Mean Aortic Pressure Gradient Research Articles

The Ross Procedure: Clinical and Echocardiographic Follow-Up in 219 Consecutive Patients

The replacement of the diseased aortic valve with a pulmonary autograft has been shown to provide excellent hemodynamic results and to be associated with low morbidity and mortality rates. From 1991 to 2005, 219 patients undergoing the Ross operation were identified. All patients underwent transthoracic echocardiography at discharge and were scheduled for a yearly study thereafter. The echocardiographic study consisted of a morphologic analysis of the pulmonary autograft with measurement of end-systolic diameters at three levels: annulus, sinuses of Valsalva, and origin of the ascending aorta 2 cm above the sinotubular junction. The dynamic analysis evaluated the function of the aortic autograft and the pulmonary homograft. Maximal and mean aortic and pulmonary transvalvular pressure gradients were investigated. The 30-day mortality was 1.8% (n = 4). Cardiac deaths were not related to the autograft. The 10-year actuarial survival was 95.7% +/- 2.1%. Six patients (2.8%) had grade 2 autograft valve regurgitation. No grade 3 or 4 pulmonary regurgitation was identified. At their most recent follow-up, 28 patients (13.1%) had grade 1 insufficiency of the pulmonary homograft, and 10 patients (4.6%) had a peak transvalvular gradient of 17.9 +/- 10.2 mm Hg. Our current experience suggests that replacement of the aortic root with a pulmonary autograft can be safely performed in infants, children, and adults and is associated with low mortality and morbidity rates. It constitutes an elegant alternative to the use of prosthetic valves in the treatment of aortic valve diseases.

Long-term prognostic factors after aortic valve replacement of severe aortic stenosis

Background:The long term prognostic factors of aortic valve replacement (AVR) in patients with severe aortic stenosis (AS) with normal and low left ventricular function are not well known in the Korean population. Methods:Between 1990 and 1999, 73 patients (52 male, 21 female, mean age:58±10.7) with severe AS underwent AVR at Yonsei Cardiovascular Hospital. Patients were excluded if they had concomitant valvular operations other than AVR, previous AVR, or more than a moderate amount of aortic valve regurgitation, or were under 18 years old. Overall survival was estimated by the Kaplan-Meier method, and the Cox proportional hazards model was used to analyze the predictors that influence long-term survival. Results:The causes of aortic stenosis were degenerative (44 case, 60%), congenital (26 case, 36%), and rheumatic (3 case, 4%) in nature. The preoperative characteristics (mean±SD) included ejection fraction (EF), 58±16.5%; mean aortic pressure gradient, 63±20 mmHg;aortic valve area, 0.62±0.13 cm. Simultaneous coronary artery bypass surgery and percutaneous transluminal coronary angioplasty were performed in 8 and 2 cases, respectively. The comparative results in all total patients of the pre/post operative echocardiography showed a significant improvement;EF of 58±17/64±12%, aortic valve area (AVA) of 0.64±0.15/1.54±0.63 cm, mean pressure gradient (MPG) of 63±21/23±13 mmHg, left ventricular end-diastolic dimension (LEEDD) of 54± 9/50±9 mmHg, and a left ventricular posterior wall thickness in systole (LV-PW) of 18±2/16±2 mm. The comparative results of the pre/post operative echocardiography of low EF patients (<35%) also showed a significant improvement;EF of 30±4/55±15%, AVA of 0.59±0.14/1.67±0.85 cm, MPG of 52±20/21±12 mmHg, LVEDD of 58±8/51±6 mm. Operative (30-day) mortality was 2.7% (2 of 73 patients). Six additional patients died during follow-up. The survival of the patient group was 86% at 5 years and 78% at 10 years. The predictors of long-term postoperative survival were preop-EF (p<0.05, R=0.26) and the presence of significant coronary artery disease (CAD) (p<0.01, R=0.35). Conclusion:Postoperative long-term survival of severe AS after AVR was negatively related to reduced preop-EF and the presence of significant CAD. Therefore, the early operative treatment before the occurrence of irreversible left ventricular dysfunction and co논문접수일:2001년 5월 18일 심사완료일:2001년 7월 20일 교신저자:하종원, 120-749 서울 서대문구 신촌동 134 연세대학교 의과대학 심장혈관센터 심장내과학교실 전화:(02) 361-7071·전송:(02) 393-2041 E-mail:ha.jongwon@mayo.edu

Mechanisms of regional ischaemic changes during dipyridamole echocardiography in patients with severe aortic valve stenosis and normal coronary arteries.

Vasodilator stress echocardiography can cause myocardial ischaemia in patients with severe aortic valve stenosis and angiographically normal coronary arteries. The aim of the study was to determine the mechanism of ischaemia in this clinical model. The study group comprised patients with severe aortic valve stenosis and normal coronary arteries: 25 patients (17 males, eight females; age 63 (SD 11) years) underwent a high dose (up to 0.84 mg/kg over 10 min) dipyridamole echocardiography test both before (2-4 d) and after (10-15 d) aortic valve replacement. Mean aortic pressure gradient was 96 (15) mm Hg, with a left ventricular mass index of 228 (49) g/m2. The dipyridamole echocardiography test was well tolerated and interpretable in all patients. Dipyridamole infusion induced chest pain in seven patients before and in no patient after surgery (28 v 0%, P < 0.01), ST segment depression in 12 patients before and two after surgery (48 v 8%, P < 0.01), and a transient regional dyssynergy in 10 patients before and two after surgery (40 v 8%, P < 0.01). In the preoperative evaluation, patients with an echocardiographically positive dipyridamole echocardiography test were comparable with patients with negative test as far as left ventricular mass index [240 (67) v 230 (64) g/m2, NS] and mean aortic pressure gradient [95 (22) v 92 (21) mm Hg, NS] were concerned. When compared to the preoperative assessment, the resting echo assessment in the postoperative evaluation showed unchanged values of left ventricular mass index [pre 228 (49) g/m2 v post 220 (36) g/m2, NS], but markedly decreased values of mean aortic gradient [pre 95 (15) mm Hg v post 22 (5) mm Hg, P < 0.01] and left ventricular wall stress index [pre 134 (30) g/cm2 v post 89 (19) g/cm2]. Dipyridamole echocardiography is a suitable clinical technique for assessing the ischaemic vulnerability of the left ventricle in severe aortic valve stenosis with angiographically normal coronary arteries. The frequent disappearance of the ischaemic response early after aortic valve replacement suggests that haemodynamic factors such as compressive diastolic wall stress or afterload reduction are important components of myocardial ischaemic vulnerability under these circumstances.

Hypertension-enhanced monocyte adhesion in experimental atherosclerosis

Hypertension is a known clinical risk factor for atherosclerosis. In experimental atherosclerosis, monocyte adhesion to the endothelial surface is enhanced and is considered to be an important early stage in plaque formation. We tested the hypothesis that hypertension enhances monocyte adhesion in experimental atherosclerosis. Twenty-two New Zealand White rabbits were fed an atherogenic diet for 3 weeks to induce plaque formation. Aortic coarctation was created in eight rabbits by wrapping a Dacron band around the midportion of the descending thoracic aorta (stenosis group), whereas six rabbits underwent banding without aortic constriction (no stenosis group). Eight rabbits served as nonoperated controls. Monocyte binding to the aortic endothelial surface was counted with epifluorescent microscopy on standard aortic segments proximal and distal to the band. Immunohistochemistry was performed for the following antibodies: VCAM-1, RAM11, CD11b, and factor VIII. Mean blood pressure was 89 +/- 3 mm Hg in the aorta proximal to the stenosis, compared with 64 +/- 4 mm Hg in the no stenosis group and 74 +/- 3 mm Hg in the control group (p < 0.01). The mean aortic blood pressure gradient across the stenosis was 16 +/- 2 mm Hg in the stenosis group, whereas the aortic blood pressure gradient was 0.2 +/- 0.6 mm Hg in the no stenosis group and -0.3 +/- 0.4 mm Hg in the control group (p < 0.001). Monocyte adhesion to the aortic endothelial surface proximal to the stenosis was increased twofold compared with adhesion to the aorta distal to the stenosis and compared with the proximal aorta in the control group (p < 0.02). The proximal-to-distal aortic ratio of monocyte binding was enhanced in the stenosis group (2.2) compared with the no stenosis (0.76) and control (0.83) groups (p < 0.01). The intima area of the aorta proximal to the stenosis was significantly increased compared with the proximal aortas in the no stenosis and control groups (p < 0.01). RAM11, CD11b, and endothelial VCAM-1 expression were enhanced in the hypertensive region proximal to the stenosis. In the hypertensive region in the aorta proximal to the stenosis, monocyte adhesion and endothelial VCAM-1 expression were increased, with intimal thickening and accumulation of macrophages. These findings suggest that hypertension may promote atherosclerotic plaque formation by enhancing monocyte adhesion.

Sex-dependent differences in left ventricular function and structure in chronic pressure overload.

To evaluate gender-related differences in left ventricular (LV) structure and function in aortic stenosis, LV biplane cineangiography, micromanometry and endomyocardial biopsies were carried out in 56 patients with aortic stenosis and normal coronary arteries. Patients were divided into males (M: n = 35), and females (F: n = 21). Sixteen normal subjects 8 M, 8 F) served as haemodynamic controls. Control biopsy data were obtained from six pre-transplantation donor hearts (3 M and 3 F). LV systolic function was evaluated by ejection fraction and its relationship to mean systolic circumferential wall stress, diastolic function by the time constant of LV pressure decay, peak filling rates and passive myocardial stiffness constant. Biopsy samples were evaluated for interstitial fibrosis, muscle fibre diameter and volume fraction of myofibrils. In a subset of 27 consecutive patients, biopsy samples were evaluated with a morphometric-morphological method, for total collagen volume fraction, endocardial fibrosis and the extension and thickness of orthogonal collagen fibres (cross-hatching). In patients with aortic stenosis, aortic valve area, aortic valve resistance and mean aortic pressure gradient were comparable in males and females, whereas end-systolic and end-diastolic volumes were larger in males than females. Ejection fraction was lower (56%) in males than females (64%) (P < 0.05); 20 of 35 males and four of 21 females had depressed systolic contractility when assessed with regard to the relationship ejection fraction-mean systolic stress (P < 0.01). Myocardial stiffness constant was higher in males than in females (P < 0.01). Nine of 14 males and two of 13 females had endocardial fibrosis (P < 0.009), whereas increased cross-hatching (> 1.5 grade) was present in 11 males and four females with aortic stenosis (P < 0.01). An abnormal collagen architecture was present in 13/14 males and 5/13 females (P < 0.002). In aortic stenosis, males have a depressed systolic function and abnormal passive elastic properties when compared to females with valve lesions of similar severity. Changes in collagen architecture may account, at least in part, for these differences.

Changes in phasic coronary blood flow velocity profile in relation to changes in hemodynamic parameters during stress in patients with aortic valve stenosis.

Alterations in phasic coronary flow profile have been demonstrated at rest in patients with aortic valve stenosis (AVS) but have never been studied under conditions of hemodynamic stress. Thirty-four patients with significant pure AVS (21 with exertional symptoms [group 1], 13 asymptomatic [group 2]) and 9 control subjects (group 3), all with normal coronary arteries, were studied successively at rest, during rapid atrial pacing, and after dobutamine infusion (5 to 30 micrograms.kg-1.min-1 i.v.) by proximal left anterior descending (LAD) intracoronary Doppler flow velocimetry concomitant with hemodynamic measurements. Systolic retrograde coronary flow velocity (CFV) was recorded only in patients with AVS, and its resting peak value was positively correlated with peak aortic pressure gradient (APG) (r = .63, P < .001). In group 1, there was lower aortic valve area (0.58 +/- 0.10 versus 0.75 +/- 0.08 cm2, P < .001) and higher resting APG and peak systolic retrograde CFV than in group 2, and also higher resting peak diastolic and mean CFV than in groups 2 and 3. In the two AVS groups, there were no changes from rest in APG and retrograde CFV at peak pacing rate; however, these parameters increased concomitantly and significantly at peak dobutamine stress. The ratio of the resting systolic to diastolic CFV curve area was inversely correlated with mean APG (r = -.54, P < .001); it was significantly lower in group 1 than in groups 2 and 3 (0.19 +/- 0.07 versus 0.29 +/- 0.10 and 0.30 +/- 0.04, respectively, both P < .005) and increased at peak pacing (group 1, to 0.29 +/- 0.14; group 2, to 0.39 +/- 0.12; group 3, to 0.38 +/- 0.07; all P < .001). At peak dobutamine stress, it decreased in patients with AVS (group 1, to 0.05 +/- 0.05; group 2, to 0.08 +/- 0.03; both P < .001) but did not change in group 3 (0.25 +/- 0.05). From rest to peak dobutamine stress, in both AVS groups there was increased retrograde systolic (group 1, 441 +/- 483%; group 2, 681 +/- 356%; both P < .001), decreased total systolic (group 1, -66 +/- 25%, P < .001; group 2, -19 +/- 24%; P = NS), and increased diastolic (group 1, 33.4 +/- 31.7%; group 2, 197.7 +/- 105.1%; both P < .001; group 1 versus group 2, P < .001) CFV curve area. In contrast, group 3 showed comparable increases in both systolic (143.5 +/- 44.4%) and diastolic (197.1 +/- 75.2%) CFV area (both P < .001). The stress-induced increases in the mean CFV and blood flow exceeded or were comparable with the concomitant increases in the estimated myocardial metabolic demand in groups 2 and 3 but were significantly lower in group 1. Stress-induced changes in LAD phasic CFV profile differ significantly between patients with and without AVS. In AVS, these changes are closely related to the concomitant stress-induced changes in hemodynamic parameters.

Impaired vagal heart rate control in aortic valve stenosis

Impaired reflex control of heart rate seems to be associated with increased risk of sudden cardiac death. To assess the effect of aortic valve stenosis on parasympathetic heart rate control we measured the heart rate responses to deep breathing and to standing up, non-invasive measures of cardiac parasympathetic activity, in 24 patients with valvular aortic stenosis and in 24 healthy asymptomatic subjects of the same age group. All but one of the patients were symptomatic and the mean aortic valve pressure gradients ranged from 32 to 114 mmHg. The heart rate response to deep breathing was significantly (P less than 0.05) lower in valve patients than in the healthy subjects. The heart rate changes evoked by standing up, however, did not differ significantly between the groups. The heart rate response to deep breathing was inversely weakly related to the left ventricular end-diastolic pressure (r = -0.41, P less than 0.05), but not significantly to the aortic valve pressure gradient, valve area, left ventricular ejection fraction or presence of coronary artery disease. Our results suggest that the impairment of reflex heart rate control is common in patients with significant aortic valve stenosis.

Aortic valve replacement with the Carpentier-Edwards pericardial bioprosthesis: clinical and hemodynamic results.

From 1981 to 1987, 189 patients underwent isolated aortic valve replacement with the Carpentier-Edwards bovine pericardial bioprosthesis. There were 9 early deaths (30-day mortality of 4.8%) and 18 late deaths (3.3% pt-yr). After 5 years, the actuarial survival rate was 81.9%. All patients but one were followed for an average of 37 months after operation, and follow-up totaled 551 patient-years. Valve-related complications included 12 thromboembolic episodes (2.2%/pt-yr), 7 endocarditis (1.3%/pt-yr), 2 hemorrhages due to anticoagulation (0.4%/pt-yr), and 3 reoperations (0.5%/pt-yr). After five years, freedom from thromboembolic events was 91%, that from reoperation was 98%, and 87% for all valve-related complications. There was no primary tissue failure of the valve. Before operation, 55% of the patients were in functional Class III or IV, 97% of the survivors were in Class I or II after valve replacement. Hematological evaluation of 77 patients, an average of 18 months postoperatively, showed no clinically significant hemolysis. Postoperative hemodynamic studies in 28 patients showed mean aortic pressure gradients across the prosthesis at rest ranging from 24 mmHg with the smaller (19 mm) to 11 mmHg with the larger (25 mm and more) valves, and effective orifice areas ranging from 1.0 to 1.9 cm2, respectively. Thus, the Carpentier-Edwards pericardial bioprosthesis appears to be a reliable and hemodynamically effective substitute for replacement of the aortic valve.

Protection from atherosclerotic lesion formation by reduction of artery wall motion

We have studied mechanical factors that could determine how stenosis protects against distal atherosclerosis in cynomolgus monkeys fed an atherogenic diet. Critical aortic stenosis was produced by coarctation of the thoracic aorta. After 3 months, coarcted monkeys had a mean aortic pressure gradient of 25 ± 1 mm Hg and a 76% ± 2% lumen stenosis. Aortic wall motion was measured by means of in vivo ultrasonic sonomicrometry. Dynamic tracings of aortic pressure and diameter were recorded simultaneously at standard locations proximal and distal to the stenosis and at comparable sites in noncoarcted control animals. In the proximal aorta, mean blood pressure and pulse pressure were increased (p < 0.05), but wall motion and intimal lesion area were not different from those determined in control monkeys. In the aorta distal to the coarct, mean blood pressure was no different from that in control animals but pulse pressure was diminished; in addition, there was marked reduction of arterial wall motion (p < 0.001). This was accompanied by a significant reduction of intimal plaque area (p < 0.05) and acid lipase activity (p < 0.001). Thus, inhibition of plaque formation in the distal-aorta coincided with reduction of pulse pressure and aortic wall motion rather than with blood pressure or hypercholesterolemia. Inhibition of arterial wall motion may account for the sparing effect often encountered in human arteries distal to stenosing atherosclerotic plaques.

Duration of ejection in aortic stenosis: Effect of stroke volume and pressure gradient

The theoretical effect of variable ventricular function on left ventricular ejection time in aortic stenosis was predicted by applying data measured in 52 patients with pure aortic stenosis to equations derived from the relations of Gorlin and Gorlin and Weissler et al. Ejection time and aortic valve area are not, of necessity, linearly related because (Formula: see text) where LVET is left ventricular ejection time, k is a constant, SV is stroke volume, PG is mean aortic pressure gradient and AVA is aortic valve area. When the patients were separated into performance groups on the basis of cardiac index (at 2.8 liters/min per m2), the linear regression relating the measured SV/square root PG with valve area in 18 patients with normal function (SV/square root PG = 11.1 AVA + 2.0, r = 0.969, p less than 0.001) predicted ejection time prolongation with decreasing valve area. In 34 patients with poor function, however, the decrease in SV/square root PG with decreasing valve area was more marked (SV/square root PG = 12.6 AVA + 0.4, r = 0.894, p less than 0.001), predicting a shorter ejection time at any given valve area in this group. As predicted by the effect of valve area on the equation, ejection time becomes most variable at a small aortic valve area. Independent ejection time measurement in these patients validated the predicted effect.

Progression of Aortic Stenosis

We assessed progressive stenosis of the aortic valve in 11 adult patients (mean age of 48 years) with aortic stenosis who had undergone two cardiac catheterizations without intervening aortic valve surgery. The mean time between cardiac catheterization was 59 months (range 20 to 133). No patients had mitral valve disease. Two patients had coronary artery disease. The results showed that progressive stenosis of the aortic valve occurred in 10 of 11 patients with a significant decrease in the calculated mean aortic valve area from 1.2 +/- 0.2 sq cm to 0.7 +/- 0.1 sq cm (P less than 0.005); a significant increase in mean left ventricular peak systolic pressure from 149 +/- 8 mm Hg to 199 +/- 3 mm Hg (P less than 0.01), and a significant increase in mean left ventricular aortic pressure gradient from 31 +/- 4 mm Hg to 75 +/- 13 mm Hg (P less than 0.005). On an individual basis, the change in left ventricular pressure and the left ventricular-aortic gradient did not always reflect the decrease in aortic valve area because of variations in cardiac output. The shortest period of time in which progression of aortic stenosis occurred was 27 to 29 months. Thus, progressive stenosis of the aortic valve occurs in adults with isolated aortic valvular stenosis. Significant decrease in the aortic valve area can develop in as short a period as 27 to 29 months.