Causes of Heart Valve Dysfunction Congenital defects (bicuspid aortic valve) Infections (rheumatic fever and bacterial endocarditis Coronary artery disease (papillary muscle rupture) Senile calcification (most common) Tricuspid or Pulmonary = right heart failure Aortic or Mitral = left heart failure Mitral Valve .. Keep inr= 2.5-3.5 Aortic Valve.. Keep inr= 2-3 Bioprosthetic= use aspirin Mechanical prosthetic= warfarin
Aortic Stenosis Age 75-84= 35% have aortic senile stenosis Aortic Stenosis results from the accumulation of calcium with the cusps of the valve and is the most predominant form of Valve Disorders. Age is the primary fisk factor, but hypertension, hyperlipidemia, male sex can also play a role. Classic symptoms: syncope, angina, and heart failure- occur when the left ventricle can no longer overcome the excessive afterload imposed by the malfunctioning aortic valve. Clinical manifestations begin when the aortic valve area has decreased to less than 1 cm2 Surgery is indicated when the patient is in stage C2 whith reduced EF < 50% or are in stage D. Age 75-84= 35% have aortic senile stenosis Age over 85= 48% have aortic senile stenosis
Mitral Valve Stenosis Mitral stenosis occurs far less than aortic stenosis. 80% of Mitral Valve stenosis are caused from rheumatic heart disease, whereas only 3% are from senile calcification. Classic Symptoms include dyspnea, hemoptysis, thromboembolism, AF, and right sided heart failure. Physiologic problems: increased pressure within the left atrium, pulmonary vasculature, and right side of the heart MR (Mitral regurgitation) can be caused from Mitral valve prolapse.
Diagnostics Transthoracic echocardiograpy Transesophageal echocardiography Coronary angiography Cardiac magnetic resonance imaging STAGE A – Normal – symptoms-absent STAGE B- Progression- mild to moderate grade lesion—symptoms=absent STAGE C- severe grade lesion – symptoms absent STAGE D= severe grade lesion and SYMPTOMATIC. In general, stage A and B – lifetime coagulation Surgery is required for EJ < 50% who are in Stage D.
Types of Valves BIOPROSTHETICS= deteriorate with time more than mechanical. Mitral Valves deteriorate after about 5 years and aortic after about 8 years. For 61-75yo, the probability of being alive after AVR was 30.9% vs 16.1% after MVR. Bioprosthetics are recommended in patients > 70 YO, or in pts who can’t take warfarin, or who have a short life expectancy–----- recommend lifelong aspirin 81 mg q day PROSTHETICS= Recommended in patients < 60 YO. Require lifelong warfarin and antiplatelet medications. (incidence of major embolism or death between warfarin & aspirin 100mg vs warfarin alone was 1.9% vs 8.5%) Mitral prosthetic valves are more thromoembolic than aortic. GUIDELINES: ACCP GUIDELINES ACC /AHA Bioprosthetics asa 50-100mg q day for at least 3 months 75-100mg asa-warfarin INR= 2-3 for first 3 months Mechanical AVR Warfarin INR goal= 2-3 warfarin INR 2-3 low risk 2.5-3.5 high risk Aortic valve repair. Asa 50-100 mg q day no addressed. Bioprosthetic MVR Warfarin INR 2-3 x 3 mo, then asa warfarin inr=3-3 x 3 month Mechanical MVR Warfarin inr= 2.5=3.5 warfarin 2.5-3.5 Mitral valve repair asa 81 mg x 3 months Consider warfarin inr= 2-3 x 3 months Ring placement Mitral valve
Heart Valves Remember: We treat only MECHANICAL PROSTHETIC VALVES with anticoagulants. (Bioprosthetics valves.. Treat with warfarin x 3 months.. Then aspirin) ONLY ANTICOAGULANT FOR VALVES IS WARFARIN RE-ALIGN STUDY actually found an increased risk of stroke and bleeding in patients with mechanical heart valve treated with dabigatran compared with warfarin (Eikelboom 2013). Additionally,a subanalysis of ENGAGE AF-TIMI 48 found a higher rate of ischemic stroke in patients treated with edoxaban 60 mg daily
Management of suspected prosthetic valve thrombosis
Disruption of VKA - Don’t need to stop warfarin for minor procedures such as cataract removal or dental procedures. ACCP recommends parenteral bridging during warfarin initation. Start 6 hrs after procedure Reduced thrombosis from 6.1 to 2%
Transcatheter Aortic Valve Replacement 1 year mortality for TAVR vs traditional surgery was 24.2% vs 26.8% with complications, rate of death at 1 year was 30.7% for TAVR and 50.7% for standard surgery. TAVR are bioprosthetics…… recommend 6 months of dual antiplatelet (aspirin and clopidogrel) followed by long term ASA 81 mg. New onset AF can effect as many as 30% of TAVR pts. Strokes are much higher in the AF population.
Mitral vs Aortic Mitral valve disorders occur far less than aortic. 80% of Mitral stenosis is caused by rheumatic heart disease. vs only 3% are due from senile calcification
For Atrial Fibrillation Management Scoring system Interpretation ATRIAL FIB- untreated is assoc with 5% chance of stroke per year.. Treated with warfarin, there is a 64% risk reduction in stroke and systemic embolism and a 25% reduction in mortality. DOACs have been shown to be as effective as warfarin for stroke prevention in patients with AF and are associated with less intracranial hemorrhage and reduced all-cause mortality. However, the DOACs, except apixaban, are associated with a 25% increase in risk of GI bleeding CHA2DS2VASc has replaced CHAD2
Use of D-dimer to stop/continue anticoagulant Utility of D-dimer Testing D-dimer testing performed several weeks after 3-6 months of warfarin therapy has been completed is a strategy identified to predict the likelihood of recurrent VTE and the need for continuing anticoagulation. A positive D-dimer (typically >0.5 mg/dL) at the time of warfarin discontinuation or shortly thereafter was shown in several meta-analyses to identify patients at higher risk of developing recurrent VTE (Bruinstroop 2009; Douketis 2010; Marcucci 2013; Verhovsek 2008), independent of the timing of D-dimer testing, patient age, and the assay cut point used (Douketis 2010). A low D-dimer value in this setting may identify patients at low risk of recurrence who can discontinue warfarin, whereas a positive D-dimer test may identify patients with a persistent prothrombotic tendency. However, one consideration to note is that D-dimer is an acute-phase reactant that is nonspecific and may be elevated by other conditions
Comparisons Pearls For Initial treatment of VTE. Use Parenteral Anticoag FIRST.. Then edoxaban or dabigatran or Start Rivaroxaban or Apixaban Without parenteral anticoags. Apixaban is the drug of choice In Renal Failure. Last 3 agents have CYP3A4 drug Interactions
Reversal Agents For Anticoagulants Idarucizumab (Praxbind) was recently granted accelerated approval by the FDA for patients on dabigatran warranting anticoagulation reversal for emergent procedure or life-threating and uncontrolled bleeding. This agent is a humanized monoclonal antibody fragment with >350-fold preferential binding to dabigatran Andexanet alfa is a recombinant modified human factor Xa decoy protein that binds to and sequesters with high specificity direct and indirect factor Xa inhibitors (apixaban, edoxaban, rivaroxaban, LMWH, fondaparinux) Ciraparantag (formerly known as aripazine and PER977), is a water-soluble synthetic molecule designed to bind to LMWH and UFH; it has been shown to bind in a similar way to fondaparinux, direct thrombin inhibitors, and direct factor Xa inhibitors, inhibiting their anticoagulant effect in animal studies.