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Biomedical subjects

D Bialostozky

Publications and source records attributed to D Bialostozky.

At least 19 recordsLinked to original sources
PubMed1982

The role of hydralazine therapy for pulmonary arterial hypertension of unknown cause.

Hydralazine was administered acutely to 12 patients who had pulmonary arterial hypertension of unknown cause. All of the patients were studied at rest and nine during exercise. On the basis of hydralazine response at rest, the patients were divided in two groups. In six patients (group A), pulmonary arteriolar resistance (Rp) decreased from 8.4 +/- 1.4 to 4.8 +/- 1.4 U/m2 (p less than 0.001), cardiac index (CI) increased from 3.47 +/- 0.3 to 5.86 +/- 0.5 1/min/m2 (p less than 0.005) and systemic resistance (Rs) decreased from 25 +/- 4 to 14 +/- 2 U/m2 (p less than 0.01). The Rp/Rs ratio did not change significantly after hydralazine (0.32 +/- 0.03 vs 0.33 +/- 0.07, NS). In the other six patients (group B), Rs decreased from 25 +/- 2 to 17.0 +/- 1 U/m2 (p less than 0.01), but the other variables did not change significantly. Our results suggest that the pulmonary vasodilatory effect of hydralazine caused a marked reduction in right ventricular afterload in group A. In group B, a marked systemic vasodilatory effect occurred and right ventricular afterload was not reduced. On the basis of the previous hemodynamic response, only group A patients were treated with oral hydralazine (50 mg every 6 hours). Hemodynamic measurements were repeated 48 hours after hydralazine, both at rest and during exercise, as well as 8 months later in five of the six patients in whom the beneficial hemodynamic effects persisted. These data suggest that hydralazine can reduce Rp in selected patients (pulmonary arterial pressure less than 60 mm Hg, Rp less than 15 U/m2 and Rp/Rs ratio less than 0.7) with pulmonary hypertension of unknown cause.

Administration, Oral↗
PubMed1982

Behavior of the pulmonary circulation in chronic obstructive pulmonary disease. Pathogenesis of pulmonary arterial hypertension at an attitude of 2,240 meters.

The hemodynamics of the pulmonary circulation were examined in 28 patients with severe and stable chronic obstructive pulmonary disease (COPD) who were born and raised at high altitude (2,240 meters) (COPD-A). All patients had mean pulmonary pressures (PAP) greater than 16 mmHg. We observed: (1) a low correlation between pulmonary arterial diastolic pressure (PAd) and arterial oxygen saturation (r = 0.38, p less than 0.05); (2) similar PAP in patients with COPD living at sea level (COPD-S) and patients with COPD-A (COPD-S, 32 +/- 7 mmHg; COPD-A, 27.5 +/- 11 mmHg; p = NS), despite more unsaturation in patients with COPD-A (COPD-S, 84.6 +/- 6%; COPD-A, 77.5 +/- 9%; p less than 0.05) and similar arterial pH; (3) lower levels of PAP in COPD-A (COPD-S, 51.7 +/- 10 mmHg; COPD-A, 33.6 +/- 12 mmHg; p less than 0.001) for the same degree of unsaturation (COPD-S, 71 +/- 6%; COPD-A, 71 +/- 8%; p = NS) and a lower arterial pH in COPD-S (COPD-S, 7.34 +/- 0.03; COPD-A, 7.39 +/- 0.04; p less than 0.01). We conclude that pulmonary hypertension caused by chronic alveolar hypoxia is present in COPD-A, but it seems to be decreased when compared with that observed in COPD-S.

Adult↗
PubMed1982

The role of isoproterenol in the preoperative evaluation of high-pressure, high-resistance ventricular septal defect.

The experience we describe derives from the short-term administration of isoproterenol in 15 patients with ventricular septal defect (VSD) and severe pulmonary artery hypertension (PAH). For the whole study group, mean pulmonary artery pressure (PAP) was 68.5 +/- 2.6 mm Hg, pulmonary vascular resistance (Rp) was 11.6 +/- 0.9 U/m2, pulmonary vascular resistance/systemic vascular resistance ratio (Rp/Rs) was 0.9 +/- 0.03, and the pulmonary vascular gradient (PAd-PWP) was 45 +/- 3.5 mm Hg. Infusions of isoproterenol decreased PAP, Rp, Rp/Rs ratio, and PAd-PWP an average of 10.2 mm Hg, 2.88 U/m2, 0.13 and 6.6 mm Hg, respectively, for the whole group (P less than 0.001). On the basis of isoproterenol response, the patients could be divided into two groups: A (n = 4) and B (n = 11). In group A, the PAP decreased from 61.7 +/- 1 to 45 +/- 4 mm Hg, the Rp from 8.9 +/- 0.3 to 4.62 +/- 0.5 U/m2, the Rp/Rs from 0.84 +/- 0.02 to 0.55 +/- .05, and the PAd-PWP from 34.5 +/- 0.9 to 24 +/- 2 mm Hg (mean +/- 1 SE). In group B a less significant change in these measurements was observed. Group A patients underwent VSD repair, and the mean average postoperative decrease in PAP was 31 mm Hg (P less than 0.001). Our findings suggest that in patients with VSD and severe PAH, in whom surgical treatment is controversial, a trial with isoproterenol should be routinely attempted. If the preceding hemodynamic parameters improve significantly, the VSD repair should be performed.

Adolescent↗
PubMed1981

Extrinsic allergic alveolitis caused by pigeon breeding at a high altitude (2,240 meters). Hemodynamic behavior of pulmonary circulation.

The hemodynamic characteristics of the pulmonary circulation were examined in 10 patients with proved extrinsic allergic alveolitis caused by pigeons (EAA-P) raised at a high altitude. All patients had lung biopsies that showed an interstitial inflammatory response with vascular lesions. At rest, all patients had mean pulmonary pressures (PAP) greater than 16 mmHg; the average PAP was 22 +/- 12 mmHg for the whole group. Pulmonary vascular resistance was high and the mean for the whole group was 225 +/- 25 d.s.cm-5. The pulmonary artery diastolic-pulmonary wedge pressure (PAd-PWP) difference was elevated and averaged 8.5 +/- 2 mmHg. All patients were hypoxemic with elevated AaDO2. With exercise, both PAP and PAd-PWP increased abnormally. While breathing oxygen (FIO2, 99.6%) PAP decreased an average of 7 mmHg (p less than 0.05) and PAd-PWP decreased an average of 5 mmHg (p less than 0.05) without a significant change in PWP. The calculated compliance of the elastic pulmonary arteries in EAA-P was not different from that in normal subjects. Alveolar hypoxia produced mainly by EAA-P and presumably enhanced by living at a high altitude appeared to be the factors in the genesis of pulmonary hypertension, because pulmonary artery diastolic pressure and PAd-PWP difference were correlated with arterial oxygen saturation.

Adult↗
PubMed1981

The role of isoproterenol in pulmonary artery hypertension of unknown etiology (primary): short- and long-term evaluation.

The experience derived from the administration of isoproterenol in six patients with pulmonary hypertension of unknown etiology (PAH-UE) is presented. The diagnosis was made after exclusion of other known diseases capable of producing hypertension in the pulmonary circuit. Catheterization was performed, and basal cardiopulmonary parameters, mean pulmonary artery pressure (PAP), pulmonary arteriolar resistance (PAR), cardiac index (CI), alveolar-arterial oxygen tension difference P(A-a)O2, and PaO2 were investigated. The effect of infusing 3 micrograms/min of isoproterenol into the pulmonary artery was studied in five cases. Isoproterenol was given sublingually to one patient who had previously received it intravenously; in another case it was given only sublingually. Significant P values (P less than .05) as a group were obtained, in relation to heart rate, CI, PAR, and mean PAP after isoproterenol. A favorable effect on the heart and lungs was seen in two cases, maintained for three years with sublingual isoproterenol with a favorable cardiorespiratory effect. Use of isoproterenol in PAH-UE is justified at present in those cases with a favorable cardiopulmonary response while no specific therapy is available.

Adolescent↗
PubMed1980

Behavior of the pulmonary circulation in the grossly obese patient. Pathogenesis of pulmonary arterial hypertension at an altitude of 2,240 meters.

Twenty persons living at an altitude of 2,240 meters were studied in order to examine the relative roles of passive and active factors in the genesis of pulmonary arterial hypertension in obesity (overweight, 75 +/- 39 percent). Pulmonary arterial hypertension was present in 80 percent (16) of the patients (mean pulmonary arterial systolic pressure, 45 +/- 17 mm Hg). In 95 percent (19) of the 20 patients, resistance to pulmonary flow at the end of diastole was increased (estimated mean pulmonary arteriolar resistance, 210 +/- 144 dynes.sec.cm-5; mean pulmonary arterial diastolic-pulmonary wedge pressure gradient 7.86 +/- 1.40 mm Hg). The mean arterial oxygen pressure was 50 +/- 9 mm Hg, the arterial carbon dioxide tension was 37 +/- 6 mm Hg and the arterial pH was 7.42 +/- 0.08. Since the pulmonary arterial systolic pressure has been reasonably predicted (r = 0.91; P < 0.001), it would appear that the compliance of the elastic pulmonary arteries in obese patients follows a normal pattern. The behavior of the right ventricular end-diastolic pressure at rest (mean change, 4.6 mm Hg; P < 0.001) and of the pulmonary wedge pressure (mean change, 4.7 mm Hg; P < 0.001) during passive lifting of the legs was indirect evidence of the increase in pulmonary blood volume. The presence of an abnormal resistance to pulmonary blood flow at the end of diastole is suggestive of a decrease in the distention of the pulmonary microcirculation. The pulmonary arterial diastolic-pulmonary wedge pressure gradient and the pulmonary arterial diastolic pressure were related to arterial oxygen unsaturation (r = 0.70; P < 0.05) but not to the concentration of hydrogen ions; thus hypercapnic acidemia appears as a secondary factor in the genesis of pulmonary arterial hypertension at high atitudes. The explanation could be the relative hyperventilation of high altitudes, with a compensatory metabolic alkalosis. The increased pulmonary blood volume and the alveolar hypoxia are the main causes in the pathogenesis of pulmonary arterial hypertension in the grossly obese patient at this altitude.

Altitude↗
PubMed1975

Coronary insufficiency in children. Coronary arteriographic studies in two siblings from a family with hyperbetalipoproteinemia.

A family affected with hyperbetalipoproteinemia was studied. Two siblings, a boy 11 and a girl 9 years of age, with characteristic findings of homozygous type II hyperlipoproteinemia are described. The highly atherogenetic nature of this disorder is illustrated by the occurrence of progressive coronary atheromatosis in the boy, in whom two coronary arteriographic studies documented the development of progressive obstruction of two coronary arteries in the course of 2 years. During this interval angina pectoris developed followed by myocardial infarction, cardiomegaly and congestive heart failure. The sister has remained asymptomatic, with apparently normal coronary arteries at age 9 years. Phonocardiograms were suggestive of aortic valve involvement although no aortic valve gradient was demonstrated by cardiac catheterization.

Child↗
PubMedDate not supplied

[Cardiac involvement in ankylosing spondylitis].

Ankylosing spondylitis is a rheumatic disease that affects the axial skeleton and has predilection for young men. Of its extraarticular manifestations, the cardiac involvement, reported up to 48%, has been pointed out in recent years. It seems to exist a racial variation in the features of the spondylitis and since most of the studies have been performed in northern countries therefore it appears inadequate to extrapolate the conclusions of such studies to our society. We studied 23 patients with definitive diagnosis of ankylosing spondylitis. All of them had a complete physical examination, electrocardiography and X-ray of the chest; eight patients underwent a Holter study of 24 hours and seven patients were examined by echocardiography. The mean age of the group was 36 years; there were 21 men and two women. The mean duration of the rheumatic disease was 11.5 years. In only 4 (17.4%) of the patients we found cardiac involvement that would not be related to another etiology. By the clinic examination we found two patients with isolated aortic insufficiency; one case had a right bundle branch block. The Holter study did not show modifications, except in the one with isolated aortic insufficiency and right bundle branch block, in whom this block became of variable degree. The echocardiographic study showed the mentioned aortic valvular lesions and did reveal the same lesion in another patient in which the other studies were normal. It is emphasized that it is adequate to search for signs of ankylosing spondylitis in every patient with isolated aortic insufficiency or/and conduction disturbances of unknown etiology and also to performe cardiac careful in each patient with ankylosing spondylitis examination.

Aortic Valve Insufficiency↗
PubMedDate not supplied

[Study, using non-invasive methods, of prostheses manufactured at the Instituto Nacional de Cardiología Ignacio Chávez].

We study the phonocardiogram, M mode, two-dimensional and Doppler pulsed echocardiogram of 30 patients, who underwent implantation of a bovine pericardial bioprosthesis manufactured at the Instituto Nacional de Cardiología Ignacio Chávez. We describe 26 patients with prosthesis in mitral position, 22 females and 4 males, with age between 19 to 60 years. After surgery, 22 were in functional I and 2 in class II of the New York Heart Association Criteria. Two patients (6.6%) died of extracardiac complications. Phonocardiogram: Mitral prosthesis closing click (MPCC) were recorded at all, the interval Q wave-MPCC was of 0.09 +/- 0.02 sec. The interval second sound-mitral prosthesis opening click (S2-MPOC) measured 0.10 +/- 0.01 sec. Mid-diastolic murmur were recorded in 8 patients (30.7%). The O-F slope of the apexcardiogram was of 82 +/- 40 mm/sec. Ten patients had tricuspid insufficiency. Echocardiogram: The D-E velocity of mitral prosthesis opening was of 318 +/- 99 mm/sec and the E-F slope velocity of 15 +/- 6.2 mm/sec. All patients except one showed paradoxical motion of the intraventricular septum. The prosthesis stents distance was of 14.1 +/- 2 mm, the internal diameter of 17.8 +/- 2.9 mm and the valvular area was calculated in 2.5 +/- 0.08 cm2. The flow velocity/diameter was 62.6 +/- 26.8 cm/sec/mm and the flow velocity/opening area of 52.5 +/- 26.1 cm/sec/cm2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Pulmonary eosinophilia and pulmonary arterial hypertension].

Pulmonary artery hypertension is a rare feature in the eosinophilic pulmonary syndrome, it had been observed only in some cases of tropical pulmonary eosinophilia. A case of prolonged pulmonary eosinophilia with reversible pulmonary hypertension is presented.

Humans↗