Do All Critical Aortic Stenosis with Chest Pain need Aortic Valve Replacement?

 

Article by:

M. Sharma

D. Mascarenhas

 

Abstract

Aortic valve replacement (AVR) remains the cornerstone of treatment for symptomatic critical Aortic Stenosis (AS). It is a Class I indication that symptomatic patients with critical AS undergo either surgical or Transcatheter Aortic Valve Replacement (TAVR). We present a patient with critical AS and new angina that was managed successfully with percutaneous coronary angioplasty of the right coronary artery. Physicians should consider that not all patients with critical AS and angina necessarily require AVR. Concomitant pathology leading to the symptoms should be carefully ruled out. This leads to a less invasive, cost effective care plan especially in patients with advanced age and comorbidities for which any type of surgical valvular intervention may pose high risk.

 

Introduction :

Aortic valve stenosis (AS) is the most common cause of left ventricular outflow obstruction in children and adults.  It is the most common type of valvular heart disease in Europe and North America, occurring in 2–7% of the population over 65 years of age.[1] Medical therapy alone is not effective for the long-term management of aortic valve disease, thus valve replacement remains the standard of care in patients with an acceptable risk profile. Symptomatic patients with “Critical AS” are highly recommended to undergo  either surgical or  Transcatheter  Aortic Valve Replacement (TAVR).[2,3] The term “critical” was defined based upon theoretical considerations showing that the aortic valve area must be reduced to one-fourth of its natural size before significant changes in circulation occur. This has been discussed later. We present a case of critical AS with significant symptoms manifested as chest pain that was managed successfully without aortic valve replacement. We will also briefly review incidence, etiology, grading of AS and current guidelines for Aortic valve replacement (AVR).

 

Case report :

A 91-year-old male presented to our office in July 2015 with a complaint of a new-onset substernal burning pain of six weeks’ duration. He had been following up with us regularly in the past for his valvular heart disease (AS), hypertension and dyslipidemia. This pain was worse with exertion and was relieved by rest. The patient would have pain on walking, even around 100 yards. Prior to six weeks, he could walk a distance of about two street blocks on level ground without any shortness of breath or chest pain. Patient denied any history of radiation or referral of pain. It was not related to breathing or positional changes. On examination, blood pressure was 140/90 mm Hg and pulse was regular at 60 beats per minute. Cardiovascular exam revealed a Grade 4/6 ejection systolic murmur best heard in the right second intercostal region radiating bilaterally to the neck.

Echocardiography (ECHO) done in May of 2014 had revealed severe AS with aortic valve area of 0.6-0.7 cm2 (centimeter square) and an ejection fraction of 65% (percent). Notably, in 2014 patient was asymptomatic. In view of his new symptoms, the patient was sent for a cardiac catheterization to evaluate his coronary anatomy prior to aortic valve replacement (AVR).

Complete heart catheterization was performed. Hemodynamic measurements revealed (in mmHg) left ventricle (LV) pressure as 240/0 and a LVEDP (left ventricular end diastolic pressure) of 10. Central aortic pressure (AO) was 166/59. There was a 55 mmHg gradient across the aortic valve. The pulmonary artery (PA) wedge pressure, mean of 24, RA (Right atrium) mean of 8, RV (Right ventricle) 60/10 with an RVEDP (Right ventricular end diastolic pressure) of 14, PA (pulmonary artery) 60/70. The aortic valve area was calculated at 0.6 cm2, which was unchanged from the ECHO finding that was done in May 2014.

The left ventriculogram in the right anterior oblique view revealed normal LV systolic motion and ejection fraction of 55-60%. Left main coronary artery revealed a common ostium giving rise to the LAD (Left anterior descending) and the circumflex artery. Right coronary artery (RCA) revealed a 99% ostial narrowing (Figure 1). LAD revealed a 60% narrowing in its proximal segment and a 90% ostial diagonal narrowing (Figure 2). Circumflex coronary artery had a 90% stenosis (Figure 3).

TC- Oct 2016 - 007 - RCA revealing a 99% ostial narrowing TC- Oct 2016 - 008 - Left anterior descending (LAD) TC- Oct 2016 - 009 - Circumflex coronary artery had a 90% stenosis

 

After a detailed discussion involving the patient, his son, the interventional cardiologist and the cardiothoracic surgeon, the patient requested that only Percutaneous Coronary Intervention (PCI) of the RCA be considered, as the chest pain was of recent duration with no change in the aortic valve finding. Thus, a successful percutaneous transluminal coronary angioplasty (PTCA) with stent placement was done in the proximal RCA with a bare metal stent (Figure 4). Patient was recommended anti-platelet therapy only for 6 months.

TC- Oct 2016 - 010 - After PTCA (shown by arrow)

Patient did extremely well after PTCA and stenting of the RCA and the patient has remained asymptomatic to date. Thus, this new onset chest pain in patient with critical AS was due to concomitant coronary artery lesion and was amenable to stenting and thus spared this elderly patient from the aortic valve replacement which would have been a high risk surgery for him.

 

Discussion:

Aortic stenosis (AS) is the most common valvular heart condition in the western world, affecting 3% of people between ages 75 and 85 and 4% of people over age 85. ​ Congenitally unicuspid, bicuspid, tricuspid, or even quadricuspid valves may be the cause of aortic stenosis.[4] In adults who develop symptoms from congenital aortic stenosis, the problem is usually a bicuspid valve.[5] The main causes of acquired aortic stenosis include degenerative calcification and less commonly, rheumatic heart disease.[6,7] Other infrequent causes of aortic stenosis include obstructive vegetations, homozygous type II hypercholesterolemia, Paget disease, Fabry disease, ochronosis, and irradiation.

Based upon a variety of hemodynamic and natural history data, clinicians generally grade the severity of stenosis as mild, moderate, severe, or critical. Grading of AS[8] are as follows:

Mild: Valve area exceeds 1.5 cm2; transvalvular velocity 2.0 to 2.9 m/s; mean gradient < 20 mm Hg. ​

Moderate: Valve area of 1.0 to 1.5 cm2; transvalvular velocity 3.0 to 3.9 m/s; mean gradient 20 to 39 mm Hg. ​

Severe: Valve area is less than 1.0 cm2; transcavitary velocity ≥ 4 m/s; mean gradient ≥ 40 mm Hg.

The term “critical” stenosis was defined based upon theoretical considerations showing that the   aortic   valve   area   must   be   reduced   to one-fourth of its natural size before significant changes in circulation occur. ​As a result, since the triangular orifice area of the normal (adult) aortic valve is approximately 3.0 cm2, an area exceeding 0.75 cm2 would not be defined as critical. Aortic valve replacement (surgical and transcatheter aortic valve replacement, TAVR) remain the only treatment proven to reduce the rates of mortality and morbidity in this condition.

Under current guidelines, the onset of symptoms of exertional angina, syncope and dyspnea in a patient who has severe aortic stenosis is a class I indication for surgery.[9] High gradient, severe aortic stenosis that is asymptomatic often poses a dilemma.[7] ​The annual rate of sudden death in patients with this condition is estimated at 1% to 3% ​but the surgical mortality rate in aortic valve replacement has been as high as 6%.[10-15] With improvements in surgical techniques and prostheses, mortality rates have been reduced to 2.42 % making a case for earlier intervention.[16]  Transcatheter aortic valve replacement (TAVR) has become widely available, but further investigation into its use in this patient cohort is warranted.[17] While assessing the cases of asymptomatic aortic stenosis, we have both traditional as well as novel markers at our disposal now. Left ventricular ejection fraction (LVEF) < 50%, peak aortic jet velocity > 4.0 m/s, valve area < 1 cm2 and mean pressure gradient > 40 mm Hg are the traditional markers to denote severe AS in asymptomatic patients. While, indexed left atrial size > 12.2 cm2 /m2, left ventricular hypertrophy (LVH) with wall thickness >15 mm​, global left ventricular longitudinal strain < 15.9, B-natriuretic peptide (BNP) level > 130 pg/ml and increase in mean pressure gradient of > 20 mm Hg during exercise testing are the novel markers of asymptomatic severe AS.

The American College of Cardiology and American Heart Association (ACC/AHA) have issued the following recommendations for aortic valve replacement, based on the severity of stenosis and on whether the patient has symptoms or not.[18-21]

1) Severe stenosis, with symptoms: class I recommendation (surgery should be done). Without surgery, these patients have a very poor prognosis, with an overall mortality rate of 75% at 3 years. ​

2) Severe stenosis, no symptoms, in patients undergoing cardiac surgery for another indication (example coronary artery bypass grafting, ascending aortic surgery, or surgery on other valves): class I recommendation for concomitant aortic valve replacement.

3)  Moderate stenosis, no symptoms, in patients undergoing cardiac surgery for another indication: class II a recommendation (i.e., aortic valve replacement “is reasonable”). ​

​4)  Very severe stenosis (aortic peak velocity > 5.0 m/s or mean pressure gradient ≥ 60 mm Hg), no symptoms, and low risk of death during surgery: class II a recommendation.

5) Severe stenosis, no symptoms, and an increase in transaortic velocity of 0.3 m/s or more per year on serial testing or in patients considered to be at high risk for rapid disease progression, such as elderly patients with severe calcification: class II b recommendation (surgery “can be considered”).

 

On revisiting the above case description we realize that the patient did have “Critical” AS but was asymptomatic.​ His chest pain was only due to  concomitant  coronary artery  disease and was  not due  to  aortic  stenosis  per  se. Age  and comorbidity of the patient posed a high risk for coronary artery bypass graft (CABG) with aortic valve surgery.​ Besides, the patient’s symptoms were of new onset and subsequent cardiac catheterization revealing critical RCA stenosis encouraged us to think otherwise. The decision to perform PCI alone with the belief that this chest pain and coronary artery disease (CAD) would be amenable to the minimal risk procedure paid dividends.

 

Conclusion:

Awareness amongst the physicians about the  fact that “ all critical aortic stenosis with chest pain may not require aortic valve replacement” is important. This can lead to less invasive treatment methodology tailored to the need of the patient especially those with advanced age, significant comorbidities and an extremely high risk for CABG, with AVR. Hence, careful history taking and  physical examination is extremely important prior to intervention.

 

TC- Oct 2016 - 011 - Writers Art pg 14

 

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