Mitral Stenosis

Mitral Stenosis


Today, I will present a VAP on mitral stenosis. After viewing this VAP, you’ll be able to identify the epidemiology and typical presentation of mitral stenosis understand the clinical evaluation and diagnosis of mitral stenosis, and finally, understand the various management strategies of mitral stenosis. This VAP will cover epidemiology, etiology, pathophysiology, clinical diagnosis, evaluation, medical therapy, and surgical slash interventional therapy of mitral stenosis. Mitral stenosis is an instruction to the flow of blood into the left ventricle at the mitral valve. There’s a high prevalence of mitral stenosis in developing countries, due to the large amount of rheumatic fever rheumatic heart disease. In India, for example, rheumatic heart disease was found in 6 out of 1,000 schoolchildren, while only being found in 0.5 per 1,000 in developed countries. The rate of progression is also significantly faster in developing countries, with most patients becoming symptomatic as either teenagers or young adults. In developed countries, there’s often 20 to 40 years between the initial infection with rheumatic fever and clinical presentation. The difference in timing is felt to be due to recurring episodes of rheumatic fever in developing countries. In developed countries, there’s usually a prolonged asymptomatic phase, followed by progressive worsening after the onset of symptoms. Unfortunately, 10 year survival in symptomatic patients with MS is only about 50 to 60%. The most common cause of mitral stenosis is inflammatory change after rheumatic heart disease, though only about half of affected patients remember having rheumatic fever. Patients with rheumatic mitral valve disease typically develop mitral regurgitation first, and then subsequently progress to mitral stenosis. Isolated mitral stenosis is found in 40% of patients who present with rheumatic heart disease. In developed countries, degenerative changes of the mitral valve also relatively common, specifically calcium deposition on the mitral valve leaflets. Other less common causes of mitral stenosis include congenital malformations of the mitral valve in systemic diseases, such as Fabry’s disease, systemic lupus, or erythematosus, and rheumatoid arthritis. MS is caused by thickening and calcification of valve leaflets, subsequent commissural and chordal fusion in valvular modularity. This leads to a narrowing of the mitral valve orifice, shown as number seven in the diagram. As the stenosis of the valve increases and the valve area decreases, there’s is an increase in the pressure gradient across the mitral valve. This causes decreased blood flow across the mitral valve. The final development of symptoms in many patients is often related to the loss of an atrial kick, often associated with atrial fibrillation. Mitral stenosis typically follows a slow progression, and symptoms are related to the amount of diastolic blood flow across the mitral valve. As heart rate increases. There’s a decrease in the amount of diastolic filling time, and consequently flow across the mitral valve. This causes symptoms in the physiologic states associated with increased heart rates, including exertion, as well as other causes of tachycardia. Dyspnea with exertion is the most common symptom at presentation. It is present in 70% of patients. Atrial fibrillation occurs in about 47% of patients with MS, and often is associated with development of symptoms after the lost of the atrial kick. Enlargement of the left atrium, due to obstruction of flow occurs in many patients, and contributes to the development of atrial fibrillation. Patients with MS are at risk for thromboembolism, especially those who have atrial fibrillation. Finally, due to the increased resistance to flow across the mitral valve, there is pulmonary vascular congestion, and this can cause hemoptysis in some patients. Additionally, any physiologic state that causes increased cardiac output can lead to symptom onset and subsequent diagnosis. The most common example of this pregnancy. Exam findings of mitral stenosis can be somewhat difficult to identify in mild disease, but are usually easily identified in more severe disease. An opening snap can be heard after the second heart sound. This is best appreciated at the apex in the left lower sternal border, when the leaflets are still mobile. It is distinguished from a split S2 because the split S2 is usually loudest at the base. A diastolic rumble is also appreciated at the apex, best in the left lateral decubitus position, and in increase by exercise. A late diastolic murmur is associated with mild MS, because it is only heard during atrial systole, while a continuous murmur is associated with more advanced disease. Decreased arterial pulses can be felt due to decreased cardiac output. Mitral facies are pinkish purple spots on the cheeks that are caused by poor perfusion. Additionally, if pulmonary hypertension has developed as a result of the vascular disease, elevated JVP, with a prominent A wave, and an RV heave, may be evident as well as signs of right sided heart failure. Several tests are often performed in the work of mitral stenosis. EKG findings usually include left atrial enlargement. Atrial fibrillation is also easily identifiable, if present. Chest x-rays can show pulmonary congestion, as evidenced by cephaliation, left atrial enlargement, and signs of pulmonary hypertension, including enlargement of the main pulmonary artery. Echocardiography is typically the study of choice to diagnose mitral stenosis, as it can assess for similar and associated conditions, describe valve area, shape, and motion, determine the gradient across the valve, and measure the degree of left atrial enlargement. Stress echocardiography can also be useful, as it assesses exercise capacity and can elicit symptoms in otherwise inactive patients. Mitral stenosis is most appropriately described as a disease continuum, and no isolated value can consistently and accurately define severity. The 2008 ACC/AHA Guidelines use mean gradient, pulmonary arteries systolic pressure in valve area. To classify severity with severe MS, having a mean gradient greater than 10 millimeters of mercury, a pulmonary artery systolic pressure greater than 50, and a valve area less than one square centimeter. While there’s variability in the hemodynamic progression between patients, serial echocardiographic studies have demonstrated an annual loss of mitral valve area between 0.1 and 0.3 square centimeters per year. As such, asymptomatic patients with mild MS should be screened with a transthoracic echocardiogram every three to five years. Those with moderate MS should be screened every one to two years, and those with severe MS should be screened every year. Symptomatic patients should be screened if they develop a change in their symptoms. Transesophageal echocardiogram is indicated if data from transthoracic echocardiogram is not adequate. Since mitral stenosis is a mechanical disease, its natural history is only altered by mechanical interventions, such as balloon valvotomy or surgery. Nonetheless, symptomatic improvement can be obtained using pharmacologic therapy in patients who are waiting for intervention, and in those with persistent symptoms after intervention. As described above, many of the symptoms associated with MS are worsened with tachycardia. In order to address this, beta blockers, or calcium channel blockers, are often used for rate control and to decrease cardiac output. Diuresis can be effective if there is evidence of pulmonary congestion. If the patient is in atrial fibrillation, attempts at pharmacologic rhythm control may be beneficial, due to the importance of the atrial kick in patients who have MS. Given the morbidity and mortality of embolic phenomena, any patient with a history of atrial fibrillation, prior embolic event, or left atrial thrombus should undergo systemic anticoagulation. Anticoagulation should also be considered in patients with severe MS, left atrial enlargement greater than 55 millimeters, or spontaneous echo contrast. In patients with rheumatic heart disease, antibiotic prophylaxis is recommended, typically with penicillin. Prophylaxis should be continued for at least 10 years after the last episode of rheumatic fever and until the age of 40. Lifelong prophylaxis is indicated for patients who are at high risk, including teachers and daycare workers. Interventional therapy with percutaneous mitral balloon valvuloplasty is indicated for patients with moderate or severe MS with symptoms, or for asymptomatic patients with pulmonary hypertension. In order to proceed with PMBV, the patient should have favorable valve morphology, as evidenced by valve mobility, self valvular thickening, valvular thickening, and calcification. Scoring systems exist to formally quantify about morphology, with less of all of the named factors being more favorable. Additionally, PMBV should not be attempted if there’s LA thrombus or moderate to severe mitral regurgitation, as documented transesophageal echocardiogram . There is some controversy regarding whether patients with severe MS and severe pulmonary hypertension should undergo PMVBV, mitral valve replacement, but this is beyond the scope of this presentation. 80% to 95% of PMBV procedures are successful, and the procedure typically doubles valve area. Possible complications include development of severe MR in up to 10% of patients, creation of an ASD, and LP perforation. Surgical therapy is indicated for symptomatic patients with moderate to severe MS if PMBV is not available, or contraindicated, due to valve morphology, thrombus, or mitral regurgitation. In general, repair is favored over replacement, due to the risk for complications associated with replacement. In summary, mitral stenosis is usually caused by rheumatic fever, and is significantly more common in the developing world than in the developed world. It is typically diagnosed with history, physical, and an echocardiogram. Finally, interventional management is indicated in appropriate patients with moderate to severe disease. I would like to acknowledge my wife, Dr. Anna Dolgner, for her help reviewing this presentation.

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