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Biomedical subjects

M Komeda

Publications and source records attributed to M Komeda.

At least 73 records · Page 4Linked to original sources

Mitral valve opening in the ovine heart.

To study the three-dimensional size, shape, and motion of the mitral leaflets and annulus, we surgically attached radiopaque markers to sites on the mitral annulus and leaflets in seven sheep. After 8 days of recovery, the animals were sedated, and three-dimensional marker positions were measured by computer analysis of biplane videofluorograms (60/s). We found that the oval mitral annulus became most elliptical in middiastole. Both leaflets began to descend into the left ventricle (LV) during the rapid fall of LV pressure (LVP), before leaflet edge separation. The anterior leaflet exhibited a compound curvature in systole and maintained this shape during opening. The central cusp of the posterior leaflet was curved slightly concave to the LV during opening. Markers at the border of the "rough zone" were separated by 10 mm during systole. We conclude that coaptation occurs very near the leaflet edges, that the annulus and leaflets move toward their open positions during the rapid fall of LVP, and that leaflet edge separation, the last event in the opening sequence, occurs near the time of minimum LVP.

Animals↗

Estimation of regional left ventricular wall stresses in intact canine hearts.

Left ventricular (LV) wall stress is an important element in the assessment of LV systolic function; however, a reproducible technique to determine instantaneous local or regional wall stress has not been developed. Fourteen dogs underwent placement of twenty-six myocardial markers into the ventricle and septum. One week later, marker images were obtained using high-speed biplane videofluoroscopy under awake, sedated, atrially paced baseline conditions and after inotropic stimulation (calcium). With a model taking into account LV pressure, regional wall thickness, and meridional and circumferential regional radii of curvature, we computed average midwall stress for each of nine LV sites. Regional end-systolic and maximal LV wall stress were heterogeneous and dependent on latitude (increasing from apex to base, P < 0.001) and specific wall (anterior > lateral and posterior wall stresses; P = 0. 002). Multivariate ANOVA demonstrated only a trend (P = 0.056) toward increased LV stress after calcium infusion; subsequent univariate analysis isolated significant increases in end-systolic LV wall stress with increased inotropic state at all sites except the equatorial regions. The model used in this analysis incorporates local geometric factors and provides a reasonable estimate of regional LV wall stress compared with previous studies. LV wall stress is heterogeneous and dependent on the particular LV site of interest. Variation in wall stress may be caused by anatomic differences and/or extrinsic interactions between LV sites, i.e., influences of the papillary muscles and the interventricular septum.

Animals↗

[Coronary stenosis and mechanisms of collateral vessel growth].

The presence or absence of collateral circulation significantly impacts the natural history of coronary artery disease. Collateral growth involves two different mechanism; capillary collaterals develop by sprouting (angiogenesis) and muscular collaterals develop in situ from preexisting arterioles (arteriogenesis). The process is mediated by various angiogenic growth factors such as VEGF, FGFs, IGF-1 and PDGF. Although these growth factors have been studied extensively, controversies still exist as to whether angiogenesis depends on increased supply of these growth factors or their receptors are upregulated by the underlying pathological situation. An increased understanding of the basic biology of collateral vessel development would be instrumental in the establishment of therapeutic angiogenesis.

Angiogenesis Inducing Agents↗

The road to complete arterial grafting for coronary artery disease.

In 1984, our department moved to the use of single, and subsequently, bilateral internal thoracic artery grafting which, when reviewed after 12 years, suggest the addition of a second internal thoracic artery is beneficial. The 10-year survival using all-cause mortality was 86.9% for bilateral internal thoracic artery grafting compared with 74.2% for the use of a single internal thoracic artery graft. The mortality rate ratio for single versus bilateral internal thoracic artery grafts was 1.4 (P=0.009). In 1995, we entered an era of total arterial grafting using combinations of radial and internal thoracic arteries. There have been no additional early complications in the first 2 years, furthermore the early results show that the postoperative creatinine kinase MB isoenzyme and the myocardial infarction rates were lower in patients receiving at least one radial artery graft compared with those not receiving a radial artery graft. Continued use of internal thoracic and radial arteries to achieve complete arterial revascularisation for patients with coronary artery disease appears justified.

Aged↗

Most ovine mitral annular three-dimensional size reduction occurs before ventricular systole and is abolished with ventricular pacing.

BACKGROUND: Conventional surgical thinking indicates that mitral annular (MA) size reduction plays a key role in mitral valve closure, and most MA size and shape changes are thought to occur during left ventricular (LV) systole. The influences of left atrial (LA) and LV systole on MA size and shape, however, remain debated. METHODS AND RESULTS: Eight radiopaque markers were placed equidistantly around the MA and imaged using high-speed simultaneous biplane videofluoroscopy in seven closed-chest, sedated sheep before and during asynchronous LV pacing. Marker images were used to compute the three-dimensional coordinates of each marker every 16.7 ms throughout the cardiac cycle, allowing calculation of three-dimensional MA area, septal-lateral (SL) dimension, and commissure-commissure (CC) dimension under control and LV pacing conditions. Maximum MA area occurred in early diastole, and minimum MA area near end-diastole; maximum area reduction was 12+/-1% (P< or =.001). Interestingly, 89+/-3% of area reduction occurred before LV systole. During this "presystolic" period, SL decreased by 8+/-1% and CC by 2+/-1%; the SL/CC ratio fell from 0.73+/-0.02 to 0.69+/-0.01 (P< or =.005), indicating a less circular shape at end-diastole. With LV pacing, total MA area reduction was similar (13+/-2 versus 12+/-1%, P=NS versus control); however, all MA area reduction occurred during LV systole with minimum MA area occurring at end-systole. Presystolic shortening in both SL and CC dimensions was lost, and presystolic ellipticalization disappeared. CONCLUSIONS: Changes in MA size and shape coincident with LA systole included area reduction and shape change prior to the onset of LV contraction. These presystolic changes vanished when LA systole was absent (LV pacing). Thus, LA systole plays a pivotal role in MA size reduction and shape alteration. The unexpected timing of these MA dynamics should be taken into account during mitral valve reparative procedures.

Animals↗

Geometric determinants of ischemic mitral regurgitation.

BACKGROUND: The precise geometric determinants of ischemic mitral regurgitation (MR) are incompletely understood, although such knowledge is important to improve mitral valve reparative techniques. METHODS AND RESULTS: The three-dimensional geometry of the mitral apparatus was studied using radiopaque markers in eight closed-chest dogs with acute posterior left ventricular wall ischemia either with (MR) or without (no-MR) MR as assessed by using color Doppler. Using a cylindrical coordinate system (origin at the midpoint between the mitral annulus commissures [anterolateral and posteromedial] and z-axis directed toward the left ventricular apex), we measured the distance to the midpoint (z, in millimeters), radial distance from the z-axis (r, in millimeters), and angle from the intercommissural line (theta) of each marker. A multivariate analysis of variance showed the following differences (P < .005) between the MR and the no-MR groups: 1) markedly increased r of the posterior papillary muscle tip (10.3 versus 6.4 mm, MR versus no-MR, at end-systole) and increased r of the anterior papillary muscle tip; 2) dilation (in the septal-lateral direction) of the midpart of the mitral annulus and near the anterolateral region; 3) increased posterior mitral leaflet r near both commissures (eg, 8.3 versus 6.2 mm on the posteromedial side) and increased z (ie, shifted toward the left ventricular apex) of the posterior leaflet on the anterolateral side (eg, 7.0 versus 6.2 mm), which is analogous to restricted (or type III) leaflet motion. CONCLUSIONS: These findings indicate that the geometric determinants of ischemic MR in dogs are complex and involve many parts of the mitral valve apparatus. This complexity suggests that surgical attention to the entire annulus and excursion of the posterior leaflet may be helpful when annuloplasty alone is inadequate.

Animals↗

Septal function during left ventricular unloading.

BACKGROUND: Left ventricular (LV) unloading with mechanical support devices alters biventricular geometry and impairs right ventricular (RV) contractility, but its effect on septal systolic function remains unknown. METHODS AND RESULTS: To evaluate the effects of LV volume and pressure unloading on septal geometry and function, LV preload was abruptly reduced by clamping left atrial pressure between 0 and -2 mm Hg in seven open-chest, anesthetized dogs by use of a pressure-control servomechanism to withdraw blood from the left atrium. With left atrial pressure clamping, maximal LV pressure decreased 30 +/- 12% (mean +/- SD) (P < .0001) and LV end-diastolic cross-sectional area (determined by two-dimensional echocardiography) decreased by 53 +/- 16% (P < .0001). This caused the septum to shift toward the left (RV septal free-wall dimension increased; P < .004) and flatten (radius of curvature increased; P < .0002), while LV septal free-wall dimension fell (P < .0001). Septal end-diastolic thickness increased 23 +/- 15% (P < .0005), reflecting a decline in septal preload. Systolic septal thickening decreased (P < .002), while systolic septal output (Septal Output = Septal Thickening x Heart Rate) fell from 30 +/- 17 to 15 +/- 22 cm/min (P < .002). This was associated with movement along the septal Frank-Starling equivalent (septal output versus end-diastolic septal thickness [preload] relation) to a less productive portion of the curve. CONCLUSIONS: LV unloading not only altered interventricular septal geometry but also reduced septal systolic thickening and output, all of which may contribute to impaired RV contractility during mechanical LV support.

Animals↗

Complete unloading alone may not adequately protect the left ventricle.

BACKGROUND: The benefit of left ventricular (LV) unloading for preserving LV function is commonly accepted, but its efficacy remains incompletely defined. METHODS: We studied the influence of complete LV unloading on LV systolic and diastolic mechanics using an in situ isovolumic preparation with two different coronary perfusion pressures (CPPs) in 12 dogs during prolonged normothermic cardiopulmonary bypass. RESULTS: Multivariate analysis of covariance with time as a covariate revealed that a high CPP (143 +/- 36 mm Hg; n = 6) was associated with better preservation of systolic LV function over time as assessed by LV end-systolic elastance (p < 0.001) and the end-systolic pressure-volume relation physiologic intercept (p < 0.001) compared with a moderate CPP (107 +/- 18 mm Hg; p < 0.005 versus a high CPP by t-test; n = 6). Dobutamine (2 micrograms.kg-1.min-1) improved LV end-systolic elastance (p < 0.005) and LV physiologic intercept (p < 0.01) only in the high-CPP group. Conversely, impaired LV diastolic function (as measured by LV stiffness) was observed (p < 0.001) with a high CPP, but did not change with a moderate CPP. CONCLUSIONS: These observations in canine hearts suggest that complete LV unloading may not preserve LV systolic function adequately over time when CPP is maintained in the accepted clinical range. A higher CPP is required to prevent deterioration over prolonged cardiopulmonary bypass times, but diastolic dysfunction still occurs.

Animals↗

Papillary muscle-left ventricular wall "complex".

OBJECTIVES: Mitral valve homografts, despite theoretical advantages, are not widely used, in part because of lack of basic information about the three-dimensional geometry of the mitral apparatus. METHODS: Radiopaque markers were used in the study of eight closed-chest dogs under four conditions: (1) baseline, (2) caval occlusion, (3) tachycardia (atrial pacing), and (4) nitroprusside infusion. Using a cylindrical coordinate system. defined with the origin at the midpoint between the anterior and posterior commissures, and the left ventricular long axis (z-axis), defined by the origin and the left ventricular apex, DTIP-MA (the z-coordinate [millimeters] of the papillary muscle tip), was measured at 10 time points throughout the entire cardiac cycle. DBASE-MA (the z-coordinate of the papillary muscle base) and LPM (the length of the papillary muscle [millimeters]) were also measured. RESULTS: DTIP-MA varied slightly with time (p < 0.001 by analysis of variance), but the magnitude of change was negligible (< 0.9 mm) (e.g., DTIP-MA of the anterior papillary muscle was 20.7 +/- 2.7/20.8 +/- 2.8 [end-diastolic/end-systolic, mean +/- 1 standard deviation]; DTIP-MA of the posterior papillary muscle was 25.8 +/- 4.8/25.5 +/- 4.5). DTIP-MA was minimally influenced by the above perturbations. DBASE-MA and LPM of each papillary muscle, however, changed throughout the cardiac cycle (p < 0.001 by analysis of variance) by about 4 mm, and both parameters were dependent on loading conditions. CONCLUSIONS: Papillary muscle length changed to keep the DTIP-MA distance constant such that the papillary muscle and left ventricular wall functioned together as a unit ("J-shaped complex"). These results provide a physiologic rationale for measuring DTIP-MA, define its potential surgical usefulness, and imply that using the entire length of the donor's papillary muscle (i.e., maintaining the entire J-shaped complex) is important in operations in which homograft or stentless xenograft mitral valves are used.

Animals↗

Further evidence for supporting cell conversion in the damaged avian basilar papilla.

Two lines of evidence suggested that a process other than supporting cell divisions may give rise to new hair cells in the bird inner ear injured by either noise or ototoxic drugs. This process, supporting cell conversion, occurs when non-dividing supporting cells transdifferentiate into hair cells. First, noise-exposed chicks received zero, one or two daily i.p. injections of cytosine arabinoside (a DNA synthesis blocker), as well as two daily intraperitoneal injections of bromodeoxyuridine, for four days. Following sacrifice, the papillae were processed for bromodeoxyuridine immunocytochemistry. All the ears demonstrated dividing cells, but increasing the number of cytosine arabinoside injections decreased the number of labeled cells. Indeed, two cytosine arabinoside injections per day nearly completely blocked supporting cell divisions in the short hair cell region within the sound-induced lesion. This suggested that unpaired, immature cells observed in a similar region with scanning electron microscopy, despite the presence of cytosine arabinoside, may have been products of supporting cell conversion. In the second experiment, birds were treated with gentamicin for three days. Upon sacrifice at 6 days post-treatment, papillae were processed for light and transmission electron microscopy. Several unusual cells were observed with phenotypic features of both hair cells and supporting cells. The peculiar cells may be in a transition from the supporting cell phenotype to that of a hair cell.

Animals↗

Gentamicin distribution in the basilar papilla: possible association with regenerated hair cell orientation.

Gentamicin-specific immunolabeling was examined in the regenerating chick basilar papilla following gentamicin treatment. Surviving hair cells were labeled in the infracuticular area, predominantly in the basal body region. Label intensity in short hair cells (SHCs) was greater than tall hair cells (THCs). Quantitative examination of stereociliary bundle orientation in regenerated hair cells revealed a considerable degree of variability from normal. The orientation of SHC stereocilia was more varied than that of THC. The results suggest an association between the accumulation of gentamicin in the region of the basal body and the degree of disorientation of the cell surface. It is possible that gentamicin accumulation around the basal body compromises the ability of the centrosome to orient hair cells correctly.

Animals↗

Loss of three-dimensional canine mitral annular systolic contraction with reduced left ventricular volumes.

BACKGROUND: We have recently described an inhomogeneous pattern of systolic contraction of the mitral annulus (MA) in normovolemic dogs: the posterior annulus shortens, and the anterior annulus lengthens. MA dynamics, however, have not been studied in volume-depleted hearts. METHODS AND RESULTS: Eight radiopaque markers were placed equidistant from each other around the MA in seven dogs. As viewed from the left atrium, the segment between markers 1 and 2 (seg12) began at the posteromedial commissure, and remaining segments were numbered sequentially clockwise around the MA (ie, posterior MA encompassed seg12, seg23, seg34, and seg45; anterior MA encompassed seg56, seg67, seg78, and seg81). Marker images were obtained in sedated dogs by simultaneous biplane videofluoroscopy 7 to 12 days after marker implantation, and three-dimensional marker coordinates at end diastole (ED) and end systole (ES) were computed. Vena caval occlusion (VCO) was used to reduce left ventricular end-diastolic volume to 70 +/- 5% of baseline (BL). With VCO, mean MA area did not change from ED to ES (3.4 +/- 0.8 versus 3.6 +/- 0.7 cm2, P = NS) during the cardiac cycle. MA segmental systolic shortening values (negative values indicate lengthening) were as follows for BL and VCO, respectively (mean +/- SD): seg12, 7 +/- 9% and 0 +/- 13%; seg23, 8 +/- 10%* and 1 +/- 11%; seg34, 16 +/- 6%* and 4 +/- 9% seg45, 10 +/- 7%* and 2 +/- 13%; seg56, -4 +/- 5%* and -16 +/- 11%*; seg67, -7 +/- 7%* and -14 +/- 7%*; seg78, 3 +/- 2%* and -1 +/- 6%; and seg81, 6 +/- 5%* and -5 +/- 11% (*P < or = .05 versus zero changes, paired t test). CONCLUSIONS: With acute volume depletion, the five annular segments that shortened at BL no longer changed length; two anterior segments (seg56 and seg67) that lengthened at BL continued to lengthen significantly, and to a greater extent. These findings indicate that the anterior MA is a more dynamic structure than previously thought. Such dynamic motion may be important for normal mitral valvular function and possibly needs to be taken into account in the design of mitral valve reparative techniques.

Animals↗

Three-dimensional dynamic geometry of the normal canine mitral annulus and papillary muscles.

BACKGROUND: Despite an incomplete knowledge of the geometry and dynamics of the mitral annulus (MA), papillary muscle (PM), and the chordae tendineac, chordal-sparing MVR is popular. METHODS AND RESULTS: The systolic reduction in three-dimensional distance between each PM tip and eight MA sites (DT-A) was measured in nine normal closed-chest dogs by use of surgically implanted radiopaque markers. Three loci (tip, junction, and base) on each PM were also projected onto the MA plane at end diastole and end systole to assess PM dynamics. The anterior PM tip showed significant shortening of DT-A toward the opposite side of the MA or the midanterior MA region (P < .005 or P < .05, respectively, versus same MA side [MANOVA]); conversely, the posterior PM tip DT-A shortened toward the opposite side of the MA near the anterior commissure or the area between the anterior commissure and midposterior MA (P < .005 versus same MA side). Annular projection revealed three-dimensional motion (relative to the MA) of the anterior PM tip, junction, and base toward the right trigone, while posterior PM motion was oriented toward the opposite side of the MA. CONCLUSIONS: Both PMs in normal canine hearts demonstrated systolic relative motion in a direction compatible with the "oblique" chordal configuration, ie, from the anterior PM to the anterior MA near the right trigone and from the posterior PM to the opposite side of the posterior MA. These observations warrant further investigation of three-dimensional PM-MA dynamics with various methods of chorda preservation during MVR to assess their impact on left ventricular systolic and diastolic function.

Animals↗

Results of represervation of the chordae tendineae during redo mitral valve replacement.

BACKGROUND: Previous studies have shown that preservation of the chordae tendineae improves early and late postoperative left ventricular function after mitral valve replacement. This report describes the results of represervation of the chordae tendineae during redo mitral valve replacement in patients who had their chordae tendineae preserved during their initial operation. METHODS: Fifty-four patients undergoing reoperative mitral valve replacement with preservation of their chordal annular attachments (chordae group) were compared with 187 patients who had redo mitral valve replacement without preservation of the chordae (nonchordae group). The interval between the initial operation and the reoperation was 8.7 +/- 4.4 years in the chordae group and 8.6 +/- 4.9 years in the nonchordae group (p = 0.315). Seventy-three patients underwent aortic valve replacement during their redo mitral valve replacement compared with 168 patients who had mitral valve replacement alone. There were 15 patients who had their chordal attachments represerved during redo double-valve replacement. RESULTS: In the chordae group, intraoperative assessment revealed excellent chordal connection between the preserved papillary muscles and the mitral annulus in all patients. One patient had adhesions between the preserved chordae and the stent of the tissue valve. The chordal attachments were preserved during insertion of the second valve in all patients. The incidence of low output syndrome and operative mortality in the chordae group was 16.7% and 7.4%, respectively. In the nonchordae group, the incidence of low output syndrome was 27.3% (p = 0.112 compared with the chordae group) and the operative mortality was 13.4% (p = 0.236 compared with the chordae group). In patients with double-valve replacement, represervation of the chordae was associated with a reduction in low output syndrome (0% versus 24%; p = 0.034) and mortality (6.7% versus 15.5%; p = 0.374). CONCLUSIONS: Preservation of the chordal attachments between the papillary muscles and the mitral annulus can be accomplished during reoperative mitral valve replacement. Represervation of the chordae tendineae may reduce postoperative low output syndrome, especially in high-risk patients undergoing redo double-valve replacement.

Aortic Valve↗

Three-dimensional dynamics of the canine mitral annulus during ischemic mitral regurgitation.

BACKGROUND: It has been suggested that ischemic mitral regurgitation results, at least in part, from generalized end-systolic mitral annulus (MA) dilatation, but the role of the MA is incompletely understood and the segmental dynamics of the MA during left ventricular ischemia have not been described. METHODS: We used radiopaque markers and simultaneous biplane videofluoroscopy to measure three-dimensional in vivo lengths of eight MA segments in 7 sedated dogs before and after induction of ischemic MR (produced by circumflex coronary artery balloon occlusion and verified by Doppler echocardiography). As viewed from the left atrium, the MA segment between markers 1 and 2 (S12) was defined as starting at the posteromedial commissure, and remaining segments were numbered sequentially clockwise around the MA (ie, the posterior MA encompassed S12, S23, S34, S45,; the anterior MA included S56, S67, S78, S81). Marker images obtained 7 to 12 days after implantation were used to construct x, y, and z coordinates of each marker at end-diastole and end-systole. RESULTS: During regional (posterolateral walls) left ventricular ischemia, the end-systolic MA area increased (4.9 +/- 0.8 cm2 [control] versus 5.9 +/- 0.6 cm2; p = 0.005). End-systolic MA segment lengths were as follows (control, ischemia [mm, mean +/- standard deviation]): S12 = 9 +/- 2, 10 +/- 3; S23 = 10 +/- 2, 12 +/- 3; S34 = 13 +/- 1, 15 +/- 1; S45 = 8 +/- 2, 9 +/- 2; S56 = 11 +/- 2, 11 +/- 2; S67 = 12 +/- 2, 12 +/- 2; S78 = 10 +/- 3, 11 +/- 2; and S81 = 11 +/- 1, 12 +/- 1. Values for S12, S23, S34, and S81 were significant (p < or = 0.05 for control versus ischemia by paired t test). CONCLUSIONS: During ischemic mitral regurgitation, the MA enlarged at end-systole, but in an asymmetric manner; most posterior annular segments lengthened, whereas most anterior annular segment lengths did not change. These data suggest that alterations in regional MA mechanics may be important in the pathogenesis of ischemic mitral regurgitation. Further three-dimensional studies of MA dynamics and shape should be conducted so that new knowledge may result in improved mitral valve surgical techniques.

Animals↗

Left ventricular diastolic suction with zero left atrial pressure in open-chest dogs.

We investigated left ventricular (LV) diastolic volume changes (suction inflows) with left atrial pressure (LAP) clamped to ambient pressure in six open-chest, anesthetized dogs. The left atrium was cannulated and connected to a servo pump, and LAP was clamped to a set point near 0 mmHg for four beats by withdrawing blood. LAP averaged 5.88 +/- 1.44 mmHg before the clamp and fell to 0.74 +/- 0.61 mmHg (P < 0.0001) after the clamp. During the first clamped beat a transmitral pressure gradient of 1.0 +/- 0.6 mmHg was observed, resulting in LV filling of 2.6 +/- 1.8 ml. Subsequent beats developed suction-driven (mean negative LV pressure: -1.5 +/- 1.3 mmHg; P < 0.005 vs. zero) LV filling of 4.5 +/- 2.8 ml/beat with a peak transmitral pressure gradient of 1.7 +/- 0.6 mmHg. These data are consistent with the hypothesis that LV suction can be an important filling mechanism under condition in which LV end-systolic volume is reduced, e.g., reduced filling pressures, high heart rates, exercise, or increased inotropic drive.

Animals↗

Results of combined pulmonary resection and cardiac operation.

BACKGROUND: Concomitant lesions of the heart and lung are uncommon, but when present they pose a therapeutic challenge for thoracic surgeons. A combined procedure avoids the need for a second major thoracic procedure and may improve outcomes and provide economic benefit. However, cardiopulmonary bypass may adversely affect the natural history of pulmonary malignancies. METHODS: The clinical records of 30 patients were reviewed who underwent simultaneous lung resection and cardiac operations between January 1982 and July 1995. Follow-up was obtained on all 30 patients (mean follow-up, 22 months; range, 1 to 100 months). RESULTS: Twenty-four patients underwent coronary artery bypass grafting in conjunction with pulmonary resection. Six patients underwent aortic (n = 4) or mitral (n = 2) valve replacement. The pulmonary resections consisted of pneumonectomy (n = 3), lobectomy (n = 14), wedge excision (n = 12), and tracheal resection (n = 1). Twenty-one patients had pathologic findings that confirmed adenocarcinoma (n = 10), squamous cell carcinoma (n = 5), small cell carcinoma (n = 2), or other malignancy (n = 4). Tumor stage of primary lung cancers was stage I, n = 12; stage II, n = 3; and stage IIIa, n = 2. Pathologic examination revealed benign disease in 9 patients. There were two operative deaths, one due to aspiration and one due to stroke. There were three late deaths, two cardiac and one of metastatic disease. Overall late survival was 85% +/- 7% and 73% +/- 16% at 1 and 5 years, respectively. Actuarial survival for patients with malignant disease was 64% at 5 years. CONCLUSIONS: Simultaneous cardiac operation and lung resection was not associated with increased early or late morbidity or mortality. Cardiopulmonary bypass does not adversely affect survival in patients with malignant disease. Cardiac valve replacement can be performed safely in conjunction with pulmonary resection.

Actuarial Analysis↗