aortic regurge AHA guidlines 2014


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  • Change symtoms, click, ecg, x ray
  • Fluroscopy—> prosthesisCT coronaries
  • aortic regurge AHA guidlines 2014

    1. 1. D . B A S E M E L S A I D E N A N Y L E C T U R E R O F C A R D I O L O G Y A I N S H A M S U N I V E R S I T Y Chronic Aortic regurge
    2. 2. CAUSES --Aortic regurgitation may be due to disease of the valve leaflets or to enlargement of the aortic root. --In the developing world, the most common cause of AR is rheumatic heart disease. --However, in developed countries, AR is most often due to aortic root dilation or a congenital bicuspid aortic valve
    3. 3. PATHOPHYSIOLOGY --Added volume of regurgitant blood produces an increase in left ventricular end-diastolic volume and an elevation in wall stresscompensatory myocardial hypertrophy increase SV, end-diastolic pressure remains normal due to an increase in ventricular compliance
    4. 4. AHA 2014
    5. 5. CLINICAL MANIFESTATIONS --Asymptomatic for decades --Due to increased mass of the enlarged left ventricle: A sense of pounding and an uncomfortable awareness of the heartbeat. Atypical chest pain induced by a mechanical interaction between the heart and the chest wall. Palpitations due to tachycardia or premature beats. --Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and eventual pulmonary edema) --Angina pectoris is uncommon  coronary arteries are typically large. underlying coronary artery disease marked left ventricular hypertrophy, subendocardial ischemia At night when the heart rate slows and arterial diastolic pressure falls to very low levels
    6. 6. Physical examination --Increased SV abrupt distension of the peripheral arteries and an elevation in systolic pressure. --Regurgitation  rapid fall in pressure with quick collapse of the arteries and a low diastolic pressure --wide pulse pressure= "water hammer" or Corrigan pulse. This finding may be best appreciated by palpation of the radial or brachial arteries (exaggerated by raising the arm) or the carotid pulses --deMusset's sign — A head bob occurring with each heart beat. Traube's sign — A pistol shot pulse (systolic and diastolic sounds) heard over the femoral arteries. Duroziez's sign — A systolic and diastolic bruit heard when the femoral artery is partially compressed. Quincke's pulses — Capillary pulsations in the fingertips or lips. Mueller's sign — Systolic pulsations of the uvula. Becker's sign — Visible pulsations of the retinal arteries and pupils. Hill's sign — Popliteal cuff systolic pressure exceeding brachial pressure by more than 60 mmHg. Mayne's sign — More than a 15 mmHg decrease in diastolic blood pressure with arm elevation from the value obtained with the arm in the standard position. Rosenbach's sign — Systolic pulsations of the liver. Gerhard's sign — Systolic pulsations of the spleen. --DD=sympathetic hyperactivity, anemia, fever, pregnancy, thyrotoxicosis, large arteriovenous fistula, patent ductus arteriosus, and severe bradycardia
    7. 7. What is the significance of a brisk carotid arterial upstroke? It depends on whether it is associated with normal or widened pulse pressure. ==If associated with normal pulse pressure, a brisk carotid upstroke usually indicates two conditions: Simultaneous emptying of the left ventricle into a high-pressure bed (the aorta) and a lower pressure bed: The latter can be the right ventricle (in patients with ventricular septal defect [VSD]) or the left atrium (in patients with mitral regurgitation [MR]). Both will allow a rapid left ventricular emptying, which, in turn, generates a brisk arterial upstroke. The pulse pressure, however, remains normal. Hypertrophic cardiomyopathy (HCM): Despite its association with left ventricular obstruction, this disease is characterized by a brisk and bifid pulse, due to the hypertrophic ventricle and its delayed obstruction. ==If associated with widened pulse pressure, a brisk upstroke usually indicates aortic regurgitation (AR). In contrast to MR, VSD, or HCM, the AR pulse has rapid upstroke and collapse. Others: anemia, fever, exercise, thyrotoxicosis, pregnancy, cirrhosis, beriberi, Paget disease, arteriovenous fistulas, patent ductus arteriosus
    8. 8. Cardiac examination --Apical impulse being displaced laterally and inferiorly and being diffuse and hyperdynamic. A prominent pulsation (and occasionally a thrill) may be felt at the sternal notch due to concurrent dilatation of the ascending aorta --Cardiac auscultation: S1 may be soft, often reflecting a long PR interval S2 is variable; it may be soft, absent, or single A2 is often soft or absent while P2 may be normal, but obscured by the diastolic murmur A systolic ejection sound may be due to abrupt aortic distension caused by the large stroke volume A third heart sound (S3 gallop) is heard when left ventricular function is severely depressed --Diastolic murmur begins immediately after A2. It is high pitched, often blowing in quality, and may be sustained in intensity or decrescendo. It may be soft and barely audible, often appreciated only when the patient is sitting up, leaning forward, and holding his or her breath in expiration, the murmur increases with squatting and decreases with the Valsalva maneuver -The intensity of the murmur does not correlate well with the severity of AR. However, the timing and duration of the murmur may be helpful. --In very severe regurgitation with ventricular decompensation, and acute AR the murmur may become soft or even absent (increase enddiastolic pressure)
    9. 9. There are two golden and three silver rules: & The first golden rule is to always judge (systolic) murmurs like people: by the company they keep. Hence, murmurs that keep bad company (like symptoms; extra sounds; thrill; and abnormal arterial or venous pulse, electrocardiogram [ECG], or chest radiograph) should be considered pathologic until proven otherwise. These murmurs should receive lots of evaluation, including technology based. & The second golden rule is that a diminished or absent S2 usually indicates a poorly moving and abnormal semilunar (aortic or pulmonic) valve. This is the hallmark of pathology. As a flip side, functional systolic murmurs are always accompanied by a well- preserved S2, with normal split. The three silver rules are: & All holosystolic (or late systolic) murmurs are pathologic. & All diastolic murmurs are pathologic. & All continuous murmurs are pathologic.
    10. 10. --The murmur is heard best along the left sternal border, at the third and fourth intercostal space, when AR is due to valvular disease. In contrast, abnormalities of the aortic root produce murmurs that are best heard at the right sternal border and apex. --Systolic murmur can be heard in many patients functional AS --Second diastolic murmur (the Austin Flint murmur) may also be appreciated mid to late diastolic rumble, heard at the apex (competing with mitral flow) absence of both a loud S1 and an opening snap of the mitral valve
    11. 11. Electrocardiogram --Left ventricular hypertrophy --Isolated atrial and ventricular premature beats are common. --Conduction abnormalities, sustained supraventricular or ventricular tachyarrhythmiasare usually not seen.
    12. 12. Chest radiograph --Cardiomegaly due to the dilatation of the left ventricle --The ascending aorta (and often the aortic arch or knob) are typically markedly dilated --Left atrial enlargement significant left ventricular dysfunction. Thus, its presence in patients with mild to moderate AR suggests associated mitral valve disease
    13. 13. Echocardiograrhy --The valve leaflets may be normal or abnormal (thickening, vegetations, calcification, and prolapsed or flail leaflets). --The aortic root is often dilated and there may be evidence of an aneurysm (dissecting or saccular). --There is often high frequency, diastolic fluttering of the anterior leaflet of the mitral valve which is due to the diastolic regurgitant jet of blood from the aorta. --Doppler echocardiography detecting the regurgitant jet AR. --The left ventricular end-systolic and end-diastolic volumes are increased in chronic AR ---TOE for good assessment of valve leaflet, Ao root, intraoperative is mandatory in aortic valve repair, to assess the functional results and identify patients who are at risk of early recurrence of AR
    14. 14. AHA 2014
    15. 15. Aortic:EROA= regurg V/VTI ar jet Regurge V= vol transaortic (CSA lvotX VTI lvot) -vol transmitral (CSA mitral annulusX VTI mitral annulus) Regurg fraction=rgeurge V/vol transaortic
    16. 16. AHA2014: Class IIa 1. Exercise testing is reasonable in selected patients with asymptomatic severe VHD to 1) confirm the absence of symptoms, or 2) assess the hemodynamic response to exercise, or 3) determine Prognosis . (Level of Evidence: B) Class I CMR is indicated in patients with moderate or severe AR (stages B, C, and D) and suboptimal echocardiographic images for the assessment of LV systolic function, systolic and diastolic volumes, and measurement of AR severity. (Level of Evidence: B)
    17. 17. Follow up -In addition to symptom status, prognosis in patients with AR is assessed by measurements of LV size and function, usually by echocardiography, as recommended by the 2006 ACC/AHA valvular guidelines (with 2008 update) -Echocardiography every one to two years -Yearly testing (CT or MRI) is recommended in patients with an aortic root or ascending aortic diameter greater than 40 mm ---Marfan patients, bicuspid with aortic root diseasefirst-degree relatives should be scanned
    18. 18. PHYSICAL ACTIVITY AND EXERCISE -Asymptomatic patients with mild or moderate AR with a left ventricular end-diastolic diameter that is normal (≤55 mm) or mildly increased can participate in all competitive sports. -Patients with asymptomatic nonsustained ventricular tachycardia at rest or with exercise should only participate in low-intensity competitive sports. -Patients with AR and significant dilatation of the ascending aorta (>45 mm, normal ≤35 mm) should participate only in low- intensity competitive sports. ---This recommendation does not apply to patients with Marfan syndrome in whom any degree of aortic dilatation should prohibit competitive sports because of the risk of aortic dissection and rupture.
    19. 19. MEDICAL THERAPY 1-Vasodilators: Vasodilators such as nifedipine and angiotensin converting enzyme (ACE) inhibitors may influence LV size and function and slow the rate of progression of AR. 2-Medical therapy, other than vasodilators, has a limited role in AR because symptomatic patients should be treated with valve replacement HF, not candidates for surgery digoxin for symptoms, diuretics for fluid control, ACE inhibitors and/or angiotensin II receptor blockers to improve survival. 3-BB relative CI as increase diastole, regurge The 2006 ACC/AHA guidelines on the management of valvular heart disease concluded that beta blocker therapy was reasonable in patients with bicuspid aortic valves who have an aortic root diameter greater than 40 mm and do NOT have moderate or severe aortic regurgitation 4-ENDOCARDITIS PROPHYLAXIS NO LONGER 5---Rheumatic fever prophylaxis: Till 40, or 10 y after last attack
    20. 20. PREGNANCY --AR is considered high risk if associated with NYHA class III to IV symptoms, an LVEF less than 40%, or Marfan syndrome definitive surgery up to termination if refuse: -- symptomatic diuretics, VD as nifedipine (CI of ACEI, ARBs) --Marfan BB esp dialted aortic root (labetalol) Operate in refarctory NYHA III, IV symptoms
    21. 21. RF in Marfan -Family history of dissection -Size increase >2 mm/year in repeated examinations using the same technique and confirmed by another technique -Severe AR -Desire to become pregnant
    22. 22. AHA 2014 Class IIa 1. Operative intervention to repair the aortic sinuses or replace the ascending aorta is reasonable in patients with bicuspid aortic valves if the diameter of the aortic sinuses or ascending aorta is greater than 5.0 cm and a risk factor for dissection is present (family history of aortic dissection or if the rate of increase in diameter is ≥0.5 cm per year). (Level of Evidence: C) 2. Replacement of the ascending aorta is reasonable in patients with a bicuspid aortic valve who are undergoing aortic valve surgery because of severe AS or AR if the diameter of the ascending aorta is greater than 4.5 cm. (Level of Evidence: C)
    23. 23. 2006 ACC/AHA guidelines recommended that patient age, ability to tolerate warfarin, and patient preference all be taken into account: --Patients with a projected long life-span generally receive a mechanical valve because of far greater durability and improved patient survival at 15 years. --The main indications for a bioprosthesis are patients who cannot or will not tolerate warfarin or for whom compliance is uncertain, and patients ≥65 years of age who do not have risk factors for thromboembolism since valve durability is less of an issue.
    24. 24. AHA 2014 The patient and family should be sufficiently educated by the Heart Valve Team about all alternatives for treatment so that their expectations can be met as fully as possible using a shared decision- making approach.
    25. 25. Heart Valve Centers of Excellence 1) are composed of experienced healthcare providers with expertise from multiple disciplines; 2) offer all available options for diagnosis and management, including complex valve repair, aortic surgery, and transcatheter therapies; 3) participate in regional or national outcome registries; 4) demonstrate adherence to national guidelines; 5) participate in continued evaluation and quality improvement processes to enhance patient outcomes; and 6) publicly report their available mortality and success rates.
    26. 26. --Echocardiogrambefore hospital discharge or at the first postdischarge outpatient visitreduction in left ventricular end-diastolic dimension in the first 10 to 14 days after surgery --Increasing experience in some centers with aortic valve repair in selected patients. --Moderate AR, who undergo CABG or mitral valve surgery, the decision to treat the aortic valve should be based on: Aetiology of the AR Age Worsening of LV function Possibility of valve repair
    27. 27. --Fluroscopy: in prosthetic valves --CT for coronaries in low risk patients
    28. 28. Other valvular lesions --When either stenosis or regurgitation is predominant, management follows the recommendations concerning the predominant VHD --Interaction between the different valve lesions ex. associated MR may lead to underestimation of the severity of AS --Indications for intervention are based on global assessment of the consequences of the different valve lesions, i.e. symptoms or presence of LV dilatation or dysfunction --The decision to intervene on multiple valves should take into account the extra surgical risk --The choice of surgical technique should take into account the presence of the other VHD.
    29. 29. Noncardiac surgery --Asymptomatic patients with severe MR or AR and preserved LV function, non-cardiac surgery can be performed safely. --The presence of symptoms or LV dysfunction should lead to consideration of valvular surgery, but this is seldom needed before non-cardiac surgery. --If LV dysfunction is severe (EF <30%), non-cardiac surgery should only be performed if strictly necessary, after optimization of medical therapy for HF. --Control heart rate (particularly in MS), to avoid fluid overload as well as volume depletion and hypotension (particularly in AS)
    30. 30. Thank you