Gadolinium prevents stretch-mediated contractile dysfunction in isolated papillary muscles.

We tested the hypothesis that overstretching the myocardium could induce and/or exacerbate contractile dysfunction via stretch-activated (SA) ion channels. Maximum developed tension (T(max)), normalized to a control value, was compared in guinea pig papillary muscles held at one of three resting lengths (physiological stretch, overstretch, and unloaded) for 85 min. Overstretched muscles exhibited decreased contractile force (T(max) = 0.77 +/- 0.03) compared with physiological and unloaded muscles (T(max) = 0.93 +/- 0.05 and 1.03 +/- 0.07, respectively). Gd(3+), an SA channel antagonist, eliminated the adverse effect of overstretching (T(max) = 0.98 +/- 0.06), but nifedipine, a dihydropyridine (DHP) antagonist of L-type calcium channels, did not (T(max) = 0.82 +/- 0.04). Exposure to modified hypoxia-reoxygenation (MHR) during physiological stretch resulted in decreased contractility (T(max) = 0.63 +/- 0.07), an effect that was exacerbated by overstretching (T(max) = 0.44 +/- 0.04). Gd(3+) mitigated the effects of overstretch during MHR (T(max) = 0.64 +/- 0.05), but DHP did not (T(max) = 0.48 +/- 0.04). These data suggest that overstretching of the myocardium contributes to contractile abnormalities via SA channels that are distinct from L-type calcium channels.

Fibrous ball: a new manifestation of chronic defibrillator and pacemaker infection.

Two patients with unusual manifestation of long-term infection of implantable cardioverter defibrillator and pacemaker were examined. Complete explanation of the defibrillator and pacemaker was done in both patients. New devices were subsequently implanted.

Effects of postischemic left ventricular pressure-volume unloading on contractile recovery and myocardial blood flow in the regionally stunned canine heart.

OBJECTIVE: Myocardial stunning remains a clinical problem without definitive therapy. This study tested the hypothesis that mechanical therapy with a ventricular assist device would accelerate recovery of contractility in stunned myocardium by increasing the postischemic myocardial blood flow. METHODS: Regional stunning was induced in dogs (25 kg) by 15 minutes of coronary occlusion and 180 minutes of reperfusion. One group (ventricular assist device; n = 10) was reperfused in conjunction with left ventricular unloading with a centrifugal-pump ventricular assist device. A second group (control; n = 8) underwent unmodified reperfusion. Hemodynamic and regional function data were acquired in all dogs with the heart in the working state before and during ischemia and after 180 minutes of reperfusion. Regional myocardial blood flow was measured at these same intervals and after 30 minutes of reperfusion, at which time the left ventricle was mechanically unloaded in animals with a ventricular assist device. RESULTS: Regional stunning was observed in all animals, but cardiogenic shock developed in none of them. After 180 minutes of reperfusion, animals with a ventricular assist device had greater systolic shortening in the risk segment than did control animals (11.5% +/- 2.8% vs 1.1% +/- 1.3%; P <.05) and had no differences in either the slope or x-axis intercept of regional preload recruitable stroke work relations compared with preischemic values. Differences in contractile recovery did not correlate, however, with postischemic myocardial blood flow. Hyperperfusion mediated by the ventricular assist device was not observed in either stunned or remote segments. CONCLUSIONS: Mechanical left ventricular unloading attenuates regional myocardial stunning within 3 hours in normotensive dogs, independent of effects on myocardial blood flow. The mechanism underlying this effect remains undefined, but these data support expanded use of mechanical therapy for stunned myocardium in clinical settings.

CT diagnosis of an unusual aortic dissection with intimointimal intussusception: the wind sock sign.

A unique combination of CT findings is reported in a rare case of aortic dissection with intimointimal intussusception. The CT showed a wind sock-like appearance in the contrast column of the aortic arch, which was felt to be characteristic of the intussuceptum. Complementary CT findings, including proximal flap in the dilated root of the aorta, no mid-ascending aortic flap, a descending aortic flap, and pericardial effusion, enabled establishment of the preoperative diagnosis.

Both dietary fish-oil supplementation and aspirin fail to inhibit atherosclerosis in long-term vein bypass grafts in moderately hypercholesterolemic nonhuman primates.

BACKGROUND: Aortocoronary vein bypass grafts are vulnerable to late atherosclerotic occlusion. Conventional platelet inhibitor therapy provides early but not persistent protection against graft failure. Evidence suggests that consumption of marine foods may reduce cardiovascular disease, possibly because of the unique long-chain unsaturated omega-3 fatty acids present in these foods. We hypothesized that dietary fish-oil supplementation would protect against atherosclerosis in vein bypass grafts. METHODS AND RESULTS: Thirty-three moderately hypercholesterolemic cynomolgus macaques were divided into four groups: control, control+aspirin, fish oil, and fish oil+aspirin. Each control group received olive oil as placebo to equalize calorie and fat consumption with that of the fish-oil groups. Both oils were in ethyl ester form, with the fish oil providing 0.88 g/d eicosapentaenoic acid. The aspirin dose was 40 mg/d. Cephalic vein grafts were interposed bilaterally in the carotid arteries and excised for analysis at 4 years. Bleeding time was significantly prolonged in all groups receiving fish oil or aspirin (P<.05). Plasma cholesterol levels were similar among groups, averaging 6.9+/-2.4 mmol/L (267+/-94 mg/dL). The extent of atherosclerosis in vein grafts did not differ among groups as evaluated both by Sudan IV staining of intimal lipid lesions (27+/-21% of total surface area, P=.89) and analysis of cholesterol content (236+/-203 nmol/mg, 9.1+/-7.8 microg/mg, P=.85). Vein graft connective tissue composition was also unaffected by treatment. CONCLUSIONS: Our findings do not support the use of concentrated dietary fish-oil supplements or aspirin for the prevention of atherosclerosis in long-term vein bypass grafts. Consumption of fish flesh or less refined oil preparations could have effects different from those of the purified fish-oil ethyl esters we used.

Functional and oximetric assessment of patients after lung reduction surgery.

OBJECTIVE: The goal of this study was to clarify the issue of functional oxygen requirement by regimented exercise oximetry in patients undergoing lung reduction surgery. METHODS: Thirty-seven patients underwent lung reduction surgery and were followed up for at least 3 months. Patients routinely completed a 6-week program of cardiopulmonary rehabilitation. Preoperative and postoperative spirometry, dyspnea scores, 6-minute walk distances, respiratory mechanics, and exercise oximetry were recorded. RESULTS: After the operation, patients had a 37% increase in forced vital capacity and a 59% increase in forced expiratory volume in 1 second. Six-minute walk distance increased from 913 +/- 310 feet before the lung reduction operation to 1202 +/- 274 feet 6 months after the operation (p < 0.001). Maximal inspiratory and expiratory pressures were significantly increased in 16 patients after lung reduction surgery. Perceived dyspnea was significantly improved. Exercise pulse oximetry demonstrated that 83% of patients met American Thoracic Society criteria for supplemental oxygen use before lung reduction surgery. After the operation, 70% of patients continued to meet American Thoracic Society criteria for supplemental oxygen use. Notably, 10 patients with exertional desaturation while breathing room air discontinued supplemental oxygen use because of a reduction in dyspnea. CONCLUSIONS: These findings demonstrate significant subjective and functional improvements related to lung reduction surgery. Exercise-induced hypoxia was not reversed by lung reduction surgery. Discontinuance of supplemental oxygen use owing to reduction in dyspnea and improved physical performance may not be warranted in lieu of continued exertional desaturation.

Increased tolerance of the chronically hypoxic immature heart to ischemia. Contribution of the KATP channel.

BACKGROUND: Hypoxia from birth in immature rabbits increases the tolerance of isolated hearts to ischemia compared with age-matched normoxic rabbits. We determined whether this increased tolerance to ischemia was due to an alteration in the ATP-sensitive potassium (KATP) channel and whether increased KATP channel activation was associated with increases in intracellular lactate. METHODS AND RESULTS: Isolated immature rabbit hearts (7 to 10 days old) were perfused with bicarbonate buffer at 39 degrees C in the Langendorff mode at a constant pressure. Saline-filled latex balloons were placed in the left and right ventricles for measurement of developed pressure. A KATP channel agonist (bimakalim) or a KATP channel antagonist (glibenclamide) was added 15 minutes before a global ischemic period of 18 minutes, followed by 35 minutes of reperfusion. Rabbits raised from birth in hypoxic conditions (FIO2 = 0.12) displayed significantly enhanced recovery of developed pressure. The right ventricle was more tolerant of ischemia than the left ventricle in normoxic and hypoxic hearts. Bimakalim (1 mumol/L) increased the recovery of left ventricular developed pressure in normoxic hearts to values not different from those of hypoxic controls (43 +/- 3% to 67 +/- 5%) and slightly increased developed pressure in hypoxic hearts (67 +/- 5% to 72 +/- 5%). Glibenclamide (3 mumol/L) abolished the cardioprotective effect of hypoxia (67 +/- 5% to 43 +/- 5%). Constant-flow studies indicated that the effects of bimakalim and glibenclamide were independent of their actions on coronary flow. Ventricular lactate and lactate dehydrogenase concentrations were elevated in hypoxic hearts compared with normoxic control hearts. CONCLUSIONS: Increased tolerance to ischemia exhibited by chronically hypoxic rabbit hearts is associated with increased activation of the KATP channel. This increased KATP activity may be the result of increased intracellular concentrations of lactate.

Single-channel and functional characteristics of a KCa channel in vascular muscle membranes of human saphenous veins.

The saphenous vein is used extensively to test for the effects of vasodilator substances on venous reactivity, but the K+ channel types that mediate vasodilation have not been identified. Thus the goal of this study was to identify K+ channel types in vascular smooth muscle membranes of human saphenous vein (HSV), which may contribute to membrane repolarization and control of venous tone. Fourteen HSVs obtained from bypass surgery were enzymatically dissociated into single vascular myocytes for patch-clamp analysis of inside-out patches (n = 81). HSV membranes showed primarily high-conductance (226 pS) K+ channels, which accounted for > or = 95% of total patch current at physiologic voltages. Channels were highly K+ selective, showed steep voltage and Ca2+ sensitivity, and were blocked by 100 nM iberiotoxin and < or = 1 mM tetraethylammonium (TEA). These Ca(2+)-sensitive channels (KCa) also showed stacked openings in depolarized patches exposed to 300-1,000 nM calcium, suggesting multiple functional KCa channels in a single membrane patch. In tension-recording studies, isolated segments of HSV exposed to 100 nM norepinephrine contracted further during progressive block of KCa channels by 0.1-3 mM TEA, suggesting that KCa channels are pathways for repolarization and vasodilation in HSV smooth muscle cells. Our finding of KCa channels in smooth muscle membranes of HSV, if extended to the plasma membranes of other human peripheral veins, suggests that this channel may represent a therapeutic site for alleviation of conditions of increased venous tone.

Mortality and neurologic morbidity after repair of traumatic aortic disruption.

BACKGROUND: Traumatic disruption of the thoracic aorta frequently results in death before operative repair. The determinants of mortality after repair, however, are uncertain. In addition, intraoperative strategies for reducing the incidence of spinal cord injury remain controversial. METHODS: The records of 45 consecutive patients undergoing repair of traumatic disruption of the thoracic aorta at a single institution during a 9-year period were reviewed in a retrospective fashion. Patient age ranged from 15 to 81 years (mean age, 33.9 years). Twenty-two patients (49%) had multiple associated injuries, and 8 (18%) had isolated aortic injuries. Nine patients (20%) experienced preoperative hypotension (systolic blood pressure of less than 90 mm Hg). Repair was performed with partial bypass in 22 patients, a heparinized shunt in 2, and no distal perfusion (clamp and sew technique) in 21. RESULTS: Nine patient (20%) died after operation. Multivariate logistic regression analysis of preoperative and intraoperative variables identified advancing age and preoperative hypotension as independent predictors of operative death. The presence of associated injuries was not an independent predictor of operative death. All 4 patients with injuries proximal to the aortic isthmus died. Ten patients were excluded from analysis of spinal cord injury either because of preoperative neurologic deficit or because of death before postoperative evaluation. Six (17%) of the remaining 35 patients had development of paraplegia: 5 of the 15 patients having the clamp and sew technique, 1 of the 2 with a shunt, and 0 of the 18 patients with bypass (p < 0.05, clamp and sew versus bypass). In the clamp and sew group, patients in whom paraplegia developed had significantly longer aortic clamp times than those without neurologic injury (40.6 +/- 4.4 minutes versus 28.7 +/- 2.9 minutes, respectively; p < 0.05). CONCLUSIONS: Advancing age, preoperative hypotension, and perhaps injury location are important determinants of death after repair of traumatic disruption of the thoracic aorta. Adjunctive perfusion with partial bypass should be used during repair to reduce the incidence of spinal cord injury.

Endothelium and vascular smooth muscle function in internal mammary artery after cryopreservation.

An optimal cryopreserved arterial conduit should have anatomic and physiologic characteristics similar to those of the fresh artery. We have cryopreserved canine internal mammary artery (IMA) with intact, prostacyclin (PGI2)-producing endothelial cells, but the underlying vascular smooth muscle appeared nonfunctional. Thus the aim of this study was to evaluate which steps of the cryopreservation method compromise vascular smooth muscle function in cryopreserved IMA. Isometric tension recording responses to vasoconstrictor agonists were used to evaluate the level of vascular muscle integrity, while endothelial function was assessed by relaxation responses to acetylcholine and by PGI2 production. These variables were measured in vessels rewarmed to 37 degrees C, following initial exposure to different stages of an eight-step computerized cryopreservation protocol (n = 10). In this protocol, tissue temperature was lowered to -10 degrees C (steps 1-2), rapidly reduced to -12 degrees C (steps 3-4), reduced further to -40 degrees C at a rate of -0.5 degrees C/min (steps 5-6), lowered to -70 degrees C (step 7), and finally equilibrated at - 196 degrees C by immersion in liquid nitrogen (step 8). Compared to fresh IMA, the amplitude of dose-dependent contractions to norepinephrine (NE 10(-9) to 10(-4) M) was step-wise depressed after cooling to < or = -12 degrees C (steps 3-4), showing only 75 and 19% of maximal contraction after steps 3-4 and step 7, respectively. Similarly, depolarization-induced contractions to KCl (10 to 60 mM) also were progressively depressed after step-wise cryopreservation, showing reduced contractile amplitudes even after steps 1-2 (-10 degrees C). Vascular muscle agonist sensitivity was unchanged (KCl) or only mildly influenced (NE) by these same temperature reductions. In contrast, endothelial-dependent relaxation to acetylcholine and PGI2 production were maintained after all steps in the cryopreservation process, and baseline PGI2 production was higher in cryopreserved IMA. These data indicate that IMA smooth muscle cell viability is poorly preserved after cooling to below -10 to -12 degrees C of the cryopreservation process, whereas endothelial cell function appears intact after profound cooling to -196 degrees C. The loss of vascular smooth muscle responsiveness coupled with the protection afforded by an intact endothelium may provide an arterial conduit less susceptible to vasospasm. Such a graft, however, would lack the dynamic properties of flow regulation in response to the metabolic needs of the myocardium.

Intraoperative epiaortic ultrasound during cardiac surgery.

BACKGROUND AND AIMS: Recent evidence suggests that the incidence of stroke during cardiac surgery may be reduced by using intraoperative epiaortic ultrasound (IEU) to detect ascending aortic atherosclerosis (AAA). To better define the role of this modality, IEU was performed in 89 patients during elective cardiac procedures. METHODS: The ascending aorta and proximal arch were divided into four segments that were graded (0 to 2) on the extent of disease both by palpation and IEU. A patient score (range 0 to 8) was determined for each modality by summing the segmental scores. Operative plan was determined in part by IEU findings. Preoperative variables were evaluated for associated risk of AAA. Palpation and IEU scores were compared for their ability to identify AAA. RESULTS: Operative technique was modified to avoid AAA in ten (11.2%) patients (mean age 68.3 +/- 2.2 years; mean IEU score = 4.40 +/- 0.40). Stroke occurred in two patients (2.2%), one whose operation was modified to avoid severe AAA and another who had minimal AAA. Mean IEU scores were significantly higher for patients > or = 65 years compared with younger patients (1.35 +/- 0.26 vs 0.66 +/- 0.21; p < 0.05) and for smokers compared with nonsmokers (1.15 +/- 0.19 vs 0 +/- 0; p < 0.05). Mean patient IEU score was greater than mean palpation score (1.06 +/- 0.18 vs 0.74 +/- 0.16; p < 0.05). Sensitivity of palpation (based on 356 segments) was 0.46; however, specificity was 0.96, predictive power of a negative palpation exam was 0.88, and overall accuracy of palpation was 0.86. Thirty of the 38 false negatives resulted from failure to detect 1+ disease. None of the 63 (71%) patients with a palpation score of zero required a technical modification or had a stroke. CONCLUSIONS: These data suggest that AAA may be more severe in older patients and smokers. Aortic palpation may not identify mild AAA. IEU can confirm and clearly define both the extent and distribution of suspected AAA and is useful for determining optimal operative strategy in patients with aortic disease.

Reactivity of human saphenous veins at arterial perfusion pressures.

Vasospasm of human saphenous vein grafts has been reported after aorta-coronary bypass operations. However, it is unknown whether veno-arterial grafts are inherently responsive to vasoconstrictor stimuli after implantation into the arterial circulation or whether their vasomotion is secondary to hemodynamic changes. Thus in this study we used in vitro methods to directly evaluate whether isolated human saphenous vein segments respond to vasoconstrictor agents at arterial pressure levels. External diameter and intraluminal flow were monitored in 12 human saphenous vein segments, which were perfused at 30 ml/min with physiologic salt solution at 90, 70, and 50 mm Hg. Increasing intraluminal pressure higher than 50 mm Hg or exposing the vein to Ca(2+)-free media did not increase vessel external diameter or intraluminal flow, which suggests that human saphenous veins were fully distended at pressures of 50 mm Hg or greater. However, all human saphenous veins were activated by a 1 mumol/L dose of norepinephrine at 50 mm Hg and dilated during subsequent intraluminal infusion of a 1 mumol/L dose of acetylcholine, showing intact vascular smooth muscle and endothelial cell function. In the same vessels, a 1 mumol/L concentration of 5-hydroxytryptamine constricted human saphenous veins by 19%, 22%, and 26% at intraluminal pressures of 90, 70, and 50 mm Hg, respectively, and reduced vessel flow by 6%, 24%, and 42% at the same pressure levels. Similarly, a 1 mumol/L concentration of norepinephrine constricted vessels pressurized at 90, 70, and 50 mm Hg by 9%, 12%, and 17%, respectively, and attenuated vessel flow by as much as 32%. We conclude that human saphenous vein segments are fully distended at perfusion pressures greater than 50 mm Hg, but can dynamically constrict to vasoactive agonists and regulate graft flow at intraluminal pressures as high as 90 mm Hg. Our findings in isolated human saphenous vein segments lend support to clinical observations that human saphenous vein grafts should be regarded as vasoactive conduits after implantation at arterial pressure levels.

Tolerance of the developing heart to ischemia: impact of hypoxemia from birth.

Many infants who require cardiac surgery have cyanotic heart disease. We assessed the relative tolerances to ischemia of hearts from immature normoxemic rabbits versus hearts from immature rabbits subjected to hypoxemia since birth. Normoxemic animals were raised from birth in an environment where the inspired fractional concentration of oxygen (FIO2) was 0.21; for the hypoxemic studies FIO2 was reduced to 0.09. Hearts (n = 6/group) from normoxemic and chronically hypoxemic rabbits at 7-12, 21-28, 35-44, and 51-56 days of age underwent aerobic "working" perfusion with Krebs bicarbonate buffer, and cardiac function was measured. Hearts were then arrested by a 3-min infusion with either cold (14 degrees C) Krebs buffer (hypothermia alone group) or St. Thomas' Hospital II solution (hypothermia plus cardioplegia group) before 6 h of hypothermic (14 degrees C) global ischemia. Hearts were reperfused, and postischemic creatine kinase leakage and recovery of function were measured. For hearts protected with hypothermia alone, recovery of aortic flow was better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (78 +/- 7 vs. 60 +/- 6%, P < 0.05) and 21-28 days old (81 +/- 12 vs. 26 +/- 28%, P < 0.05). Protection with hypothermia plus cardioplegia was also better in hearts hypoxemic from birth compared with normoxemic controls at 7-12 days (74 +/- 8 vs. 63 +/- 10%, P < 0.05) and 21-28 days old (84 +/- 3 vs. 71 +/- 5%, P < 0.05). Protection with hypothermia alone and hypothermia plus cardioplegia was no different within chronically hypoxemic age groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of saphenous vein graft relaxation between Plasma-Lyte solution and normal saline solution.

Venospasm of saphenous vein grafts may damage endothelial cells and compromise early and late graft performance. Hence it is desirable to identify and use storage solutions that minimize vascular spasm during vein preparation. In view of this, we initiated isometric tension-recording studies in isolated canine and human saphenous vein to evaluate the acute, vasoactive effects of two storage solutions, Plasma-Lyte solution and normal saline solution. In initial experiments, canine saphenous veins were mounted in tissue baths containing physiologic salt solution and tonically constricted by 2 x 10(-6) mol/L norepinephrine. The physiologic salt solution in the bath was then replaced by Plasma-Lyte solution or normal saline solution containing the same norepinephrine concentration, and changes in contraction amplitude were recorded for 90 minutes. Storage in Plasma-Lyte solution at 37 degrees C completely relaxed norepinephrine-activated canine saphenous vein within 20 minutes, whereas veins remained partially constricted in normal saline solution. Both Plasma-Lyte solution and normal saline solution relaxed canine saphenous vein less at room temperature (25 degrees C) than at 37 degrees C, implying that warming of storage solutions in the operating room may promote graft dilation. To identify the mechanism by which Plasma-Lyte solution induced relaxation, we replaced its putative vasodilator components of gluconate and acetate with NaCl, but this alteration did not reduce relaxation induced by Plasma-Lyte solution. However, adding 1.6 mmol/L CaCl2 to Plasma-Lyte solution completely reversed the venodilation, suggesting that the low Ca2+ content of Plasma-Lyte solution confers its relaxant action. Finally, we tested the vasoactive effect of Plasma-Lyte solution on human saphenous vein obtained by discard from coronary bypass operations. Plasma-Lyte solution at 37 degrees C effectively dilated norepinephrine-activated human saphenous vein, inducing complete relaxation within 20 minutes. On this basis, we recommend the use of Plasma-Lyte solution as a venodilating storage solution during coronary bypass operations to optimize vein graft relaxation before implantation.

Management of patients with intramural hematoma of the thoracic aorta.

BACKGROUND: Intramural hematoma of the thoracic aorta (IMH) is a diagnosis of exclusion and represents spontaneous, localized hemorrhage into the wall of the thoracic aorta in the absence of bona fide aortic dissection, intimal tear, or penetrating atherosclerotic ulcer. This process may arise from primary vasa vasorum hemorrhage within the aortic media or rupture of an atherosclerotic plaque. The clinical presentation of patients with IMH mimics that of acute aortic dissection; moreover, considerable diagnostic confusion exists despite the use of many different imaging modalities. The optimal mode of management of patients with IMH (medical versus medical plus surgical) remains problematic because of the paucity of information available. METHODS AND RESULTS: Thirteen patients with IMH were managed at two medical centers between 1983 and 1992. Patients with IMH caused by giant penetrating atherosclerotic ulcers were specifically excluded. There were 8 women and 5 men (mean age, 70 years [range, 54 to 82 years]). The admitting clinical diagnosis was acute aortic dissection, and all patients had a history of hypertension. There was no evidence of aortic dissection or intimal disruption as assessed by computed tomographic (CT) scan (n = 11), aortography (n = 10), magnetic resonance imaging (MRI) scan (n = 9), transesophageal echocardiography (TEE) (n = 6), or intravascular ultrasound (n = 1). The diagnosis of IMH was established by exclusion. The descending thoracic aorta was involved in 10 cases and the ascending/arch in 3. Conservative medical management was attempted initially. All 3 patients with IMH involving the ascending aorta ultimately required operative intervention, and 2 individuals died; 2 of 10 patients with descending aortic involvement eventually underwent surgery. Average hospital stay was 11 days; the mean follow-up interval for discharged patients was 29 months. CONCLUSIONS: IMH is a distinct pathological entity, should not be confused with aortic dissection, and probably will be identified more frequently in the future. All patients with IMH should be monitored carefully and treated with aggressive antihypertensive therapy. Frequent serial assessment is necessary using TEE or MRI/CT scans. Based on this small experience, patients with ascending/arch IMH, ongoing pain, or IMH expansion should probably undergo early graft replacement. Patients with IMH involving the descending thoracic aorta who have no evidence of progression and become pain free can probably be treated conservatively but require antihypertensive therapy and serial aortic imaging surveillance indefinitely.

Validity of cardiac output measurement by the thermodilution method in the presence of acute tricuspid regurgitation.

Evaluation of patients with acute tricuspid insufficiency may include assessment of cardiac output by the thermodilution method. The accuracy of estimates of thermodilution-derived cardiac output in the presence of tricuspid insufficiency has been questioned. This study was designed to determine the validity of the thermodilution technique in a canine model of acute reversible tricuspid insufficiency. Cardiac output as measured by thermodilution and electromagnetic flowmeter was compared at two grades of regurgitation. The relationship between these two methods (thermodilution/electromagnetic) changed significantly from a regression slope of 1.01 +/- 0.18 (mean +/- standard deviation) during control conditions to a slope of 0.86 +/- 0.23 (p < 0.02) during severe regurgitation. No significant change was observed between control and mild regurgitation or between the initial control value and a control measurement repeated after tricuspid insufficiency was reversed at the termination of the study. This study shows that in a canine model of severe acute tricuspid regurgitation the thermodilution method underestimates cardiac output by an amount that is proportional to the level of cardiac output and to the grade of regurgitation.