A. What are the most common causes of aortic stenosis?

The three most common causes of aortic stenosis are

congenital abnormalities (unicuspid, bicuspid, or fused leaflets)

Congenital aortic stenosis generally presents before age 30 years,

rheumatic heart disease,

and degenerative valve disease resulting from calcium deposition.

egenerative aortic stenosis is the most common cause in persons older than 70 years.

B. How does aortic stenosis cause syncope?

C. What is the pathophysiologic mechanism by which aortic stenosis causes angina pectoris?

D. How does aortic stenosis result in the physical findings described previously?

 

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Syncope in aortic stenosis is usually due to decreased cerebral perfusion from the fixed obstruction, but it may also occur because of transient atrial arrhythmias with loss of effective atrial contribution to ventricular filling. Arrhythmias arising from ventricular tissue are also more common in patients with aortic stenosis and can result in syncope.

Angina can be caused by a number of different mechanisms. Approximately half of all patients have comorbid significant coronary artery disease, which can lead to angina. Even without coronary artery disease, aortic stenosis causes compensatory ventricular hypertrophy. Ventricular hypertrophy causes an increase in oxygen demand as well as compression of the vessels traversing the cardiac muscle, resulting in decreased oxygen supply. The result is relative ischemia of the myocytes. Finally, in the case of calcified aortic valves, calcium emboli can cause coronary artery obstruction, although this is rare.

Carotid upstroke is decreased (pulsus parvus) and late (pulsus tardus) because of the fixed obstruction to flow. Left ventricular hypertrophy causes the apical impulse to be displaced laterally and to become sustained. The increased dependence on atrial contraction is responsible for the prominent S4. Flow through the restricted aortic orifice results in the midsystolic murmur, whereas regurgitant flow causes the diastolic murmur.

 

Time course of calcific aortic stenosis
Image
This conceptual framework for the natural history of calcific aortic valve disease illustrates the spectrum of disease from the 'at risk' patient to the patient with end-stage severe symptomatic aortic stenosis. Once aortic sclerosis is detectable, there is an increased risk of cardiovascular events, as shown by deviation of the survival curve (solid black line) from the expected event-free survival (dashed black line). At the onset of even mild symptoms, survival deviates even more from expected, with a dramatic decline in survival with severe symptomatic aortic stenosis. Aortic valve replacement (AVR) at the onset of early symptoms prevents these late adverse outcomes.
Reproduced from: Otto CM. Calcific aortic valve disease: outflow obstruction is the end stage of a systemic disease process. Eur Heart J 2009; 30(16):1940-2. By permission of the European Society of Cardiology. Copyright © 2009 Oxford University Press.

 

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Mortality Reduction With Early Surgery For Severe Aortic Stenosis

Asymptomatic patients do better than with wait-and-see policy

https://www.medpagetoday.com/meetingcoverage/aha/83417?xid=nl_mpt_ACC_Reporter_2019-11-18&eun=g5674783d2r

 

 

 

First Appropriate Use Criteria Issued for Severe Aortic Stenosis

  • Posted: 10/17/2017
  • Author: 

    Nicole Lou,Reporter, MedPage Today/CRTonline.org

Multi-society guide OKs intervention for most symptomatic cases

Cardiology professional societies combined forces to issue the first appropriate use criteria (AUC) for the treatment of patients with severe aortic stenosis.

The document outlining 95 common clinical scenarios and the treatments deemed “rarely appropriate,” “may be appropriate,” or “appropriate” appeared online in the Journal of American College of Cardiology and flagship journals of certain other of the 11 collaborating societies.

Treatments addressed included transcatheter aortic valve replacement (TAVR), surgical aortic valve replacement (SAVR), and balloon aortic valvuloplasty as a bridge to valve replacement or to palliative care; but the AUC also considered when no intervention is best.

Intervention was deemed generally appropriate in symptomatic patients, though in “scenarios in which expected survival is less than one year and overall health status is influenced more by comorbidities than aortic stenosis, a less aggressive option (medical management) is considered Appropriate.”

“In scenarios in which the patient has reduced ejection fraction, intervention is generally considered ‘appropriate,’ with the decision for TAVR or SAVR based predominantly on surgical risk,” the AUC stated, “the only exceptions being situations in which stress test results suggest that the stenosis is pseudosevere rather than severe or in which LV systolic function is profoundly impaired without contractile reserve. In these patients, medical management is considered ‘appropriate.’

“In the asymptomatic patient, a positive stress test effectively identifies the patient as symptomatic, with intervention again considered ‘appropriate’ regardless of surgical risk. In asymptomatic patients with findings suggesting likelihood of symptom onset but not sudden death, intervention is rated ‘appropriate,’ whereas medical management is considered ‘may be appropriate.’”

Writing group chair Robert Bonow, MD, of Northwestern University’s Feinberg School of Medicine in Chicago, and colleagues emphasized that the scenarios presented were at the “extremes of comorbidity as black and white examples” and acknowledged that real-life patients usually “present in shades of gray.”

“There needs to be flexibility in interpreting the nuances of many of these scenarios, just as there needs to be sound clinical judgment in making treatment decisions given the increasing complexity of patients with aortic stenosis,” the authors emphasized. “The writing group recognizes that this field is evolving very rapidly, and hence this document will need to be updated in a timely manner in order to reflect advances in technology and clinical outcomes.”

Societies that signed on to the AUC were the American College of Cardiology, American Association for Thoracic Surgery, American Heart Association, American Society of Echocardiography, European Association for Cardio-Thoracic Surgery, Heart Valve Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, and Society of Thoracic Surgeons.

 

Disclosures

Bonow disclosed representing the American College of Cardiology, conducting personal research at Harvard Clinical Research Institute, and having institutional ties to Gilead Sciences.

Source:

Journal of the American College of Cardiology

http://www.onlinejacc.org/

Bonow RO, et al “ACC/AATS/AHA/ASE/EACTS/ HVS/SCA/SCAI/SCCT/SCMR/STS 2017 appropriate use criteria for the treatment of patients with severe aortic stenosis” J Am Coll Cardio 2017; DOI: 10.1016/j.jacc.2017.09.018.

 

Content 4

E. Based on the way this patient presented, what is his life expectancy if left untreated?

Once symptoms occur in aortic stenosis, without treatment the prognosis is poor. Life expectancy is 2 years if aortic stenosis causes angina and 3 years if aortic stenosis causes syncope.

 

A 72-year-old man with a history of hyperlipidemia presents with a syncopal episode and is noted to have a systolic murmur on exam.

  • What valvular abnormality is concerning in the presentation of syncope?

    — Aortic stenosis (AS)

  • What are the typical characteristics of the murmur of AS? (Listen to Audio)

    — Timing: Mid-systolic; Shape: crescendo-decrescendo; Location of maximal intensity: Right 2nd intercostal space (base of heart);Radiation: Upward to the carotid arteries; Pitch: Low; Quality: Rough

    (Listen to Audio)

 

A 59-year-old man is brought to the emergency department by ambulance after experiencing a syncopal episode. He states that he was running in the park when he suddenly lost consciousness. He denies any symptoms preceding the event, and he had no deficits or symptoms upon arousing. On review of systems, he does say that he has had substernal chest pressure associated with exercise for the past several weeks. Each episode was relieved with rest. He denies shortness of breath, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. His medical history is notable for multiple episodes of pharyngitis as a child. He is otherwise well. He has no significant family history. He was born in Mexico and moved to the United States at age 10 years. He does not smoke, drink alcohol, or use drugs. On examination, his blood pressure is 110/90 mm Hg, heart rate 95 bpm, respiratory rate 15/min, and oxygen saturation 98%. Neck examination reveals both pulsus parvus and pulsus tardus. Cardiac examination reveals a laterally displaced and sustained apical impulse. He has a grade 3/6 midsystolic murmur, loudest at the base of the heart, radiating to the neck, and a grade 1/6 high-pitched, blowing, early diastolic murmur along the left sternal border. An S4 is audible. Lungs are clear to auscultation. Abdominal examination is benign. He has no lower extremity edema. Aortic stenosis is suspected.

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