Objectives

We seek to identify predictors of 30-day mortality after balloon aortic valvuloplasty (BAV).

Background

To date, there is no validated method of predicting patient outcomes after percutaneous aortic valve interventions.

Methods

Data for consecutive patients with severe aortic stenosis who underwent BAV at the Mount Sinai Medical Center from January 2001 to July 2007 were retrospectively reviewed. Cox proportional hazards regression was used to identify significant predictors of 30-day mortality and the resultant model was compared to the EuroSCORE using Akaike's Information Criterion and area under the receiver-operating curve (AUC).

Results

The analysis included 281 patients (age 83 ± 9 yrs, 61% women, aortic valve area: 0.64 ± 0.2 cm2), 36 (12.8%) of whom died within 30 days of BAV. Identified risk factors for 30-day mortality, critical status, renal dysfunction, right atrial pressure, and cardiac output, we used to construct the CRRAC the AV risk score. Thirty-day survival was 72% in the highest tertile versus 94% in the lower two tertiles of the score. Compared to the additive and logistic EuroSCORE, the risk score demonstrated superior discrimination (AUC = 0.75 vs. 0.60 and 0.63, respectively).

Conclusions

We derived a risk score, the CRRAC the AV score, that identifies patients at high-risk of 30-day mortality after BAV. Validation of the developed risk prediction score, the CRRAC the AV score, is needed in other cohorts of post-BAV patients and potentially in patients undergoing other catheter-based valve interventions.

Objectives

To determine whether nitrogen-containing bisphosphonate (NCBP) therapy is associated with the prevalence of cardiovascular calcification.

Background

Cardiovascular calcification correlates with atherosclerotic disease burden. Experimental data suggest that NCBP may limit cardiovascular calcification, which has implications for disease prevention.

Methods

The relationship of NCBP use to the prevalence of aortic valve, aortic valve ring, mitral annulus, thoracic aorta, and coronary artery calcification (AVC, AVRC, MAC, TAC, and CAC, respectively) detected by computed tomography was assessed in 3,636 women within the Multi-Ethnic Study of Atherosclerosis (MESA) using regression modeling.

Results

Analyses were age-stratified because of a significant interaction between age and NCBP use (interaction p-values: AVC p<0.0001; AVRC p<0.0001; MAC p=0.002; TAC p<0.0001; CAC p=0.046). After adjusting for age, body mass index, demographics, diabetes, smoking, blood pressure, cholesterol levels, and statin, hormone replacement, and renin-angiotensin inhibitor therapy, NCBP use was associated with a lower prevalence of cardiovascular calcification in women ≥65 years old (prevalence ratio [95% confidence interval]: AVC 0.68 [0.41, 1.13]; AVRC 0.65 [0.51, 0.84]; MAC 0.54 [0.33, 0.93]; TAC 0.69 [0.54, 0.88]; CAC 0.89 [0.78, 1.02]), whereas calcification was more prevalent in NCBP users among the 2,181 women <65 years old (AVC 4.00 [2.33, 6.89]; AVRC 1.92 [1.42, 2.61]; MAC 2.35 [1.12, 4.84]; TAC 2.17 [1.49, 3.15]; CAC 1.23 [0.97, 1.57]).

Conclusions

Among women in the diverse MESA cohort, NCBPs were associated with decreased prevalence of cardiovascular calcification in older subjects, but more prevalent cardiovascular calcification in younger ones. Further study is warranted to clarify these age-dependent NCBP effects.

Fibrocalcific aortic stenosis (AS) results from an active process similar to atherosclerosis that involves basement membrane disruption, lipid deposition, inflammatory cell infiltration, and calcification. Consequently, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been extensively studied as potential therapeutic agents capable of slowing the progression of AS. However, two randomized trials, SALTIRE and the SEAS study, showed no benefit with statin therapy for AS. These results have shed doubt over the efficacy of statin therapy for AS, although their potential efficacy at early stages of aortic valve disease remains possible. In this article, we review the pathophysiology of fibrocalcific AS and discuss future directions for its nonsurgical management in the post-SEAS era.