Absence Of Significant Mitral Regurgitation Research Articles

Aortic Stenosis and the Evolution of Cardiac Damage after Transcatheter Aortic Valve Replacement.

Background/Objectives: Severe aortic stenosis (AS) is the most frequent valvular heart disease. Models for stratifying cardiac damage associated with aortic stenosis have been developed to predict outcomes following valve replacement. However, evidence regarding morphological and functional evolution, as well as potential changes in the degree of cardiac damage, is limited. We aim to provide information on the evolution of cardiac morphology and the function of patients undergoing transcatheter aortic valve replacement (TAVR) who have been classified using a cardiac damage staging system. Methods: In total, 496 patients were included in the analysis, and were classified into four stages based on the extent of cardiac damage as follows: Stage 0, no cardiac damage: left ventricle global longitudinal strain (LV-GLS) < -17%; right ventricular-arterial coupling (RVAc) ≥ 0.35), and absence of significant mitral regurgitation (MR). Stage 1, left-sided subclinical damage: LV-GLS ≥ -17%. Stage 2, left-sided damage: significant MR. Stage 3, right-sided damage: RVAc < 0.35. Results: The mean age was 82.1 ± 5.9 years, and 53.0% were female. In total, 24.5% of patients met the criteria for Stage 0, and Stage 1 included 42.8% of patients, Stage 2 included 16.5%, and Stage 3 comprised 16.2% of patients. Mortality was 8.4% for stage 0, 17.4% for stage 1, 25.6% for stage 2, and 28.6% for stage 3 patients (p = 0.004). Diabetes mellitus (DM) (p = 0.047) and chronic kidney disease (CKD) (p = 0.024) were the only clinical predictors of no change or worsening in the stage of cardiac damage. Regarding echocardiographic variables, concomitant tricuspid, and mitral regurgitation, ≥ 2 were both significantly associated with no change or worsening, also (p < 0.001). Conclusions: Cardiac damage that is secondary to severe aortic stenosis has morphological and functional repercussions that, even after valve replacement, persist and might worsen the prognosis.

363 TRICUSPID ANNULUS DISJUNCTION: THE MISSING PIECE IN THE ARRHYTHMIC MITRAL VALVE PROLAPSE?

Abstract Background Arrhythmic mitral valve prolapse (MVP) is characterized by left ventricular (LV) fibrosis, due to an excessive myocardial stretch on the LV basal-mid inferolateral wall. Mitral annulus disjunction (MAD) and curling are common findings in arrhythmic MVP patients, thus representing the excessive traction of mitral apparatus on myocardium. Cardiac magnetic resonance (CMR) demonstrated to clearly identify these typical morpho-functional alterations, as well as LV fibrosis, in MVP patients. The involvement of right-sided annulus disease recently emerged as an interesting missing piece in the natural history of MVP patients. However, its role in a population of arrhythmic MVP patients in absence of significant mitral regurgitation (MR) has not been evaluated. Purpose The primary aim of the study was to evaluate the prevalence and the role of tricuspid annulus disjunction (TAD) in the arrhythmic MVP patients. Secondly, we evaluated the role of TAD in the prevalence and severity of the common morpho-functional alterations of MVP, MAD and curling. Methods Consecutive MVP patients with normal systolic function and without significant MR, referred for palpitations, were enrolled. Morpho-biventricular evaluations, including MAD and curling assessment, as well as LV fibrosis were evaluated using CMR. Results 66 patients met the inclusion criteria (29% male, median age 44 years). TAD was identified in 22 MVP patients (27% male, median age 52 years). No differences for ventricular arrhythmias (p: 0.459) between MVP patients without (n: 44) and with TAD (n: 22) were identified. MVP patients with TAD were older (52 vs 42 years, p: 0.009) and presented reduced biventricular end-diastolic volumes, despite normal, in comparison with those without TAD (left ventricle: 80.5 vs 93.5 ml/m2, p: 0.002; right ventricle: 72.5 vs 85.5 ml/m2, p: 0.018). MAD and curling were more common in patients without TAD (respectively, 25 vs 19, p:0.014 and 24 vs 20, p: 0.002) than in those with TAD. Conversely, MAD and curling are more severe in patients with TAD (respectively, 5.9 vs 4.7 mm and 4 vs 3 mm, both p: 0.034) than in those without TAD. No differences for LGE distribution were identified in the two groups (p: 0.062). Conclusion In arrhythmic MVP patients, presence of TAD was associated with a great severity of MAD and curling. So, despite uncommon, the contextual presence of TAD and MAD in arrhythmic MVP patients suggests a more severe biannular disease, characterized by an increased biventricular myocardial stretch. Conversely to MAD, TAD wasn't associated with ventricular arrhythmias. Thus, its role in ventricular arrhythmogenesis in MVP patients appeared limited.

Left ventricular remodelling in mitral valve prolapse patients: implications of apical papillary muscle insertion.

Mitral valve prolapse (MVP) causes left ventricular (LV) remodelling even in the absence of significant mitral regurgitation. To evaluate whether apical insertion of the papillary muscle (PM) influences the pattern and severity of MVP-related LV remodelling. All MVP patients who underwent CMR at our institution between December 2008 and December 2019 were included, thoroughly reviewed and grouped according to apical/non-apical PM insertion. Apical PM insertion was found in 53/92 patients (58%) and associated with mitral leaflet thickening (P < 0.01) and a trend towards higher prevalence of mitral annular disjunction (P = 0.05). Whereas no differences in ventricular volumes or ejection fraction were found, patients with apical PM insertion showed more lateral wall remodelling with mid lateral wall thinning [2.1 (1.8-2.5) vs. 4.0 (3.5-5.0) mm, P < 0.01], increased LV eccentricity and a lower GCS at this level (15 ± 3% vs. 20 ± 3%, P < 0.01). In long-axis direction, increased end-diastolic mid lateral wall angulation was found (i.e. angle <155° measured in the thinnest point of the mid lateral wall in four-chamber view) with a higher angle variation during systole (25 ± 11° vs. 17 ± 8°, P < 0.01). Remarkably, PM fibrosis was significantly more frequent in patients with apical PM insertion (i.e. 66% vs. 28%, P < 0.01). Finally, a higher burden of premature ventricular complexes (>5%) and non-sustained ventricular tachyarrhythmias was found in patients with apical PM insertion: 53% vs. 25% (P = 0.04) and 38% vs. 18% (P = 0.04), respectively. Apical PM insertion is part of the phenotypic spectrum of MVP, impacts significantly LV remodelling, and potentially may be related to increased ventricular arrhythmogenicity.

Left ventricular remodeling in mitral valve prolapse patients: implications of apical papillary muscle implantation

Abstract Funding Acknowledgements Type of funding sources: None. BACKGROUND Mitral valve prolapse (MVP) causes left ventricle (LV) remodeling even in the absence of significant mitral regurgitation. PURPOSE We sought to evaluate whether apical implantation of the papillary muscle (PM) has an influence on the pattern and severity of MVP-related LV remodeling. METHODS All MVP patients who underwent Cardiovascular Magnetic Resonance at our institution between December 2008 and December 2019 were included, thoroughly reviewed and grouped according to apical/non-apical PM implantation. RESULTS Apical PM implantation was found in 53/92 patients (58%) and associated with mitral leaflet thickening (p &amp;lt; 0.01) and a trend toward higher prevalence of mitral annular disjunction (p = 0.05). Whereas there were no differences between groups concerning ventricular volumes and ejection fraction, mitral valve prolapse location or severity of mitral valve insufficiency, patients with apical PM implantation showed more lateral wall remodeling with mid lateral wall thinning (2.1 [1.8-2.5]mm vs. 4.0 [3.5-5.0]mm, p &amp;lt; 0.01), increased LV eccentricity and a lower Global Circumferential Strain at this level (15 ± 3% vs. 20 ± 3%, p &amp;lt; 0.01). In long-axis direction, increased end-diastolic mid lateral wall angulation was found (i.e., angle &amp;lt;155° measured in the thinnest point of the mid lateral wall in 4-chamber view) with a higher angle variation during systole (25 ± 11° vs. 17 ± 8° p &amp;lt; 0.01). Remarkably, PM fibrosis was significantly more frequent in patients with apical PM implantation (i.e., 66% vs. 28%, p &amp;lt; 0.01). Importantly, PM fibrosis was observed in the apically implanted PM in the vast majority of cases (86%), showing a strong association between PM fibrosis and its apical implantation. Finally, a higher burden of premature ventricular complexes (&amp;gt;5%) and non-sustained ventricular tachyarrhythmias was found in patients with apical PM implantation: 53% vs. 25% (p = 0.04) and 38% vs. 18% (p = 0.04), respectively. CONCLUSIONS Apical PM implantation is part of the phenotypic spectrum of MVP, significantly impacts LV remodeling and potentially may be related to increased ventricular arrhythmogenicity.

Mitral valve prolapse morphofunctional features by cardiovascular magnetic resonance: more than just a valvular disease

IntroductionMitral valve (MV) prolapse (MVP) is a primary valvular abnormality. We hypothesized that additionally there are concomitant abnormalities of the left ventricle (LV) and MV apparatus in this entity even in the absence of significant mitral regurgitation (MR).ObjectiveTo characterize MV and LV anatomic and functional features in MVP with preserved LV ejection fraction, with and without significant MR, using cardiovascular magnetic resonance (CMR).MethodsConsecutive MVP patients (n = 80, mean 52 years, 37% males) with preserved LV ejection fraction, and 44 controls (46 years, 52% males) by CMR were included, as well as 13 additional patients with “borderline” MVP. From cine images we quantified LV volumes, MV and LV anatomic measurements (including angle between diastolic and systolic annular planes, annular displacement, and basal inferolateral hypertrophy) and, using feature tracking, longitudinal and circumferential peak systolic strains.ResultsSignificant MR was found in 46 (56%) MVP patients. Compared with controls, MVP patients had LV enlargement, basal inferolateral hypertrophy, higher posterior annular excursion, and reduced shortening of the papillary muscles. LV basal strains were significantly increased, particularly in several basal segments. These differences remained significant in patients without significant MR, and many persisted in “borderline” MVP.ConclusionsIn patients with MVP and preserved LV ejection fraction there is LV dilatation, basal inferolateral hypertrophy, exaggerated posterior annular displacement and increased basal deformation, even in the absence of significant MR or overt MVP. These findings suggest that MVP is a disease not only of the MV but also of the adjacent myocardium.

Abstract 16798: Evidence of Abnormal T1 Mapping in Arrhythmic Mitral Valve Prolapse Without Significant Mitral Regurgitation

Background: Prior cardiac magnetic resonance (CMR) studies have reported abnormal T1 mapping, reflective of diffuse myocardial fibrosis, in patients with mitral valve prolapse (MVP) and ventricular arrhythmias. However, T1 mapping was derived from conventional Look-Locker sequences and/or obtained in selected MVP patients with severe mitral regurgitation (MR) and a clinical indication for CMR. Hypothesis: We hypothesize that extracellular volume (ECV) fraction, a marker of diffuse fibrosis derived from research-based, MOLLI T1 mapping sequences, is increased in MVP subjects with ventricular arrhythmias, even in the absence of significant MR. Methods: We performed CMRs in 10 consecutive, randomly selected MVP patients identified through our echocardiographic database, age/gender matched to 10 controls free of significant cardiac disease. All 10 MVPs underwent ambulatory EKG monitoring. CMR images were acquired using a GE 3.0T Discovery MR750w scanner. Global ECV fraction was calculated using pre- and 10 minutes post-contrast T1 times after administration of 0.1 mmol/kg of gadobutrol (Gadavist). Late gadolinium enhancement (LGE) was also obtained. MR fraction was quantified by velocity encoded CMR. Mild MR was defined as MR fraction &lt; 16%. Results: MVP patients had significantly higher ECV fraction compared to controls (mean ECV (%) 32 ± 4 vs 20 ± 6, p = 0.0002), with 5/10 demonstrating non-sustained VT on ambulatory EKG monitoring. The majority (9/10 or 90%) of MVPs had mild or no MR (MR fraction &lt; 16%), and 1/10 or 10% had moderate MR (MR fraction 18%). Only one individual in the MVP group had late gadolinium enhancement (LGE) in the papillary muscles. Conclusion: MVP with ventricular arrhythmias is associated with increased global ECV reflective of diffuse myocardial fibrosis, even in the absence of significant MR or LGE. Our preliminary findings highlight for the first time a primary interstitial derangement in MVP. Larger studies are needed to understand the mechanisms and prognostic significance of primary diffuse fibrosis in MVP.

Effect of Guideline-Based Therapy on Left Ventricular Systolic Function Recovery After ST-Segment Elevation Myocardial Infarction

Little is known about the proportion of ST-segment elevation myocardial infarction (STEMI) patients treated with primary percutaneous coronary intervention, who have reduced left ventricular ejection fraction (LVEF) within 48 hours (baseline) of admission and exhibit LVEF recovery under optimal guideline-based medical treatment. Therefore, the present study evaluates the evolution of LVEF in patients after STEMI and under guideline-based medical therapy. In 2,853 STEMI patients treated with primary percutaneous coronary intervention, echocardiography was performed at baseline and at 6 months follow-up. Patients with previous myocardial infarction, reinfarction, coronary artery bypass grafting or incomplete echocardiographic data at 6 months follow-up were excluded. Reduced LVEF at baseline was defined as <40%. LVEF recovery was defined as LVEF >50% at 6 months follow-up. The prevalence of LVEF <40% at baseline was 13% (n = 371 patients; mean age 60 [range 33 to 88] years; 76% men). At follow-up, 31% of patients remained with a LVEF <40%, 30% showed a LVEF between 41% and 49% and in 39% of patients LVEF improved to >50%. There were no differences in usage of guideline-based medications at discharge across groups. On multivariable analysis, peak troponin T levels (odds ratio [OR] 0.895; p < 0.001), baseline LVEF (OR 1.069; p = 0.023) and absence of significant mitral regurgitation (OR 0.376; p = 0.018) were independently associated with LV recovery at follow-up. In conclusion, the prevalence of LVEF <40% is low. With optimal medical therapy, LVEF normalizes in 39% of patients. Smaller enzymatic infarct size, baseline LVEF and absence of mitral regurgitation were independently associated with LVEF recovery at follow-up.

Incidence and prognosis implications of long term left ventricular reverse remodeling in patients with dilated cardiomyopathy

BackgroundLeft ventricular reverse remodeling (LVRR) in dilated cardiomyopathy is poorly known within the context of current therapeutic approach. Our goal is to describe the present incidence of LVRR, the factors able to predict it and the long term prognosis of these patients. Methods and resultsWe performed a retrospective analysis of a cohort or 387 consecutive outpatients. Mean follow-up was 50.4±28.4months. Sustained LVRR occurred in 57.6% of patients.The number of coronary arteries with severe stenosis (HR 0.69, 95% CI 0.55–0.86; p=0.001), New York Heart Association Functional Class (NYHA FC) (HR 0.39, 95% CI 0.27–0.54; p<0.001) as well as the severity of mitral regurgitation (MR) at the end of follow-up (HR 0.42, 95% CI 0.30–0.58; p<0.001) and the time until first event (HR 1.02, 95% CI 1.01–1.03; p<0.001) were independent predictors of left ventricular ejection fraction improvement.LVRR was tightly related to prognosis due to the fact that both improvement in cardiac function achieving normal or slightly impaired LVEF (HR 0.31, 95% CI 0.17–0.56; p<0.001) and shorter time to achieve LVRR (HR 0.99, 95% CI 0.98–0.99; p=0.017) formed part of the best model for predicting events in DCM. ConclusionMore than half of the patients showed sustained LVRR associated with a significantly better prognosis.Fewer numbers of coronary arteries with severe stenosis, milder NYHA FC and the absence of significant MR at the end of follow-up as well as longer event free period formed a simple model to prognosticate LVRR.LVRR and the time to achieve it were strongly related to long term prognosis in patients with DCM.

Abstract 19824: Percutaneous Mitral Balloon Comissurotomy versus Surgical Comissurotomy in the Treatment of Severe Symptomatic Mitral Stenosis

Introduction: Percutaneous mitral balloon comissurotomy (PMBC) and surgical comissurotomy can be used for treatment of stage D mitral stenosis. Randomized controlled trials (RCTs) comparing PMBC and surgery have shown inconsistent results. Hypothesis: PMBC is associated with better hemodynamic and clinical results for the treatment of stage D mitral stenosis. Methods: Databases were searched for RCTs that compared double-balloon PMBC to surgical comissurotomy. Inclusion criteria were no left atrial clot, a favorable valve morphology and absence of significant mitral regurgitation. Clinical and hemodynamic outcomes were evaluated within short-term (less than 6 months) and long-term (over 6 months) follow up. Random-effects model was used due to anticipated heterogeneity. Results: A total of 6 RCTs with 474 patients were included, of whom 222 (46.8%) underwent PBMC. In short-term follow up, PMBC was associated with a larger mitral valve area (MVA) compared to surgical comissurotomy (mean difference 0.41 cm2; 95% CI 0.16-0.67; p=0.002; figure 1A), but also a higher incidence of moderate to severe mitral regurgitation (MR; OR 2.63; 95% CI 1.04-6.70; p=0.04; figure 1B). Short-term symptomatic (NYHA II-IV) heart failure (p=0.40) and new MR (p=0.32), as well as long-term MVA (p=0.23), restenosis (p=0.39), symptomatic heart failure (p=0.11), new MR (p=0.64) and need for reintervention (p=0.21) were not significantly different between groups. Conclusions: Our meta-analysis of RCTs suggests that PMBC is associated with an increased MVA as well as a higher incidence of moderate to severe MR when compared to surgery in the treatment of stage D MS. Therefore, the decision to proceed with PMBC or surgery in patients suitable for both procedures must rely on patient preferences, physician experience and risk of procedure-specific complications, such as left-to-right shunt with PMBC and wound infection/dehiscence with surgical comissurotomy.

Anomalous Origin of Left Coronary Artery from Main Pulmonary Artery (ALCAPA) Who Underwent Two Coronary System Repair with a Novel Technique

We report clinical, CT, invasive coronary angiography and intra-operative findings of a symptomatic elderly man with anomalous origin of left coronary artery from pulmonary artery (ALCAPA). ALCAPA is a rare syndrome with anomalous origin of left main coronary artery (LMCA) from main pulmonary artery (MPA). Survival into adulthood is rare and our case is probably the oldest survivor who has undergone two coronary system repairs for this anomaly. The unique features of our case include: 1) Absence of “q” wave myocardial infarction on ECG; 2) Absence of significant mitral regurgitation; 3) Demonstration of stress induced perfusion defects in nuclear imaging which as per our knowledge has been done for the first time in the literature; 4) A unique technique of closing anomalous LMCA origin by a pericardial patch, sutured on the internal aspect of MPA is the hallmark of this case.

Classic Mitral Valve Prolapse Causes Enlargement in Left Ventricle Even in the Absence of Significant Mitral Regurgitation

The aim of this study was to evaluate whether left ventricular size was increased in patients with classic bileaflet mitral valve prolapse (MVP) in the absence of significant mitral regurgitation (MR). Patients with classic bileaflet MVP were included as the case group. Two different control groups were established. The first control group was composed of the patients with mild MR caused by the reasons except MVP. The second control group consisted of healthy individuals whose echocardiograms were normal. The patients with moderate or severe MR and having abnormality in the other valves were excluded. There were 20 patients in each group. Systolic and diastolic diameters and volumes of left ventricle (LV) in the MVP group were significantly higher than those in the control groups. In 10 of the patients in the MVP group, LV internal diastolic diameter (LVIDD) values were measured as ≥5.7 cm, whereas increased LVIDD value was detected in only one patient in the other two control groups. There was a significant difference in terms of the presence of increased LVIDD values between the MVP group and the control groups. Despite this enlargement in the LV dimension, the LV ejection fractions were found similar in all groups. Furthermore, it was found that the lengths of both anterior and posterior mitral leaflets in MVP group were significantly higher than those in the control groups. The LV diameters and volumes of patients with classic bileaflet MVP were found to be increased even in the absence of significant MR. These results need to be supported by large-scale clinical studies.

Assessment of left ventricular function using mitral annular velocities in patients with congestive heart failure with or without the presence of significant mitral regurgitation

Myocardial velocities in patients with congestive heart failure (CHF) were studied using pulsed wave Doppler tissue imaging. Velocities were recorded at the mitral and tricuspid annulus. Four sites at the mitral annuli were selected corresponding to the septal, lateral, inferior, and anterior walls of the left ventricle from apical 4- and 2-chamber views. A mean value from the above 4 sites was selected to describe the mitral annular velocities. Only one site of the tricuspid annulus was selected, corresponding to the right ventricular free wall. Three different annular velocities were recorded: the peak systolic, and the peak early and late diastolic velocities. A total of 96 patients were compared with 12 age-matched healthy participants. Patients with CHF had significantly decreased mitral and tricuspid systolic velocities compared with healthy participants (4.9 vs 9.3 cm/s, P <.001, for the mitral annulus and 10.4 vs 14.6 cm/s, P <.001, for the tricuspid annulus). The early diastolic velocity was also reduced in patients compared with healthy participants (5.9 vs 10.9 cm/s, P <.001, for the mitral annulus and 8.6 vs 12.9 cm/s, P <.001, for the tricuspid annulus). Patients with CHF had a severely depressed left ventricular ejection fraction (EF) (27%). The correlation the between systolic mitral annular velocity and EF was relatively good (r = 0.59 and P <.001). The patients with CHF were divided into 2 subgroups depending on the presence or absence of significant mitral regurgitation. There was a correlation between EF and the systolic mitral annular velocity both in patients with (r = 0.61, P <.001) and without (r = 0.59, P <.001) significant mitral regurgitation. In conclusion, compared with healthy participants, the mitral and tricuspid annular velocities are significantly decreased in patients with CHF. The correlation between EF and the systolic mitral annular velocity is relatively good irrespective of the presence or absence of significant mitral regurgitation. Measurements of annular velocities constitute a simple and useful method for evaluating patients with CHF. (J Am Soc Echocardiogr 2003;16:240-5.)

Effect of Atrial Fibrillation on Pulmonary Venous Flow Patterns Assessed by Doppler Transesophageal Echocardiography

To investigate the effect of atrial fibrillation (AF) on pulmonary venous flow (PVF) patterns in a cohort with nonrheumatic AF. A prospective and controlled study undertaken at a tertiary referral medical center. The echocardiographic parameters of left superior PVF as assessed by Doppler transesophageal echocardiography in 40 patients with chronic AF (group 1) were compared to those of 33 volunteers with sinus rhythm (group 2) and well-matched baseline characteristics. : All group 1 patients presented with single systolic forward flow (SFF) patterns. In contrast, single and double SFF patterns were found equally in group 2. With regard to reverse flow (RF), most group 1 patients (33 of 40) had an early systolic RF and none had atrial RF; however, most group 2 subjects (29 of 33) had an atrial RF. Some of the group 1 patients (17%) had a late systolic RF in the absence of significant mitral regurgitation. In group 1, the SFF appeared later and disappeared earlier than in group 2. The mean systolic peak velocity and time-velocity integral (TVI) of the SFF were significantly lower in group 1 compared to group 2. The diastolic peak velocity and TVI were not significantly different between groups. : Our data indicate that AF independently and significantly affects the PVF and leads to characteristic flow patterns different from sinus rhythm. The presence of AF reduces SFF in addition to the absence of atrial RF. These changes in the flow patterns should be taken into account while interpreting the implications of PVF in the presence of AF.

Rheumatic mitral stenosis associated with hypertrophic cardiomyopathy and anomalous muscle bundle in the right ventricle

Clinical, echocardiographic, haemodynamic and angiographic features of a patient with rheumatic mitral stenosis, hypertrophic cardiomyopathy and anomalous muscle bundle in the right ventricle are presented. At the bedside, the presence of left ventricle type apex beat, left ventricle S 4 gallop, ejection systolic murmur at the left mid sternal border and electrocardiographic evidence of left ventricular hypertrophy in a patient with classical findings of mitral stenosis in the absence of significant mitral regurgitation and aortic valve disease should suggest this extremely rare association of mitral stenosis with hypertrophic cardiomyopathy.

Transesophageal echocardiographic characterization of pulmonary vein flow not due to atrial contraction or mitral regurgitation

In normal human subjects who are in normal sinus rhythm, transthoracic echocardiographic studies have demonstrated that blood flows from the pulmonary veins into the left atrium during both systole and diastole. 1 Using transesophageal echocardiography, we have demonstrated that a brief period of flow reversal characterized by retrograde left atrial to pulmonary vein flow is seen in most normal subjects during left atrial contraction. 2 Recent studies have demonstrated the importance of recognition of pulmonary vein flow reversal occurring during systole as a marker of severe mitral regurgitation. 3 In patients in atrial fibrillation, however, we have noted pulmonary vein flow reversal which appears systolic in timing in the absence of significant mitral regurgitation. The current study characterizes this nonatrial flow reversal and compares its flow characteristics with the flow reversal noted in sinus rhythm.

Limitations of pulmonary wedge V waves in diagnosing mitral regurgitation

To study the usefulness of large V waves in pulmonary capillary wedge tracings in establishing the diagnosis of mitral regurgitation, data on 1,021 consecutive cardiac catheterizations were reviewed. Wedge tracings were obtained by Swan-Ganz catheterization in 208 patients, usually because of suspected valve disease. One hundred two patients had no trace of mitral regurgitation angiographically, 69 had mild to moderate and 37 had severe regurgitation. V waves were graded as trivial (less than 5), intermediate (5 to 10) or large (10 or more mm Hg above mean wedge pressure). Of 50 patients with large V waves, 18 (36 percent) had no or trace mitral regurgitation; these included 5 with mitral stenosis, 3 with a mitral valve prosthesis, 4 with coronary disease and congestive failure, 2 with aortic valve disease and congestive failure and 2 with a ventricular septal defect. Of 37 patients with severe mitral regurgitation, 16 (43 percent) had large and 12 (32 percent) had trivial V waves. Thus, mitral regurgitation is the most common cause of large V waves; however, large V waves are neither highly sensitive nor specific for severe regurgitation. Increased left atrial compliance may be associated with trivial V waves in the presence of severe regurgitation. Mitral obstruction, congestive heart failure and ventricular septal defect may all be associated with large V waves in the absence of significant mitral regurgitation.