NT-proBNP cut-off value for ruling out heart failure in atrial fibrillation patients - A prospective clinical study.

STUDY OBJECTIVE: N-terminal pro-brain natriuretic peptide (NT-proBNP) measurements can be used to rule out heart failure in patients with sinus rhythm. Atrial fibrillation often coexists with heart failure but affects NT-proBNP levels. This study aims to identify the optimal NT-proBNP cut-off value for ruling out heart failure among atrial fibrillation patients. METHODS: This prospective study included 409 atrial fibrillation patients admitted to the emergency department. The inclusion criterion was documented atrial fibrillation on a 12­lead electrocardiogram. All patients completed a NT-proBNP blood sample, a chest X-ray and an echocardiogram. Heart failure was defined as a left ventricular ejection fraction of <40%. RESULTS: In total, 409 patients were included (mean age: 75.2 ± 11.6). The median NT-proBNP level was 2577 ng/L (quartiles: 1185-5438) and 21% had heart failure. We found a lower median NT proBNP level of 3187 ± 3973 ng/L in patients without heart failure compared to 9254 ± 8008 ng/L in patients with heart failure (absolute difference: 4131, 95% (CI): 3299-4986, p < 0.001). The area under the receiver operating characteristic curve for diagnosing heart failure was 0.82 (95% confidence interval: 0.77-0.87). The optimal cut-off value for ruling out heart failure was 739 ng/L with a sensitivity of 99%, a specificity of 18%, and a negative predictive value of 98%. CONCLUSIONS: NT-proBNP can be used to rule out heart failure in atrial fibrillation patients with a high negative predictive value, but low specificity. TRIAL REGISTRATION NUMBER: NCT04125966. https://clinicaltrials.gov/ct2/show/NCT04125966.

Reverse remodeling of tricuspid valve morphology and function in chronic thromboembolic pulmonary hypertension patients following pulmonary thromboendarterectomy: a cardiac magnetic resonance imaging and invasive hemodynamic study.

BACKGROUND: To investigate changes in tricuspid annulus (TA) and tricuspid valve (TV) morphology among chronic thromboembolic pulmonary hypertension (CTEPH) patients before and 12 months after pulmonary thromboendarterectomy (PEA) and compare these findings to normal control subjects. METHODS: 20 CTEPH patients and 20 controls were enrolled in the study. The patients were examined with echocardiography, right heart catherization and cardiac magnetic resonance imaging prior to PEA and 12 months after. RESULTS: Right atrium (RA) volume was significantly reduced from baseline to 12 months after PEA (30 ± 9 vs 23 ± 5 ml/m2, p < 0.005). TA annular area in systole remained unchanged (p = 0.11) and was comparable to controls. The leaflet area, tenting volume and tenting height in systole were significantly increased at baseline but decreased significantly with comparable values to controls after 12 months (p < 0.005). There was correlation between the changes of right ventricular-pulmonary artery coupling and changes of TV tenting height (r = - 0.54, p = 0.02), TV tenting volume (r = - 0.73, p < 0.001) and TV leaflet area (- 0.57, p = 0.01) from baseline to 12 months after PEA. Tricuspid regurgitation jet area/RA area was significantly (p < 0.01) reduced from baseline (30 ± 13%) to 12 months after PEA (9 ± 10%). CONCLUSION: In CTEPH patients selected for PEA, TV tenting height, volume and valve area are significantly increased whereas annulus size and shape are less affected. The alterations in TV morphology are fully reversed after PEA and correlates to improvements of right ventricular-pulmonary arterial coupling.

Pulmonary vasodilation by sildenafil in acute intermediate-high risk pulmonary embolism: a randomized explorative trial.

BACKGROUND: To investigate if acute pulmonary vasodilation by sildenafil improves right ventricular function in patients with acute intermediate-high risk pulmonary embolism (PE). METHODS: Single center, explorative trial. Patients with PE were randomized to a single oral dose of sildenafil 50 mg (n = 10) or placebo (n = 10) as add-on to conventional therapy. The time from hospital admission to study inclusion was 2.3 ± 0.7 days. Right ventricular function was evaluated immediately before and shortly after (0.5-1.5 h) randomization by right heart catheterization (RHC), trans-thoracic echocardiography (TTE), and cardiac magnetic resonance (CMR). The primary efficacy endpoint was cardiac index measured by CMR. RESULTS: Patients had acute intermediate-high risk PE verified by computed tomography pulmonary angiography, systolic blood pressure of 135 ± 18 (mean ± SD) mmHg, increased right ventricular/left ventricular ratio 1.1 ± 0.09 and increased troponin T 167 ± 144 ng/L. Sildenafil treatment did not improve cardiac index compared to baseline (0.02 ± 0.36 l/min/m2, p = 0.89) and neither did placebo (0.00 ± 0.34 l/min/m2, p = 0.97). Sildenafil lowered mean arterial blood pressure (- 19 ± 10 mmHg, p < 0.001) which was not observed in the placebo group (0 ± 9 mmHg, p = 0.97). CONCLUSION: A single oral dose of sildenafil 50 mg did not improve cardiac index but lowered systemic blood pressure in patients with acute intermediate-high risk PE. The time from PE to intervention, a small patient sample size and low pulmonary vascular resistance are limitations of this study that should be considered when interpreting the results. TRIAL REGISTRATION: The trial was retrospectively registered at www.clinicaltrials.gov (NCT04283240) February 2nd 2020, https://clinicaltrials.gov/ct2/show/NCT04283240?term=NCT04283240&draw=2&rank=1 .

Long-term changes of resting and exercise right ventricular systolic performance in patients with chronic thromboembolic pulmonary hypertension following pulmonary thromboendarterectomy - A two-dimensional and three-dimensional echocardiographic study.

AIMS: To characterize right ventricular (RV) geometry and function in chronic thromboembolic pulmonary hypertension (CTEPH) patients at rest and during exercise before pulmonary thromboendarterectomy (PEA), and at 3 and 12 months after PEA using two-dimensional and three-dimensional echocardiography with reference to clinical performance and exercise capacity. METHODS AND RESULTS: Forty subjects (20 CTEPH patients and 20 controls) were enrolled between December 2014 and January 2017. Three-dimensional echocardiography demonstrated a significant reduction and normalization of end-diastolic and end-systolic RV volumes in CTEPH patients 12 months after PEA. RV systolic function improved after PEA; however, tricuspid annular plane systolic excursion (TAPSE) (baseline 18 ± 6 mm vs 15 ± 3 mm at 12 months after PEA, P < .05) and tricuspid lateral annular systolic velocity (RV-S') (baseline -8.3 ± 2.1 cm/s vs -7.2 ± 1.3 cm/s at 12 months after PEA, P < .05) declined significantly after PEA. Tricuspid regurgitation gradient was 64 ± 21 mm Hg at baseline, 40 ± 14 mm Hg at 3 months, and 30 ± 13 at 12 months, P < .00001. RV free-wall longitudinal strain at peak exercise was significantly increased from baseline (-10.6 ± 5.5%) to 12 months of follow-up (-15.8 ± 5.2%), P < .005. Physical exercise capacity, measured as peak oxygen uptake, was significantly increased and correlated directly with improvement of resting and exercise-induced RV-EF. CONCLUSION: Improvement of RV geometry and systolic function, along with the reduction of systolic pulmonary pressure, can be expected following PEA in CTEPH patients during long-term follow-up. Improvement of RV myocardial contractility after PEA was only revealed at peak exercise over time. Importantly, physical exercise capacity was significantly increased and was found to be directly correlated with improvement of resting and exercise-induced RV-EF.

Porcine Tricuspid Valve Anatomy and Human Compatibility: Relevance for Preclinical Validation of Novel Valve Interventions.

BACKGROUND: Tricuspid regurgitation may be a precursor for heart failure, reduced functional capacity, and poor survival. A human compatible experimental model is required to understand the pathophysiology of the tricuspid valve disease as a basis for validating novel tricuspid valve interventions before clinical use. The study aim was to evaluate and compare the tricuspid valve anatomy of porcine and human hearts. METHODS: The anatomy of the tricuspid valve and the surrounding structures that affect the valve during a cardiac cycle were examined in detail in 100 fresh and 19 formalin-fixed porcine hearts obtained from Danish Landrace pigs (body weight 80 kg). All valvular dimensions were compared with human data acquired from literature sources. RESULTS: No difference was seen in the tricuspid annulus circumference between porcine and human hearts (13.0 ± 1.2 cm versus 13.5 ± 1.5 cm; p = NS), or in valve area (5.7 ± 1.6 cm2 versus 5.6 ± 1.0 cm2; p = NS). The majority of chordae types exhibited a larger chordal length and thickness in human hearts compared to porcine hearts. In both species, the anterior papillary muscle (PM) was larger than other PMs in the right ventricle, but muscle length varied greatly (range: 5.2-40.3 mm) and was significantly different in pigs and in humans (12.2 ± 3.2 mm versus 19.2 mm; p <0.001). CONCLUSIONS: The porcine tricuspid valve was determined to be a valid model for preclinical animal studies, despite various anatomic differences being noted between porcine and human hearts.

Impaired left and right systolic ventricular capacity in corrected atrial septal defect patients.

Resting right ventricular (RV) systolic function has in some studies been shown to be impaired after correction of an atrial septal defect (ASD) whereas impairment of left ventricular (LV) systolic function is uncertain. In the present study we examine the LV and RV systolic response to exercise in patients with a previously corrected ASD in order to investigate the myocardial capacity. Thirty-six adult ASD patients with a corrected isolated secundum ASD and eighteen adult age-matched controls underent a semi-supine exercise stress echocardiographic examination. At rest, LV parameters were comparable between groups, and RV global longitudinal strain (RV-GLS) was lower for the ASD group (-18.5%, 95% CI -20.0--17.0%) compared with controls (-24.5%, 95% CI -27.7--22.4%, p < 0.001). At peak exercise, LV ejection fraction (LVEF) was lower for ASD patients (61%, 95% CI 58-65%) compared with controls (68%, 95% CI 64-73% p = 0.01). Peak LV global longitudinal strain (LV-GLS) was borderline significantly lower (ASD: -18.4%, 95% CI -20.2--16.6%, controls: -21.3%, 95% CI -23.6--19.0%, p = 0.059). Both RVEF (ASD: 64%, 95% CI 60-68%, controls: 73%, 95% CI 65-80%, p = 0.05) and tricuspid annular plane systolic excursion (TAPSE) (ASD: 2.5 cm, 95% CI 2.3-2.7 cm, controls: 3.2 cm, 95% CI 2.9-3.6 cm, p < 0.001) at peak exercise were lower for ASD patients. Exercise assessed peak oxygen uptake was comparable between groups (ASD: 32.8 mL O2/kg/min, 95% CI 30.3-35.5 mL O2/kg/min, controls: 35.2 mL O2/kg/min, 95% CI 31.6-38.8 mL O2/kg/min, p = 0.3). Corrected ASD patients demonstrate a reduced LV and RV systolic exercise response decades after ASD correction whereas resting parameters of LV and RV systolic function were within normal range. The presence of subclinical systolic myocardial dysfunction during exercise might be associated with the long-term morbidities documented in this patient group.

Elevated Left and Right Atrial Pressures Long-Term After Atrial Septal Defect Correction: An Invasive Exercise Hemodynamic Study.

Background Despite correction of the atrial septal defect (ASD), patients experience atrial fibrillation frequently and have increased morbidity and mortality. We examined physical capacity, cardiac performance, and invasive hemodynamics in patients with corrected ASD. Methods and Results Thirty-eight corrected patients with isolated secundum ASD and 19 age-matched healthy controls underwent right heart catheterization at rest and during exercise with simultaneous expired gas assessment and echocardiography. Maximum oxygen uptake was comparable between groups (ASD 32.7±7.7 mL O2/kg per minute, controls 35.2±7.5 mL O2/kg per minute, P=0.3), as was cardiac index at both rest and peak exercise. In contrast, pulmonary artery wedge v wave pressures were increased at rest and peak exercise (rest: ASD 14±4 mm Hg, controls 10±5 mm Hg, P=0.01; peak: ASD 25±9 mm Hg, controls 14±9 mm Hg, P=0.0001). The right atrial v wave pressures were increased at rest but not at peak exercise. The transmural filling pressure gradient (TMFP) was higher at peak exercise among patients with ASD (10±6 mm Hg, controls 7±3 mm Hg, P=0.03). One third of patients with ASD demonstrated an abnormal hemodynamic exercise response defined as mean pulmonary artery wedge pressure ≥25 mm Hg and/or mean pulmonary artery pressure ≥35 mm Hg at peak exercise. These patients had significantly elevated peak right and left atrial a wave pressures, right atrial v wave pressures, pulmonary artery wedge v wave pressures, and transmural filling pressure compared with both controls and patients with ASD with a normal exercise response. Conclusions Patients with corrected ASD present with elevated right and in particular left atrial pressures at rest and during exercise despite preserved peak exercise capacity. Abnormal atrial compliance and systolic atrial function could predispose to the increased long-term risk of atrial fibrillation. Registration Information clinicaltrials.gov. Identifier: NCT03565471.

The relation of structural valve deterioration to adverse remodelling and outcome in patients with biological heart valve prostheses.

AIMS: Native valve aortic stenosis is associated with adverse remodelling of the left ventricle and remodelling is stopped or even reversed with aortic valve replacement (AVR). However, the degeneration of bioprostheses and development of structural valve deterioration (SVD) may affect this. METHODS AND RESULTS: To assess the association with SVD, remodelling and outcome 451 patients from a single surgical centre who had undergone AVR with a Mitroflow pericardial bioprosthesis were studied. All patients were assessed in 2014 and a subgroup of patients (N = 327) were re-exanimated again after at least 18 months [median time of 27 (interquartile range, IQR 26-33) months] including echocardiography, measurements of N-terminal pro-brain natriuretic peptide, and assessment of functional status. SVD was based on echocardiography. Moderate SVD was present in 63 patients (14%) and severe SVD in 19 (4%), in the subgroup with follow-up echocardiography 48 patients (15%) patients had moderate to severe SVD at first examination. Patients with SVD had significantly greater increase in left ventricular (LV) mass index [21.6 g/m2 (IQR 5.7-48.3 g/m2) vs. 9.1 g/m2 (-8.6 to 27.3 g/m2), P = 0.01]. Further, patients with SVD had lower LV ejection fraction [55% (IQR 51-62%) vs. 60% (IQR 54-63%), P = 0.01] at follow-up. During follow-up, 94 patients (21%) met the composite endpoint of death or reoperation due to SVD and 41 patient readmitted for heart failure. In multivariable Cox regression analysis, severe SVD [hazard ratio (HR) 2.64 (1.37-5.07), P = 0.004] was associated with composite endpoint, and readmission for heart failure [HR 3.82 (1.53-9.51), P = 0.004]. CONCLUSION: SVD in aortic bioprostheses is associated with adverse LV remodelling and adverse outcome.

Magnetic resonance hyperpolarization imaging detects early myocardial dysfunction in a porcine model of right ventricular heart failure.

AIMS: Early detection of heart failure is important for timely treatment. During the development of heart failure, adaptive intracellular metabolic processes that evolve prior to macro-anatomic remodelling, could provide an early signal of impending failure. We hypothesized that metabolic imaging with hyperpolarized magnetic resonance would detect the early development of heart failure before conventional echocardiography could reveal cardiac dysfunction. METHODS AND RESULTS: Five 8.5 kg piglets were subjected to pulmonary banding and subsequently examined by [1-13C]pyruvate hyperpolarization, conventional magnetic resonance imaging, echocardiography, and blood testing, every 4 weeks for 16 weeks. They were compared with a weight matched, healthy control group. Conductance catheter examination at the end of the study showed impaired right ventricular systolic function along with compromised left ventricular diastolic function. After 16 weeks, we saw a significant decrease in the conversion ratio of pyruvate/bicarbonate in the left ventricle from 0.13 (0.04) in controls to 0.07 (0.02) in animals with pulmonary banding, along with a significant increase in the lactate/bicarbonate ratio to 3.47 (1.57) compared with 1.34 (0.81) in controls. N-terminal pro-hormone of brain natriuretic peptide was increased by more than 300%, while cardiac index was reduced to 2.8 (0.95) L/min/m2 compared with 3.9 (0.95) in controls. Echocardiography revealed no changes. CONCLUSION: Hyperpolarization detected a shift towards anaerobic metabolism in early stages of right ventricular dysfunction, as evident by an increased lactate/bicarbonate ratio. Dysfunction was confirmed with conductance catheter assessment, but could not be detected by echocardiography. Hyperpolarization has a promising future in clinical assessment of heart failure in both acquired and congenital heart disease.

Long-term changes of exercise hemodynamics and physical capacity in chronic thromboembolic pulmonary hypertension after pulmonary thromboendarterectomy.

BACKGROUND: A substantial number of chronic thromboembolic pulmonary hypertension (CTEPH) patients experience dyspnea on exertion and limited exercise capacity despite surgically successful pulmonary endarterectomy (PEA). We sought to prospectively evaluate resting and peak exercise hemodynamics before, 3 and 12 months after PEA in consecutive CTEPH-patients and correlate it to physical functional capacity. METHODS AND RESULTS: Twenty consecutive CTEPH-patients were examined. Twelve months after PEA, 75% of patients with severely increased pre-PEA mean pulmonary arterial pressure (mPAP) at rest had normal or mildly increased mPAP. However, mPAP reduction was less pronounced during exercise where only 45% had normal or mildly increased mPAP at 12 months. Hemodynamic changes during exercise were tested using the pressure-flow relationship (i.e. mPAP/cardiac output (CO) slope). The average mPAP/CO slope was 7.5 ± 4.2 mm Hg/L/min preoperatively and 3.9 ± 3.0 mm Hg/L/min at 12 months (p < .005). CO reserve (CO increase from rest to peak exercise) was increased (5.7 ± 2.9 L/min) 12 months after PEA compared with pre-PEA (2.5 ± 1.8 L/min), p < .0001. However, 12 months after PEA, the CO reserve was only 49% of that of healthy controls, p < .0001. Changes in cardiac output (∆CO), calculated as the difference between CO before PEA and 12 months later, were significantly correlated with six-minute-walk-test and peak oxygen uptake (VO2), both at rest and peak exercise. CONCLUSION: Invasive exercise hemodynamic examination in CTEPH-patients demonstrates that after otherwise successful PEA surgery, >50% of patients have a significant increase in exercise mPAP, and the CO reserve remains compromised 12 months after PEA. Improvement in physical capacity is correlated with ∆CO.

Entire mitral reconstruction with porcine extracellular matrix in an acute porcine model.

OBJECTIVE: The objective of our study was to investigate the feasibility of reconstructing the entire mitral valvular and subvalvular apparatus in pigs using a modified tube graft design made of 2-ply small intestinal submucosa extracellular matrix. METHODS: The reconstructions were performed in an acute 80-kg porcine model with 8 pigs, each acting as its own control. A modified tube graft was designed from a sheet of 2-ply small intestinal submucosa extracellular matrix. Before and after mitral valve reconstruction, echocardiography was used to assess mitral regurgitation, left ventricular outflow tract obstruction due to systolic anterior motion, mitral stenosis, leaflet mobility, and leaflet geometry. RESULTS: The reconstructed mitral valves were fully functional without any observable echocardiographic signs of regurgitation. We did not observe any left ventricular outflow tract obstruction due to systolic anterior motion nor any mitral valve stenosis, despite a diminished septal-lateral distance after reconstruction. The reconstruction had a reduced tenting area, a reduced coaptation length (9.6 ± 1.7 mm vs 7.9 ± 1.0 mm, P = .010, diff = -1.7 mm, 95% confidence interval, -3.1 to -0.4 mm), and atrial bending of both leaflets. CONCLUSIONS: In this acute porcine study, entire mitral valvular and subvalvular apparatus reconstruction using a modified tube graft design made from 2-ply small intestinal submucosal extracellular matrix was feasible. The 2-ply small intestinal submucosa extracellular matrix could withstand the pressure exerted by the left ventricle without any signs of tearing or rupture. These promising results warrant further assessment of both the annular geometry and the long-term durability.

Long-term changes of right ventricular myocardial deformation and remodeling studied by cardiac magnetic resonance imaging in patients with chronic thromboembolic pulmonary hypertension following pulmonary thromboendarterectomy.

BACKGROUND: Right ventricular (RV) afterload in patients with chronic thromboembolic pulmonary hypertension (CTEPH) is associated with reduced myocardial contractility and ventriculoarterial coupling. The impact of increased afterload on RV myocardial deformation was assessed by comparing the characteristics of CTEPH patients to healthy controls at baseline, and by comparing characteristics of CTEPH patients before and 12 months after pulmonary endarterectomy (PEA). METHODS: Cardiac deformation and function of CTEPH patients (n = 20) and healthy controls (n = 20) were assessed by cardiac magnetic resonance (CMR). CTEPH patients were also examined with right heart catheterization before and 12 months after PEA. RESULTS: PEA resulted in significant improvement of invasive hemodynamics and normalization of RV hypertrophy and right atrial, RV and left ventricular dimensions and volumes. RV ejection fraction improved from 30 ±â€¯13% at baseline to 44 ±â€¯10% at 12 months (p < 0.0001) but remained decreased compared with control subjects (54 ±â€¯4%, p < 0.05). RV global circumferential strain (GCS) normalized 12 months after PEA, but RV global longitudinal strain (GLS) remained significantly lower in CTEPH patients than controls (baseline -12.9 ±â€¯3.3% vs. -16.5 ±â€¯3.6% at 12 months p < 0.01, vs. controls -19.3 ±â€¯3.2%, p < 0.05). RV mass changes were significantly correlated with RV-ejection fraction, RV-GLS, and RV-GCS. RV-pulmonary arterial coupling with the volume method improved at 12 months (0.49 ±â€¯0.30 vs. 0.84 ±â€¯0.31, p < 0.0005), but remained significantly reduced compared with healthy controls (1.19 ±â€¯0.20, p < 0.0005). CONCLUSION: RV global longitudinal and circumferential myocardial three-dimensional strain by CMR improved significantly in CTEPH patients 12 months after PEA. Improvements in myocardial deformation were associated with regression of RV hypertrophy and decrease in pulmonary artery pressure.

Influence of Mitroflow bioprosthesis structural valve deterioration on cardiac morbidity.

BACKGROUND: This study investigated the extent and nature of cardiac morbidity and cause of mortality in patients with Mitroflow structural valve deterioration (SVD). METHODS: A retrospective study was performed examining the medical records of patients who had received Mitroflow bioprosthesis between February 2001 and April 2014 and died during this period. A total of 211 patients were identified and included in the analyses. To determine the cause of mortality, cases were divided into three predefined groups: cardiovascular death due to SVD (group 1), cardiovascular death with no SVD (group 2) and non-cardiovascular death without SVD (group 3). RESULTS: Overall mortality in this study was 7.6% at 1 year, 46.4% at 5 years and 97.2% at 10 years. In group 1, 53 patients (25%) died; in group 2, 59 patients (28%) died; and in group 3, 99 patients (47%) died. Hospitalisation for congestive heart failure was observed in 49.1% in the SVD group vs. 10.2 and 13.1% in the two other groups, p < 0.001. Hospitalisation for endocarditis was also significantly higher in the SVD group (11.3%) than in the two other groups (6.8 and 0%), p < 0.05. Hospitalisation due to myocardial infarction, cerebral stroke, arrhythmia or other cardiac-related diseases was not significantly different between groups. CONCLUSION: Structural valve deterioration in Mitroflow bioprosthesis was associated with a high prevalence of hospital admissions due to congestive heart failure and endocarditis. Patients with Mitroflow bioprosthesis should be systematically and routinely followed with echocardiography, and reoperation should be considered if SVD has developed.

Structural valve deterioration in the Mitroflow biological heart valve prosthesis.

OBJECTIVES: Concern has been raised regarding the long-term durability of the Mitroflow biological heart valve prosthesis. Our aim was to assess the incidence of structural valve degeneration (SVD) for the Mitroflow bioprosthesis in a nationwide study in Denmark including all patients alive in Denmark who had received a Mitroflow aortic bioprosthesis since 2000. METHODS: Patients alive in Denmark with a Mitroflow bioprosthesis implanted since January 2000 were invited to participate in a nationwide cross-sectional study with a predefined definition of SVD. Of 1552 patients, 861 patients had died and 47 patients had been reoperated with 40 reoperations due to SVD. The remaining 644 patients were invited for evaluation; 574 patients accepted and were evaluated for SVD. The incidence of SVD was calculated using competing risk regression analysis with death as the competing event. RESULTS: A total of 173 patients were diagnosed with SVD by echocardiography. Of these, 64 (11%) patients had severe SVD and 109 (19%) patients moderate SVD. Severe SVD was associated with the age of the prosthesis and small prosthesis size [Size 21: hazard ratio (95% confidence interval, CI) 2.72 (0.97-8.56), P = 0.06; Size 19: 6.26 (1.63-24.06), P = 0.008]. The cumulative incidences of reoperation or severe SVD at Year 9 were 12.5% for Size 19, 7.6% for Size 21 and 3.1 (1.2-6.4)% for Size 23. Median survival in patients with prosthesis Sizes 23-29 was 6.4 (95% CI 5.7-7.0) years, with Size 21 it was 6.5 (95% CI 5.9-7.1) years and with Size 19 it was 6.9 (95% CI 5.7-8.2) years (P = 0.78). CONCLUSIONS: The incidence of undetected severe SVD was as high as the incidence of operated SVD. The overall risk for SVD is high for the Mitroflow bioprosthesis, especially if the prosthesis is small and older than 5 years.

Mitral valve posterior leaflet reconstruction using extracellular matrix: an acute porcine study.

OBJECTIVES: To investigate mitral valve posterior leaflet and subvalvular reconstruction using a 2-ply small intestinal submucosal extracellular matrix sheet. METHODS: Mitral valve posterior leaflet and subvalvular reconstruction was characterized in an acute 80-kg porcine model with 7 pigs acting as their own controls. The characterization was based on pressure catheter measurements of pressure differences to identify mitral regurgitation, stenosis and systolic anterior motion. Furthermore, echocardiography was used for the evaluation of leaflet mobility and geometry, whereas sonomicrometry was used to describe annular and subvalvular geometry. RESULTS: The reconstructed mitral valve was fully functional without any signs of regurgitation (peak left atrial pressure for baseline and reconstruction 12 ± 2 mmHg vs 11 ± 2 mmHg, P = 0.550), mitral valve stenosis (mean pressure difference across the mitral valve 4.8 ± 2.3 mmHg vs 4.1 ± 2.3 mmHg, P = 0.589) or systolic anterior motion. The echocardiographic characterization revealed septal-lateral downsizing, reduced tenting area, increased coaptation length (6.0 ± 0.6 mm vs 8.7 ± 2.3 mm, P = 0.002) and an atrial bend of the reconstructed posterior leaflet. A ballooning effect of the patch material was present at the posterior annular segment. CONCLUSIONS: Mitral valve posterior leaflet and subvalvular reconstruction using a 2-ply small intestinal submucosal extracellular matrix sheet as patch material was possible in an acute porcine model. The reconstructed mitral valve was fully functional without signs of mitral valve stenosis, valve regurgitation, stenosis or systolic anterior motion. The ballooning appearance of the patch material might, however, constitute an altered leaflet stress distribution in this area.

Transapical neochord implantation: is tension of artificial chordae tendineae dependent on the insertion site?

OBJECTIVE: Transapical chordae tendineae replacement is a promising new approach for mitral leaflet prolapse. However, animal studies have raised concerns that the tension of the transapically fixated artificial neochordae might be greater than the tension in the neochordae attached to papillary muscle tips, thereby reducing repair durability. METHODS: In eight 80-kg pigs, the primary anterior leaflet chordae were replaced by a 5-0 polytetrafluoroethylene neochord using a miniature in-line force transducer. The neochord was attached first to the anterior papillary muscle and, on a second cardiac bypass, transapically to the left ventricle apex. Occlusion of the inferior vena cava was performed to examine the effect of left ventricle pressure changes on neochord tension to adjust the crude data to 95 mm Hg. The maximum slope of the chordal tension curve was calculated to compare curve patterns. The data are presented as the mean ± standard deviation. RESULTS: The following tension was measured in the neochordae during papillary muscle and transapical fixation, respectively: peak tension (crude, 0.39 ± 0.32 vs 0.50 ± 0.25 N, P = .17; adjusted, 0.41 ± 0.30 vs 0.46 ± 0.27 N, P = .22), mid-systolic tension (crude, 0.19 ± 0.12 vs 0.19 ± 0.15 N, P = .96; adjusted, 0.28 ± 0.16 vs 0.19 ± 0.11 N, P = .12). There was a significantly lower maximum slope (dF/dtmax) of the neochord tension curves after papillary muscle fixation compared with transapical fixation (7.4 ± 6.9 vs 10.3 ± 7.7 N/s, P = .028). CONCLUSIONS: Overall, the chordal insertion site had little influence on the tension in the artificial neochordae compared with the interindividual variation. However, abnormal tension fluctuations in the transapically fixated neochordae might predispose to leaflet tears and early repair failure.