EHR519 202430 Week 5A Lecture 2 Valvular Diseases PDF

Warning This material has been produced and communicated to you by or on behalf of Charles Sturt University in accordance with section 113P of the copyright act (Act). The material in this communication may by subject to copyright under the act. Any further reproduction or c...

Warning This material has been produced and communicated to you by or on behalf of Charles Sturt University in accordance with section 113P of the copyright act (Act). The material in this communication may by subject to copyright under the act. Any further reproduction or communication of this material by you may be the subject of copyright protection under this act. Do not remove this notice Valvular disorders 2  Valve Disorders/Valvular Heart Disease (VHD) Damage or defect in one of the four heart valves Aortic, mitral, tricuspid or pulmonary Congenital or acquired Risk factors Smoking Gender Age Hypercholesterolemia Hypertension T2DM Almost one-third of elderly individuals have echocardiographic or radiological evidence of calcific aortic valve (CAV) sclerosis, an early and subclinical form of CAV disease (CAVD) (Zeng et al. 2016) 3  Valves have an outer layer of endothelial cells, surrounding 3 layers of matrix, all with specialised functions. Matrix has collagens, proteoglycans, elastin Valves open/ close 100,000 day Healthy valves ensure that blood flows with suitable force in the proper direction at the correct time. In valvular heart disease, the valves become too narrow and hardened (stenotic) to open fully, or are unable to close completely (incompetent). Stenotic: forces blood to back up in the adjacent heart chamber Incompetent: allows blood to leak back into the chamber that it has just exited. To compensate for poor pumping action, the heart muscle enlarges and thickens, i.e. LVH. In some cases, blood pooling in the chambers of the heart has a greater tendency to clot, ↑ risk of stroke or pulmonary embolism. 4  Mitral Valve Regurgitation The most common cause of chronic mitral regurgitation is myxomatous changes seen in mitral valve prolapse (MVP). The middle layer of the valve leaflets become thickened, frequently causing leaflet redundancy, which makes it difficult for them to close properly. The chordae tendinae may also be affected, disrupting support of the mitral valve apparatus. 5  Mitral Valve Stenosis Mitral valve is narrowed and does not close properly Blocks blood flow coming into the LV Common cause is infection, calcification (due to inflammation) or genetic 6 Aortic Valve Regurgitation Aortic valve does not close completely and allows some of the blood back into the left ventricle LVH and dilation gradually occur over time if left untreated in order to maintain LV pressures and Q Largest LV end-diastolic volumes Eventually leads to arrhythmias, LV impairment and heart failure 7 Aortic Valve Stenosis Narrowing of the aortic valve which restricts blood flow from the LV to the aorta and thus systemic circulation Increase workload on the LV, leading to hypertrophy and heart failure 8 Inflammation Inflammation is known to play a significant role in many types of macrovascular calcification, including CAVD. A number of the inflammation-associated factors, including Tumor necrosis factor (TNF-α) Interleukin 1-β CRP Advanced glycosylation-end products, and Oxidized low-density lipoprotein (oxLDL) cholesterol activate vascular biomineralization and vascular osteogenic signalling processes Reactive oxygen species (ROS), has a pro-osteogenic and pathogenic role in CAVD and that a number of the enzymatic mechanisms that counteract oxidative stress are downregulated in valves during the pathogenesis of CAVD Advances in genomic technologies = identification of many genetic abnormalities 9 Signs and Symptoms Shortness of breath (SOB) Fatigue, (during PA) Swollen feet or legs Heart palpitations Dizziness or fainting Coughing up blood Chest pain 11 Treatment Calcific aortic valve disease and other types of Valvular heart diseases are reaching epidemic status Although the incidence of VHD is high, therapeutic approaches for this disease are limited The primary clinical approach for valve repair or replacement is surgery Aortic valve replacement is the second most frequent cardiac surgery following coronary artery bypass grafting 12  Effects on/of Exercise Training Heart valve stenosis and regurgitation reduce Q Hypertrophy, ventricular dispensability and diastolic dysfunction The mechanical function of a valve cannot improve with exercise However exercise is recommended to improve overall quality of life and ADLs Only when disease progresses to the point of affecting resting or exertional symptoms, or compromised hemodynamics is exercise restricted Aware of contraindications if other co-morbidities are present Effects on the Exercise Response Exercise responses will be dependent on the type and severity of the VHD and which valve(s) are affected Asymptomatic milder forms usually have few restrictions Because of the risk of sudden death, it is recommended that patients with moderate-to-severe aortic stenosis not participate in vigorous or competitive exercise Some abnormal hemodynamics during exercise include: Tachycardia Atrial fibrilation Blunted cardiac output Hypotension Limited exercise capacity Management & Medications Often on medications that: Widen blood vessels Lower BP Decrease heart’s work rate Maintain a regular heart rhythm Lower HR Reduce risk of blood clots Increase force of the heart’s contractions  Recommendations for Exercise Testing Testing primarily completed on asymptomatic patients Difficult to use as a diagnostic tool due to the co-morbidities including left ventricular hypertrophy and exercise-induced S-T segment depression Testing should include assessment of HR and BP responses and exercise-induced symptoms Quantify the extent of hemodynamic impairments (chest pain, dyspnoea, arrhythmias) Recommendations for exercise prescription No prospective studies examining the impact of regular exercise on the progression of valvular heart disease. AHA and ACC, suggest symptomatic individuals not participate in competitive sport Asymptomatic individuals, lesions considered safe and compatible with exercise include the mild stenotic and mild regurgitant lesions Gentle walking or cycling for 20–30 min 5 x wk @ HR correlating to ventilatory anaerobic threshold assessed by cardiopulmonary exercise testing or at 80% MHR (60%–70% for individuals taking beta-blockers). 3–6 repetitions up to 20% of the body weight on upper limbs and 50% of the body weight on the lower limbs. Exceptions include individuals with severe aortic stenosis or pulmonary stenosis. Patients must be advised to stop exercising immediately in the event of angina, palpitations or dizziness Gati, et al., Heart 2019