Effect of percutaneous balloon valvuloplasty on pulmonary hypertension in mitral stenosis.

Percutaneous mitral balloon valvuloplasty (PMBV) has been useful in decreasing mitral valve obstruction in mitral stenosis; however, the long-term effects of valvuloplasty on pulmonary artery pressure have not been extensively studied. Thirty-three patients underwent PMBV in our institution between January 1988 and December 1991. There were significant reductions in peak (19 +/- 1 to 12 +/- 1 mm Hg) and mean (10 +/- 0.7 to 6 +/- 0.4 mm Hg) mitral valve gradients estimated by Doppler techniques immediately after PMBV. The mitral valve area, as assessed by the pressure half-time method, increased from 1.06 +/- 0.05 to 1.98 +/- 0.08 cm2 (p < 0.001) after the procedure and remained significantly greater (1.68 +/- 0.11 cm2) at 17 +/- 2 months. Right ventricular systolic pressure (RVSP) was estimated in patients with tricuspid regurgitation (TR) using the modified Bernoulli equation. There was a good correlation between Doppler and catheterization for RVSP (r = 0.83 pre valvuloplasty; r = 0.87 post valvuloplasty). Right ventricular systolic pressure by Doppler was 56 +/- 4 mm Hg before valvuloplasty and 48 +/- 4 mm Hg immediately afterwards (p < 0.001). Nine patients had TR on follow-up Doppler studies with an estimated RVSP of 53 +/- 9 mm Hg (p = NS compared with pre- and post-valvuloplasty values). Six of these nine patients had moderate or severe mitral regurgitation (MR), compared with one patient without TR at follow-up (p < 0.05). There appears to be a good correlation between the RVSP determined by Doppler and measured at catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic effects of octreotide in patients with autonomic neuropathy.

BACKGROUND: The somatostatin analogue, ectrootide, is being used to treat postprandial hypotension in patients with autonomic neuropathy. Although the therapeutic effect of the drug is presumably secondary to a splanchnic vasoconstrictor action, its effect on splanchnic hemodynamics has never been characterized in patients with autonomic neuropathy. Moreover, it is unknown whether octreotide acts on other vascular beds in this group of patients or whether it affects cardiac output. We, therefore, measured splanchnic, forearm, and systemic vascular resistance and cardiac output before and after administering octreotide (0.4 microgram/kg s.c.) to patients with idiopathic autonomic neuropathy and diabetic autonomic neuropathy. METHODS AND RESULTS: Splanchnic blood flow was determined from the clearance of indocyanine green in seven patients. We observed that octreotide decreased splanchnic blood flow (from 850 +/- 77 to 664 +/- 48 ml/min, p less than 0.005), increased mean blood pressure (from 97 +/- 6 to 115 +/- 3 mm Hg, p less than 0.005), and increased splanchnic vascular resistance (from 0.118 +/- 0.012 to 0.18 +/- 0.018 mm Hg/ml/min, p less than 0.005). Forearm blood flow was measured by plethysmography in 13 patients. Octreotide increased forearm vascular resistance in patients with idiopathic autonomic neuropathy (n = 8) from 19.1 +/- 1.0 to 27.2 +/- 3.8 mm Hg/ml/min/100 ml forearm volume (p less than 0.01) and from 25.2 +/- 3.9 to 41.0 +/- 6.8 mm Hg/ml/min/100 ml (p less than 0.01) in patients with diabetic autonomic neuropathy (n = 5). Cardiac output was measured by two-dimensional echocardiography. Octreotide administration increased cardiac output in five of six patients with idiopathic autonomic neuropathy (from 4.4 +/- 0.4 to 5.0 +/- 0.5 l/min, p less than 0.02) and five of five patients with diabetic autonomic neuropathy (from 3.8 +/- 0.4 to 5.1 +/- 0.4 l/min, p less than 0.02). Systemic vascular resistance increased in patients with idiopathic autonomic neuropathy from 21.2 +/- 2 to 24.9 +/- 2.6 (p less than 0.05) but did not change in patients with diabetic autonomic neuropathy. CONCLUSION: The pressor effect of octreotide in patients with autonomic neuropathy is associated with increased splanchnic and forearm vascular resistance and with increased cardiac output.

Dynamic changes in left ventricular outflow tract flow velocities after amyl nitrite inhalation in hypertrophic cardiomyopathy.

Doppler echocardiography was performed in 21 patients with hypertrophic cardiomyopathy (HC), in nine patients with no evidence of left ventricular (LV) hypertrophy by two-dimensional echocardiography, and in five patients with systemic hypertension and concentric LV hypertrophy. The LV outflow tract (LVOT) peak velocity was recorded by continuous wave Doppler technique at rest and after amyl nitrite inhalation. The LVOT pressure gradient was calculated by the modified Bernoulli equation. A significant increase in heart rate and a drop in systolic blood pressure were observed in all patients after amyl nitrite inhalation; no adverse effects were encountered. The peak LVOT velocity and pressure gradient increased significantly after provocation in all patients, but the increase was much more pronounced in patients with HC (peak LVOT velocity increased from 2.2 +/- 0.8 to 4.3 +/- 1.0 m/sec and peak gradient increased from 22 +/- 17 to 78 +/- 36 mm Hg). The Doppler spectral signal in patients with HC demonstrated a characteristic contour, with peak velocity occurring in late systole. However, the observed increase in LVOT peak velocity was not statistically different between treated (with beta-blockers and calcium blockers) and untreated patients with HC. We conclude that LVOT peak velocity and pressure gradients in patients with HC can be readily assessed by Doppler echocardiography both at rest and after amyl nitrite inhalation. The dynamic changes in LVOT velocity induced by this provocation have certain characteristic features in obstructive HC but appear to be independent of the medical regimen used, at least in the dosages tested in our study.

Normal and abnormal prosthetic valve function as assessed by Doppler echocardiography.

Doppler echocardiography was performed in 136 patients with a normally functioning prosthetic valve in the aortic (n = 59), mitral (n = 74) and tricuspid (n = 3) positions. These included patients with St. Jude (n = 82), Björk-Shiley (n = 18), Beall (n = 13), Starr-Edwards (n = 7) or tissue (n = 16) valves. Peak and mean pressure gradients across the prostheses were measured using the simplified Bernoulli equation. The prosthetic valve orifice (PVO, in square centimeters), only in the mitral position, was calculated by the equation: PVO = 220/pressure half-time. In the aortic position, the St. Jude valve had a lower peak velocity (2.3 +/- 0.6 m/s, range 1.0 to 3.9), peak gradient (22 +/- 12 mm Hg, range 4 to 61) and mean gradient (12 +/- 7 mm Hg, range 2 to 32) than the other valves (p less than 0.05) when compared with Starr-Edwards). In the mitral position, the St. Jude valve had the largest orifice (3.0 +/- 0.6 cm2, range 1.8 to 5.0) (p less than 0.0001 compared with all other valves). Insignificant regurgitation was commonly found by pulsed mode Doppler technique in patients with a St. Jude or Björk-Shiley valve in the aortic or mitral position and in patients with a Starr-Edwards or tissue valve in the aortic position. In 17 other patients with a malfunctioning prosthesis (four St. Jude, two Björk-Shiley, four Beall and seven tissue valves) proven by cardiac catheterization, surgery or autopsy, Doppler echocardiography correctly identified the complication (significant regurgitation or obstruction) in all but 2 patients who had a Beall valve. It is concluded that 1) the St. Jude valve appears to have the most optimal hemodynamics; mild regurgitation can be detected by the Doppler technique in normally functioning St. Jude and Björk-Shiley valves in the aortic or mitral position and in Starr-Edwards and tissue valves in the aortic position, and 2) Doppler echocardiography is a useful method for the detection of prosthetic valve malfunction, especially when the St. Jude, Björk-Shiley and tissue valves are assessed.

Value and limitations of Doppler ultrasound in the evaluation of aortic stenosis: a statistical analysis of 70 consecutive patients.

Continuous-mode Doppler ultrasound and cardiac catheterization were performed within 1.4 +/- 2.0 days in 70 patients, aged 26 to 84 (mean 67 +/- 11) years, with suspected aortic stenosis. Optimal Doppler spectral display signal was recorded from the apical window in 43% of the patients, the second or third right parasternal area in 34%, and from the suprasternal notch view in 20% of the patients. Aortic valve gradients by Doppler ultrasound were calculated by the simplified Bernoulli equation: pressure gradient = 4X (velocity). There was an overall fair correlation between the peak gradient by Doppler technique and both the maximal instantaneous (r = 0.66) and peak-to-peak aortic pressure gradient (r = 0.68) obtained at catheterization and a good correlation (r = 0.75) between mean gradient by Doppler technique and catheterization. These correlation coefficients improved significantly in the last 51 patients as compared to the initial 19 patients of the study. Of the last 51 patients, correlation was better in those in normal sinus rhythm as compared to those in atrial fibrillation, and in patients with no or insignificant coexistent AR as compared to those with greater than or equal to 2+ AR. The age of the patient and the status of cardiac output did not significantly affect the accuracy of correlations. We conclude that measurements of aortic valve gradient by continuous-mode Doppler ultrasound may not correlate closely with those by catheterization when the experience with the Doppler technique is limited and when patients in atrial fibrillation or with significant coexistent AR are studied.

Hemodynamic consequences of left atrial myxomas as assessed by Doppler ultrasound.

Seven patients with left atrial (LA) myxoma who were studied by M-mode, two-dimensional, and Doppler echocardiography and who underwent surgical excision of the tumor are described. In six patients, the myxoma was attached to the lower interatrial septum and was protruding through the mitral valve (MV) during diastole. Significant MV obstruction (mean diastolic gradient of 16 mm Hg) was detected by Doppler in only one patient and was confirmed by hemodynamic studies; another patient had only a small gradient (peak 8 and mean 4 mm Hg). Mild mitral regurgitation (MR) was found preoperatively in four of five patients who underwent left ventriculography, but was not detected by Doppler. Postoperatively, however, five patients were found to have mild MR and one patient had moderate MR by Doppler. The use of Doppler echocardiography can provide important additional information regarding the hemodynamic consequences of LA myxomas.

Prevalence and severity of mitral regurgitation in the mitral valve prolapse syndrome: a Doppler echocardiographic study of 80 patients.

Doppler echocardiography was performed in 80 consecutive patients (22 men, 58 women), aged 38 +/- 16 years, who had mitral valve prolapse diagnosed by two-dimensional echocardiography. Of the 80 patients, 16 (20%) were asymptomatic and 11 (14%) had a normal physical examination (no click or murmur). The M-mode echocardiogram was negative for mitral valve prolapse in 11 patients (14%) and equivocal or nondiagnostic in 19 patients (24%). Mitral regurgitation was evaluated using pulsed mode Doppler echocardiography and was quantified by the mapping technique as minimal or mild when a holosystolic regurgitant jet was recorded just below the mitral valve into the left atrium, and as moderate or severe when the jet was detected at the mid- or distal left atrium. Mitral regurgitation was found in 55 (69%) of the 80 patients and it was minimal or mild in 47 patients (59%) and moderate or severe in 8 (10%). In 20 (36%) of the 55 patients with mitral regurgitation by Doppler technique, a systolic murmur was not detected and each of the 20 had only mild mitral regurgitation. Left atrial and left ventricular size were significantly smaller in patients with mild or no regurgitation as compared with the eight patients with moderate or severe regurgitation. These eight patients were all men (six over 50 years of age) who usually presented with dyspnea and a holosystolic murmur; the mitral valve prolapse was holosystolic by M-mode and involved both leaflets by two-dimensional echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)

Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: a common finding by Doppler echocardiography.

M-mode and Doppler echocardiography were performed in 16 patients with first degree atrioventricular (AV) block, 1 patient with second degree (Wenckebach type) and 3 patients with third degree AV block; 20 individuals with a normal PR interval served as control subjects. The time from the onset of the P wave to the mitral valve closure by M-mode and to the end of mitral flow by Doppler echocardiography were obtained. In 20 normal subjects, the P wave to mitral valve closure interval measured 220 +/- 30 ms by M-mode and to the end of mitral flow 225 +/- 29 ms by Doppler technique (p = NS). In patients with first degree AV block, these intervals measured 242 +/- 41 and 249 +/- 36 ms, respectively (p = NS). Late diastolic (before the onset of the QRS complex) mitral regurgitation was detected by pulsed mode Doppler imaging in 9 (56%) of the 16 patients with first degree AV block but in none with a normal PR interval. In the four patients with advanced AV block, intermittent mid or late diastolic mitral regurgitation was found to depend on the position of the P wave in diastole. With early diastolic P waves, the end of mitral valve flow by Doppler technique occurred 230 to 250 ms after the onset of the P wave and was followed by mild diastolic mitral regurgitation of variable duration. With P waves falling in systole, the mitral valve remained open throughout diastole; during most of diastole, however, there was neither forward mitral flow (diastasis) nor diastolic mitral regurgitation detected by Doppler technique.(ABSTRACT TRUNCATED AT 250 WORDS)