Rheumatic heart disease (RHD), a sequela of Group A beta-hemolytic streptococcal infection, is a major acquired cardiac disease predominantly affecting the younger population. A history of rheumatic fever during childhood, often presenting with joint involvement, precedes the development of RHD [1,2]. The bacterial antigen cross-reacts immunologically with valvular tissue, resulting in immune-mediated damage that leads to scarring or annular deformity, thereby altering normal cardiac physiology.

Valve damage in RHD typically manifests as stenosis due to thickening and fibrosis, restricting left ventricular inflow. Alternatively, regurgitation may occur due to leaflet elongation or inadequate coaptation. Chronic stenotic valves may also become regurgitant due to calcific fixation of the mitral orifice.

While RHD has declined significantly in prevalence in developed nations, it remains a major cause of valvular heart disease in developing regions. According to the World Heart Federation, RHD predominantly affects impoverished and vulnerable populations, placing a significant burden on healthcare systems. Globally, it is estimated that approximately 33 million people are affected, with around 320,000 RHD-related deaths annually [3]. If untreated, RHD can lead to serious complications including arrhythmias, stroke, infective endocarditis, and systemic embolization, all of which significantly impair quality of life and survival.

In the South Asian population, the mitral valve is most frequently affected, followed by the aortic valve. Mitral stenosis is more common than mitral regurgitation in this demographic. In contrast, aortic valve involvement is more prevalent in Western populations, typically due to degenerative etiologies.

RHD is a chronic, debilitating, and potentially fatal condition that is largely preventable. Patients often remain asymptomatic after the initial episode of rheumatic fever; however, symptoms usually emerge once moderate-to-severe valvular damage has occurred. Common symptoms include progressive breathlessness, orthopnea, atypical chest pain, generalized weakness, and peripheral edema.

Long-standing mitral valve disease often leads to left atrial dilation and the development of post-capillary pulmonary arterial hypertension (PAH), complicating both diagnosis and management. PAH presents a challenge in surgical planning, particularly in deciding whether to concurrently address the tricuspid valve during mitral valve surgery [4,5]. Double valve interventions are associated with higher morbidity, including increased risk of prosthetic valve dysfunction, need for anticoagulation, prolonged cardiopulmonary bypass and aortic cross-clamp time, and extended hospitalization.

There are limited studies evaluating the long-term outcomes in patients with untreated tricuspid lesions undergoing isolated mitral valve replacement in the context of PAH. While earlier literature indicates that both mitral valve and pulmonary vasculature are involved in a significant subset of RHD patients, current guidelines do not advocate for prophylactic tricuspid intervention in cases of mild disease.

This study aims to evaluate the behavior and rate of improvement in pulmonary arterial pressures following mitral valve replacement, using echocardiographic indices and clinical parameters. We also aim to assess pulmonary vascular resistance to quantify the hemodynamic changes post-surgery.

Surgical or minimally invasive correction of mitral valve pathology requires a multidisciplinary approach. Mitral valve replacement remains the standard treatment for symptomatic primary mitral stenosis, typically yielding excellent outcomes when performed in a timely manner. Involvement of multiple valves can significantly alter hemodynamics, often resulting in volume overload, which can be accurately assessed by echocardiography.

Pulmonary arterial pressures are expected to change following surgical correction of mitral pathology, but few studies have systematically evaluated this phenomenon [6]. It is increasingly recognized that pulmonary hypertension is, to some extent, reversible following mitral valve intervention. Through this study, we aim to analyze echocardiographic indices reflecting pulmonary pressures and vascular resistance, thereby elucidating the extent of pulmonary hemodynamic recovery post-mitral valve surgery. Notably, pulmonary hypertension is also a recognized predictor of poor postoperative outcomes in this patient group.

RHD remains the predominant cause for valve replacement surgeries in countries like India, with mitral valve replacement constituting the majority of cases [7,8]. Although RHD can involve all four cardiac valves, its progression may vary between valves due to multiple influencing factors. Recent studies conducted on larger cohorts have increasingly demonstrated favorable surgical outcomes, challenging earlier assumptions about the risks of surgical intervention in the presence of PAH [9,10].

Aims and Objectives

The present study was conducted with the following objectives:

1. To assess the change in pulmonary arterial pressure among patients undergoing mitral valve replacement.
2. To correlate clinical improvement following mitral valve surgery with changes in pulmonary arterial pressures.
3. To identify clinical factors associated with the degree of change in pulmonary arterial pressure among patients undergoing mitral valve replacement.

Study Design and Setting

This retrospective observational study was conducted in the Department of Cardiothoracic and Vascular Surgery (CTVS) between February 2018 and December 2019. Patient records were reviewed for individuals diagnosed with pulmonary arterial hypertension (PAH) who underwent mitral valve replacement (MVR). Ethical clearance was obtained from the Postgraduate Research Monitoring Committee and the Institutional Ethics Committee prior to data collection.

Study Participants

Inclusion Criteria

• Patients diagnosed with mitral stenosis and/or mitral regurgitation with baseline PAH
• Underwent elective mitral valve replacement

Exclusion Criteria

• Severe left ventricular dysfunction (ejection fraction <30%)
• Concomitant coronary artery disease or myocardial pathology
• Co-existent intracardiac shunt lesions
• Active infective endocarditis
• Emergency mitral valve replacement
• Non-cardiac causes of PAH (e.g., parenchymal/interstitial lung disease, systemic vasculitis, hepatic failure, pulmonary arteriovenous malformations)
• Severe systemic comorbidities

Sampling

Sampling Population

Patients with mitral valvular heart disease and associated PAH undergoing MVR during the study period.

Sample Size Estimation

Based on historical records, an estimated five eligible patients underwent MVR per month. Over a 12-month recruitment window, a maximum of 60 patients was expected and included.

Sampling Technique

Patient data were collected retrospectively from the Medical Records Department. Only de-identified records of patients meeting inclusion criteria were reviewed. Severe mitral stenosis was defined by a mitral valve area ≤1 cm² (assessed by planimetry or pressure half-time), while severe mitral regurgitation was defined as a regurgitant jet area ≥40% of left atrial area or evidence of volume overload on echocardiography. Pulmonary hypertension was defined as systolic pulmonary artery pressure (PASP) ≥40 mmHg on preoperative echocardiography.

Study Procedure

Preoperative and postoperative transthoracic echocardiographic parameters were recorded from patient files. Echocardiographic views included standard parasternal long and short axis, apical four-chamber, and subcostal views. Color Doppler and spectral Doppler data of mitral, tricuspid, pulmonary, and aortic valves were reviewed.

Key Hemodynamic Measurements

• PASP was estimated using the tricuspid regurgitation (TR) jet velocity with the simplified Bernoulli equation:

PASP=4×(TR velocity)2+Right Atrial Pressure(RAP)PASP=4×(TR velocity)2+Right Atrial Pressure(RAP)

RAP was assumed based on right atrial and inferior vena cava size (10 mmHg for normal RA, 15 mmHg for dilated RA, and 20 mmHg for dilated RA with dilated IVC).

• Pulmonary Artery Diastolic Pressure (PADP) was estimated from pulmonary regurgitation velocity at end-diastole using the formula:

PADP=4×(PR velocity)2+RAPPADP=4×(PR velocity)2+RAP

• Pulmonary Vascular Resistance (PVR) was calculated as:

PVR=(TR velocityTime Velocity Integral)×10+0.16PVR=(Time Velocity IntegralTR velocity​)×10+0.16

Derived from apical four-chamber view.

Severity Classification

• PASP:
• Normal: <40 mmHg
• Mild: 40–50 mmHg
• Moderate: 50–60 mmHg
• Severe: >60 mmHg

• PADP:
• Normal: <10 mmHg
• Mild: 10–20 mmHg
• Moderate: 20–30 mmHg
• Severe: >30 mmHg

• PVR (Wood units):
• Normal: 1–3
• Mild: 3–4
• Moderate: 4–6
• Severe: >6

Timing of Assessments

• Preoperative: 5–7 days before surgery
• Postoperative: At 1 month and 6 months after MVR
  Due to suboptimal echocardiographic windows in the early postoperative period (e.g., chest wall edema), only data from 1-month and 6-month follow-ups were considered for postoperative comparisons.

MVR was performed via median sternotomy with cardiopulmonary bypass and prosthetic valve implantation. Follow-up echocardiograms were obtained during routine outpatient visits at the valve clinic.

Data Collection Tools

Echocardiographic data were obtained using Philips iE33 and Siemens cardiovascular ultrasound systems in the echocardiology lab and CTVS ICU.

Variables and Measurements

• Independent Variables: Age, sex, BMI, clinical status (NYHA class)
• Primary Outcome Variables: PASP, PADP, and PVR
• Confounding/Interacting Variables: None explicitly identified

Statistical Analysis

Categorical variables (e.g., gender, comorbidities) were expressed as frequencies and percentages. Continuous variables (e.g., age, PA pressures) were summarized using means with standard deviations or medians with ranges, as appropriate. Changes in pulmonary hemodynamics over time were assessed using one-way and two-way repeated measures ANOVA. Statistical significance was defined as a two-tailed p-value <0.05. Analyses were conducted at a 5% level of significance.

A total of 60 patients who had pulmonary arterial hypertension (PAH) at the time of mitral valve surgery and satisfied the inclusion and exclusion criteria were included in this study. Postoperative changes in pulmonary pressures and clinical outcomes were assessed using echocardiographic records and clinical documentation, as per the predefined statistical methodology.

Demographic and Baseline Characteristics

The age of the patients ranged from 18 to 66 years, with a mean age of 37.72 years. The highest number of patients (n = 28, 46.7%) belonged to the 31–40 years age group, followed by 10 patients (16.6%) each in the 21–30 years and >50 years categories.

The majority of the cohort were female patients.

Valve Prosthesis and NYHA Functional Class

A total of four sizes of TTK Chitra prosthetic valves were used:

• 25 mm valve: 9 patients (15%)
• 27 mm valve: 31 patients (51.7%)
• 29 mm valve: 12 patients (20%)
• 31 mm valve: 8 patients (13.3%)

At presentation, the functional status of patients based on the New York Heart Association (NYHA) classification was as follows:

• NYHA Class II: 14 patients (23.3%)
• NYHA Class III: 40 patients (66.6%)
• NYHA Class IV: 6 patients (10%)
  No patients presented in NYHA Class I.

Anthropometric Data

• Mean height of male patients: 158.3 cm
• Mean weight of male patients: 58.2 kg
• Mean height of female patients: 150.2 cm
• Mean weight of female patients: 46.6 kg
• Mean BMI:
• Males: 23.9 kg/m²
• Females: 19.8 kg/m²

There was no statistically significant difference in height, weight, or BMI between male and female patients (p > 0.05).

Echocardiographic Findings

Echocardiographic measurements were used to assess pulmonary hemodynamic parameters preoperatively and at follow-up intervals of 1 month and 6 months post-mitral valve replacement (MVR).

• The mean pulmonary artery systolic pressure (PASP) decreased significantly over time:
• Preoperative PASP: 51.28 mmHg
• 1-month postoperative PASP: 44.98 mmHg
• 6-month postoperative PASP: 41.83 mmHg
• The mean pulmonary artery diastolic pressure (PADP) also showed a consistent reduction:
• Preoperative PADP: 18.2 mmHg
• 1-month postoperative PADP: 15.5 mmHg
• 6-month postoperative PADP: 13.8 mmHg
• Similarly, the mean pulmonary vascular resistance (PVR) demonstrated a marked decline:
• Preoperative PVR: 5.2 Wood Units (WU)
• 1-month postoperative PVR: 3.7 WU
• 6-month postoperative PVR: 3.1 WU

These trends indicate a significant and sustained reduction in pulmonary pressures and resistance following mitral valve replacement, suggesting an improvement in pulmonary hemodynamics over the six-month follow-up period.

This retrospective observational study was conducted in the Department of Cardiothoracic and Vascular Surgery (CTVS) at JIPMER, Puducherry, covering the period from February 2018 to December 2019. The primary objective was to evaluate the progression and improvement of pulmonary arterial hypertension (PAH) in patients undergoing mitral valve replacement (MVR) for mitral valve disease. The study also aimed to assess the temporal improvement in pulmonary hemodynamic parameters at 1-month and 6-month follow-up using transthoracic echocardiography.

A total of 60 patients with mitral valve disease and preoperative PAH were included in the study. The majority were female (71.6%), and the mean age was 37.72 years, which is consistent with findings from previous literature. For instance, a study by Vaturi et al. involving 131 patients with rheumatic mitral valve disease also demonstrated a predominance of female patients and a similar age distribution (mean age 45 ± 15 years). That study showed that although many patients presented with PAH at the time of mitral valve surgery, the majority did not progress to severe disease.

In the present study, most patients were in NYHA class III at the time of presentation, and a large proportion had only mild PAH preoperatively (80%), while 11.6% had moderate PAH and 8.3% had severe PAH. Postoperative echocardiographic data revealed a significant reduction in pulmonary artery pressures and pulmonary vascular resistance at the 1-month follow-up, which remained stable through the 6-month follow-up. Specifically, mean PASP decreased from 51.28 mmHg preoperatively to 41.83 mmHg at 6 months; mean PADP declined from 18.2 mmHg to 13.8 mmHg, and PVR dropped from 5.2 to 3.1 Wood Units.

These findings are consistent with a study by Choudhary et al., which reported that in patients with severe PAH undergoing mitral valve surgery, only a small percentage regressed to moderate or mild PAH over a longer follow-up period of 3–5 years. Interestingly, our study found that most of the hemodynamic improvement occurred within the first month after surgery, and there was minimal further regression between 1 and 6 months. This suggests that the initial postoperative period may be critical in determining long-term pulmonary vascular outcomes.

Similarly, Ho Young Hwang et al. observed that mitral valve replacement for rheumatic mitral stenosis resulted in a significant reduction in pulmonary artery pressures, although these changes were not immediate [29]. Our findings align with this, showing significant early improvements in PA pressures by the 1-month mark. According to Jong-Won Ha et al., survival rates in patients with mild to moderate PAH undergoing MVR are comparable to those without PAH, further reinforcing the potential benefit of early surgical intervention in this group [36].

Additionally, it is worth noting that delayed surgery in patients with even mild PAH may result in progression to more severe disease, as noted by Choudhary et al., who reported worsening of PAH over time in untreated patients [39,40]. This underlines the importance of timely surgical intervention in patients with mitral valve disease and early-stage PAH.

In our cohort, atrial fibrillation (AF) was present in 33.3% of patients, predominantly among those in NYHA class III. There was no statistically significant gender difference in the incidence of AF or heart rate, nor in other clinical variables such as dyspnea, which was the most common presenting symptom.

Overall, this study demonstrates that mitral valve replacement leads to significant short-term reductions in pulmonary arterial pressures and vascular resistance in patients with rheumatic mitral valve disease and PAH. Early surgical intervention, particularly in patients with mild or moderate PAH, may prevent progression to severe disease and improve postoperative outcomes [45]. However, long-term follow-up is essential to evaluate the durability of these improvements and their impact on functional status and survival.

The results are consistent with earlier studies that suggest early surgical intervention can reverse pulmonary vascular changes, especially if irreversible remodelling has not yet occurred. Patients with higher preoperative pressures experienced greater absolute reductions, suggesting potential reversibility even in advanced PAH stages [49]. However, some patients retained elevated pressures postoperatively, indicating persistent pulmonary vascular changes. The findings support the role of early MVR to prevent the progression of PAH and reduce postoperative morbidity. It also emphasizes the importance of echocardiographic monitoring of PA pressures pre- and post-surgery.

Limitations

This study has several limitations. First, the follow-up period was limited to approximately two years post-mitral valve surgery, which restricted the assessment of long-term outcomes and the durability of pulmonary pressure improvements. Second, as a retrospective observational study, it was constrained by the availability and completeness of existing records, limiting the collection of additional variables that might have provided deeper insights or influenced the results. Lastly, the study cohort included relatively few patients with atrial fibrillation and severe pulmonary arterial hypertension, despite most patients presenting with NYHA class III symptoms, which may limit the generalizability of the findings to these subgroups.

There is a relative scarcity of studies examining the progression of mild pulmonary arterial hypertension (PAH) in patients undergoing mitral valve surgery for rheumatic heart disease (RHD). This study observed that although PAH is commonly present in these patients, the improvement in pulmonary arterial pressures following mitral valve replacement is gradual. The initial postoperative reduction in pulmonary artery pressures was statistically significant, with a more gradual decline thereafter. Pressure measurements obtained via catheterization could potentially provide more precise data. A larger sample size and longer follow-up would help to better characterize these trends. Close follow-up with echocardiographic and clinical assessments is essential for optimal management. A prospective study design would facilitate collection of additional variables and enable extended monitoring, allowing more robust comparisons with existing literature. Overall, mitral valve replacement has a favourable impact on pulmonary arterial pressures in patients with PAH.

Tables:

Acknowledgements: The authors thank Dr Saichandran, Dr Sreevathsa Prasad and Dr Hemachandren for their valueable inputs. The study was conducted in the department of Cardiovascular and Thoracic Surgery along with the department of Cardiology at Jawaharlal Institute of Post Graduate Medical Education and Research, Pondicherry (an institute of national importance)

1. Simonneau G, Gatzoulis MA, Adatia I, et al. Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol. 2013;62:34.
2. Bayat F, Aghdaii N, Farivar F, Bayat A, Kord Valeshabad A. Early hemodynamic changes following mitral valve replacement in patients with severe and mild pulmonary arterial hypertension. Ann Thorac Cardiovasc Surg. 2013;19:201-206.
3. Ward C, Hancock BW. Extreme pulmonary hypertension caused by mitral valve disease—Natural history and results of surgery. Br Heart J. 1975;37:74-78.
4. Bendjaballah S, Lakehal R, Aimar F, Bouharraga R, Bouzid A. Results of mitral valve surgery with pulmonary arterial hypertension: Analysis of a retrospective study. J Cardiovasc Dis Diagn. 2017;5:1-6.
5. Tandon HD, Kasturi J. Pulmonary vascular changes associated with isolated mitral stenosis in India. Br Heart J. 1975;37:26-36.
6. Jorge E, Baptista R, Faria H, Calisto J, Matos V, Gonçalves L, et al. Mean pulmonary arterial pressure after percutaneous mitral valvuloplasty predicts long-term adverse outcomes. Rev Port Cardiol. 2012;31:19-25.
7. Bossone E, D’Andrea A, D’Alto M, Citro R, et al. Echocardiography in pulmonary arterial hypertension: from diagnosis to prognosis. J Am Soc Echocardiogr. 2013;26:1-14.
8. Elway SE, Mohamed AH, Abu El-Hussein AK. Outcome after mitral valve replacement in patients with rheumatic mitral valve regurgitation and severe pulmonary hypertension. Egypt J Cardiovasc Anesth. 2013;7:74-78.
9. Manners JM, Munro JL, Ross JK. Pulmonary hypertension in mitral valve disease. Thorax. 1977;32:691-696.
10. Aryanpur I, Padyar M, Shakibi JG, Siassi B. Regression of pulmonary hypertension after mitral valve surgery in children. Chest. 1977;71:354-360.
11. Salzberg SP, Filsoufi T, Anyanwu A, von Harbou K, Gass A, Pinney SP, Carpentier A. High risk mitral valve surgery. Ann Thorac Surg. 2005;80:502-506.
12. Abbas AE, Fortuin FD, Schiller NB. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol. 2003;41:1021-1027.
13. Reference values in hemodynamics. Edwards Lifesciences. Available at: edwards.com
14. Iung B, Vahanian A. Epidemiology of acquired valvular heart disease. Can J Cardiol. 2014;30:962-970.
15. Wilkins GT, Weyman AE, Abascal VM, et al. Percutaneous balloon dilatation of the mitral valve: an analysis of echocardiographic variables related to outcome and the mechanism of dilatation. Br Heart J. 1988;60:299-308.
16. Gordis L. The virtual disappearance of rheumatic fever in the United States: lessons in the rise and fall of disease. Circulation. 1985;72:1155-1162.
17. Markowitz M, Kaplan EL. Reappearance of rheumatic fever. Adv Pediatr. 1989;36:39-65.
18. Kaplan EL, Hill HR. Return of rheumatic fever: consequences, implications and needs. J Pediatr. 1987;111(2):244-246.
19. Dodu SR, Bothing S. Rheumatic fever and rheumatic heart disease in developing countries. World Health Forum. 1989;10(2):203-212.
20. Saxena A. Increasing detection of rheumatic heart disease with echocardiography. Expert Rev Med Devices. 2014;11(5):491-497.
21. Paar JA, Berrios NM, Rose JD, et al. Prevalence of rheumatic heart disease in children and young adults in Nicaragua. Am J Cardiol. 2010;105:1809-1814.
22. Shankar J, Jaiswal PK, Cherian KM. Rheumatic involvement of all four cardiac valves. Heart. 2005;91(6):e50.
23. Iung B, et al. A prospective survey of patients with valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease. Eur Heart J. 2003;24:1231-1243.
24. Lee R, et al. Fifteen-year outcome trends for valve surgery in North America. Ann Thorac Surg. 2011;91:677-684.
25. Agarwal A, et al. Results of repeat balloon valvuloplasty for treatment of aortic stenosis in patients aged 59 to 104 years. Am J Cardiol. 2005;95:43-47.
26. Vassileva CM, et al. Outcome characteristics of multiple-valve surgery: comparison with single-valve procedures. Innovations (Phila). 2014;9:27-32.
27. Roberts WC, Virmani R. Aschoff bodies at necropsy in valvular heart disease. Evidence from an analysis of 543 patients over 14 years of age that rheumatic heart disease is, at least anatomically, a disease of the mitral valve. Circulation. 1978;57(4):803-807.
28. Vaturi M, Porter A, Adler Y. The natural history of aortic valve disease after mitral valve surgery. J Am Coll Cardiol. 1999;33:2003-2008.
29. Manjunath CN, Srinivas P, Ravindranath KS, Dhanalakshmi C. Incidence and patterns of valvular heart disease in a tertiary care high-volume cardiac center: A single center experience. Indian Heart J. 2014;66(3):320-326. doi:10.1016/j.ihj.2014.03.010
30. Unger P, et al. Mitral regurgitation in patients with aortic stenosis undergoing valve replacement. Heart. 2009.
31. Unger P, et al. Effects of valve replacement for aortic stenosis on mitral regurgitation. Am J Cardiol. 2008;102:1378-1382.
32. Otto CM, Bonow RO. In: Libby P, Bonow RO, Mann DL, Zipes DP, editors. Braunwald’s Heart Disease. Philadelphia, PA: Saunders Elsevier; 2008. p. 1625-1693.
33. Cohn LH, Mason DT, Ross J Jr, Morrow AG, Braunwald E. Preoperative assessment of aortic regurgitation in patients with mitral valve disease. Am J Cardiol. 1967;19:177-182.
34. Niles N, et al. Preoperative left and right ventricular performance in combined aortic and mitral regurgitation and comparison with isolated aortic or mitral regurgitation. Am J Cardiol. 1990;65:1372-1378.
35. Jeong DS, et al. Fate of functional tricuspid regurgitation in aortic stenosis after aortic valve replacement. J Thorac Cardiovasc Surg. 2014;148:1328-1333.
36. Dahou A, et al. Tricuspid regurgitation is associated with increased risk of mortality in patients with low-flow low-gradient aortic stenosis and reduced ejection fraction: results of the multicenter TOPAS study. JACC Cardiovasc Interv. 2015;8:588-596.
37. Singh JP, Evans JC, Levy D, et al. Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study). Am J Cardiol. 1999;83:897-902.
38. Fedak PWM, Verma S, David TE, et al. Clinical and pathophysiological implications of a bicuspid aortic valve. Circulation. 2002;106:900-904.
39. Pnina V, Walter M, Yael W, Levi J, Abraham B. Clinical-echocardiographic correlations in acute rheumatic fever. Pediatrics. 1983;71(5):830-834.
40. Remenyi B, Wilson N, Steer A, et al. World Heart Federation criteria for echocardiographic diagnosis of rheumatic heart disease—an evidence-based guideline. Nat Rev Cardiol. 2012;9:297-309.
41. Saxena A, Zuhlke L, Wilson N. Echocardiographic screening for rheumatic heart disease: issues for the cardiology community. Glob Heart. 2013;8:197-202.
42. Arom KV, Nicoloff DM, Kersten TE, et al. Ten-year follow-up study of patients who had double valve replacement with the St Jude Medical prosthesis. J Thorac Cardiovasc Surg. 1989;98:1008-1015.
43. Nakano K, Koyanagi H, Hashimoto A, et al. Twelve years’ experience with the St Jude Medical valve prosthesis. Ann Thorac Surg. 1994;57:697-703.
44. Jamieson ER, Marchand MA, Pelletier CL, et al. Structural valve deterioration in mitral replacement surgery: comparison of Carpentier-Edwards supra-annular porcine and perimount pericardial bioprostheses. J Thorac Cardiovasc Surg. 1999;118:297-304.
45. Bourguignon T, Espitalier F, Pantaleon C, et al. Bioprosthetic mitral valve replacement in patients aged 65 years or younger: long-term outcomes with the Carpentier-Edwards PERIMOUNT pericardial valve. Eur J Cardiothorac Surg. 2018;53:745-753.
46. Hufnagel CA, Harvey WP, Rabil PJ, McDermott TF. Surgical correction of aortic insufficiency. Surgery. 1954;35:673-683.
47. Nair K, Muraleedharan CV, Bhuvaneshwar GS. Developments in mechanical heart valve prosthesis. Sadhana. 2003;28(3 & 4):575-587.
48. Butchart EG, Gohlke-Bärwolf C, Antunes P, et al. Recommendations for the management of patients after heart valve surgery. Eur Heart J. 2005;26(22):2463-2471.
49. Ha JW, et al. Is prophylactic aortic valve replacement indicated during mitral valve surgery for mild to moderate aortic valve disease? Ann Thorac Surg. 2002;74(4):1115-1119.