| What are etiologies causing mitral valve stenosis? | Rheumatic fever (leading cause), congenital, severe calcification, SLE, RA. |
| How is pathology of MS? | RF (Chronic inflammation of valve leaflets lead to thickening and fibrosis and calcification, commissures fuse, chorodae tendenae fuse, become rigid, and lead to narrowing at apex of the funnel-shaped, calcification immobilizes the leaflets and narrows the orifice. |
| How is pathophysiology of MS? | Normal adults Mitral valve is 4-6 cm2, in obstruction <2cm2 blood flows from LA to LV if elevated LA pressure (hemodynamic hallmark of MS).
<1.5cm2 severe MS need LA pressure 25mmHg to maintain normal CO.
Elevated pulmonary artery pressure reduces pulmonary compliance thus exertional dyspnea, which is precipitated by clinical event increasing blood flow in orifice elevating LA pressure.
For assessment transvalvular pressure gradient and flow rate should be measured, isolated MS LV EDP and EF are normal, influences are important at level of PAP |
| How does MS cause pulmonary hypertension? | Passive backward transmission of elevated LA pressure, pulmonary arteriolar constriction (second stenosis) triggered by LA and pulmonary venous hypertension, interstitial edema in walls of small pulmonary vessels, organic obliterative changes in pulmonary vascular bed in end stages.
Severe pulmonary HTN leads to RV enlargement , secondary tricuspid regurgitation and pulmonary regurgitation and right sided heart failure |
| What are symptoms of MS? | Once pt became seriously symptomatic disease progresses to death in 2-5 years, dyspnea, persistent AF accelerates the symptoms progression, hemoptysis, pulmonary infection |
| What are physical findings in MS? | Opening snap (OS) of mitral valve in expiration near cardiac apex, follows aortic valve closure by 0.05-0.12 s.
Time interval between A2 and OS varies inversely with severity of MS, OS followed by low pitch rumbling diastolic murmur heard best at apex with pt in left lateral recumbent position. |
| What are labs done for MS? | ECG, Echocardiogram (TTE/TEE), CXR, cardiac cath (assesses lesions such as AS and AR) |
| How is tx of MS? | Penicillin prophylaxis of group A strep for secondary prevention of RF, infective endocarditis prophylaxis restricted for pt at high risk of complications from infection like pt with hx of endocarditis.
Indication for percutaneous mitral commissurectomy and mitral valve surgery in clinically significant mitral stenosis (area <1.5cm2); PMC symptomatic pt w/out unfavorable characteristic for PMC/symptomatic pt with contraindication for high risk surgery.
Mitral valve surgery in symptomatic pt not suitable for PMC in absence of futility |
| What are contraindications for PMC in RF? | • MVA> 1.5 cm2
• LA thrombus
• More than mild regurgitation
• Severe or bi-commissural calcification
• Absence of commissural fusion
• Severe concomitant aortic valve disease, or severe combined tricuspid stenosis and regurgitation requiring surgery
• Concomitant CAD requiring bypass surgery |
| Give algorithm of management of Rheumatic mitral valve stenosis? | . |
| How is etiology of mitral regurgitation? | Disease of any of the five mitral valve apparatus (leaflets, annulus, chorodae tendinae, papillary muscles, subjacent myocardium.
Acute mitral regurgitation (endocarditis, papillary muscle rupture post-MI, trauma, chordal rupture/leaflet flail (MVP/IE))
Chronic mitral regurgitation (myxomatous, RF, endocarditis, mitral annular calcification, congenital celft/AV canal, HOCM with SAM, ischemic LV remodeling, dilated cardiomyopathy, radiation) |
| What are different types of MR? | • primary (degenerative organic) MR, in which the leaflets and/or chordae tendineae are primarily responsible for abnormal valve function,
• functional (secondary) MR, in which the leaflets and chordae tendineae are structurally normal but the regurgitation is caused by annular enlargement, papillary muscle displacement, leaflet tethering, or their combination |
| How is pathophysiology of MR? | • The resistance to LV emptying (LV afterload) is reduced in patients with MR as a consequence, the LV is decompressed into the LA during ejection, and with the reduction in LV size during systole, there is a rapid decline in LV tension.
• The initial compensation to MR is more complete LV emptying. However LV volume increases progressively with time as the severe of the regurgitation increases and as LV contractile function deteriorates.
• This increase in LV volume is accompanied by a reduced forward CO. LV compliance is often increased, and thus, LV diastolic pressure does not increase until late in the course，
• The regurgitant volume varies directly with the LV systolic pressure and the size of the regurgitant orifice; the latter, in turn, is influenced by the extent of LV and mitral annular dilation. Because EF rises in severe MR in the presence of normal LV function, even a modest reduction in this parameter (<60%) reflects significant dysfunction |
| What are symptoms of MR? | Chronic mild-moderate pt isolated MR is usually asymptomatic.
Chronic severe MR (fatigue, exertional dyspnea, orthopnea, right side HF, painful hepatic congestion, ankle edema, distended neck vein, ascites, secondary TR, in pt with associated pulmonary vascular disease and pulmonary HTN) |
| How is physical exam of pt with MR? | Chronic severe MR (systolic murmur grade III/IV, holosystolic, systolic murmur usually prominent at apex and radiates to axilla)
Acute severe MR (systolic murmur decrescendo and ceases mid to late systole)
Ruptured chorodae tendina/ primary involvement of posterior mitral leaflet/prolapse/flail (regurg jet is eccentric directed anteriorly and strikes LA wall adjacent to aortic root, systolic murmur transmitted to base of heart) |
| What are labs done in case of MR? | ECG, TTE, TEE, CXR.
Asymptomatic pt with severe MR LVEF>60% should be followed every 6 months in heart valve center, measurement of BNP levels, exercise electrocardiography, are useful diagnostic and risk strat tools.
Asymptomatic pt with moderate MR and preserved LV function can be followed on a yearly basis and echocardiography should be performed every 1-2 years |
| How is tx of MR? | medical, surgical (repair: valve reconstruction via valvuloplasty techniques and insertion of annuloplasty ring, MVR bio/mechanical)
Transcatheter mitral valve repair |
| How is management of MR algorithm? | . |
| What is recommendation indication for mitral valve intervention in chronic severe secondary MR? | • Valve surgery/intervention is recommended only in patients with severe SMR who remain symptomatic despite GDMT (including CRT if indicated) and has to be decided by a structured collaborative Heart Team
• Valve surgery is recommended in patients undergoing CABG or other cardiac surgery |
| What is mitral valve prolapse? | • MVP is a relatively common but highly variable clinical syndrome resulting from diverse pathologic mechanisms of the mitral valve apparatus
• The cause is unknown, but in some, it appears to be genetically determined
• MVP is a frequent finding in patients with heritable disorders of connective tissue
• In MVP myxomatous degeneration is confined to the mitral valve, although the tricuspid and aortic valves may also be affected |
| What are clinical features of MVP? | • MVP is more common in women and occurs most frequently between the ages of 15 and 30 years
• The clinical course is most often benign
• Most patients are asymptomatic and remain so for their entire lives
• MVP varies in its clinical expression, ranging from only a systolic click and murmur with mild prolapse of the posterior leaflet to severe MR
• Arrhythmias
• Sudden death is a very rare complication and occurs most often in patients with severe MR and depressed LV systolic function |
| How is auscultation for MVP? | • Mid or late (nonejection) systolic click
• Systolic clicks may be multiple and may be followed by a high-pitched, mid-late systolic crescendo-decrescendo murmur and is heard best at the apex |
| What are labs for MVP? | ECG, TTE |
| What is tricuspid stenosis? | • Tricuspid stenosis (TS), which is much less prevalent than mitral stenosis (MS) in North America and Western Europe
(generally rheumatic in origin, and is more common in women than men)
• A mean diastolic pressure gradient of 4 mmHg is usually sufficient to elevate the mean RA pressure to levels that result in systemic venous congestion.
• TS is almost always accompanied by significant TR. (Operative repair may permit substantial improvement of tricuspid valve function. If repair cannot be accomplished, the tricuspid valve may have to be replaced ) |
| What is tricuspid regurgitation? | • Primary (organic)
(Rheumatic, Endocarditis, Myxomatous (TVP), Carcinoid, Radiation, Congenital (Ebstein's), Trauma, Papillary muscle injury (post-MI))
• Secondary (functional)
RV and tricuspid annular dilatation due to multiple causes of (RV enlargement (e.g., long-standing pulmonary HTN， remodeling post-RV MI), Chronic RV apical pacing]) |
| How are cases of TR? | • In at least 80% of cases, TR is secondary to marked dilation of the tricuspid annulus from RV enlargement due to PA hypertension
• The incompetent tricuspid valve allows blood to flow backward from the RV into the RA
• Significant degrees of TR will lead to RA enlarge ment and elevation of the RA and jugular venous pressures
• Fatigue and exertional dyspnea owing to reduced forward CO are early symptoms of isolated, severe TR
• The disease progresses and RV function declines :
• cervical pulsations, abdominal full ness/bloating， diminished appetite, and muscle wasting, although with progressive weight gain and painful swelling of the lower extremities
• Tricuspid valve surgery is most often comprises repair rather than replacement |
| What is pulmonary stenosis? | • Pulmonic valve stenosis (PS) is essentially a congenital disorder
• Much less common etiologies include carcinoid and obstructing tumors or bulky vegetations. The pulmonic valve is only very rarely affected by the rheumatic process
• PS is defined hemodynamically by a systolic pressure gradient between the RV and main PA. RV hypertrophy develops as a consequence of sustained obstruction to RV outf1ow, and systolic ejection is prolonged |
| What are auscultations of PS? and how is tx? | The murmur
• mild or moderate PS is mid-systolic in timing，
• crescendo-decrescendo in configuration heard best in the left second interspace
• usually introduced by an ejection sound (click) in younger adults whose valves are still pliable
• increases in intensity during inspiration.
• Pulmonic balloon valvotomy is recommended
• Surgery may be required when the valve is dysplastic |
| What is pulmonary regurgitation? | Primary valve disease (congenital, postvalvotomy, endocarditis, carcinoid)
Annular enlargement (pulmonary HTN, idiopathic dilation, marfan's syndrome) |
| How is PR clinically? | • Severe PR results in RV chamber enlargement and eccentric hypertrophy
• Mild or moderate degrees of PR do not, by themselves, result in symptoms
• PA hypertension, may dominate the clinical picture
• Reduce PA vascular resistance and pressure should be optimized.
• pharmacologic/ vasodilator
• and/or surgical/interventional strategies, depending on the cause of the PA hypertension |
