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Results for “PULMONARY HEART DISEASE”

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PubMed1989

[Correlative evaluation of electrocardiographic changes and spirometric parameters in pulmonary cardiopathy secondary to chronic obstructive bronchopneumopathy].

EKG is not considered a sensitive procedure for diagnosis of chronic pulmonary heart disease (CPHD). We performed a correlative study between EKG signs and spirometry in chronic obstructive pulmonary disease (COPD). Fifty-six consecutive in-patients (M 52, F 4, age 59.1 +/- 13.1 yrs) with COPD and echocardiographic/roentgenologic signs of right ventricular enlargement were studied. An EKG score system (0-6) was developed considering: 1) AQRS greater than or equal to 90 degrees; 2) P waves greater than or equal to 2.5 mm; 3) R wave V1 greater than or equal to 7 mm or R/S V1 greater than or equal to 1; 4) R/S V5 less than or equal to 1; 5) RV strain pattern; 6) RBBB. Significant (p less than 0.01) linear correlations were observed between: a) AQRS vs FEV1 (r = -0.59); b) AQRS vs FEV1/FVC% (r = -0.61); c) R/S V5 vs FEV1, (r = +0.38); d) EKG score vs FEV1 (r = -0.42); e) EKG score vs FEV1/FVC% (r = -0.40). Significant relationship between EKG score and spirometry suggests that this criterium can be useful for a more reliable ecg diagnosis of CPHD.

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PubMed2003

Pulmonary blood pressure, not flow, is associated with net endothelin-1 production in the lungs of patients with congenital heart disease and normal pulmonary vascular resistance.

OBJECTIVE: Endothelin-1 concentrations are increased in patients with increased mean pulmonary arterial pressure, pulmonary blood flow, and pulmonary vascular resistance. However, endothelin-1 concentrations have not been well characterized in patients with congenital heart disease and normal pulmonary vascular resistance. In particular, it is unclear whether pressure or flow is the key regulator of endothelin- 1 in this setting. We tested the hypothesis that pulmonary blood pressure and not flow is associated with net endothelin-1 production in patients with congenital heart disease and normal pulmonary vascular resistance. METHODS: With a commercially available immunoassay, we measured endothelin-1 concentrations in pulmonary arterial and pulmonary venous plasma of 56 consecutive patients with congenital heart disease and pulmonary vascular resistance less than 2 U. m(2) undergoing cardiac catheterization. We used multiple linear regression to analyze the effect of demographic and hemodynamic variables on pulmonary arterial and venous endothelin-1 concentrations and on the change of endothelin-1 concentration over the pulmonary vascular bed. RESULTS: Multiple linear regression revealed that of all the hemodynamic variables tested, mean pulmonary arterial pressure had the greatest effect on increasing the change of endothelin-1 concentration over the pulmonary vascular bed (P <.0001). Pulmonary blood flow did not have any effect on endothelin-1 concentrations or on the change of endothelin-1 concentration over the pulmonary vascular bed. CONCLUSIONS: This study shows that pulmonary blood pressure and not flow is associated with net endothelin-1 production in patients with congenital heart disease and normal pulmonary vascular resistance.

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