Prognostic implications of left ventricular diastolic dysfunction with preserved systolic function following acute myocardial infarction

The contribution of diastolic dysfunction in patients with preserved left ventricular (LV) systolic function to impaired functional status and cardiac mortality in myocardial infarction (MI) is unknown. In the present study, assessment of LV diastolic function was performed by Doppler analysis of the mitral and pulmonary venous flow, and the propagation velocity of early mitral flow by color M-mode Doppler echocardiography in 183 consecutive patients at day 5-7 following their first acute MI. Patients were classified into four groups: group A: preserved LV systolic and diastolic function (n = 73); group B: LV systolic dysfunction with preserved diastolic function (n = 10); group C: LV diastolic dysfunction with preserved systolic function (n = 60); group D: combined LV systolic and diastolic dysfunction (n = 40). The cardiac mortality rate at 1 year was significantly higher in groups C (13%) and D (38%) compared to A (2%) (p < 0.01). Multivariate regression analysis identified LV diastolic dysfunction (p = 0.001), Killip class >or=II (p = 0.006), and age (0.008) as predictors of cardiac death or readmission due to heart failure. The presence of LV diastolic dysfunction with preserved systolic dysfunction is associated with increased morbidity and mortality following acute MI.     

利用QTVI技术评价心肌梗死患者局部收缩功能

目的 :超声评价三支病变的心肌梗死患者局部收缩功能。方法 :超声测量 3 0例心肌梗死患者 (MI组 )和 3 0例正常人 (control组 )局部心肌各时相的峰值速度 (Sm 、Em、Am)、收缩期应变率峰值(SRS)、最大时间 速度积分 (TVImax)以及最大应力 (εmax)、二尖瓣最大下移距离 (D)。结果 :心肌梗死患者局部Sm、Em、Am 、TVImax、εmax、SRS 和D均较对照组明显下降。对照组应变率曲线较一致 ,而梗死组较杂乱。结论 :三支病变的心肌梗死患者局部收缩功能明显减低 ,其中TVImax和D是评价局部收缩功能的良好指标     

Induction of myocardial hypertrophy after coronary ligation in rats decreases ventricular dilatation and improves systolic function.

BACKGROUND. Previous studies have shown that hypertrophy of surviving myocytes after myocardial infarction (MI) is limited. Progressive ventricular dilatation after MI may occur when compensatory hypertrophy cannot restore left ventricular (LV) wall stress to normal. METHODS AND RESULTS. To test whether induction of additional myocyte hypertrophy might prevent pathological LV remodeling after large MI, we administered 2-tetradecylglycidic acid (TDGA) 20 mg/kg/day to sham-operated (n = 12) and MI (n = 10) rats for 10 days, beginning the third day after infarction. We have previously shown that chronic inhibition of long-chain fatty acid oxidation with TDGA in rats results in myocardial hypertrophy without any apparent impairment of LV systolic function. When compared with untreated MI rats (n = 9), we found that TDGA-treated MI rats had increases in LV weight/body wt, myocyte cross-sectional area, and peak developed LV pressure during abrupt aortic occlusion. MI rats treated with TDGA had lower LV end-diastolic pressures and smaller end-diastolic volumes, whereas stroke volume was maintained. The ex vivo passive LV pressure-volume relation was shifted toward the pressure axis compared with untreated infarct rats. In sham-operated rats, TDGA caused increases in LV weight/body wt, myocyte size, peak developed LV pressure, cardiac index, and stroke volume index, and a shift of the passive LV pressure-volume relation toward the pressure axis. CONCLUSIONS. Induction of myocardial hypertrophy with an inhibitor of long-chain fatty acid oxidation retarded the process of LV dilatation and produced beneficial effects on systolic function after large myocardial infarction. These data support the hypothesis that inadequate hypertrophy of residual myocardium after infarction may contribute to LV dilatation and the development of congestive heart failure.     

The atrioventricular plane displacement as a means of evaluating left ventricular systolic function in acute myocardial infarction.

Displacement of the atrioventricular (AV) plane toward the cardiac apex in systole was studied quantitatively by echocardiography in 37 patients with first-time acute myocardial infarction (MI) in order to evaluate left ventricular systolic function. The amplitude of AV plane displacement was recorded from the apex at four different sites corresponding to the septal, lateral, anterior, and posterior walls of the left ventricle from apical 4- and 2-chamber views. The patients had a decreased displacement of the AV plane compared with controls which was more pronounced at the sites of infarction. The mean value of the AV plane displacement (AV mean) correlated linearly with the left ventricular (LV) ejection fraction calculated by radionuclide angiography (r = 0.87, p less than 0.001, SEE = 6.2). An AV mean of 10 mm or more had a high sensitivity (95%) and specificity (82%) in defining a normal ejection fraction (greater than or equal to 50%). A high correlation coefficient was found between LV wall motion index and the AV plane displacement. Thus, in acute MI the LV function can be assessed noninvasively using AV plane displacement.     

Detection of abnormal left ventricular function by Doppler tissue imaging in patients with a first myocardial infarction and showing normal function assessed by conventional echocardiography.

AIMS: The aim of the study was to characterize left ventricular (LV) function by Doppler tissue imaging (DTI) after a first myocardial infarction (MI) where the conventional echo-Doppler parameters showed no abnormalities. METHODS: Out of 202 patients who were referred for an echocardiogram, 19 patients were previously healthy and had a normal ejection fraction and no wall motion abnormalities at echocardiogram. These 19 patients were compared with 16 age-matched healthy subjects (HS). The longitudinal LV function was assessed using the mitral annular velocities (mean value from four different sites of the LV) determined by DTI. RESULTS: The patients with MI had significantly reduced peak systolic and peak early diastolic mitral annular velocities compared to HS (8.6 v. 9.7 cm/s, P<0.001 for systolic velocity, and 10.9 v. 12.3 cm/s, P<0.01 for diastolic velocity, respectively). The patients had normal diastolic LV function assessed by the conventional Doppler echocardiogram (e.g. transmitral flow, IVRT and pulmonary venous flow patterns). To assess the LV filling pressure, the ratio of the transmitral early wave velocity assessed by conventional echo-Doppler and peak early diastolic mitral annular velocity determined by DTI (E/Edti) was used. The E/Edti was significantly higher in patients than in HS (7.0 v. 5.7, P<0.05). CONCLUSION: Previously healthy subjects who are suffering from a first MI and showing normal systolic and diastolic LV function, determined by conventional echo-Doppler methods, show decreased mitral annular systolic and diastolic velocities determined by DTI compared to healthy subjects. This is probably evidence of mild subendocardial damage due to MI that remains undetected by conventional echo-Doppler methods.     

Analysis of the left ventricular early diastolic function in old myocardial infarction by gated radionuclide angiography

In order to determine the validity of the left ventricular (LV) diastolic function for evaluation of ischemic heart disease, gated radionuclide angiography was performed in 37 patients with transmural myocardial infarction (MI) [18: anterior, 19: inferior infarction] and 10 normal control subjects. LV ejection fraction (LVEF) was decreased in patients with anterior MI but not in those with inferior MI. Time to peak filling rate was not significantly prolonged in both anterior MI and inferior MI. Filling fraction was apparently reduced only in anterior MI. However, peak filling rate (PFR) was significantly reduced even in inferior MI as well as in anterior MI. PFR correlated well with LVEF in normal control, anterior MI and inferior MI. In both anterior MI and inferior MI, their coefficients were smaller than in controls. The normal PFR always indicated normal LVEF, while normal LVEF was not necessarily indicative of normal PFR. Results indicated that LV diastolic function estimated by equilibrium radionuclide angiography might reflect more precisely LV dysfunction in old MI than LV systolic function. The reduction of LV diastolic function in old MI was more prominent than that of LV systolic function. Therefore, it may be deduced that evaluation of LV diastolic function is essential to the estimation of the degree of ischemic myocardial cell damage and the efficacy of drugs on ischemia-induced LV dysfunction.     

Longitudinal changes and prognostic implications of left ventricular diastolic function in first acute myocardial infarction

BACKGROUND: Left ventricular (LV) diastolic dysfunction contributes to signs and symptoms of clinical heart failure and may be related to prognosis in heart diseases. LV diastolic dysfunction is reported to be present in acute myocardial infarction (MI); however, little is known about the time course of changes in LV diastolic function and its relation to prognosis after acute MI. METHODS AND RESULTS: Two-dimensional and Doppler echocardiographic examinations were performed in 58 consecutive patients with first acute MI. The patients were studied serially within 1 hour and at days 5, 90, and 360 after arrival to the coronary care unit. LV diastolic function was assessed by Doppler measurements of transmitral and pulmonary venous flow. On the basis of mitral inflow, patients with MI were stratified at baseline to 3 LV diastolic filling patterns: normal, impaired relaxation, or pseudonormal/restrictive. Patients with MI were observed for development of congestive heart failure (Killip class >I) during hospitalization and for death during 1-year follow-up, and these complications were related to LV diastolic function. LV diastolic dysfunction was present in the very early phase of acute MI, with signs of impaired relaxation or restrictive LV filling dynamics in 38% and 24% of the patients, respectively, whereas 38% had normal LV filling characteristics. Impaired relaxation of the LV was most pronounced and found in 60% after 1-year follow-up. In-hospital congestive heart failure (Killip class >I) was found in 50% of the patients with initial impaired LV relaxation and in 71% of the patients with initially pseudonormal or restrictive LV filling dynamics, whereas patients with normal LV filling were free of heart failure. Patients with initial impaired relaxation and restrictive LV filling dynamics demonstrated a significant LV dilation during 1-year follow-up. Patients with initial pseudonormal/restrictive LV filling pattern were more frequently readmitted to the hospital for heart failure and had significant higher New York Heart Association class score compared with patients with normal or impaired relaxation during follow-up. Cardiac death was (n = 6) only observed in patients with pseudonormal or restrictive LV filling pattern. In a multivariate stepwise regression analysis, mitral E deceleration time 相似文献   

Significance of a mitral regurgitation systolic murmur complicating a first acute myocardial infarction in the coronary care unit--assessment by colour Doppler flow imaging.

To determine the prevalence and significance of a systolic mitral murmur heard after a first acute myocardial infarction (MI), we studied 186 consecutive patients in the coronary care unit (CCU) during a one-year period. Fifteen patients had a murmur as a result of mitral regurgitation (MR) (prevalence 8%) documented by colour Doppler flow imaging. It was heard before the third day of hospitalization in 10 (67%) patients, and on the third day itself in the remainder. The severity of MR was graded semi-quantitatively: moderate in 12 (80%) patients, and mild, moderate to severe and severe in three respectively. The direction of the MR jet, determined by colour flow imaging, improved the information obtained by two-dimensional echocardiography (2D echo) that could only diagnose mitral leaflet abnormality in seven (47%) patients. In 10 of 15 (67%) patients, the 2D echo ejection fraction was greater than or equal to 40% and in eight (53%) the wall motion score obtained by analysing 11 left ventricular (LV) segments was less than or equal to 8. Two (13%) patients died in the CCU, four (27%) had LV failure, one angina and eight (53%) remained asymptomatic in the hospital. Of 171 patients without a systolic murmur, 22 (13%) had LV failure, 13 (8%) angina and 25 (15%) died during the in-hospital stay (P-NS for these complications between patients with and without MR murmur). During a follow-up of 12-24 months, one MR patient died, and seven (47%) remained asymptomatic. We conclude that the prevalence of MR systolic murmurs in acute MI patients is low.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise-induced changes in mitral regurgitation in patients with prior myocardial infarction and left ventricular dysfunction: relation to mitral deformation and left ventricular function and shape.

AIMS: The aim of this study was to assess the relationship between exercise-induced changes in mitral regurgitation (MR) and echocardiographic characteristics of mitral deformation, global left ventricular (LV) function and shape at rest and after exercise. METHODS AND RESULTS: Forty consecutive patients with ischaemic MR due to prior myocardial infarction (MI), ejection fraction <45% in sinus rhythm underwent exercise-echocardiographic testing. Exercise-induced changes in effective regurgitant orifice (ERO) were compared with baseline and exercise-induced changes in mitral deformation and global LV function and shape. There was significant correlation between exercise-induced changes in ERO and changes in coaptation distance (r=0.80, P<0.0001), tenting area (r=0.79, P<0.0001) and mitral annular diameter (r=0.65, P<0.0001), as well as in end-systolic sphericity index (r=-0.50, P=0.001, respectively), and wall motion score index (r=0.44, P=0.004). In contrast, exercise-induced changes in ERO were not related to the echocardiographic features at rest. By stepwise multiple regression model, the exercise-induced changes in mitral deformation were found to independently correlate with exercise-induced changes in ERO (generalized r(2)=0.80, P<0.0001). CONCLUSION: Exercise-induced changes in severity of ischaemic MR in patients with LV dysfunction due to prior MI were independently related to changes in mitral deformation.     

Specific tissue Doppler predictors of preserved systolic and diastolic left ventricular function after an acute anterior myocardial infarction

The degree of left ventricular (LV) dysfunction determines the outcome of patients suffering an acute anterior myocardial infarction (AAMI). Many recent studies have utilized tissue Doppler echocardiography (TDE) parameters in the assessment of LV function. We sought to investigate whether some variables easily obtained from TDE profiles of mitral annulus corners would predict a relatively preserved LV global function traditionally assessed with ejection fraction (EF) and deceleration time (DT), within the acute phase of AAMI. Included were 50 consecutive patients with a first AAMI. Standard echocardiography and TDE of mitral annulus were performed within 36 hours of admission. Pulsed wave sample volumes were set at the septal, lateral, anterior, and inferior corners of the mitral annulus. Preserved LV function was defined as an EF > 40% together with a DT > or = 140 ms and < 220 ms. An inferior annular systolic velocity of > 7.5 cm/s predicts preserved global left ventricular function with a sensitivity of 81% and specificity of 71%. An anterior mitral annular early diastolic velocity of > 8cm/s had a sensitivity of 69% and specificity of 85%. When these two velocities both exceed the limits above, such a combined index yielded a sensitivity of 69%, specificity of 94%, and an overall diagnostic accuracy of 86% for the estimation of preserved LV global function. The parameters derived from TDE profiles of inferior and anterior mitral annulus comers provide valuable information to predict preserved global left ventricular function during the early period of AAMI.     

Role of nitrates after acute myocardial infarction.

Apart from their ability to relieve myocardial ischemia, nitrates have an important role to play on preservation of left ventricular (LV) geometry and function after acute myocardial infarction (MI). In the first 48 hours after acute MI, intravenous nitroglycerin infusion titrated to a low-dose regimen produces multiple benefits, including smaller infarct size, better regional and global LV function, less remodeling, fewer in-hospital complications, and fewer deaths in-hospital and up to 1 year. This regimen might be an effective adjunct during reperfusion therapy for salvaging ischemic myocardium, LV geometry, and function. Recent studies indicate that prolonged therapy with nitrates during the healing phase after acute MI can effectively further limit progressive LV remodeling (less LV dilation, expansion, thinning, and aneurysm formation) and preserve LV function. Tolerance with chronic therapy is avoided by an eccentric dose regimen to provide a nitrate-free interval.     

心肌梗死后室壁瘤形成伴严重二尖瓣返流对左室附壁血栓形成的影响

目的:探讨心肌梗死后室壁瘤形成伴严重二尖瓣返流对左室附壁血栓形成的影响。方法: 回顾性分析340例心肌梗死后室壁瘤形成患者的临床资料,根据是否并发严重二尖瓣返流分为严重二尖瓣返流组与非严重二尖瓣返流组,严重二尖瓣返流组84例,二尖瓣返流较轻或无返流256例,归为非严重二尖瓣返流组,比较两组左房直径、左室舒张末期直径、左室收缩末期直径、室间隔及左室后壁厚度、左室射血分数及左室附壁血栓发生率。结果: 分析结果显示,严重二尖瓣返流组的左室附壁血栓发生率明显低于非严重二尖瓣返流组(11% vs. 22%,P<0.05)。严重二尖瓣返流组的左房直径、左室舒张末期直径、左室收缩末期直径均大于非严重二尖瓣返流组（均P<0.01)。严重二尖瓣返流组的左室射血分数低于非严重二尖瓣返流组。左室舒张期室间隔厚度及后壁厚度两组无显著差异。结论: 心肌梗死后室壁瘤形成伴严重二尖瓣返流时可能有降低左室附壁血栓形成的作用。     

The relationship between renal function and cardiac structure, function, and prognosis after myocardial infarction: the VALIANT Echo Study.

OBJECTIVES: The purpose of this study was to determine whether alterations in cardiac structure or function contribute to the increased risk associated with renal impairment after myocardial infarction (MI). BACKGROUND: Renal impairment is associated with adverse cardiovascular outcomes after MI. METHODS: Echocardiography was performed on 603 patients with left ventricular (LV) dysfunction, heart failure (HF), or both after MI. Patients were grouped according to their estimated glomerular filtration rate (eGFR), and measures of cardiac structure and function were related to baseline eGFR. The relationship between eGFR and cardiac structure and function and clinical outcomes of death or HF was assessed with multivariable Cox regression. RESULTS: Ejection fraction, infarct segment length, right ventricular function, and mitral deceleration time were not influenced by renal function. Patients with reduced eGFR had smaller LV and larger left atrial (LA) volumes and higher left ventricular mass index (LVMI) and LV mass/LV volume ratio. A greater proportion of the patients with reduced eGFR had LV hypertrophy. The relationship between eGFR and the outcome of death or HF was attenuated by including baseline differences in LVMI, and both LVMI and LA volume conferred additional prognostic information in a multivariable model. CONCLUSIONS: Renal impairment was associated with smaller LV and larger LA volumes and increased LVMI. Systolic function was similar when compared with patients with normal renal function. Thus, reduced systolic function cannot account for worse outcomes in patients with renal impairment after MI. Indirect measures of diastolic function suggest that diastolic dysfunction might be an important mediator of increased risk in this population.     

Prognostic importance of systolic and diastolic function after acute myocardial infarction

Background Although risk stratification after acute myocardial infarction (AMI) often is focused on systolic left ventricular (LV) function, it appears that a more complete study of ventricular function including assessment of LV filling would be useful. Doppler echocardiography allows assessment of LV filling, and with the use of the Tei index (sum of isovolumic relaxation and contraction times divided by ejection time), a global estimate of ventricular function may be obtained. Therefore, the aim of this study was to determine the prognostic importance of LV systolic, diastolic, and overall LV function in a large consecutive population with AMI.Methods Echocardiography was performed within 6 days of AMI. LV systolic, diastolic, and global function was assessed by means of wall motion index (WMI), mitral flow pattern, and Tei index. The primary end point was all-cause death.Results Of 799 enrolled patients, 197 died during a median follow-up of 34 months. In a multivariate model including WMI and clinical parameters, WMI had important prognostic information. When mitral filling pattern and quartiles of Tei index were added to the model, restrictive filling (mitral deceleration time <140 ms) was associated with a risk ratio of 1.9 (95% CI 1.3-2.7, P < .0001, Tei index values of >0.68/0.56-0.68/0.46-0.55/<0.46 were associated with risks of 4.0 [2.1-6.9]/2.3 [1.5-3.9]/2.1 [1.2-3.6]/1.0, P < .001). In this model, WMI had no prognostic value (P = .18).Conclusions Mitral deceleration time and the Tei index have independent and important prognostic value after AMI. (Am Heart J 2003;145:147-153.)     

Long-term caspase inhibition ameliorates apoptosis, reduces myocardial troponin-I cleavage, protects left ventricular function, and attenuates remodeling in rats with myocardial infarction

OBJECTIVES: This study was designed to evaluate whether in vivo caspase inhibition can prevent myocardial contractile protein degradation, improve myocardial function, and attenuate ventricular remodeling. BACKGROUND: Apoptosis is thought to play an important role in the development and progression of heart failure (HF) after a myocardial infarction (MI). However, it is not known whether inhibiting apoptosis can attenuate left ventricular (LV) remodeling and minimize systolic dysfunction. METHOD: A 28-day infusion of caspase inhibitor (n = 12) or vehicle (n = 9) was administered to rats immediately after an anterior MI. In addition, five sham-operated rats given the caspase inhibitor were compared with 17 untreated sham-operated animals to study effects in non-MI rats. Left ventricular function, remodeling parameters, and hemodynamics were studied four weeks later. Myocardial caspase 3 activation and troponin-I contractile protein cleavage were studied in the non-infarct, remote LV myocardium using Western blots. Apoptosis was assessed using immunohistochemistry for activated caspase-positive cells as well as the TUNEL method. Collagen volume was estimated using morphometry. RESULTS: Caspase inhibition reduced myocardial caspase 3 activation. This was accompanied by less cleavage of troponin-I, an important component of the cardiac contractile apparatus, and fewer apoptotic cardiomyocytes. Furthermore, caspase inhibition reduced LV-weight-to-body-weight ratio, decreased myocardial interstitial collagen deposition, attenuated LV remodeling, and better preserved LV systolic function after MI. CONCLUSIONS: Caspase inhibition, started soon after MI and continued for four weeks, preserves myocardial contractile proteins, reduces systolic dysfunction, and attenuates ventricular remodeling. These findings may have important therapeutic implications in post-MI HF.     

辛伐他汀对家兔心肌梗死后心室重构及心功能的影响

目的研究辛伐他汀对家兔心肌梗死后(MI)心室重构及心功能的影响。方法家兔20只采用结扎冠状动脉左前降支的方法建立急性心肌梗死模型,随机分MI组(10只)和辛伐他汀组(10只)。MI组术后不给任何处理和干预,辛伐他汀干预组在MI术后3d口服辛伐他汀(10mg.kg-1.d-1)10周。术前和术后10周进行超声心动图检查。术后10周进行有创血液动力学测定,而后摘取心脏称重。取两组家兔左心室进行HE染色,做组织细胞学检查。结果10周后辛伐他汀组家兔左室重量、左室舒张期末径、左室收缩期末径、左房直径及左室舒张期末压显著低于MI组,射血分数、缩短分数明显高于MI组(P<0.05)。HE染色辛伐他汀组与MI组比较,心肌细胞变性坏死明显减轻,炎性细胞浸润减少,间质纤维化减轻,非梗死区心肌细胞的代偿性肥大增生较MI组为低。结论辛伐他汀能够改善心肌梗死后家兔心室重构和心功能。     

Relation of B-type natriuretic peptide early after acute myocardial infarction to left ventricular diastolic function and extent of myocardial damage determined by magnetic resonance imaging

Early after acute myocardial infarction, the relation between plasma B-type natriuretic peptide (BNP) and extent of myocardial scar formation and diastolic dysfunction remains unclear. In 32 consecutive patients early (5 +/- 3 days) after a first acute myocardial infarction, delayed contrast-enhanced magnetic resonance (MR) imaging was performed to define myocardial scar. Diastolic function was assessed using phase-contrast MR measurements of mitral flow and septal tissue velocities (tissue MR imaging) to estimate left ventricular (LV) filling pressures. MR study was immediately followed by BNP measurement. BNP related to LV ejection fraction (r = -0.52, p = 0.002), extent of myocardial scar (percent delayed hyperenhancement of LV mass, r = 0.49, p = 0.005; transmural index, r = 0.58, p <0.001), and estimated LV filling pressures (ratio of early diastolic mitral flow velocity to early diastolic mitral annular velocity, r = 0.51, p = 0.003). In multivariate analysis, transmural index and early diastolic mitral flow velocity/early diastolic mitral annular velocity were independent predictors of BNP levels (p <0.05, power of 0.99 at alpha = 0.05). In conclusion, among patients with recent myocardial infarction, high BNP levels are independently associated with extent of myocardial scar tissue and estimated LV filling pressures.     

The effect of the localization of Q wave myocardial infarction on ventricular electromechanics

BACKGROUND: The exact location of a Q wave myocardial infarction has an important effect on overall left ventricular function. OBJECTIVES: To assess the effect of localization of Q wave infarction on left ventricular minor and long axis function, with particular reference to electromechanical disturbances. METHODS: We studied 72 patients with Q wave myocardial infarction; 35 anterior, age 61+/-15 years and 37 inferior, age 62+/-12 years. ECG intervals were automatically measured by Hewlett-Packard Pagewriter and LV dimension and filling velocities studied by transthoracic echocardiography and simultaneous phonocardiogram. Findings were compared with 21 controls of similar age. RESULTS: Heart rate and all ECG intervals were similar in the two patient groups and controls. QRS axis was more to the left in patients with inferior MI. Normal septal q wave was absent in lead V5 and V6 in 33/35 (94%) patients with anterior MI and in only 3/37 (8%) with inferior MI, p<0.001. LV minor axis dimensions were enlarged vs. normal (p<0.001) in the two patient groups and to a greater extent in anterior MI compared with inferior MI, p<0.05. Isovolumic relaxation time was prolonged only in-patients with an inferior MI, p<0.01. Long axis amplitude was globally reduced (p<0.001) in the two patient groups as were shortening and lengthening velocities (p<0.001). The onset of septal long axis shortening with respect to the q wave was delayed by 30 and 40 ms in inferior MI and anterior MI and that of lengthening with respect to A2 by 20 and 30 ms, respectively, compared to normal (p<0.001 for both). Post ejection shortening was localized to the septal long axis in 32/35 patients with anterior MI but was generalized involving all three LV long axes in inferior MI, p<0.001. Transmitral Doppler flow velocities and the frequency of mild mitral regurgitation were similar in the two groups. CONCLUSION: These results confirm a close association between anterior Q wave infarction, septal incoordination and absent septal q waves. The global incoordinate long axis behaviour in inferior Q wave MI may be due to significant papillary muscle dysfunction, and results in significant shape change in early diastole. This disturbance in electromechanical behaviour might play an important role in the differing outcomes between the two different sites of myocardial infarction.     

Effects of long-term renal sympathetic denervation on heart failure after myocardial infarction in rats

The purpose of the present study was to investigate the effects of long-term renal denervation (RD) on heart failure due to myocardial infarction (MI). Wistar rats were anesthetized and the bilateral renal nerves were surgically denervated 2 days before MI was induced by coronary artery ligation. Four weeks later, left ventricular (LV) function and sodium excretion were determined. In MI rats, RD improved the reduced sodium excretion. MI + RD rats revealed lower LV end-diastolic pressure and greater maximum dP/dt as compared with those of MI+ innervation (INN) rats. LV end-diastolic and end-systolic dimensions were significantly smaller and LV fractional shortening was greater in MI + RD rats than in MI + INN rats (20.9% ± 3.2% vs 14.9% ± 3.0%). In rats without MI, RD did not affect either sodium excretion or LV function and dimensions. The present results suggest that the long-term RD reduces LV filling pressure and improves LV function after MI, probably due to a restoration of impaired natriuresis. Increased renal sympathetic nerve activity might contribute to the progression of heart failure after MI. Received: June 11, 2001 / Accepted: September 22, 2001     

Long-term captopril treatment improves diastolic filling more than systolic performance in rats with large myocardial infarction

Objectives. This study sought determine the effects of long-term angiotensin-converting enzyme (ACE) inhibition on left ventricular (LV) diastolic filling in postinfarction heart failure.Background. Long-term treatment with ACE inhibitors is beneficial in experimental animals and patients with heart failure. Because this treatment typically produces only small improvements in LV systolic function, we hypothesized that improvements in LV diastolic filling might contribute to the overall beneficial effects of ACE inhibitors after myocardial infarction (MI).Methods. We performed transthoracic echocardiographic-Doppler examinations in rats 1 and 6 weeks after transmural MI or sham operation. Rats with MI were randomized to no treatment (n = 10) or captopril (2 g/liter in drinking water, n = 8) after the baseline echocardiogram.Results. Six weeks after MI, untreated rats bad significant LV dilation compared with sham-operated rats (LV diastolic dimension [mean ± SEM] 10.7 ± 0.3 vs. 8.5 ± 0.3 mm, p < 0.05). Rats with untreated MI also had impaired fractional shortening (9 ± 1% vs. 34 ± 2%, p < 0.05) and depressed systolic thickening of the noninfarcted posterior wall (37 ± 3% vs. 65 ± 9%, p < 0.05). Rats with MI showed progressively restricted LV diastolic filling as assessed by transmitral Doppler recordings. At 6 weeks, peak early filling velocity (E) was increased (97 ± 3 vs. 77 ± 2 cm/s, p < 0.05), E wave deceleration was more rapid (23 ± 3 vs. 12 ± 1 m/s², p < 0.05), isovolumetric relaxation time was decreased (18 ± 1 vs. 24 ± 1 ms, p < 0.05), and late filling velocity was lower (26 ± 7 vs. 34 ± 1 cm/s, p < 0.05) in rats with MI versus sham-operated rats. Compared with rats with untreated MI, rats receiving captopril had similar LV diastolic dimensions (10.5 ± 0.35 vs. 10.7 ± 0.35 mm), slightly higher fractional shortening (16 ± 2% vs. 9 ± 1%, p < 0.05 [captopril MI vs. untreated MI]) and unchanged posterior wall thickening (49 ± 12% vs. 37 ± 3%, p = 0.3). In contrast, captopril almost completely normalized diastolic filling abnormalities (E velocity 82 ± 5 cm/s, p < 0.05 [captopril MI vs. untreated MI]; E wave deceleration rate 15 ± 2 m/s², p < 0.05 [captopril MI vs. untreated MI]; isovolumetric relaxation time 20 ± 1 ms).Conclusions. Long-term captopril treatment in rats with a large MI modestly limits LV remodeling and the development of systolic dysfunction but markedly improves the restrictive diastolic filling abnormalities that are seen in untreated rats.