A second locus for Marfan syndrome maps to chromosome 3p24.2-p25.

Marfan syndrome (MFS) is an autosomal dominant connective-tissue disorder characterized by skeletal, ocular and cardiovascular defects of highly variable expressivity. The diagnosis relies solely on clinical criteria requiring anomalies in at least two systems. By excluding the chromosome 15 disease locus, fibrillin 1 (FBN1), in a large French family with typical cardiovascular and skeletal anomalies, we raised the issue of genetic heterogeneity in MFS and the implication of a second locus (MFS2). Linkage analyses, performed in this family, have localized MFS2 to a region of 9 centiMorgans between D3S1293 and D3S1283, at 3p24.2-p25. In this region, the highest lod score was found with D3S2336, of 4.89 (theta = 0.05). By LINKMAP analyses, the most probable position for the second locus in MFS was at D3S2335.

Central pulse pressure is a major determinant of ascending aorta dilation in Marfan syndrome.

BACKGROUND: In patients with Marfan syndrome (MFS), brachial pulse pressure (PP) has been recognized as a risk factor for aortic dilatation, leading to aortic dissection, the main cause of premature death. However, the relationships between aortic PP, aortic stiffness, and aortic root dilation have not been investigated. Our main objective was to determine whether central PP, which takes into account wave reflections and aortic stiffness, is a better determinant of ascending aorta diameter than brachial PP in MFS patients. METHODS AND RESULTS: Twenty patients with confirmed MFS and 20 age- and sex-matched control subjects were included in this cross-sectional, noninvasive study. Elastic properties of the abdominal aorta and common carotid, common femoral, and radial arteries were calculated from the pulsatile changes in arterial diameter and pressure. The ascending aorta diameter, measured with conventional echocardiography, was 37% larger in MFS than in control subjects (P<0.001). Arterial distensibility was 38% lower in MFS than in control subjects at the site of the abdominal aorta (P<0.01) but not at other sites (common carotid, common femoral, and radial arteries). Independently of age and body surface area, ascending aorta diameter was positively correlated with carotid PP in MFS (P<0. 01) and negatively in control subjects (P<0.01) but was not correlated with brachial PP and mean blood pressure. CONCLUSIONS: In patients with MFS, local PP, estimated from carotid PP, was a major determinant of ascending aorta diameter, whereas brachial PP was not. Increased arterial stiffness was confined to the aorta.

Quantitative two-dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement.

In 14 patients requiring aggressive therapy for circulatory failure resulting from massive pulmonary embolism, hemodynamic and two-dimensional echocardiographic data were obtained at bedside (acute phase) and again after circulatory improvement (intermediate phase) and during recovery. The acute stage was characterized by a low cardiac output state despite inotropic support (cardiac index 1.9 +/- 0.6 liters/min per m2) associated with increased right atrial pressure (12.4 +/- 4.2 mm Hg), increased right ventricular end-systolic and end-diastolic area (12.4 +/- 3.4 and 15.4 +/- 4.1 cm2/m2, respectively) and reduced right ventricular fractional area contraction (20.1 +/- 8.6%). Two-dimensional echocardiography also revealed interventricular septal flattening at both end-systole and end-diastole and markedly decreased left ventricular end-diastolic dimensions. Left ventricular fractional area contraction remained normal. Hemodynamic improvement occurred during the intermediate phase as shown by restoration of cardiac index (3.3 +/- 0.6 liters/min per m2), decrease in right atrial pressure (8.3 +/- 4.8 mm Hg), reduction in right ventricular end-systolic area (9.0 +/- 3.6 cm2/m2 at the intermediate stage and 6.1 +/- 1.8 cm2/m2 at recovery) and end-diastolic area (10.5 +/- 3.6 cm2/m2 at the intermediate stage and 8.9 +/- 2.9 cm2/m2 at recovery) and improvement in right ventricular fractional area contraction (31.5 +/- 16.4%). The interventricular septum progressively returned to a more normal configuration at both end-systole and end-diastole, and left ventricular diastolic dimension steadily increased. It is concluded that circulatory failure secondary to massive pulmonary embolism was mediated through a profound decrease in left ventricular preload, resulting from both pulmonary outflow obstruction and reduced left ventricular diastolic compliance.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of full-dose heparin anticoagulation on the development of left ventricular thrombosis in acute transmural myocardial infarction.

The incidence of left ventricular thrombosis after acute transmural myocardial infarction has been evaluated with two-dimensional echocardiography. To assess the preventive action of early anticoagulation with full-dose heparin, 90 patients, admitted within 5.2 +/- 4.6 hours after the onset of symptoms of their first episode of acute myocardial infarction (46 anterior and 44 inferior), were prospectively studied. Patients were randomly assigned either to therapeutic anticoagulation with heparin or to no anticoagulant therapy. Serial two-dimensional echocardiograms were recorded on the day of admission, the next day, days 4 to 7 and days 20 to 50 to detect left ventricular thrombus and to assess global left ventricular performance. On the first echocardiogram (10.3 +/- 8.0 hours after the onset of symptoms) no thrombus was visualized. In 44 patients with inferior myocardial infarction (23 receiving heparin and 21 not receiving heparin) no further left ventricular thrombus developed. In 46 patients with anterior myocardial infarction, 21 additional thrombi developed (45.6%) within 4.3 +/- 3.0 days after the acute event. Thrombus developed in 8 (38%) of 21 patients receiving heparin, compared with 13 (52%) of 25 patients not receiving heparin. This difference in ventricular thrombosis was not statistically significant (chi-square with the Yates correction = 0.76; NS). No difference was found between the subgroups in terms of clinical variables, infarct size, hemodynamic impairment, intensity of the inflammatory process and quantitative two-dimensional echocardiographic and cineangiographic left ventricular function. It is concluded that early anticoagulation with heparin reduced by 27% the incidence of left ventricular thrombus formation in anterior acute transmural myocardial infarction, and this relative risk reduction was not statistically significant when compared with findings in the untreated group.

Aneurysms of sinus of Valsalva: two-dimensional echocardiographic diagnosis and recognition of rupture into the right heart cavities.

The aim of this study was to evaluate the role of echocardiography in the diagnosis of sinus of Valsalva aneurysms projecting toward the right heart cavities. Three patients who had a ruptured aneurysm of a sinus of Valsalva diagnosed by echocardiography and confirmed by catheterization underwent cardiac surgery. In two patients, the aneurysm originated from the right coronary sinus and had perforated into either the inflow or outflow tract of the right ventricle. In the third patient, the aneurysm, which originated from the noncoronary sinus, ruptured into the atrium. A fourth patient was also investigated and had an unruptured aneurysm of the right coronary sinus projecting into the right ventricular outflow tract. M-mode, two-dimensional and contrast echocardiographic studies were performed before cardiac catheterization in all patients and after surgery in three patients. M-mode echocardiography was useful only when the aneurysm had an anterior projection, whether or not the aneurysm was ruptured. Conversely, two-dimensional echocardiography was always able to identify the aneurysmal sac which appeared as an abnormal circular thin-walled structure protruding into the right heart cavities. By using multiple views, it was possible to investigate the whole abnormal structure and locate the sinus from which the aneurysm originated. The use of the echo contrast technique allowed more precise definition of the aneurysmal sac and diagnosis of a left to right shunt by demonstrating a negative contrast image in the right cavities. On the other hand, no negative contrast image was recorded in the patient with an unruptured aneurysm or in the two instances of a successful surgically reconstructed aorta.

Regional specificity of peak hyperemic response in patients with congestive heart failure: correlation with peak aerobic capacity.

OBJECTIVES: The aim of this study was to compare peak reactive hyperemic blood flows in the forearm and calf of patients with congestive heart failure and in age- and gender-matched normal subjects. In addition, we attempted to correlate peak oxygen consumption with forearm and calf peak reactive hyperemic flows in the patients with heart failure. BACKGROUND: Disparate results have been reported regarding forearm peak reactive hyperemia in patients with congestive heart failure. Because training significantly increases peak reactive hyperemic flow in normal subjects, we hypothesized that in patients with congestive heart failure who curtail walking because of exertional symptoms, calf peak reactive hyperemic flow would be preferentially attenuated and that impairment of calf vasculature may correlate with peak oxygen consumption. METHODS: Forearm and calf blood flows were measured by venous occlusive plethysmography at rest and after 5 min of arterial occlusion in 46 patients with congestive heart failure and 7 age- and gender-matched normal subjects. Peak oxygen consumption was measured during graded exercise on a bicycle ergometer. RESULTS: Calf peak reactive hyperemic flow was lower in patients with congestive heart failure than in normal subjects (22 +/- 1 vs. 32.5 +/- 3.5 ml/min per 100 ml, p < 0.001), whereas forearm peak reactive hyperemic flows were similar in the two groups. Calf peak reactive hyperemic flow was linearly related to peak oxygen consumption (r = 0.58, p < 0.0001), but forearm peak reactive hyperemic flow was not. Forearm and calf peak reactive hyperemic flows were not related at rest or after 5 min of arterial occlusion in the patients with heart failure. CONCLUSIONS: Calf peak reactive hyperemic flow is reduced in patients with congestive heart failure, whereas forearm peak reactive hyperemic flow is identical to that of age- and gender-matched normal subjects. Calf peak reactive hyperemic flow is linearly related to peak oxygen consumption in patients with congestive heart failure, but forearm peak reactive hyperemic flow is not.

Dynamic cardiomyoplasty: effect of discontinuing latissimus dorsi muscle stimulation on left ventricular systolic and diastolic performance and exercise capacity.

OBJECTIVES: This study sought to assess the short-term effect of discontinuing latissimus dorsi muscle stimulation on left ventricular systolic and diastolic performance and exercise tolerance in patients with improved functional status by cardiomyoplasty, in whom latissimus dorsi muscle was fully conditioned. BACKGROUND: Cardiomyoplasty has consistently improved the functional status of patients, but the short-term effect of latissimus dorsi muscle contraction has not been assessed in these patients. METHODS: Right-heart catheterization, Doppler-echocardiography and maximal exercise testing with expired gas analysis were performed in 10 patients with congestive heart failure who had undergone cardiomyoplasty at least 6 months earlier. Data were obtained when the latissimus dorsi muscle was stimulated every other systole and after stimulation was discontinued for 1 h. The power of this study to detect a 10% difference was > 80%. RESULTS: After cardiomyoplasty, left ventricular ejection fraction increased from 0.22 +/- 0.08 (mean +/- SD) to 0.27 +/- 0.07 after 6 months (p < 0.02 vs. before cardiomyoplasty) and to 0.24 +/- 0.09 after 1 year; functional class went from 3.0 +/- 0.0 to 2.0 +/- 0.5 after 6 months and to 2.0 +/- 0.7 after 1 year (both p < 0.001 vs. before cardiomyoplasty). After discontinuation of latissimus dorsi muscle stimulation, cardiac index did not change (2.28 +/- 0.45 vs. 2.30 +/- 0.46 liters/min per m2). Mean systemic arterial and pulmonary capillary wedge pressures were also similar (85.2 +/- 6.0 vs. 88.4 +/- 5.6 mm Hg and 14.9 +/- 7.1 vs. 13.6 +/- 6.8 mm Hg, respectively). Doppler E/A ratio decreased from 1.04 +/- 0.33 to 0.83 +/- 0.25 (p < 0.02), suggesting that left ventricular diastolic function may have been improved by latissimus dorsi muscle stimulation. Peak oxygen consumption was unaltered (1,633 +/- 530 vs. 1,596 +/- 396 ml/min). CONCLUSIONS: Alterations in left ventricular diastolic rather than systolic function may be responsible for the long-term clinical benefits of cardiomyoplasty.

Contrast echocardiographic visualization of cough-induced right to left shunt through a patent foramen ovale.

In a series of 24 consecutive patients referred to the echocardiography laboratory because of suspected patent foramen ovale, contrast two-dimensional and M-mode echocardiographic studies were performed during normal breathing and during two provocative tests: the Valsalva maneuver and cough. A right to left shunt was visualized in 8 patients during normal breathing, in 11 patients during the Valsalva maneuver and in 17 patients during the cough test. Cardiac catheterization performed in all 24 patients and postmortem examination available in 3 patients confirmed the patency of the foramen ovale in only 15 patients. In these 15 patients, echo contrast appeared in the left heart cavities in early systole and almost simultaneously with complete right heart opacification. In contrast, for the two false positive results during the cough test, ultrasound contrast appeared at any time of the cardiac cycle when the right heart cavities had been partially cleared of contrast material. Right and left atrial pressures were simultaneously measured in four patients, and the normal interatrial pressure gradient was reversed during the Valsalva maneuver and the cough test. Echocardiography during both provocative tests showed that the interatrial septum flattened or became convex toward the left atrium. The cough test appears to be more reliable and easier to perform in critically ill patients than the Valsalva maneuver for the detection of right to left shunting through a patent foramen ovale.

Left ventricular compliance in acute myocardial infarction in man.

Left ventricular end-diastolic pressure (P) and volume (V) were measured in 12 patients with acute myocardial infarction. It was assumed that the diastolic P-V relationship was exponential and corresponded to the formula P=be KV. In 7 patients submitted to volume loading, several data points of this relationship were obtained and at zero volume, the mean intercept with the ordinates was 0.037+/-0.015 kPa (SEM) (0.28+/-0.12 mmHg). In the other 5 patients, the P-V curve was plotted through this intercept and the pressure and volume co-ordinates obtained by control. The K coefficient (passive elastic modulus) was greater, and the normalised left ventricular compliance index (dV/VdP) was smaller in the infarct group than in the control group. This suggests decreased left ventricular compliance during the acute phase of myocardial infarction. By comparing left ventricular function curves plotted using either end-diastolic pressure or end-diastolic volume as the stretch index it is possible to evaluate the relative participation of decreased compliance and depressed contractility in global left ventricular function.

Fibulin-2: genetic mapping and exclusion as a candidate gene in Marfan syndrome type 2.

Fibulin-2 (FBLN2) is a new extracellular matrix protein that has been considered a candidate gene for Marfan syndrome type 2 (locus MFS2) based on chromosomal colocation at 3p24.2-p25 and disease phenotype. In the absence of polymorphic markers reported for FBLN2, direct sequencing of the gene was performed and two intragenic polymorphisms were identified. Linkage was excluded between FBLN2 and the MFS2 gene. Furthermore, two-point lod scores were generated between these markers and anonymous markers arrayed on the genetic map of 3p and closely linked to MFS2. These analyses placed FBLN2 at marker D3S1585.

Relation of functional improvement in congestive heart failure after quinapril therapy to peripheral limitation.

Angiotensin-converting enzyme inhibitors have been shown to increase maximal muscle blood flow in parallel to peak VO2 in patients with congestive heart failure (CHF). Whether this increase shifts factors limiting peak aerobic capacity from periphery (skeletal muscle or vessels) to central factors (cardiac or respiratory) is unknown. Comparison of peak oxygen consumption (VO2) obtained during leg cycling (VO2 leg) with peak VO2 obtained during combined leg cycling and arm cranking (VO2 arm + leg) allows determination of the relative role of central or peripheral factors. We compared VO2 leg with VO2 arm + leg before and after 3 months of therapy with quinapril 40 mg in 16 patients with CHF (age 53 +/- 13 years) due to left ventricular systolic dysfunction (ejection fraction 0.25 +/- 0.07). Before quinapril, VO2 arm + leg was significantly higher than VO2 leg (19.0 +/- 3.3 vs 16.9 +/- 3.8 ml/kg/min, p < 0.001), whereas after therapy these 2 values were similar (20.3 +/- 4.3 vs 21.0 +/- 4.3 ml/kg/min; p = NS), indicating that patients were no longer limited by peripheral factors. Besides, VO2 leg increase after therapy was higher in patients in whom difference between VO2 arm + leg and VO2 leg was the greatest (i.e., in patients who were initially more limited by peripheral factors). Simultaneously, calf peak reactive hyperemia and circumference significantly increased, indicating an improvement in vascular dilating capacity and an increase in skeletal muscle mass. No significant modification occurred in the forearm. Thus, patients who improved the most after 3 months of quinapril therapy were those who were initially limited by peripheral factors. The restricting role of these factors was reduced after quinapril therapy.

Vasodilator synchronized retroperfusion: quantitative assessment of flow-function relation in acutely ischemic canine myocardium.

To investigate whether addition of vasodilator drugs can increase the beneficial effects on the ischemic myocardium of diastolic synchronized retroperfusion (DSR), low doses of verapamil (2 micrograms/kg/min) or nitroglycerin (0.7 microgram/kg/min) were infused through DSR in open-chest dogs undergoing 180 minutes of proximal left anterior descending coronary artery occlusion. Verapamil-DSR (n = 6), nitroglycerin-DSR (n = 6) or DSR alone (n = 8, controls) were started 10 minutes after the onset of occlusion and maintained for 170 minutes. Regional myocardial blood flow (MBF) (microspheres) and left ventricular function (endocardial ultrasonic crystals) were simultaneously assessed in nonischemic and ischemic zones in the 3 groups, before and after 10 and 180 minutes of coronary occlusion. DSR alone significantly increased ischemic regional MBF, endocardial/epicardial flow ratio and endocardial segmental length shortening. Verapamil DSR increased both nonischemic and ischemic regional MBF but reduced the endocardial/epicardial flow ratio and worsened ischemic contractile function. Nitroglycerin DSR did not modify ischemic transmural flow compared with DSR alone, but abolished the beneficial endocardial/epicardial blood flow redistribution, resulting in no additional improvement of contractile function. Thus, ischemic MBF and function are not improved by addition of small amounts of verapamil or nitroglycerin to the arterial retroperfusate in this model of acute myocardial ischemia.

Two dimensional echocardiographic visualization of ventricular septal rupture after acute anterior myocardial infarction.

In three consecutive cases of ventricular septal rupture after acute anterior myocardial infarction, wide angle two dimensional echocardiography readily visualized the septal defect, permitting the defect to be localized and its size estimated. In addition, negative contrast echoventriculography identified a left to right shunt at the ventricular level. The echocardiographic findings were corroborated by cardiac catheterization data in all patients, by perioperative examination in two and by postmortem findings in one patient. Postoperative echocardiographic studies afforded demonstration of the patch closing the defect. In patients with acute myocardial infarction associated with the sudden appearance of a systolic murmur, two dimensional echocardiography should be performed promptly in order to guide the diagnosis and management of these critically ill patients. In some patients with severe cardiogenic shock, in whom a favorable prognosis depends on rapid treatment, two dimensional echocardiography may allow the patient to be taken to surgery immediately without further study.

Diastolic synchronized retroperfusion versus reperfusion: effects on regional left ventricular function and myocardial blood flow during acute coronary occlusion in dogs.

The effects of 170 minutes of diastolic synchronized retroperfusion of the coronary sinus with arterial blood during 180 minutes of coronary artery occlusion on regional myocardial contractility (ultrasonic crystals) and blood flow (microspheres) were investigated in open-chest dogs. These effects were compared with those of 180 minutes of coronary occlusion and those of 170 minutes of anterograde reperfusion after 10 minutes of coronary occlusion in separate groups of dogs. Retroperfusion was able to almost restore transmural blood flow in the moderately ischemic zones and to increase it back to 47% of its preocclusion value in the severely ischemic zones with, in both zones, a favorable redistribution of flow toward the endocardium. Simultaneously, retroperfusion significantly improved segment length shortening in the moderately ischemic zones and significantly reduced the extent of paradoxical bulging in the severely ischemic zones. These partial recoveries in regional contractility and blood flow during retroperfusion were intermediate between those induced by 170 minutes of anterograde reperfusion and those of 180 minutes of coronary artery occlusion. Thus, in the presence of coronary artery occlusion, retroperfusion appears to exert a beneficial effect by improving both regional perfusion and function in the ischemic zones and may be proposed as a medical circulatory support to the jeopardized myocardium.

A dose-response study of intravenous enoximone in congestive heart failure.

Previous clinical studies with intravenous enoximone have used cumulative dosing to quantify enoximone's hemodynamic effects. The magnitude and duration of the hemodynamic effects of single intravenous doses of enoximone were evaluated in patients with congestive heart failure. Sixty patients, who were in New York Heart Association functional classes III and IV, received single intravenous doses of enoximone, either 0.25 (12 patients), 0.5 (13 patients), 1 (14 patients), 1.5 (10 patients) or 2 mg/kg (11 patients). Cardiac index was increased by 20% with the 0.25 mg/kg dose and by 48% and 42% with the 1.5 and 2 mg/kg doses, respectively. These increases were statistically significant (Student's paired t test with Bonferroni's correction, p less than 0.007) for 1 hour after 0.25 and 0.5 mg/kg, for 2 hours after 1 mg/kg and for 4 hours after 1.5 and 2 mg/kg. Enoximone also reduced pulmonary artery diastolic pressure by 19% with 0.25 mg/kg and by 29% with 2 mg/kg. The duration of effect varied from 1 hour with 0.25 mg/kg to 4 hours with 2 mg/kg. Enoximone produced no consistent or dose-related effects on heart rate or blood pressure. Eighteen adverse reactions were reported by 15 patients, of which 11 were minor and transient (vein pain, flushes, nausea). In 5 patients ventricular or supraventricular arrhythmias were observed, including nonsustained ventricular tachycardia and extrasystoles; 3 of these patients had evidence of arrhythmias before enoximone. Laboratory studies before and after treatment showed no drug-related effects. Dose-related effects on the magnitude and duration of hemodynamic responses to intravenous enoximone were evident within the dose range of 0.25 to 2 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Doppler-derived aortic maximal acceleration. A reliable index of left ventricular systolic function.

We compared maximal acceleration of aortic blood flow (aortic Amax), calculated from maximal aortic velocity obtained with a conventional echo-Doppler machine with the invasive inotropic index left ventricular end-systolic pressure/left ventricular end-systolic volume (LVESP/LVESV) ratio and left ventricular ejection fraction (LVEF). Continuous wave (CW) and pulsed wave (PW) Doppler aortic blood flows were recorded from the apical view in 16 patients (age, 62.3 +/- 6.4 years) within 24 h of left-sided catheterization. The theoretical exponential relationship between LVEF and LVESP/LVESV was confirmed in our study population (r = 0.92; p < 0.0001). The relationship between aortic Amax determined either by CW or PW and LVESP/LVESV was linear (r = 0.92 and 0.93, respectively, p < 0.001), whereas the relationship between aortic Amax and angiographic LVEF was exponential (PW: r = 84; CW: r = 0.85; both p < 0.001). We conclude that (1) aortic Amax, derived from maximal velocity obtained with a conventional machine, can be used as an index of left ventricular systolic function, and (2) PW as well as CW Doppler signals can be used for this calculation.

Treatment of early postinfarction ventricular aneurysm by intra-aortic balloon pumping and surgery.

In nine patients with medically refractory left ventricular failure and/or ventricular arrhythmias, secondary to acute formation of a ventricular aneurysm, intra-aortic balloon pumping (IABP) was instituted 24 to 36 hours before diagnostic angiographic studies. Ventricular irritability was reduced and heart failure was controlled in all patients. Eight patients underwent operation, four within 3 weeks of an acute myocardial infarction and four within 3 months. All had resection of the recent infarction and two had myocardial revascularization as well. Two of the eight patients died in the early postoperative period from intractable ventricular fibrillation. All six patients who survived the operation (mean follow-up 12 months) had excellent clinical results. Ventricular irritability was suppressed and only one patient had residual heart failure. However, there was one late death 7 months after operation. The results suggest that surgical therapy may be effective in the management of medically unresponsive arrhythmias and/or congestive heart failure in the acute or intermediate postinfarction phase. IABP assistance was helpful in supporting the circulation and reducing ventricular irritability during the preoperative and postoperative periods.

Influence of lung and chest wall compliances on transmission of airway pressure to the pleural space in critically ill patients.

Nineteen patients with acute respiratory failure were divided into three groups according to their total compliance (CT). Transmission of airway pressure to the pleural space was then evaluated by measurement of esophageal pressure at both end-expiration and end-inspiration, and at three levels of PEEP. Chest wall (CW) and lung complicance (CL) were also calculated from simultaneous measurements of lung volume changes induced by tidal delivery. In group 1 (CT greater than 45 ml/cmH2O), 37 percent of airway pressure was transmitted to pleural space. In group 2 (CT between 45 and 30 ml/cmH2O), 32 percent of airway pressure was transmitted to the pleural space. In group 3 (CT less than 30 ml/cmH2O), only 24 percent of airway pressure was transmitted to the pleural space. These differences are statistically significant (p less than 0.001) and illustrate the influence of a progressive increase in lung stiffness (CL = 100.3 +/- 17.2 ml/cmH2O in group 1, CL = 45.0 +/- 6.3 ml/cmH2O in group 2, and CL = 28.6 +/- 8.9 ml/cmH2O in group 3) on transmission of airway pressure to the pleural space. Despite lesser transmission of airway pressure to the pleural space in the most damaged lungs, no significant difference was found between groups with regard to transmural venous pressure changes throughout the study.

Inspiratory impairment in right ventricular performance during acute asthma.

Right ventricular function was investigated in seven asthmatic patients during an acute attack, using simultaneous bedside right heart catheterization and two-dimensional echocardiography (2DE). Hemodynamic and echocardiographic data were compared during four successive periods of the respiratory cycle: inspiration, early expiration, mid-expiration, and late expiration. During inspiration, 2DE showed a significant increase in right ventricular area at both end-systole and end-diastole. This inspiratory right ventricular enlargement coexisted with a significant reduction in 2DE stroke area and pulmonary artery pulse pressure suggesting an inspiratory reduction in right ventricular stroke output. A transient depression of right ventricular function during deep inspiratory effort in asthma was thus strongly suggested. The negative pressure surrounding the right ventricle at inspiration is advocated as the causative factor enabling reduction in the hydraulic force effecting right ventricular ejection. The highly negative pleural pressure probably holds the right ventricular free wall and restrains its systolic inward motion, as suggested by the finding of a concomitant inspiratory reduction in right ventricular developed pressure and 2DE fractional area contraction.

Incidence of tricuspid regurgitation and vena caval backward flow in mechanically ventilated patients. A color Doppler and contrast echocardiographic study.

In 40 patients requiring mechanical ventilation for an episode of respiratory failure of various causes, prevalence of tricuspid regurgitation (TR) or other cause of vena caval backward flow (VCBF) was systematically investigated using transthoracic Doppler echocardiography. Quantification of TR was obtained from planimetry of the regurgitant jet during color Doppler examination. The influence of cyclic mechanical lung inflation was examined by contrast echography of the inferior vena cava and hepatic veins. All the 40 patients studied had TR, which was mild in 21, moderate in 9 and severe in 10. Using a planimetric scale, TR was more marked during mechanical ventilation, when compared with a brief period of spontaneous breathing. Moreover, contrast echocardiography demonstrated that systolic TR reached inferior vena cava and hepatic veins in 16 cases, and also evidenced direct mechanical action of lung inflation producing a pancardiac VCBF in 15 cases. This high incidence of TR and VCBF partially may explain the relatively poor reliability of the thermodilution method for measurement of cardiac output when used in ventilated patients.