February 17th, 2010

Which Strategy for Severe Calcific Aortic Stenosis?


The patient is a 72-year-old man with a history of ischemic cardiomyopathy (LV ejection fraction, 30%–35%) and NYHA class II/III heart-failure symptoms at baseline. Over the previous month, he had experienced recurrent episodes of volume overload and sustained ventricular tachycardia (VT) requiring intravenous diuretics and up-titration of his amiodarone therapy. He then presented in VT storm, requiring intravenous lidocaine in addition to amiodarone, and was transferred to a tertiary care facility for potential VT ablation.

His additional medical history is noteworthy for hypertension, hyperlipidemia, insulin-dependent type II diabetes mellitus, paroxysmal atrial fibrillation, chronic renal insufficiency (serum creatinine, 1.5 mg/dL), mild chronic obstructive lung disease, and Parkinson’s disease. He underwent bypass surgery for coronary atherosclerosis in 2004 and received a biventricular pacemaker/defibrillator in 2005.

At the tertiary facility, an echocardiogram revealed an LVEF of 30%–35% (LV end-diastolic diameter, 5.1 cm) with global hypokinesis. Moderate-to-severe RV dysfunction was identified. The patient had a heavily calcified, trileaflet aortic valve with a peak gradient of 29 mm Hg, a mean gradient of 18 mm Hg, and a calculated valve area of 0.6 cm2. He also had moderate mitral regurgitation (regurgitant volume, 52 mL). His estimated pulmonary-artery systolic pressure was 21 mm Hg + RA.

A subsequent catheterization confirmed severe aortic stenosis and revealed native 3-vessel disease with patent grafts. A FDG-PET scan showed a small area of inferior scar but no ischemia.



  • Is the patient’s aortic stenosis a major contributor to his recent HF decompensation and recurrent VT?
  • Which would better serve the patient: aortic valve surgery or balloon valvuloplasty?
  • Should he be considered for an experimental percutaneous valve replacement?

James Fang, MD

This man appears to have significant aortic stenosis despite his modest gradient. Although the cath lab findings are not reported, they appear to corroborate the echocardiographic findings. No comment is made of assessing contractile reserve, which would help to rule out pseudo-aortic stenosis; this assessment can be done either in the cath lab or using echocardiography. Assuming that such an assessment would confirm severe aortic stenosis, I would recommend surgical aortic valve replacement.

Two other issues should also be resolved before surgery is entertained. The presence of a “porcelain” aorta would temper the enthusiasm for surgical AVR. In addition, the moderate-to-severe RV dysfunction is of concern and needs to be further clarified in the cath lab. The CVP, RVSWI, and TR are not commented on. This degree of RV dysfunction is not typically seen with severe aortic stenosis.

The patient’s comorbidities and the redo nature of an AVR increase his operative mortality. Based on publicly available risk scoring tools, his predicted mortality is in the range of 9% (STS) to 25% (EuroScore). Although these scores have been validated in various populations, they appear, to many clinicians, to overestimate risk in clinical practice. This issue has limited the interpretation of the published TAVI experience, and we await large randomized (albeit not blinded) studies such as PARTNER.

If surgical expertise is not available, a percutaneous AVR could be offered as an alternative but should be done in the context of a clinical trial. The durability of percutaneous valves is not clear and cannot be compared to conventional AVR in this regard at this time. Certainly, the recently published Canadian experience (with both transapical and transfemoral approaches) is encouraging. A “bridging” strategy could include valvuloplasty, with the understanding that the results would be temporary; this approach would primarily serve to reassure the clinicians that AVR of any sort is worth undertaking, while also potentially improving the baseline hemodynamic status of the patient.

There is reasonable evidence that wall stress and decompensated heart failure are arrhythmogenic; the patient’s aortic stenosis appears to be significant enough to contribute to this scenario. It would also be important to assess his CRT. LV stimulation can be pro-arrhythmic in certain substrates — particularly in ischemic heart disease, due to the nature of the scarring involved.


The patient underwent aortic valve replacement with a bioprosthetic valve. The total bypass time was 224 minutes with a cross clamp time of 114 minutes. On post-operative day 2, the patient was successfully weaned off pressor and intra-aortic balloon pump support. However, he was massively volume overloaded and remained somnolent, despite lack of sedation, making extubation difficult. An attempt at diuresis with escalating doses of intravenous furosemide was unsuccessful. CVVH was started but diuresis was limited by fever and hypotension. In this context, the patient developed recurrent ventricular tachycardias, requiring anti-tachycardia pacing by his device. Due to the his continued ventilator dependence, a tracheostomy and percutaneous endoscopic gastrostomy tube were placed on post-operative day 12. A chest CT revealed multifocal pneumonia and the patient was treated with broad spectrum antibiotics. He developed a spontaneous pneumothorax, requiring chest tube placement. He then developed progressive hypotension with evidence of Staphylococcus aureus bactermia. Despite escalating support, the patient suffered an asystolic arrest and died on post-operative day 20.

James Fang, MD

It would be interesting to know what the surgical findings were and the intraoperative course, particularly in light of the close to 4-hour bypass time. If right ventricular dysfunction was an intra- or immediately postop issue, I wonder if RVAD support was entertained, especially since massive volume overload is commented on early after surgery. The prolonged pump time likely played a large role in his postoperative neurologic state. The source of this man’s postoperative infection would also be of interest since it ultimately led to his death. Although the ultimate outcome might temper my preoperative comments, I would still not change my overall preoperative assessment. Valvuloplasty again may have been a reasonable “bridging strategy.”

5 Responses to “Which Strategy for Severe Calcific Aortic Stenosis?”

  1. Determining the “true risk”…
    This is definitely an interesting and rather challenging case. In regards to the patient’s clinical presentation, it seems that the calcific AS is playing a major component. After ruling-out ischemia as a precipitant, it is very likely that the etiology of heart failure and ventricular arrhythmias are secondary to severe AS. It is also likely that the patient has a poorly compliant left ventricle secondary to chronic pressure overload hypertrophy and this could be leading to significantly elevated filling pressures with exercise due to worsening MR. In regards to his treatment options, to help add some more perspective, and assuming the best case scenario that the patient has only mild chronic kidney disease, mild obstructive lung disease, no peripheral vascular disease, no history of TIA/CVA, and isolated AV replacement, his mortality risk from traditional AVR surgery would be: ~6% using the STS risk score, ~8% using the EuroSCORE, and ~25% using the Parsonnet risk score. I think the discrepancy tells us something about the limitations of these risk scores in the real world setting. Clinically, it seems evident that he’s high risk. Finally, I think the question of whether he might be considered for a percutaneous aortic valve also depends on additional factors that would make him more or less amenable, e.g. peripheral vascular disease, adequate femoral vascular access, aortic annular size, etc.

  2. This clearly is a very complex case of significant ischemic cardiomyopathy, valvular disease as well as other comorbidities. Given low velocities and low mean gradient across the aortic valve I am not convinced whether AS is a major contributor to patient’s symptoms. I agree, contractile reserve assessment would be very helpful but also results of the right heart catheterization. Assuming, AS is severe, given several risk factor as well as severely decreased right ventricular function suggested by 2D echo but also relatively low RVSP, I would favor percutanous valvuloplasty over open heart AVR. Given history of ischemic cardiomyopathy and minimal viability on FDG-PET, I would be concerned about scar mediated VT and therefore refer for EP evaluation and possible VT ablation.

  3. I wonder if there was severe aortic stenosis in 2004. If done in conjunction with the AVR and CABG in 2004 the patient’s condition could have been better later in life.
    Patient volume overload seems to be important. Biventricular failure and aortic stenosis may be the causes of volume overload. However, renal artery stenosis should be considered also. There are many potential causes for the formation of renal artery stenosis in this patient. It would be better if the patient were analyzed in this situation before operation.
    In my opinion, seems to have been rushed to surgery. The moderate-to-severe RV dysfunction is important to be present as a risk factor. It would be better if it is continued medical treatment rather than surgery.

  4. Unfortunate outcome-Here are my 2 cents in chronological order:

    1. Map and ablate VT with impella support
    2. BAV and stabilization of heart failure
    3. Assess response-clinically and quantitatively-Echo/RHC
    4. The judgement call regarding surgical vs. percutaneous AVR requires more than what can be described on paper.

    I have yet to see a great outcome with RVAD support except when the underlying etiology was reversible/transient in the first place. The RV failure deserved more attention than given to it-uniformly fatal.

  5. David Powell , MD, FACC says:

    A hemodynamic assessment of the AS with dobutamine was indicated. I believe this would be required for TAVI. In my experience, a peak transaortic velocity of 2.7 m/sec is about the lowest seen for severe AS and only with extremely hypokinetic ventricles. The pre-existing CHF and systolic dysfuction also mandates particular attention to the true severity of the AS and its relationship to symptoms and right heart failure. Absence of contractile reserve along with RV failure would place this patient at much higher surgical risk.