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Results for “PULMONARY HEART DISEASE”

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At least 757 records · Page 42Linked to original sources
PubMed1987

[Left heart ventricle in chronic cor pulmonale patients. Etiological, pathomorphological and organ weight measurement studies].

The histories and the results of the postmortem examinations of 507 patients with chronic pulmonary heart disease were studied. In 62.6% of them left ventricular hypertrophy was found. As probable causes for this left ventricular hypertrophy are suggested: arterial hypertension, ischemic heart disease, hypoxemia, hypercapnia, heart failure, diabetes mellitus. The weight measurement correlations between the left and the right heart ventricles were studied in: "normal hearts", hearts with right ventricular, hypertrophy only, hypertrophy of both ventricles, left ventricular hypertrophy only. A correlation between the mass increase and the wall thickness of the ventricles was established. In the patients with chronic pulmonary heart disease and hypertrophy of both ventricles the mass and the wall thickness of the ventricles increase simultaneously. The possible pathogenetic mechanisms of the left ventricular involvement in patients with chronic pulmonary heart disease are discussed.

Cardiomegaly↗
PubMed1993

Impairment of endothelium-dependent pulmonary artery relaxation in children with congenital heart disease and abnormal pulmonary hemodynamics.

BACKGROUND: Endothelial injury may be an important event in the pathophysiology of pulmonary hypertension. We therefore investigated whether endothelial dysfunction occurs early in children with congenital heart defects who are at risk of developing pulmonary vascular disease. METHODS AND RESULTS: In 25 children aged 3-16 years, we studied the response of the pulmonary circulation to graded infusions of acetylcholine (an endothelium-dependent vasodilator) and nitroprusside (a dilator not dependent on endothelial function). Diameter of a bronchopulmonary segment artery and pulmonary blood flow velocity were measured using quantitative angiography and intra-arterial Doppler catheters in 10 children aged 4-16 years with normal pulmonary hemodynamics (controls), seven children aged 3-12 years with left-to-right shunt lesions resulting in increased pulmonary flow, and eight children aged 3-14 years with established pulmonary vascular disease. In the controls, there was a dose-dependent increase in flow velocity in response to acetylcholine (maximal increase, 93 +/- 7%) and in response to nitroprusside (51 +/- 8%). In contrast, in patients with pulmonary vascular disease, the response of flow velocity to similar doses of acetylcholine (33 +/- 7%, p < 0.01) and nitroprusside (7 +/- 13%, p < 0.01) were impaired. In the patients with high pulmonary flow, there was an impaired response to acetylcholine (46 +/- 9%, p < 0.01), but response to nitroprusside was preserved (42 +/- 8%, p > 0.10), consistent with endothelial dysfunction. Arterial diameter was unchanged during acetylcholine infusion in all subjects and increased only modestly in response to nitroprusside (< or = 10%), indicating that the major site of action of each agent is distal to the segmental pulmonary arteries. CONCLUSIONS: Endothelium-dependent pulmonary artery relaxation can be demonstrated in vivo and is impaired in young patients with increased pulmonary flow secondary to congenital heart disease. This impairment may be an important early event in the pathogenesis of pulmonary vascular disease.

Acetylcholine↗
PubMed1988

Balloon pulmonary valvotomy: palliation for cyanotic heart disease.

Balloon pulmonary valvotomy was attempted in eight children with cyanotic congenital heart disease and pulmonic stenosis who were scheduled for a palliative procedure (shunt). In seven patients the balloon could be positioned across the pulmonary anulus, and valvotomy was performed. Five of the patients had tetralogy of Fallot with multiple levels of pulmonary outflow obstruction. For all patients in whom the balloon could be properly positioned the valvotomy was successful, as judged by arterial hemoglobin saturation, which increased from 72% +/- 5% to 83% +/- 5% (p less than .005). Valvotomy was followed by an immediate rise in mean pulmonary artery pressure (12.6 +/- 2.8 to 18.3 +/- 4.8 mm Hg, p less than 0.05) and a decline in hematocrit level at 2 months (54% +/- 5% to 47% +/- 4%, p less than 0.05). There was no mortality or complication from the valvotomy, and the need for a systemic to pulmonary artery shunt was eliminated in six of eight patients. Follow-up has ranged from 0.5 to 2.8 years. This trial indicates that balloon pulmonary valvotomy can be safely performed and is effective palliation in selected patients with cyanotic heart disease that is not suitable for primary repair. The increased pulmonary flow may improve oxygenation and growth of the pulmonary arteries without the need of a systemic to pulmonary artery shunt.

Catheterization↗
PubMed2000

Comparison of hyperventilation and inhaled nitric oxide for pulmonary hypertension after repair of congenital heart disease.

BACKGROUND: Pulmonary hypertension is associated with congenital heart lesions with increased pulmonary blood flow. Acute increases in pulmonary vascular resistance (PVR) occur in the postoperative period after repair of these defects. These increases in PVR can be ablated by inducing an alkalosis with hyperventilation (HV) or bicarbonate therapy. Studies have shown that these patients also respond to inhaled nitric oxide (iNO), but uncertainty exists over the relative merits and undesirable effects of HV and iNO. HYPOTHESIS: Alkalosis and iNO are equally effective in reducing PVR and pulmonary artery pressure (PAP) in children with pulmonary hypertension after open heart surgery. SETTING: Critical care unit of a tertiary care pediatric hospital. DESIGN: Prospective, randomized, crossover design. PATIENTS: Twelve children with a mean PAP > 25 mm Hg at normal pH after biventricular repair of congenital heart disease. INTERVENTIONS: Patients were assigned to receive iNO or HV (pH > 7.5) in random order, and the effect on hemodynamics was measured. Each treatment was administered for 30 mins with a 30-min washout period between treatments. Finally, both treatments were administered together to look for a possible additive effect. MEASUREMENTS AND MAIN RESULTS: Cardiac output and derived hemodynamic parameters using the dye dilution technique. Hyperventilation, achieved by an increase in ventilator rate without a change in mean airway pressure, decreased Pa(CO2) from a mean (SD) of 43.7+/-5.3 to 32.3+/-5.4 mm Hg and increased pH from 7.40+/-0.04 to 7.50+/-0.03. This significantly altered both pulmonary and systemic hemodynamics with a reduction in PAP, PVR, central venous pressure, and cardiac output and an increase in systemic vascular resistance. In comparison, iNO selectively reduced PAP and PVR only. The reduction in PVR was comparable between treatments, although addition of iNO to HV resulted in a small additional reduction in PVR. An additional decrease in PAP was seen when HV was added to iNO, attributable to a reduction in cardiac output rather than a further decrease in PVR. CONCLUSIONS: Inhaled NO and HV are both effective at lowering PAP and PVR in children with pulmonary hypertension after repair of congenital heart disease. The selective action of iNO on the pulmonary circulation offers advantages over HV because a decrease in cardiac output and an increase in SVR are undesirable in the postoperative period.

Administration, Inhalation↗
PubMed1996

Cancer mortality among silicotics in China's metallurgical industry.

BACKGROUND: We conducted a retrospective cohort study of lung cancer among silicotics in China's metallurgical industries. The study cohort consisted of 4372 male silicotics diagnosed and alive before 1 January 1980. The follow-up period was 1 January 1980 to 31 December 1989. RESULTS: Standardized mortality ratios (SMR) of all deaths, all cancers, chronic bronchopneumonia, pneumonia and pulmonary heart disease, and pulmonary tuberculosis showed statistically significant excesses. The SMR for lung cancer for the total cohort was 237 (P < 0.01). When the total study cohort was divided into various categories by occupation (including iron ore mining, ore-sintering, refractory brick manufacturing, iron and steel smelting, and steel casting), significant excess lung cancer risk was observed among silicotics in all categories (SMR > 200, P < 0.01) except for casting (SMR = 157, P > 0.05). Excess lung cancer was not related to years since diagnosis of silicosis or years of exposure to silica. There was more than twofold excess lung cancer risk among both smoking (SMR = 257, P < 0.01) and non-smoking silicotics (SMR = 209, P < 0.01). Silicosis increased the risk of lung cancer.

China↗