Exercise-induced Mitral Regurgitation Research Articles

Change in Lung Fluid Volume during Exercise in Patients with Exercise-Induced Mitral Regurgitation

Exercise-induced mitral regurgitation (MR) can be diagnosed during stress echocardiography testing. Remote dielectric sensing (ReDSTM) is a noninvasive electromagnetic-based modality to measure lung fluid levels. The change in lung fluid levels in patients with MR during stress echocardiography remains unknown. Patients with symptomatic MR at baseline and suspected worsening exercise-induced MR underwent stress echocardiography. ReDS values were measured before and after the tests. A total of four patients (ages ranging between 74 and 84 years old, three women) underwent stress echocardiography testing using a bicycle ergometer. In patient A, MR effective regurgitant orifice area (EROA) remained unchanged and ReDS values decreased. EROA increased significantly with a small incremental change in ReDS values in patient B and patient C, who underwent valve repair with MitraClip later. Patient D had a mild increase in MR EROA but a considerable increase in ReDS values (from 22% to 32%), and eventually received valve repair with MitraClip. The ReDS system may be a complementary tool to conventional stress echocardiography in the evaluation of clinically significant MR and considering mitral valve intervention.

Determinants of Exercise-Induced Mitral Regurgitation Using Three-Dimensional Transesophageal Echocardiography Combined With Isometric Handgrip Exercise

Using three-dimensional (3D) transesophageal echocardiography (TEE) and isometric handgrip exercise (IHE), we investigated the determinants of exercise-induced mitral regurgitation (MR) according to MR etiologies. Seventy-six patients with more than moderate MR, 40 patients with functional MR (FMR) and 36 patients with degenerative MR (DMR), underwent 3D TEE combined with IHE. Mitral valve (MV) geometry and 3D vena contracta area (3D VCA) were simultaneously evaluated at baseline and during IHE. With regard to exercise-induced MR, Δ3D VCA was calculated as the difference between 3D VCA at baseline and 3D VCA during IHE. IHE caused different changes in MV geometry between etiologies and led to exacerbation of 3D VCA at baseline. Larger Δ3D VCA was observed in the FMR group compared with the DMR group (15.9 ± 10.3 mm2 versus 7.3 ± 4.2 mm2; p < 0.0001). In multivariate analyses, tenting height and 3D VCA were selected as independent factors associated with Δ3D VCA in the FMR group (p = 0.0135 and p = 0.0201, respectively), while flail width was selected as an independent factor associated with Δ3D VCA in the DMR group (p = 0.0066). In conclusion, IHE alters mitral valve geometry and causes exacerbation of MR regardless of MR etiology and the determinants of exercise-induced MR differed between MR etiologies.

Exercise-induced mitral regurgitation and right ventricle to pulmonary circulation uncoupling across the heart failure phenotypes.

Exercise-induced mitral regurgitation (Ex-MR) is one of the mechanisms that contribute to reduced functional capacity in heart failure (HF). Its prevalence is not well defined across different HF subtypes. The aim of the present study was to describe functional phenotypes and cardiac response to exercise in HFrEF, HFmrEF, and HFpEF, according to Ex-MR prevalence. A total of 218 patients with HF [146 men, 68 (59-78) yr], 137 HFrEF, 41 HFmrEF, 40 HFpEF, and 23 controls were tested with cardiopulmonary exercise test combined with exercise echocardiography. Ex-MR was defined as development of at least moderate (≥2+/4+) regurgitation during exercise. Ex-MR was highly prevalent in the overall population (52%) although differed in the subgroups as follows: 82/137 (60%) in HFrEF, 17/41 (41%) in HFmrEF, and 14/40 (35%) in HFpEF (P < 0.05). Ex-MR was associated with a high rate of ventilation (VE) to carbon dioxide production (VCO2) in all HF subtypes [31.2 (26.6-35.6) vs. 33.4 (29.6-40.5), P = 0.004; 28.1 (24.5-31.9) vs. 34.4 (28.2-36.7), P = 0.01; 28.8 (26.6-32.4) vs. 32.2 (29.2-36.7), P = 0.01] and with lower peak VO2 in HFrEF and HFmrEF. Exercise right ventricle to pulmonary circulation (RV-PC) uncoupling was observed in HFrEF and HFpEF patients with Ex-MR [peak TAPSE/SPAP: HFrEF 0.40 (0.30-0.57) vs. 0.29 (0.23-0.39), P = 0.006; HFpEF 0.44 (0.28-0.62) vs. 0.31 (0.27-0.33), P = 0.05]. HFpEF with Ex-MR showed a distinct phenotype characterized by better chronotropic reserve and peripheral O2 extraction.NEW & NOTEWORTHY Ex-MR is a common mechanism across the spectrum of HF subtypes and combines with ventilatory inefficiency and RV-PC uncoupling. Interestingly, in HFpEF, Ex-MR emerged as unexpectedly prevalent and peculiarly associated with increased chronotropic response and peripheral O2 extraction as potential adaptive mechanisms to backward flow redistribution.

The MitraClip Procedure in Patients With Moderate Resting but Severe Exercise-Induced Mitral Regurgitation.

Optimal timing for percutaneous mitral regurgitation (MR) treatment using MitraClip (Abbott Vascular) remains unclear. We evaluated the outcome after MitraClip in patients with moderate resting MR, progressing to severe exercise- induced MR (MR2+) compared to patients with severe resting MR (MR3). We retrospectively investigated 221 patients undergoing MitraClip. All-cause deaths and heart failure (HF) hospitalizations were assessed as the combined primary endpoint. We identified 55 MR2+ and 166 MR3 patients. At baseline, MR3 patients showed higher STS scores (6.7 ± 7.3 vs 4.4 ± 5.5; P<.01), more HF hospitalizations in the 2 years prior to the procedure (51% vs 29%; P<.01), worse left ventricular ejection fraction (44.9 ± 16.5% vs 52.5 ± 14.3%; P<.01), larger left ventricular end-diastolic diameter (LVEDd; 57.0 ± 9.3 mm vs 51.7 ± 8.2 mm; P<.001), and larger left atrial volumes (118.3 ± 55.8 mL vs 98.6 ± 35.2 mL; P=.02). Long-term outcome according to the combined endpoint was significantly worse in MR3 patients (P=.01). HF hospitalizations significantly declined in both groups 2 years after MitraClip (P<.001 in MR3 patients, P=.03 in MR2+ patients). Multivariate Cox regression analysis revealed LVEDd (hazard ratio, 1.035; 95% confidence interval, 1.005-1.066; P=.02) and previous HF hospitalizations (hazard ratio, 1.813; 95% confidence interval, 1.016-3.234; P=.04) as strong outcome predictors. Symptomatic patients with moderate resting and severe exercise-induced MR during handgrip echocardiography may represent an MR cohort at an earlier disease stage with improved treatment response following MitraClip implantation compared to individuals with severe resting MR. Larger left ventricular diameters and preprocedural HF hospitalizations were identified as independent adverse outcome predictors.

Exercise-induced in Secondary Mitral Regurgitation: Analysis of Echocardiographic Parameters at Rest Predicting the Onset of Significant Exercise-induced Mitral Regurgitation

Exercise-induced in Secondary Mitral Regurgitation: Analysis of Echocardiographic Parameters at Rest Predicting the Onset of Significant Exercise-induced Mitral Regurgitation

Abstract 16657: Role of Exercise Induced Mitral Regurgitation and Its Prevalence in Functional Limitation of Heart Failure Patients With Preserved Ejection Fraction

Background: Functional limitation in heart failure (HF) patients recognize multiple mechanisms. Exercise-induced mitral regurgitation (Ex-MR) has been extensively studied in HF population with reduced ejection fraction (HFrEF, EF &lt; 40%), as responsible of right ventricle (RV) to pulmonary circulation (PC) uncoupling phenomenon. The relative role of this hemodynamic determinant has not been investigated so far in HF patients with preserved (HFpEF, EF &gt; 50%) and mid-range EF (HFmrEF, EF 40 - 49%). Aim: To describe functional phenotypes and cardiac response to exercise in HF patients, with respect to the development of Ex-MR. Methods: 179 HF patients and 23 controls were tested with cardiopulmonary exercise test (CPET) combined with exercise-echocardiography. Based on current guidelines, we identified 114 HFrEF, 34 HFmrEF and 31 HFpEF, further divided according with the presence of at least moderate (&gt;2+/4+) Ex-MR. Results: Ex-MR rate was 58%, 41% and 42% in HFrEF, HFmrEF and HFpEF, respectively. Ex-MR was associated with echocardiographic signs of RV-PC uncoupling (TAPSE/PASP ratio), particularly enhanced by the exercise in HFpEF patients. HFpEF with Ex-MR showed a distinct phenotype with chronotropic competence and increased peripheral oxygen extraction, compared to Ex-MR - cohort, possible expression of a compensatory mechanism to significant reduction in contractile reverse. The Ex-MR was associated with lower peak VO2 and workload in HFrEF and HFmrEF, while there were no differences related to HFpEF. The presence of Ex-MR significantly compromised also ventilatory efficiency (VE/VCO2) in all HF classes. Conclusion: Ex-MR emerged as a new mechanism of functional limitation in HFpEF, sharing a common pathophysiological basis with other HF patients. The RV-PC uncoupling is the best haemodynamic correlate of Ex-MR.

Impact of exercise-induced mitral regurgitation on hypertrophic cardiomyopathy outcomes.

Rest echocardiography plays a role in hypertrophic cardiomyopathy (HCM) diagnosis and risk stratification because left atrial enlargement, severe left ventricle (LV) hypertrophy, and rest LV outflow tract (LVOT) gradients ≥50 mmHg are sudden cardiac death risk factors that have been highlighted in recent guidelines. Conversely, the lack of evidence makes that exercise-echocardiography findings play a limited role. In clinical practice, LVOT gradient, but also mitral regurgitation (MR) or pulmonary pressure, seems relevant parameters to look for, during the exercise. Therefore, we sought to determine whether exercise-induced changes in myocardial and valvular functions could improve HCM risk stratification. Consecutive primitive HCM patients with a preserved LV ejection fraction underwent standardized exercise echocardiography (including the assessment of myocardial function, dynamic left intraventricular gradient, and valvular regurgitations) at baseline and were clinically followed for a median of 29.3 months. The primary endpoint was a composite criterion that included death from any cause, cardiorespiratory arrest, and hospitalization for a cardiovascular event. A total of 126 patients were included. Eighteen patients reached the primary endpoint. According to univariate Cox regression analysis, exercise LVOT gradient ≥50 mmHg [hazard ratio (HR) = 3.31, P = 0.01] and significant (≥2/4) exercise MR (HR = 3.64, P < 0.01) were associated with the primary endpoint. Patients with significant MR had significantly higher rest and exercise LVOT gradients (P = 0.001 and P = 0.001) and larger left atria volumes (P < 0.001). Significant exercise-induced MR appears to significantly impact the prognoses of HCM patients, and it is also associated with higher LVOT rest and exercise gradients.

Abstract 13745: Severity of Functional Mitral Regurgitation During Maximal Exercise Testing in Heart Failure: Additional Value of Combining Echocardiography with Cardiopulmonary Exercise Testing

Background: In heart failure (HF) patients the severity of mitral regurgitation (MR) at rest has a well established prognostic value and its increase during exercise further adds to an increased risk. Our goal was to define the relationship between the degree of exercise MR severity with cardiopulmonary and echocardiographic related phenotypes in a cohort of HF patients. Methods: 71 HF reduced ejection fraction patients (mean age 67±11; male 72%; ischemic etiology 61%; NYHA class I, II, III and IV 13%, 36%, 39% and 12%, mean ejection fraction 33±9%) underwent cardiopulmonary exercise test (CPET) on tiltable cycle-ergometer combined with echocardiography at rest and during exercise. The population was divided into two groups according to the degree of functional peak MR: no to mild/moderate MR (no MR, MR1+ and MR2+) vs moderate/severe MR (MR3+ and MR4+). Results: A good correlation (ρ coefficient= 0.49) was found between the degree of dynamic MR and PASP at peak exercise. Despite similar echocardiographic profile at rest patients with significant peak MR (MR≥3+) had worse exercise performance (lower peak VO2, O2 pulse and workload) and impaired ventilatory efficiency (higher VE/VCO2 slope). Conclusions: In HF patients the severity of exercise-induced MR is associated with the most unfavorable performance and pulmonary hemodynamic response. A combined approach with CPET and echocardiographic assessment can help to early unmask and target functional MR and its related unfavorable phenotypes.

Heart Failure With Preserved Ejection Fraction in Outpatients With Unexplained Dyspnea: A Pressure-Volume Loop Analysis

The aim of the present study was to diagnose heart failure with preserved ejection fraction (HFPEF) in outpatients with unexplained chronic dyspnea and to elucidate its underlying mechanisms in this population using invasive pressure-volume loop analysis. The diagnosis of HFPEF in stable outpatients with unexplained dyspnea is difficult. Thirty patients (age 67 +/- 8.6 years, 27% males) with preserved left ventricular (LV) ejection fraction (>50%) and unexplained chronic New York Heart Association functional class II to III dyspnea underwent heart catheterization. Patients with significant coronary artery stenosis (>50%) were excluded. Pressure-volume loops were assessed using a conductance catheter at rest, hand-grip exercise, leg lifting, and nitroprusside and dobutamine infusion. Twenty (66%) patients showed LV end-diastolic pressure >16 mm Hg (HFPEF), whereas the remaining 10 patients served as controls. Patients with HFPEF had significantly higher end-diastolic stiffness (0.205 +/- 0.074 vs. 0.102 +/- 0.017, p < 0.001) at rest, and their end-diastolic pressure-volume relationship showed a consistent upward and leftward shift during all hemodynamic interventions compared with controls. Regarding the underlying mechanism of HFPEF, 14 (70%) patients had markedly increased end-diastolic stiffness, which was considered a sufficient single pathology to induce increased LV end-diastolic pressure. Four (20%) patients showed a concomitant presence of moderately increased stiffness and severe LV dyssynchrony, and the remaining 2 (10%) patients, with normal stiffness, showed significant exercise-induced mitral regurgitation at hand-grip exercise. If the invasive pressure measurements were absent, only 5 (25%) of the outpatients with HFPEF fulfilled the European Society of Cardiology definition of HFPEF. A significant proportion of stable outpatients with unexplained chronic dyspnea may have HFPEF. In the patients whom we studied, increased LV stiffness, dyssynchrony, and dynamic mitral regurgitation were the major mechanisms underlying development of HFPEF.

Abstract 1603: Factors and Mechanisms Associated with Improved Cardiopulmonary Performance after Cardiac Resynchronization Therapy. An Exercise Echocardiography Study.

Background: Cardiac resynchronization therapy (CRT) leads to better cardiopulmonary performance in congestive heart failure (CHF) patients (pts). Mechanisms underlying the benefits are not fully elucidated. Aim: To investigate factors and mechanisms associated with improved cardiopulmonary performance after CRT. Methods: Twenty-three pts (EF 26±7%, QRS complex 170±26 msec) were studied by simultaneous quantitative semi-supine exercise echocardiography and cardiopulmonary exercise testing before and 3 months after CRT. Pts with an increase (Δ) in peak VO 2 ≥1.1 ml/kg/min were considered clinical responderes. Effective regurgitant orifice (ERO) of the mitral regurgitation (MR) was assessed using the PISA method. Results: In the entire population, CRT was associated with a decrease in LV dyssynchrony from 53±2 to 23±9 msec (p&lt;0.001), increase LV ejection fraction (EF) from 26±7 to 36±9% (p&lt;0.001) and ERO reduction from 0.24±0.11 to 0.13±0.06 cm 2 (p&lt;0.001) In addition, peak VO 2 increased from 11.6±2.3 to 12.9±3.6 ml/kg/min (p&lt;0.01) and Nt-pro BNP decreased from 2795±1644 to 2021±1353 pg/ml (p&lt;0.05). At follow-up (Table ), ERO at rest was similar but exercise-induced ERO and Nt-pro BNP were significantly lower in responders vs nonresponders. Change in peak VO 2 correlated inversely with the extent of exercise-induced MR at follow-up (r=−0.47, p&lt;0.05), with baseline Nt-pro BNP levels (r=−0.53, p&lt;0.05) and change in LVESV (r=−0.49, p&lt;0.05). Conclusions. Improved cardiopulmonary performance after CRT is related to changes in exercise-induced MR rather than resting MR. Thus, effects on the exercise-induced MR in parallel to reverse LV remodelling appear to contribute to improved cardiopulmonary performance and clinical benefits of the CRT.

Early and late effects of cardiac resynchronization therapy on exercise-induced mitral regurgitation: relationship with left ventricular dyssynchrony, remodelling and cardiopulmonary performance

Exercise-induced mitral regurgitation (MR) bears a poor prognosis in patients with congestive heart failure (CHF). Cardiac resynchronization therapy (CRT) is associated with improved clinical outcome but its effects on exercise-induced MR remain undetermined. We investigated serial changes in functional MR in relation to left ventricular (LV) remodelling and cardiopulmonary performance after CRT. Twenty-eight patients with CHF (LV ejection fraction 25 +/- 7%), broad QRS complex (171 +/- 27 ms), and at least mild MR [effective regurgitant orifice (ERO) 0.25 +/- 0.12 cm2] were studied with quantitative exercise echocardiography and cardiopulmonary exercise testing prior, within 1 week, and 3 months after CRT. Early after CRT, a decrease in LV dyssynchrony (from 54 +/- 21 to 19 +/- 7 ms, P < 0.001) and in MR at rest (ERO from 0.25 +/- 0.12 to 0.20 +/- 0.10 cm2, P = 0.047) was observed. However, no change in exercise-induced increase in MR was observed (ERO from 0.34 +/- 0.12 to 0.31 +/- 0.16 cm2, NS). Three months after CRT, a decrease in the mitral valve tenting area (from 3.3 +/- 1.2 to 2.0 +/- 0.6 cm2, P < 0.001) and an increase in LV sphericity index (from 1.5 +/- 0.3 to 1.8 +/- 0.5, P < 0.001) were paralleled by an attenuation of exercise-induced MR (ERO 0.19 +/- 0.06 cm(2), P = 0.001 vs. prior CRT). This was associated with an increase in LV ejection fraction (from 25 +/- 7 to 35 +/- 9%, P < 0.001), peak oxygen uptake (from 11.7 +/- 2.4 to 13.7 +/- 3.8 mL/kg/min, P = 0.001), and a decrease in Nt-pro-BNP (from 2777 +/- 1681 to 1963 +/- 1361 pg/mL, P = 0.067). CRT is associated with acute decrease in resting MR but does not immediately attenuate exercise-induced MR. In contrast, only late, CRT-induced reversed LV remodelling and reduced mitral apparatus deformation are associated with a reduction in both resting and exercise-induced MR and with an improvement in cardiopulmonary performance.

Prognostic value of mitral regurgitation assessment during exercise echocardiography in patients with left ventricular dysfunction: A follow-up study of 1.7±1.5 years☆

The value of exercise echocardiography (EE) over resting echocardiography when this last incorporates information on mitral regurgitation (MR) is only partially known. Furthermore, limited data exist regarding the value of MR worsening during exercise in patients with left ventricular (LV) dysfunction. We investigate whether EE has incremental value over a resting echo-Doppler study; and whether post-exercise MR increments the value of EE for predicting outcome in patients with LV dysfunction. Three hundred and twenty-three consecutive patients with LV dysfunction (LV ejection fraction < or =45%) referred for EE were followed for 1.7 +/- 1.5 years. There were 43 hard events (myocardial infarction in 9 and cardiac death in 34). Resting MR, peak heart rate x blood pressure, and number of involved territories at exercise were independently associated to hard events (incremental P-value of EE =0.02). Independent variables associated to cardiac death were resting MR, peak heart rate x blood pressure, peak wall motion score index, and MR worsening (incremental P-value of MR worsening = 0.04). EE maintains its prognostic value over resting echocardiography even when this last incorporates information on MR. Exercise-induced MR worsening has independent prognostic value for cardiac death in patients with LV dysfunction.

Contribution of exercise-induced mitral regurgitation to exercise stroke volume and exercise capacity in patients with left ventricular systolic dysfunction.

Functional mitral regurgitation (MR) is common in patients with heart failure and left ventricular (LV) dysfunction, and its severity may vary over time, depending primarily on the loading conditions. Because dynamic changes in the severity of functional MR may affect forward stroke volume, we hypothesized that exercise-induced changes in MR severity influence the stroke volume response of patients with LV dysfunction to exercise, and hence their exercise capacity. Heart failure patients (n=25; mean age 53+/-12 years) with LV dysfunction underwent dynamic bicycle exercise at steady-state levels of 30%, 60%, and 90% of predetermined peak VO2. During each exercise level, right heart pressures, cardiac output, VO2, and MR severity were measured simultaneously. During exercise, MR severity, as evaluated by the ratio of MR jet over left atrium area, increased from 15+/-8% to 33+/-15%. Peak VO2, exercise-induced changes in stroke volume, and those in capillary wedge pressure correlated with the changes in MR (r=-0.55, -0.87, and 0.62, respectively, P<0.01). The changes in MR severity also correlated with those in end-diastolic (r=-0.75, P<0.01) and end-systolic (r=-0.72, P<0.01) sphericity indexes and those in the coaptation distance (r=0.86, P<0.01). Our data indicate that in patients with LV dysfunction, exercise-induced changes in MR severity limit the stroke volume adaptation during exercise and therefore contribute to limitation of exercise capacity.

Exercise-induced mitral regurgitation is a predictor of morbid events in subjects with mitral valve prolapse: M.F. Stoddard, C.R. Prince, S. Dillon, R.A. Longaker, G.T. Morris, N.E. Liddell. Noninvasive Cardiology, Cardiology Division, University of Louisville, Louisville, KY. J Am Coll Cardiol 1995;25:693–9.

Exercise-induced mitral regurgitation is a predictor of morbid events in subjects with mitral valve prolapse: M.F. Stoddard, C.R. Prince, S. Dillon, R.A. Longaker, G.T. Morris, N.E. Liddell. Noninvasive Cardiology, Cardiology Division, University of Louisville, Louisville, KY. J Am Coll Cardiol 1995;25:693–9.

Exercise-induced mitral regurgitation in patients with congestive heart failure. Correlations with exercise capacity and hemodynamics

Exercise-induced mitral regurgitation in patients with congestive heart failure. Correlations with exercise capacity and hemodynamics

Exercise-Induced Mitral Regurgitation is a Predictor of Morbid Events in Subjects with Mitral Valve Prolapse

Exercise-Induced Mitral Regurgitation is a Predictor of Morbid Events in Subjects with Mitral Valve Prolapse

Exercise-induced mitral regurgitation is a predictor of morbid events in subjects with mitral valve prolapse

This study attempted to determine whether a subset of patients with mitral valve prolapse and no mitral regurgitation at rest will develop mitral regurgitation during exercise and have a higher than anticipated risk of morbid cardiovascular events. Mitral regurgitation in patients with mitral valve prolapse identifies a subset of patients at higher risk for morbid events. However, mitral regurgitation in patients with mitral valve prolapse may be intermittent and could go unrecognized. A provocative test to unmask mitral regurgitation in these patients would be useful. Ninety-four adult patients with mitral valve prolapse and no mitral regurgitation at rest were studied during supine bicycle ergometry using color flow Doppler echocardiography in the apical four-chamber and long-axis views. Patients were prospectively followed up for morbid events. Thirty (32%) of 94 patients had exercise-induced mitral regurgitation. Prospective follow-up (mean 38 months) showed more morbid events in the group with than without mitral regurgitation and included, respectively, syncope (43% vs. 5%, p < 0.0001), congestive heart failure (17% vs. 0%, p < 0.005) and progressive mitral regurgitation requiring mitral valve replacement surgery (10% vs. 0%, p < 0.05). Cerebral embolic events, endocarditis or sudden death were rare and not different between groups. In patients with mitral valve prolapse without mitral regurgitation at rest, exercise provokes mitral regurgitation in 32% of patients and predicts a higher risk for morbid events.

Exercise-Induced Mitral Regurgitation in Mitral Valve Prolapse

In patients with mitral valve prolapse (MVP), mitral regurgitation (MR) increases risk of valve replacement, endocarditis, and sudden death. This study examined the outcome of patients with MVP and no MR at rest who developed MR during exercise. Ninety-four subjects fulfilled entrance criteria and underwent supine bicycle exercise tests with echocardiographic evaluation every 2 to 3 minutes. …

Postural exercise abnormalities in symptomatic patients with mitral valve prolapse

The hemodynamics of the supine and upright exercise response in 16 symptomatic women with mitral valve prolapse (Group I) was compared with that in 8 asymptomatic normal control women (Group II). All subjects had supine and upright echocardiography and phonocardiography at rest and none demonstrated mitral regurgitation. All participants then underwent same day graded bicycle exercise, with simultaneous radionuclide angiography in both the upright and the supine posture. Catecholamines were measured, and a variety of volumetric and hemodynamic data were obtained.Group I (patients with mitral valve prolapse) demonstrated a reduced exercise tolerance, especially during upright exercise, as measured by both total exercise duration and maximal work load achieved. Mean total catecholamine measurements were similar between the two study groups at comparable mean heart rate, mean blood pressure and mean rate-pressure (double) product. No difference was observed in the ratio of right to left ventricular stroke counts at rest or during exercise regardless of posture, suggesting that exercise-induced mitral regurgitation did not occur.A difference was noted, however, in left ventricular end-diastolic volume index. At rest, Group I patients exhibited a 42% decrease in this index when sitting upright, and this difference from supine values persisted at submaximal (300 kpm/min) and peak work loads (34 and 29% difference, respectively). This contrasted with the control subjects whose upright end-diastolic volumes at rest, at 300 kpm/min and at peak exercise were reduced 21, 10 and 3%, respectively, compared with supine values. Cardiac index measurements reflected the reduced left ventricular end-diastolic volume observed. Other measurements, including ejection fraction, left ventricular end-systolic volume index and peak systolic pressure/end-systolic volume ratio, were similar between the two groups at each posture and level of exercise. The percent stroke volume ejected during each third of systolic ejection was also not remarkably different between the groups.In summary, as compared with control subjects, patients with mitral valve prolapse exhibit an exaggerated reduction in left ventricular end-diastolic volume throughout upright exercise. The associated redaction in cardiac output at each level of exercise may contribute to the reduction in exercise tolerance observed in this symptomatic patient subset.

Color Doppler assessment of mitral regurgitation induced by supine exercise in patients with coronary artery disease

Development of mitral regurgitation (MR) during acute myocardial ischemia is a well known occurrence. To assess the feasibility and clinical utility of detecting MR during exercise testing, color Doppler examinations were performed in 22 patients with angiographically proved coronary artery disease (CAD) and in 17 normal subjects before, during and after graded supine bicycle exercise. Not only was MR visualized using color Doppler during dynamic testing, but it was also slightly more sensitive (59% vs 54%) and specific (100% vs 88%) than the electrocardiographic response in identifying patients with CAD. When the appearance of MR or diagnostic electrocardiographic changes or both were used to identify patients with CAD, the sensitivity of exercise tolerance testing increased to 82%, although the specificity was 88%. In addition, exercise-induced MR was observed to be as sensitive and specific as exercise-induced wall motion abnormalities. Combining exercise-induced MR with wall motion abnormalities also increased the sensitivity to 82%, with the specificity remaining at 100%. With use of exercise-induced MR, wall motion abnormalities or electrocardiographic changes, the sensitivity and specificity of the exercise test in diagnosing CAD was 91% and 88%, respectively. The degree of MR as estimated by maximal area of regurgitation signals, as well as by its ratio to left atrial area, did not correlate with extent of CAD. However, the presence of exercise-induced MR suggested an increased likelihood of 3-vessel CAD because it was found in 9 of 11 patients with 3-vessel CAD, compared with 2 of 5 patients with 2-vessel and 2 of 6 patients with 1-vessel CAD. Thus, assessment of MR by color Doppler during exercise testing may provide an additional diagnostic criterion for detecting patients with CAD.