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Objectives: The aim of this study was to investigate the long-term clinical and hemodynamic outcomes after aortic valve replacement with the Carpentier-Edwards Perimount bioprosthesis (Edwards Lifesciences, Irvine, Calif), which has been used in our institution since 1984. Methods: From January 1984 to December 1995, the Carpentier-Edwards pericardial bioprosthesis was used for aortic valve replacement in 254 patients (male/female ratio 117:137) with a mean age of 71 years (range 25-87 years). Before the operation, 216 patients (85%) were in New York Heart Association functional class III or IV. The predominant diagnosis was aortic stenosis (n = 219, 86%). Associated surgical procedures included coronary artery bypass grafting in 130 cases (51%), mitral valve replacement in 11 cases (4%), and tricuspid or mitral valve repair in 12 cases (5%). Previous cardiac operations had been performed in 36 cases (14%). Follow-up was 100% complete at a mean of 60 ± 31 months. Univariate estimates of time-related cumulative probabilities were calculated by the Kaplan-Meier method. Multivariable adjustment was performed by Cox proportional hazards regression. Echocardiography was performed in 61% of long-term survivors. Results: There were 11 early deaths (4%) and 58 late deaths. Actuarial survivals at 5, 10, and 12 years were 80% ± 3%, 50% ± 8%, and 36% ± 9%, respectively. At 12 years the freedom from cardiac death was 73% ± 7%, the freedom from valve-related death was 84% ± 11%, the freedom from valve reoperation was 83% ± 9%, the freedom from primary tissue failure was 86% ± 9%, the freedom from thromboembolism was 67% ± 13%, and the freedom from endocarditis was 98% ± 1%. Echocardiography was performed on long-term survivors (mean follow-up 67 ± 25 months) and showed that transvalvular peak and mean pressure differences measured with Doppler echocardiography were 23.2 ± 9.6 and 12.3 ± 4.8 mm Hg, respectively. Aortic regurgitation was found by Doppler echocardiography to be none or trivial, mild, moderate, and severe in 64%, 30%, 3%, and 1% of patients, respectively. Mean left ventricular mass index was 107.2 ± 35.3 g/m 2 (118.9 ± 40.2 g/m 2 in men and 98.8 ± 28.8 g/m 2 in women) at late follow-up. One third of all patients, regardless of sex (n = 26/64 women and n=14/45 men), had evidence of left ventricular hypertrophy. However, our analyses indicate that the residual left ventricular hypertrophy was not caused by valve mismatch but was probably multifactorial. Conclusion: The Carpentier-Edwards Perimount bioprosthesis has provided satisfactory clinical and hemodynamic outcome. However, at long-term follow-up about one third of the patients being investigated still had left ventricular hypertrophy examined by echocardiography. J Thorac Cardiovasc Surg 2002;124:146-54

days after an acute myocardial infarction, the LC and R arose from the RM and the RM was severely narrowed by an atherosclerotic plaque (Fig. 1). In the second patient, a 60-year-old man who died shortly after aortocoronary bypass grafting for severe angina pectoris, the LAD and R arose from the RM which also was severely narrowed by atherosclerotic plaque (Fig. 2), as were all major coronary arteries. Origin of the LC from the R coronary artery is the most frequent major congenital anomaly of the coronary arteries. Origin of the LAD from the RM, however, is extremely rare. Reports of five necropsy patients with this type anomaly appear only in a thesis’ and, to our knowledge, in no published reports. Severe narrowing by atherosclerotic plaque of the RM coronary artery-the true equivalent of severe narrowing of the LM coronary artery-has not been reported previously, and indeed the concept of a RM coronary artery, except possibly in the congenital condition, corrected transposition of the great arteries (ltransposition), has not been presented previously.

We performed simultaneous echocardiographic and hemodynamic studies in 11 patients with muscular subaortic stenosis to determine whether systolic anterior motion (SAM) of the anterior mitral leaflet and the pressure gradient are related quantitatively. SAM without septal contact was associated with either no gradient or a small impulse gradient of less than 10 mm Hg. SAM with septal contact was always associated with a pressure gradient of more than 10 mm Hg. The size of the pressure gradient correlated inversely with the time periods: (1) onset of SAM-septal contact (r = .79, p less than .001) and (2) onset of aortic ejection to onset of SAM-septal contact (r = -.89, p less than .001). Size also correlated directly with the time period: (3) duration of SAM-septal contact (r = .80, p less than .001). Thus when the time from the onset of SAM to the onset of SAM-septal contact was long, SAM-septal contact developed late in systole, the duration of SAM-septal contact was brief and the pressure gradient was low. When SAM-septal contact developed in early systole, the duration of SAM-septal contact was long and the pressure gradient was high. With the index of time period (3) divided by time period (1), a regression equation was devised to predict the size of the pressure gradient (pressure gradient [mm Hg] = 25 [ratio] + 25; r = .90, p less than .001; SE +/- 15 mm Hg). The echocardiographic time period index was validated prospectively in nine other patients and the significant correlation with the hemodynamically determined gradient persisted (r = .89, p less than .01). We conclude that SAM and the pressure gradient are related quantitatively in muscular subaortic stenosis. These observations have implications regarding the mechanism and significance of the pressure gradient in muscular subaortic stenosis.

Two dimensional echocardiography is now commonly used in the Coronary Care Unit as a first line tool in the diagnosis of serious complications of acute myocardial infarction. The complications which will be discussed are severe left ventricular (LV) dysfunction, right ventricular (RV) dysfunction, left ventricular pseudoaneurysm, post-infarction ventricular septal defects (VSD), mitral regurgitation and left ventricular thrombus.

Echocardiographic and Doppler studies are invaluable in the detection and management of patients with hypertrophic cardiomyopathy, since virtually all aspects of the disorder can be evaluated. Echocardiography is the primary method of diagnosis, and hemodynamic studies are required usually only when surgery is contemplated. All patients should if possible undergo complete M-mode, two-dimensional, Doppler, and color flow studies to define the extent of hypertrophy, the hemodynamic subgroup, quantitation of left ventricular outflow obstruction, mitral regurgitation when present, and an assessment of diastolic function. Patients undergoing medical or surgical therapy for this disorder should have repeat studies performed to assess the effects of therapy on the degree of obstruction and diastolic dysfunction.

A wide angle phased array sector scanner was used to find the optimal method, the reliability and the reproducibility of measuring the mitral valve area with two dimensional echocardiography in patients with rheumatic mitral stenosis. Initial experience with 18 patients revealed that tracing the early diastolic actual black-white interface of the perceived orifice was the most reliable method for drawing the mitral valve orifice area. Good interobserver correlation was obtained when two observers used either method to calculate the mitral valve area ( r = 0.93). Similarly good intrastudy reliability was obtained when any one observer applied one measurement method to different diastolic cycles within the same study ( r = 0.89). The phased array two dimensional echocardiogram properly differentiated patients with critical mitral stenosis from those with non-critical mitral stenosis, but the correlation between the echocardiographically and the hemodynamically derived mitral valve areas was less good than previously reported ( r = 0.83). Imaging a test object with varied known orifice sizes and excised stenotic mitral valves of known orifice size with a phased array and mechanical sector scanner failed to reveal superiority of either instrument. Further testing with a phased array instrument revealed that the perceived orifice was critically dependent on receiver gains settings for any transmitted power level. Receiver gain settings too low led to image dropout, indicating a falsely large orifice. Receiver gain settings too high led to image saturation, indicating a falsely narrowed orifice. Six additional patients with predominant mitral stenosis later underwent imaging with strict attention paid to individual receiver gain settings. Combining the data from these 6 patients with those from the initial 18 patients gave a better correlation between the echocardiographic and hemodynamic calculated mitral valve areas ( r = 0.92). Accurate noninvasive measurement of the mitral valve area with two dimensional echocardiography in patients with mitral stenosis appears to depend on use of the proper echocardiographic technique to localize the true commissural edge of the valve in early diastole, the correct instrument settings and the appropriate method for drawing the perceived orifice. The noninvasive measurement of the mitral valve orifice with two dimensional echocardiography in mitral stenosis provides clinically useful data that are reliable and reproducible if these factors are taken into account.

Sixteen patients had two-dimensional echocardiographic diagnosis of the presence or absence of left ventricular thrombi and anatomical, radiological, or clinical confirmation of the diagnosis. Eleven patients had positive diagnoses, which were confirmed in 10 and possibly incorrect in one. Five other records were reviewed because the patients had undergone aneurysmectomy after two-dimensional echocardiograms: three were true negative and two were false negative studies.

Although the postoperative hemodynamic and echocardiographic features of idiopathic hypertrophic subaortic stenosis have been studied, the expected consistent postoperative thinning of the interventricular septum has not been reported. In this study, the short-term effects of septal myectomy were evaluated in 16 patients. All patients were assessed with pre- and postoperative hemodynamic studies and M-mode echocardiograms, and six of the 16 patients had pre- and postoperative two-dimensional echocardiograms. The mean resting preoperative gradient of 74 mm Hg (range 10--190 mm Hg), which fell to a mean resting postoperative gradient of 8 mm Hg (range 0--25 mm Hg), was associated with decreased end-diastolic interventricular septal thickness at the midventricular level in 14 of 16 patients and at the subaortic level in 16 of 16 patients by M-mode echocardiography. The group also demonstrated changes in left ventricular outflow tract configuration and dimension, mitral valve systolic anterior motion, mitral E-F0 slope and left ventricular percent fractional shortening by both M-mode and two-dimensional studies. In the two patients who did not show midventricular septal thinning on M-mode echocardiography, the two-dimensional echocardiograms revealed that the area of myectomy extended only through the subaortic region and not down to the midventricular septum. Thus, we have observed consistent postmyectomy septal thinning at both the midventricular and subaortic levels by M-mode echo. By defining the geometry of the septal myectomy in vivo with two-dimensional echocardiography, we can better interpret M-mode studies and identify factors that influence echocardiographic visualization of the region of myectomy.

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic entity that involves principally the left ventricle and is caused by asymmetric or concentric hypertrophy of unknown cause. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the apex, at the midventricular level, or, rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by upper septal hypertrophy narrowing the outflow tract and setting the stage for Venturi forces to cause systolic anterior motion of the anterior or posterior mitral leaflets. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyotomy-myectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. This form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy available today. The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness (decreased compliance) that characterize diastole in hypertrophic cardiomyopathy. Relaxation is impaired by the contraction load (the obstruction), by a decrease in the principal relaxation loads, by a pathologic degree of nonuniformity of contraction and relaxation, and in all likelihood, by impaired inactivation of the biochemical processes responsible for contraction (? due to primary or ischemia-induced calcium overload). Calcium channel-blocking agents may dramatically improve left ventricular relaxation by speeding up the inactivation process, by decreasing the degree of nonuniformity, or by altering the contraction and relaxation loads in a favorable manner. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their occurrence also appears to depend on the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole as well as the disturbances of rhythm appear to be related to the site and/or extent of the hypertrophic process.(ABSTRACT TRUNCATED AT 400 WORDS)

Restrictive cardiomyopathy is far less common in North America than the congestive and hypertrophic myopathies. The terms refers to a condition characterized by a ‘stiff heart’ due to rigid ventricular walls with impaired diastolic filling. Infiltration or fibrosis of the myocardium is the usual cause [1]. Hemodynamic studies demonstrate a characteristic dip and plateau configuration typical of diastolic dysfunction, while systolic function is often normal. All of the restrictive cardiomyopathies are infiltrative, however, the converse is not always true as not all infiltrative cardiomyopathies are primarily restrictive. The clinical and hemodynamic characteristics of infiltrative cardiomyopathies occupy a spectrum from the classic restrictive type to the purely congestive.

Surgical ventriculomyectomy and ventriculomyotomy by the aortic approach are safe and effective methods of relieving symptoms and obstruction to left ventricular outflow in patients with hypertrophic obstructive cardiomyopathy. With the addition of Doppler ultrasound to the routine follow-up assessment of these patients an unexpectedly high occurrence of aortic regurgitation was found in the postoperative patients. Because aortic regurgitation has been reported to rarely accompany this condition, 67 patients with hypertrophic obstructive cardiomyopathy were studied clinically and with Doppler echocardiography for the presence and severity of aortic regurgitation. Severity of the regurgitation was quantitated by pulsed or color Doppler echocardiography according to the length and width of the regurgitant jet in at least two views. In 37 patients with hypertrophic obstructive cardiomyopathy who did not undergo surgery, aortic regurgitation was detected in only 1 (3%) by Doppler ultrasound and in none clinically. In 52 patients who did undergo surgery and were studied a mean of 7.8 years postoperatively, aortic regurgitation of trivial to moderate degree was common, being detected in 28 (54%) by Doppler ultrasound and in 6 (12%) clinically. In a subgroup of 22 patients who were studied preoperatively and again early postoperatively (mean 6 weeks), new aortic regurgitation was found in 8 (36%) and was graded as trivial in all. Aortic regurgitation is a common complication related to ventriculomyectomy and ventriculomyotomy in patients with hypertrophic obstructive cardiomyopathy. Although initially trivial, the regurgitation may progress in severity over time. The regurgitation has been well tolerated in all patients studied to date.

We prospectively studied 14 patients with the carcinoid syndrome to determine if two-dimensional echocardiography could detect the nature and extent of valvular abnormalities. Eight of the 14 patients had definite abnormalities of the right-sided cardiac valves. The tricuspid valve had a characteristic appearance, similar to previously described pathologic findings. The leaflets appeared diffusely thickened, shortened and stiff without evidence of commissural fusion. Saline contrast studies demonstrated tricuspid regurgitation, which corresponded to the severity of the tricuspid valve involvement. The pulmonary valve could only be adequately assessed in seven of 14 patients, and morphologic abnormalities similar to those in the tricuspid valve were found. Follow-up studies have shown progression of cardiac disease in six of eight patients. We conclude that two-dimensional echocardiography can detect the characteristic cardiac abnormalities in the carcinoid syndrome and may be a useful tool for following their progression.

Infarct expansion and aneurysm (LVA) formation has a poor prognosis. Traditional techniques of LVA resection may be associated with suboptimal results, and do not fully restore LV geometry. LV endoaneurysmorrhaphy(LVEA) is a newer operative technique which utilizes an endocardial patch to exclude the aneurysm and normalize LV geometry. Late clinical and echocardiographic features of these patients (pts) is unknown. We prospectively followed 51 consecutive pts who had undergone LVEA. Average duration of follow-up (F/U) was 4.6 years (range 2-10 years). All pts had clinical evaluation and review of medical records. Results There were 2 (4%) peri-operative deaths, 2 (4%) in-hospital deaths, and 13 (24%) late deaths. Clinical improvement was noted in all 34 survivors: NYHA Class Pre-op F/U CCS Pre-op F/U n (%) n (%) n (%) n (%) I 5 (15) 21 (62) I 12 (35) 29 (85) II 9 (26) 8 (24) II 3 (9) 5 (15) III 13 (38) 4 (12) III 5 (15) 0 IV 7 (21) 1 (3) IV 14 (41) 0 30 surviving pts had F/U 2D echocardiograms (2DE). Near normal LV geometry was restored in all pts, and no patch aneurysms were noted at late F/U. 24/30 2DEs were adequate for quantitative analysis. The average LVEF post-op was 40.2% using the modified biplane analysis. Conclusions LV endoaneurysmorrhaphy was associated with a 72% overall survival after average 4.6 year F/U. All survivors had improvement in clinical status and normalization of LV geometry.

Aortic stenosis (AS) induces chronic pressure overload on the left ventricle (LV) with alterations in myocardial structure and function. We aimed to study the impact of transcatheter aortic valve implantation (TAVI) on the recovery of myocardial mechanics and the influence of post-procedural aortic