Search

Introduction: Guideline directed medical therapy (GDMT) can result in improvement in left ventricular (LV) size and function following heart failure with reduced ejection fraction (HFrEF) diagnosis. Some therapies, such as device based interventions, are thus delayed in hopes of achieving recovery. We report remodeling and clinical outcomes in a large, consecutive series of patients presenting with a severely dilated and dysfunctional LV following 3-6 months of initial GDMT. Hypothesis: Patients with HFrEF and LVEDD ≥ 6.5cm at initial diagnosis will have a low likelihood of myocardial recovery in 3-9 months and a high burden of associated morbidity and mortality. Methods: Patients were retrospectively identified by a database search of echocardiogram studies obtained at Emory Healthcare hospitals between 2008-2018. Chart review was done to select patients’ with a new diagnosis of HFrEF and LVEDD ≥ 6.5 cm. Myocardial recovery was defined as LVEF > 35% at a follow-up echocardiogram done at least 3 months after initial study. Primary endpoint for Kaplan-Meier survival analysis was freedom from composite of death, enrollment in hospice, left ventricular assist device, or cardiac transplantation. Results: 339 patients with a median follow-up of 3.4 years were identified. The mean age was 49.0 ± 14.9 year and 68 (20.1%) were female. The mean LVEF at diagnosis was 16.9 ± 7.9% with a mean LVEDD of 7.0 ± 0.4 cm. Median time to repeat echocardiogram was 6.0 months. LVEF at follow-up was 18.3 ± 8.8% with a mean LVEDD of 6.9 ± 0.6 cm. Only 8 (2.5%) patients had myocardial recovery. 1- and 5-year primary event survival was 82.4% and 55.4% respectively. The median event free time was 5.9 years. Conclusions: Patients with de novo diagnosis of HFrEF and moderate or severe left ventricular enlargement have very low rates of myocardial recovery. Low survival estimate at 5 years suggests a potential benefit for early consideration of advanced therapies and device based therapies in this cohort.

Background: The N-Terminal of pro-B-type natriuretic peptide (NT-proBNP) is a potent biomarker for heart failure (HF), reflecting left ventricular dilation and stress. The association among obesity, HF, and NT-proBNP is complex, with paradoxically lower levels of NT-proBNP in obese individuals, despite their elevated HF risk. Furthermore, a few studies have reported decreased HF risk, but also increases in NT-proBNP, after weight loss via bariatric surgery. However, studies have not simultaneously evaluated changes in NT-proBNP and cardiac function after bariatric surgery. Hypothesis: There will be discordance between improvements in cardiac filling pressures (as reflected by E/e’) and increases in NT-proBNP with weight loss following bariatric surgery. Methods: We conducted a single-center analysis of participants in the BARI-Heart Study who underwent bariatric surgery and attended study visits 3-6 months and 2 weeks before surgery, and 6 and 12 months after surgery. We examined pre- and post-surgery changes in NT-proBNP and in echocardiographic measures of cardiac function. We also assessed the correlation between NT-pro-BNP and E/e’, at 2 weeks pre- and 6 months post-surgery. Results: Among 71 BARI-Heart participants (mean age 45 years, 74% female, 87% white, mean BMI 47.0 kg/m 2 ), there were no significant pre-surgery changes in BMI, NT-proBNP, or E/e’. By 6-12 months, there were marked reductions in BMI and significant increases in NT-proBNP, but decreases in E/e’ ( Figure ). Changes from surgery to the 6 month visit in NT-proBNP and E/e’ were associated (r=0.295; p=0.02). There was a tendency towards stronger correlations between NT-proBNP and E/e’ post- (r= 0.436; p Conclusions: Weight loss is associated with increases in NT-proBNP despite reduced LV filling pressures, suggesting a non-cardiac etiology underlying increases in NT-proBNP after weight loss. The interpretation of NT-proBNP for cardiac dysfunction may change with decreasing adiposity.

Background— Surgery for severe mitral regurgitation is indicated if symptoms or left ventricular dilation or dysfunction occur. However, prognosis is already reduced by this stage, and earlier surgery on asymptomatic patients has been advocated if valve repair is likely, but identifying suitable patients for early surgery is difficult. Quantifying the regurgitation may help, but evidence for its link with outcome is limited. Cardiovascular magnetic resonance (CMR) can accurately quantify mitral regurgitation, and we examined whether this was associated with the future need for surgery. Methods and Results— One hundred nine asymptomatic patients with echocardiographic moderate or severe mitral regurgitation had baseline CMR scans and were followed up for up to 8 years (mean, 2.5±1.9 years). CMR quantification accurately identified patients who progressed to symptoms or other indications for surgery: 91% of subjects with regurgitant volume ≤55 mL survived to 5 years without surgery compared with only 21% with regurgitant volume >55 mL ( P 40%. CMR-derived end-diastolic volume index showed a weaker association with outcome (proportions surviving without surgery at 5 years, 90% for left ventricular end-diastolic volume index 2 versus 48% for ≥100 mL/m 2 ) and added little to the discriminatory power of regurgitant fraction/volume alone. Conclusions— CMR quantification of mitral regurgitation was associated with the development of symptoms or other indications for surgery and showed better discriminatory ability than the reference-standard CMR-derived ventricular volumes. CMR may be able to identify appropriate patients for early surgery, with the potential to change clinical practice, although the clinical benefits of early surgery require confirmation in a clinical trial.

Background— Current indications for surgery in patients with significant aortic regurgitation (AR) focus on symptoms and left ventricular dilation/dysfunction. However, prognosis is already reduced by this stage, and earlier identification of patients for surgery could be beneficial. Quantifying the regurgitation may help, but there are limited data on its link with outcome. Cardiovascular magnetic resonance (CMR) can accurately quantify AR, and we examined whether this was associated with the future need for surgery. Methods and Results— One hundred thirteen patients with echocardiographic moderate or severe AR were monitored for up to 9 years (mean 2.6±2.1 years) following a CMR scan, and the progression to symptoms or other indications for surgery was monitored. AR quantification identified outcome with high accuracy: 85% of the 39 subjects with regurgitant fraction >33% progressed to surgery (mostly within 3 years) in comparison with 8% of 74 subjects with regurgitant fraction ≤33% ( P P 246 mL had good, although lower, discriminatory ability (area under the curve 0.88), but the combination of this measure with regurgitant fraction provided the best discriminatory power. Conclusions— High degrees of CMR-quantified AR were associated with the development of symptoms or other indications for surgery. Quantifying AR showed slightly better discriminatory ability than “gold standard” CMR ventricular volume assessment. This could provide a new paradigm for the timing of surgical intervention but requires confirmation in a clinical trial.

Whether cardiac ventricles can acutely dilate during septic myocardial dysfunction.A prospective echocardiographic study was performed to assess changes of left ventricular dimensions over time in patients with septic shock.A 20-bed surgical intensive care unit of Pitié-Salpêtrière university hospital in Paris.Forty-five patients were studied over the first 10 days of septic shock.None.Left ventricular end-diastolic area (LVEDA), fractional area change (FAC), velocity time integral of the aortic flow, echocardiographic indices of left ventricular relaxation, and cardiac troponin I (cTnI) were measured at day 1, 2, 3, 4, 7, and 10. Three groups were defined: 29 patients without increased cTnI and cardiac impairment (group 1), eight patients with increased cTnI and left systolic ventricular dysfunction (group 2), and eight patients with increased cTnI and isolated impairment of left ventricular relaxation (group 3). At day 1, LVEDA was significantly higher in group 2 (13 +/- 3 cm/m, p0.05) compared with groups 1 (10 +/- 2 cm/m) and 3 (11 +/- 2 cm/m). LVEDA did not change in groups 1 and 3. In group 2, LVEDA and FAC returned within 10 days to values observed in groups 1 and 2. A significant correlation was found between aortic velocity time integral and LVDEA (r =.78, p = 0.022) and FAC (r =.89, p = 0.003) only in group 2.Acute and reversible left ventricular dilation accompanies septic shock-induced systolic left ventricular dysfunction. When septic myocardial abnormalities are limited to reversible impairment of left ventricular relaxation, left ventricular dimensions remain unchanged.

The purpose of this study was to determine the effects of exercise training on LV geometry and LV diastolic function in a rat model of MI.One month after MI induced by ligation of the left anterior descending artery (N = 45) or sham operation (N = 26), rats were randomized to either a sedentary or exercise group. Exercise consisted of treadmill running at 24 m.min-1, 1 h.d-1, 5 d.wk-1, for 3 wk. Passive LV pressure volume relationships were established with an isolated, red-cell-perfused Langendorff preparation. Infarct size was determined histologically and categorized as small (30% of LV) or large (or =30% of LV).LV end-diastolic pressure-volume relationships were shifted rightward with increasing infarct size (P0.05). Exercise training further shifted the LV end-diastolic pressure-volume relationships rightward in sham, small MI and large MI (P0.05). Peak LV developed pressure was comparable in sedentary and exercised-trained hearts in sham, small MI, and large MI. LV diameter and septal wall thickness were greatest in large MI (P0.05). Exercise-trained hearts showed a tendency for a greater LV diameter and septal wall thickness in sham, small MI, and large MI. Scar thinning was most notable in large MI (P0.05).Moderate-intensity treadmill running induces myocardial remodeling and a rightward shift in the LV end-diastolic pressure-volume relationship after MI, an adaptation similar to what is observed with exercise training in sham hearts without MI.

OBJECTIVE To examine the effects of early angiotensin-converting enzyme (ACE) inhibitor therapy after myocardial infarction on infarct expansion in an experimental rat model. BACKGROUND ACE inhibitor therapy within 24 h of acute myocardial infarction (AMI) reduces mortality by unknown mechanism(s). METHODS Rats underwent permanent coronary artery occlusion. A treated group received enalapril (1.9+/-0.2 mg/kg) daily in drinking water beginning 2 h after coronary artery occlusion, a time too late to reduce infarct size. Rats were sacrificed 2 days or 2 weeks after myocardial infarction. Hearts were arrested and fixed at a constant pressure, then sectioned and photographed for morphometric analysis. RESULTS Infarcts in the control group expanded between 2 days and 2 weeks after myocardial infarction (expansion index 0.7+/-0.1 versus 2.5+/-0.4, P< 0.05). However, infarct expansion remained unchanged in the enalapril group between 2 days and 2 weeks after myocardial infarction (expansion index 0.8+/-0.1 versus 1.3+/-0.1, NS). Two weeks after myocardial infarction, the enalapril group had fewer expanded infarcts than the control group (expansion index 1.3+/-0.1 versus 2.5+/-0.4, P< 0.05). While left ventricular volume increased in the control group between 2 days and 2 weeks after myocardial infarction (0.17+/-0.01 ml versus 0.36+/-0.03 ml, P< 0.05), it remained constant in the enalapril group (0.22+/-0.02 ml versus 0.25+/-0.03 ml, NS). Two weeks after myocardial infarction, the left ventricles were larger in the control group than in the enalapril group (0.36+/-0.03 ml versus 0.25+/-0.03 ml, P< 0.05). CONCLUSIONS Treatment with enalapril initiated 2 h after AMI prevented left ventricular dilation by limiting infarct expansion. This may explain the mechanism by which ACE inhibitor therapy started within 24 h of an AMI improves survival 5-6 weeks after infarction.

Background Left ventricular dilation after acute myocardial infarction (MI) is mainly determined by infarct size. In addition, this detrimental structural adaptation seems to be augmented in patients with the ACE DD genotype. The ACE DD genotype is associated with increased ACE activity. The aim of the present study was to evaluate whether ACE activity per se may carry prognostic significance for subsequent left ventricular dilation as assessed by echocardiography during 1-year follow-up after acute MI. Methods and Results Left ventricular end-systolic and end-diastolic volume indexes were assessed by two-dimensional echocardiography. In 102 consecutive patients, plasma ACE activity was determined 3.7±0.1 hours after the onset of MI. In 64 of these patients, left ventricular volume indexes obtained at baseline and 1 year after MI were used for the present analysis. Patients were divided into a group having low ACE activity (≤12 IU/L, n=15) and a group having high ACE activity (>12 IU/L, n=49). Infarct size was a significant predictor of the increase in left ventricular volume indexes ( P =.0001) in these patients. Multivariate regression analysis, after correction for infarct size, demonstrated that elevated plasma ACE activity is a significant predictor of the increase in left ventricular end-diastolic and end-systolic volume indexes ( P =.0006 and P =.02, respectively) 1 year after MI. Conclusions Elevated plasma ACE activity determined soon after the onset of MI may be a significant predictor of the development of left ventricular dilation and may identify patients at risk.

To the Editor: I was impressed by the follow-up and detailed study by Bolognese et al1 on left ventricular remodeling …

Aortic-mitral valve discontinuity has previously been described in double outlet right ventricle, endocardial cushion defect, single ventricle, tetralogy of Fallot, and prolapse of the mitral valve. We are reporting two additional examples of aortic-mitral valve discontinuity including 15 cases of gross left ventricular dilation and a case of acute pneumococcal bacterial endocarditis with a large subannular erosion. While nonspecific, aortic-mitral valve discontinuity is a clinically important sign that should be sought with slow-M-mode scanning and strip chart recording.