Clinical and noninvasive hemodynamic results after aortic balloon valvuloplasty for aortic stenosis.

Balloon valvuloplasty has been shown to be an effective treatment for adults with aortic stenosis, typically providing a 50 to 80% increase in aortic valve area and marked improvement in exertional dyspnea, angina and syncope. However, the duration of this hemodynamic and clinical improvement is uncertain. Forty-two patients were followed for 10.2 +/- 0.5 months. Balloon valvuloplasty caused dramatic immediate reduction in the number of patients with moderate or severe dyspnea (80 to 14%), moderate or severe angina (39 to 2%) and syncope (30 to 2%). Furthermore, this improvement in symptoms continued for the duration of the follow-up period in most patients. Echocardiographic aortic valve mean gradient and area determined at 3-month intervals, however, showed a trend toward or return to prevalvuloplasty levels by 9 months' follow-up in 13 of 25 patients (52%), whereas 12 of 25 patients showed no deterioration in their hemodynamic parameters. This trend toward restenosis was accompanied by symptomatic deterioration in 5 of 13 patients (38%). This tendency toward restenosis in greater than 50% of patients by 9 months underscores the need for further technical improvements if balloon valvuloplasty is to be widely applied. Even with these limitations, however, balloon valvuloplasty seems to provide a significant improvement in actuarial survival compared with the natural history of elderly patients with severe aortic stenosis.

Treatment of cardiogenic shock by emergency aortic balloon valvuloplasty.

We used aortic balloon valvuloplasty to successfully treat two patients who had cardiogenic shock associated with calcific aortic stenosis. In both patients, the resulting reduction in mean aortic valve gradient and increase in calculated aortic valve area allowed prompt discontinuation of treatment with pressors and a return to near normal renal function. Both patients were discharged within 10 days after valvuloplasty and showed significant, long-lasting clinical improvement. Aortic balloon valvuloplasty can reverse cardiogenic shock associated with calcific aortic stenosis.

Mechanism of aortic balloon valvuloplasty: fracture of valvular calcific deposits.

Balloon valvuloplasty has been shown to acutely reduce the hemodynamic and symptomatic severity of calcific aortic stenosis. The mechanism by which this improvement is accomplished is not known. At necropsy, three patients who died after hemodynamically successful aortic balloon valvuloplasty were found to have aortic valve calcific deposits fractured at one or more sites. These findings suggest that fracture of leaflet calcium represents the basis for successful aortic balloon valvuloplasty.

Dual balloon technique for valvuloplasty of aortic stenosis in adults.

A dual balloon technique was studied in 16 patients with aortic stenosis in whom results with a single balloon (up to 20 mm, 5.5 cm or 25 mm, 3.0 cm in diameter and length, respectively) were judged to be suboptimal. Dual balloon valvuloplasty was performed using 2 balloons advanced and inflated simultaneously across the stenotic aortic valve orifice. For the group as a whole, the average peak transvalvular gradient was reduced from 79 +/- 8 to 57 +/- 7 mm Hg (mean +/- standard error) using a single balloon (p less than 0.0005), and reduced further to 36 +/- 4 mm Hg using dual balloons (p less than 0.0005 compared with single balloon results). Similarly, calculated aortic valve orifice area was increased from 0.45 +/- 0.04 to 0.57 +/- 0.05 cm2 using a single balloon (p less than 0.0005), and further increased to 0.77 +/- 0.06 cm2 using dual balloons (p less than 0.0005). Dual balloon dilation caused no complications directly attributable to the use of 2 balloons, including no exacerbation of aortic regurgitation. These results suggest that dual balloon valvuloplasty is safe and efficacious in selected patients with aortic stenosis.

Treatment of calcific aortic stenosis by balloon valvuloplasty.

Recent reports have established the feasibility of using balloon valvuloplasty to reduce left ventricular outflow tract obstruction due to a calcified aortic valve. The present study summarizes experiences with this technique in 9 patients (7 women, 2 men, mean age 78 years) in whom balloon valvuloplasty was used to treat calcific aortic stenosis. Peak aortic valve gradient (mm Hg) decreased from 68 +/- 8 (mean +/- standard error of the mean) before valvuloplasty to 35 +/- 5 after valvuloplasty (p = 0.003). Mean aortic valve gradient decreased from 57 +/- 7 before valvuloplasty to 30 +/- 5 after valvuloplasty (p = 0.006). Calculated aortic valve area increased from 0.42 +/- 0.04 to 0.81 +/- 0.06 cm2 (p = 0.005). Balloon valvuloplasty failed to diminish aortic valve obstruction in only 1 patient who, at subsequent surgery, had a congenitally bicuspid aortic valve. Significant aortic regurgitation was not observed in any of the 9 patients after valvuloplasty. One patient did have a highly focal, presumably embolic, brain stem infarct during the procedure. Femoral arterial blood loss, related to wire-guided exchange of balloon catheters too large for a 12Fr introducer sheath, was minimized by direct arterial exposure in 8 of the 9 patients. Thus, these findings confirm the efficacy of balloon valvuloplasty for the treatment of calcific aortic stenosis. The procedure, however, is not without hazard.

Pulmonary hemorrhage in lupus erythematosus without evidence of an immunologic cause.

Intra-alveolar hemorrhage is a known complication of lupus erythematosus (LE), but its cause is controversial. Some authors have shown immune complexes (ICs) deposited at various sites in the alveolar septae and postulated that these deposits result in pulmonary hemorrhage (PH). A patient with LE and PH had no detectable IC deposits at a time when IC disease was present in the kidney and vasculitis was active in the skin. Reviewing the literature, we show that IC deposits in the lung are nonspecific and are not correlated with PH. We propose that classification schemes that differentiate between IC-mediated PH and idiopathic PH are arbitrary, and that patients thought to have idiopathic PH should be followed up prospectively to monitor the development of possible immunologic disease.