Systolic anterior motion of mitral valve - SAM


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  • Systolic anterior motion of mitral valve - SAM

    1. 1. Critical Case Conference Gagan Kumar MD
    2. 2. HPI • Admitted on 1/26/2011 • 80 Y female – weakness and nausea x 1 day. – Had troponin leak • • • • Ruled out for ACS Started CPAP and Nocturnal oxygen Cardiology consulted for Troponin leak Planned for RHC & LHC – Not done due to high INR – Then again for candidiasis in groin area.
    3. 3. Past Medical History • RA (rheumatoid arthritis) • Atrial fibrillation • Right Diaphragm paralysis with right middle lobe collapse. 2008 ? probably had since birth. admission 6/08 for hypoxia, multifactorial sectondary to right phrenic nerve palsy. On home oxygen therapy 2L NC • OSA with hypoventilation, does not use CPAP • DVT (deep venous thrombosis) 5/08 • Aortic stenosis • • • • • Unspecified essential hypertension BCC (basal cell carcinoma of skin) Depression RA (refractory anemia) Hyperlipidemia
    4. 4. Family history • Mother: HTN, CAD (died at 94) • Father: melanoma • Social history: – 5 pack years, quit 1972 – No EtOH – Retired homemaker
    5. 5. Medications • ClonazePAM (KLONOPIN) 0.5 mg tablet Take 0.5 mg by mouth nightly. • Escitalopram (LEXAPRO) 20 MG tablet Take 1 Tab by mouth daily. • Lisinopril (PRINIVIL OR ZESTRIL) 40 MG tablet Take 1 Tab by mouth daily. • Metoprolol (LOPRESSOR) 25 MG tablet Take 1 Tab by mouth 2 times daily. pt needs f/u visit for further refills. • Potassium chloride SA 20 MEQ tablet Take 20 mEq by mouth daily. • Warfarin (COUMADIN) 3 MG tablet Take 6 mg by mouth every Monday. Take 3 mg by mouth every Sunday, Tuesday, Wednesday, Thursday, Friday & Saturday.
    6. 6. Hospital course • ECHO done 1/27/2011 LV size is upper normal. There is severe asymmetric basal septal hypertrophy, with an approximate 2:1 septal to inferolateral wall ratio. There also appears to be systolic anterior motion of the mitral chords. There is at least a 40 mm Hg peak LVOT dynamic gradient, which is probably underestimated due to technical limitation of study. Visually estimated LVEF is 65-70%. The right ventricle appears moderately enlarged with normal systolic function. The left atrium visually appears severely enlarged. enlarged The right atrium is severely enlarged. There are moderate fibrocalcific changes of the aortic valve which does not appear to be significantly stenotic.Mild to moderate aortic regurgitation. The mitral leaflets appear mildly thickened. There is moderate mitral annular calcification present.There is mild to moderate mitral regurgitation. regurgitation There is mild to moderate tricuspid regurgitation. Estimated PA systolic pressure by tricuspid regurgitant Doppler velocity is 60 mmHg. No obvious significant pericardial effusion.
    7. 7. Hospital course • On 1/30/2011 – increasing oxygen requirements & found unresponsive. • She was found to be in Atrial fibrillation • ABG shows – respiratory acidosis & hypoxia. • Transferred to MICU
    8. 8. Vitals 1/30/2011
    9. 9. EKG on admission 1/26/2011
    10. 10. EKG on the day of transfer to MICU 1/30/2011
    11. 11. I&O
    12. 12. Labs
    13. 13. Problem list • Acute hypercapnic respiratory failure, superimposed on chronic respiratory acidosis • Acute neurologic failure (no drugs) • Atrial fibrillation with RVR • Urinary retention • Hypertrophic cardiomyopathy with SAM • SIRS possible sepsis (fever of 101 Of)
    14. 14. Hospital course • She was intubated A/C 18/600/5/70 • Started on amiodarone drip • Started on Norepinephrine which was weaned off in 5 hours. • CVP 8-13 • Started on Vancomycin + Zosyn • Given IVF ~ 2L
    15. 15. Hospital course • Antibiotics changed as per culture reports – Urine grew enterococcus – Sputum miniBAL grew MRSA • Extubated on 2/1/2011 • BiPAP at night after extubation • Beta blockers added: metoprolol increased to 150mg BID to control HR
    16. 16. Questions? • Was the hypotensive crisis due to atrial fibrillation with some role of sepsis? • What was ‘SAM’? Did it have any role in the events? • Is the management any different in tachyarrhythmia with SAM?
    17. 17. Systolic Anterior Motion of the Mitral Valve
    18. 18. Anatomy
    19. 19. Anatomy
    20. 20. What is SAM? • Anterior movement of mitral valve (either of the leaflets) during systole. – Mostly involves anterior leaflet • Maximal anterior motion in HCM patients occurs before maximal posterior wall contraction—approximately two-thirds of the way through systole
    21. 21. Why does it happen? • Venturi effect: increased flow velocity in effect LVOT • Anterior and inward displacement of papillary muscle with elongation of valve leaflet → creates slack in leaflet. leaflet • Flow drag: Pushing force of the flow drag • Timing of papillary muscle contraction
    22. 22. Three following features are necessary for SAM • Mitral-septal contact and obstruction: anterior position of mitral coaptation • Angle of flow onto the mitral valve, such that flow gets behind the mitral valve (angle of attack) • Chordal slack FLOW DRAG
    23. 23. Time course through systole after ‘flow drag’ Once the mitral valve touches the septum  a narrowed orifice occurs Pressure difference across the orifice becomes the new hydrodynamic force across the mitral leaflet This pressure difference pushes the leaflet further into the septum, narrowing the orifice further amplifying feedback loop is established that cycles for much of ejection (longer in systole that it cycles, the higher the gradient)
    24. 24. What accentuates SAM? • Decreased preload – Dehydration – Orthostasis – Valsalva • Decreased afterload – Vasodilators • Increased LV ionotropy – Fever / Exercise / Dobutamine
    25. 25. Clinical findings • On examination: – LV heave – S1 normal; S2 paradoxical splitting; S4 – Systolic ejection murmur – left sternal border – Increases with valsalva, vasodilators – Decreases with squatting, vasopressors
    26. 26. ECHO Parasternal long axis view
    27. 27. ECHO • Parasternal long axis view • HCM shows significant hypertrophy of – the interventricular septum (IVS) – posterior left ventricular wall (PWLV); the echofree space behind the posterior wall is a pericardial effusion (PE). RV: right ventricle Ao: aorta LV: left ventricle LA: left atrium.
    28. 28. M – mode ECHO ECG time
    29. 29. Hemodynamics in HCM with fixed left ventricular outflow obstruction LV LVOT Aorta
    30. 30. HCM with variable left ventricular outflow tract obstruction LVOT gradient
    31. 31. Brockenbrough–Braunwald–Morrow sign AO = Descending aorta; LV = Left ventricle; After the third QRS complex, the ventricle has more time to fill. Since there is more time to fill, the left ventricle will have more volume at the end of diastole (increased preload). Due to the Frank–Starling law of the heart, the contraction of the left ventricle (and pressure generated by the left ventricle) will be greater on the subsequent beat (beat #4 in this picture). Because of the dynamic nature of the outflow obstruction in HCM, the obstruction increases more than the left ventricular pressure increase. This increase causes a fall in the aortic pressure as the left ventricular pressure rises (seen as the yellow shaded area in the picture).
    32. 32. History • SAM was reported in late 1960’s with Hypertrophic Cardiomyopathy (HCM) – Thought to be specific for this entity – Associated with LVOT obstruction • Later both the findings were proven wrong – SAM is present in 30-60% of HCM – HCM with SAM: only 25-50% have LVOT obstruction – SAM can be present in absence of HCM
    33. 33. Hemodynamic consequences • Diastolic dysfunction • Prolongation of systolic ejection • Reduction in stroke volume • Disrupts MV functioning → MR • Microvascular dysfunction • Intolerant to tachyarrythmias
    34. 34. Medical Treatment • Negative ionotropes – Decrease LV ejection acceleration ↓ Decrease hydrodynamic force on mitral valve ↓ Decreased feedback loop β-blockers Disopyramide Verapamil
    35. 35. Medical Treatment • Start with β-blockers : – prolonging diastole → prolongs filling time. But doesn’t decrease LVOT gradient. • Verapamil: causes vasodilation. Verapamil
    36. 36. Medical Treatment • Disopyramide: Disopyramide – use in combination with β-blockers. – Reduces gradient and prolongs exercise time • Side effects – Anticholinergic side effects (BPH) – Can accelerate AV conduction ( hence always used with beta blockers) – Prolongs QT interval (stop if QTc increases by > 25%) • Avoid with amiodarone/ sotalol etc.
    37. 37. Things to avoid • Use diuretics with extreme caution !!! – Reduce preload → increase obstruction • Hemodynamics can be compromised by vasodilators – – – – ACEI ARBs Nitrates Nifedipine • Positive inotropes – Digoxin
    38. 38. Non-Surgical Treatment • DDD pacing with short AV delay – Reduced LVOT gradient by 50% – Not much difference in exercise capacity – Can use in elderly or who have contraindication to surgery. – Can use more negatively ionotropic medications since they are now protected against bradycardia.
    39. 39. Non-Surgical Treatment • Alcohol ablation of septum – Small balloon catheter is placed into a proximal septal artery – Contrast is injected into the target septal perforator – After occlusion of a septal perforator by a small balloon to prevent back leakage, 1 to 4 mL of absolute alcohol in injected into the distal perforator – Balloon is left inflated for 5 to 10 minutes • 36% reduction in acceleration • Complications – Death in 0% to 4% – LAD dissection – Leakage of alcohol back into the LAD with LAD occlusion and large infarction – Complete heart block in 9% to 38%
    40. 40. Schematic Diagram of Alcohol Septal Ablation
    41. 41. Classical myotomy-myectomy is the ‘gold standard’ therapy for patients with severely symptomatic hypertrophic obstructive cardiomyopathy more than three quarters of all long-term survivors are in functional class I or II (New York Heart Association) and overall survival after 18 years (mean follow up 8.1 years) was 68%, with a linearized mortality rate of 1.9% per patient-year.
    42. 42. Patients with obstructive HCM and mild or no symptoms have only slight excess mortality. However, patients with markedly elevated resting LVOT gradients are at a high risk of heart failure and death. These findings may have important implications for therapy, including the timing of septal reduction therapy
    43. 43. ‘SAM’ in common situations
    44. 44. SAM & HTN • Frequency: 1% to 30% of patients with Frequency LVH from HTN • Maximal SAM occurred at the end of systole with the mitral valve still anteriorly displaced • “Venturi effect” may be more pronounced in this subgroup
    45. 45. SAM & HTN • Implications?? – Vasodilators may increase SAM & LVOT obstruction – Negatively ionotropes have beneficial effects
    46. 46. SAM & Diabetes • In poorly controlled diabetics (HbA1c > 13) – SAM occurred in 65% of diabetics with β-stimulation (10% in controls) – Possibly related to greater LV mass in those who exhibit SAM – May have implications in septic patients on pressors – especially Norepinephrine
    47. 47. SAM & ACS Compensatory hyperkinesis in non-infarcted ventricular segments Reduced systolic diameter of the outflow tract Provides substrate for obstruction SAM
    48. 48. SAM & ACS • Causes new murmur & can be confused with VSD or papillary muscle rupture • Clinical Implications !!! – Inotropes & Vasodilators will WORSEN the shock & increase LVOT obstruction – Control heart rate & decrease hyperadrenergic & hypercontractile state – use BB or Vasoconstrictors ( to increase afterload) – like phenylephrine
    49. 49. Stress Echocardiography • SAM present in 8-35% • Especially Dobutamine stress test* • Mostly caused by mid cavity obstruction but may have SAM & LVOT obstruction • Consensus is that the changes are due to catecholamine effect rather than a physiological response (like exercise) * The Effect of Dobutamine Stress on Left Ventricular Outflow Tract Gradients in Hypertensive Patients. ANGIOLOGY 2004 55: 295
    50. 50. Approximately two-thirds of patients with symptomatic nonobstructive HCM have latent LVOTO. This study suggests that all patients with symptomatic non-obstructive HCM should have exercise stress echocardiography. echocardiography
    51. 51. General anesthesia !! Vasodilator Effect of drugs Peri-operative hypotension Ventricular under-filling Hypovolemia Altered ventricular and papillary muscle geometry + increased ventricular contraction and outflow tract velocity increase drag forces on the mitral valve leaflets SAM
    52. 52. SAM after mitral valve surgery • Up to 5% of mitral valve repair • Mechanism: anterior displacement of the mitral Mechanism coaptation point, shifting the mitral leaflets towards the LVOT • Increased risk if – excess of redundant tissue in the posterior leaflet – ratio of anterior leaflet length to posterior leaflet length of less than 1.3 – Insertion of an annuloplasty ring
    53. 53. SAM after mitral valve surgery • What to do in these cases? – Discontinuation of inotropes. – Give appropriate fluid therapy. • Reassess
    54. 54. SAM: Take home points • SAM of Mitral Valve can be present in conditions other than HOCM with important clinical applications. • Hypovolemia/ Increased adrenergic flow/ Vasodilators can accentuate latent SAM. • ECHO is useful in diagnosis. • Management consists of – – – – Negative inotropes Avoid vasodilators Give fluids Increase Afterload.
    55. 55. Comments & Questions
    56. 56. 00548171