Observations on blood pressure and aortic valve disease.
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27 patients with following diagnoses were examined by ultrasound: ASD; Aortic valve disease; Mitral valve disease with predominant insufficiency; Mitral stenosis; right heart failure; patients without evidence of cardiac disease. The right ventricular dimension (RVD Index) was assessed representing the distance between the right ventricular epicardial echoes and echoes from the right side of the interventricular septum divided by the patient's body surface area, analogue measurements were done to obtain the left ventricular dimension (LVD Index). The ratio from LVD to RVD was calculated. The motion of the interventricular septum was classified as Normal, Abnormal A and Abnormal B, according to known criteria. Three groups of patients could be differentiated: Patients without cardiac disease; Patients with right ventricular enlargement and ASD; Patients with left ventricular enlargement with aortic and mitral valve disease. In patients with cardiac enlargement, echocardiography provides better information concerning the ratio of the left ventricular to the right ventricular diameter compared to a routine chest X ray.
A group of patients with minor aortic valve disease and inappropriately severe left ventricular hypertrophy is described. Clinical, electrocardiographic and echocardiographic assessment of the degree of left ventricular hypertrophy suggested that they had haemodynamically severe aortic stenosis but this was not borne out at cardiac catheterisation. Although a chance association between non-obstructive hypertrophic cardiomyopathy and mild aortic stenosis may have been responsible, an abnormally severe hypertrophic response to minor aortic outflow obstruction is proposed as another possible explanation. The association between minor aortic valve disease and severe left ventricular hypertrophy should be considered when assessing aortic stenosis since the prognosis with medical management seems good and valve replacement is likely to be of no benefit in such cases.
BACKGROUND: Aortoplasty has been advocated for moderate dilatation of the ascending aorta associated with aortic valve disease. We report our results with this conservative approach. METHODS: Seventeen consecutive patients with unsupported aortoplasty were reviewed. Twelve patients had aortic valve regurgitation and 5 had stenosis. The aortic wall was analyzed histologically in 14 patients. Follow-up was complete, with a mean time of 6 years (range, 2.3 to 10.5 years). RESULTS: Two patients among the 15 hospital survivors died during follow-up of causes unrelated to aortic pathology. Survival at 7 years was 86.7% (+/- 8.8%). Recurring aortic aneurysms developed in 4 patients after a mean time of 63 months, with an event-free survival at 7 years of 41% (+/- 21%). All of these 4 patients had aortic valve regurgitation and cystic medial necrosis. CONCLUSIONS: The recurrence rate of aneurysms after unsupported aortoplasty and aortic valve replacement is high in patients with aortic regurgitation. This strongly suggests that in these patients, the aortic dilatation is related to an underlying wall deficiency, associated with the aortic valve pathology, rather than to the hemodynamic stress imposed by the aortic valve disease.
BACKGROUND AND AIM OF THE STUDY: The effect of concurrent disease and cardiac comorbidity on survival after bioprosthetic valve replacement in elderly patients was assessed retrospectively. Risk factors were categorized as general, non-cardiac (age, diabetes, previously treated carcinoma) and cardiac (LVEF, three-vessel disease, previous CABG or valve replacement, and endocarditis). METHODS: A total of 400 elderly patients (median age 73 years; range: 71-76 years) was studied. Medical history included diabetes, previous CABG or aortic valve replacement (AVR), endocarditis and treatment of previous carcinoma. A left ventricular ejection fraction (LVEF) of <0.66 and presence of three-vessel disease were also investigated. Hospital deaths (and cause) were recorded; survival or date and cause of death after discharge were obtained by questionnaire. Kaplan-Meier univariate and Cox proportional hazards multivariate regression analyses were carried out. RESULTS: Mortality during follow up was 28.3%; hospital mortality was 3.8%. Univariate analysis showed five factors significantly to affect survival: LVEF, history of endocarditis, carcinoma, age and three-vessel disease. Fifteen of 38 patients with history of carcinoma died, 10 due to a malignancy. Of 76 patients with three-vessel disease, 26 died. A history of diabetes and previous CABG did not influence survival significantly. Four of eight patients with preoperative endocarditis died, all in hospital. Six of 11 patients died after redo-AVR, none before 36 months follow up. By Cox regression analysis, LVEF and histories of carcinoma and endocarditis remained significant. CONCLUSION: AVR should be performed before ventricular deterioration occurs. Previous CABG is not a contraindication for AVR. Endocarditis impaired survival. Long-term mortality after redo-AVR in this population was relatively high, but acceptable. AVR should also be performed in elderly patients with aortic valve disease. Since prognosis of symptomatic aortic valve disease is poor in the short term, AVR is indicated in patients treated for carcinoma.
One hundred and twenty stable patients with pure and severe aortic valve disease and without coronary lesions (aortic stenosis, 43 patients; aortic regurgitation, 45 patients; combined aortic stenosis and regurgitation, 32 patients) who had been submitted to haemodynamic studies were prospectively studied with standard electrocardiograms, M-mode echocardiograms, and 24-hour ambulatory electrocardiography (Holter recording). The frequency and complexity of ventricular arrhythmias were related to clinical parameters such as functional class, type of lesion and presence of syncope, and to parameters of left ventricular hypertrophy and function. Ventricular arrhythmias were present in 92% of patients. A high number of ventricular premature beats was directly correlated with parameters of complexity of the arrhythmia. A significant relation was found between electrocardiographic left ventricular hypertrophy and Ryan class (P less than 0.05), and an inverse relation between maximal number of ventricular premature beats in any hour and left ventricular ejection fraction (P less than 0.05). The group of patients with aortic regurgitation showed a higher total number of ventricular premature beats per 24 hours (P less than 0.001), a higher maximal number of these in any hour (P less than 0.01), a higher number of patients with pairs (P less than 0.001), and a higher number of patients in Ryan classes 3, 4A, 4B (P less than 0.01). This study shows a high incidence of ventricular arrhythmias in aortic valve disease, and especially in aortic regurgitation, with a significant relation between left ventricular hypertrophy and function, and number and complexity of arrhythmias.
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A high speed electric rasp was used to remove fibrous thickening from the aortic valve in conjunction with aortic valve commissurotomy in ten patients. All patients had moderate rheumatic aortic valve disease combined with severe mitral valve disease, and were treated by mitral valve replacement and aortic valve repair. All patients survived the operative procedure. There were no deaths or complications during hospitalization related to the valve repair process. The transaortic valve gradient was relieved from an average of 21.0 +/- 8.6 mmHg to 5.6 +/- 4.0 mmHg (catheterization), and from moderate to less-than-mild stenosis (echocardiography). Aortic valve regurgitation was reduced from an average of 2.2+ to 0.7+ on a scale of 0 to 4+ (aortography), and from an average of 2.5+ to 1.1+ on a scale of 0 to 4+ (echocardiography). During the follow-up period, no patients were reoperated on because of aortic valve dysfunction. Follow-up echocardiographic study demonstrated that the transaortic pressure gradient and valvular regurgitation had not progressed, and immediate postoperative conditions were maintained. There were two late deaths not related to the aortic valve. One patient died of prosthetic valve endocarditis in the mitral prosthesis 14 months postoperatively, and the other of a cerebrovascular accident 21 months postoperatively. Based on these data, we believe that aortic valve repair with a high speed electric rasp can effectively relieve aortic stenosis, reduce valvular regurgitation, and provide an excellent hemodynamic result at early and mid-term follow-up.
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Left ventricular biopsies from 126 patients with advanced (EF less than 50%, n = 45) and mild (EF 50-60%, n = 21) and latent cardiomyopathy (EF greater than 60%, n = 60) and 18 additional patients with aortic valve disease and 22 cases with hypertrophic cardiomyopathy were analyzed to define possible correlations between myocardial structure and function. Deterioration of ventricular function was combined with increasing muscle cell diameters (r = 0.47) and increasing nuclear size of the myocytes (r = 0.74) in latent and dilative cardiomyopathies and in patients with aortic valve disease (cell diameter, r = 0.6; nuclear size, r = 0.9). Patients with HCM showed a wide range of cell diameter and nuclear size. 24% of the latter patients had no bioptic evidence of myocardial hypertrophy. The mitochondrial volume of the myocytes was 23% in the normal and hypertrophied myocardium independent of the kind of disease and ventricular function. The volume fraction of the myofibrils continuously decreased with worsening of the left ventricular function in patients with latent and dilative cardiomyopathy (from 45 +/- 6.9 to 37.6 +/- 6.3%) and aortic valve disease (from 46.2 +/- 3.4 to 27.9 +/- 9.3%). Patients with hypertrophic cardiomyopathy presented with normal or slightly decreased values of myofibrils consistent with normal ventricular function (42.5 +/- 5.0). The data demonstrate that the degree of myocardial hypertrophy and certain ultrastructural findings are inversely correlated with left ventricular function.
The problems posed by asymptomatic aortic valve disease with regards to surgery differ according to whether the lesion is aortic stenosis or regurgitation. In stenotic lesions, even severe, the risk of spontaneous evolution is very small when the subject is totally asymptomatic. However, the quality of the results of surgery in asymptomatic or pauci-symptomatic patients and the increased difficulties in the very elderly are incentives not to differ surgery when the stenosis is severe, and especially when left ventricular function begins to degrade. In aortic regurgitation, the risk of progression is also low in asymptomatic patients but left ventricular dysfunction may develop before symptoms occur: this explains the necessity for regular clinical, echocardiographic and eventually radioisotopic examination of patients with severe aortic regurgitation. In dystrophic aortic regurgitation, an aneurysm of the sinuses of Valsalva and/or of the ascending aorta, or progressive fusiform dilatation of the ascending aorta are reasons for not postponing surgery for replacement of the aortic valve and the ascending aorta.
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We determined stimulation rates of cardiac adenylate cyclase activity by isoproterenol and impromidine in particulate sarcolemmal membrane preparations from human papillary muscles resected during open heart replacement of mitral and aortic valves. In addition, specific receptor binding studies with [3H]dihydroalprenolol [( 3H]DHA) to cardiac beta-receptors and [3H]tiotidine [( 3H]TIOT) to cardiac H2-receptors were carried out in the same preparations. Compared with the response in patients with pure mitral valve stenosis, the response of cardiac adenylate cyclase activity to isoproterenol showed a marked decrease (-90%) in patients with combined mitral and aortic valve disease, corresponding to the severity of degree of insufficiency at both valves. Similar changes were observed in receptor binding studies with [3H]DHA, in which the reduction of beta-receptor density was of the same order of magnitude. In contrast, stimulation of the enzyme by impromidine and binding capacity of [3H]TIOT to cardiac H2-receptors were found to be unaltered in the same membrane preparations of all 16 patients. We conclude that treatment with H2-agonists may be a new therapeutic approach to congestive heart failure, especially in patients not responding to beta-adrenoceptor stimulation with beta-sympathomimetic drugs.
OBJECTIVES: We studied the expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and endothelial selectin (E-selectin) on aortic valve endothelium in patients undergoing valve replacement. We also assessed the relation between serum levels and endothelial expression and also the changes in serum levels following surgery. BACKGROUND: Nonrheumatic aortic valve disease is believed to be a degenerative condition. Increased tissue and soluble adhesion molecule levels are described in inflammatory conditions. METHODS: Aortic valves from 22 surgical (16 bicuspid, 6 tricuspid) and 6 autopsy (4 normal, 2 thickened) cases were studied by immunohistochemistry. Soluble adhesion molecules were measured in peripheral blood preoperatively, and at 6 and 18 months postoperatively, and compared with controls. RESULTS: The majority of the surgically removed tricuspid and bicuspid valves expressed adhesion molecules (E-selectin, 75% and 100%; ICAM-1, 75% and 80%; VCAM-1, 69% and 60%, respectively). The normal postmortem valves did not express these, while the diseased ones did. Endothelial expression of E-selectin correlated strongly with serum levels (r = 0.695, p = 0.004). Soluble E-selectin levels were significantly higher at baseline compared with controls (p = 0.017) and fell significantly at 18 months postoperatively (p = 0.005). CONCLUSIONS: Adhesion molecule expression on diseased valves supports an inflammatory component in "degenerative" aortic valve disease. The diseased valves may be the main source of elevated soluble E-selectin in this condition as blood levels correlate with endothelial expression and blood levels fall at 18 months postoperatively.
The diagnosis and treatment of aortic valve disease can be challenging for the clinician. Aortic regurgitation (AR) may be evaluated with Doppler echocardiography or catheterization. Medical therapy consists of vasodilators. Surgery may be appropriate for patients with symptoms, left ventricular dilatation or diminished left ventricle systolic function. Aortic stenosis (AS) can be evaluated with the same modalities as AR. There is evidence that statin therapy may slow the progression of AS. Contrary to conventional wisdom, vasodilators are safe and effective in certain patients. Surgical valve replacement is performed for symptoms and in certain asymptomatic patients.
In order to investigate the incidence of severe ventricular arrhythmias, the 24-h ambulatory ECG of 55 patients with aortic valve disease (NYHA classes I-IV; stenosis: n = 24; regurgitation: n = 18; mixed lesions: n = 13) without coronary heart disease were evaluated with regard to the number of premature ventricular beats and according to the Lown classification. Ventricular arrhythmias were found in 73% of all patients (Lown classes III-V: 38%; Lown classes IV-V: 20%). A significant relation between the degree of arrhythmias and the gradient or severity of regurgitation of the aortic valve could not be established. However, there was a significant linear correlation between the left ventricular ejection fraction and the degree of arrhythmias (stenosis: r = 0.60; regurgitation: r = -0.72; mixed lesions: r = 0.78; all p less than 0.005). Complex arrhythmias of Lown classes III-IV are rare (less than 10%) in patients with good left ventricular function (LVEF greater than 60%). There was a history of palpitations in 81% of patients with Lown classes III-V. According to these data, ventricular arrhythmias are present in a large number of patients with aortic valve disease. The degree of arrhythmia does not correlate to the transvalvular stenosis or the severity of regurgitation, but is strongly influenced by the myocardial performance. Therefore in patients with aortic valve disease significant arrhythmias are frequently a sign of impaired LV function.
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