Progressive worsening of aortic regurgitation due to detachment of the aortic valve commissure with multimodality imaging to elucidate pathogenesis: a case report.

Background: Aortic regurgitation (AR) associated with detachment of the aortic valve commissure is extremely rare. We present a case of progressively worsening severe chronic AR due to detachment of the aortic valve commissure during hospitalization that was confirmed with multimodality imaging. Case summary: A 50-year-old male with Marfan syndrome visited our hospital to receive treatment for cholelithiasis. Pre-operative examination revealed severe AR and aortic root aneurysm. Because the patient was asymptomatic, it was decided that cholecystectomy should be performed first. However, the patient's heart failure worsened acutely when his blood pressure increased just before induction of anaesthesia. The patient required intubation and management of heart failure. Five days later, the patient underwent cholecystectomy. He was treated for heart failure and underwent open heart surgery on the 35th hospital day. Intraoperative transoesophageal echocardiography revealed that his AR was caused by both enlargement of the aortic root and localized dissection of the aortic valve commissure, which was supported by intraoperative findings and histopathological evaluation. Aortic regurgitation was exacerbated by a new localized dissection, resulting in acute worsening of heart failure. Discussion: Aortic valve commissure detachment can easily lead to sudden onset of severe AR, deteriorating haemodynamics, and acute pulmonary oedema. Since delayed medical treatment leads to poor clinical outcomes, prompt and accurate diagnosis and appropriately timed surgical intervention are essential. This very rare case of severe AR worsening due to spontaneous aortic valve commissure dissection was evaluated with multiple modalities during hospitalization. Understanding this clinical condition will help cardiologists provide better medical care.

Potential Effects of Mild Atrial Secondary Mitral Regurgitation in Patients With Isolated Atrial Fibrillation.

BACKGROUND: Patients with only moderate atrial secondary mitral regurgitation (asMR) frequently develop heart failure (HF). Mechanisms of HF with moderate asMR and the impact of mild asMR remain unclarified. Although mild/moderate primary mitral regurgitation is compensated by left ventricular (LV) dilatation, the LV is not dilated in asMR. We hypothesized that patients with mild asMR without LV dilatation may have impaired hemodynamics and higher risks of subsequent symptomatic HF deterioration. METHODS: Stroke volume, cardiac output, and systolic pulmonary artery pressure were measured by echocardiography in 142 patients with isolated atrial fibrillation and 30 healthy controls. The prognosis of patients with isolated atrial fibrillation was followed up. RESULTS: In the 142 patients with isolated atrial fibrillation, asMR was no/trivial in 55, mild in 83, moderate in 4, while none had severe asMR. Compared with controls and patients with no/trivial asMR, LV end-diastolic volume index was not increased and hemodynamic parameters were abnormal in patients with mild asMR (LV end-diastolic volume index, 65±6 versus 58±8 versus 60±8 mL/m²; stroke volume index, 42±4 versus 35±4 versus 29±6 mL/m²; P<0.001 versus other 2 groups; cardiac output index, 2.8±0.4 versus 2.8±0.5 versus 2.3±0.6 L/min per m²; P<0.001; systolic pulmonary artery pressure, 21±3 versus 26±5 versus 37±9 mm Hg; P<0.001). Although the event-free rate of HF symptomatic deterioration or hospitalization in patients with no/trivial asMR during a median 13.9 months follow-up was 86.9% and 100%, the rate in mild asMR was 59.4% and 85.0% (P<0.001 or P=0.032), respectively. CONCLUSIONS: In the presence of isolated AF and no compensatory LV dilatation, impaired hemodynamics and higher risks of symptomatic HF deterioration were associated with mild asMR, requiring further studies of causalities.

Guideline-Directed Medical Therapy for Elderly Patients With Acute Myocardial Infarction Who Undergo Percutaneous Coronary Intervention　- Insights From a Retrospective Observational Study.

BACKGROUND: The efficacy of guideline-directed medical therapy (GDMT) in the elderly remains unclear. This study evaluated the impact of GDMT (aspirin or a P2Y12inhibitor, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, ß-blocker, and statin) at discharge on long-term mortality in elderly patients with acute myocardial infarction (AMI) who had undergone percutaneous coronary intervention (PCI).Methods and Results: Of 2,547 consecutive patients with AMI undergoing PCI in 2009-2020, we retrospectively analyzed 573 patients aged ≥80 years. The median follow-up period was 1,140 days. GDMT was prescribed to 192 (33.5%) patients at discharge. Compared with patients without GDMT, those with GDMT were younger and had higher rates of ST-segment elevation myocardial infarction and left anterior descending artery culprit lesion, higher peak creatine phosphokinase concentration, and lower left ventricular ejection fraction (LVEF). After adjusting for confounders, GDMT was independently associated with a lower cardiovascular death rate (hazard ratio [HR] 0.35; 95% confidence interval [CI] 0.16-0.81), but not with all-cause mortality (HR 0.77; 95% CI 0.50-1.18). In the subgroup analysis, the favorable impact of GDMT on cardiovascular death was significant in patients aged 80-89 years, with LVEF <50%, or with an estimated glomerular filtration rate ≥30 mL/min/1.73 m2. CONCLUSIONS: GDMT in patients with AMI aged ≥80 years undergoing PCI was associated with a lower cardiovascular death rate but not all-cause mortality.

Intra- and Postprocedural Management of Coronary Artery Perforation During Percutaneous Coronary Intervention.

Background: Little is known regarding the postprocedural management of coronary artery perforation (CAP). Methods and Results: The characteristics, outcomes, and management of 115 CAP cases among 13,453 patients undergoing percutaneous coronary intervention (PCI) between 2001 and 2017 at Miyazaki Medical Association Hospital were analyzed retrospectively. The incidence of CAP was 0.85% (25 [0.19%] coronary ruptures [CRs], 90 [0.67%] wire perforations [WPs]). The most prevalent causes of CRs and WPs were rotational atherectomy (36.0%) and polymer-jacketed wires (41.1%), respectively. Fifty-two percent of CRs were treated using prolonged balloon inflation, whereas 50% of WPs were treated through embolization. Immediate and delayed cardiac tamponade (CT) occurred in 20% and 24% of CRs, respectively, and in 2.2% and 10% of WPs, respectively. The mean (±SD) right atrial pressure (RAP) during delayed CT in the CR and WP groups was 16.0±1.2 and 14.0±3.0 mmHg, respectively. New-onset atrial fibrillation developed in 24.0% and 11.1% of patients in the CR and WP groups, respectively, whereas late-onset coronary artery aneurysm (CAA) occurred in 24.0% and 0% of patients, respectively. One-year mortality rates in patients with immediate and delayed CT were 28.6% and 20.0%, respectively. Conclusions: Special attention should be paid to delayed CT, new-onset atrial fibrillation, and late-onset CAA after CAP treatment. Continuous monitoring of RAP after CAP during PCI may be useful for the early detection of delayed CT.

Outcomes of Elderly Patients With Acute Myocardial Infarction and Heart Failure Who Undergo Percutaneous Coronary Intervention.

Background: As life expectancy rises, percutaneous coronary intervention (PCI) is being performed more frequently, even in elderly patients with acute myocardial infarction (AMI). This study evaluated outcomes of elderly patients with AMI complicated by heart failure (AMIHF), as defined by Killip Class ≥2 at admission, who undergo PCI. Methods and Results: We retrospectively analyzed 185 patients with AMIHF aged ≥80 years (median age 85 years) who underwent PCI between 2009 and 2019. The median follow-up period was 572 days. The rates of in-hospital major bleeding (Bleeding Academic Research Consortium Type 3 or 5) and in-hospital all-cause mortality were 20.5% and 25.9%, respectively. The proportion of frail patients increased during hospitalization, from 40.6% at admission to 59.2% at discharge (P<0.01). The cumulative incidence of all-cause mortality was 36.3% at 1 year and 44.1% at 2 years. After adjusting for confounders, advanced age, Killip Class 4, final Thrombolysis in Myocardial Infarction flow grade <3, and longer door-to-balloon time were associated with higher mortality, whereas higher left ventricular ejection fraction and cardiac rehabilitation were associated with lower mortality (all P<0.05). Progression of frailty during hospitalization was an independent risk factor for long-term mortality in hospital survivors (P<0.01). Conclusions: The management of patients with AMIHF aged ≥80 years who undergo PCI remains challenging, with high rates of in-hospital major bleeding, frailty progression, and mortality.

Dynamic changes in the three-dimensional mitral complex geometry in a case of takotsubo cardiomyopathy with transient systolic anterior movement of the mitral valve.

A 57-year-old female presented to us with takotsubo cardiomyopathy. Echocardiogram revealed systolic anterior movement of the mitral valve (SAM) and severe mitral regurgitation (MR) with left ventricular (LV) dysfunction. After intensive medical treatment, SAM and MR almost disappeared along with the restoration of LV wall motion abnormality. We quantitatively analyzed three-dimensional mitral complex geometry at the acute phase and the recovery phase. At the initial examination when the transient SAM was observed, annulus diameters and area were significantly smaller, compared with the recovery phase. Excessive systolic movement of the annulus along with hyperdynamic LV basal wall may contribute to the transient SAM with severe MR. Learning objective: Recent studies have suggested systolic anterior movement of the mitral valve (SAM) causes acute mitral regurgitation in patients with takotsubo cardiomyopathy. However, the mechanism of transient SAM in Takotsubo cardiomyopathy remains unclear. This is the first report that assessed the unique geometric mechanisms of transient SAM in Takotsubo cardiomyopathy.

Left atrial appendage orifice dimensions in Japanese atrial fibrillation population measured by multiplane transesophageal echocardiography.

BACKGROUND: Successful implantation of the WATCHMAN device requires an accurate understanding of left atrial appendage (LAA) anatomy and orifice dimensions. Racial differences are observed in LAA size when comparing Asians with non-Asians. METHODS: A total of 170 patients (123 male, 67.4 ± 9.2 years) with paroxysmal or persistent atrial fibrillation (AF) underwent transesophageal echocardiography before catheter ablation or cardioversion (September 2018 to September 2019). As per the recommendations of the WATCHMAN device, the maximal LAA ostial diameters were measured at multiplane angles of 0°, 45°, 90°, and 135°. RESULTS: The majority of patients (121/170, 71%) had an LAA orifice size within 17-25 mm. Fifteen (8.8%) patients had undersized (< 17 mm) and eight (0.5%) had oversized (> 31 mm) LAA. One patient in this population had no LAA. LAA size was significantly larger in patients with persistent AF than in those with paroxysmal AF (23.3 ± 4.2 mm vs. 20.0 ± 3.0 mm, p < 0.001) and in male patients than in female patients (22.4 ± 4.2 vs. 20.9 ± 3.7 mm, p = 0.03). LAA orifice dimension was significantly correlated with CHADS2 score, the left atrial volume (LAV), E/e', and the left ventricular ejection fraction. Persistent AF, body mass index, and LAV were independently associated with LAA orifice dimension in multivariate analysis. CONCLUSION: This study demonstrated the distribution of LAA orifice dimension in the Japanese AF patients. This finding should be used as a reference to understand the racial characteristics of LAA size for the WATCHMAN procedure.

Non-rheumatic giant left atrium: An illustrative case successfully treated by surgical intervention.

A 45-year-old male presented to us with decompensated heart failure. He had been diagnosed as having atrial fibrillation when he was 31 years old. Transthoracic and transesophageal echocardiography revealed an excessive left atrial (LA) enlargement with left ventricular dysfunction and severe functional mitral regurgitation. There were no specific findings of rheumatic valve disease. He underwent surgical mitral valve replacement and LA volume reduction surgery after optimal medical therapy. Surgically-removed specimens of the LA and the anterior mitral leaflet were examined and there were no specific histopathological findings suggesting the specific etiology of the giant LA in this patient. The patient's condition significantly improved after the surgery without any cardiac events ever since. .

Impact of osteogenic activity on degenerative aortic valve disease in patients with osteoporotic hip fracture.

BACKGROUND: Previous studies have proposed that osteogenic and apoptotic processes of valve interstitial cells contribute to the mineralization and then calcification of the aortic valve. Osteoblast-like cells subsequently mediate calcification of the aortic valve as part of a highly regulated process analogous to skeletal bone formation. The objective of this study was to evaluate the pathogenesis of the sclerotic/calcific changes in the aortic valve from histological and biological findings, and investigate the role of osteoblasts in the calcified pathway of aortic stenosis. METHODS: Preoperative echocardiography in 550 consecutive patients with osteoporotic hip fracture were retrospectively examined (475 females, mean 25th-75th, 89 [85-93] years). One hundred sixteen patients were under medical treatment with anti-osteoporosis drugs. We evaluated the prevalence and degree of degenerative changes in the aortic valve and examined the associations of bone turnover biomarkers N-terminal pro-peptide of type 1 collagen (P1NP) and serum tartrate-resistant acid phosphatase (TRACP-5b) with degenerative calcific changes in the aortic valve. RESULTS: Of 550 patients, 112 patients (20.9%) showed no leaflet calcification; 296 (53.8%), 1 leaflet calcification; and 142 (25.8%), 2 ≥ leaflets calcification. Significant (peak velocity ≥ 3.0m/s) Aortic stenosis was found in 43 patients (7.8%). In patients who were not taking anti-osteoporotic drugs, P1NP was higher in the 2 ≥ leaflets calcification group than in the other groups (p < 0.01). TRACP-5b was not significantly different among the three groups (p = 0.15). CONCLUSIONS: Degenerative changes in the aortic valve were related to bone biomarker activation in osteoporotic hip fracture patients.

Longitudinal Evaluation of Mitral Valve Leaflet Remodeling After Acute Myocardial Infarction: Serial Quantitation of Valve Geometry Using Real-Time 3-Dimensional Echocardiography.

BACKGROUND: Recent animal studies have suggested that mitral valve (MV) leaflet remodeling can occur even without significant tethering force and that the postinfarct biological reaction would contribute to the histopathologic changes of the leaflet. We serially evaluated the MV remodeling in patients with anterior and inferior acute myocardial infarction (MI), by using 2- and 3-dimensional transthoracic echocardiography. Additional histopathologic examinations were performed to assess the leaflet pathology. METHODS: Sixty consecutive first-onset acute MI (anterior MI, n=30; inferior MI, n=30) patients who underwent successful primary percutaneous coronary intervention were examined (1) before primary percutaneous coronary intervention, (2) at 6-month follow-up, and (3) at follow-up 1 year or later after onset. MV complex geometry including MV leaflet area and thickness was analyzed using dedicated software. Additional histopathologic study compared 18 valves harvested during surgery for ischemic mitral regurgitation (MR). RESULTS: MV area and thickness incrementally increased during the follow-up period. MV leaflet area significantly increased (anterior MI: 5.59 [5.28-5.98] to 6.54 [6.20-7.26] cm2/m2, P<0.001; inferior MI: 5.60 [4.76-6.08] to 6.32 [5.90-6.90] cm2/m2, P<0.001), and leaflet thickness also increased (anterior MI: 1.09 [0.92-1.24] to 1.45 [1.28-1.60] mm/m2, P<0.001; inferior MI: 1.15 [1.03-1.25] to 1.44 [1.27-1.59] mm/m2, P<0.001); data represent onset versus ≥1 year. Larger annuls, larger tenting, and a reduced leaflet area/annular ratio with smaller coaptation index were observed in patients with persistent ischemic MR compared with those without significant ischemic MR. Histopathologic examinations revealed that MV thickness was significantly greater in chronic ischemic MR compared with acute ischemic MR (1432.6±490.5 versus 628.7±278.7 µm; P=0.001), with increased smooth muscle cells and fibrotic materials. CONCLUSIONS: MV leaflet remodeling progressed both in area and thickness after MI. This is the first clinical study to record the longitudinal course of MV leaflet remodeling by serial echocardiography.

Relations of Augmented Systolic Annular Expansion and Leaflet/Papillary Muscle Dynamics in Late-Systolic Mitral Valve Prolapse Evaluated by Echocardiography with a Speckle Tracking Analysis.

The mechanism of systolic annular expansion in mitral valve prolapse (MVP) is not clarified. Since annular expansion is systolic outward shift of MV leaflet/chorda tissue complex at superior and outer ends, annular expansion could be related to inward (superior) shift of the complex at another inferior and inner end of the papillary muscle (PM) tip and/or systolic lengthening of the tissue complex, especially MV leaflets.MV annulus systolic expansion, PMs' systolic superior shift, and MV leaflets' systolic lengthening were evaluated by echocardiography with a speckle tracking analysis in 25 normal subjects, 25 subjects with holo-systolic MVP and 20 subjects with late-systolic MVP.PMs' superior shift, MV leaflets' lengthening, MV annular area at the onset of systole and subsequent MV annulus expansion were significantly greater in late-systolic MVP than in holo-systolic MVP (4.6 ± 1.6 versus 1.5 ± 0.7 mm/m2, 2.5 ± 1.4 versus 0.6 ± 2.0 mm/m2, 6.8 ± 2.5 versus 5.7 ± 1.0 cm2/m2 and 1.6 ± 0.8 versus 0.1 ± 0.5 cm2/m2, P < 0.001, respectively). Multivariate analysis identified MV leaflets' lengthening and PMs' superior shift as independent factors associated with MV annular expansion.Conclusions: These results suggest that systolic MV annular expansion in MVP is related to abnormal MV leaflets' lengthening and PMs' superior shift.

Anatomical and physiological assessment of a symptomatic anomalous origin of the right coronary artery from the pulmonary artery by noninvasive imaging examinations.

A 58-year-old female visited our hospital complaining of fatigue and repetitive pre-syncope during exercise. She had suffered with those symptoms for decades and had visited some hospitals where she did not get conclusive diagnosis. She was ultimately diagnosed as having subclinical ventricular septal defect unrelated to her symptoms. Echocardiography revealed normal ventricular function, but color Doppler showed multiple abnormal intramyocardial blood flow signals in ventricular septum and moderator band, which suggested abnormally developed coronary perfusion. Dilated left main trunk and abnormal color Doppler signal running into the main pulmonary trunk were also observed. Coronary computed tomography angiography revealed that right coronary artery originated from pulmonary artery and made connection to distal left anterior descending artery, which led to the final diagnosis of anomalous origin of the right coronary artery from the pulmonary artery. Exercise stress echocardiography showed wall motion abnormalities in inferior region which suggested ischemia in right coronary artery (RCA) territory. Her symptoms could be derived from the myocardial ischemia. She was referred to surgical intervention considering the possible risk of cardiac events including sudden death. Re-implantation of the abnormal RCA to the aorta was performed successfully. Her long-year persistent symptoms were completely alleviated, and repeat exercise stress echocardiography showed no evidence of ischemia. .

Unique mechanism of mitral valve prolapse in atrial septal defect: Three-dimensional insights into mitral complex geometry using real-time transesophageal echocardiography.

BACKGROUND: Mitral valve prolapse (MVP) is often identified in patients with atrial septal defect (ASD), which occasionally require surgical intervention at the time of ASD closure or even long after the surgery. Ventricular and valvular geometric characteristics in preoperative ASD patients were evaluated by three-dimensional (3D) transesophageal echocardiography. METHODS AND RESULTS: Mitral valve (MV) complex geometry was quantitatively measured by 3D transesophageal echocardiography in 11 ASD patients (Qp/Qs > 1.5) and 11 controls. The ASD group had a significantly larger indexed prolapse volume and height, with a larger anterior mitral leaflet than controls (0.53 [0.33-0.75] vs 0.057 [0.027-0.11] mL/m2 , P = .0001; 2.89 [2.13-3.50] vs 0.92 [0.48-1.32] mm/m2 , P < .0001; 391.3 [346.4-445.1] vs 295.3 (281.9-330.0) mm2 /m2 , P = .011, respectively). The right ventricular (RV)-to-left ventricular (LV) end-systolic diameter ratio was larger in the ASD group than in the control group (1.34 [0.96-1.45] vs 0.85 [0.75-0.88], P = .004). The indexed inter-papillary muscle distance (IPMD) was significantly shorter in the ASD group than in the control group (7.77 [6.55-8.24] vs 9.71 [8.64-10.8] mm/m2 , P = .011). IPMD was significantly correlated with the RV-LV end-systolic diameter ratio (r = -.70, P = .017). CONCLUSIONS: Inward shift of the LV papillary muscle tips due to RV dilation may be a major mechanism of MV prolapse in ASD. At the same time, positive remodeling of the anterior leaflet was observed in the ASD group, which may compensate for the billowing leaflet geometry to maintain effective coaptation. Three-dimensional assessment of the MV apparatus geometry will help to further understand perioperative mitral regurgitation in patients with ASD.

Reverse Remodeling of the Mitral Valve Complex After Radiofrequency Catheter Ablation for Atrial Fibrillation: A Serial 3-Dimensional Echocardiographic Study.

BACKGROUND: Mitral regurgitation is frequently complicated with atrial fibrillation without apparent organic changes in the leaflet, which occasionally improves after successful radiofrequency catheter ablation. We aimed to evaluate a possible geometric effect of radiofrequency catheter ablation on the mitral valve apparatus. METHODS: Forty-three consecutive patients who underwent successful catheter ablation for persistent atrial fibrillation (maintaining sinus rhythm for 6 months after their procedure) were examined by serial real-time 3-dimensional transesophageal echocardiography before and 6 months after catheter ablation. Mitral valve complex geometry was measured using dedicated software for 3-dimensional transesophageal echocardiography. RESULTS: Mitral valve apparatus showed significant reverse remodeling along with left atrial reverse remodeling 6 months after successful catheter ablation (50.5 [39.2-61.0] versus 36.4 [28.9-43.1] mL/m2; P<0.001). The degree of mitral regurgitation decreased in a majority of patients (mitral regurgitation jet area; 1.83 [0.78-3.09] versus 0.77 [0.36-1.47] cm2; P<0.001). Annular area significantly decreased (5.32±0.91 versus 4.73±0.76 cm2/m2; P<0.001) in both anterior-posterior and medial-lateral directions. Mitral annular contraction significantly recovered after maintaining sinus rhythm for 6 months (7.51 [4.82-9.62]% versus 9.71 [6.27-13.85]%; P=0.008). There were no significant changes in tenting volume or tenting height (0.46 [0.27-0.89] versus 0.51 [0.32-0.72] mL/m2, P=0.744; 2.34 [1.75-3.48] versus 2.76 [1.99-3.08] mm/m2, P=0.717). The leaflet surface area also significantly decreased after catheter ablation (5.74 [5.01-6.33] versus 5.19 [4.63-5.64] cm2/m2; P<0.001). CONCLUSIONS: Maintaining sinus rhythm after successful catheter ablation promotes reverse remodeling in the mitral valve apparatus and improves so-called atrial functional mitral regurgitation. The positive geometric effect of catheter ablation would be expected to be a possible contributor to better outcomes in patients with atrial fibrillation, in addition to the postprocedural freedom from rhythm disturbance.

Significance of preoperative right ventricular function on mid-term outcomes after surgical ventricular restoration for ischemic cardiomyopathy.

OBJECTIVES: To analyze our surgical experiences with surgical ventricular restoration (SVR) for dilated ischemic cardiomyopathy (ICM) and to determine the significance of preoperative right ventricular (RV) function on outcomes. METHODS AND RESULTS: This study retrospectively analyzed 19 patients who underwent SVR between April 2010 and May 2016. Their mean age and New York Heart Association functional class were 62 ± 11 years and 2.9 ± 0.8, respectively. The preoperative mean left ventricular (LV) end-systolic volume index and LV ejection fraction (LVEF) were 134 ± 56 mL/m2 and 24 ± 7%, respectively. The preoperative mean RV fractional area change (RVFAC) to quantify RV systolic function was 33 ± 13%, as assessed by transthoracic echocardiography. The mean follow-up period was 47 ± 20 months. Three patients died of cardiac causes during the follow-up, with the 3-year and 5-year freedoms from cardiac-related death of 89% and 79%, respectively. Major adverse cardiac events (MACEs) occurred in ten patients, with the 3-year and 5-year MACE-free survival rates of 58% and 41%, respectively. RVFAC (risk ratio [RR] = 0.92, 95% confidence interval [CI] 0.86-0.98, p = 0.01) and LVEF (RR = 0.83, 95% CI 0.68-0.97, p = 0.02) were significant predictors of MACEs in the multivariate analysis. Patients with RVFAC of < 35% had significantly poorer MACE-free survival rates (33% at 3 years) than those with RVFAC of ≥ 35% (80% at 3 years). CONCLUSION: SVR for ICM provided acceptable freedom from cardiac-related death; however, MACEs commonly occurred and was associated with RV dysfunction.

The unique mechanism of functional mitral regurgitation in acute myocardial infarction: a prospective dynamic 4D quantitative echocardiographic study.

AIMS: Mechanisms of chronic ischaemic mitral regurgitation (IMR) are well-characterized by apically tethered leaflet caused by papillary muscles (PMs) displacement and adynamic mitral apparatus. We investigated the unique geometry and dynamics of the mitral apparatus in first acute myocardial infarction (MI) by using quantified 3D echocardiography. METHODS AND RESULTS: We prospectively performed 3D echocardiography 2.3 ± 1.8 days after first MI, in 174 matched patients with (n = 87) and without IMR (n = 87). 3D echocardiography of left ventricular (LV) volumes and of mitral apparatus dynamics throughout cardiac cycle was quantified. Similar mitral quantification was obtained at chronic post-MI stage (n = 44). Mechanistically, acute IMR was associated with larger and flatter annulus (area 9.29 ± 1.74 cm2 vs. 8.57 ± 1.94 cm2, P = 0.002, saddle shape 12.7 ± 4.5% vs. 15.0 ± 4.6%, P = 0.001), and larger tenting (length 6.36 ± 1.78 mm vs. 5.60 ± 1.55 mm, P = 0.003) but vs. chronic MI, mitral apparatus displayed smaller alterations (all P < 0.01) and annular size, PM movement remained dynamic (all P < 0.01). Specific to acute IMR, without PM apical displacement (P > 0.70), greater separation (21.7 ± 4.9 mm vs. 20.0 ± 3.4 mm, P = 0.01), and widest angulation of PM (38.4 ± 6.2° for moderate vs. 33.5 ± 7.3° for mild vs. 31.4 ± 6.3° for no-IMR, P = 0.0009) wider vs. chronic MI (P < 0.01). CONCLUSIONS: 3D echocardiography of patients with first MI provides insights into unique 4D dynamics of the mitral apparatus in acute IMR. Mitral apparatus remained dynamic in acute MI and distinct IMR mechanism in acute MI is not PM displacement seen in chronic IMR but separation and excess angulation of PM deforming the mitral valve, probably because of sudden-onset regional wall motion abnormality without apparent global LV remodelling. This specific mechanism should be considered in novel therapeutic strategies for IMR complicating acute MI.

Possible mechanism of late systolic mitral valve prolapse: systolic superior shift of leaflets secondary to annular dilatation that causes papillary muscle traction.

Progressive superior shift of the mitral valve (MV) during systole is associated with abnormal papillary muscle (PM) superior shift in late systolic MV prolapse (MVP). The causal relation of these superior shifts remains unclarified. We hypothesized that the MV superior shift is related to augmented MV superiorly pushing force by systolic left ventricular pressure due to MV annular dilatation, which can be corrected by surgical MV plasty, leading to postoperative disappearance of these superior shifts. In 35 controls, 28 patients with holosystolic MVP, and 28 patients with late systolic MVP, the MV coaptation depth from the MV annulus was measured at early and late systole by two-dimensional echocardiography. The PM tip superior shift was monitored by echocardiographic speckle tracking. MV superiorly pushing force was obtained as MV annular area × (systolic blood pressure - 10). Measurements were repeated after MV plasty in 14 patients with late systolic MVP. Compared with controls and patients with holosystolic MVP, MV and PM superior shifts and MV superiorly pushing force were greater in patients with late systolic MVP [1.3 (0.5) vs. 0.9 (0.6) vs. 3.9 (1.0) mm/m2, 1.3 (0.5) vs. 1.2 (1.0) vs. 3.3 (1.3) mm/m2, and 487 (90) vs. 606 (167) vs. 742 (177) mmHg·cm2·m-2, respectively, means (SD), P < 0.001]. MV superior shift was correlated with PM superior shift ( P < 0.001), which was further related to augmented MV superiorly pushing force ( P < 0.001). MV and PM superior shift disappeared after surgical MV plasty for late systolic MVP. These data suggest that MV annulus dilatation augmenting MV superiorly pushing force may promote secondary superior shift of the MV (equal to late systolic MVP) that causes subvalvular PM traction in patients with late systolic MVP. NEW & NOTEWORTHY Late systolic mitral valve prolapse (MVP) is associated with mitral valve (MV) and papillary muscle (PM) abnormal superior shifts during systole, but the causal relation remains unclarified. MV and PM superior shifts were correlated with augmented MV superiorly pushing force by annular dilatation and disappeared after surgical MV plasty with annulus size and MV superiorly pushing force reduction. This suggests that MV annulus dilatation may promote secondary superior shifts of the MV (late systolic MVP) that cause subvalvular PM traction.