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In aortic stenosis, severe ventricular arrhythmias may be linked to left ventricular dysfunction and are a factor to be considered when a surgical decision is to be made. Conduction disturbances are frequent, sometimes not related to the severity of the stenosis and may endanger patient's life.
Supravalvular aortic stenosis is characterized by obstruction of the left ventricular outflow tract distal to the aortic valve, and may result in diminished coronary artery blood flow. This report describes the cases of 2 patients in whom obstruction to left coronary artery flow was caused by obliteration of the coronary ostium itself. This mechanism differs from the more commonly recognized cause--valve leaflet adhesion to the obstructing ridge of aortic tissue. The coronary artery obstruction found in these 2 patients required direct enlargement of the left coronary ostium in both. This mechanism of impaired coronary artery flow deserves emphasis, as traditional methods of extended patch aortoplasty may fail to relieve the coronary ostial narrowing.
In aortic stenosis (AS), postextrasystolic potentiation (PESP), a measure of contractile reserve, has been demonstrated by an increased aortic valve gradient (AVG) after a ventricular extrasystole (VE). We studied age-related changes in PESP in 20 consecutive patients (age, 65-89 years) with significant AS (aortic area <or= 1.0 cm(2)) on cardiac catheterization with VE on AVG pressure recording. Hemodynamics and LV systolic time intervals were averaged from three consecutive beats and from the post-VE beat. Changes (Delta) in AVG, pre-ejection period/LV ejection time ratio (PEP/LVET), aortic diastolic pressures (AoDP), and LV end-diastolic pressures (LVEDP) were calculated. Age was inversely correlated with DeltaAVG (r = -0.84, P = 0.0001), with DeltaPEP/LVET (r = -0.87, P = 0.0001), and with DeltaAoDP (r = -0.89, P = 0.0001), but not with DeltaLVEDP (r = 0.23, P = 0.31). On multivariate analysis, only age was associated with DeltaAVG (r(2) = 0.72, P = 0.0001). There was an age-related decline in PESP in patients with AS, which was accompanied by changes in contractile reserve and afterload reduction, but independent of preload reserve.
Balloon aortic valvuloplasty has been used as treatment for selected patients with severe aortic stenosis. We report our experience of 11 procedures, performed on ten patients between October 1987 and June 1988. The peak aortic systolic gradient was reduced by 53% from 77 +/- 22 to 37 +/- 14 mmHg (p less than 0.0001) whilst cardiac output did not change significantly (4.1 +/- 1.7 to 3.8 +/- 1.6 (p less than 0.0001) whilst cardiac output did not change significantly (4.1 +/- 1.7 to 3.8 +/- 1.6 L/min). Aortic valve area was increased by 50%, from 0.4 +/- 0.2 to 0.6 +/- 0.2 cm2 (p less than 0.0001). Initial symptomatic improvement was achieved in eight patients. Echocardiographically demonstrated aortic regurgitation did not increase after valvuloplasty. There were no deaths during the procedure, no embolic events and no femoral artery complications. The mean follow-up for survivors was 9 +/- 3 months. Five patients died and three had symptom recurrence at an average of 13 weeks (six-24 weeks). Only two patients reported a continued improvement in symptoms. Balloon aortic valvuloplasty produced a small increase in aortic valve area and a satisfactory initial clinical response, but there was a high incidence of symptom recurrence. The procedure may have a role in the short-term palliation of severely symptomatic patients who are unable to have aortic valve replacement.
In aortic stenosis (AS), conventional indexes of severity vary with changes in transvalvular flow. It is important to determine the true severity of obstruction because AS in the presence of low cardiac output and low gradient is associated with high mortality during aortic valve replacement. This study compares 3 indexes of stenosis severity at different transvalvular flow rates in patients with low-flow, low-gradient critical AS. Eight patients with critical AS (valve area < or = 0.7 cm2), low cardiac output (< 4.0 L/min), and low mean transvalvular gradient (< or = 40 mm Hg) underwent hemodynamic assessment at baseline, after transvalvular flow was augmented with dobutamine, and after the valve opening was increased with percutaneous balloon aortic valvuloplasty. Severity of obstruction was assessed using 3 different measures: Gorlin formula calculated valve area, valvular resistance, and percentage left ventricular stroke work loss. Dobutamine infusion increased cardiac output by 35% and mean transvalvular gradient by 27%. The mean Gorlin formula calculated aortic valve area increased from 0.5 to 0.6 cm2 (p = 0.002). Percentage left ventricular stroke work loss increased from 23% to 28% (p = 0.03). Valve resistance was unchanged by dobutamine (350 to 310 dynes X sec X cm(-5); p = NS). Balloon valvuloplasty increased cardiac output 13% and decreased the gradient 31%; this resulted in an increase in the calculated valve area from 0.6 to 0.9 cm2 (p = 0.001). Percentage left ventricular stroke work loss decreased from 28% to 20% (p = 0.002), and valve resistance decreased from 310 to 181 dynes X sec X cm(-5) (p = 0.001) after valvuloplasty. We conclude that in patients with low-flow, low-gradient critical AS, valve resistance is the most flow-independent measure of severity of stenosis. All measures improve with percutaneous balloon aortic valvuloplasty.
BACKGROUND: Calcific aortic stenosis has many characteristics in common with atherosclerosis, including hypercholesterolemia. We hypothesized that intensive lipid-lowering therapy would halt the progression of calcific aortic stenosis or induce its regression. METHODS: In this double-blind, placebo-controlled trial, patients with calcific aortic stenosis were randomly assigned to receive either 80 mg of atorvastatin daily or a matched placebo. Aortic-valve stenosis and calcification were assessed with the use of Doppler echocardiography and helical computed tomography, respectively. The primary end points were change in aortic-jet velocity and aortic-valve calcium score. RESULTS: Seventy-seven patients were assigned to atorvastatin and 78 to placebo, with a median follow-up of 25 months (range, 7 to 36). Serum low-density lipoprotein cholesterol concentrations remained at 130+/-30 mg per deciliter in the placebo group and fell to 63+/-23 mg per deciliter in the atorvastatin group (P<0.001). Increases in aortic-jet velocity were 0.199+/-0.210 m per second per year in the atorvastatin group and 0.203+/-0.208 m per second per year in the placebo group (P=0.95; adjusted mean difference, 0.002; 95 percent confidence interval, -0.066 to 0.070 m per second per year). Progression in valvular calcification was 22.3+/-21.0 percent per year in the atorvastatin group, and 21.7+/-19.8 percent per year in the placebo group (P=0.93; ratio of post-treatment aortic-valve calcium score, 0.998; 95 percent confidence interval, 0.947 to 1.050). CONCLUSIONS: Intensive lipid-lowering therapy does not halt the progression of calcific aortic stenosis or induce its regression. This study cannot exclude a small reduction in the rate of disease progression or a significant reduction in major clinical end points. Long-term, large-scale, randomized, controlled trials are needed to establish the role of statin therapy in patients with calcific aortic stenosis.
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The present investigation was designed to derive an accurate pulsed Doppler method of assessing aortic stenosis severity that does not rely on measurement of aortic jet velocity. Left ventricular ET and SV were determined from pulsed Doppler recordings of flow velocity at the aortic anulus in 44 mostly normotensive patients with aortic stenosis. Aortic valve area at catheterization ranged between 0.3 and 2.13 cm2. A predicted ET was derived from Doppler-determined SV with the use of a regression equation previously described by Harley et al. A significant inverse quadratic relation was observed between the ET difference (delta ET), defined as measured ET minus predicted ET, and valve area at catheterization (r = -0.87; valve area = 1.4 - 15 delta ET + 60 delta ET2; SEE = 0.23 cm2). An ET difference of greater than or equal to 0.060 second was 88% sensitive, 89% specific, and 89% accurate for detecting critical aortic stenosis. Thus the ET difference, derived from measurements of SV and ET by pulsed Doppler, is a sensitive index for detection of critical aortic stenosis that is independent of determination of aortic jet velocity. This index should complement the Doppler evaluation of aortic stenosis, especially in cases where interrogation of the stenotic jet with continuous wave Doppler is inadequate.
Calcified aortic stenosis (CAS) is an unusual cause of cerebral infarct. The presence of cerebral intra-vascular or intra-parenchymatous calcifications, symptomatic or not, is suggestive of the diagnosis of CAS. We report two patients who experienced stroke induced by spontaneous calcic emboli from a calcified aortic valve and underline the importance of brain CT scan.
Neonatal aortic stenosis is a complex and heterogeneous condition, defined as left ventricular outflow tract obstruction at valvular level, presenting and often requiring treatment in the first month of life. Initial presentation may be catastrophic, necessitating hemodynamic, respiratory and metabolic resuscitation. Subsequent management is focused on maintaining systemic blood flow, either via a univentricular Norwood palliation or a biventricular route, in which the effective aortic valve area is increased by balloon dilation or surgical valvotomy. In infants with aortic annular hypoplasia but adequately sized left ventricle, the Ross-Konno procedure is also an attractive option. Outcomes after biventricular management have improved in recent years as a consequence of better patient selection, perioperative management and advances in catheter technology. Exciting new developments are likely to significantly modify the natural history of this disorder, including fetal intervention for the salvage of the hypoplastic left ventricle; 3D echocardiography providing better definition of valve morphology and aiding patient selection for a surgical or catheter-based intervention; and new transcutaneous approaches, such as duel beam echo, to perforate the valve.
Supravalvular aortic stenosis (SVAS) may occur as an isolated autosomal dominant trait or as a feature of Williams syndrome. It has been suggested that a defect in calcitonin function may play a role in Williams syndrome. We have excluded calcitonin as a candidate gene for SVAS using a gene specific probe.
Supravalvular aortic stenosis (SVAS) occurs as an autosomal dominant trait or as part of the phenotype of the usually sporadic condition Williams syndrome. SVAS is the result of mutation or deletion of the elastin gene (ELN), located at chromosome 7q11.23. Thus, SVAS may be more appropriately termed an elastin arteriopathy. Studies have demonstrated various point mutations and intragenic deletions of ELN resulting in nonsyndromic SVAS. Individuals with Williams syndrome are hemizygous for the elastin gene, owing to a 1 to 2 megabase deletion of a portion of the long arm of chromosome 7 that encompasses ELN. This submicroscopic deletion is readily detected by fluorescent in-situ hybridization, useful in the diagnosis of Williams syndrome. The severity of SVAS is quite variable, both in series of Williams syndrome patients and within SVAS kindreds, suggesting that other genetic factors are involved in expression of the phenotype. Experiments with elastin knockout mice will likely yield clues regarding the role of elastin in arterial morphogenesis and the pathogenesis of obstructive vascular disease.
Supravalvular aortic stenosis (SVAS) is an inherited obstructive vascular disease that affects the aorta, carotid, coronary and pulmonary arteries. Previous molecular genetic data have led to the hypothesis that SVAS results from mutations in the elastin gene, ELN. In these studies, the disease phenotype was linked to gross DNA rearrangements (35 and 85 kb deletions and a translocation) in three SVAS families. However, gross rearrangements of ELN have not been identified in most cases of autosomal dominant SVAS. To define the spectrum of ELN mutations responsible for this disorder, we refined the genomic structure of human ELN and used this information in mutational analyses. ELN point mutations co-segregate with the disease in four familial cases and are associated with SVAS in three sporadic cases. Two of the mutations are nonsense, one is a single base pair deletion and four are splice site mutations. In one sporadic case, the mutation arose de novo. These data demonstrate that point mutations of ELN cause autosomal dominant SVAS.
BACKGROUND: Aortic stenosis (AS) and atrial fibrillation (AF) are commonly encountered in clinical practice. Natriuretic peptides (NP) are endogenous cardiac hormones, which have been shown to increase in patients with heart failure, and valvular or congenital heart disease. We aimed to determine the association between atrial NP (ANP) and late postoperative AF after surgery for AS along with temporal changes in plasma ANP levels and left atrial (LA) volumes. METHODS: 22 patients (16 males/6 females, mean age: 61 years) with symptomatic AS and 8 healthy volunteers (5 males/3 females) were enrolled into our study. All the patients studied underwent transthoracic echocardiography, which was repeated during the follow-up. N-terminal ANP (N-ANP) was studied initially and at the 2-month follow-up. Postoperatively, the patients were followed up for 12 months for AF attacks. RESULTS: Patients with AS had significantly higher levels of N-ANP, left ventricular (LV) end-diastolic pressure, E/A ratio, LV mass and LA volumes compared to the controls. Patients with postoperative AF attacks were significantly older, had higher N-ANP levels and LV end-diastolic pressure in addition to higher LA volumes and longer symptom duration compared to patients without AF. Age at the time of operation (p = 0.011) and N-ANP at the 2nd month (p = 0.047) were found to be independent predictors for late AF attacks during follow-up in regression analysis. Besides, N-ANP (p < 0.001) at the 2-month follow-up independently predicted impaired LA remodeling. CONCLUSION: ANP might be an important factor to identify AS patients at risk for late postoperative AF attacks.
After a patient had aortic valvotomy and aortotomy for the relief of valvar aortic stenosis supravalvar stenosis developed over the next six years.
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BACKGROUND: The aim of the study was to assess the value of Pulsed-wave Doppler tissue imaging (DTI) in assessing diastolic and systolic function in patients with severe aortic value stenosis. METHODS: Thirty-five patients with aortic stenosis (AS) (valve orifice < or = 1 cm 2 , mean age 71.8 +/- 6.2) and 35 comparable healthy subjects were studied. All subjects performed conventional 2-dimensional Doppler echocardiography and DTI at mitral annulus level. Patients with AS were divided into 2 groups: 16 patients who presented initial signs of HF and a depressed left ventricular systolic function (AS I) (EF: 35%-50%) and 19 patients were asymptomatic and had normal left ventricular systolic function (EF > 50%) (ASII). The 16 symptomatic AS patients underwent surgical aortic valve replacement and were examined after 1 year. RESULTS: DTI was able to detect abnormalities of systolic and diastolic function in AS: the significantly lower peak S velocity in AS I than in AS II and in controls, both at septum and lateral wall level; the significantly lower peak E velocity in AS I than in AS II and in controls both at septum and lateral wall level; the significantly higher peak A velocity in AS I than in AS II and in controls both at septum and lateral wall level; the significant lower E/A ratio in AS I than in AS II and in controls both at septum and lateral wall level. CONCLUSION: We found a significant inverse correlation between DTI lateral S velocity, DTI peak E velocity, lateral DTI E/A ratio, and AS peak and mean gradient. According to the results of this study we can affirm that DTI parameters surely had an important physiopathological impact in the knowledge of myocardial function in patients with severe aortic stenosis.
Subvalvular aortic stenosis (SAS) is a congenital heart defect that causes fixed form of hemodynamically significant left ventricular outflow tract (LVOT) obstruction with progressive course. It has a spectrum of anatomy. It appears usually beyond infancy, causes left ventricular hypertrophy and myocardial dysfunction, and tends to involve the aortic and mitral valves in its progressive course. Although most of the patients are asymptomatic, careful monitoring is essential. Moderate to severe SAS requires surgical resection and septal myomectomy. There is a high rate of postoperative recurrence of the lesion. Recurrent lesions and the complex type of lesions with aortic valve involvement should have aortoseptoplasty (to enlarge the outflow tract) and Ross procedure (removal of the damaged aortic valve and placement of a pulmonary autograft in the aortic position and a pulmonary homograft in the pulmonary position).