis of the left ventricle as the diameter of a sphere; and (3) analysis of wall motion by the centerline method 7 ; the percentages of the diastolic left ventricular circumference that were dyskinetic or akinetic, hypokinetic, and normal were calculated. 3 The percentage of akinetic or dyskinetic segments was determined in patients who had successful left ventriculography. This was defined as the number of severely hypokinetic, akinetic, or dyskinetic segments divided by the total number of segments viewed from a standard 30 right anterior oblique view (visualizing the anterobasal, anterolateral, apical, inferior, and posterobasal segments). The extent of coronary artery occlusion was quantified for each major coronary artery (from 0% 100%), and for this analysis significant coronary 210 LVEDP and HF post-mi july. august 2007 Congestive Heart Failure (ISSN ) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT Copyright 2007 by Le Jacq. All rights reserved. No part of

3 Table II. LVEDP and Presence of Significant Coronary Artery Disease on Coronary Angiography CORONARY ARTERY NO. (%) (N=744) MEAN LVEDP, MM HG P VALUE Left main Lesion >70% 23 (3) 24.1± No lesion 731 (97) 22.8±9.0 LAD Lesion >70% 143 (19) 21.8± No lesion 601 (81) 23.0±8.7 LCX Lesion >70% 152 (20) 22.8± No lesion 592 (80) 22.8±8.9 RCA Lesion >70% 279 (38) 23.4± No lesion 465 (62) 21.9±9.1 Significant coronary artery disease was defined as any coronary occlusion >60% along any portion of the coronary artery. Abbreviations: LAD, left anterior descending artery; LCX, left circumflex artery; LVEDP, left ventricular end-diastolic pressure; RCA, right coronary artery. disease was considered as any obstruction >60%. The presence and extent of mitral regurgitation were graded on a standard scale (0 to 4). 8 Statistical Methods. Baseline characteristics between the SAVE trial population and the LVEDP cohort or among the 3 groups of LVEDP were compared by using t tests or analysis of variance for continuous variables and chi-square test for trend for categoric variables. The relationship between LVEDP and other hemodynamic and angiographic measures was assessed with Pearson correlation coefficients. Linear regression was used to determine whether coronary anatomy was a significant predictor of LVEDP. Kaplan- Meier curves were employed to display the time-dependent cardiac events based on the unadjusted LVEDP tertiles and compared with the log rank test. Univariate and multivariate Cox proportional hazard models were constructed to evaluate the association between LVEDP group and specific cardiac event. The baseline covariates included in the multivariate model were sex; age; previous AMI; presence of diabetes mellitus; current smoking; LVEF; peak creatinine kinase level; serum creatinine level; randomization assignment (placebo or angiotensinconverting enzyme [ACE] inhibitor); history of hypertension; baseline Killip class; and the use of diuretics, vasodilators, or β-blockers 72 hours before randomization. The results of the regression analyses are presented as hazard ratios along with 95% confidence intervals and P values. All P values are 2-sided and a P value <.05 was considered significant. All statistical analyses were performed using STATA software, version 8.0 (Stata, College Station, TX). Outcomes. The primary clinical outcome in this study was the occurrence of severe HF or death. Severe HF was defined in the SAVE trial as a composite of either hospitalization for HF or HF requiring open-label ACE inhibition. In addition, data on HF requiring intensification of medical therapy were also collected; this was defined as HF requiring the addition or increase in digoxin or diuretic dose. Results The baseline characteristics of patients in the LVEDP cohort were slightly but significantly different than the non-lvedp population (Table I). This cohort was significantly younger (57.1±11 years vs 60.5±10; P<.001), had more patients in Killip class I (489/744 [66%] vs 854/1472 [58%]; P<.001), and had a greater LVEF (32%±6% vs 31%±7%; P<.001) than did patients in the general SAVE trial population. Factors Associated With a High LVEDP. Hemodynamic and Volumetric Factors. Mean LVEDP was 22.9±9.0 mm Hg and was closely correlated with other hemodynamic measures obtained during the same cardiac catheterization. Information on right heart hemodynamics was available in 204 (27%) of participants. LVEDP most closely correlated with mean pulmonary artery pressure (r=0.63; P<.001) and pulmonary capillary wedge pressure (r=0.58; P<.001) and was less strongly related to central venous pressure (r=0.39; P<.001). LVEDP was positively correlated to increases in left ventricular enddiastolic volume (r=0.37; P=.0002) and end-systolic volume (r=0.32; P=.0013). The degree of mitral regurgitation (MR) was not related to abnormalities of LVEDP (mean LVEDP if no MR, 22.1±9 mm Hg; mild MR, 23.4±9 mm Hg; moderate to severe MR, 23.6±10 mm Hg; P=.32 for comparison). When left ventriculography was used, qualitative abnormalities of left ventricular distortion were related to higher LVEDP; however, the extent of akinetic-dyskinetic segments visualized on angiography was not related to LVEDP. Coronary Angiographic Findings. The extent of proximal disease in the major epicardial coronary arteries was not a significant predictor of LVEDP (left main disease r 2 =0.0003, P=.62; proximal left anterior descending r 2 =0.0001, P=.85; proximal right coronary artery r 2 =0.001, P=.40; proximal left circumflex r 2 =0.005, P=.54). The presence of significant coronary disease (any lesion >70% or >50% in the left main coronary artery) along any portion of the major epicardial arteries was also not significantly related to LVEDP (Table II). LVEDP and HF post-mi july. august Congestive Heart Failure (ISSN ) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT Copyright 2007 by Le Jacq. All rights reserved. No part of

4 Table III. Baseline Characteristics Among LVEDP Cohorts LVEDP <15 MM HG LVEDP MM HG LVEDP >30 MM HG P VARIABLE (N=166) (N=437) (N=141) Mean age, y 57.8± ± ± Men 129 (78) 375 (84) 109 (77).06 White 133 (92) 395 (89) 125 (89).58 CLINICAL HISTORY AT ENROLLMENT Previous MI 68 (41) 141 (32) 37 (26).03 Previous cardiac surgery 20 (12) 49 (11) 12 (8.5).30 Smoking 3 weeks prior 62 (42) 215 (57) 60 (51).13 Diabetes 27 (16) 87 (20) 39 (27).03 Family history of heart disease 79 (47) 200 (46) 63 (45).69 Hypertension 66 (40) 188 (43) 66 (47).17 History of CHF 9 (5) 18 (4) 6 (4).58 History of significant valve disease 8 (5) 13 (2.9) 3 (2.1).13 INITIAL PHYSICAL EXAMINATION HR, beats per minute 79±13 77±13 80±13.05 SBP, mm Hg 110±14 111±13 111±14.76 DBP, mm Hg 69±11 70±9 70±10.77 Killip class (69) 286 (65) 89 (63) (31) 151 (35) 52 (37) Peak creatinine kinase level, mg/dl 2102± ± ±2682 <.001 Serum creatinine, mg/dl 1.14± ± ± LVEF 33.2± ± ± EVENTS BETWEEN INDEX MI AND RANDOMIZATION HF 48 (29) 166 (38) 64 (46).01 PTCA post-angiogram 30 (18) 114 (26) 51 (36).01 CABG post-angiogram 24 (14) 43 (9.7) 20 (14).97 Thrombolytic therapy 61 (36) 211 (48) 50 (35).88 Hypotension requiring intervention 36 (21) 100 (23) 31 (22).88 MEDICATION USE WITHIN 72 HOURS OF RANDOMIZATION β-blockers Diuretics Non-ACE vasodilators ACE Inhibitors Mean time from MI to catheterization, d 8.2± ± ±16.62 Values are expressed as No. (%) unless otherwise indicated. Abbreviations: ACE, angiotensin-converting enzyme; CABG, coronary artery bypass graft; CHF, congestive heart failure; DBP, diastolic blood pressure; HF, heart failure; HR, heart rate; LVEDP, left ventricular end-diastolic pressure; LVEF, left ventricular ejection fraction; MI, myocardial infarction; PTCA, percutaneous transluminal coronary angioplasty; SBP, systolic blood pressure. VALUE Clinical Characteristics. Patients with the highest LVEDP had significantly higher creatinine kinase peaks, lower LVEF as measured noninvasively by radionuclide ventriculography, and a trend for more patients in Killip class >2 and were more likely to have been revascularized between the index AMI and randomization. The average time between the index AMI and measurement of LVEDP was 8.0±21 days and was not significantly different among the cohorts of LVEDP (Table III). LVEDP and Clinical Outcomes. Clinical event rates increased with increasing LVEDP, although these differences were not statistically significant (Table IV). Using time-dependent Kaplan- Meier analyses and log rank testing, we noted a trend for the cohort of LVEDP >30 mm Hg to have the greatest event rate of death or severe HF (Figure, log rank, P=.05) as well as for the individual HF-related end points: intensification of therapy (log rank, P=.0006), severe HF (log rank, P=.01), hospitalization for HF (log rank, P=.03), and HF requiring open-label ACE inhibition (log rank, P=.02). Baseline LVEDP >30 mm Hg was not related to the risk of total mortality (log rank, P=.22), cardiovascular mortality (log rank, P=.41), or risk of death/recurrent MI or HF (log rank, P=.23). With the Cox proportional hazards model, an LVEDP 30 mm Hg was associated with a greater hazard for 212 LVEDP and HF post-mi july. august 2007 Congestive Heart Failure (ISSN ) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT Copyright 2007 by Le Jacq. All rights reserved. No part of

5 Table IV. Clinical Event Rates Based on Baseline LVEDP EVENT LVEDP <15 MM HG (N=166) LVEDP MM HG (N=437) LVEDP >30 MM HG (N=141) P VALUE Death or severe HF 37 (22) 108 (25) 43 (30).23 Death 24 (15) 69 (16) 27 (19).54 Severe HF 27 (16) 74 (17) 34 (24).14 HF requiring intensification of 46 (28) 141 (32) 57 (41).06 therapy or death HF requiring intensification of therapy or death 32 (19) 97 (22) 42 (30).07 Values are expressed as No. (%). Abbreviations: HF, heart failure; LVEDP, left ventricular end-diastolic pressure. death or severe HF (unadjusted hazard ratio [HR], 1.40; 95% confidence interval [CI], ), HF requiring intensification of therapy (unadjusted HR, 1.62; 95% CI, ), hospitalization for HF (unadjusted HR, 1.58; 95% CI, ), HF requiring ACE inhibition (unadjusted HR, 1.66; 95% CI, ), and severe HF alone (unadjusted HR, 1.60; 95% CI, ) when compared with LVEDP <30 mm Hg. After adjustment for other predictors of HF outcome, however, LVEDP >30 mm Hg no longer remained a significant predictor of any of the 3 HF outcomes (Table V). Discussion Survivors of AMI are at increased risk for subsequent fatal and nonfatal cardiovascular events. 9 In this prospective cohort analysis from the SAVE trial, LVEDP correlated closely with other hemodynamic measures of filling pressures; angiographic volume measurement and high LVEDP were associated with lower ejection fraction, but not related to the extent of coronary artery disease or the percentage of akinetic-dyskinetic segments at the time of cardiac catheterization. Although an LVEDP >30 mm Hg was a significant univariate predictor of death or HF, after adjustment for known predictors of increased cardiac risk, LVEDP did not remain an independent marker. Following AMI, short-term mortality increases linearly with the development and progression of pulmonary congestion and HF Previous clinical studies have suggested that LVEDP measured at or near the time of AMI may have prognostic significance. Figure. Kaplan-Meier analysis of the primary outcome, death, or severe heart failure based on left ventricular end-diastolic pressure (LVEDP). Log rank test for LVEDP >30 mm Hg compared with 30 mm Hg; P=.05. Elevated LVEDP has been associated with incomplete coronary reperfusion, and LVEDP >18 mm Hg has been demonstrated to be a predictor of in-hospital mortality and the development of HF at 30 days in patients with AMI. 13 In addition, noninvasive estimation of left ventricular filling pressures has also been demonstrated to be a significant predictor of mortality in a cohort of post-ami patients. 14 The range of LVEDP values in this study varied from 2 to 52 mm Hg, with a median of 22 mm Hg. Using a cutoff of 15 mm Hg as an acceptable threshold of normality, these data suggest that 75% of the patients in this cohort had an abnormal LVEDP at baseline. Patients with LVEDP >30 mm Hg were more likely to have higher creatinine kinase peaks, significantly worse left ventricular function at baseline, and a trend for a greater proportion to be in Killip class 2 or greater. There are multiple influences of LVEDP early in the post-ami period. Early myocardial stunning may transiently increase LVEDP with subsequent normalization of filling pressures over the long term. 15 LVEDP may also have been decreased by the use of vasodilating and diuretic drugs. Captopril therapy has been shown to significantly reduce LVEDP and volumes in a cohort of anterior-wall AMI patients observed over a period of 1 year. 16 It is possible that randomization to ACE inhibitors or chronic administration of other vasodilators or diuretics may have attenuated the long-term effect of a single LVEDP measurement. This study was not adequately powered LVEDP and HF post-mi july. august Congestive Heart Failure (ISSN ) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT Copyright 2007 by Le Jacq. All rights reserved. No part of

6 Table V. Cox Proportional Hazards Analysis for LVEDP >30 mm Hg (n=141) Compared With LVEDP 30 mm Hg (n=612) OUTCOME UNADJUSTED HR 95% CI ADJUSTED HR a 95% CI Death or HF HF requiring intensification with digoxin or diuretics Severe HF b HF requiring ACE inhibitor Hospitalization for HF a P value refers to the comparison among all 3 groups. b HF requiring admission or open-label ACE inhibitor treatment. Abbreviations: ACE, angiotensin-converting enzyme; CI, confidence interval; HF, heart failure; HR, hazard ratio; LVEDP, left ventricular end-diastolic pressure. to assess the influence of captopril randomization on clinical outcomes. Finally, it is possible that LVEDP is not a long-term independent predictor in a cohort of patients with low ejection fraction in which the majority have elevated LVEDP at baseline. There are a few important limitations to discuss regarding this analysis. Primarily, LVEDP measurements were taken in a select group of patients felt to have ongoing or high-risk ischemia and may not be generalizable to all cohorts of AMI survivors. All cardiac catheterizations were performed by the treating physicians. Although the analysis of all data was standardized by a catheterization core laboratory, the acquisition of hemodynamic data including the timing of LVEDP measurement to ventriculography was not standardized. It is possible that variations in technique or interpretation of the hemodynamic results may have affected the quality or reliability of LVEDP measurement. In addition, this study may have lacked statistical power to detect clinically meaningful differences in the 3 groups of LVEDP. Although the event rates were similar in patients with an LVEDP <15 mm Hg and 15 to 30 mm Hg, there was a trend for death and all HF events to be greater for the group with LVEDP >30 mm Hg, with the time-dependent outcome of death or HF significant on univariate analysis. Further studies with more patients may confirm that an independent threshold of risk does exist at LVEPD >30 mm Hg. Despite these limitations, this analysis demonstrates that abnormalities of LVEDP are common in the early post-ami period and correlate well with other measures of filling pressures and ventricular volumes. Although the LVEDP was correlated to creatinine kinase peak, it was not related to the percentage of akinetic-dyskinetic segments or to the extent of coronary disease at the time of cardiac catheterization. These data suggest that myocardial infarction size and atherosclerotic burden are not enough to explain the variability in LVEDP. 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N Engl J Med. 1988;319: LVEDP and HF post-mi july. august 2007 Congestive Heart Failure (ISSN ) is published bimonthly (Feb., April, June, Aug., Oct., Dec.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT Copyright 2007 by Le Jacq. All rights reserved. No part of