Left ventricular thrombus formation after first anterior wall acute myocardial infarction

The characteristics of the left ventricle and coronary arteries associated with left ventricular (LV) thrombus in patients with recent anterior acute myocardial infarction were defined. Of 77 patients studied, 35 (46%) had LV thrombi. The presence of LV thrombus was not correlated to the extent of coronary artery disease. The frequency of LV thrombus progressively increased with groups of increasing wall motion abnormality as determined by the extent of akinesia and dyskinesia (%AD) (%AD 0 to 14, thrombus present in 3 of 16 [19%], %AD 15 to 29, thrombus in 8 of 27 [30%]; %AD greater than or equal to 30%, thrombus in 24 of 34 [71%]; p less than 0.001) and with increasingly severe degrees of early ventricular shape change (normal or mildly abnormal contour, 16% with thrombus; moderately abnormal contour, 36% with thrombus; severely abnormal contour, 70% with thrombus; p less than 0.001). Patients with thrombi had higher diastolic (249 +/- 55 vs 225 +/- 48 ml; p less than 0.05) and systolic (158 +/- 48 vs 120 +/- 45 ml; p less than 0.001) volumes than patients without thrombi, respectively. A stepwise discriminant analysis identified ejection fraction, extent of early shape change and LV end-diastolic pressure as independent correlates of LV thrombus after acute myocardial infarction.     

Left ventricular remodeling after myocardial infarction in antecedent hypertensive patients.

Antecedent hypertension adversely affects mortality and heart failure after myocardial infarction (MI). In addition, accelerated ventricular remodeling is a contributor to the increased mortality observed after MI. The purpose of this study was to assess the relationship of antecedent hypertension to ventricular remodeling after MI. Ninety-four patients presenting with a first acute MI who were treated with reperfusion therapy within 12 h of their symptom onset were enrolled in this study. All of them underwent left ventriculography immediately after reperfusion therapy and again at 6 months after the occurrence of MI. Patients were divided into two groups: a hypertensive group and a normotensive group. End-diastolic volume index (EDVI), end-systolic volume index (ESVI), and ejection fraction (EF) values in the acute phase were compared to those at 6 months after acute MI in either group. The hypertensive group showed a significant increase in both EDVI and ESVI after 6 months, whereas the normotensive group did not. In addition, there was no change in EF in the hypertensive group, whereas EF increased significantly after 6 months in the normotensive group. As a result, the percent changes in ESVI and EF were significantly different between the hypertensive group and normotensive group. The results demonstrated that antecedent hypertension interacts with ventricular cavity dilatation after MI.     

Left ventricular dyssynchrony acutely after myocardial infarction predicts left ventricular remodeling.

OBJECTIVES: We sought to identify predictors of left ventricular (LV) remodeling after acute myocardial infarction. BACKGROUND: Left ventricular remodeling after myocardial infarction is associated with an adverse long-term prognosis. Early identification of patients prone to LV remodeling is needed to optimize therapeutic management. METHODS: A total of 178 consecutive patients presenting with acute myocardial infarction who underwent primary percutaneous coronary intervention were included. Within 48 h of intervention, 2-dimensional echocardiography was performed to assess LV volumes, LV ejection fraction (LVEF), wall motion score index, left atrial dimension, E/E' ratio, and severity of mitral regurgitation. Left ventricular dyssynchrony was determined using speckle-tracking radial strain analysis. At 6-month follow-up, LV volumes, LVEF, and severity of mitral regurgitation were reassessed. RESULTS: Patients showing LV remodeling at 6-month follow-up (20%) had comparable baseline characteristics to patients without LV remodeling (80%), except for higher peak troponin T levels (p < 0.001), peak creatine phosphokinase levels (p < 0.001), wall motion score index (p < 0.05), E/E' ratio (p < 0.05), and a larger extent of LV dyssynchrony (p < 0.001). Multivariable analysis demonstrated that LV dyssynchrony was superior in predicting LV remodeling. Receiver-operating characteristic curve analysis demonstrated that a cutoff value of 130 ms for LV dyssynchrony yields a sensitivity of 82% and a specificity of 95% to predict LV remodeling at 6-month follow-up. CONCLUSIONS: Left ventricular dyssynchrony immediately after acute myocardial infarction predicts LV remodeling at 6-month follow-up.     

Left ventricular remodeling in the first year after acute myocardial infarction and the predictive value of N-terminal pro brain natriuretic peptide

Background Left ventricular (LV) remodeling after myocardial infarction (MI) has received much attention because of its severe impact on morbidity and mortality rates. However, the incidence and extent of LV remodeling in a modern infarct population who were offered antiremodeling treatment in compliance with daily clinical practice is unknown. The purpose of this study was to clarify this issue and to evaluate the predictive value of N-terminal pro brain natriuretic peptide (NT-proBNP). Methods Forty-two patients with a first transmural MI were examined after 1 week, 1 month, 3 months, 6 months, and 1 year with blood samples and magnetic resonance imaging. Results In 12 patients (29%), LV end-diastolic volume index (LVEDVI) and LV end-systolic volume index (LVESVI) increased by 24% and 22% (P <.0001; P = .01). In 12 patients (29%), LVEDVI and LVESVI decreased by 19% and 23% (P <.0001; P = .0005), whereas the remaining 18 patients (43%) had stable conditions regarding these LV measures. LV ejection fraction at baseline was significantly reduced in all patient categories but was unchanged over time. Elevated NT-proBNP level at baseline was identified as an independent predictor of increase in LVEDVI during follow-up examination (P = .007). A baseline level of NT-proBNP >115 pmol/L identified patients who later had LV dilatation develop with a sensitivity and specificity of 89% and 68% (area under curve = 0.77). Conclusion In this 1-year follow-up study of patients with a first transmural MI, approximately 30% had significant increments develop in LVEDVI and LVESVI, and LV ejection fraction remained unchanged. Patients in whom LV dilatation developed could be identified early after the MI with elevated plasma levels of NT-proBNP. (Am Heart J 2002;143:696-702.)     

Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p less than .01), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p less than .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p less than .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p less than .05) and significant increases in angiographic cardiac index (p less than .01) and LVESV index (p less than .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akinetic-dyskinetic segments and volume-overload hypertrophy of noninfarcted segments.(ABSTRACT TRUNCATED AT 400 WORDS)     

急性心肌梗死后左心室重构及其防治

本文简述了急性心肌梗死后左心室重构的发生机制、时间、后果、影响因素及防治措施等     

Left atrial remodeling in acute anterior myocardial infarction

BACKGROUND: Our goal in this study was to examine the changes in the left atrial functions over a period of 3 months by using left atrial volume measurements in patients with anterior myocardial infarction (MI). METHODS AND RESULTS: Seventy-three patients with anterior MI who consulted our hospital in the first 12 hours starting from the onset of the chest pain and who exhibited ST elevation were enrolled in the study. The left atrial functions of the patients were evaluated by transthoracic echocardiography for a total number of four times; first at the time of the visit to the hospital, then in the first week, and then in the first and third months. Eight (10.95%) of the 73 patients included in the study died during the follow-up. The remaining 65 patients completed the 3-month study period. Of these 65 patients, primary percutaneous transluminal coronary angioplasty (PTCA) was performed for 24 (36.9%) patients and thrombolytic therapy was given to 13 (20%), whereas 28 (43.1%) patients were given only medical treatment. Left atrium (LA) maximum transverse diameter, LA maximum, minimum, and presystolic volume, LA active emptying volume and fraction were found to increase significantly in comparison to baseline detected for this parameter in the first and third months (P < 0.001). However, LA passive emptying volume and fraction was found to decrease significantly in comparison to baseline detected for this parameter in the first and third months (P < 0.001). CONCLUSIONS: An increase in the diameter, volume, and dimensions of LA during atrial remodeling was detected. LA passive emptying fraction was found to decrease, whereas atrial active emptying function was found to increase to compensate for this change.     

Relationship between heart rate variability and left ventricular remodeling after reperfused first anterior wall acute myocardial infarction.

The aim of the present study was to test the hypothesis that inadequate improvement in heart rate variability (HRV) in the healing stage of acute myocardial infarction (AMI) is associated with left ventricular (LV) remodeling. The study group comprised 20 patients (14 men, 6 women; mean age, 61+/-12 years) with a reperfused first anterior AMI (相似文献   

Left ventricular myocardial remodeling and contractile state in chronic aortic regurgitation

BACKGROUND: In chronic aortic regurgitation, eccentric hypertrophy, with combined concentric hypertrophy of the left ventricle, is an important adaptive response to volume overload, which in itself is a compensatory mechanism for permitting the ventricle to normalize its afterload and to maintain normal ejection performance (physiologic hypertrophy). However, progressive dilatation of the left ventricle leads to depressed left ventricular (LV) contractility and myocardial structural changes, including cellular hypertrophy and interstitial fibrosis (pathological hypertrophy). HYPOTHESIS: The study was undertaken to determine the relationship between left ventricular myocardial structure and contractile function in 14 patients with chronic aortic regurgitation by cardiac catheterization and endomyocardial biopsies. METHODS: Myocardial cell diameter and percent interstitial fibrosis were obtained from biopsy samples. Contractile function was evaluated from the ratio of end-systolic wall stress to end-systolic volume index (ESS/ESVI) and the ejection fraction-end-systolic stress (EF-ESS) relationship, which was obtained from 30 normal control subjects. RESULTS: Myocardial cell diameter correlated significantly with the ESVI (r = 0.72, p < 0.005), ejection fraction (r = -0.58, p < 0.05), and ESS/ESVI (r = -0.58, p < 0.05). The percent interstitial fibrosis also correlated inversely with ESS/ESVI (r = -0.71, p < 0.005). Compared with very few patients with an ESVI < 70 ml/m2, the majority of patients with ESVI > or = 70 ml/m2 had a cell diameter of > or = 30 microns and a percent interstitial fibrosis of > or = 10%. The nine patients who had depressed contractile function, as assessed from the EF-ESS relationship, had a higher percent interstitial fibrosis (p < 0.05) than five patients showing a normal EF-ESS relationship, despite the fact that there was no significant difference in myocardial cell diameter between them. Thus, advanced cellular hypertrophy and excessive interstitial fibrosis were significantly and independently associated with myocardial contractile dysfunction and appeared to be responsible for ventricular remodeling. CONCLUSION: Our findings suggest that in many patients with aortic regurgitation, eccentric hypertrophy changes its nature from physiologic to nonphysiologic during the earlier stages in the course of the disease rather than during the stage described previously.     

Left ventricular remodeling in patients with stress hyperglycemia after acute myocardial infarction

Background To investigate the association between left ventricular remodeling and stress hyperglycemia (SH) inpatients with acute anterior wall myocardial Infarction. Methods Patients with acute anterior myocardial infarction and a successful primary percutaneous coronary intervention (PCI) were enrolled and divided into two groups according to the presence or absence of SH. Patients with diabetes mellitus were excluded. Echocardiographic studies were performed on discharge and at 6 month follow-up. Left ventricular (LV) ejection fractions (EF), LV end-diastolic volume (EDV) and LV end-systolic volume (ESV) were obtained at baseline and at 6 month. Differences between changes of ESV (ΔESV) and changes of EDV (ΔEDV) in the two groups as well as EF improvement rate (ΔEF %) over six month were obtained. Correlation between SH and LV remodeling was investigated. Results (1) At baseline, the level of hemoglobin A1c was significantly higher in SH group (6.9±1.4 vs 6.2±0.8 P=0.04). Other baseline characteristics, including peak serum creatine kinase MB and LV function, were similar between two groups; (2) EF increased significantly over 6 months in both group with SH((41.1±7.2)% vs (52.7±8.4)%, P=0.02) and group without SH. ((43.6±8.7)% vs (54.5±9.3)%, P=0.03) (3) Only in SH group, EDV increased significantly at 6 month (139.6±26.7 vs 126.1±26.7 P=0.04); (4) There was a weak correlation between ΔEDV and the level of fasting plasma glucose on admission.(Pearson's r=0.35, P0.01). Conclusions (1) Previous glucose metabolism disorder is at least partially responsible for hyperglycemia on admission; (2) Given successful primary PCI within recommended time interval, left ventricular function improved regardless of whether SH is present or not; (3) The degree of glucose metabolic dysfunction on admission is weakly associated with the remodeling process in 6 months     

Left ventricular remodelling and brain natriuretic peptide after first myocardial infarction

OBJECTIVE—To investigate the relation between brain natriuretic peptide (BNP) concentrations and left ventricular remodelling characteristics after acute myocardial infarction.
DESIGN—Consecutive sample prospective cohort study.
SETTING—District general hospital coronary care unit in the north of England.
PATIENTS—133 initial survivors of a first myocardial infarction who received thrombolytic treatment.
INTERVENTIONS—Patients had transthoracic echocardiography and BNP concentrations measured at three to seven days (early) and two months (late).
MAIN OUTCOME MEASURES—Wall motion index  1.2, end systolic left ventricular volume index and mortality at one year.
RESULTS—Patients with an early wall motion index of  1.2 had higher early and late BNP concentrations (early BNP mean (SEM) 629 (76.2) pg/ml v 334 (20.8) pg/ml, p = 0.001 and late BNP 584 (79.5) pg/ml v 343 (25.0) pg/ml, p = 0.001). Patients with an increase in end systolic left ventricular volume index of > 10% also had higher early and late BNP concentrations (early BNP p = 0.034 and late BNP p = 0.001). Early BNP was significantly associated with one year mortality (p = 0.003).
CONCLUSIONS—Higher BNP concentrations early after first myocardial infarction are associated with adverse left ventricular remodelling characteristics. This may help explain why BNP is such a strong predictor of outcome after myocardial infarction.


Keywords: brain natriuretic peptide; wall motion index; left ventricular volume index; myocardial infarction