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Biomedical subjects

S Rich

Publications and source records attributed to S Rich.

At least 109 records · Page 6Linked to original sources
PubMed1987

High-dose calcium channel-blocking therapy for primary pulmonary hypertension: evidence for long-term reduction in pulmonary arterial pressure and regression of right ventricular hypertrophy.

In an attempt to produce substantial reductions in pulmonary arterial pressure and pulmonary vascular resistance in patients with primary pulmonary hypertension, a new treatment strategy using high doses of calcium channel-blocking drugs was developed. Thirteen patients were given an initial test dose of 60 mg diltiazem or 20 mg nifedipine followed by consecutive hourly doses until a 50% fall in pulmonary vascular resistance and 33% fall in pulmonary arterial pressure was achieved or untoward side effects developed. The initial drug challenges failed to produce significant reductions in mean pulmonary arterial pressure or pulmonary vascular resistance. In eight of 13 patients, continued hourly doses produced a reduction in mean pulmonary arterial pressure of 48% (61 to 35 mm Hg, p less than .01) and a reduction in pulmonary vascular resistance of 60% (15 to 6 units, p less than .01). These patients were discharged on high-dose (up to 720 mg/day diltiazem or 240 mg/day nifedipine) calcium channel-blocking drugs as long-term therapy. Five patients have returned for restudy after 1 year. In four of five the reductions in pulmonary arterial pressure and pulmonary vascular resistance were sustained and were associated with regression of right ventricular hypertrophy as assessed by electrocardiography and echocardiography. One patient who reduced her dose to a conventional level had a return of her pulmonary arterial pressure and pulmonary vascular resistance toward previous levels. We conclude that substantial reductions in pulmonary arterial pressure and pulmonary vascular resistance that are associated with regression of right ventricular hypertrophy are possible in some patients with primary pulmonary hypertension by use of calcium channel-blocking drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Thromboxane synthetase inhibition in primary pulmonary hypertension.

Thromboxane synthetase inhibitors have been shown to reduce thromboxane, a potent vasoconstrictor, and increase prostacyclin, a potent vasodilator, in normal subjects. We evaluated the acute and chronic (three months) effects of the thromboxane synthetase inhibitor CGS13080 administered 200 mg every six hours on the resting hemodynamics in ten patients with primary pulmonary hypertension (PPH), and on their response to 20 mg of nifedipine given sublingually before and after the thromboxane synthetase inhibitor treatment. It was concluded that one can modulate the levels of endogenous thromboxane and prostacyclin in patients with primary pulmonary hypertension using a thromboxane synthetase inhibitor. Although the thromboxane synthetase inhibitor alone produced only modest hemodynamic changes over time, the addition of nifedipine was able to produce a further lowering of pulmonary artery pressure and pulmonary vascular resistance.

Adult↗
PubMed1987

Primary pulmonary hypertension. A national prospective study.

A national registry was begun in 1981 to collect data from 32 centers on patients diagnosed by uniform criteria as having primary pulmonary hypertension. Entered into the registry were 187 patients with a mean age (+/- SD) of 36 +/- 15 years (range, 1 to 81), and a female-to-male ratio of 1.7:1 overall. The mean interval from onset of symptoms to diagnosis was 2 years. The most frequent presenting symptoms included dyspnea (60%), fatigue (19%), and syncope (or near syncope) (13%). Raynaud phenomenon was present in 10% (95% of whom were female) and a positive antinuclear antibody test, in 29% (69% female). Pulmonary function studies showed mild restriction (forced vital capacity [FVC], 82% of predicted) with a reduced diffusing capacity for carbon monoxide (DLCO), and hypoxemia with hypocapnia. The mean (+/- SD) right atrial pressure was 9.7 +/- 6 mm Hg; mean pulmonary artery pressure, 60 +/- 18 mm Hg; cardiac index, 2.3 +/- 0.9 L/min X m2; and pulmonary vascular resistance index, 26 +/- 14 mm Hg/L/min X m2 for the group. Although no deaths or sustained morbid events occurred during the diagnostic evaluation of the patients, the typically long interval from initial symptoms to diagnosis emphasizes the need to develop strategies to make the diagnosis earlier.

Adolescent↗
PubMed1986

Determination of left ventricular ejection fraction using ultrafast computed tomography.

We evaluated ultrafast CT as a method to measure left ventricular ejection fraction in 16 adults with congenital or acquired heart disease who underwent cardiac catheterization. CT scanning of the left ventricle was performed at 4 to 12 adjacent 1 cm levels (depending on heart size) at 50 msec/scan for one cardiac cycle, with the table positioned with an axial tilt of 10 to 20 degrees and a lateral slew of 5 to 10 degrees to best approximate the long axis of the left ventricle. Image enhancement was achieved by an injection of 25 ml of Renografin-76 via a peripheral vein, with scanning timed to coincide with maximal enhancement of the left ventricular cavity. Ejection fraction was computed by measuring the percent change in area of the left ventricle from diastole (largest area) to systole (smallest area) in a single slice at the mid-left ventricular level. Mean ejection fraction for the group was 58.1 +/- 15.1% (range 24% to 84%). The ejection fraction from left ventriculography, computed from biplane images using the Dodge (area-length) formula, was 59.6 +/- 12.3% (range 28% to 77%). There was an excellent correlation between left ventricular ejection fraction by CT and ventriculography (r = 0.91, y = 1.1x - 8.5, p less than 0.001). This study demonstrates that ultrafast CT can provide an accurate measure of left ventricular ejection fraction by simple methodology.

Adult↗
PubMed1986

Nonoperative control of retroperitoneal hemorrhage secondary to placement of an inferior vena cava occluding device in a patient with recurrent pulmonary emboli.

A woman with multiple recurrent pulmonary emboli and iatrogenic inferior vena cava perforation caused by the Hunter-Sessions introducer was treated successfully by placement of a Hunter-Sessions balloon to control the ensuing retroperitoneal hemorrhage and interrupt the inferior vena cava. Full anticoagulation therapy was continued throughout the operation and postoperatively.

Catheterization↗
PubMed1986

Doppler echocardiographic assessment of impaired left ventricular filling in patients with right ventricular pressure overload due to primary pulmonary hypertension.

In patients with primary pulmonary hypertension, competition between the right and left ventricles for the limited pericardial space results in distortion of left ventricular geometry reflected in displacement of the ventricular septum toward the left ventricular cavity. Left ventricular shape is most dramatically deranged at end-systole and early diastole, suggesting the possibility that the distribution of left ventricular diastolic filling might be altered. To investigate this hypothesis, nine patients with primary pulmonary hypertension and nine normal individuals were studied with echocardiographic techniques. Left ventricular isovolumic relaxation time was significantly prolonged in patients with primary pulmonary hypertension by comparison with normal individuals (129 +/- 36 versus 53 +/- 9 ms, p less than 0.005) and the fraction of the transmitral flow velocity integral occurring in the first half of diastole was significantly less than in normal individuals (38 +/- 14% versus 70 +/- 9%, p less than 0.005). Measurement of fractional changes in short-axis left ventricular cavity area similarly demonstrated that in patients with primary pulmonary hypertension fractional early diastolic cavity expansion (32 +/- 11%) was significantly less than in normal individuals (78 +/- 9%, p less than 0.005). In patients with primary pulmonary hypertension, the ventricular septum was abnormally flattened toward the left ventricular cavity at end-systole (normalized septal curvature 0.04 +/- 0.19) and remained that way throughout early diastolic filling but returned toward normal at end-diastole (normalized septal curvature 0.68 +/- 0.19, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Antinuclear antibodies in primary pulmonary hypertension.

The association of positive antinuclear antibodies with the clinical and hemodynamic features of 43 patients with primary pulmonary hypertension and 16 patients with secondary pulmonary hypertension was investigated. Each patient had determinations of antinuclear antibodies using a KB cell substrate immunofluorescent test. Of the patients with primary pulmonary hypertension, 40% had positive antinuclear antibodies at titers of 1:80 dilutions or greater. There were no differences between patients with primary pulmonary hypertension and positive antinuclear antibodies compared with those with negative antinuclear antibodies in relation to clinical or hemodynamic status. A 6% incidence rate of antinuclear antibodies was found in patients with secondary pulmonary hypertension, similar to that in the normal population. The clinical, hemodynamic, serologic and histologic similarity between patients with primary pulmonary hypertension and those with unexplained pulmonary hypertension associated with collagen vascular disorders suggests that primary pulmonary hypertension in some patients may represent a collagen vascular disease confined to the lungs. The frequency of positive antinuclear antibody tests would place primary pulmonary hypertension between rheumatoid arthritis and scleroderma in the spectrum of collagen vascular diseases. Further studies are necessary, however, before one might expect that immunosuppressive therapy would be beneficial to these patients.

Adult↗
PubMed1986

Flexible fiberoptic pericardioscopy for the diagnosis of pericardial disease.

Pericardiocentesis provides an etiologic diagnosis for pericardial effusions approximately 25% of the time. In seven patients with evidence of a large pericardial effusion of unknown origin without cardiac tamponade, a flexible fiberoptic bronchoscope was inserted through a subxiphoid incision after the effusion was drained. Pericardioscopy allowed visualization of all pericardial surfaces and made it possible to perform selective biopsy not limited to a subxiphoid window. It is a safe procedure that can permit distinction among benign, malignant and tuberculous origins of pericardial effusion.

Adolescent↗
PubMed1986

Verapamil infusions in the treatment of atrial tachyarrhythmias.

Ten patients with symptomatic atrial tachyarrhythmias were treated with an iv verapamil bolus (mean 8.5 mg) followed by a continuous verapamil infusion (mean dose 9.4 mg/h). The infusions were titrated to ventricular rate and continued for an average of 20 h, until oral therapy could be instituted. All patients had a significant, sustained reduction in ventricular rate during the infusion, without a significant reduction in mean arterial pressure. Although one patient complained of dizziness after 8 h of infusion therapy, the regimen was generally well tolerated and no patient had clinical worsening of heart failure. These preliminary data suggest that continuous verapamil infusions can safely and effectively control ventricular rate in patients with rapid atrial tachyarrhythmias, until oral medications can be started.

Adult↗
PubMed1986

Automated morphologic evaluation of pulmonary arteries in primary pulmonary hypertension.

Pulmonary wedge angiograms have been shown to reflect the severity of pulmonary vascular disease in congenital heart disease. Thirteen pulmonary wedge angiograms with a balloon occlusion catheter were performed in 11 adult patients (five normals and six with primary pulmonary hypertension [PPH]) and their features related to the resting pulmonary artery pressure (PAP). Individual cine frames from each study were selected and digitized with a computer-assisted operator-interactive program. By fitting densitometric profiles from the vessel segments, serial arterial cross-sectional diameters were calculated from mathematically derived points. There was a strong correlation between arterial taper (T, change in vessel caliber per unit axial length) and a power function of mean PAP with T = 0.304 X PAP-0.59, R = .91, P less than .001. These results demonstrate a correlation between an angiographically derived morphologic characteristic of the pulmonary vasculature (taper) and a hemodynamic parameter (PAP) in PPH. This offers a method to follow the course of the disease and the effects of drug therapy by assessing anatomic changes in the vessels.

Humans↗
PubMed1986

Primary pulmonary hypertension: radiographic and scintigraphic patterns of histologic subtypes.

The chest radiograph and perfusion lung scans were evaluated in 39 consecutive patients with primary pulmonary hypertension to see if these noninvasive methods could distinguish among the histologic subtypes. Chest radiographs were categorized as having either normal lung fields or increased bronchovascular markings. Blood flow on lung scans was graded as normal or as having diffuse, nonsegmental, patchy abnormalities. These patterns were then correlated against pathologic specimens obtained from 19 patients, which were graded on vascular changes and microthrombi. Plexogenic arteriopathy was characterized by a normal chest radiograph and normal distribution of tracer on lung scan. Thromboembolism was characterized by a normal chest radiograph but patchy distribution of tracer on lung scan. Pulmonary veno-occlusive disease was characterized by increased bronchovascular markings on chest radiograph as well as patchy distribution of tracer on lung scan. Distinguishing patients on the basis of their histologic characteristics may be important so that vasodilators or anticoagulants can be selected as therapy.

Adult↗
PubMed1986

Primary pulmonary hypertension: recent advances.

This review highlights newer insights into possible pathogenic mechanisms, clinical features, and treatment of primary pulmonary hypertension. A disease once believed to be found only in younger women, it has now been well documented to occur in both the young and elderly, with a female to male distribution of approximately 1.7:1 at all ages. Several possible etiologic mechanisms have recently been elucidated. Evidence has been forthcoming suggesting a possible role for thromboxane being produced by the pulmonary vascular bed, an underlying abnormality in clot lysis, the presence of antinuclear antibodies which could represent a collagen vascular disorder involving the lung, and a potential aggravating role of female hormones. Unfortunately, the major frustration with primary pulmonary hypertension remains its treatment. Some investigators suggest that anticoagulation may have beneficial effects on long-term survival, although this remains controversial. Most of the recently published articles on therapy have dealt with the use of vasodilators. A careful review of the effectiveness of vasodilators in these patients has failed to show that their chronic use alters either the patient's clinical course, survival, or the disease process itself. It does appear, however, that sustained beneficial effects can be realized in some patients if a substantial reduction in the pulmonary artery pressure is achieved with drug treatment. A thorough understanding of the physiologic characteristics of the pulmonary vascular bed is necessary in order to avoid misinterpreting the effects of vasodilators, which can also be detrimental. The development of vasodilators that are more specific for the pulmonary vascular bed may lead to better clinical results. Strategies for making an earlier diagnosis, however, may be equally important in our attempts to improve the prognosis.

Antibodies, Antinuclear↗
PubMed1985

Magnitude and implications of spontaneous hemodynamic variability in primary pulmonary hypertension.

The pulmonary artery (PA) pressure and pulmonary resistance at rest have been noted to vary spontaneously in patients with primary pulmonary hypertension. To evaluate this variation, in 12 patients (8 women, 4 men, aged 43 +/- 13 years), hourly measurements were made for 6 consecutive hours of heart rate, systemic and PA pressures, cardiac output, systemic and pulmonary resistance. After these baseline measurements the patients were tested with hydralazine and nifedipine therapy. Spontaneous variability in pulmonary pressures and resistances occurred in each patient, with the amount of variation (coefficient of variation) in PA pressure averaging 8% and in total pulmonary resistance 13% over the 6 hours. The patients with the most variability in mean PA pressure also had the most variability in cardiac output (r = 0.69, p = 0.02). Variability also correlated with the severity of the disease, as the patients with the highest total pulmonary resistances also had the most variation for that factor (r = 0.91, p less than 0.01). The amount of variability did not correlate, however, with the acute response to either hydralazine or nifedipine administration. Based on the average coefficients of variation in these 12 patients, estimates were obtained of the percent change needed for an observed change to be attributed to a drug effect with 95% confidence. From these estimates, it was projected that for a single patient, a mean change in pulmonary resistance of 36% or a mean change in PA pressure of 22% would be required in order to attribute the changes to a drug effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Reduced training intensities and loss of aerobic power, endurance, and cardiac growth.

Twelve subjects participated in an exercise program of cycling and running 40 min/day, 6 days/wk. After 10 wk, they continued to train with either a one-third or two-thirds reduction in work rates for an additional 15 wk. Frequency and duration for the additional training remained the same as during the 10 wk of training. The average increases in maximum O2 uptake (VO2 max) were between 11 and 20% when measured during cycling and treadmill running after 10 wk of training. VO2 max was not maintained at the 6-day/wk training levels with a one-third reduction in training intensity but was still higher than pretraining levels. With a two-thirds reduction in intensity, VO2 max declined to an even greater extent than with the one-third reduction. Short-term endurance (approximately 5 min) was maintained in the one-third reduced group but was markedly reduced in the two-thirds reduced group. Long-term endurance was decreased significantly from training by 21% in the one-third reduced group (184-145 min) and by 30% in the two-thirds reduced group (202-141 min). Calculated left ventricular mass, obtained from echocardiographic measurements, increased approximately 15% after training but returned to control levels after reduced training in both groups. These results demonstrate that training intensity is an essential requirement for maintaining the increased aerobic power and cardiac enlargement with reduced training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗