Effect of prostacyclin on vascular capacity in the dog.

Since the discovery of prostacyclin (PGI2) in 1976, there has been great interest in its vascular effects and potential clinical applications. High infusion rates of PGI2 markedly depress arterial blood pressure both in animal studies and in clinical trials. This fall in pressure may result entirely from a decrease in arterial resistance. However, it is possible that the administration of PGI2 may decrease ventricular filling due to an increase in vascular capacity. To investigate whether or not PGI2 affects vascular capacity, we infused PGI2 intraarterially at both 10 and 25 micrograms/min into 15 dogs on total cardiopulmonary bypass. These infusions were associated with a 25 +/- 3 mmHg decrease in arterial pressure and an increase in vascular capacity of 155 +/- 29 ml (SE, P less than 0.005). This increase in capacity was greater (P less than 0.02) than the increase of 23 +/- 42 ml resulting from infusions of nitroglycerin into eight dogs at 2 mg/min, which produced a decrease in arterial pressure of 23 +/- 4 mmHg, which was the maximal effect that could be achieved. Neither bilateral cervical vagotomy nor beta adrenergic blockade with propranolol significantly diminished the increase in vascular capacity associated with infusions of PGI2. The results from studies in four eviscerated dogs indicated that PGI2 acts on both splanchnic and extrasplanchnic capacity vasculature. To compare the direct effects of PGI2 with those of nitroglycerin and nitroprusside on venous tone, we used an isolated canine spleen preparation. Infusions of PGI2 (100 mcg/min) increased spleen weight in this preparation by 9.0 +/- 2.4% (n = 10, P less than 0.001); this increase was significantly greater than increases of 3.6 +/- 2.2% (P less than 0.001) and 3.5 +/- 2.3% (P less than 0.001) caused by high dose infusions of nitroglycerin (1 mg/min) and nitroprusside (400 micrograms/min), respectively. Thus, PGI2 substantially increases vascular capacity by a mechanism that appears to involve a direct action on vascular smooth muscle. Furthermore, these results suggest that PGI2 might be useful in clinical conditions in which an increase in vascular capacity is indicated.

Prevalence and prognostic significance of atrial arrhythmias after orthotopic cardiac transplantation.

OBJECTIVES: We studied the duration and prognostic significance of atrial arrhythmias in the denervated transplanted heart, specifically the occurrence of atrial fibrillation in the absence of vagal modulation. BACKGROUND: Substantial animal data indicate that vagally induced dispersion of atrial refractoriness plays a central role in the induction and maintenance of atrial fibrillation. METHODS: We studied the occurrence of atrial arrhythmias in the denervated hearts of 88 consecutive orthotopic transplantations in 85 patients by means of continuous telemetry and all available electrocardiographic tracings. RESULTS: Fifty percent of recipients (44 of 88) developed at least one atrial arrhythmia. Atrial fibrillation occurred 23 times (21 recipients), atrial flutter 39 times (26 recipients), ectopic atrial tachycardia 3 times (3 recipients) and supraventricular tachycardia 18 times (11 recipients). The number of atrial fibrillation and atrial flutter episodes did not differ (23 vs. 39, p = 0.072), but the mean duration of atrial flutter was longer than that of atrial fibrillation (37.0 +/- 10 vs. 6.6 +/- 3.6 h, p = 0.014). Atrial fibrillation was associated with an increased risk of subsequent death (10 of 21 recipients with vs. 15 of 67 without atrial fibrillation, risk ratio 3.15 +/- 0.18, p = 0.005 by Cox proportional hazards model). All 5 recipients who developed "late" atrial fibrillation (> 2 weeks after transplantation) died versus 5 of 16 who developed atrial fibrillation within the first 2 weeks (p = 0.007). Causes of death included rejection (three recipients), allograft failure (two recipients), infection (three recipients) and multiorgan failure (two recipients). Atrial fibrillation was not associated with age, gender, ischemic time, reason for transplantation, echocardiographic variables, invasive hemodynamic variables or biopsy grade. Mean time from atrial arrhythmia to echocardiography was 2.7 +/- 3.3 days; that to biopsy was 4.8 +/- 6.3 days. Atrial flutter was not associated with subsequent death. Only 7 (15.9%) of 44 recipients demonstrated moderate or severe allograft rejection at the time of the arrhythmia. CONCLUSIONS: Atrial arrhythmias occur frequently in the denervated transplanted heart, often in the absence of significant rejection. Late atrial fibrillation may be associated with an increased all-cause mortality.

Quantitative relation between increased intrapericardial pressure and Doppler flow velocities during experimental cardiac tamponade.

To establish whether a quantitative relation exists between pericardial pressure and respiratory variation in intracardiac blood flow velocities, a spontaneously breathing closed chest canine model of pericardial tamponade was created. In seven dogs, pericardial pressure was sequentially increased in stages from a mean of -4 +/- 1 to 10 +/- 2 mm Hg while aortic and pulmonary Doppler flow velocities, pleural pressure changes (respiratory effort), blood pressure and cardiac output were measured. The variation in the Doppler-detected peak transaortic velocity (AV) during inspiration (IV) increased linearly from -5 +/- 3% at baseline (pericardial pressure -4 mm Hg) to -32 +/- 9% at a pericardial pressure of 10 mm Hg [IVAV = -2 (pericardial pressure)--13.1; r = 0.78, p less than 10(-6)]. The inspiratory variation in the peak transpulmonary velocity increased from 13 +/- 3% at baseline to 71 +/- 19% at a pericardial pressure of 10 mm Hg. The inspiratory variation in the pulmonary Doppler peak velocity (IVPV) was dependent on both pericardial pressure and degree of respiratory effort [IVPV = 3.8 (pericardial pressure) + 2.6 (respiratory effort) + 10.9; r = 0.88, p less than 10(-8)]. Thus, quantitative relations exist between increases in intrapericardial pressure and increases in inspiratory variation of peak aortic and pulmonary flow velocities. Additionally, pulmonary artery flow velocity is influenced more than aortic velocity by intrathoracic pressure.

Reconsideration of echocardiographic standards for mitral valve prolapse: lack of association between leaflet displacement isolated to the apical four chamber view and independent echocardiographic evidence of abnormality.

Mitral valve prolapse by current echocardiographic criteria can be diagnosed with surprising frequency in the general population, even when preselected normal subjects are examined. In most of these individuals, however, prolapse is present in the apical four chamber view and absent in roughly perpendicular long-axis views. Previous studies have shown that systolic annular nonplanarity can cause apparent prolapse in the four chamber view without actual leaflet displacement above the most superior points of the anulus, and there is evidence for such nonplanarity in vivo. It is then reasonable to ask whether superior leaflet displacement limited to the four chamber view has any pathologic significance or complications. The purpose of this study, therefore, was to address the following hypothesis: that patients with superior leaflet displacement confined to the four chamber view have no higher frequency of associated echocardiographic abnormalities than do patients without displacement in any view. Such abnormalities, which would provide independent evidence of mitral valve pathology or dysfunction, include leaflet thickening, left atrial enlargement and mitral regurgitation. Leaflet displacement was measured in the parasternal long-axis and apical four chamber views in 312 patients who were studied retrospectively and selected for the absence of forms of heart disease other than mitral valve prolapse. Leaflet thickness and left atrial size were measured and mitral regurgitation was graded. Patients with leaflet displacement limited to the four chamber view were no more likely to have associated abnormalities than were patients without displacement in any view (0 to 2% prevalence, p greater than 0.5). In contrast, patients with leaflet displacement in the long-axis view were significantly more likely to have associated abnormalities (12 to 24%, p less than 0.005), the frequency of which increased with the extent of leaflet displacement in that view (p less than 0.0001). These results suggest that displacement limited to the apical four chamber view is, in general, a normal geometric finding unassociated with echocardiographic evidence of pathologic significance.

Regional variability in the myocardial clearance of thallium-201 and its importance in determining the presence or absence of coronary artery disease.

There are several limitations in using absolute myocardial clearance of thallium-201 for the detection of coronary artery disease. Noncardiac factors such as peak exercise heart rate and blood level of thallium can affect its absolute myocardial clearance. However, because all myocardial segments in a given heart are exposed to the same noncardiac factors, a relative difference in myocardial clearance of thallium between segments could reflect the presence of coronary artery disease. Accordingly, myocardial clearance of thallium was analyzed in 370 patients. Patients in Group I (n = 45) had less than 1% probability of having coronary artery disease, patients in Group II (n = 44) had normal coronary arteries and patients in Group III (n = 281) had coronary artery disease. Although mean myocardial clearance of thallium in 15 myocardial segments in three views in Group I subjects was 3.4 +/- 0.7 hours, the variability between the slowest and fastest clearing segments in the same subject was as much as 98%. This variability was systematic, suggesting technical reasons associated with imaging as the cause of the variability: 78% of the slowest clearing segments were basal whereas 53% of the fastest clearing segments were apical (p less than 0.01). When Group II and III patients were compared based on Group I values, the absolute myocardial clearance of thallium had a sensitivity and specificity of 92 and 16%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Contrast echocardiography in acute myocardial ischemia. III. An in vivo comparison of the extent of abnormal wall motion with the area at risk for necrosis.

To define the in vivo relation between abnormal wall motion and the area at risk for necrosis after acute coronary occlusion, 11 open chest dogs were studied. Five dogs underwent left anterior descending coronary artery occlusion and six underwent left circumflex artery occlusion. Area at risk was defined at five short-axis levels (mitral valve, chordal, high and low papillary muscle and apex) using myocardial contrast echocardiography. Wall motion was measured in the cycles preceding injection of contrast medium. Two observers used two different methods to measure wall motion. In method A, end-diastolic to end-systolic fractional radial change for each of 32 endocardial targets was determined. The extent of abnormal wall motion was then calculated using three definitions of wall motion abnormality: akinesia/dyskinesia, fractional inward endocardial excursion of less than 10%, and fractional inward endocardial excursion of less than 20%. In method B, the information from the entire systolic contraction sequence was analyzed and correlated with a normal contraction pattern. The best linear correlation between area at risk (AR) and abnormal wall motion (AWM) was achieved using method B and expressed by the following linear regression: AWM = 0.92 AR + 3.0 (r = 0.92, p less than 0.0001, SEE = 1.7%). Of the three definitions of abnormality used in method A, the best correlation was achieved between area at risk and less than 10% inward endocardial excursion and was expressed by the following polynomial regression: AWM = -0.01 AR2 + 1.5 AR -0.14 (r = 0.92, p less than 0.001, SEE = 1.7%). These data demonstrate that there is a definite relation between area at risk and abnormal wall motion but that this relation varies depending on the method used to analyze wall motion. However, wall motion during acute ischemia is also influenced by the loading conditions of the heart. Because these may vary in a manner that is independent of the ischemic process, measurement of both risk area and abnormal motion may provide a more comprehensive assessment of cardiac function in myocardial ischemia than is provided by the measurement of either alone.

Prevalence and timing of regional myocardial dysfunction after rotational coronary atherectomy.

OBJECTIVES: This study aimed to evaluate the prevalence and time course of wall motion abnormalities associated with rotational coronary atherectomy. BACKGROUND: Although initial clinical studies found evidence of transient wall motion abnormalities after rotational coronary atherectomy, the prevalence and duration of these wall motion abnormalities are unknown. METHODS: Using simultaneous echocardiography, we prospectively evaluated 22 patients undergoing rotational atherectomy and compared their wall motion abnormalities with those of 10 patients undergoing coronary angioplasty alone. The extent of wall motion abnormality was quantified and plotted against time to produce curves of abnormal wall motion development and recovery for the two groups. RESULTS: The cumulative ischemic time was similar for the two groups ([mean +/- SD] 10.3 +/- 6 min for rotational atherectomy vs. 9.6 +/- 4.2 min for coronary angioplasty, p = 0.73). The rate of return to baseline function was significantly lower in the rotational atherectomy group than in the coronary angioplasty group (rotational atherectomy rate constant 0.069 +/- 0.079/min vs. coronary angioplasty rate constant 1.250 +/- 0.47/min, p = 0.0001). The mean time to recovery of baseline wall motion in the rotational atherectomy group (153 min, 95% confidence interval [CI] 6.5 to 3,600) was significantly longer than in the coronary angioplasty group (2.6 min, 95% CI 1.3 to 5.5, p = 0.0001). Rotational atherectomy burr time was longer in the patients who developed myocardial infarction than in those without myocardial infarction (4.7 +/- 2.4 vs. 3 +/- 1.4 min, p = 0.045). CONCLUSIONS: Transient wall motion abnormalities are common after rotational coronary atherectomy and have a longer duration than those observed after coronary angioplasty. This disparity may be a consequence of differences in the mechanisms by which rotational coronary atherectomy and coronary angioplasty produce their effect.

Functional relation between infarct thickness and regional systolic function in the acutely and subacutely infarcted canine left ventricle.

Specific information regarding the relation between infarct thickness and regional systolic function is important to the overall understanding of both the pathophysiology of acute and subacute myocardial infarction and the functional benefits of myocardial salvage interventions designed to limit the transmural extent of infarction and thereby preserve left ventricular function. In the present study, quantitative computer-assisted two-dimensional echocardiography was used to define the relation between infarct thickness and systolic function in the acutely and subacutely infarcted canine left ventricle. Echocardiograms were obtained at the mid-papillary muscle level at baseline and 6 h after occlusion (acute infarction) in eight animals and at baseline and 72 h after occlusion (subacute infarction) in nine animals. Systolic function was assessed by measuring the extent of fractional radial shortening along each of 36 evenly spaced endocardial targets from end-diastole to end-systole; the transmural extent of infarction was determined from the triphenyltetrazolium chloride-staining deficit at 6 and 72 h. The relation between systolic function and transmural extent of infarction was analyzed in two ways. First, the extent of fractional radial shortening in each group was examined as a function of quartile (25%) increments in transmural infarct thickness. This analysis revealed 1) a significant overall loss of fractional radial shortening with increasing transmural extent of infarction in both groups; and 2) significant differences in the extent of systolic dysfunction between successive quartile increments of infarction. Second, the relation between infarct thickness and systolic dysfunction was modeled mathematically by fitting the data from each infarct series to linear, logarithmic and exponential functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Percutaneous mitral balloon valvotomy in patients with calcific mitral stenosis: immediate and long-term outcome.

OBJECTIVES: This study analyzed the immediate and long-term outcome of percutaneous balloon mitral valvotomy in patients with and without fluoroscopically visible mitral valve calcification. BACKGROUND: Mitral valve calcification has been shown to be an important factor in determining immediate and long-term outcome of patients undergoing surgical mitral commissurotomy. Patient selection has an important impact on the outcome of percutaneous balloon mitral valvotomy. METHODS: The immediate and long-term results of percutaneous balloon mitral valvotomy were compared in 155 patients with and 173 patients without mitral valve calcification. The patients with calcified valves were assigned to four groups according to severity of calcification. RESULTS: Patients with calcified mitral stenosis more frequently were in New York Heart Association functional class III or IV and more frequently had atrial fibrillation, previous surgical commissurotomy, echocardiographic score > 8, higher pulmonary artery and left atrial pressures, higher pulmonary vascular resistance and mean mitral valve gradient and lower cardiac output and smaller mitral valve area. Mitral valve area after valvotomy was significantly smaller in patients with calcified valves (1.8 +/- 0.06 vs. 2.1 +/- 0.06 cm2) and was > or = 1.5 cm2 in 65% of patients with and 83% of patients without calcified valves (p = 0.004). A successful outcome, defined as mitral valve area > 1.5 cm2 without significant mitral regurgitation and left to right shunting, was achieved in 52% of patients with and 69% of patients without uncalcified valves (p = 0.001). The success rate was 59%, 48%, 35% and 33% in subgroups with 1+, 2+, 3+ and 4+ calcification, respectively. The rates of significant left to right shunting and mitral regurgitation after valvuloplasty were similar in the two groups. Estimated survival rate (80% vs. 99%, respectively, p = 0.0001), survival rate without mitral valve replacement (67% vs. 93%, respectively, p < 0.00005) and event-free survival rate (63% vs. 88%, respectively, p < 0.00005) at 2 years were significantly better in the patients with uncalcified valves. Survival rate curves became progressively worse as the severity of calcification increased. CONCLUSIONS: These findings indicate that immediate and long-term results of mitral valvuloplasty are not as successful in patients with fluoroscopically visible mitral valve calcification as in those without calcification.

The role of percutaneous aortic balloon valvuloplasty in patients with cardiogenic shock and critical aortic stenosis.

OBJECTIVES: The goal of this study was to evaluate the role of percutaneous aortic valvuloplasty in patients with cardiogenic shock due to severe aortic stenosis and associated major comorbid conditions and to establish predictors of survival. BACKGROUND: The prognosis for patients in cardiogenic shock with severe aortic stenosis is poor. Aortic valve replacement can be lifesaving, but the presence of multiorgan failure precludes these patients from operation. Percutaneous aortic balloon valvuloplasty has been used in these patients with short-term improvement and could be an alternative therapeutic option. METHODS: Of 310 patients undergoing percutaneous aortic balloon valvuloplasty, 21 were in cardiogenic shock and were included in this study. All 21 patients had associated major comorbid conditions at the time of presentation. RESULTS: After percutaneous aortic balloon valvuloplasty, systolic aortic pressure increased from 77 +/- 3 (mean +/- SEM) to 116 +/- 8 mm Hg (p = 0.0001); aortic valve area increased from 0.48 +/- 0.04 to 0.84 +/- 0.06 cm2 (p = 0.0001); and cardiac index increased from 1.84 +/- 0.13 to 2.24 +/- 0.15 liters/min per m2 (p = 0.06). Nine patients died in the hospital, two during the procedure and seven after successful percutaneous aortic balloon valvuloplasty (five from multiorgan failure). Five patients had vascular complications. Stroke, cholesterol emboli and aortic regurgitation requiring aortic valve replacement occurred in one patient each. Twelve patients (57%) survived and were followed up for 15 +/- 6 months; five patients subsequently died. The Kaplan-Meier survival curve showed a 38 +/- 11% survival rate at 27 months. The only predictor for longer survival rate was the postprocedure cardiac index. CONCLUSIONS: 1) Emergency percutaneous aortic balloon valvuloplasty can be performed successfully as a lifesaving procedure. 2) Morbidity and mortality remain high despite successful percutaneous aortic balloon valvuloplasty. 3) For nonsurgical candidates, percutaneous aortic balloon valvuloplasty may be the only therapeutic alternative.

Evidence for a rebound coagulation phenomenon after cessation of a 4-hour infusion of a specific thrombin inhibitor in patients with unstable angina pectoris.

OBJECTIVES: In a Phase I clinical trial, we studied the antithrombotic and clinical effects of the synthetic competitive thrombin inhibitor, argatroban, in 43 patients with unstable angina pectoris. BACKGROUND: Thrombin has a pivotal role in platelet-mediated thrombosis associated with atheromatous plaque rupture in patients with an acute ischemic coronary syndrome. However, the efficacy of conventional heparin therapy to prevent ischemic events is limited and has been surpassed by that of specific thrombin inhibitors in experimental models of arterial thrombosis. METHODS: Intravenous infusion of the drug (0.5 to 5.0 micrograms/kg per min) for 4 h was monitored by sequential measurements of coagulation times and of indexes of thrombin activity in vivo followed by a 24-h clinical observation period. RESULTS: Significant dose-related increases in plasma drug concentrations and activated partial thromboplastin times (aPTT), but no bleeding time prolongation or spontaneous bleeding, was observed. Myocardial ischemia did not occur during therapy but, surprisingly, 9 of the 43 patients experienced an episode of unstable angina 5.8 +/- 2.6 h (mean +/- SD) after infusion. This early recurrent angina was correlated significantly with a higher argatroban dose and with greater prolongation of aPTT but not with other demographic, clinical, laboratory and angiographic characteristics. Pretreatment plasma concentrations of thrombin-antithrombin III complex and fibrinopeptide A were elevated two to three times above normal values. During infusion, thrombin-antithrombin III complex levels remained unchanged, whereas a significant 2.3-fold decrease in fibrinopeptide A concentrations was observed. By contrast, 2 h after infusion, thrombin-antithrombin III complex concentrations increased 3.9-fold over baseline measurements together with return of fibrinopeptide A levels to values before treatment with argatroban. CONCLUSIONS: In patients with unstable angina, argatroban inhibits clotting (aPTT prolongation) and thrombin activity toward fibrinogen (fibrinopeptide A decrease), but in vivo thrombin (thrombin-antithrombin III complex) formation is not suppressed. However, cessation of infusion is associated with rebound thrombin (thrombin-antithrombin III complex) generation and with an early dose-related recurrence of unstable angina. Although the mechanism of this clinical and biochemical rebound phenomenon remains to be determined, its implication for the clinical use of specific thrombin inhibitors in the management of ischemic coronary syndromes may be significant.

Echocardiography can predict which patients will develop severe mitral regurgitation after percutaneous mitral valvulotomy.

OBJECTIVES: Using two-dimensional echocardiography, we sought to identify features that are associated with severe mitral regurgitation after percutaneous mitral valvulotomy and combine them into a predictive score. BACKGROUND: Severe mitral regurgitation after percutaneous mitral valvulotomy is a major complication carrying an adverse prognosis that, to date, has not been predictable in advance. METHODS: In a consecutive series of 566 patients who underwent percutaneous mitral valvulotomy, 37 (6.5%) developed severe mitral regurgitation (assessed by angiography) after the procedure, 31 of whom had an echocardiogram available before percutaneous mitral valvulotomy. These 31 patients were matched by age, gender, mitral valve area and degree of mitral regurgitation before valvulotomy with 31 randomly selected patients who did not develop severe mitral regurgitation after percutaneous mitral valvulotomy. An echocardiographic score was developed on the basis of the pathologic studies of valves of patients who developed severe regurgitation after percutaneous mitral valvulotomy (leaflet rupture of relatively thin portions of nonhomogeneously thickened leaflets in the presence of commissural and subvalvular calcification) and evaluated uneven distribution of thickness in the anterior and posterior mitral leaflets, degree of commissural disease and subvalvular disease involvement, with each component graded from 0 to 4 (total, 0 to 16). Intraobserver and interobserver variability for score assessment were 6% and 7%, respectively. RESULTS: The total mitral regurgitation echocardiographic score was significantly greater in the severe mitral regurgitation group (11.7 +/- 1.9 [mean +/- SD] vs. 8.0 +/- 1.2, p < 0.001). In addition, the component grades for the anterior leaflet (3.2 +/- 0.7 vs. 2.3 +/- 0.6, p < 0.001), commissures (2.6 +/- 0.7 vs. 1.6 +/- 0.6, p < 0.001) and subvalvular apparatus (3.2 +/- 0.6 vs. 2.3 +/- 0.7, p < 0.001) were also higher in the mitral regurgitation group. With a total score > or = 10 as a cutoff point for predicting severe mitral regurgitation after percutaneous mitral valvulotomy, a sensitivity of 90 +/- 5% and a specificity of 97 +/- 3% were obtained. Stepwise logistic regression analysis identified the mitral regurgitation echocardiographic score as the only independent predictor for developing severe mitral regurgitation after percutaneous mitral valvulotomy (p < 0.0001). CONCLUSIONS: This new mitral regurgitation echocardiographic score can predict the development of severe mitral regurgitation after percutaneous mitral valvulotomy and can be useful in the selection of patients for this technique.

Significant tricuspid regurgitation is a marker for adverse outcome in patients undergoing percutaneous balloon mitral valvuloplasty.

OBJECTIVES: This study examined the association between the presence of tricuspid regurgitation and immediate and late adverse outcomes in patients undergoing balloon mitral valvuloplasty. BACKGROUND: Significant tricuspid regurgitation has an adverse impact on morbidity and mortality in patients undergoing mitral valve surgery for mitral stenosis. METHODS: We studied 318 consecutive patients (mean [+/- SD] age 54 +/- 15 years) who underwent balloon mitral valvuloplasty and had color Doppler echocardiographic studies before the procedure. Patients were classified into three groups: 221 with no or mild (69%), 60 with moderate (19%) and 37 with severe (12%) tricuspid regurgitation. Clinical follow-up ranged from 6 to 62 months. RESULTS: Before mitral valvuloplasty, increasing degrees of tricuspid regurgitation were associated with a smaller initial mitral valve area (p < 0.05), higher echocardiographic score (p < 0.05), lower cardiac output (p < 0.01) and higher pulmonary vascular resistance (p < 0.01). Although the initial success rate did not differ significantly between groups, patients with a higher degree of tricuspid regurgitation had less optimal results, as reflected by a smaller absolute increase in mitral valve area (1.02 vs. 0.9 vs. 0.7 cm2, p < 0.01). The estimated 4-year event-free survival rate (freedom from death, mitral valve surgery, repeat valvuloplasty and heart failure) was lower for the group with severe tricuspid regurgitation (68% vs. 58% vs. 35%, p < 0.0001). At 4 years, 94% of patients with mild tricuspid regurgitation were alive compared with 90% and 69%, respectively, of patients with moderate or severe tricuspid regurgitation (p < 0.0001). Cox proportional analysis identified tricuspid regurgitation as an independent predictor of late outcome (p < 0.001). CONCLUSIONS: Patients with mitral stenosis and severe tricuspid regurgitation undergoing mitral valvuloplasty have advanced mitral valve and pulmonary vascular disease, suboptimal immediate results and poor late outcome.

Echocardiographic assessment of patients with infectious endocarditis: prediction of risk for complications.

To enhance the echocardiographic identification of high risk lesions in patients with infectious endocarditis, the medical records and two-dimensional echocardiograms of 204 patients with this condition were analyzed. The occurrence of specific clinical complications was recorded and vegetations were assessed with respect to predetermined morphologic characteristics. The overall complication rates were roughly equivalent for patients with mitral (53%), aortic (62%), tricuspid (77%) and prosthetic valve (61%) vegetations, as well as for those with nonspecific valvular changes but no discrete vegetations (57%), although the distribution of specific complications varied considerably among these groups. There were significantly fewer complications in patients without discernible valvular abnormalities (27%). In native left-sided valve endocarditis, vegetation size, extent, mobility and consistency were all found to be significant univariate predictors of complications. In multivariate analysis, vegetation size, extent and mobility emerged as optimal predictors and an echocardiographic score based on these factors predicted the occurrence of complications with 70% sensitivity and 92% specificity in mitral valve endocarditis and with 76% sensitivity and 62% specificity in aortic valve endocarditis.

Quantitative analysis of dipyridamole-thallium images for the detection of coronary artery disease.

To determine if the detection of coronary artery disease by dipyridamole-thallium imaging is improved by quantitative versus qualitative analysis, and combining quantitative variables, 80 patients with chest pain (53 with and 27 without coronary artery disease) who underwent cardiac catheterization were studied. Segmental thallium initial uptake, linear clearance, monoexponential clearance and redistribution were measured from early, intermediate and delayed images acquired in three projections. Normal values were determined from 13 other clinically normal subjects. When five segments per view were used for quantitative analysis, sensitivity and specificity were 87 and 63%, respectively, for uptake, 77 and 67% for linear clearance, 60 and 60% for monoexponential clearance and 62 and 56% for redistribution. Of the four variables, uptake and linear clearance were the most sensitive (p less than 0.01) and specificity did not differ significantly. Using three segments per view, the specificity of uptake increased (p less than 0.05) to 78% without a significant change in sensitivity (85%). With this approach, sensitivity and specificity did not differ from those of qualitative analysis (85 and 78%, respectively). Stepwise logistic regression analysis demonstrated that the best quantitative thallium correlate of the presence of coronary artery disease was a combination variable of "either abnormal uptake or abnormal linear clearance, or both." Using five segments per view, the model's specificity (85%) was greater than that of uptake alone (p less than 0.02), with similar sensitivity (92%). Using three segments per view, the model's specificity (93%) was greater than that of uptake alone (p less than 0.05) and of qualitative analysis (p less than 0.05), with similar sensitivity (85%).(ABSTRACT TRUNCATED AT 250 WORDS)

Determination of the quantitative thallium imaging variables that optimize detection of coronary artery disease.

Although quantification of exercise thallium images has been previously reported, the relative value of different imaging variables for detection of coronary artery disease has not been analyzed in a large group of patients with cardiac catheterization data. Regional initial thallium uptake, redistribution and clearance on thallium study were measured in 325 patients also undergoing cardiac catheterization (281 patients with and 44 patients without coronary artery disease). Normal values were defined in 55 other clinically normal subjects. When five myocardial segments were analyzed in each view, the respective values for sensitivity and specificity were 95 and 50% for initial thallium uptake, 60 and 87% for redistribution and 74 and 66% for clearance. Initial thallium uptake was the most sensitive but least specific (p less than 0.001), whereas redistribution was the least sensitive and most specific (p less than 0.001). Using stepwise logistic regression analysis, the best correlate of coronary artery disease was initial thallium uptake. Addition of redistribution to a mathematical model of the probability of coronary artery disease did not alter sensitivity, but increased specificity from 50 to 70% (p less than 0.001). Once initial uptake and redistribution were considered, myocardial thallium clearance provided no additional improvement in the correlation. Excluding the two basal segments in each view from the analysis increased the specificity from 70 to 80% (p less than 0.001) without affecting sensitivity. Of the 15 patients (5%) with coronary disease not detected using this approach, none had left main disease and 10 (67%) had one vessel disease. A combination of variables derived from quantification of exercise thallium images provides a superior sensitivity and specificity for the detection of coronary artery disease compared with the use of a single variable.

Prognostic value of exercise thallium-201 imaging in patients presenting for evaluation of chest pain.

Accurate prognostic information is important in determining optimal management of patients presenting for evaluation of chest pain. In this study, the ability of exercise thallium-201 myocardial imaging to predict future cardiac events (cardiovascular death or nonfatal myocardial infarction) was correlated with clinical, coronary and left ventricular angiographic and exercise electrocardiographic data in 139 consecutive, nonsurgically managed patients followed-up over a 3 to 5 year period (mean follow-up, 3.7 +/- 0.9), using a logistic regression analysis. Among patients without prior myocardial infarction (100 of 139), the number of myocardial segments with transient thallium-201 defects was the only statistically significant predictor of future cardiac events when all patient variables were evaluated. Among patients with myocardial infarction before evaluation (39 of 139), angiographic ejection fraction was the only significant predictor of future cardiac events when all variables were considered. This study suggests an approach to evaluate the risk of future cardiac events in patients with possible ischemic heart disease.

Quantitation of acute myocardial infarct size by nuclear magnetic resonance imaging.

Nuclear magnetic resonance (NMR) imaging has shown potential in the detection and characterization of acute myocardial infarction in humans. This study was performed to evaluate the capability of NMR imaging in the measurement of infarct size in patients with recent myocardial infarction. Electrocardiographic (ECG)-gated spin-echo NMR imaging was performed in 26 patients a mean of 9 +/- 3 days (range 5 to 20) after infarction. The imaging technique used provided single-slice, spin-echo (time to echo [TE] = 60 ms) images of the left ventricle in its true short axis, allowing direct correlation of NMR infarct location and size with the region of severe hypokinesia on left ventriculography. In all 20 patients with complete NMR studies, infarct location was correctly identified by using specific, objective criteria. The correlation between the mean infarct volume (29 +/- 11 ml) and the quantitated left ventricular hypokinetic segment (7.5 +/- 4.0 cm) was good (r = 0.84, p = 0.0002), suggesting that NMR imaging of the heart may have a role in the noninvasive assessment of myocardial infarct size in patients.

Evolution of the temporal contraction sequence after acute experimental myocardial infarction.

The effect of infarct maturation on the temporal sequence of contraction within infarct zones has not previously been described. Accordingly, the time-varying pattern of contraction within ischemic/infarct zones was studied with use of cross-sectional echocardiography in 17 dogs at 10 min to 6 weeks after acute experimental myocardial infarction. Left ventricular short-axis images were digitized from end-diastole to end-systole and endocardial fractional radial change along 36 evenly spaced rays was calculated. The circumferential extent of dyskinesia and the number of rays that exhibited maximal dyskinesia were determined for each decile of the normalized contraction sequence. Between 10 min and 1 week after infarction, the greatest circumferential extent of dyskinesia occurred between the 3rd and 4th deciles of the normalized contraction sequence. However, as the infarct matured, the greatest spatial expanse of dyskinesia was noted to occur progressively earlier in the contraction sequence (second decile at 6 weeks), and the extent of mid- to late-systolic dyskinesia decreased markedly. Whereas end-systolic dyskinesia was present in 30% to 50% of ischemic/infarct zone rays from 10 min to 48 h, end-systolic dyskinesia was no longer observed at 6 weeks. Similarly, the maximal amplitude of dyskinesia was most commonly observed during midsystole from 10 min to 48 h, but occurred progressively earlier as the infarct matured, falling during the first decile at 6 weeks after infarction. These data suggest that maximal circumferential extent and amplitude of dyskinesia occur progressively earlier in the systolic contraction sequence as the infarct matures.(ABSTRACT TRUNCATED AT 250 WORDS)

Classification of mouse VK groups based on the partial amino acid sequence to the first invariant tryptophan: impact of 14 new sequences from IgG myeloma proteins.

Fourteen new VK sequences derived from BALB/c IgG myeloma proteins were determined to the first invariant tryptophan (Trp 35). These partial sequences were compared with 65 other published VK sequences using a computer program. The 79 sequences were organized according to the length of the sequence from the amino terminus to the first invariant tryptophan (Trp 35), into seven groups (33, 34, 35, 36, 39, 40 and 41aa). A distance matrix of all 79 sequences was then computed, i.e. the number of amino acid substitutions necessary to convert one sequence to another was determined. From these data a dendrogram was constructed. Most of the VK sequences fell into clusters or closely related groups. The definition of a sequence group is arbitrary but facilitates the classification of VK proteins. We used 12 substitutions as the basis for defining a sequence group based on the known number of substitutions that are found in the VK21 proteins. By this criterion there were 18 groups in the Trp 35 dendrogram. Twelve of the 14 new sequences fell into one of these sequence groups; two formed new sequence groups. Collective amino acid sequencing is still encountering new VK structures indicating more sequences will be required to attain an accurate estimate of the total number of VK groups. Updated dendrograms can be quickly generated to include newly generated sequences.