Serial changes in left ventricular size after acute myocardial infarction.

The prognosis is poor for patients with left ventricular enlargement associated with large infarcts. We studied 78 patients using gated single-photon emission computed tomography (SPECT, to assess left ventricular volumes), right heart catheterization (to measure pulmonary wedge pressure and cardiac output), and conventional planar radionuclide ventriculography (to estimate ejection fraction), 2-6 days, 3-5 weeks, and 5-8 months after their first myocardial infarction. Patients were assigned to a large or small infarct-size group based on creatine kinase analysis. In 37 patients with large infarcts, left ventricular volume increased and was greater than 27% after 5-8 months than after 2-6 days (p less than 0.05). Although ejection fraction remained significantly depressed, stroke volume, which initially declined, was restored as a result of dilation and thus returned to normal by 3-5 weeks, indicating that enlargement of the left ventricle compensated for the loss of contractile myocardium and depression of global ejection fraction. The progressive nature of left ventricular dilation suggested that this process is of major pathophysiologic importance and that it plays an etiologic role in the genesis of heart failure and perhaps of sudden death following myocardial infarction. Dilation preceded hemodynamic deterioration, which became evident on exercise after 5-8 months in patients with large infarcts.     

Arrhythmias and left ventricular function after defibrillation during acute myocardial infarction in the intact dog

The purpose of this study was to assess the recovery of the left ventricular pressure (P_LV), and the incidence and type of arrhythmias after effective low-dose defibrillation (I_max = 18 ? 70 A) in healthy hearts and in hearts with acute myocardial infarction (AMI) in the intact dog. In fifteen dogs 84 episodes of fibrillation-defibrillation were studied in the healthy heart and 53 episodes were studied in the acute phase of myocardial infarction $\text{1}\text{2}$ to 3 hours after occlusion of a part of the left anterior descending artery by a catheter technique. Time to recovery of P_LV depended on duration of fibrillation (t_F) and cumulative defibrillation current ($\text{I}\text{1}\text{2}$), and became critical at t_F > 45 seconds and $\text{I}\text{1}\text{2}\text{> 45 A}$. Total duration of arrhythmias due to defibrillation increased with increasing t_F and $\text{I}\text{1}\text{2}$. Arrhythmias which have a relative greater chance of resulting in refibrillation or which may seriously decrease the cardiac output occurred more often with $\text{I}\text{1}\text{2}\text{> 55 A}$ (p < 0.001), when 50% of episodes were followed by these arrhythmias. No differences were found in responses between the healthy heart and the heart with AMI.     

Hemodynamic changes after experimental reduction of the left atrium.

Two experimental models were studied to determine the hemodynamic consequences of atrial volume reduction as observed after operative correction of transposition of the great arteries. The volume of the left atrium (LA) was reduced either by inflation of an intracavitary balloon (group A) or by surgical intervention (group B) to 50--60% of the control values as determined by angiography. The angiographic data correlated well with the true volumes obtained by water displacement. This major reduction of LA volume caused small but constant hemodynamic changes. Although the LA stroke volume decreased by 50% and the LA/LV volume relation was reduced by 50% (from 0.42 to 0.21), there was only a slight increase of pulmonary artery pressure (7% in group A and 14% in group B) and a slight decrease in cardiac index (13% in group A and 10% in group B) and in left ventricular end-diastolic pressure (9% in group A and 11% in group B). The reduction of atrial volume results in only minor functional alteration of the intact heart.     

Relationship between the changes in myocardial perfusion and left ventricular ejection fraction after acute myocardial infarction. Study with myocardial contrast echocardiography.

BACKGROUND AND OBJECTIVE: Myocardial contrast echocardiography has recently been proposed as a valid technique in the evaluation of myocardial perfusion after myocardial infarction. The objective of this study was to evaluate the relation between changes in myocardial perfusion assessed by myocardial contrast echocardiography and left ventricular ejection fraction after myocardial infarction. PATIENTS AND METHODS: We prospectively studied 17 patients with acute myocardial infarction, on whom two echocardiographic studies were performed, at 48-72 hours and at 6 months. Left ventricular ejection fraction and myocardial perfusion were evaluated with myocardial contrast echocardiography (Multiple-Frame Triggering and Harmonic Angio). Basal, medial and distal segments of the interventricular septum (anterior location infarction) and inferior wall (inferior infarction) were assessed. Myocardial perfusion was classified semi-quantitatively as grade 0, 1 or 2 (absent, heterogeneous or homogeneous opacification, respectively), giving a perfusion score. RESULTS: Left ventricular ejection fraction improved in 9 patients (53%), the proportion of grade 0 segments decreasing by 11 +/- 17%; by contrast, this proportion increased by 9 +/- 13% in patients with no improvement in ejection fraction (p = 0.028). Additionally, a significant correlation was observed between changes in ejection fraction and both perfusion score (r = 0.625; p = 0.007) and the proportion of grade 2 segments (r = 0.649; p = 0.005). CONCLUSION: After myocardial infarction, there is a significant relation between changes in left ventricular ejection fraction and myocardial perfusion assessed by myocardial contrast echocardiography with i.v. agents.     

心肌梗死后心房结构重构的实验研究

心房颤动（房颤）是心肌梗死病程中较为常见的并发症，文献报道其发生率为7％～20％。越来越多的证据表明心房缝隙连接通道的改变在房性心律失常的发生中起重要作用，有研究发现缝隙连接蛋白40（connexin 40，Cx40）敲除小鼠的房性心动过速的易患性增加，提示心房Cx40的改变可能有助于房性心律失常的发生。本研究的目的是观察慢性心肌梗死后心房结构的改变，尤其是Cx40的空间分布和基因表达的变化，以阐明房颤发生的可能基质。     

Acute changes of global and regional left ventricular function immediately after direct myocardial revascularization.

Direct myocardial revascularization (DMR) has been proposed to treat patients with severe coronary artery disease who are not amenable for classical revascularization techniques such as percutaneous coronary intervention (PCI) or bypass surgery (CABG). Although recent reports suggest its benefit in alleviating patients' complaints in the long term, there is still a paucity of data on the immediate impact on regional and global myocardial functioning following this treatment. In this overview we discuss our own experience and provide a summary of other data currently available.     

Hemodynamic complications of ventricular septal rupture after acute myocardial infarction.

Ventricular septal rupture (VSR) is a rare but serious complication following acute myocardial infarction (MI). Patients may present with a new murmur associated with a thrill. Right heart catheterization will demonstrate elevated right atrial and pulmonary artery pressures as well as an oxygen step-up at the right ventricular level. Patients with a right ventricular infarction or cardiogenic shock and a ventricular septal rupture have high in-hospital mortality rates. Prompt diagnosis followed by surgical repair is essential for patients with VSR following MI.     

Relationship between changes in left ventricular bipolar electrograms and regional myocardial blood flow during acute coronary artery occlusion in the dog.

The purpose of this study was to determine whether a quantitative relationship existed between a reduction in regional myocardial blood flow, measured by radiolabeled microspheres, and the degree and type of changes in myocardial activation recorded in bipolar left ventricular subepicardial and subendocardial electrograms, in open-chest dogs following acute coronary artery occlusion. We found that the degree of regional myocardial ischemia was related quantitatively to the reduction in amplitude recorded with bipolar electrograms in the subepicardium and subendocardium, and to the increase in duration of subepicardial electrograms. Other characteristics measured in electrograms did not relate to the degree of ischemia. Despite a comparable reduction in regional myocardial blood flow, subepicardial conduction delay exceeded that recorded in the subendocardium, which often exhibited accelerated conduction.     

Infarct artery perfusion and changes in left ventricular volume in the month after acute myocardial infarction

The relation between perfusion of the infarct-related artery and changes in left ventricular volume and function during the month after a first myocardial infarction was examined in 40 patients who did not receive thrombolytic therapy. Infarct artery perfusion was documented at predischarge coronary angiography, and left ventricular volume was measured by nongeometric analysis of radionuclide angiograms performed within 48 hours of infarction and at 1 month. Left ventricular dilation (greater than or equal to 20% increase in volume) developed in 16 patients, whereas 5 patients had a decrease in left ventricular volume of greater than or equal to 20% by 1 month. Left ventricular dilation occurred in all 14 patients without perfusion of the infarct-related artery, compared with only 2 of 26 patients with perfusion of this artery due to subtotal occlusion or collateral vessels. All five patients whose left ventricular volume decreased by greater than or equal to 20% had a perfused infarct artery. Multiple linear regression analysis confirmed that the degree of perfusion of the infarct artery (partial r = 0.58, p = 0.001) was a more important predictor of volume change than was infarct size measured by peak creatine kinase (partial r = 0.30, p = 0.009) or QRS score (partial r = 0.20, p = 0.087). Left ventricular ejection fraction decreased from 0.38 +/- 0.10 to 0.30 +/- 0.16 (p = 0.05) in 11 patients with an anterior infarct and ventricular dilation; it increased from 0.45 +/- 0.10 to 0.62 +/- 0.07 (p = 0.02) in the 5 patients with a greater than or equal to 20% decrease in volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early and late changes in left ventricular filling after acute myocardial infarction and the effect of infarct size.

To characterize the early (1 week) and late (6 weeks) changes in left ventricular (LV) filling pattern associated with acute myocardial infarction (AMI) 45 patients (mean age 65 +/- 2 years) were studied by Doppler echocardiography. Based on clinical criteria, patients were divided into those with large (group L; n = 12) and those with small (group S; n = 33) infarcts and then compared with 16 age-matched control subjects. The following parameters were calculated from the mitral velocity waveform: (1) peak early and peak atrial velocities and their integrals; (2) peak early to atrial velocity ratio and velocity integral ratio; and (3) the pressure half-time of the early wave. One week after AMI, group L showed a decreased atrial and increased early velocity, velocity ratio and integral ratio, whereas the pressure half-time of the early wave was shorter than that in group S and in control subjects. At 6 weeks group L showed a reduction in early velocity, early to atrial velocity ratio and integral ratio, whereas pressure half-time increased. When groups S and L were combined there was a good inverse correlation between pressure half-time and infarct size as measured by peak enzyme release (r = -0.64, p < 0.001). These data suggest that, depending on infarct size, patients exhibit a "restrictive" filling pattern early after the acute event. This is manifested by the greater proportion of filling occurring in early diastole, reflecting an overall increase in chamber stiffness. At 6 weeks, this pattern is less pronounced presumably due to the remodeling process.     

Hemodynamic changes in patients with myocardial infarct complicated by acute left ventricular failure during combined nitroglycerin and dobutamine therapy

A total of 18 patients with acute myocardial infarction complicated by acute left ventricular failure were examined for their central hemodynamics. Intravenous nitroglycerin was shown to cause positive changes in central hemodynamic parameters, but it failed to normalize the hemodynamics in patients with baseline low blood pressure, as nitroglycerin induced a further reduction in blood pressure. A combined administration of nitroglycerin and dobutamine solutions contributes to hemodynamic normalization and is indicated for patients with acute myocardial infarction complicated by acute left ventricular failure at a baseline low blood pressure.     

Early sequential changes in left ventricular dimensions and filling pressure in patients after myocardial infarction

Early consecutive changes in pulmonary arterial end-diastolic pressure (PAEDP) and echocardlographic left ventricular dimensions were measured in 14 patients within the first 8 days after acute myocardial infarction. Left ventricular volumes were estimated from echocardiographic left ventricular dimensions. Left ventricular compliance was assessed by three formulas, $\text{ΔV}\text{ΔP}$, ΔV/ESV/ΔP and $\text{LVID}{}_{\mathrm{d}}\text{PAEDP}$, where AV = echocardiographic stroke volume, ΔP = a derived left ventricular diastolic pressure change from the lowest level of early diastolic to the end-diastolic pressure, ESV = left ventricular end-systolic volume, and LVID_d = echocardiographic left ventricular end-diastolic dimension. To compare pressure, dimension and compliance values, linear relations were assumed between values for left ventricular end-diastolic volume, end-systolic volume, pulmonary arterial end-diastolic pressure and the day after infarction. The estimated third day values for the variables obtained from these linear relations were used so that each patient's values would contribute equal weight to the statistical analysis.The estimated third day compliance values from each formula correlated highly with one another (r = 0.69 ? 0.82). Neither $\text{ΔV}\text{ΔP}$ nor ΔV/ESV/ΔP had a significant correlation with LVID_d. Echocardiographic end-diastolic volume correlated with both end-systolic volume (r = 0.89) and echocardiographic stroke volume (r = 0.62) but not with pulmonary arterial end-diastolic pressure. When the first and last measurements for each patient are used, large changes in pulmonary arterial end-diastolic pressure associated with no or small alterations in echocardiographic left ventricular end-diastolic dimension in 12 patients imply acute changes in ventricular compliance. Sequential compliance values ($\text{ΔV}\text{ΔP}$) increased in seven survivors and decreased in one. $\text{ΔV}\text{ΔP}$ decreased in the five patients who died or had electrocardiographic evidence of extension of infarction. Early sequential changes in filling pressure, echocardiographic dimensions, and left ventricular compliance had a close correlation with the clinical course of the patients in our series and these data may assist in the management of patients with hemodynamic instability after acute myocardial infarction.