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PubMed1993

Relation of phasic coronary flow velocity profile to clinical and hemodynamic characteristics of patients with aortic valve disease.

BACKGROUND: Our objective was to assess phasic coronary blood flow and velocity characteristics of the proximal portion of the left anterior descending artery and to evaluate their relation to the clinical and hemodynamic manifestations in patients with aortic valve disease. METHODS AND RESULTS: We examined 26 patients with chronic aortic regurgitation (AR), 12 patients with predominant aortic stenosis (AS), and 11 control subjects using an intravascular Doppler catheter with spectral analysis. Angiographic assessment of AR identified 10 patients with mild regurgitation and 16 with severe regurgitation. The resting systolic coronary flow velocity-time integral (VTI) was significantly higher and the diastolic VTI was slightly but significantly higher in patients with severe regurgitation than in those with mild regurgitation (11.8 +/- 4.2 vs 4.1 +/- 1.1 cm, P < .001; 18.5 +/- 5.8 vs 13.2 +/- 3.2 cm, P < .05) and control subjects (4.0 +/- 1.0 cm, P < .001 and 13.3 +/- 3.6 cm, P < .05), respectively. Patients with AS had a slightly lower resting systolic VTI (3.8 +/- 1.4 cm) and a higher diastolic VTI (14.6 +/- 3.7 cm) than control subjects. Resting coronary blood flow was greater in patients with aortic valve disease than in control subjects. There was a significant correlation between the ratio of the resting systolic to diastolic VTI (S/D ratio) and the ratio of the aortic systolic to diastolic pressure (r = .75, P < .001) in patients with AR. The S/D ratio was inversely correlated with left ventricular systolic pressure (r = -.92, P < .001) and positively correlated with the ratio of the aortic systolic to diastolic pressure (r = .68, P < .05) in patients with AS. CONCLUSIONS: Our results indicate that hemodynamic changes related to aortic valve disease contribute to alterations in the resting phasic coronary blood flow and velocity profiles observed in these patients.

Aortic Valve Insufficiency↗
PubMed2001

Activation of the cardiac renin-angiotensin system and increased myocardial collagen expression in human aortic valve disease.

OBJECTIVES: We sought to determine whether the cardiac renin-angiotensin system (RAS) is activated in human aortic valve disease depending on left ventricular function, and we analyzed the concomitant regulation of the extracellular matrix components. BACKGROUND: In animal models with pressure or volume load, activation of the cardiac RAS increases fibrosis. In human aortic valve disease, the ventricular collagen protein content is increased, but only scarce data on the activation state of the cardiac RAS and its effects on collagen and fibronectin messenger ribonucleic acid (mRNA) are available. METHODS: In left ventricular biopsies from patients with aortic valve stenosis (AS) and aortic valve regurgitation and from control subjects, we quantitated mRNAs for angiotensin-converting enzyme (ACE), chymase, transforming growth factor-beta1 (TGF-beta1), collagen I, collagen III and fibronectin by reverse-transcription polymerase chain reaction. Proteins were localized by immunohistochemistry; ACE activity was determined by high performance liquid chromatography; and TGF-beta protein by quantitative enzyme immunoassay. RESULTS: Protein, ACE and TGF-beta1 mRNA were significantly increased in patients with AS and AR (1.5- to 2.1-fold) and correlated with each other. The increase occurred also in patients with normal systolic function. Collagen I and III and fibronectin mRNAs were both upregulated about twofold in patients with AS and AR. In AS, collagen and fibronectin mRNA expression levels were positively correlated with left ventricular end-diastolic pressure and inversely with left ventricular ejection fraction (LVEF). CONCLUSIONS: In human hearts, pressure and volume overload increases cardiac ACE and TGF-beta1 in the early stages. This activation of the cardiac RAS may contribute to the observed increase in collagen I and III and fibronectin mRNA expression. The increase in extracellular matrix already exists in patients with a normal LVEF, and it increases with functional impairment.

Aged↗
PubMed1975

[Long-term course of tricuspid insufficiency operated during the surgical correction of mitral and mitro-aortic valve diseases].

This study concerns 120 patients with tricuspid incompetence (TI) combined with mitral or mitral-aortic valve disease. This second part is devoted to the 72 patients whose TI was corrected together with the mitral-aortic valve lesions, and the long-term post-operative course (average 40 months) was analysed. The results were correlated with pre-operatice clinical intensity of the TI: un unfavourable course (persistent TI and right ventricular failure) was noted in 56% of the cases of TI judged to be intense and in 29% only of the cases of TI judged to be clinically negligible (p is less than 0.5). The course varied according to the mode of tricuspid valve repair with a good long-term result in 37% of the 30 cases with Kay's annuloplasty, 62% of the 26 prosthetic valve replacements and 69% of the 13 cases treated by Carpentier's annuloplasty. This latter technique seems to represent the most efficient means of correction for TI, when the anatomical lesions allow for it. In the group of the patients studied, the course is independent from the degree of heart enlargement and from the pulmonary artery pressure level before operation.

Aortic Valve↗
PubMed1975

Myocardial ultrastructure in patients with chronic aortic valve disease.

Light and electron microscopic observations were made on left ventricular myocardium removed at operation from 16 patients with chronic aortic valve disease. In all 16 patients most cardiac muscle cells were hypertrophid, and surrounded by small amounts of fibrous tissue. In two of the six patients with pure aortic regurgitation and in four of the five patients with combined aortic stenosis and regurgitation, cardiac muscle cells with evidence of degeneration were present in addition to hypertrophied, nondegenerated cells. Degenerated cardiac muscle cells were not observed in the six patients with predominant aortic stenosis. Cardiac muscle cells with mild degeneration showed focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. More severely degenerated muscle cells showed a marked decrease in the numbers of myofibrils and T tubules and proliferation of sarcoplasmic reticulum or mitochondria, or both. Severly degenerated cells usually were present in areas of marked fibrosis, often were atrophic, had thickened basement membranes and had lost their intercellular connections. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic aortic valve disease.

Adolescent↗
PubMed1991

[Severe disorders of auriculoventricular conduction after aortic valve replacement. A postoperative electrophysiological study in 36 patients and the long-term follow-up].

Cardiac conduction defects (CD) are common in patients with aortic valve diseases. Several studies have suggested that the occurrence of complete heart block at the time of valve replacement is related with preoperative conduction defects and with other factors like calcium deposits, aortic gradient or poor left ventricular function. We evaluated 36 patients undergoing isolated aortic valve replacement in 29 of them, combined mitroaortic in four, isolated mitral valve replacement in two and subvalvular myectomy in one. In all of them an electrophysiologic study was done at the postoperative period. In group 2 (with preoperative CD) patients were older (mean age +/- SEM; 56.57 +/- 8.90) than in group 1 (without CD) (45.64 +/- 14.79) (p less than 0.02). Surgical times were higher in group 1 than in group 2 (p less than 0.01 and p less than 0.005). The site of block was distal to the His bundle in 59% of patients in group 1 and in 47% in group 2 (p-NS). Complete AV block occurred in 70.5% of patients in group 1 while was of 36.8% in group 2 (p less than 0.05). Severity of conduction defects was unrelated with the type of valve disease, aortic valve calcification or gradient or with poor left ventricular function. Preoperative conduction defects were not responsible of more severe postoperative conduction defects. On late follow-up permanent pacemakers were unnecessary in 33% of patients in group 1 and in 75% in group 2 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Aortic valve replacement and the senior citizen.

The elderly patient, regardless of age, faces an early demise from progressive cardiac decompensation secondary to aortic valve disease. Aortic valve replacement can be carried out at a reasonable operative risk and extend the longevity to very close to that of normal life expectancy. It is our feeling, based on these results, that patients with significant symptoms secondary to aortic valvular disease, regardless of age and without other major organ problems, should be given the choice of aortic valve replacement to enhance the quality and quantity of their lives.

Age Factors↗
PubMedDate not supplied

Left ventricular aneurysm, aortic valve disease and coronary narrowing in a patient with Hunter's syndrome.

Hunter's syndrome (mucopolysaccharidosis type 2, MPS 2) is an inherited disorder of glycosaminoglycan degradation commonly associated with cardiac disease. We present the case of a young man with unusual cardiac manifestations of this syndrome. When mixed aortic valve disease was noted in childhood, other classical features of the milder form of Hunter's syndrome were present. There was no symptomatic or echocardiographic cardiovascular deterioration until age 27 when the patient presented in severe biventricular failure. Investigations demonstrated cardiomegaly and a large apical left ventricular aneurysm. The patient died suddenly soon after this diagnosis. Post mortem examination demonstrated a hypertrophied left ventricle with a 6-cm apical aneurysm. Coronary arterial walls were diffusely thickened but with only mild lumenal stenosis. Mitral and aortic valve disease was also present. There is one previous report of ventricular aneurysm in Hunter's syndrome. Pathophysiological contributions to aneurysm formation may include abnormal coronary flow, the presence of aortic stenosis and abnormal myocardium. This patient's sudden deterioration after a long period of clinical stability reinforces the need for careful follow-up of patients with cardiac manifestations of Hunter's disease.

Adult↗
PubMed1992

Ventricular arrhythmias in aortic valve disease before and after surgery.

In order to evaluate the incidence and prognostic value of ventricular arrhythmias in patients with aortic valve disease, 24 hour ambulatory electrocardiographic recordings were obtained in 374 patients without coronary artery disease (aortic stenosis n = 194, aortic regurgitation n = 103, combined aortic stenosis and regurgitation n = 77). Following aortic valve replacement, repeat recordings were obtained in a subgroup of 96 patients at 13 +/- 4 days and 18 +/- 7 months. Ventricular arrhythmias were classified in all cases according to Lown and were compared with clinical, echocardiographic and hemodynamic data. Preoperatively, ventricular premature beats were observed in 329 patients (88%), and were found to be frequent (>30 ventricular premature beats/hour) in 83 (22%). Multiformity was found in 105 (28%), couplets in 75 (20%) and ventricular tachycardia in 45 (12%). The occurrence of ventricular arrhythmias was not related to the type or severity of the valve lesions. Patients with severe ventricular arrhythmias (Lown class 3 or 4: 36.5%) had a higher ventricular wall thickness (interventricular septum thickness 14.2 +/- 1.8 mm vs. 11.9 +/- 2.0 mm, p < 0.01, a higher LV mass (178 +/- 32 g/m2 vs. 142 +/- 35 g/m2, p < 0.001) and a lower left ventricular ejection fraction (48% +/- 9% vs. 56.5% +/- 10%, p < 0.001); while in patients with aortic regurgitation a higher end-diastolic LV volume (224 +/- 38 ml/m2 vs. 178 +/- 42 ml/m2, p < 0.02) and a higher end-systolic LV diameter (56 +/- 7 mm vs. 46 +/- 8 mm, p < 0.02) were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗
PubMed1993

New observations on the etiology of aortic valve disease: a surgical pathologic study of 236 cases from 1990.

Among 236 aortic valves surgically excised at the Mayo Clinic in 1990 (mean patient age, 66 years; age range, 10 to 92 years), 154 (65%) were stenotic, 58 (25%) were insufficient, and 24 (10%) were both stenotic and insufficient. Pure stenosis was related to calcification, and causes included degenerative (51%), bicuspid (36%), post-inflammatory (9%), and other (4%) reasons. Fourteen (9%) valves with pure stenosis also underwent ventricular septal myectomy, 12 for hypertrophy and two for co-existent hypertrophic cardiomyopathy. Pure insufficiency was not related to calcification, and causes included aortic root dilatation (50%), bicuspid valve (14%), post-inflammatory (14%), post-therapeutic (14%), and other (8%) reasons. Combined stenosis and insufficiency was secondary to degenerative calcification (46%), bicuspid and post-inflammatory etiologies (17% each), post-therapeutic (13%), and indeterminate (8%) causes. New observations include the following findings: (1) degenerative (senile) disease is the most common cause of aortic stenosis and combined stenosis and insufficiency at the Mayo Clinic, (2) aortic root dilatation is the most common cause of pure aortic insufficiency, (3) post-therapeutic aortic valve disease now leads to valve replacement in a substantial percentage of patients, particularly among those with insufficiency, (4) post-inflammatory (presumably rheumatic) disease is relatively uncommon in all three functional categories, (5) septal myectomy may be performed for hypertrophic states other than hypertrophic cardiomyopathy, and (6) adults with operated congenital heart disease are undergoing valve replacement for annular dilatation with insufficiency. Because of the increasing age of the general population, the prominence of age-related degenerative aortic valve calcification and aortic root dilatation may have important implications concerning future health care costs.

Adolescent↗
PubMed2005

Extracellular matrix remodelling in human aortic valve disease: the role of matrix metalloproteinases and their tissue inhibitors.

AIMS: Aortic valve diseases are characterized by pathological remodelling of valvular tissue but the cellular and molecular effectors involved in these processes are not well known. The role of matrix metalloproteinase (MMP)-2, MMP-9, MMP-3, MMP-7, and tissue inhibitor of matrix metalloproteinase (TIMP)-1 and TIMP-2 are investigated here. METHODS AND RESULTS: Histological analysis of pathological valves [aortic stenosis (AS) (n=49), aortic regurgitation (AR) (n=23)] and control valves (n=8) was performed. The main tissue abnormalities (calcification, inflammatory cells, and capillaries) observed in AS were less severe or absent in AR. However, both groups of pathological valves displayed similar histological signs of extracellular matrix (ECM) remodelling. Biochemical analysis of MMPs and TIMPs (gelatin and casein zymography and ELISA) was performed on valve extracts. MMP-2 activity was not significantly different in control and pathological valves. Increases in MMP-9 and MMP-3 in AS demonstrated an inflammatory state. Finally, there was a four- to seven-fold increase of TIMP-1 in pathological valves. TIMP-1, TIMP-2, and MMP-2 were synthesized by the valvular interstitial cells in primary culture. CONCLUSION: This study demonstrates the involvement of the MMP/TIMP system in ECM remodelling of both AS and AR. These findings provide evidence of inflammatory injury more severe in AS than in AR and involvement of mesenchymal cell response.

Adult↗
PubMed1975

[Long-term course of nonoperated tricuspid insufficiency following surgical correction of mitral and mitro-aortic valve diseases].

This study concerns 120 patients with tricuspid incompetence (TI) combined with mitral or mitral-aortic valve disease. This first part is devoted to the 48 patients TI of whom was not corrected, and the long-term course (average 40 months) after mitral-aortic lesions correction was analysed. Assessment of the degree of TI at operation differed markedly from its pre-operative clinical assessment; surgical findings agreed with the clinical estimations in 10 of 12 cases of TI considered to be negligible, but only in 4 of 24 cases with a TI considered as intense clinically. The long-term unfavourable courses (TI with persistent right ventricular failure) were more common in the group of TI considered intense clinically (59%) than in the TI considered clinically as negligible (23%). Assessment by the surgeon during operation of the degree of TI seemed a less accurate element of valuation of the long-term prognosis. The mean pulmonary artery pressure measured at operation did not have, in the patients studied, a significant influence on the long-terme course after mitral-aortic valve correction. On the contrary, the results were less favourable in the group of patients whose TI was old-standing and in the group of patients with a cardio-thoracic ration higher than 0.65. It seems therefore legitimate to recommend correction of both the cases of TI considered to be intense by the surgeon, and those considered to be intense clinically, even if the surgeon finds them to be negligible. This attitude is the more justified the older the TI and the larger the heart enlargement.

Aortic Valve↗
PubMed1993

Familial calcification of aorta and calcific aortic valve disease associated with immunologic abnormalities.

We report three patients of the same family with linear calcification of the ascending aorta, severe calcific mixed aortic valve disease associated with increased levels of globulins, lambda-chain gammopathy, an increased T4/T8 lymphocyte ratio, and other immunologic abnormalities. None of the patients had syphilis, atherosclerosis, abnormalities of calcium or phosphorus metabolism, lymphadenopathy, or other systemic diseases. It is postulated that these cases and some previously reported in the literature as idiopathic represent a distinct pathologic entity, familial or sporadic, in which localized vascular and valvular calcific disease is associated with an underlying immunologic disorder or autoimmune process.

Adult↗
PubMed1982

A new method to treat fusiform aneurysms of the ascending aorta associated with aortic valve disease: an alternative to radical resection.

A new method designed to deal with special forms of fusiform aneurysms of the ascending aorta associated with aortic valve disease is presented. The procedure consists of replacing the aortic valve, decreasing the aortic diameter by excision of an oval segment, placing a well-tailored Dacron vascular graft around the ascending aorta, and anchoring it with previously placed sutures driven through the sewing ring of the valve prosthesis through the aortic wall. The technique has been applied in 6 patients with postoperative observation ranging from six weeks to two and a half years. Technically the operation was carried out without difficulty, and all the patients are doing well.

Aorta↗
PubMed2006

[Symptomatic severe chronic aortic valve disease: a comparative study of cardiac magnetic resonance imaging and echocardiography].

OBJECTIVE: To show the real value of cardiac magnetic resonance imaging (CMRI) in the evaluation of patients with symptomatic chronic aortic valve disease. METHODS: Seventy patients--35 with aortic stenosis (AoS) and 35 with aortic regurgitation (AoR) with surgical indication, who underwent preoperative echocardiogram (ECHO) and CMRI to assess ventricular function, volumes, and left ventricular mass index using cine magnetic resonance imaging, were studied. RESULTS: No statistically significant difference was observed between the AoS and AoR groups when ECHO and CMRI variables were compared. When compared with the type of symptom, ECHO and CMRI variables showed the same pattern. CONCLUSION: CMRI data were in agreement with ECHO data regarding the assessment of left ventricular volume and ejection fraction, and with the clinical presentation of patients with chronic aortic valve disease.

Adolescent↗
PubMedDate not supplied

Subaortic flow profiles in aortic valve disease: a two-dimensional color Doppler study.

With time-corrected color Doppler echocardiography, the aortic subvalvular spatial flow velocity profile was registered in two perpendicular planes in 10 patients with aortic valve disease and in 5 healthy control subjects. Patients with predominant aortic valve stenosis had a fairly flat profile, and the subvalvular diameter, obtained from left parasternal two-dimensional tissue imaging, provided a good estimate of the mean of the two transverse flow axes. This explains the accuracy in determination of stroke volume and aortic valve area that is reported in studies on patients with aortic valve stenosis when the continuity equation is used. However, the use of apical pulsed Doppler ultrasound registrations from the left ventricular outflow tract and parasternal two-dimensional echocardiography for flow area calculation may introduce large errors in calculated stroke volume in certain patients with aortic regurgitation and in normal subjects, because of a non-flat spatial velocity profile or an inaccurate estimate of flow area.

Aged↗
PubMed1979

Gastrointestinal angiodysplasia associated with aortic valve disease: part of a spectrum of angiodysplasia of the gut.

Twelve patients with angiodysplasia of the gastrointestinal tract were seen at The Mary Imogene Bassett Hospital are presented. Six share the features of gastric or duodenal angiodysplasia, advanced age, and aortic valve disease. Of these 6 patients, 4 who bled repeatedly were treated with endoscopic coagulation of areas of gastric and duodenal angiodysplasia. Six patients with other types of gastrointestinal angiodysplasia are presented for comparison. Two had gastric angiodysplasia and no aortic valve disease, 2 had hereditary hemorrhagic telangiectasia, 1 had received irradiation, and 1 could not be classified. We suggest that angiodysplasia of the gastrointestinal tract can be regarded as a spectrum with a clearly inherited etiology on one extreme and an acquired etiology on the other. A subset of these patients may be associated with aortic valve disease. Angiodysplasia of the upper gastrointestinal tract may account for a significant fraction of previously unexplained bleeding. It is hoped that this paper will aid in their more frequent recognition.

Aged↗