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.     

Evaluation of left ventricular function three years after percutaneous recanalization of chronic total coronary occlusions

We investigated early and late effects of percutaneous revascularization for chronic total coronary occlusion on left ventricular (LV) function and volumes. Magnetic resonance imaging was performed in 21 patients before and 5 months and 3 years after recanalization. Global LV function and volumes and segmental wall thickening (SWT) were quantified on cine images. The 2 viability indexes used were the transmural extent of infarction (TEI) on delayed contrast enhancement images and end-diastolic wall thickness at baseline. Significant decreases in mean end-diastolic (86 +/- 14 to 78 +/- 15 ml/m2; p = 0.02) and mean end-systolic volume indexes (35 +/- 13 to 30 +/- 13 ml/m2; p = 0.03) were observed 3 years after recanalization. Mean ejection fraction tended to improve (60 +/- 9% to 63 +/- 11%; p = 0.11). SWT significantly increased at 5-months' follow-up (p <0.001), and an additional improvement was found at 3 years' (p = 0.04) follow-up in segments with TEI <25%. In segments with TEI of 25% to 75%, SWT was unchanged at 5-month follow-up (p = 0.89), but improved at 3 years (p = 0.04). SWT was unchanged in segments with transmural scars. For segmental functional recovery, TEI was a better predictor than end-diastolic wall thickness at baseline (odds ratio 5.6, 95% confidence interval 1.5 to 21.1, p = 0.01 vs odds ratio 2.5, 95% confidence interval 0.7 to 8.3, p = 0.14). In conclusion, a positive effect on LV remodeling and ejection fraction was observed up to 3 years after recanalization. Both early and late improvements in regional LV function were observed in the perfusion territory of chronic total coronary occlusion and were related to the transmural extent of infarction on pretreatment magnetic resonance imaging.     

Left ventricular remodeling after anterior wall acute myocardial infarction in modern clinical practice (from the REmodelage VEntriculaire [REVE] study group)

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) has been well described in previous studies. However, there is a paucity of data on the incidence of and risk factors for LV remodeling in modern clinical practice that incorporates widespread use of acute reperfusion strategies and almost systematic use of "antiremodeling" medications, such as angiotensin-converting enzyme inhibitors and beta blockers. We enrolled 266 patients with anterior wall Q-wave AMI who had >or=3 segments of the infarct zone that were akinetic on echocardiography before discharge. Echocardiographic follow-up was performed 3 months and 1 year after AMI. LV volumes, ejection fraction, wall motion score index, and mitral flow velocities were determined in a blinded analysis at a core echocardiographic laboratory. Acute reperfusion was attempted in 220 patients (83%; primary angioplasty in 29% and thrombolysis in 54%). During hospitalization, 99% of patients underwent coronary angiography and 87% underwent coronary stenting of the infarct-related lesion. At 1 year, 95% of patients received an antiplatelet agent, 89% a beta blocker, 93% an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker, and 93% a statin. Echocardiographic follow-up was obtained in 215 patients. There was recovery in LV systolic function as shown by a decrease in wall motion score index and an increase in ejection fraction. There was a significant increase in end-diastolic volume (EDV; 56.4 +/- 14.7 ml/m2 at baseline, 59.3 +/- 15.7 ml/m2 at 3 months, 62.8 +/- 18.7 ml/m2 at 1 year, p <0.0001). LV remodeling (>20% increase in EDV) was observed in 67 patients (31%). Peak creatine kinase level, systolic blood pressure, and wall motion score index were independently associated with changes in EDV. In conclusion, recent improvements in AMI management do not abolish LV remodeling, which remains a relatively frequent event after an initial anterior wall AMI.     

Clinical implication of persistent ischemic chest pain on admission in patients with late reperfused acute myocardial infarction

OBJECT: Although previous studies reported that late reperfusion might prevent left ventricular dilation after acute myocardial infarction (AMI), implication of persistent ischemic chest pain on admission remains to be investigated. This study was undertaken to assess the implication of persistent ischemic chest pain on in-hospital outcome and left ventricular function after late reperfused AMI. METHODS AND PATIENTS: We studied 63 patients with a first anterior AMI who underwent percutaneous coronary intervention 6 to 24 hours (11.2+/-4.5 hours) after the onset. Of 63 patients, 48 (76%) had persistent ischemic chest pain on admission. RESULTS: Incidence of in-hospital death, reinfarction or congestive heart failure was similar between the 2 groups. Pretreatment left ventricular ejection fraction and end-diastolic volume were similar between the 2 groups. Predischarge angiography was performed at 17+/-5 days after the onset. Late reperfusion prevented the dilation of left ventricular end-diastolic volume in patients with chest pain (78+/-12 to 75+/-17 ml/m2, p=0.15), but did not in those without (75+/-20 to 93+/-28 ml/m2, p=0.03). A multivariate analysis revealed that absence of persistent ischemic chest pain was an independent predictor of predischarge left ventricular end-diastolic volume >100 ml/m2 (odds ratio 0.10, p=0.04). CONCLUSIONS: Our data demonstrated that absence of persistent ischemic chest pain appears to be a simple and reliable marker which predicts left ventricular dilation after late reperfused AMI.     

Effect of intravenous metoprolol on left ventricular performance in Q-wave acute myocardial infarction

To determine the effects of intravenous metoprolol on left ventricular (LV) function in acute myocardial infarction (AMI), 16 patients were studied within 48 hours of Q-wave AMI (mean ejection fraction 47 +/- 6%, mean pulmonary artery wedge pressure 22 +/- 6 mm Hg) with high fidelity pressure and biplane cineventriculography before and after intravenous metoprolol (dose 12 +/- 4 mg). Heart rate decreased from 90 +/- 13 to 74 +/- 11 beats/min (p less than 0.001), pulmonary arterial wedge pressure and LV end-diastolic pressure were unchanged (22 +/- 6 to 21 +/- 6 and 27 +/- 8 to 26 +/- 8 mm Hg, respectively), despite impaired LV relaxation (P = Poe-t/T) after intravenous metoprolol (T from 59 +/- 13 to 72 +/- 12 ms, p less than 0.001). Peak systolic circumferential LV wall stress decreased after beta-adrenergic blockade (330 +/- 93 to 268 +/- 89 g/cm2, p less than 0.05) and LV contractility decreased (dP/dtmax from 1,480 +/- 450 to 1,061 +/- 340 mm Hg/s, p less than 0.001). The ejection fraction decreased (48 +/- 7 to 43 +/- 7%, p less than 0.05) due to an increase in LV end-systolic volume (85 +/- 19 to 93 +/- 19 ml, p less than 0.05) since LV end-diastolic volume was unchanged (161 +/- 30 to 163 +/- 30 ml, difference not significant). In patients with Q-wave AMI, intravenous metoprolol reduces the major determinants of myocardial oxygen demand including heart rate, contractility and peak systolic wall stress. Further, despite decreased heart rate, (+)dP/dtmax, ejection fraction, isovolumic relaxation, LV end-diastolic pressure and end-diastolic volume remain unchanged.     

Effects of percutaneous coronary arterial thrombectomy during acute myocardial infarction on left ventricular remodeling

The benefit of primary angioplasty for acute myocardial infarction (AMI) is limited by the no-reflow phenomenon, resulting in chronic left ventricular (LV) remodeling. The aim of this study was to evaluate the impact of thrombectomy with the Rescue percutaneous thrombectomy catheter on LV function after AMI. We performed a retrospective study comparing conventional angioplasty with the combination of angioplasty and thrombectomy using the Rescue catheter. The study population was comprised of 109 consecutive patients with AMI who underwent angioplasty and thrombectomy and 86 controls treated with conventional angioplasty. Baseline clinical and lesion characteristics were similar in the 2 groups. Postprocedural restoration of normal flow (Thrombolysis In Myocardial Infarction grade 3) was more frequent in the thrombectomy group (82% vs 69%, p = 0.03). No differences were observed in cardiac events, including death, reinfarction, and target vessel revascularization (thrombectomy vs controls, 27% vs 33%; p = 0.44) or changes in ejection fraction (p = 0.22) during 6-month follow-up. The incidence of LV remodeling, defined as an increase in LV end-diastolic volume index of >20%, was significantly lower in the thrombectomy group (22% vs 44%; p = 0.01). Multiple logistic regression analysis revealed that thrombectomy with the Rescue catheter contributed significantly to reduction of both no-reflow and LV remodeling. In the setting of primary angioplasty, adjunctive pretreatment with a rescue catheter reduces the no-reflow phenomenon and protects against LV remodeling.     

粒细胞集落刺激因子动员自体外周血干细胞移植治疗急性心肌梗死的临床研究

目的观察经皮经腔冠状动脉内移植自体外周血干细胞(PBSC)治疗急性心肌梗死(AMI)的疗效。方法自2003年11月至2005年1月共入选AMI患者70例,随机分为干细胞移植组和对照组,两组均为35例。干细胞治疗组在常规AMI治疗(药物与介入治疗)基础上应用粒细胞集落刺激因子(GCSF)皮下注射动员自体骨髄干细胞,连用5天,第6天分离外周血干细胞悬液,将采集后的干细胞悬液经OVERTHEWIRE球囊导管中心腔注入梗死相关动脉(IRA),进行外周血干细胞移植;对照组经AMI常规方法(药物与介入)治疗。在外周血干细胞动员、采集及经冠状动脉回输过程中观察其不良反应。两组患者在移植前及移植后6个月应用超声心动图评价左室形态及心功能变化,室壁节段性运动积分;比较两组患者生存率及心脏事件发生率。结果6个月时干细胞移植组心脏收缩末容积(ESV)明显减小[(63.8±23.9)ML比(52.6±20.3)ML,P=0.01],舒张末容积(EDV)无显著性变化[(134.2±36.7)ML比(119.2±30.3)ML,P=0.07];左室射血分数(LVEF)显著增高[(50.0±8.2)%比(57.1±7.8)%,P<0.001];左室壁节段性运动积分指数(WMSI)明显减低[(1.219±0.190)比(1.101±0.118),P<0.001]。对照组介入术前及术后6个月随访ESV、EDV、LVEF及WMSI均无统计学差异(P=0.490、0.259、0.117、0.395)。两组术后6个月生存率及心脏事件发生率无统计学差异。不良反应:在PBSC动员、分离、采集及回输中总的不良反应共25例次,其中动员时不良反应占37.1%(13/35),分离和采集中的不良反应占14.3%(5/35),经冠状动脉回输过程中出现的不良反应占20.0%(7/35)。结论经皮经腔冠状动脉内移植自体PBSC治疗AMI可以在近期有效地减少心肌梗死缺血面积,减轻左室重构,改善心功能。     

Comparison of two- and three-dimensional echocardiography with sequential magnetic resonance imaging for evaluating left ventricular volume and ejection fraction over time in patients with healed myocardial infarction

Echocardiographic follow-up of left ventricular (LV) volumes is difficult because of the test-retest variation of 2-dimensional echocardiography (2DE). We investigated whether the accuracy and reproducibility of real-time 3-dimensional echocardiography (RT3DE) would make this modality more feasible for serial follow-up of LV measurements. We performed 2DE and RT3DE and cardiac magnetic resonance imaging (MRI) in 50 patients with previous infarction and varying degrees of LV function (44 men; 61 +/- 11 years of age) at baseline and after 1-year follow-up. Images were obtained during breath-hold and measurements of LV volumes and ejection fraction were made offline. Over follow-up, end-diastolic volume decreased from 192 +/- 53 to 187 +/- 60 ml (p <0.01), end-systolic volume decreased from 104 +/- 51 to 95 +/- 53 ml (p <0.01), and ejection fraction increased from 48 +/- 12% to 51 +/- 12% (p <0.01). MRI showed that LV mass shrank from 183 +/- 39 to 182 +/- 37 g (p <0.01). The correlation between change in RT3DE and change in MRI was greater than the correlations of 2DE with MRI for measurement of end-diastolic volume (r = 0.47 vs 0.02, p <0.01), end-systolic volume (r = 0.44 vs 0.17, p <0.01), and ejection fraction (r = 0.58 vs -0.03, p <0.01). The change in end-diastolic volume between baseline and follow-up with RT3DE (-4 +/- 20, p <0.01) was similar to that with MRI but was unrecognized by 2DE (4 +/- 19, p = 0.09). There was good test-retest and inter- and intraobserver correlation within RT3DE for volumes, ejection fraction, and mass. In conclusion, if sequential measurement of LV volumes is used to guide management decisions, 3DE appears preferable to 2DE.     

Effect of quinapril initiated during progressive remodeling in asymptomatic patients with healed myocardial infarction

Approximately 20% of patients with healed myocardial infarction develop asymptomatic progressive left ventricular (LV) dilation and remodeling and are at increased risk for progression to symptomatic congestive heart failure and premature death. It was the goal of this study to test whether quinapril may interrupt this process and to analyze potential mechanisms. Of 138 patients with an average infarct age of 56 months, 25 had asymptomatic progressive LV dilation and were randomized in a prospective, double-blind study to placebo or quinapril. At baseline (mean +/- SEM) ejection fraction was reduced (35 +/- 3% and 39 +/- 3%) and end-diastolic volume (gated single-photon emission computed tomography) increased (104 +/- 9 and 117 +/- 12 ml/m(2)) with placebo (n = 13) and quinapril (n = 12), respectively. Progressive dilation continued in patients taking placebo (6 months: 9.4 +/- 5.2 ml/m(2), 12 months 24.6 +/- 5. 4 ml/m(2); change from baseline: p <0.05 vs baseline; p <0.05 vs 6 months), but not with quinapril (6 months: -0.9 +/- 4.0 ml/m(2); 12 months: 4.1 +/- 5.2 ml/m(2) [p <0.05] vs placebo). Wedge pressure during bicycle exercise was similar at baseline, but at 12 months tended to be lower with quinapril (17 +/- 1 mm Hg) than with placebo (24 +/- 4 mm Hg, p = 0.1673). Thus, quinapril prevented further progression of asymptomatic LV dilation and remodeling after remote myocardial infarction, possibly due to attenuation of an exercise-induced increase in LV filling pressure.     

Influence of transmurality, infarct size, and severe microvascular obstruction on left ventricular remodeling and function after primary coronary angioplasty

Infarct size has been considered an established marker of left ventricular (LV) remodeling. We assessed the predictive value of myocardial/microvascular injury assessed by delayed enhanced magnetic resonance imaging (MRI) on LV remodeling and LV ejection fraction after primary coronary intervention (PCI) compared with peak troponin levels, an established index of myocardial infarct size. We performed MRI in 76 patients with first acute myocardial infarction 6 +/- 2 days after successful PCI. Necrosis was judged as transmural when delayed enhancement was extended to >or=75% of LV segment thickness. Severe microvascular obstruction was identified as areas of late hypoenhancement surrounded by delayed enhancement. Infarct size was expressed as an index by dividing the total percentage of delayed enhancement involvement by the number of LV segments. LV end-diastolic volume index and function were quantified by 2-dimensional echocardiography at 6 +/- 1 months after acute myocardial infarction. Remodeling was evaluated as a change in LV end-diastolic volume index at follow-up compared with baseline. At univariate analyses, transmural necrosis, severe microvascular obstruction, infarct size, and troponin level were correlated directly with remodeling and inversely with LV function at follow-up (p <0.001). At multiple regression, only transmural necrosis and troponin level remained independent predictors of LV remodeling and function. With respect to troponin, transmural necrosis improved the predictive power of LV remodeling (R2 for change = 0.19) and function (R2 for change = 0.16). In conclusion, in patients with acute myocardial infarction undergoing PCI, the amount of transmural necrosis as assessed by MRI is a major determinant of LV remodeling and function, with significant additional predictive value to infarct size and severe microvascular obstruction.     

Intravenous atrial natriuretic peptide prevents left ventricular remodeling in patients with first anterior acute myocardial infarction

OBJECTIVES: The study evaluates the effect of atrial natriuretic peptide (ANP) compared with nitroglycerin (GTN) on left ventricular (LV) remodeling after first anterior acute myocardial infarction (AMI). BACKGROUND: Compared with GTN, ANP suppresses the renin-angiotensin-aldosterone system and endothelin-1 (ET-1), which stimulate LV remodeling. METHODS: Sixty patients with a first anterior AMI were randomly divided into the ANP (n = 30) or GTN (n = 30) groups after direct percutaneous transluminal coronary angioplasty. We evaluated LV ejection fraction (LVEF), end-diastolic volume index (LVEDVI) and end-systolic volume index (LVESVI) at the acute phase and after one month. We also measured neurohumoral factors during study drug infusion. RESULTS: There was no difference in the baseline characteristics or LVEF (46.9+/-1.0 vs. 46.8+/-1.3%) between the two groups. Although there was no difference in hemodynamics during the infusion periods, the LVEF was significantly improved after one month compared with the baseline value in both groups, but it was improved more in the ANP group than in the GTN group (54.6+/-1.1%, 50.8+/-1.3%, p < 0.05). Left ventricular enlargement was prevented in the ANP group (LVEDVI, 85.8+/-3.1 ml/m2 to 87.3+/-2.7 ml/m2; p = ns, LVESVI, 45.6+/-1.8 ml/m2 to 41.0+/-2.1 ml/m2, p < 0.05) but not in the GTN group (LVEDVI, 86.2+/-4.1 to 100.2+/-3.7, p < 0.01; LVESVI, 46.3+/-2.8 ml/m2 to 51.1+/-3.0 ml/m2, p = ns). During the infusion, ANP suppressed plasma levels of aldosterone, angiotensin II and ET-1 compared with GTN. CONCLUSIONS: These findings indicate that in patients with a first anterior AMI, an ANP infusion can prevent LV remodeling better than can GTN, and effectively suppresses aldosterone, angiotensin II and ET-1.     

Effects of reperfusion on left ventricular ejection fraction and volume after acute myocardial infarction.

The effects of reperfusion on left ventricular (LV) function and volume were studied in patients with evolving acute myocardial infarction (AMI). We analyzed the LV ejection fraction and volume in patients who had been admitted within 24 h of the onset of their first AMI with culprit lesion of #6, #7 and #1 (American Heart Association classification). Sixty-five patients (Re group) received successful reperfusion therapy within 6 h after the AMI. The other 60 patients (Oc group), who were admitted from 6 to 24 h after the AMI, received conservative therapy. Patients with re-obstruction of the culprit lesion after reperfusion therapy were excluded from the Re group. Patients with spontaneous recanalization following conservative therapy were excluded from the Oc group. The LV ejection fraction (LVEF), LV end-systolic volume index (LVESVI), and LV end-diastolic volume index (LVEDVI) were measured using a modified Dodge's formula by left ventriculography performed 4 weeks after the AMI. LVEF in the Re group was significantly greater than in the Oc group (57 +/- 12 vs 49 +/- 11%) (mean +/- SD, p less than 0.01). LVESVI in the Re group was significantly smaller than in the Oc group (30 +/- 13 vs 38 +/- 16 ml/m2, p less than 0.01). Although LVEDVI was not significantly different between the 2 groups, in patients with a responsible coronary lesion of segment #6, LVEDVI in the Re group was significantly smaller than in the Oc group (67 +/- 14 vs 77 +/- 18 ml/m2, p less than 0.05). Although LVEF and LV volume correlated in both groups, the correlation was weak (r = 0.40-0.42), suggesting that LV volume was not dependent solely on LV functional recovery. The incidence of ventricular aneurysm in the Re group was significantly lower than in the Oc group (15.4 vs 45.0%, p less than 0.01). Multivariate analysis selected reperfusion of the responsible coronary artery as one of the factors significantly associated with a reduction of LVEDVI, LVESVI, an improvement of LVEF, and a decrease in the rate of aneurysm formation. In summary, our results indicated that reperfusion improved EF, reduced LV volume, and decreased the rate of aneurysm formation as compared to non-reperfusion, which suggests that reperfusion therapy is beneficial for both functional recovery and ventricular remodeling.     

Prediction of functional recovery of the left ventricle after coronary revascularization in patients with prior anterior myocardial infarction: a myocardial integrated backscatter study.

Cyclic variation (CV) of myocardial integrated backscatter (IBS), which reflects intrinsic contractile performance, can predict myocardial viability in patients with a reperfused acute myocardial infarction (MI), but the use of this method has not been validated for chronic left ventricular (LV) dysfunction. The aim of this study was to examine whether myocardial IBS was useful for predicting LV functional recovery after coronary revascularization in 17 patients with prior anterior MI and LV dysfunction (ejection fraction <50%). Within 24 h of the revascularization procedure (percutaneous transluminal coronary angioplasty or coronary stenting), IBS curves were obtained by placing the region of interest on the anterior wall on the short-axis IBS image. The patients had repeat left heart catheterization at 3 or 6 months after the revascularization procedure, and were grouped according to the patterns of the IBS curve within the anterior wall. In 8 patients (group A), the IBS curve had a synchronized pattern with the magnitude of CV > or = 3.5, and in the remaining 9 patients (group B), the curve had either an asynchronized pattern or the magnitude of CV was less than 3.5 dB even in the case of synchronized pattern, or both. At baseline, there were no significant differences in LV functional indices between the 2 groups. After the follow-up period, the LV end-systolic volume decreased (75 +/- 21 ml to 56 +/- 20ml, p = 0.05), LV ejection fraction increased (35 +/- 12% to 50 +/- 14%, p = 0.014), and LV end-diastolic pressure decreased (19 +/- 10 mmHg to 13 +/- 6 mmHg, p = 0.02) in group A, whereas only the LV ejection fraction increased (34 +/- 9% to 40 +/- 11%, p = 0.03) in group B; LV end-systolic volume (72 +/- 19 ml to 66 +/- 16 ml, p = 0.126) and LV end-diastolic pressure (18 +/- 12 mmHg to 14 +/- 8 mmHg, p = 0.184) showed no significant changes. In conclusion, IBS is valuable for predicting LV functional recovery after coronary revascularization in patients with LV dysfunction caused by a remote anterior MI. A large-scale study is be needed to establish these data.     

Serum C-reactive protein elevation in left ventricular remodeling after acute myocardial infarction--role of neurohormones and cytokines

BACKGROUND: We previously reported that increased peak serum C-reactive protein (CRP) level after acute myocardial infarction (AMI) was a major predictor of cardiac rupture and long-term outcome. The aim of this study was to clarify the role of serum CRP elevation as a possible marker of left ventricular (LV) remodeling after AMI. METHODS: We prospectively studied 31 patients who underwent primary angioplasty for a first anterior Q-wave AMI. Peak serum CRP level was determined by serial measurements after admission. LV volume and the plasma levels of various neurohormones and cytokines were measured on admission, and 2 weeks and 6 months after AMI. RESULTS: Patients with higher peak CRP levels (above the median) had a greater increase in LV end-diastolic volume during 2 weeks after AMI (+21+/-14 vs. +5+/-6 ml/m(2), P=0.001) and a lower ejection fraction (45+/-11 vs. 53+/-7%, P=0.02) than those with lower CRP levels, associated with a higher incidence of pump failure, atrial fibrillation, and LV aneurysm. Plasma levels of norepinephrine, brain natriuretic peptide, and interleukin-6 2 weeks after AMI were higher in the high CRP group than in the low CRP group. CONCLUSIONS: Increased peak serum CRP level was associated with a greater increase in LV volume after anterior AMI. Plasma norepinephrine and interleukin-6 levels were increased in patients with higher CRP levels, suggesting a possible role of sympathetic activation and enhanced immune response in the development of LV remodeling after AMI.     

ST-segment re-elevation unrelated to left ventricular ejection fraction or volume after anterior wall acute myocardial infarction treated with successful reperfusion

Ventricular remodeling is a major determinant of the long-term prognosis of patients with acute myocardial infarction (AMI). No previous study examined the relation of ST-segment re-elevation to left ventricular (LV) volume and function in patients with successful reperfusion. We examined the relation of ST-segment re-elevation to LV function and volume indices in 51 patients with anterior wall AMI who underwent successful reperfusion by direct coronary angioplasty. A 12-lead electrocardiogram was recorded once a day until 7 days after the onset of AMI. ST-segment shift was measured and Sigma ST was defined as the sum of ST-segment elevation obtained from leads V2, V3, and V4. ST-segment re-elevation was defined as present when the difference between maximal and minimal Sigma ST (Delta ST) was >0.3mV. LV indices were obtained from left ventriculography performed approximately 1 month after the onset of AMI. ST-segment re-elevation was observed in 15 patients (29%). No significant differences were observed between the ST- re-elevation group and non-ST-re-elevation group in LV ejection fraction (49.4+/-14.0 vs. 51.2+/-11.5%), LV end-systolic volume index (35.8+/-13.1 vs. 33.8+/-12.5 mL/m(2)) or LV end-diastolic volume index (69.7+/-12.8 vs. 68.3+/-14.4 mL/m(2)). The difference between maximal and minimal Sigma ST (Delta ST) was not significantly correlated with any LV index examined. In conclusion, the present study revealed that ST-segment re-elevation after successful reperfusion in anterior wall AMI patients was not related to LV volume or function, indicating that ST-re-elevation is not a clinically meaningful indicator of LV remodeling.     

Doppler-derived mitral deceleration time as a strong prognostic marker of left ventricular remodeling and survival after acute myocardial infarction: results of the GISSI-3 echo substudy

OBJECTIVES: The goal of this study was to assess the impact of left ventricular (LV) diastolic filling on remodeling and survival after acute myocardial infarction (AMI). BACKGROUND: Little is known regarding the link between LV filling, its changes over time, and six-month remodeling and late survival in uncomplicated AMI. METHODS: Doppler mitral profile, end-diastolic volume index (EDVi) and end-systolic volume index (ESVi), ejection fraction (EF), and wall motion abnormalities (%WMA) were evaluated in 571 patients from the GISSI-3 Echo substudy at baseline, pre-discharge, and six months after AMI. Patients with baseline early mitral deceleration time (DT) 130 ms were assigned to the restrictive group (n = 147), and those with DT >130 ms to the nonrestrictive group (n = 424). RESULTS: Restrictive group patients had greater baseline ESVi and %WMA and lower EF than nonrestrictive group, and six-month greater LV dilation (EDVi, ESVi: p < 0.001 for EDVi and ESVi), smaller decrease in %WMA decrease (p < 0.01), and larger EF impairment (p < 0.008). Among the restrictive group, patients (n = 56) with pre-discharge persistent restrictive filling (n = 56) showed six-month greater LV enlargement (p < 0.001) and EF impairment (p < 0.009) than those (n = 91) with reversible restrictive filling. Baseline %WMA and EDVi, together with pre-discharge persistent restrictive filling, predicted severe (>20%) LV dilation. Four-year survival was 93% in nonrestrictive patients versus 88% in the restrictive group (p < 0.06), and 93% in pre-discharge reversible restrictive versus 79% in persistent restrictive (p < 0.0003). The single best predictor of mortality, by Cox analysis, was pre-discharge persistent restrictive filling (chi-square 14.88). CONCLUSIONS: Left ventricular dilation may occur even after uncomplicated AMI and may be paralleled by an improvement in LV filling. However, a baseline restrictive filling that persists at pre-discharge identifies more compromised patients at higher risk for six-month remodeling and four-year mortality.     

Effects of percutaneous transluminal septal myocardial ablation for obstructive hypertrophic cardiomyopathy on systolic and diastolic left ventricular function assessed by pressure-volume loops

The aim of the present study was to determine the long-term effects of percutaneous transluminal septal myocardial ablation (PTSMA) on systolic and diastolic left ventricular (LV) functions in patients with obstructive hypertrophic cardiomyopathy (HC). Ten consecutive patients with symptomatic HC despite optimal medical treatment were referred for PTSMA at our center. LV systolic and diastolic functions were assessed by online LV pressure-volume loops obtained by conductance catheter at baseline and at 6 months after the procedure. At follow-up, the mean gradients at rest and after extrasystole were significantly decreased compared with baseline (88 +/- 29 to 21 +/- 11 mm Hg and 130 +/- 50 to 35 +/- 22 mm Hg, respectively, p <0.01 for the 2 comparisons). End-systolic and end-diastolic pressures significantly decreased (p <0.01), whereas end-systolic and end-diastolic LV volumes significantly increased (p <0.01 for the 2 comparisons). Cardiac output and stroke volume were unchanged, as were ejection fraction (p = 0.25) and maximum dP/dt (p = 0.13). The slope of the end-systolic pressure-volume relation was not decreased, indicating a preserved contractility. The relaxation constant time, end-diastolic stiffness, projected volume of the end-diastolic pressure-volume relation at 30 mm Hg, and diastolic stiffness constant showed a significant improvement of active and passive myocardial diastolic properties. In conclusion, PTSMA is an effective method in the treatment of symptomatic patients with HC. At 6-month follow-up, the LV-aortic gradient was decreased and active and passive LV diastolic properties were increased. Myocardial contractility was not decreased and general hemodynamics was maintained.     

Cardioprotective effects of magnesium sulfate in patients undergoing primary coronary angioplasty for acute myocardial infarction.

BACKGROUND: Experimental evidence indicates that magnesium sulfate may have potential cardioprotective properties as an adjunct to coronary reperfusion. The present study was designed to examine the hypothesis that magnesium might have beneficial effects on left ventricular (LV) function and coronary microvascular function in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: The study population of 180 consecutive patients with a first AMI (anterior or inferior) underwent successful primary coronary intervention. Patients were randomized to treatment with either intravenous magnesium (magnesium group, n=89) or normal saline (control group, n=91). Pre-discharge left ventriculograms were used to assess LV ejection fraction (LVEF), regional wall motion (RWM) within the infarct-zone and LV end-diastolic volume index. The Doppler guidewire was used to assess coronary flow velocity reserve (CFVR) as an index of coronary microvascular function. Magnesium group subjects showed significantly better LV systolic function (LVEF 63+/-9% vs 55+/-13%, p<0.001; RWM: -1.01+/-1.29 SD/chord vs -1.65+/-1.11 SD/chord, p=0.004), significantly smaller LV end-diastolic volume index (63+/-17 ml/m(2) vs 76+/-20 ml/m(2), p<0.001), and significantly higher CFVR (2.95+/-0.76 vs 2.50+/-0.99, p=0.023) than controls. CONCLUSION: Magnesium sulfate as an adjunct to primary coronary intervention shows favorable functional outcomes in patients with AMI.     

Effect of intraaortic balloon pumping on left ventricular function in patients with persistent ST segment elevation after revascularization for acute myocardial infarction.

The purpose of the present study was to assess the impact of intraaortic balloon pumping (IABP) in patients with persistent ST elevation who underwent revascularization within 6 h of their first acute anterior myocardial infarction (AMI). Persistent ST elevation after revascularization was defined as being > or =50% of the initial value on return to the coronary care unit. Twenty-four patients were treated without IABP (control group) and 27 patients were treated with IABP (IABP group). There was no significant difference between the 2 groups in pretreatment left ventricular ejection fraction (LVEF), end-diastolic volume index or end-systolic volume index. After 137+/-46 days, the change in the LVEF was significantly higher in the IABP group than in the control group (5+/-13% vs 13+/-15%, p=0.04). However, the left ventricular end-diastolic volume index was similar between the 2 groups during follow-up (pretreatment: 77+/-19 ml/m(2) vs 74+/-13 ml/m(2), p=0.54; follow-up: 86+/-22 ml/m(2) vs 83+/-18 ml/m(2), p=0.60). These data suggest that IABP enhances the improvement in LVEF independent of remodeling in AMI patients with persistent ST elevation after revascularization.     

Prediction of remote left ventricular volumes and functions after acute myocardial infarction with successful coronary intervention.

BACKGROUND: The scintigraphic perfusion defect size (DS) at 1 week after acute myocardial infarction (AMI) predicts remote left ventricular (LV) volumes and LV ejection fraction (LVEF). The present study examined whether LV volumes and LVEF 6 months after AMI may be better predicted by the combination of LV volumes and LVEF just after reperfusion, and DS at 1 week, after AMI in patients with Thrombolysis In Myocardial Infarction (TIMI) grade III reperfusion by percutaneous coronary intervention. METHODS AND RESULTS: In 48 patients with AMI and TIMI grade III reperfusion, quantitative gated SPECT (QGS) was performed just after reperfusion, and at 1 week and 6 months after AMI. LV end-diastolic volume index decreased (108+/-8 to 93+/-6 ml/m(2), p<0.05) and LVEF increased (44+/-3 to 50+/-2%, p<0.05) 6 months after AMI. In addition, they were better predicted by a combination of LV volumes and LVEF just after reperfusion and DS at 1 week after AMI. CONCLUSIONS: In AMI with TIMI grade III reperfusion, LV volumes and LVEF at 6 months after MI correlate with the values obtained just after reperfusion. Myocardial perfusion imaging combined with QGS at reperfusion may predict these late-phase parameters.