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

We directly measured the net pulmonary extraction of circulating norepinephrine, epinephrine and dopamine in control patients and patients with primary or secondary pulmonary hypertension. Mixed pulmonary artery norepinephrine, epinephrine and dopamine were 314 +/- 13 pg/ml, 102 +/- 9 pg/ml, 51 +/- 5 pg/ml, respectively, for the control group; values were similar in patients with pulmonary hypertension. The pulmonary extraction of norepinephrine was 25.4 +/- 2.6% (clearance 266 +/- 62 ng/min) in control patients; epinephrine and dopamine were not extracted. There was no net extraction or production of any of the three catecholamines by the lungs in any of the patients with pulmonary hypertension. We conclude that the lungs play a significant role in the inactivation of circulating norepinephrine in man. This metabolic function of the lungs appear to be lost in pulmonary hypertension.

The clinical experience with 37 patients with acute transmural inferior wall myocardial infarction who were assessed for evidence of right ventricular involvement is reported. On the basis of currently accepted hemodynamic criteria, 29 patients (78%) had evidence suggestive of right ventricular infarction. However, only 5 (20%) of 25 patients demonstrated right ventricular uptake of technetium pyrophosphate on scintigraphy. Two-dimensional echocardiography or isotope nuclear angiography, or both, were performed in 32 patients; 20 studies (62%) showed evidence of right ventricular wall motion disturbance or dilation, or both. Twenty-one patients demonstrated a late inspiratory increase in the jugular venous pressure (Kussmaul's sign). The presence of this sign in the clinical setting of inferior wall myocardial infarction was predictive for right ventricular involvement in 81% of the patients in this study. It is suggested that right ventricular involvement in this clinical setting is common and includes not only infarction but also dysfunction without detectable infarction, which is likely on an ischemic basis.

SUMMARY Thirteen patients who had ventricular septal defects (VSDs) after myocardial infarction (MI) underwent two-dimensional echocardiography (2-D echo), with confirmation of the VSD by oximetry. Eight of the patients were male and five were female, ages 51-76 years. Five had anterior and eight inferior MIs. Two-dimensional echocardiography revealed akinesis or dyskinesis of the interventricular septum (IVS) in all 13 patients. In only six could a defect in the IVS be directly visualized. Two-dimensional echocardiographic left ventricular (LV) wall motion abnormalities correlated with ECG and angiographic site of infarction in all patients. Twelve patients had adequate saline contrast studies. Positive LV contrast (microbubbles entering the left ventricle through the VSD) was seen in 11 patients, and negative right ventricular (RV) contrast (washout of the RV bubbles by LV blood crossing the VSD) in five patients; at least one abnormality was present in every patient. The location of the VSD was determined by visualizing a VSD or by the site of the positive LVor negative RV contrast. Oximetry showed VSD shunts of 1.4:1 to 7:1, with no correlation between the degree of negative RV contrast and shunt size. Surgical or pathologic confirmation of VSD was obtained in 12 patients, with agreement of VSD location by 2-D echo in all. Four of the 11 patients who underwent surgical repair died, and two patients died before surgery could be attempted. We conclude that 2-D echo is a sensitive, rapid and safe technique for diagnosing VSD after MI. Positive LV contrast, with or without negative RV contrast, is more sensitive in the diagnosis and localization of post-MI VSD than direct echocardiographic visualization of the defect.