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Pathophysiology and natural history of mitral stenosis

Pathophysiology and natural history of mitral stenosis
Literature review current through: Jan 2024.
This topic last updated: Dec 19, 2023.

INTRODUCTION — The hemodynamic consequence of mitral stenosis (MS) is an increased impedance or resistance to transmitral flow. MS attenuates the atrial contribution to left ventricular filling and it also poses a hydraulic opposition or resistance to early filling. Unlike other valvular lesions, which are often attributable to many etiologies, MS alone, or in combination with other valvular pathology, is mostly secondary to rheumatic heart disease. However, the prevalence of calcific MS in resource-abundant countries has increased as populations age [1]. Progression of MS eventually leads to the development of disabling symptoms (eg, dyspnea, hemoptysis, thromboembolism, pulmonary hypertension, and right-sided heart failure). (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)

The natural history and pathophysiology of MS will be reviewed here. Given the widespread use of surgical and percutaneous interventions, information on the natural history of MS comes from older studies and other limited observations of patients in resource-limited countries who have not undergone a corrective procedure.

The roles of medical and surgical therapy and the use of percutaneous balloon valvotomy are discussed separately. (See "Rheumatic mitral stenosis: Overview of management" and "Surgical and investigational approaches to management of mitral stenosis" and "Percutaneous mitral balloon commissurotomy in adults".)

ETIOLOGY — Rheumatic heart disease (RHD) is the most common cause of mitral stenosis (MS); other causes are much less frequent [2,3]. However, only 50 to 70 percent of patients with MS report a history of rheumatic fever [4-6]. RHD remains a major public health problem in resource-limited countries [7-9]. Rheumatic MS has become less common in resource-rich countries given marked reductions in the incidence of rheumatic fever [10]. Occasional outbreaks of rheumatic fever in the United States appear to be the result of either increased virulence of a streptococcal strain or immigration from areas where RHD is prevalent [11]. Involvement of the mitral valve is present in approximately 90 percent of individuals with RHD [12]. Since rheumatic MS is a chronic condition, it is not seen during the first episode of acute rheumatic carditis. In many populations, RHD is more common in females than in males [9]. Rheumatic MS is a continuously progressive lifelong disease. (See "Acute rheumatic fever: Epidemiology and pathogenesis".)

The following are other causes of mitral stenosis:

Mitral annular calcification is a degenerative process of the fibrous support structure of the mitral valve. This form of MS is a common disorder, particularly in older adults, that may occasionally lead to hemodynamically significant MS [1,13]. (See "Clinical manifestations and diagnosis of mitral annular calcification".)

Radiation-associated valve disease, including MS, is increasingly recognized as late manifestation in survivors of Hodgkin lymphoma that is associated with thickening and fibrosis of the aortic-mitral curtain [14-16]. These valve abnormalities may only be manifested 10 to 20 years after radiation treatment. Isolated MS is a rare complication from prior radiation. (See "Cardiotoxicity of radiation therapy for breast cancer and other malignancies".)

Congenital causes of MS are uncommon and usually present in infants and children [13].

Other rare conditions include Fabry disease, Whipple disease, mucopolysaccharidosis, methysergide therapy, carcinoid valve disease, endomyocardial fibrosis, and systemic rheumatic disease (such as systemic lupus erythematosus and rheumatoid arthritis).

Other conditions may produce hemodynamic abnormalities similar to those of native valvular MS; these include atrial myxoma, large infected vegetations, ball valve thrombus, and degenerated stenotic bioprosthetic mitral valve. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

PATHOPHYSIOLOGY

The nature and development of mitral stenosis (MS) should be considered in terms of the underlying etiology and pathology, the factors that contribute to progression, and the long-term hemodynamic and structural sequelae.

Pathoanatomic considerations

Rheumatic heart disease — Rheumatic heart disease (RHD) is the result of an exaggerated immune response to specific bacterial epitopes in a susceptible host [17]. The inflammatory process in the valve leaflets is thought to be initiated by cross-reactivity between streptococcal antigen and the valve tissue; there is no evidence for active infection of the valve leaflets. Mitral disease begins with the formation of tiny nodules located along the coapting portions of the valve leaflets [5]. The leaflets thicken with eventual deposition of fibrin on the cusps and loss of normal valve morphology. Although the incidence of RHD is variable after an episode of acute rheumatic fever, approximately 50 percent of those with evidence of carditis develop organic valvular damage. In addition, up to 75 percent of patients with documented recurrences of rheumatic fever have some form of valvular disease after 45 years of follow-up (algorithm 1) [3]. (See "Acute rheumatic fever: Clinical manifestations and diagnosis" and "Acute rheumatic fever: Epidemiology and pathogenesis".)

Chronic RHD affecting the mitral valve apparatus progresses over years to decades and causes a number of pathologic changes, affecting the mitral valve apparatus, which are diagnostic for rheumatic valve disease [5,18]: fusion of the leaflet commissures; thickening, fibrosis, and calcification of the leaflet cusps [19]; and thickening, fusion, and shortening of the chordae tendineae. The net effect is transition from a mitral valve that is often regurgitant early in the disease process to a stenotic mitral valve with a symmetric, central, oval-shaped orifice and a classic pattern of "doming" of the leaflets in diastole due to fusion of the leaflet tips at the commissures. The degree of leaflet thickening and calcification and the severity of chordal involvement are variable.

Commissural fusion and chordal shortening are due to recurrent rheumatic fever with repetitive valve scarring, but leaflet thickening and calcification appear to be primarily due to the stress of chronic turbulent flow through a deformed valve. Consistent with this hypothesis is the observation in a study from South Africa that ongoing rheumatic activity was present in 2 percent of patients with pure MS compared with 47 percent of patients with pure mitral regurgitation (MR) [18]. Also supportive of this hypothesis is the observation that recurrent stenosis after mitral valvuloplasty, without intervening episodes of rheumatic fever, is due to leaflet thickening and calcification without recurrent commissural fusion [20-22].

In some patients with MS the thickened, often calcified, mitral leaflets and chordae contribute to LV diastolic dysfunction. This is manifested by higher LV diastolic pressures and smaller diastolic volumes [23], and can be particularly prominent after balloon valvotomy.

Rheumatic MS has a delayed onset compared to rheumatic MR. The interval between the episode of rheumatic fever and the clinical presentation of MS varies geographically, ranging from as little as a few years in countries with a high prevalence of rheumatic fever [18,24,25] to 20 years in countries where rheumatic fever is rare [3,5]. Most children with RHD have pure MR (as illustrated by series in 12 African countries, India and Yemen [9], South Africa [18], Cameroon [24], and Mozambique [26]), with pure MS as well as mixed MS and MR increasing into adulthood [26,27]. (See "Clinical manifestations and diagnosis of rheumatic heart disease", section on 'Chronic valve disease'.)

More rapid progression from MR to MS in areas of high prevalence may be due to the ineffective use of antibiotics and/or increased virulence of the Streptococcus organism causing a more severe primary rheumatic insult [18,25]. The ensuing acute inflammatory process can lead to commissural adhesion prior to the more common degenerative sequelae. It is therefore not uncommon in some of these countries to see symptomatic MS in patients less than 20 years of age [9,18,24,25], compared with the typical development of symptoms between the ages of 30 and 50 in developed nations [5].

Congenital MS — Congenital MS is a rare condition that often involves multiple valve components, such as rolled, thickened leaflet margins, hypoplasia or fusion of the papillary muscles (including parachute mitral valve in which the mitral chordae are attached to a single or dominant papillary muscle [28]), and short and thickened chordae tendineae [13,29,30]. Parachute mitral valve is often a component of the Shone complex (which includes other left-sided obstructive lesions such as supramitral ring, valvular aortic stenosis, subaortic stenosis, and aortic coarctation). Atrioventricular canal defects are also associated with an increased risk of parachute mitral valve deformity. Accessory mitral valve tissue is a rare cause of congenital MS [31].

Mitral annular calcification — Mitral annular calcification (MAC) develops from progressive calcium deposition along and beneath the mitral valve annulus. MAC generally follows the C-shape of the mitral annulus, so the base of the anterior mitral leaflet is generally (but not always) spared. Although data on the pathophysiology of MAC are very limited, an atherosclerotic process similar to that observed for calcific aortic valve disease has been proposed since atherosclerosis and MAC are strongly associated. Data have linked MAC to a decreased glomerular filtration rate, suggesting that associated abnormal calcium-phosphate metabolism is related to the pathogenesis of MAC [32,33].

Data have shown that MAC associated with severe calcific MS has a high burden of comorbidities. A study of 200 patients observed over a mean of 14 years demonstrated slow decrease in mean mitral valve area (by 0.05 cm2 per year) [1]. (See "Clinical manifestations and diagnosis of mitral annular calcification".)

Hemodynamic and structural sequelae

Altered filling dynamics — The abnormal filling dynamics of MS are characterized by an increased transmitral pressure gradient. This diastolic pressure gradient is dependent on the severity of MS, cardiac output, and heart rate. In patients with mild to moderate MS, left atrial (LA) pressures are only minimally elevated at rest, but may increase to produce symptoms with exercise or other conditions that increase heart rate such as atrial fibrillation. In more severe forms of MS, LA pressures are usually significantly elevated at rest. The mean transmitral pressure gradient and the pulmonary venous pressure is increased in patients with MS when the cardiac output increases, as in anemic and pregnant patients (figure 1).

Progressive MS is associated with a gradual loss of cross-sectional valve area. The normal mitral valve orifice has a cross-sectional area of 4 to 6 cm2. In general, a valve area of <2.5 cm2 must be present before exertional dyspnea can be attributed to MS. A valve area of <1.5 cm2 is usually required to produce symptoms at rest (table 1) [34]. An orifice area of ≤1.5 cm2 is considered to represent severe MS, and is associated with a significant pressure gradient that is necessary to maintain adequate filling of the left ventricle. (See "Echocardiographic evaluation of the mitral valve".)

With isolated MS, the left ventricular systolic and diastolic pressures are usually normal. However, when the stenosis is very severe, there may be a decrease in left ventricular filling and end-diastolic volume (ie, preload), leading to reductions in stroke volume and cardiac output. Furthermore, the chronically elevated LA pressure leads to marked atrial remodeling and increased pulmonary venous as well as pulmonary arterial pressures and resistance (figure 2). (See "Hemodynamics of valvular disorders as measured by cardiac catheterization".)

Left atrial remodeling — Chronic pressure overload leads to a range of adaptive processes in the LA, including myocardial hypertrophy, interstitial fibrosis, and geometric remodeling. These changes predispose to mechanical complications of LA chamber enlargement, in-situ thrombosis, and atrial fibrillation. An enlarged LA may impinge on the left recurrent laryngeal nerve, causing hoarseness (Ortner’s syndrome).

LA thrombosis is found in 17 to 24 percent of patients undergoing mitral valve surgery [35,36], and may be caused not only by stasis due to atrial fibrillation but also by endocardial injury secondary to chronic LA pressure overload. A scanning electronmicroscopy analysis of left and right atrial appendages of 35 patients who required corrective surgery for mitral valve disease showed that advanced changes were more frequently seen in the endocardium of the LA appendage compared with right atrial appendage [37]. Patients with MS had a higher proportion of advanced endocardial changes in the LA appendage compared with patients with MR. Further support for the concept that LA endothelial injury may be a mediator of LA thrombosis in MS independent of atrial fibrillation comes from a study in China that showed that the normalized expression of the von Willebrand factor gene relative to control was 3.04 in the LA appendage from 40 patients with LA thrombus and 2.16 in those without thrombosis (n = 40; p<0.01) [38].

Other factors such as the shape of the LA may also predispose to an increased risk of LA thrombosis. Data suggest that at comparable volumes, a spherical LA shape had an increased risk for embolic cerebrovascular events compared with an elliptical-shaped LA [39].

Pulmonary hypertension — Patients with MS commonly have pulmonary hypertension (PH), classified as PH due to left heart disease [40]. In most patients with PH caused by MS, the pulmonary artery pressure rises passively and maintains a normal or near-normal pulmonary arteriovenous pressure gradient. Likewise, the PA end-diastolic pressure minus the pulmonary venous pressure remains near zero. This subtype of increased pressures in the lung is also referred to as "postcapillary PH" [40]. (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults".)

A minority of patients with MS and PH have "combined pre- and postcapillary PH" [40]. This type of reactive PH is due to vasoconstriction [41] and pathological remodeling of the pulmonary vasculature [42] and may be, in part, mediated by the potent vasoconstrictor endothelin-1 (ET-1). Levels of ET-1 are threefold higher in patients with severe MS compared with healthy control subjects [43]. In a group of patients with severe MS undergoing percutaneous balloon mitral valvuloplasty or mitral valve replacement, the baseline ET-1 concentration was an independent predictor of a decrease in pulmonary capillary wedge pressure at six months following mitral valve intervention [43]. (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults", section on 'Diagnostic criteria'.)

The pulmonary vasculature remodels over time in patients with MS. There is progressive luminal narrowing due to intimal hyperplasia, enhanced proliferation and diminished apoptosis of endothelial and smooth-muscle cells, medial hypertrophy and fibrosis, and adventitial hypertrophy in small pulmonary arteries [42]. Changes are also evident in the small pulmonary veins, capillaries, and lymphatics. Veins may also exhibit thickened and fibrotic media and may be arterialized (ie, elastin fibers are condensed into internal and elastic laminae). The capillaries are often engorged, with thickened basement membranes and the lymphatics are dilated and thicker than normal. Pulmonary venous hypertension also leads to broncho-pulmonary anastomoses, which have been associated with hemoptysis. (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults", section on 'Pathogenesis'.)

Pulmonary arterial hypertension eventually leads to right ventricular hypertrophy and enlargement, tricuspid regurgitation, increased right atrial pressure, and the development of right-sided heart failure (figure 2). (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis", section on 'Right heart failure'.)

Pulmonary hypertension in patients with MS is potentially reversible. This was illustrated in a randomized comparison of balloon valvuloplasty (valvotomy) and open surgical commissurotomy in patients with severe MS [44]. The mean pulmonary artery systolic pressure was approximately 55 mmHg at baseline and fell to 49 mmHg one week after the procedure and then to 32 mmHg at three-year follow-up (figure 3).

NATURAL HISTORY — In the absence of correction of the stenotic lesion, rheumatic mitral stenosis (MS) is generally a progressive disease. Development of clinical evidence of progression is slow in asymptomatic patients but becomes more rapid after the onset of symptoms.

The number of patients with nonrheumatic MS is so small that little information is available concerning the natural history. (See "Clinical manifestations and diagnosis of mitral annular calcification", section on 'Mitral stenosis'.)

Rate of progression — The mean rate of progressive valve narrowing is approximately 0.1 cm2/year in North American series, but there is appreciable interpatient variability [45,46]. This was illustrated in a Doppler echocardiographic evaluation of 103 patients with MS (mean age 61 years) [45]. During an average 3.3-year follow-up, mitral valve area decreased at a mean rate of 0.09 cm2/year but there was marked interpatient variability. There was no decrease in 28 patients, relatively little change (<0.1 cm2/year) in 40, and more rapid (≥0.1 cm2/year) in 35. The rate of loss of valve area cannot be predicted by initial valve area [45,46].

In a study from Israel, investigators followed 36 patients with moderate MS for approximately six years [47]. The data suggest that the rate of mitral valve narrowing in patients with moderate MS is variable and cannot be predicted by patient's age, past commissurotomy, valve score, or gradient. Notably, in many patients, the valve area did not change over a long observation period.

Asymptomatic phase — The duration of the asymptomatic phase (stage B and C) (table 1) of rheumatic MS varies across geographical areas [48]. For example, in North America, it is generally a slowly progressive disease, with a latency period as long as 15 to 40 years between the initial infection and the onset of clinical symptoms [3,4,13]. In resource-limited settings, on the other hand, MS progresses much more rapidly, and may lead to symptoms in younger patients, typically in young adults, or in the teenage years, but even in children under five years of age in some countries [49].

The natural history of rheumatic MS was evaluated in a prospective study of 159 such patients from Germany [3]. The following findings were noted:

The mean interval between rheumatic fever and the onset of symptoms was 16.3 years.

At 25 years after the initial episode of rheumatic fever, 8 percent were asymptomatic, 9 percent were New York Heart Association (NYHA) class II, 33 percent were NYHA class III, and 50 percent were NYHA class IV or had undergone mitral valve surgery.

Similar findings were noted in an older report in which 49 asymptomatic patients were followed for 20 years: 24 percent remained asymptomatic, 14 percent developed symptoms or atrial fibrillation, and 62 percent died [6].

Symptomatic phase — The prognosis dramatically worsens once the patient with MS develops symptoms (stage D) (table 1). It has been estimated that progression from mild symptoms to severe disability takes only seven to nine years [3,4].

In the absence of correction of the stenosis, overall mortality increases as a patient's functional capacity decreases. This relationship can be illustrated by the following observations:

In a study published in 1962, 271 symptomatic patients with MS were followed for up to 26 years after their initial presentation [50]. The 10-year survival rate for patients in functional class I, II, III, and IV was >80, 69, 33, and 0 percent, respectively. At 20 years, 49 percent of patients in class II were still alive compared with no survivors among the patients in class III.

In a later report, patients in whom valve surgery was recommended but refused had 5- and 10-year survival rates of 44 and 32 percent, respectively [3].

Other poor prognostic indicators include the presence of atrial fibrillation [50] and the progression to severe pulmonary hypertension [51]. In one series of 586 patients with mitral valve disease, 8.2 percent had severe pulmonary hypertension, defined as a resting systolic pulmonary artery pressure of 80 mmHg or above and pulmonary vascular resistance of 10 Woods units or greater [51]. The mean survival of patients with pulmonary hypertension who did not undergo surgery was 2.4 years [51].

Effect of pregnancy — The increase in heart rate and cardiac output during pregnancy can substantially increase the resting transmitral gradient in females with MS, which can lead to symptoms in a previously asymptomatic (and perhaps undiagnosed) patient or an exacerbation of symptoms in an already symptomatic patient. These issues are discussed in detail separately. (See "Pregnancy in women with mitral stenosis".)

Complications — In addition to the gradual progression just described, as many as one-half of patients have one or more episodes of acute deterioration due to one of the complications of MS [5]. (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)

Chronic or paroxysmal atrial fibrillation occurs in approximately 45 percent of cases, making it the most common cause of disability in a previously asymptomatic patient [4-6]. As mentioned above, a rapid ventricular rate raises left atrial and pulmonary venous pressures because of the reduction in diastolic filling time. Potential complications include pulmonary edema, hemoptysis, and pulmonary hemorrhage [4,6].

Prior to surgical correction and the use of prophylactic anticoagulation, systemic thromboembolic events complicated MS in 13 to 26 percent of patients [4,6,52]. The majority of events occurred in patients with atrial fibrillation, but some had no known history of this arrhythmia. Most of these emboli arose from the left atrium. Emboli can also arise from the right atrium, leading to pulmonary embolism, when there is pulmonary hypertension and right ventricular and atrial dilatation.

Patients with MS and pulmonary hypertension may develop functional tricuspid regurgitation that often improves with successful treatment of the MS. The decrease in severity of tricuspid regurgitation parallels the decrease in pulmonary artery pressures. On rare occasions, rheumatic tricuspid stenosis and regurgitation are also found in patients with MS. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation".)

Causes of death — Death from MS is due to progressive right-sided heart failure and/or pulmonary edema in over 60 percent of cases [6,50]. Most of the remaining deaths are due to systemic thromboembolic events, 40 percent of which involve the brain, or a large pulmonary embolism [53]. In older studies, infectious complications, such as endocarditis, accounted for 5 to 8 percent of deaths [6,50]. However, the great majority of these fatal infectious complications occurred in the preantibiotic era.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

SUMMARY

Pathophysiology – Mitral stenosis (MS) is due to thickening and immobility of the mitral valve leaflets (figure 4), resulting in obstruction in blood flow from the left atrium to the left ventricle. The mechanical obstruction leads to increases in pressure within the left atrium, pulmonary vasculature, and right heart. (See 'Pathophysiology' above.)

Cause – In nearly all cases, MS is caused by rheumatic involvement of the mitral valve. (See 'Etiology' above.)

Rheumatic MS – Disease progression results in a number of pathologic changes affecting the mitral valve apparatus, which are diagnostic for rheumatic valve disease: fusion of the leaflet commissures; and thickening, fusion, and shortening of the chordae tendineae. (See 'Pathophysiology' above.)

Rate of progression – In the absence of correction of the stenotic lesion, MS is generally a progressive disease. Progression is slow in asymptomatic patients but becomes more rapid after the onset of symptoms. The rate of progression of MS varies across geographical areas. (See 'Natural history' above.)

Stages of MS – The stages of MS delineate the transition from an asymptomatic phase (stage B as and C) to a symptomatic phase (stage D) (table 1). In general, a valve area of <2.5 cm2 must be present before exertional dyspnea can be attributed to MS; a valve area of <1.5 cm2 is usually required to produce symptoms at rest (table 1). (See 'Rate of progression' above and "Echocardiographic evaluation of the mitral valve" and "Rheumatic mitral stenosis: Clinical manifestations and diagnosis", section on 'Diagnosis and evaluation'.)

Effect of atrial fibrillation – Atrial fibrillation is often the first trigger of symptoms in asymptomatic patients. (See 'Altered filling dynamics' above.)

Effect of pregnancy – The increase in heart rate and cardiac output during pregnancy can substantially increase the resting transmitral gradient in females with MS, which can lead to symptoms in a previously asymptomatic (and perhaps undiagnosed) patient or an exacerbation of symptoms in an already symptomatic patient. (See 'Effect of pregnancy' above.)

Complications – Complications of MS include atrial fibrillation, systemic thromboembolic events, secondary pulmonary hypertension, tricuspid regurgitation, and heart failure. (See 'Complications' above.)

Causes of death – Death from MS is due to progressive right-sided heart failure and/or pulmonary edema in over 60 percent of cases. Most of the remaining deaths related to MS are due to systemic thromboembolic events. (See 'Causes of death' above.)

ACKNOWLEDGMENTS

The UpToDate editorial staff acknowledges William H Gaasch, MD (deceased), who contributed to an earlier version of this topic review.

The UpToDate editorial staff acknowledges Matthew J Sorrentino, MD, FACC, who contributed to an earlier version of this topic review.

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Topic 8137 Version 23.0

References

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