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aorta stenosis regurgitasi

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Case Report aortic stenosis and AortiC RegurgitationPresented By :Dewi AngrianaMickliana Timang

Supervised by :Dr. Akhtar Fajar, Sp.JP, FIHA

Patient identityName : Mr. MDAge : 43 years oldGender : MaleAddress :KonaweMR : 718346Date of admittance : July 7th 2015

History TakingChief complaint: shortness of breathHistory taking: It has been since 2 months before admitted and worsen within the last 3 weeks before admitted to the hospital and relieved by sitting upright. Paroxysmal Nocturnal Dyspnea(+). Dyspnea On Exercise (+). Chest pain (-) palpitation (-) nausea (+) vomitus (-). Cough (+). Cough history (+) 1 month ago with sputum mixed with blood. Fever (-) and fever history was not exist. Defecation & micturition were normal.

PAST ILLNESS HISTORYHistory of cardiac disease before (+). Admitted to hospital in Kendari with Valvular Heard Disease. Recently admitted in Siloam Hospital for a week then referred to RSWS.Family history of cardiac disease (-)Cigaratte smoking (+)

Physical ExaminationPresent status: Severe illness / Poor-nourished / ConsciousVital signs:BP: 100/60 mmHgHR: 100 x/ minuteRR: 26 tpm (abdominal)T: 36.8C (axilla)

Physical ExaminationHead : Anemia (+) Icterus (+)Neck : No mass, no tenderness, JVP R+3 cmH2OChest : Rhonchi +/+ (base of lungs)Wh -/-Heart: S1/S2 regular, Murmur systolic grade 4/6 (apex)Abdominal : Ascites (+) minimalExtremities: Edema (+) minimal on pretibial and dorsum pedis

ECG (7/7/15 )

Rhythm : Sinus rhythm, reguler QRS Rate: Heart rate 100 bpm Axis : Left Axis Deviation P Wave : NormalPR Interval : 0.14 sQRS Complex : 0.08 s, poor R Wave progression, S V1+ R V6ST Segment: ST depression I aVL V5 V6 ST Elevation V3 V4T Wave : T inverted in lead I, aVL, V4, V5, V6Conclusion: Sinus Rhythm, Left Ventricular Hypertrophy Ischemic antero lateral wall

Chest X-RayConclusion :Cardiomegaly with oedem pulmonalRight diaphragm elevatedCVC in the right hemithorax with the tip at the level of Costovertebral Thoracic 8Pleural Efusion bilateralAorta Dilatation

Lab. FindingsHasilNilai NormalRBC2,87.106/mm3(3,8 5,8).106/mm3HGB8,8 g/dL12 - 16 g/dLWBC16,3 .103/mm3(4 - 10).103/mm3PLT354 103/mm3(150 - 400).103/mm3PT13,810-14INR1,33APTT24,922-30GDS136 mg/dl< 200 mg/dLUreum117 mg/dL10 - 50 mg/dLKreatinin1,0 mg/dL< 1,1 mg/dLSGOT34 U/L< 38 U/LSGPT42 U/L< 41 U/LAsam urat10,0 mg/ml2,4-5,7Natrium136 mmol/L136-145 mmolKalium3,8 mmol/L3.5-5.1 mmolKlorida98 mmol/L97-111mmolAssesmentCardiogenic ShockCHF NYHA III-IVSevere Aortic Stenosis Moderate Aortic RegurgitationMitral Regurgitation, Tricuspid Regurgitation, and Severe Pulmonary HypertensionSuspect Infective Endocarditis

ManagementO2 8 L/min via NRMIVFD NaCl 0,9% 500cc/24 jamDobutamin 5mcg/kgBBFurosemide 120 mg/24jam/SyringepumpNorephinefrin 0,1 mg/kgbbECHOCARDIOGRAPHY

ECHOCARDIOGRAPHY

ECHOCARDIOGRAPHYComplain : possible infective endocarditisLA DilatationLVH (+) Eccentric, LVPWd 20 mmSystolic function LV good, EDD 57 / ESD 37/ EF 65%Global NormokineticRV contractility good, tapse 3,35cm

Heart ValvesAorta : 3 vegetative cusps (+), destroyed cusp, AR severe with PHT 288 msMitral: PML Prolapsed ec. Rupture chordae, MR severe, with Jet EccentricTricuspid : TR moderate with TVG 51 mmHgPulmonal : PR mild

Other:SEC (+) LA and LV with thrombus LA

Conclusion : LVHSevere AR ec. Vegetation : destroyed cuspsSevere MR ec. Rupture ChordaeModerate TR, PHMild PRSystolic Function LV good, LVEF 65%: LVH (+) eccentricRV Contractility good SEC (+) LA and LV with thrombus

DISCUSSIONINTRODUCTIONObstruction to left ventricular (LV) outflow is localized most commonly at the aortic valve.AS has become the most frequent type of VHD in Europe and North America. It primarily presents as calcific AS in adults of advanced age (27% of the population >65 years).Aortic StenosisINTRODUCTIONIncidenceAffects 5 in 10,000 people80% of adults with symptomatic AS are men.PrevalenceIn adults undergoing surgery for AS in the United States, calcific AS accounts for 51% of cases, bicuspid AS 36%, and rheumatic disease 9%. The prevalence of bicuspid aortic valve in the general population may be as high as 1-2% of the general population.Risk FactorsAgeDyslipidemiaMale

ETIOLOGIESCongenital : congenital mono or bicuspid valve. (about 1% to 2% of the population)Degenerative : Calcific disease progresses causing a reduction in leaflet motion and effective valve area without commissural fusion. Calcific AS is an active disease process by lipid accumulation, inflammation, and calcification.Rheumatic : Rheumatic AS due to fusion of the commissures with scarring. Approximately 95% of patients who are found to have rheumatic AS have coexisting involvement of the mitral valve.

MAJOR TYPES OF AORTIC VALVE STENOSIS

Braunwald's Heart Disease: A Textbook Of Cardiovascular Medicine Ninth Edition. 2012;1468-78.VALVE HISTOLOGY

Braunwald's Heart Disease: A Textbook Of Cardiovascular Medicine Ninth Edition. 2012;1468-78.PATHOPHYSIOLOGY

Braunwald's Heart Disease: A Textbook Of Cardiovascular Medicine Ninth Edition. 2012;1468-78.PHYSICAL EXAMPulse: pulsus tardus and pulsus parvus.Murmur: The characteristic sign is a crescendo-decrescendo systolic murmur over the right second intercostal space. The murmur radiates to the carotids and to the apex (the latter is referred to as the Gallavardin phenomenon).

PHYSICAL EXAMThe second heart sound (S2) is diminished or absent in severe AS.A fourth heart sound (S4) is common and reflects increased atrial contribution to ventricular filling.CARDIAC IMAGINGChest RadiographyEchocardiographyCardiac CatheterizationDobutamine-Stress Echocardiography

Categories Of Aortic Stenosis Severity

Braunwald's Heart Disease: A Textbook Of Cardiovascular Medicine Ninth Edition. 2012;1468-78.Recommended Intervals For Follow-up Of Adults With Asymptomatic Aortic Stenosis

Vahanian. Alec, Catherine M. Otto. Risk stratification of patients with aortic stenosis. European Heart Journal. 2010.Natural History Of Asymptomatic Patients With Aortic Stenosis

Braunwald's Heart Disease: A Textbook Of Cardiovascular Medicine Ninth Edition. 2012;1468-78.ESC And ACC/AHA Guidelines For Management Of Aortic Valve Stenosis (1)

Vahanian. Alec, Catherine M. Otto. Risk stratification of patients with aortic stenosis. European Heart Journal. 2010.ESC And ACC/AHA Guidelines For Management Of Aortic Valve Stenosis (2)

Vahanian. Alec, Catherine M. Otto. Risk stratification of patients with aortic stenosis. European Heart Journal. 2010.Management of severe aortic stenosis.The Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal. 2012

Recommendations For The Use ofTAVI

The Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). European Heart Journal. 2012Contraindications For TAVI

PERCUTANEOUS AORTIC BALLOON DILATATIONPercutaneous balloon dilatation offers little benefit for adults with calcific AS or with secondary calcification of a bicuspid aortic valve.This procedure is reserved for patients with serious severe comorbidities that are not candidates for AVR, patients requiring urgent noncardiac surgery, and as a bridge to AVR.

Medical TherapyRecommendationsClass I : Hypertension in patients at risk for developing AS (stage A) and in patients with asymptomatic AS (stages B and C) should be treated according to standard GDMT, started at a low dose, and gradually titrated upward as needed with frequent clinical monitoring (Level of Evidence: B)Class IIb : Vasodilator therapy may be reasonable if used with invasive hemodynamic monitoring in the acute management of patients with severe decompensated AS (stage D) with NYHA class IV HF symptoms (Level of Evidence: C)2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart DiseasePROGNOSISPrognosis is similar to that for age-matched normal adults during the asymptomatic period.Development of symptoms is associated with a grave prognosis, showing a 2-year survival rate of ~50% without surgical intervention.MEDIAN SURVIVAL TIME INSYMPTOMATIC SEVERE AORTIC STENOSIS

EDUCATION Diet : Low-salt dietActivity: Asymptomatic patients with mild AS: Physical activity is not restricted and patients can participate in competitive sports.Patients with moderate AS: They should avoid competitive sports that involve high dynamic and static muscular demands. Other forms of exercise can be performed after an exercise test with no ST-segment changes or sustained arrhythmias.Patients with severe AS should be advised to limit their activity to relatively low levels.Prevention : Prophylaxis against infective endocarditis and recurrent rheumatic fever, if applicable, is indicated.

Aortic RegurgitationDEFINITIONAortic regurgitation (AR) is the abnormal retrograde flow of blood through the aortic valve during cardiac diastole.

EPIDEMIOLOGYStenosis Aorta is the most common Valvular Heart Disease. 43.1% was found among 1197 patients.Mitral Regurgitation 31.5% among 877 patientsAortic Regurgitation 13.3% among 369 patientsMitral Stenosis 12.1% among 336 patients

From the study of Framingham, 4.9% case of Aortic Regurgitation . 13% on male and 8.5% on female.Aortic Regurgitation worsen with age, especially with Marfan syndrome.ETIOLOGYDdilatiation of aortic root:Aortic aneurysm (e.g Marfan Syndrome)Annuloaortic ectasiaAorta dissectionSyphilisAbnotmalities of valve leaflets:Rheumatic Heart DiseaseEndocarditisAorta artificial congenital Ventricular Septal Defect (VSD)Aortic left ventricular tunnelRupture (trauma)PATOPHYSIOLOGY

SymptomsAcute aortic regurgitationsudden severe shortness of breath rapidly developing heart failurechest pain

SymptomsPalpitations, often described as the sensation of having forceful heart beats, due to widened pulse pressure with hyperdynamic circulationShortness of breath, which may not worsen with exertion in the early stages due to compensatory tachycardia with shortened diastoleChest pain, if LV end-diastolic pressure compromises coronary perfusion pressure gradientsChronic Aortic Regurgitation50Physical Findingsde Musset sign head bobbing with heartbeat Corrigan pulse water hammer pulse Bisferiens pulse brach/ fem arteries Hill sign popliteal > brachial by 60mmHg Traube sign pistol shot sounds over fem artery Duroziez sign sys m when femoral artery compressed proximally and diastolic m when compressed distally Quincke sign capillary pulsations Apical impulse - diffuse, hyperdynamic and displaced inf/lat systolic thrill base/suprasternal notch / carotid arteries

51Physical Findings Diastolic murmur high frequency, sitting up, leaning forward duration > intensity correlates with severity mild AR early diastole, hi pitched blowing severe AR holodiastolic, rough musical (cooing dove) eversion/perforation of Ao cusp Primary valve dz heard best LSB 3-4 intercostal Ao Root dz heard best RSBAustin Flint murmur mid-late diastolic apical rumble severe ARWide Pulse Pressure Systolic flow murmur (/thrill)52*ECG :- LVH + T inversion*Chest XR :- Cadiac dilatation Aortic dilatation Pulmonary congestion*ECHO : Dilated LV Hyperdynamic LV Fluttering AML Doppler detects reflux*Cardiac Catheterization :- Dilated LV AR Dilated aortic root

INVESTIGATION53Medical Management Vasodilators (Nifedipine, Hydralizine, ACEI, Nipride) goal is to reduce SBP, improve forward SV, reduce regurgitant volume

Diuretics for pulmonary congestion Prophylaxis against Infective Endocarditis54Criteria for Aortic Valve Replacement in Chronic Aortic RegurgitationSymptomsCongestive heart failure.Declining exercise tolerance on exercise testing.Angina

Anatomy, regardless of symptoms:Left ventricular dysfunction: EF 75 mm- Left ventricular systolic dimension >55 mm-Aortic root dimension >50 mmPROGNOSISPatient with EF 45% pre-operative survive longer post operation than EF