Transmural Anterior Myocardial Infarction Research Articles

Body Surface Potential Mapping during Atrial Depolarization in Rats with Post-Infarction Chronic Heart Failure against the Background of Fabomotizole Therapy.

Cardiac remodeling in rats with post-infarction chronic heart failure caused by anterior transmural myocardial infarction leads to an atypical location of areas of positive and negative cardioelectric potentials on the body surface before the onset of the PII-wave on the ECG in the limb leads, which is a sign of increased heterogeneity of atrial depolarization associated with the appearance of additional excitation focus in the left atrium. A course of therapy with fabomotizole leads to a decrease in the heterogeneity of atrial depolarization at the initial stages of the formation of the cardioelectric field of the atria on the body surface before the onset of the PII-wave, thereby producing an antiarrhythmic effect.

Correlation of the Left Ventricular Systolic Dysfunction and Ventricular Depolarization in a Post-Infarction Model of Chronic Heart Failure.

The body surface potential mapping of the heart during the period of ventricular depolarization and the inotropic function of the ventricles were studied in rats under conditions of a translational model of post-infarction chronic heart failure developed by us. We revealed a statistically significant (p<0.001) correlation between the left-ventricular ejection fraction and the values of the maximum positive and negative extrema of the cardioelectric field on the body surface of rats with post-infarction chronic heart failure caused by anterior transmural myocardial infarction. The calculated linear regression equations have high predictive efficiency, which makes it possible to use the amplitude characteristics of the heart cardioelectric field as a marker of the development of chronic heart failure.

Choice of Tactics for Experimental Therapy of Chronic Heart Failure with ALM-802 Compound.

The cardioprotective activity of ALM-802 compound was demonstrated in model experiments simulating postinfarction chronic heart failure in rats forming in 90 days after anterior transmural myocardial infarction. ALM-802 decreased the left ventricle and improved its inotropic function (p=0.038). This effect was observed in case of systematic administration of ALM-802 over 28 days (starting from day 91 after infarction modeling). This is apparently the minimum time for the cardioprotective effect of ALM-802 to prevent or treat the resulting heart failure, because short-term systematic therapy (15 days) produced no positive effect.

Выбор тактики экспериментальной терапии хронической сердечной недостаточности соединением АЛМ-802

The cardioprotective activity of ALM-802 compound was demonstrated in model experiments simulating postinfarction chronic heart failure in rats forming in 90 days after anterior transmural myocardial infarction. ALM-802 decreased the left ventricle and improved its inotropic function (p=0.038). This effect was observed in case of systematic administration of ALM-802 over 28 days (starting from day 91 after infarction modeling). This is apparently the minimum time for the cardioprotective effect of ALM-802 to prevent or treat the resulting heart failure, because short-term systematic therapy (15 days) produced no positive effect.

372 Left Ventricular Sphericity Index is a Predictor of Cardiovascular Events in Patients With Anterior Transmural Myocardial Infarction but not in Takotsubo Syndrome

Left ventricular sphericity index (LVSI) is a simple measure to evaluate changes in left ventricular (LV) geometry. The aim of our study was to evaluate the prognostic role of LVSI in patients with Takotsubo Syndrome (TS) and Anterior Myocardial Infarction (AMI). Consecutive patients with TS admitted to our institution in the period of Jan 2013 to Dec 2018 were evaluated (n=66). Patients with complete two-dimensional transthoracic echocardiograms were included in analysis (n=49) and matched with a cohort of AMI (n=50). Appraisal of demographic, clinical and echocardiographic parameters of patients was undertaken, and patients were followed for the composite outcome of cardiovascular death, heart failure and arrhythmia. Biplane SI was calculated as an average of the short- and long-axis length in the 4- and 2-chamber apical views. TS patients (64.3±13.7 years, 92% female) were followed for a median of 25.6 months, with a total of 9 patients reaching a primary outcome. LVSI was not predictive of cardiovascular outcomes for patients with TS (p=0.34). Patients with anterior STEMI (62.10±12.84 years, 73% male) were followed up for a median of 29.06 months with 9 patients reaching a primary outcome. In the AMI group, there was a significant association between LVSI and composite primary outcomes (p=0.04). LVSI is reflective of geometric changes in the left ventricle and is associated with adverse cardiovascular outcomes in patients with AMI but not TS (likely secondary to the reversible nature of TS). LVSI may be an important prognostication tool for patients with AMI.

A Translational Model of Chronic Heart Failure.

We created a translational model of chronic heart failure in rats that developed in 3 months after reproducing experimental anterior transmural myocardial infarction. The model simulated the basic clinicodiagnostic criteria of this disease: impaired contractility and dilatation of heart ventricles, signs of venous congestion, elevated plasma content of biochemical markers, and abnormal overexpression of AT1aR and β-adrenoceptors.

MicroRNA-214 exerts a Cardio-protective effect by inhibition of fibrosis.

The miRNAs play important roles in regulating myocardial fibrosis. The purpose of this study was to determine the potential roles of microRNA-214 (miR-214) in cardiac fibrosis in vitro and in vivo. In vitro experiment, Ang II-induced cardiac fibroblasts (CFBs) are transfected with pre-miR-214, anti-miR-214 and their oligo controls. Gene expression was checked by Quantitative realtime-PCR (qRT-PCR) and western blotting. In the present experiment, compared with controls, expressions of collagen type I (COL I), collagen type III (COL III), transforming growth factor (TGF)-β1, and tissue inhibitors of metalloproteinase (TIMP)-1 were all increased, but matrix metalloproteinase (MMP)-1 was reduced in CFB by Ang II treatment at both mRNA and protein levels, and these alterations were found reversed by miR-214 transfection. In vivo, an anterior transmural acute myocardial infarction (AMI) was created by occlusion of the left anterior descending coronary artery after Ad-pre-miR-214, Ad-anti-miR-214 or Ad-GFP was delivered separately. Four weeks after AMI, protein contents of COL I, COL III and TGF-β1 in tissue from border area were found increased after AMI, but impaired by overexpression of miR-214. While the expression of MMP-1 was increased by miR-214 stimulation but decreased by miR-214 inhibition. These results suggested that miR-214 exerts cardio-protective effects by inhibition of fibrosis and the inhibitory effect involves TGF-β1 suppression and MMP-1/TIMP-1 regulation. Anat Rec, 299:1348-1357, 2016. © 2016 Wiley Periodicals, Inc.

BLOOD LEVEL OF COLLAGEN BIOMARKERS AND SULFATED GLYCOSAMINOGLYCANS IN ACUTE TRANSMURAL MYOCARDIAL INFARCTION

Aim. To study dynamics of blood levels of carboxyterminal propeptide of I type procollagen (PICP), carboxyterminal telopeptide of type I collagen (CITP) and sulfated glycosaminoglycans (sGAG) in the dynamics, in patients with transmural transmural myocardial infarction (MI) complicated with aneurysm. Material and methods. Totally, 46 patients included with acute transmural anterior MI, who underwent the assessment of PICP, CITP and sGAG in dynamics. Results. On the 1st to 3rd days of MI without aneurysm there was increase of PICP up to 61,4 ng/mL, on 10-12th and 18-22nd days its level did not change significantly, remaining high. In aneurysm MI the level of PICP increased just from the 10-12th days and in lower grade — comparing to patients without aneurysm. Level of CITP in patients without aneurysm was comparable to controls during the entire study. Level of sGAG in non-aneurysm patients increased from 10-12th days, and in MI with aneurysm — did not differ from healthy persons during the entire study. Conclusion. Increase of CITP and lower PICP and sGAG in MI patients with aneurysm witnesses’ probable predominance of degradation processes of connective tissue over its synthesis.

THE VALUES OF MATRIX METALLOPROTEASE-9 AND TISSUE METALLOPROTEASE INHIBITOR-1 IN ACUTE MYOCARDIAL INFARCTION WITH ANEURYSM FORMATION

Aim. To study the blood levels of MMP-9 and TIMP-1 in dynamic in patients with acute transmural anterior myocardial infarction complicated by aneurysm. Material and methods. 46 patients with acute transmural anterior myocardial infarction were included into the study. The blood levels of MMP-9 and TIMP-1 were studied. Results. In 1-3 days the patients with myocardial infarction without aneurysm had a significant increase in MMP- 9 up to 229,8 ng/ml, then to 10-12th days a decrease and then increase again up to 237,3 ng/ml by 18-22th days. In patients with myocardial infarction complicated by an aneurysm at 1-3rd and 10-12th days the level of MMP-9 increased slightly, and only at 18-22th days we observed significant increases of MMP-9 up to 159,2 ng/ml. In patients with myocardial infarction without aneurysm the level of TIMP-1 gradually grew up from 1-3rd days (698,9 ng/ml) to 18-22th days (942,3 ng/ml). In patients with myocardial infarction complicated by an aneurysm at 1-3rd and 10-12th days we observed maximum values of TIMP-1, gradually decreased to 18-22th days. Conclusion. The changes found in MMP-9 and TIMP-1 levels might indicate a delay of reparation processes in patients with myocardial infarction complicated by an aneurysm.

Post myocardial infarction left ventricular dysfunction – Assessment and follow up of patients undergoing surgical ventricular restoration by the endoventricular patchplasty

Authors of this important article by D'Mello et al, have nicely presented a prospective study of clinical and echocardiographic follow up of Left Ventricular (LV) geometry of 59 consecutive patients with previous transmural anterior myocardial infarction, who underwent LV restoration, analyzed between June 2007 and May 2008.1 The authors are to be complemented for this important series which showed excellent immediate and short-term results following LV restoration surgery. The results show a progressive remodeling after ventricular reconstruction mainly by excluding the scar area. Volume reduction is more important than the post surgical shape of the ventricle. The study was done before the MRI era; and hence the images of the scar are not demonstrated in the study.2,3 Analysis of the precise mechanism of remodeling is perhaps not possible without MRI. Distinction between dyskinetic and akinetic forms of the scar are not clearly brought out; it is usually transmural with dyskinesia and subendocardial with akinesia. The size of a synergy and its extension determine the extent of remodeling.4,5 It is surprising that these 59 patients were not severe cases of ischemic failing ventricle, as the mean ejection fraction was 33.5 ± 5%, preoperative end diastolic volume index 89.7 ± 6 and end systolic volume index 48.8 ± 11.3 which are below the threshold of very severe cardiac failure. White et al have given a figure of >60 ml of end systolic volume index as the major determinant of survival after recovery from myocardial infarction.6 This work is indeed of great interest and I hope the authors with their experience will present more severe cases showing a positive interest in LV reconstruction and thereby demonstrating that the S.T.I.C.H trial was a miss organized trial.7 The global approach of heart failure by Buckberg cannot be accepted; it is apparent that Buckberg is a prisoner of his “flying fancies” trying to establish something without any serious base.7 The myocardial systolic contraction is a “twist up” like a “snake” ascension. The crux of the problem of systolic heart failure is the ventricular spherical dilatation whatever be the anatomic substrate. The surgical ventricular restoration (S.V.R) or surgical anterior ventricular restoration (S.A.V.R) are acronyms in place of left ventricular reconstruction (L.V.R.) because this technique is applied most of time only for anterior LV wall, with the objective of “volume reduction” and to get an elliptical shape of LV. Finally, I would like to emphasize the following points: Ventricular wall has a systolic concentric (centripetal contraction) confirmed by MRI video examination of left ventricular wall in 4 projections.8 Heart failure is not an entity but a syndrome with various causes; in post myocardial infarction failure, the cause is an extension of the necrotic, then fibrous and finally calcified transmural or subendocardial scar, when it reaches = or <30% of LV perimeter. The dilatation is not the cause, but the consequence; dilatation is more ovoid than spherical. LVR as proposed by as in 1984, have these main goals: to suppress or exclude the scarred asynergic wall, to abolish the mechanism of progressive dilatation i.e. the eccentric systolic motion, restoring the curvature of non-infarcted myocardium and maintain the physiological diastolic volume of the rebuilt cavity by balloon sizing before “clothing” of the cavity by a patch anchored on contractile edge of normal myocardium.9 In conclusion, this article by D'Mello et al demonstrates and emphasizes the modern approach toward post myocardial infarction heart failure which is a very prevalent disease encountered in day to day clinical practice.

Section 10: Surgical Approaches to the Treatment of Heart Failure

Section 10: Surgical Approaches to the Treatment of Heart Failure

Correlation between infarct-related coronary artery patency and predischarge electrocardiographic patterns in patients with first anterior myocardial infarction who received thrombolytic therapy.

The aim of this study was to investigate the correlation between the ST-segment and T-wave patterns in predischarge electrocardiogram and patency of left anterior descending coronary artery in patients with a first anterior myocardial infarction (AMI). One hundred and fifty-six of 175 consecutive patients who were admitted to our clinic between January 2000 and September 2002 due to a first episode of transmural AMI and who received thrombolytic therapy were enrolled. Coronary angiography was performed by the Judkins method on the 6th-10th day after the acute infarction. The corrected TIMI frame count (CTFC) was estimated according to the previously described method. According to the combination of the ST-segment and T-wave morphology on the day (6-10) of cardiac catheterization, patients were classified into four groups: group A, ST elevation <<0.1 mV and negative T waves; group B, ST elevation >or=0.1 mV and negative T waves; group C, ST elevation <<0.1 mV and positive T waves; and group D, ST elevation >or=0.1 mV and positive T waves. Of the 99 patients with negative T waves, 47 (48%) had CTFC <or=27, 32 (32%) CTFC between 27 and 40, 15 (15%) CTFC >or=40-100, and 5 (5%) CTFC >>100. Of the 57 patients with positive T waves, CTFC was <or=27 in 14 (25%), between 27 and 40 in 17 (30%), >or=40-100 in 11 (19%), and >>100 in 15 (26%) ( P << 0.001). From the 76 patients with an isoelectric ST segment, 38 (50%) had CTFC <or=27, 29 (38%) CTFC between 27 and 40, 8 (11%) CTFC >or=40-100, and 1 (1%) CTFC >>100. Of the 80 patients with an elevated ST segment, 23 (29%) had CTFC <or=27, 20 (25%) CTFC between 27 and 40, 18 (23%) CTFC >or=40-100, and 19 (23%) CTFC >>100 ( P << 0.001). Use of the combination of two electrocardiographic parameters (ST segment and T waves) also indicated that there were significant differences between groups A and D, and groups B and D ( P << 0.001 and P << 0.05, respectively). Development of an isoelectric ST segment with negative T waves may indicate a better degree of reperfusion after AMI. In contrast, patients in whom ST-segment elevation and positive T waves remain at discharge from the coronary care unit have a higher probability of a nonpatent left anterior descending artery.

Myocardial Replacement Therapy

Case Presentation: A 56-year-old farmer who experienced a transmural anterior myocardial infarction (MI) 3 years ago was referred for evaluation of progressive dyspnea and fatigue. During the acute phase of MI, he was treated with fibrinolysis, as primary angioplasty was not available at his local hospital. Angiography performed 3 months after MI revealed occlusion of the left anterior descending artery with diffuse changes distal to the occluded segment. An attempt at percutaneous recanalization had failed. Despite treatment with β-blockers and angiotensin-converting enzyme inhibitors, serial echocardiograms performed by his local cardiologist had shown a large dyskinetic area and subsequently progressive dilatation and remodeling of the left ventricle. The patient is currently presenting with New York Heart Association class III symptoms and a history of several recent episodes of pulmonary edema. The development of postinfarction congestive heart failure in survivors of the acute phase of MI is related to myocardial cell loss in the area supplied by the infarct-related artery and the subsequent formation of a scar. As the most important strategies during the acute phase of MI, primary angioplasty and fibrinolysis are aimed at the restoration of blood flow to minimize necrosis. In addition, late revascularization procedures may enable recovery of contractility, but only in areas of the hibernating myocardium that contain a minimal number of viable, reversibly injured myocytes. In patients with a large myocardial necrotic area resulting from acute MI, and especially when the necrotic zone is weakly supplied by collaterals, the loss of cardiomyocytes results in the formation of fibrous tissue and, subsequently, in left ventricular remodeling, aneurysm formation, and progression of congestive heart failure. In some patients, cardiac transplantation may be an option, but because of the shortage of organs, its practical use is limited to end-stage heart failure cases. Stem cell implants have been discovered to …

An Experimental Model of Coronary Anastomosis without Suturing

Objective The aim of the study is to explore the feasibility and mid-term patency of an easier anastomotic technique for Minimally Invasive Direct Coronary Bypass Grafting (MIDCAB). Methods Eight mongrel dogs (±15 kg) underwent direct anastomosis between the left internal thoracic artery (LITA) and the left anterior descending coronary artery (LAD) via inferior sternotomy on the beating heart. After positioning the graft, the distal part of the LAD was opened to allow retrograde filling of the LITA-graft. The anastomosis was secured by the use of biological glue (BtoGlue, Cryolife, Marietta, GA, USA). No intravascular suture material was used. Ischemic time averaged 6 min. The proximal LAD was occluded upstream the arteriotomy. All survivors were angiographically controlled for patency after 6–8 weeks. Consequently, four dogs were sacrificed after 6 weeks and the remaining after 3 months for anatomo-pathological and histological examination by light and electron microscopy of the anastomotic site. Results All procedures were successful except for one animal that died of uncontrollable bleeding at the anastomotic site. Another sustained post-operative transmural anterior myocardial infarction due to a late graft occlusion. All angiographically controlled grafts were patent with two vascular strings near the anastomotic site. Histology showed early macrophage infiltration into the glue. At post-mortem examination, new endothelialization was noticed in 80% of the cases. However, ultrastructural examination detected marked differences in endothelial fibroblastic lining compared to normal histology. Conclusions Good mid-term permeability of the LITA grafts was observed in this new anastomotic technique for MIDCAB in the canine model. Although neo-endothelialization was present in most cases, ultrastructural differences were noticed after 3 months in the neointima compared to normal.

An experimental model of coronary anastomosis without suturing

Objective: The aim of the study is to explore the feasibility and mid-term patency of an easier anastomotic technique for Minimally Invasive Direct Coronary Bypass Grafting (MIDCAB). Methods: Eight mongrel dogs (±15 kg) underwent direct anastomosis between the left internal thoracic artery (LITA) and the left anterior descending coronary artery (LAD) via inferior sternotomy on the beating heart. After positioning the graft, the distal part of the LAD was opened to allow retrograde filling of the LITA-graft. The anastomosis was secured by the use of biological glue (BioGlue, Cryolife, Marietta, GA, USA). No intravascular suture material was used. Ischemic time averaged 6 min. The proximal LAD was occluded upstream the arteriotomy. All survivors were angiographically controlled for patency after 6–8 weeks. Consequently, four dogs were sacrificed after 6 weeks and the remaining after 3 months for anatomo-pathological and histological examination by light and electron microscopy of the anastomotic site. Results: All procedures were successful except for one animal that died of uncontrollable bleeding at the anastomotic site. Another sustained post-operative transmural anterior myocardial infarction due to a late graft occlusion. All angiographically controlled grafts were patent with two vascular strings near the anastomotic site. Histology showed early macrophage infiltration into the glue. At post-mortem examination, new endothelialization was noticed in 80% of the cases. However, ultrastructural examination detected marked differences in endothelial fibroblastic lining compared to normal histology. Conclusions: Good mid-term permeability of the LITA grafts was observed in this new anastomotic technique for MIDCAB in the canine model. Although neo-endothelialization was present in most cases, ultrastructural differences were noticed after 3 months in the neo-intima compared to normal.

Ischemic mitral regurgitation: intraventricular papillary muscle imbrication without mitral ring during left ventricular restoration.

Functional mitral regurgitation in ischemic cardiomyopathy carries a poor prognosis, and its surgical management remains problematic and controversial. The aim of this study was to report the results of our surgical approach to patients who have had myocardial infarctions and have ventricular dilatation, mitral regurgitation, reduced pump function, pulmonary hypertension and coronary artery disease. This surgical approach consists of endoventricular mitral repair without prosthetic ring, ventricular reconstruction with or without patch, and coronary artery bypass grafting. Forty-six patients (aged 64 +/- 10 years) with previous anterior transmural myocardial infarction and mitral regurgitation comprised the study group. Indication for surgery was heart failure in 93% of cases; 25 patients were in New York Heart Association functional class IV and 17 were in class III. Mitral regurgitation was moderate to severe in 32 cases (69%). All patients underwent coronary artery bypass grafting, with a mean of 3.2 +/- 1.3 grafts. Associated aortic valve replacement was performed in 4 cases. Global operative mortality rate was 15.2%. End-diastolic and end-systolic volumes significantly decreased after surgery (from 140 +/- 40 to 98 +/- 36 mL/m(2) and from 98 +/- 32 to 63 +/- 22 mL/m(2), respectively, P =.001). Systolic pulmonary pressure decreased significantly (from 55 +/- 13 to 43 +/- 16 mm Hg, P =.001). Ejection fraction did not change significantly. Postoperative mitral regurgitation was absent or minimal in 84% of cases; 1 patient had severe mitral regurgitation necessitating valve replacement. New York Heart Association functional class significantly improved. The mean preoperative functional class was 3.4 +/- 0.6 (median 3, range 2-4); after the operation, this decreased to 1.9 +/- 0.7 (median 2, range 1-3, P <.001). Cumulative survival at a 30-month follow-up was 63%. Our aggressive, combined surgical approach is aimed at correcting the three components of ischemic cardiomyopathy: relieving ischemia, reducing left ventricular wall tension by decreasing left ventricular volumes, and reducing volume overload and pulmonary hypertension by repairing the mitral valve. Despite a relatively high perioperative mortality rate, surviving patients benefitted from the operation, with improved clinical functional class and thus quality of life.

Renin Expression at Sites of Repair in the Infarcted Rat Heart

Y. Sun, J. Zhang, J. Q. Zhang and K. T. Weber. Renin Expression at Sites of Repair in the Infarcted Rat Heart. Journal of Molecular and Cellular Cardiology (2001) 33, 995–1003. Angiotensin (Ang) II has autocrine and paracrine functions that contribute to structural cardiac remodeling by fibrous tissue following myocardial infarction (MI). The recruitment of angiotensin converting enzyme (ACE) and AngII receptors by inflammatory and fibroblast-like cells involved in tissue repair of the infarcted heart is now well established. On the other hand, the temporal and spatial response and cellular source of renin in infarcted hearts have not been fully elucidated. The relationship between renin synthesis and circulating renin activity have likewise not been addressed. The present study sought to assess the cellular source, spatial distribution and temporal response of renin expression and synthesis in the rat heart following anterior transmural MI, and to determine its relationship to circulating renin activity. At day 3 and weeks 1, 2, 3 and 4 following left coronary artery ligation, the localization and optical density of cardiac renin mRNA was detected by quantitative in situ hybridization; cardiac and circulating renin activity was measured by radioimmunoassay; cells expressing cardiac renin were detected by immunohistochemistry; and injury/repair was assessed by hematoxylin/eosin and collagen-specific picrosirius red staining. Unoperated rats served as normal controls. The authors found: (1) renin mRNA and activity were not detected in either normal control or non-infarcted myocardium, but were expressed at the site of infarction and other sites of repair involving visceral pericardium and endocardium of interventricular septum at all time points; (2) cells expressing renin at day 3 and weeks 1 and 2 were predominantly macrophages, while at weeks 3 and 4, they were primarily myofibroblasts; (3) renin activity in the infarcted myocardium rose progressively over the course of 4 weeks; and (4) circulating renin activity was significantly increased at day 3 and week 1, reached a peak at week 2, declined at week 3 and returned to normal levels at week 4. Thus, renin expression and activity appear at sites of repair in the infarcted rat heart on day 3 and rise progressively thereafter over 4 weeks, independent of circulating renin. Several types of cells are responsible for renin synthesis at these sites; primarily macrophages during the inflammatory phase of repair, and myofibroblasts during the subsequent fibrogenic phase. Cardiac renin production following MI contributes to local AngII generation that regulates tissue repair and structural remodeling following MI.

Effects of the Dor procedure on left ventricular dimension and shape and geometric correlates of mitral regurgitation one year after surgery

Objectives: In the present study we retrospectively analyzed ventriculographic data from symptomatic patients after myocardial infarction who underwent the Dor procedure (endoventricular circular patch plasty repair) to evaluate left ventricular shape 1 year after the operation and to analyze the geometric correlates of late mitral regurgitation. Methods: Forty-four patients with previous transmural anterior myocardial infarction comprised the study group. Left ventricular volumes, global left ventricular systolic and diastolic sphericity, the extent of wall motion abnormalities, and the presence and degree of mitral regurgitation were analyzed before and 1 year after operation. Results: Comparing preoperative diastole to systole within the cardiac cycle, left ventricular shape becomes more elliptical in systole than it was in diastole (eccentricity index closer to 1). The intervention leads to an increased diastolic sphericity, but for each cardiac cycle, the systolic shape is more elliptical relative to its diastolic counterpart in respect to basal conditions. Mitral regurgitation was detected after operations in 17 patients; 14 of them did not have mitral regurgitation before operations. Patients with late mitral regurgitation had greater preoperative volumes and more spherical chamber than did patients without late mitral regurgitation. Conclusions: Despite a more spherical postoperative left ventricular chamber, systolic pump function improves after the Dor procedure, mainly for the improvement in inferior wall shortening. The presence of late mitral regurgitation is relatively frequent in this series of patients, and this emphasizes the importance of a more accurate quantitative evaluation of preoperative functional mitral regurgitation to repair the valve when appropriate. Geometric correlates of late mitral regurgitation appeared to be greater chamber sphericity and larger ventricular volumes preoperatively. (J Thorac Cardiovasc Surg 2001;121:91-6)

Accuracy of low load exercise-induced T wave normalization in predicting the presence of contractile reserve after an anterior myocardial infarction.

BACKGROUND AND METHODS. Exercise-induced T wave normalization occurring at a low (less-than-or-equal50 watt) workload in infarct-related electrocardiographic leads was studied in 30 consecutive patients with a recent transmural anterior acute myocardial infarction. Patients underwent both ergometric stress testing (within 30 days after the infarction) and low dose dobutamine echocardiography. The T wave normalization was considered significant when it occurred in at least two infarct-related leads. A significant contractile reserve was considered present in an infarcted region when 50% or more of the dyskinetic segments functionally improved on exercise during dobutamine infusion. RESULTS. Eighteen patients showed exercise-induced T wave normalization (group 1), and 12 patients did not (group 2). Myocardial contractile reserve in the infarct area was detected in 16 patients of group 1 (88%) and in 3 patients (25%) of group 2 (p=0.004). The overall sensitivity, specificity, and diagnostic accuracy of T wave normalization, as it reflects contractile reserve in the infarct area, were 84%, 82%, and 83%, respectively. CONCLUSION. Low load exercise-induced T wave normalization in infarct-related leads appears to be an accurate marker of residual contractile reserve in the infarct area in patients with recent transmural acute anterior myocardial infarction. (c) 2000 by CHF, Inc.

Infarct‐related artery patency after transmural anterior myocardial infarction and Q wave regression + R wave development: Is there a relationship?

Infarct‐related artery patency after transmural anterior myocardial infarction and Q wave regression + R wave development: Is there a relationship?