Left Ventricular Function Status Research Articles

Low Transvalvular Flow Rate in Patients Undergoing Transcatheter Aortic Valve Implantation (TAVI) Is a Predictor of Mortality: The TFR-TAVI Study

Transvalvular flow rate (TFR) represents a better reflection of transvalvular flow than the stroke volume index (SVi), and has recently emerged as a useful prognostic tool in patients undergoing surgical aortic valve replacement. There is a paucity of data investigating the role of TFR and its relationship with other clinical or echocardiographic factors in patients undergoing transcatheter aortic valve implantation (TAVI). This was a retrospective single-centre study of 629 consecutive patients who underwent TAVI between March 2009 and September 2020. Pre-TAVI low TFR was defined as <200 c/s. The primary study end point was all-cause mortality. Low TFR was observed in 41.8% (263/629) of included patients and was associated with increasing age, low body surface area, hypertension, diabetes, atrial fibrillation, left ventricular (LV) dysfunction, and significant mitral regurgitation. LV function status and severity of aortic valve disease were independent predictors of low TFR. Low TFR was significantly associated with long-term all-cause mortality even after adjustment for other risk factors (adjusted hazard ratio [aHR] 1.44; 95% confidence interval [CI] 1.02-2.03; p=0.038). When data were stratified according to SVi, low TFR was an independent predictor of long-term all-cause mortality in patients with normal SVi (aHR 1.98; 95% CI 1.06-3.69; p=0.032) but not in patients with low SVi (HR 1.23; 95% CI 0.71-2.11; p=0.46; p=0.016 for interaction). Low TFR is common in patients undergoing TAVI and is an independent predictor of all-cause mortality, particularly in patients with normal SVi.

Comparison of de novo implantation vs. upgrade cardiac resynchronisation therapy: a multicentre experience

Background The clinical safety and consequences of upgrade procedures compared with de novo cardiac resynchronisation therapy (CRT) implantation in heart failure remain unclear. The present study aimed to assess clinical and procedural consequences of patients undergoing CRT upgrade as compared to de novo CRT implantations. Methods In this prospective cohort study, two subgroups were considered as the study population as (1) de novo group that CRT was considered on optimised medical treatment with heart failure of NYHA functional class from II to IV, left ventricular ejection fraction (LVEF) of ≤35%, and QRS width of >130 ms and (2) upgrade group including the patients with previously implantable cardioverter defibrillator (ICD) with the indications for upgrading to CRT. The two groups were compared regarding the changes in clinical outcome and echocardiography parameters. Results The procedure was successful in 95.9% of patients who underwent CRT upgrade and 100% of those who underwent de novo CRT implantation. It showed a significant improvement in LVEF, severity of mitral regurgitation and NYHA functional classification, without any difference between the two study groups. Overall procedural related complications were reported in 10.8% and 3.8% (p = .093) and cardiac death in 5.4% and 2.5% (p = .360), respectively, with no overall difference in postoperative outcome between the two groups. Conclusions Upgrading to CRT is a safe and effective procedure regarding improvement of functional class, left ventricular function status and post-procedural outcome.

Study of Left Ventricular Dysfunction In Type 2 Diabetes Mellitus Patients Without Known Co-Morbidities

Background: Subclinical left ventricular dysfunction in type 2 diabetes mellitus (DM) patients may precede the development of symptomatic heart failure. Detecting this dysfunction early could potentially prevent its progression. However, there is a scarcity of studies on this topic in Bangladesh. Therefore, this study aimed to explore the left ventricular function status in type 2 DM patients without any known co-morbid conditions in a tertiary care hospital. Methods: A cross-sectional study was conducted at the Department of Internal Medicine in Sir Salimullah Medical College &amp; Mitford Hospital over a one-year period. A total of 100 patients with a diagnosis of type 2 DM, meeting the inclusion-exclusion criteria, were enrolled. Written informed consent was obtained from each participant, followed by the collection of socio-demographic data, detailed clinical history, and routine investigations. Echocardiograms were performed on all participants to assess the presence of systolic and diastolic dysfunction using various modes. Data analysis was conducted using the statistical software SPSS 23.0. Results: The mean age of the study patients was 47.23±9.13 (SD) years, with the majority in the age group of 40-49 years (43%). Female patients accounted for 58% of the sample, while male patients comprised 42%. The frequency of left ventricular diastolic dysfunction (LVDD) was 65%. The presence of LVDD was associated with longer duration of diabetes mellitus, higher HbA1C levels, older age, and increased BMI (p&lt;.05). Conclusion: The majority of type 2 diabetic patients in this study exhibited left ventricular diastolic dysfunction, with a prevalence of 65%. Further larger-scale studies are recommended to validate these findings. Bangladesh J Medicine 2023; 34(3): 229-234

Features of erythrocyte membranes beta-adrenoreactivity in patients with resistant hypertension and type 2 diabetes mellitus

Introduction. Patients with resistant hypertension (RHTN) and type 2 diabetes mellitus (T2DM) are characterized by sympathetic hyperactivity. A promising method for the assessment is a measurement of erythrocyte membrane beta-adrenergic reactivity (β-ARM). However, little is known about β-ARM in patients with RHTN and T2DM.Purpose. To investigate the properties of β-ARM of erythrocytes in patients with RHTN and T2DM in relation to clinical, laboratory, and instrumental data.Material and Methods. The cross-sectional study comprised 38 patients with RHTN combined with T2DM with mean age of 62.1 ± 7 years (25 women (65.8%)), 24-hour systolic/diastolic blood pressure (24-BP) (SBP/DBP) of 160.3 ± 14.2/90.8 ± 10.5 mm Hg, and glycated hemoglobin (HbA1c) of 7.2 ± 1.4%. The comparison group comprised 24 patients with RHTN without T2DM, which did not significantly differ in sex and age. General clinical examinations, measurements 24-BP and office blood pressure, β-ARM, HbA1c, 24-hour urine, echocardiography, and 24-hour electrocardiography with the assessment of heart rate variability (HRV) with low-frequency (LF) and high-frequency (HF) components were performed in all patients.Research Results. In both groups, β-ARM was significantly higher than the normal value corresponding to 20 conventional units (CU): 45.9 ± 21.9 and 41.3 ± 18.9 for patients with RHTN+T2DM and RHTN without T2DM, respectively, p = 0.39. The incidence of increase in β-ARM was comparable: 82% in RHTN with T2DM patients and 88% in RHTN without T2DM patients, χ2 = 0.38, p = 0.537. The β-ARM values correlated with duration of hypertension (R = 0.31), SBP-24 variability (R = 0.36), LF (R = 0.60), and HF (R = –0.53)) values according to HRV, 24-hour urine volume (R = –0.32), left ventricular parameters (ejection fraction (R = 0.42), ventricular efficiency (R = –0.36), arterioventricular coupling (R = –0.40)), duration of T2DM (R = –0.45), and HbA1c level (R = –0.55).Conclusions. RHTN patients were characterized by a high frequency of β-ARM increase, whether or not T2DM was present, although a long and severe course of T2DM was associated with lower values of this indicator. According to the data from instrumental studies, β-ARM in patients with RHTN and T2DM was quantitatively related to the markers of sympathetic activity, which correlated with the duration of hypertension and parameters of renal and left ventricular functional status.

High leptin status indicates an increased risk of mortality and heart failure in stable coronary artery disease

Background and aimsLeptin is an adipocyte-derived peptide involved in energy homeostasis and body weight regulation. The position of leptin in cardiovascular pathophysiology remains controversial. Some studies suggest a detrimental effect of hyperleptinemia on the cardiovascular (CV) system, while others assume the role of leptin as a neutral or even protective factor. We have explored whether high leptin affects the mortality and morbidity risk in patients with stable coronary heart disease. Methods and resultsWe followed 975 patients ≥6 months after myocardial infarction or coronary revascularization in a prospective study. All-cause or cardiovascular death, non-fatal cardiovascular events (recurrent myocardial infarction, stroke, or any revascularization), and hospitalizations for heart failure (HF) we used as outcomes.High serum leptin concentrations (≥18.9 ng/mL, i.e., 4th quartile) were associated with worse survival, as well as with a higher incidence of fatal vascular events or hospitalizations for HF. Even after full adjustment for potential covariates, high leptin remained to be associated with a significantly increased 5-years risk of all-cause death [Hazard risk ratio (HRR) 2.10 (95%CIs:1.29–3.42), p < 0.003], CV death [HRR 2.65 (95%CIs:1.48–4.74), p < 0.001], and HF hospitalization [HRR 1.95 (95% CIs:1.11–3.44), p < 0.020]. In contrast, the incidence risk of non-fatal CV events was only marginally and non-significantly influenced [HRR 1.27 (95%CIs:0.76–2.13), p = 0.359]. ConclusionsHigh leptin concentration entails an increased risk of mortality, apparently driven by fatal CV events and future worsening of HF, on top of conventional CV risk factors and the baseline status of left ventricular function.

Left Ventricular Dysfunction in Outpatients with Frequent Ventricular Premature Complexes.

Frequent ventricular premature complexes (VPCs) and VPC QRS duration are risk factors for left ventricular (LV) dysfunction. To determine which clinical characteristics and electrocardiographic features are associated with LV dysfunction (ejection fraction, <50%) and frequent VPCs, we retrospectively reviewed data from a single-center registry of all patients diagnosed with frequent VPCs at a Korean outpatient clinic. We identified 412 consecutive outpatients (mean age, 54.7 ± 16.8 yr; 227 women [55.1%]) who were diagnosed with frequent VPCs and had no structural heart disease from January 2010 through December 2017. Available transthoracic echocardiograms and 24-hour Holter monitoring data were evaluated to correlate the occurrence of VPCs and symptoms. Typical VPC-related symptoms (palpitations or dropped beats) were observed in 251 patients (61.1%). Electrocardiograms revealed VPCs with a left bundle branch block-like morphology in 327 patients (79.5%) and VPCs with an inferior axis in 353 (85.8%). Twenty-six patients (6.3%) were diagnosed with VPC-related LV dysfunction. The mean VPC burden did not differ significantly by LV functional status (11.06% ± 10.13% [normal] vs 14.41% ± 13.30% [impaired]; P=0.211). Patients with impaired LV function were more often men (P=0.027), had no typical VPC-related symptoms (P=0.006), and had significantly longer VPC QRS durations (mean, 157 ms vs 139 ms; P <0.01). Our findings suggest that male sex, absence of typical VPC-related symptoms, and a VPC QRS duration >157 ms are associated with LV dysfunction in patients with frequent VPCs, findings that may be useful in predicting such dysfunction.

Abstract 8902: The High Circulating Leptin is Associated With Increased Mortality Risk in Stable Coronary Heart Disease Patients

Introduction: Leptin is an adipocyte-derived peptide, involved in energy homeostasis and regulation of body weight. The position of leptin in cardiovascular pathophysiology remained controversial, some studies suggest a detrimental effect of hyperleptinemia on the cardiovascular (CV) system, while others assume the role of leptin as protective. Hypothesis: We explore whether high leptin status affects the mortality/ morbidity risk in stable patients with coronary heart disease. Methods: 975 patients, ≥6 months after myocardial infarction (EUROASPIRE cohort) were followed in a prospective study. All-cause or CV death, non-fatal events (myocardial infarction, stroke or any revascularization) and hospitalizations for heart failure (HF) were registered as outcomes Results: High serum leptin concentrations (≥18.9 ng/mL, i.e. 4 th quartile) indicate inferior survival, as well as a higher incidence of fatal vascular event or hospitalizations for HF ( see Figure). Even after full adjustment for potential covariates, high leptin was associated with significantly increased 5-years risk of all-cause death [HRR 2.10 (95%CIs:1.29-3.42), p&lt;0.003], CV death [HRR 2.65 (95%CIs:1.48-4.74), p&lt;0.001] and HF hospitalization [HRR 1.95 (95%CIs:1.11-3.44), p&lt;0.020]. In contrast, the incidence risk of non-fatal CV events was only marginally and non-significantly influenced [HRR 1.27 (95%CIs:0.76-2.13), p=0.359] Conclusions: High leptin concentration entails an increased risk of mortality (apparently driven by fatal CV events) and future worsening of HF, on top of conventional CV risk factors and the baseline status of left ventricular function.

Peripartum Cardiomyopathy: A Case Series

Peripartum cardiomyopathy (PPCM) is a life threatening entity of peripartum period characterized by left ventricular systolic dysfunction and heart failure in absence of any known cardiac disease. Though its incidence is rising but there is still uncertainty regarding its incidence, pathogenesis, and optimum management protocol. Retrospective analysis of twenty cases of PPCM admitted, within July 20016 to June 2018 in the department of Cardiology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka is done here. Mean age of study population was 25 (6.3). Majority of the patients were multi-paras 12 (60%). 80% of the patients were diagnosed after delivery. Breathlessness was the most common symptom. Bibasal lung base crepitations was most frequent sign, which was found in 95% cases. Sinus tachycardia was most frequent electrocardiographic change which was found in 80% cases. Mean left ventricular ejection fraction (LVEF) was 35.2(2.8). All the patients had different extent of global hypokinesia of left ventricle (LV) at rest. The patients were treated with bed rest, water and salt restriction, loop diuretic, digitalis, selective Beta-blocker, vitamin B complex and an anticoagulant in relevant cases in antepartum period, Angiotensin converting enzyme inhibitor (ACEI) or Angiotensin receptor blocker (ARB) was added in postpartum period.70% patients were clinically improved and in 45% the left ventricular functional status returned to normal. 30% developed persistent cardiomyopathy beyond six months of presentation. Maternal mortality was 1 (5%). Among all live births three had intra uterine growth retardation. The pathophysiology, emerging investigations modalities, updated management protocol, and prognosis of PPCM are also discussed in this review.&#x0D; University Heart Journal Vol. 17, No. 1, Jan 2021; 71-75

Liraglutide relieves myocardial damage by promoting autophagy via AMPK-mTOR signaling pathway in zucker diabetic fatty rat

Liraglutide, a glucose-lowering agent used to treat type 2 diabetic mellitus is reported to exert cardioprotective effects in clinical trials and animal experiments. However, the cardioprotective mechanism of liraglutide on diabetic cardiomyopathy has not been fully illustrated. The present study was performed to investigate whether liraglutide alleviates diabetic myocardium injury by promoting autophagy and its underlying mechanisms. Our results show that liraglutide significantly reduced the levels of creatine kinase (CK) and lactate dehydrogenase (LDH), improved left ventricular functional status and alleviated myocardial fibrosis in the Zucker diabetic fatty (ZDF) rat model. Liraglutide also mitigated high glucose-induced injury in NRCs. However these effects were partly reversed by the autophagic inhibitor chloroquine (CQ). Liraglutide promoted myocardial autophagy in the vivo and in the vitro models. Furthermore, liraglutide-induced enhancement of autophagy was related to increased AMPK phosphorylation and decreased mTOR phosphorylation, which was partially abolished by the AMPK inhibitor compound C (Comp C). Collectively, our data provide evidence that liraglutide mediated diabetic myocardium injury by promoting AMPK-dependent autophagy.

Left ventricular systolic dysfunction is associated with adverse outcomes in acute right ventricular infarction.

In patients with acute right ventricular infarction (RVI), global right ventricular (RV) performance is dependent on compensatory left ventricular (LV)-septal contractile contributions. This study was designed to assess the influence of depressed left ventricular ejection fraction (LVEF) on hemodynamics and clinical outcomes in patients with RVI. We retrospectively identified 338 patients with acute inferior ST elevation myocardial infarction (STEMI) undergoing a primary percutaneous coronary intervention. RVI was determined echocardiographically by right ventricular free wall motion abnormalities and depressed global RV performance (fractional area change); LV function was similarly calculated. RVI was documented in 185 (55%) cases. Compared with those with inferior myocardial infarction alone, patients with RVI suffered more hemodynamic compromise (need for inotropes or vasopressors 39 vs. 15%, P<0.0001, and intra-aortic balloon pump 32 vs. 13%, P<0.0001) and higher in-hospital mortality (14 vs. 3%, P=0.0006). In cases without RVI, the status of LV function did not influence in-hospital mortality (ejection fraction≤40%=7.3% vs. ejection fraction>40%=1.8, P=0.12). In contrast, in patients with RVI, LVEF was an important determinant of outcome: those with LVEF ≤ 40% suffered more hemodynamic compromise (need for inotropes or vasopressors 63 vs. 30%, P<0.0001, and intra-aortic balloon pump 59 vs. 22%, P<0.0001) and had markedly higher in-hospital mortality (33 vs. 7%, P<0.0001). In patients with acute inferior myocardial infarction complicated by RVI, depressed LVEF is associated with greater hemodynamic compromise and higher in-hospital mortality. These findings may have clinical implications for supportive efforts in such cases.

Pregnancy and subsequent pregnancy outcomes in peripartum cardiomyopathy

To study the clinical profile and management of peripartum cardiomyopathy, and to analyze the pregnancy outcomes of pregnant women with this disorder as well as its effect on subsequent pregnancies. All patients admitted with peripartum cardiomyopathy from July 2006 to June 2009 by the Departments of Cardiology and Obstetrics and Gynecology from the Institute of Post Graduate Medical Education and Research, Kolkata, India, were considered for this observational study. Thirty-six women with 42 pregnancies (36 first pregnancies and six second pregnancies in the same patients) were evaluated. Primiparas constituted 39% (14/36) of the total study population. Twenty-six women (72%) were clinically improved and in 17 (48%) the left ventricular functional status returned to normal. Five cases (14%) developed persistent cardiomyopathy (persistent left ventricular dysfunction beyond six months of presentation), and five women (14%) presented with thromboembolic events and anticoagulation was used as secondary prophylaxis. Maternal mortality was 14% (5/36). Among all live babies two had intrauterine growth restriction (IUGR) and another two died during the neonatal period. Of the six women with subsequent pregnancies, the patient with persistent cardiomyopathy died after delivering a stillborn baby. The remaining five cases with normal left ventricular functional status had favorable fetal outcomes; however, the mothers experienced morbidities such as symptoms of heart failure (two cases) and one of them progressed to persistent cardiomyopathy. Subsequent pregnancies should be discouraged as it increases the risk of recurrence of left ventricular dysfunction. Anticoagulation may be considered as a primary prevention of thromboembolism in pregnant mothers with peripartum cardiomyopathy.

Practice viewpoints: AICD, who and when?

Automatic implantable cardioverter-defibrillator (AICD) is a costly but effective treatment modality for the prevention of sudden cardiac death (SCD). Causes of SCD are age-dependent, disease-specific and affected by racial/ethnic differences....

Role of the left ventricular cavity-to-myocardium count ratio in resting technetium-99m-Sestamibi SPECT in the recovery of myocardial function after thrombolytic therapy in patients with acute myocardial infarction

The aim of this study was to assess the value of the Cavity-to-Myocardium count ratio (CM ratio) calculated in the resting 99mTc-Sestamibi SPECT images to identify myocardial functioning status and recovery of myocardial function in patients with acute myocardial insult who have received thrombolytic therapy. The study demonstrates that the resting 99mTc-Sestamibi SPECT CM ratio can be used to approximately assess the left ventricular function status and can predict the recovery of jeopardised myocardium function after thrombolytic therapy.

The Role of Left Ventricular Long-axis Contraction in Patients with Asymptomatic Aortic Regurgitation

We aimed to investigate the role of long axis contraction in patients with asymptomatic chronic aorta regurgitation (AR). In 84 consecutive patients (48 men, mean age 55.5 +/- 13.5 years) tissue Doppler imaging was performed. During catheterization, left ventricular end-diastolic pressure (LVEDP) and end-diastolic wall stress (EDWS) were calculated. The best predictor for group membership (exercise ejection fraction increase > or < of 5%) is the systolic wave maximal velocity (Sv) at the lateral mitral annulus (9 cm/s). Patients with Sv > 9 cm/s (45 patients) formed group I, while 39 patients with Sv < 9 cm/s formed group II. LVEDP and EDWS were higher in group II (15.5 +/- 1.9 mm Hg and 214.8 +/- 233.3 g/cm2) than in group I (10.3 +/- 1.7 mmHg and 111.8 +/- 40.8 g/cm2), P = .0001 and P = .01, respectively. In patients with asymptomatic AR, the estimation of left ventricular long axis contraction at rest, can unmask a subnormal left ventricular functional status.

Impact of valve prosthesis-patient mismatch on short-term mortality after aortic valve replacement.

The prosthesis used for aortic valve replacement (AVR) can be too small in relation to body size, thus causing valve prosthesis-patient mismatch (PPM) and abnormally high transvalvular pressure gradients. This study examined if there is a relation between PPM and short-term mortality after operation. The indexed valve effective orifice area (EOA) was estimated for each type and size of prosthesis being implanted in 1266 consecutive patients and used to define PPM as not clinically significant if >0.85 cm2/m2, as moderate if >0.65 cm2/m2 and <or=0.85 cm2/m2, and as severe if <or=0.65 cm2/m2; it was correlated with 30-day mortality and compared with other relevant variables. Moderate or severe PPM was present in 38% of patients. Thirty-day mortality was 4.6% (58/1266 patients) and the strongest independent predictors in multivariate analysis were left ventricular ejection fraction <40% (P=0.007), infectious endocarditis (P=0.002), emergent/salvage operation (P=0.002), cardiopulmonary bypass time >120 minutes (P=0.001), and PPM (P=0.003). Relative risk of mortality was increased 2.1-fold (95% confidence interval, 1.2 to 3.7) in patients with moderate PPM and 11.4-fold (4.4 to 29.5) in those with severe PPM. Moreover, risk of mortality for every category of PPM was higher in patients with a left ventricular ejection fraction <40% as compared with >or=40% (nonsignificant PPM, 2.7 versus 1.0; moderate PPM, 7.1 versus 1.8; severe PPM, 77.1 versus 11.3). PPM is a strong and independent predictor of short-term mortality among patients undergoing AVR, and its impact is related both to its degree of severity and the status of left ventricular function. In contrast to other risk factors, moderate-severe PPM can be largely avoided with the use of a prospective strategy at the time of operation.

Left Atrial Functional Reserve in Patients with Nonischemic Dilated Cardiomyopathy: An Echocardiographic Dobutamine Study

To evaluate left atrial functional reserve in patients with chronic heart failure and nonischemic dilated cardiomyopathy (DCM). Left ventricular functional status has been investigated using echocardiographic dobutamine. In 35 consecutive patients (29 men and 6 women; mean +/- SD age, 42.37 +/- 13.5 years), peak oxygen consumption (O(2)max) was measured; the day after, a low-dose dobutamine (5 to 10 micro g/kg/min, of 5 min each step) study was performed. Left atrial volumes at mitral valve opening, onset of left atrial systole, and mitral valve closure were measured by using two-dimensional echocardiography. Left atrial active emptying volume (LAEV) [volume at onset of atrial systole - minimal volume] was calculated, as was left atrial active emptying fraction (LAEF): [(volume at onset of atrial systole - minimal volume)/volume at onset of atrial systole] x 100. The changes (values obtained after inotropic stimulation minus those obtained at baseline) of the above-mentioned echocardiographic variables were considered as left atrial functional reserve. In the entire study group after dobutamine infusion, increases in LAEV (3.34 +/- 7.54 mL, p = 0.01) and LAEF (6 +/- 13.2%, p = 0.01) were observed. The changes in the above-mentioned parameters were correlated with O(2)max values (r = 0.73 and r = 0.71, respectively; p < 0.001). After inotropic stimulation, LAEV and LAEF were increased in patients with O(2)max values > 14 mL/kg/min (5.62 +/- 7.28 mL and 10.04 +/- 13.13%, respectively) and decreased in patients with O(2)max values < 14 mL/kg/min (- 1.08 +/- 6.13 mL and - 1.6 +/- 9.9%, respectively; p = 0.01 for both). Echocardiographic dobutamine can evaluate left atrial functional reserve in patients with nonischemic DCM.

Pulmonary venous flow determinants of left atrial pressure under different loading conditions in a chronic animal model with mitral regurgitation

Background: The aim of our study was to quantitatively compare the changes and correlations between pulmonary venous flow variables and mean left atrial pressure (mLAP) under different loading conditions in animals with chronic mitral regurgitation (MR) and without MR. Methods: A total of 85 hemodynamic conditions were studied in 22 sheep, 12 without MR as control (NO-MR group) and 10 with MR (MR group). We obtained pulmonary venous flow systolic velocity (Sv) and diastolic velocity (Dv), Sv and Dv time integrals, their ratios (Sv/Dv and Sv/Dv time integral), mLAP, left ventricular end-diastolic pressure, and MR stroke volume. We also measured left atrial a, x, v, and y pressures and calculated the difference between v and y pressures. Results: Average MR stroke volume was 10.6 ± 4.3 mL/beat. There were good correlations between Sv ( r = −0.64 and r = −0.59, P < .01), Sv/Dv ( r = −0.62 and r = −0.74, P < .01), and mLAP in the MR and NO-MR groups, respectively. Correlations were also observed between Dv time integral ( r = 0.61 and r = 0.57, P < .01) and left ventricular end-diastolic pressure in the MR and NO-MR groups. In velocity variables, Sv ( r = −0.79, P < .001) was the best predictor of mLAP in both groups. The sensitivity and specificity of Sv = 0 in predicting mLAP 15 mm Hg or greater were 86% and 85%, respectively. Conclusion: Pulmonary venous flow variables correlated well with mLAP under altered loading conditions in the MR and NO-MR groups. They may be applied clinically as substitutes for invasively acquired indexes of mLAP to assess left atrial and left ventricular functional status. (J Am Soc Echocardiogr 2002;15:1181-8.)

The effects of acute normovolemic hemodilution on left ventricular systolic and diastolic function in the absence or presence of beta-adrenergic blockade in dogs.

Acute normovolemic hemodilution (ANH) increases cardiac output because of a reduction in blood viscosity and enhancement of left ventricular (LV) contractility. The status of LV function, especially LV diastolic function during ANH, remains controversial. We therefore examined LV systolic and diastolic function during ANH. Sixteen dogs were anesthetized with isoflurane in the absence (Group 1) and presence (Group 2) of beta-adrenergic blockade (propranolol 1 mg/kg). LV contractility was quantified by the slope (M(w)) of the stroke work and end-diastolic volume relation. Diastolic function was evaluated with the time constant of LV relaxation (T), chamber stiffness constant (K(c)), peak LV diastolic filling rate during early filling (peak E) and atrial contraction (peak A), and ratio of peak E to peak A (E/A). Normovolemic exchange of blood (50 mL/kg) for 6% hydroxyethyl starch (ANH50) significantly increased M(w) in Group 1 but not in Group 2. In both groups, ANH50 significantly decreased T. ANH50 significantly increased peak E in both groups and peak A in Group 1, and it did not change the E/A ratio or K(c) in either group. ANH causes positive inotropic effects and enhances diastolic function without beta-blockade. Even after beta-adrenergic blockade, ANH improves diastolic function through the reduction of LV ejection impedance. Acute normovolemic hemodilution enhances LV (left ventricular) diastolic function by alterations in the LV loading condition produced by hemodilution, which mainly contributes to a compensatory increase in cardiac output.

Left ventricular remodeling after aortic valve replacement

The aim of the study was the assessment of left ventricular (LV) systolic function and left ventricular mass following aortic valve replacement (AVR) due to aortic valve stenosis as well as the influence of regression of LV hypertrophy in patients with normal and impaired LV systolic function prior to surgery. 74 patients with severe aortic valve stenosis (29 female, 45 male, mean age 66 +/- 18 years) were divided into 2 groups according to LV ejection fraction (EF): Group 1 with EF > 50% (n = 40); Group 2 with EF < or = 50% (n = 34). Furthermore, patients were differentiated into a group A without (n = 53) and a group B with aortic regurgitation (< or = II degrees, n = 21). All patients were examined by transthoracic echocardiography before and 1 month after surgery. There was a significant decrease of LV enddiastolic and endsystolic volume indices following AVR in group 2 and group B. Patients with preoperatively lower EF (group 2) showed an increase in LV ejection fraction from 39 +/- 10% before AVR to 47 +/- 11% after AVR (p < 0.001), whereas patients with preoperative normal EF (group 1) showed a significant decrease in EF (from 62 +/- 8% to 57 +/- 10%, p < 0.05). Also patients with combined aortic valve disease before AVR had an increase of EF after surgery (from 45 +/- 14% to 56 +/- 14%, p < 0.03). There were significant decreases of interventricular septum thickness and LV posterior wall thickness in group 1 and group A, whereas a significant decrease of LV enddiastolic diameter index was noted only in group B. Improvement of the NYHA functional class could be demonstrated in group 2 from 2.8 +/- 0.7 before to 2.2 +/- 0.6 after AVR, as well as in group B from 2.9 +/- 0.7 before to 1.9 +/- 0.7 after surgery. In conclusion, patients with impaired LV function or combined aortic valve disease showed a significant improvement of left ventricular systolic function after AVR, while patients with normal LV function presented a slight decrease of EF. There was a significant regression of left ventricular muscle mass in all groups independent of the left ventricular functional status.

Management of Left Ventricular Aneurysm by Intracavitary Repair

Left ventricular aneurysms (LVAs) occur in up to 40% of patients after myocardial Most LVAs are caused by occlusion of the coronary arteries, most frequently the left anterior descending coronary artery, and are located in the anteroapical region of the left ventricle. They appear as circumscribed, noncontractile areas of tissue that can be identified by systolic thinning of the infarcted area of myocardium. Occasionally, LVAs result from trauma, nonspecific myocarditis, bacterial endocarditis, or congenital malformations of the heart. Whether to treat a patient with an LVA medically or surgically depends on the status of left ventricular function and on the severity of symptoms. Patients with LVAs usually have (in order of frequency) congestive heart failure (with or without angina), thromboembolism, and ventricular tachyarrhythmias. In patients with severe symptoms and medically intractable heart failure or angina, surgery is the only option. In most patients, symptoms and prognosis can be improved by repairing the aneurysm and, when necessary, by performing concomitant coronary artery bypass or valve repair. The goal of treatment is to restore normal filling volume and normal geometric chamber configuration. Until cardiopulmonary bypass became a reality, few attempts were made to correct left ventricular aneurysms. Soon after the introduction of cardiopulmonary bypass, however, we reported the first successful repair of a ventricular ane~rysm.~ In that procedure, we dissected the adherent parietal pericardium from the aneurysmal surface and then completely excised the aneurysm, trimming the edges back to the functional myocardium. Since then, we have used a variety of other techniques to repair ventricular aneurysms, including plication, septoplasty with plication, patches, septa1 patches, and overlapping and felt buttre~ses.~ Although these methods were satisfactory, each produced either distortion, papillary dysfunction, or compromised ventricular volume. In 1988, I tried a new method of repair in a few patients whose ventricular aneurysms were so large that repair by excision would have left too little normal myocardium to restore ventricular function. This technique of intracavitary repair, which I called ventricular endoaneurysmorrhaphy, differed from earlier techniques I had used4q5 and from similar techniques used by other^.^.^ Our results (detailed later) were excellent, and as our experience broadened, we began to use the endoaneurysmorrhaphy technique on even the highest-risk patients with good results. Furthermore, we found that endoaneurysmorrhaphy could be easily adapted to any situation where active myocardium was present. We now prefer this technique over any other. This report will detail the different indications and techniques of intracavitary repair that we use in the treatment of left ventricular aneurysms.