Severity Of Left Ventricular Remodeling Research Articles

Cardiac Phenotypes of Pregnant Women with Hypertensive Disorders in Different Ethnic Groups

The objective of this study was to conduct a comparative analysis of the features of LV myocardial remodeling in pregnant women with chronic arterial hypertension (CAH) and preeclampsia (PE) on the background of CAH. Methods and Results: The study cohort included pregnant women (n=547) with hypertensive disorders. All women were divided into two groups: Group 1 included 376 Caucasian patients living in the Republic of Dagestan; Group 2 included 171 patients living in the Republic of Sakha (Yakutia) (indigenous residents [Yakuts and Evenks). Later on, all patients were divided into the following subgroups: Sub1A (n=134), and Sub2A (n=69) – pregnant women with CAH; Sub1B (n=242) and Sub2B (n=102) – pregnant women with PE on the background of CAH. The diagnosis of pregnant women with CAH was made on the basis of existing national and foreign recommendations that an increase in SBP ≥140 mmHg and/or DBP ≥90 mmHg indicates CAH. Different patterns of left ventricular (LV) geometry were defined based on left ventricular mass index (LVMI) and relative wall thickness (RWT), as recommended by the American Society of Echocardiography. The observed/predicted LVM ratio was calculated as 100×(oLVM/pLVM). Participants with an oLVM/pLVM ratio of >128% were categorized as having “inappropriate” LVM (iLVM). iLVM was found in Subgroups 1B and 2B in the third trimester. The frequency of LV remodeling in pregnant women of Subgroups 1 A and 2A in the second and third trimesters did not differ significantly. In Subgroup 1B, the frequency of concentric left ventricular hypertrophy (cLVH) was higher in the third trimester (42.6%) than in the second trimester (26.9%) (P=0.000). Moreover, in the third trimester, the frequency of cLVH was significantly higher in Subgroup 1B than in Subgroup 2B (42.6% and 29.4%, respectively, P=0.022). At the same time, in the third trimester, the frequency of left ventricular concentric remodeling (LVCR) was significantly higher in Subgroup 2B than in Subgroup 1B (56.9% and 44.2%, respectively, P=0.032). In the second trimester in Subgroup 1B, the frequency of LVCR was higher than in Subgroup 1A: 50% and 38.1%, respectively, P=0.026). By the third trimester, the severity of LV remodeling has increased significantly in Subgroup 1B. Thus, in Subgroup 1B, the frequency of c LVH reached 42.6% compared to 31.3% in Subgroup 1A (P=0.03). In Subgroup 2B, in the third trimester, the frequency of LVCR was slightly higher than in Subgroup 2A (56.9% and 43.5%. respectively, P=0.08). Conclusion: Living conditions predetermine the prevalence of iLVM and LVCR in pregnant northerners with CAH. A more common type of LV remodeling in pregnant women with CAH in conditions of high-altitude hypoxia is also LVCR, which transforms into cLVH by the third trimester in pregnant women with PE on the background of CAH. The study of the type of LV geometry and the appropriateness of LVM allows us to clarify the degree of LV damage in hypertension-related pregnancy. iLVM in pregnant women with CAH appears to be a predictor of the development of PE. The revealed changes in the LV structure—LVCR and cLVH—are more significant in PE on the background of CAH.

Abstract 10671: Similar Left Ventricular Remodeling Despite Different Coupling Intervals of Frequent Premature Ventricular Contractions

Introduction: Left ventricular (LV) post-extrasystolic potentiation (PESP) and dyssynchrony (LVD) are proposed mechanisms that may trigger premature ventricular contraction-induced cardiomyopathy (PVC-CM). While long-coupled (LC) PVCs are characterized by higher LVD and lower PESP, short-coupled (SC) PVCs have higher PESP and lower LVD. Methods: Twenty-four mongrel dogs implanted with right ventricular epicardial pacemakers were randomized to short-coupled (PVC-SC; 200 to 220-ms, n = 10), long-coupled (PVC-LC; 320 to 340-ms, n = 7) bigeminal PVCs, or no PVCs (sham; n = 7). Holter monitors were obtained to confirm PVC burdens. Echocardiograms were performed at baseline and regular intervals up to 12 weeks after assignment to assess for LV remodeling by investigators blinded to group assignments. Intra- and inter-group comparisons were performed at each time point. PVC-CM was defined as LV ejection fraction < 50%. Results: Holter monitors confirmed similar PVC burdens in PVC-LC and PVC-SC groups. After 12 weeks (Table 1), PVC-CM developed in 9 (90%) PVC-SC and 5 (71%) PVC-LC animals (p = 0.5368) with similar LVEF reduction in both groups (PVC-SC: 44.4 ± 1.5%; PVC-LC: 44.7 ± 4.0%; p = 0.9953) compared to sham (62.6 ± 1.5%). LV end-diastolic volume was greater in the PVC-LC (67.5 ± 4.6 mL) compared to PVC-SC (57.5 ± 2.7 mL; p = 0.0171) and sham (52.1 ± 1.5 mL; p = 0.0004) groups. LV end-systolic volume and indices of LV mass were similarly elevated in PVC-SC and PVC-LC groups compared to sham. Conclusions: Short- and long-coupled PVCs did not differentially impact the incidence or severity of LV remodeling in this translational animal model of PVC-CM. This finding is compatible with preliminary clinical observations that PVC coupling interval does not predict the development of PVC-CM in humans. Our data suggest that PESP and LV dyssynchrony play equally important roles in the development of PVC-CM.

Speckle tracking echocardiography in patients with stroke

Abstract Introduction Global longitudinal strain (GLS) via speckle tracking echocardiography (STE) has emerged as a quantitative technique to estimate myocardial function and has been shown to have clinical utility in a variety of settings. The use of this technique in patients with a stroke is limited. Purpose Comparative analysis of myocardial deformation indicators in patients with a stroke, depending on the severity and subtype. Results 230 patients with an acute cerebrovascular accident (132 men and 98 women) were included in our study, with the mean age of 64,9±10,8. Transient ischemic attack (TIA) was diagnosed in 39 (17%), acute ischemic stroke (AIS) in 191 (83%) patients. The type of an ischemic stroke in each patient was classified as one of the following traditional stroke subtypes: large-artery atherosclerosis (LAA) was diagnosed in 85 (44,5%), cardioembolic infarcts were diagnosed in 58 (30,4%), lacunar infarcts were diagnosed in 32 (16,8%) and in 16 (8,4%) the stroke was of another determined or undetermined etiology. There was no significant difference in left ventricular (LV) ejection fraction (EF) between the subgroups of TIA and AIS - 63.0% [60.0; 65.0] and 62.0% [58.0; 65.0], respectively. The LV GLS was within normal limits and amounted to 19.9±2.6 in the TIA group where as in the group of patients with stroke there was a significant (p<0.01) decrease in GLS below standard values - 17.1±3.8. The LV EF showed no significant difference between the groups of stroke subtypes. However, a decrease in GLS was found in the series from cardioembolic infarct > lacunar infarct > LAA - 17.5±3.7 > 16.5±6.5 > 16.2±3.2 (p=0,7). A decrease in GLS was significantly more often observed in male patients. A decrease in the level of GLS in patients with a stroke is associated with duration of type 2 diabetes, stroke severity by the National Institutes of Health Stroke Scale (NIHSS) score, ECG voltage criteria for LVH, increase in heart rate, LV mass/BSA, relative wall thickness (RWT) according to echocardiography. Significant differences in GLS from the size of the stroke focus according to CT scanning/ magnetic resonance imaging were not detected. Conclusion GLS via STE in patients with a stroke correlates with the severity of a stroke, the severity of LV remodeling, risk factors for cardiovascular events and requires a further study to assess the long-term prognosis Funding Acknowledgement Type of funding source: None

Proteomic signature for early diagnosis of left ventricular remodeling after myocardial infarction

Heart failure (HF) remains a main cause of mortality worldwide. The most common cause of HF is coronary artery disease and particularly myocardial infarction (MI). Left ventricular remodelling (LVR) is a progressive dilatation of the left ventricle that occurs in response to MI and is difficult to predict in clinical practice based on infarct size, infarct location or LV ejection fraction. Several studies have identified LVR as a powerful indicator of a high risk of HF or death after MI. The aim is to identify plasmatic proteins that could predict the occurrence and severity of LVR in order to prevent HF. The REVE and REVE-2 studies have included respectively, 215 and 246 patients with a first anterior MI. The patients have been followed-up with serial echocardiography during one year to quantify LVR. Plasma samples have been collected during hospitalization for both studies, and at 1, 3 and 12 months after MI for REVE-2, allowing to measure 5284 proteins thanks to a high throughput proteomic approach (SOMASCAN). Due to the high dimension of data (more variables than individuals), we used statistical methods performing variable selection to build a proteomic signature of LVR. We showed that REVE and REVE-2 studies share common statistical characteristics (distributions, correlations) allowing us to perform analysis on REVE-2 and use REVE for validation. We confirmed the difficulty to predict LVR using only clinical data, with prediction models explaining at the best 11% of LVR (R 2 = 0.106). Using the proteomic data we explained 30% of LVR (R 2 = 0.297) using a 22-proteins based score built with nested models. We confirmed that LVR is complex to predict even with a huge number of potential biomarkers to explore. Still, we enhanced the predictability of LVR and we intend to find a protein profile of LVR during the year after MI by studying data collected during this period.

Zooming in on the Microvasculature in Heart Failure With Preserved Ejection Fraction

Heart failure (HF) with preserved ejection fraction (HFpEF) has traditionally been viewed as a form of hypertensive heart disease with increased left ventricular (LV) afterload ultimately leading to HFpEF. However, HFpEF patients typically have numerous other comorbidities.1 Although the severity of LV remodeling and ventricular vascular dysfunction2 and the rate of adverse outcomes3 are greater in patients with HFpEF than in patients with comorbidities alone, some argue that HFpEF is not a distinct syndrome but rather a collection of comorbidities masquerading as HF. See Article by Srivaratharajah et al More recently, based on integrative physiological studies in human HFpEF, the biology of nitric oxide–cyclic guanosine monophosphate–protein kinase G signaling, and elegant studies of human HFpEF myocardium, Paulus and Tschope synthesized an alternate HFpEF pathophysiologic paradigm.1 This paradigm postulates that multimorbidity creates a systemic proinflammatory milieu, coronary microvascular endothelial inflammation, and migration of inflammatory cells to the myocardium with production of proinflammatory cytokines, myocardial inflammation, and subsequent fibrosis. Further, they propose that microvascular endothelial inflammation promotes oxidative stress with generation of oxidative/nitrosative species, which limits myocardial nitric oxide–cyclic guanosine monophosphate–protein kinase G signaling by diminishing nitric oxide bioavailability and oxidizing downstream nitric oxide targets, thus promoting cardiomyocyte hypertrophy. Impaired protein kinase G activity and peroxynitrite-stimulated phosphatases are proposed to alter the phosphorylation status of proteins that influence myofiber relaxation and stiffness and, thus, further impair LV diastolic function. This paradigm has sparked great interest in therapies that target impaired myocardial cyclic guanosine monophosphate–protein kinase G signaling in HFpEF. However, the Paulus paradigm has an important correlate in that an established consequence of coronary microvascular endothelial inflammation is impaired coronary microvascular endothelial function and ultimately coronary microvascular remodeling and rarefaction with decreased microvascular density (MVD).4 The potential impact of diffuse microvascular endothelial inflammation on the functional and …

The experimental model of transition from compensated cardiac hypertrophy to failure created by transverse aortic constriction in mice

BackgroundTransverse aortic constriction (TAC) operation is used as an experimental model of left ventricular (LV) hypertrophy and LV failure in mice. The severity of LV remodeling or failure may depend on the degree of TAC, but is variable among operated animals. Therefore, we tried to identify the optimal diameter of TAC to create this model with ease and high reproducibility. Methods and resultsTo produce TAC in C57BL/6J mice (7–9weeks, body weight 19–26g, n=109), a 7–0 nylon suture ligature was tightly tied around the transverse aorta against needles with 3 different diameters (mm); 0.40, 0.385 and 0.375. LV wall thickness, end-diastolic dimension, fractional shortening were measured by echocardiography. At 4weeks after TAC, no mouse with the 0.400mm gauge progressed in LV failure. The 0.385mm pin gauge mouse kept a more survival rate compared with the 0.375mm (59% vs 48%), representing same efficient in LV failure. With the 0.385mm pin gauge, hearts of mice remained LV hypertrophy at 1week after TAC, followed by LV failure at 4weeks. ConclusionTAC with the diameter of 0.385mm can effectively induce the transition from LV hypertrophy to failure in mice with relatively preserved survival.

The Transition from Compensated Cardiac Hypertrophy to Failure Created by Transverse Aortic Constriction in Mice

Transverse aortic constriction (TAC) operation is used as an experimental model of left ventricular (LV) hypertrophy and failure in mice. The severity of LV remodeling or failure may depend on the degree of TAC, but is variable among operated animals. Therefore, we tried to identify the optimal diameter of TAC to create this model with ease and high reproducibility.

Benefits of submitral procedures for ischemic mitral regurgitation.

The surgical strategy for ischemic mitral regurgitation (MR) remains controversial. Ischemic MR is a secondary valve disease caused by left ventricular (LV) remodeling and subsequent papillary muscle displacement, usually without structural valve lesions. Reduction annuloplasty is the standard surgical procedure for this condition, though it cannot clearly provide a survival benefit for those with LV dysfunction and is associated with a high prevalence of late recurrence of MR. The valvular procedure alone could be insufficient to treat ischemic MR in terms of long-term survival and the prevention of recurrence because ischemic MR is primarily a ventricular disorder. Thus, recent studies have focused on alternative procedures that target the primary cause of ischemic MR, the papillary muscles and left ventricle. We believe that the appropriate selection of surgical procedures among valvular, subvalvular, and even ventricular ones, considering the severity of LV remodeling for each patient would be more beneficial. Here we review recent studies featuring various surgical approaches to ischemic MR, especially with submitral procedures.

DOES SEVERITY OF LEFT VENTRICULAR REMODELING INFLUENCE THE RELATION BETWEEN MYOCARDIAL VIABILITY AND SURVIVAL WITH MEDICAL OR SURGICAL THERAPY IN PATIENTS WITH CORONARY ARTERY DISEASE AND LEFT VENTRICULAR DYSFUNCTION?

Prior retrospective studies of patients with ischemic left ventricular (LV) dysfunction suggest that severity of LV remodeling affects the relation between myocardial viability and survival with surgical (CABG) or medical (MED) therapy, such that patients who benefit from CABG are those with viable

左室リモデリング進行度を考慮した虚血性僧帽弁閉鎖不全症に対する弁形成術の工夫–乳頭筋接合術および左室形成術追加の意義–

左室リモデリング進行度を考慮した虚血性僧帽弁閉鎖不全症に対する弁形成術の工夫–乳頭筋接合術および左室形成術追加の意義–

THE ROLE OF THE MATRIX METALLOPROTEINASES IN THE DEVELOPMENT OF LEFT VENTRICULAR HYPERTROPHY IN PATIENTS WITH ARTERIAL HYPERTENSION AND METABOLIC SYNDROME

Aim. To assess the role of the activation of matrix metalloproteinase-1 zymogen (ProMMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the development of left ventricular (LV) hypertrophy in patients with arterial hypertension (HT) and metabolic syndrome (MS) with varying degree of obesity. Material and methods. 108 patients with HT and MS divided into 3 groups according to body mass index, and 28 healthy women were studied. Intracardiac blood flow and ProMMP-1 and TIMP-1 levels were assessed. Results. Disbalance in the ProMMP-1 and TIMP-1 systems is associated with the severity of left ventricular remodeling and grade of obesity. The changes in LV structure and geometry and activation ProMMP-1 with a deficit of TIMP-1 were most significant in patients with HT and grade 3 obesity (respectively 7.7±0.61 and 183.6±17.2 ng/ml in grade 3 obesity vs 3.5±0.3 and 291.7±22.4 ng/ml in grade 1 obesity; p<0.05). Associations between hemodynamic parameters and levels of ProMMP-1 [withLVmass index (LVMI): r=0.47; p<0.05] and TIMP-1 (with LVMI: r=-0.39; p<0.05) were determined. Conclusion. Changes in the ProMMP-1 and TIMP-1 system in women with HT and MS are associated with the severity ofLVhypertrophy.

Impact of left ventricular remodelling on outcomes after left ventriculoplasty for ischaemic cardiomyopathy: Japanese surgical ventricular reconstruction group experience†

Surgical ventricular reconstruction (SVR) for patients with severe left ventricular (LV) remodelling due to ischaemic cardiomyopathy is still controversial, because the Surgical Treatment for Ischaemic Heart Failure (STICH) trial demonstrated that SVR not only has no beneficial effect on survival compared with coronary artery bypass grafting (CABG) alone, but also is worse for those with a larger LV. Therefore, we assessed the impact of LV remodelling on the outcomes after SVR for ischaemic cardiomyopathy in Japan, using Di Donato's LV shape classification. From 2000 to 2010, 627 patients underwent SVR for ischaemic heart failure in 11 Japanese hospitals. To assess the patients with an LV ejection fraction (LVEF) of ≤ 35% like the STICH trial, considering the severity of LV remodelling, the patients with a preoperative LVEF of >35%, no preoperative LV volume assessment and no preoperative LV shape classification were excluded. Finally, 323 patients were selected as the study subjects. The LV shape was divided into three types according to Di Donato's classification. Types 1 and 3 indicate the aneurysmal and globally akinetic LV, respectively. Type 2 is the intermediate shape. Type 1, 2 and 3 LV shapes were observed in 85 (26%), 104 (32%) and 134 (42%) of the patients, respectively. The preoperative LV volume and diameter increased if the LV became more akinetic (Type 3 > 2 > 1, P < 0.001). LVEF was lower in those with more akinetic LV (P = 0.002). The preoperative LV end-diastolic volume index and LVEF in Type 3 patients were 133 ± 47 ml/m(2) and 22 ± 7%, respectively. Mitral valve repair was more frequently performed for patients with the Type 3 LV shape (65%) than for the others (P < 0.001). The hospital mortality rates were 2.4, 2.9 and 7.4% for Type 1, 2 and 3 patients, respectively (P = 0.16). Kaplan-Meier analysis demonstrated no significant difference in mortality among the three groups (log-rank P = 0.37). The 5-year survival rates were 81, 70 and 73% for Type 1, 2 and 3 patients, respectively. The severity of LV remodelling did not affect survival after SVR plus CABG. The results of SVR were acceptable even for those with globally akinetic LV due to ischaemic cardiomyopathy.

Ultrasonographic measurement of flow-mediated vasodilation in dogs with chronic valvular disease

ObjectivesTo measure flow-mediated vasodilation (FMD) in healthy dogs and in client-owned dogs with chronic valvular disease (CVD) and to investigate possible correlations between markers of CVD severity and FMD. AnimalsTwelve dogs with CVD and 11 healthy weight-matched dogs. MethodsBrachial artery FMD following 5 min inflation of a cuff around the antebrachium was measured in 12 dogs with CVD and 11 healthy weight-matched dogs. Measurements were also obtained in the healthy dogs 5 min after cuff placement but without inflation (‘sham cuff placement’). Dogs with CVD underwent echocardiography to confirm and characterize their disease. ResultsIn healthy dogs (median age 4 [2–6] years), median FMD was 7.7% versus 3.4% with sham cuff placement (P = 0.003). In dogs with CVD (median age 8 [4–16] years) median FMD was 5.5% versus 7.7% in healthy dogs (P = 0.131). FMD showed an inverse correlation with left ventricular end-diastolic diameter normalized for body weight (r = −0.76, P = 0.0043). ConclusionsBrachial FMD in dogs with early CVD inversely correlates with severity of left ventricular remodelling.

Myocardial performance index: prediction and monitoring of remodeling and functioning of the left ventricle after first myocardial infarction

Dynamic changing of left ventricular geometry and contractile state after acute myocardial infarction is responsible for various aspects of left ventricular remodeling and dysfunction. A number of studies have shown that myocardial performance index allows prediction of acute myocardial infarction complications. The objective of our study was to determine the power of myocardial performance index to predict and assess the severity of left ventricular remodeling, systolic and diastolic dysfunction after acute myocardial infarction over the long term. Echocardiography was performed within the first week of hospitalization, after one, three and six months in 77 patients with first acute myocardial infarction. At the end of the study the patients were divided into group A and B with mild and severe left ventricular remodeling, respectively. Myocardial performance index was significantly lower in group A compared to B, at the beginning (0.62 vs. 0.75; p = 0.002), and at the end of study (0, 60 vs. 0, 69; p = 0.004). After six months, 31% of study patients developed LV systolic dysfunction with prevalence in group B (56% vs. 19%, p = 0.002). Myocardial performance index > or = 0.70 at first week after acute myocardial infarction is a strong predictive parameter for extensive early and late left ventricular remodeling and systolic dysfunction (p < 0.05), but it is not a valuable predictor of diastolic failure. MPI obtained at first week of acute myocardial infarction was predictive for early and long term left ventricular remodeling and systolic dysfunction. Myocardial performance index had doubtful clinical use in assessing dynamics of remodeling and it was without clinical value in predicting diastolic function deterioration.

Noninvasive Detection of Fibrosis Applying Contrast-Enhanced Cardiac Magnetic Resonance in Different Forms of Left Ventricular Hypertrophy: Relation to Remodeling

We aimed to evaluate the incidence and patterns of late gadolinium enhancement (LGE) in different forms of left ventricular hypertrophy (LVH) and to determine their relation to severity of left ventricular (LV) remodeling. Left ventricular hypertrophy is an independent predictor of cardiac mortality. The relationship between LVH and myocardial fibrosis as defined by LGE cardiovascular magnetic resonance (CMR) is not well understood. A total of 440 patients with aortic stenosis (AS), arterial hypertension (AH), or hypertrophic cardiomyopathy (HCM) fulfilling echo criteria of LVH underwent CMR with assessment of LV size, weight, function, and LGE. Patients with increased left ventricular mass index (LVMI) resulting in global LVH in CMR were included in the study. Criteria were fulfilled by 83 patients (56 men, age 57 +/- 14 years; AS, n = 21; AH, n = 26; HCM, n = 36). Late gadolinium enhancement was present in all forms of LVH (AS: 62%, AH: 50%; HCM: 72%, p = NS) and was correlated with LVMI (r = 0.237, p = 0.045). There was no significant relationship between morphological obstruction and LGE. The AS subjects with LGE showed higher LV end-diastolic volumes than those without (1.0 +/- 0.2 ml/cm vs. 0.8 +/- 0.2 ml/cm, p < 0.015). Typical patterns of LGE were observed in HCM but not in AS and AH. Fibrosis as detected by CMR is a frequent feature of LVH, regardless of its cause, and depends on the severity of LV remodeling. As LGE emerges as a useful tool for risk stratification also in nonischemic heart diseases, our findings have the potential to individualize treatment strategies.

Severity of left ventricular remodeling defines outcomes and response to therapy in heart failure

AbstractObjectives: The objective of this study was to test the hypothesis that the severity of left ventricular remodeling predicts the response to treatment and outcomes in chronic heart failure....

Severity of left ventricular remodeling defines outcomes and response to therapy in heart failure: Valsartan heart failure trial (Val-HeFT) echocardiographic data

ObjectivesThe objective of this study was to test the hypothesis that the severity of left ventricular remodeling predicts the response to treatment and outcomes in chronic heart failure. BackgroundReversal of remodeling should produce the most favorable outcome in patients with the most severe remodeling. MethodsIn 5,010 heart failure patients on background therapy and randomized to valsartan and placebo, serial recordings of left ventricular internal diastolic diameter (LVIDd) and ejection fraction (EF) were read at sites that had to meet qualifying standards before participating. Baseline LVIDd and EF were pooled across treatments and retrospectively grouped by quartiles Q1 to Q4, representing best to worst. Kaplan-Meier survival curves were obtained by the log-rank test. Q1 was compared with Q4 for mortality and combined mortality and morbidity (M + M) from Cox regression risk ratios (RRs). Valsartan versus placebo changes from baseline in LVIDd and EF were analyzed by quartiles from analysis of covariance. Valsartan and placebo were compared by RRs for M + M. ResultsSurvival rates were greater in the better quartiles for LVIDd and EF (p < 0.00001). The RR for Q1 versus Q4 in events approached 0.5 for both LVIDd and EF (p < 0.0001). An LVIDd decrease and EF increase were quartile-dependent and greater with valsartan than placebo at virtually all time points. The RR for M + M outcomes favored valsartan in the worse quartiles. ConclusionsStratification by baseline severity of remodeling showed that patients with worse LVIDd and EF are at highest risk for an event, yet appear to gain the most anti-remodeling effect and clinical benefit with valsartan treatment.

Preoperative Selection of Patients With Severely Impaired Left Ventricular Function for Coronary Revascularization

Both thallium imaging and low-dose dobutamine echocardiography have been proposed to predict the reversibility of left ventricular (LV) dysfunction in patients with coronary disease. The present study was designed to evaluate whether the use of these techniques during the preoperative assessment of coronary patients with depressed LV function can improve our ability to identify those likely to have improved LV function after surgery. Forty consecutive patients (age, 60 +/- 10 years) with coronary disease and an ejection fraction < or = 35% underwent dobutamine echocardiography (10 micrograms/kg per minute) and exercise-redistribution-reinjection thallium single photon emission computed tomography (SPECT) before coronary revascularization by bypass surgery (n = 33) or angioplasty (n = 7). Recovery of LV function was evaluated by echocardiography 5.3 +/- 2.4 months after revascularization. According to the changes in end-systolic volume and ejection fraction after revascularization, the patients were categorized into groups with (n = 19) and without (n = 21) postoperative functional improvement, defined as a > 5% increase in ejection fraction and > 10 mL decrease in end-systolic volume. Before revascularization, patients with improved postoperative function had smaller end-diastolic volume and less wall motion abnormalities than those with persistent dysfunction. They also showed greater improvement of wall motion score with dobutamine (6.1 +/- 2.4 versus 1.8 +/- 4.2 grades, P < .001) and smaller thallium defect score after exercise (38 +/- 12 versus 47 +/- 14 grades, P = .04). Discriminant analysis selected the improvement in wall motion score with dobutamine and baseline end-diastolic volume as independent predictors of postoperative recovery. Consideration of both parameters allowed prediction of functional outcome in 84% of the patients with and 81% of those without postoperative improvement. Among the parameters commonly available before surgery in coronary patients with depressed LV function, the maintenance of significant inotropic reserve, the severity of LV remodeling, and the magnitude of the perfusion defect after exercise can predict the reversal of LV dysfunction after revascularization.