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1.
Heart Lung Circ ; 19(1): 38-42, 2010 Jan.
Article in English | MEDLINE | ID: mdl-19783212

ABSTRACT

BACKGROUND: Left heart disease and pulmonary vascular disease (PVD) both lead to raised pulmonary artery pressure (PAP) but differ in pathophysiology, prognosis and treatment. There are currently no criteria for diagnosing PVD in the presence of left heart disease. We therefore studied the relationship between PAP and pulmonary capillary wedge pressure (PCWP, a measure of left atrial pressure) to help define when PAP should be considered 'out-of-proportion' to PCWP, thus suggestive of PVD. METHODS: Retrospective analysis of 898 consecutive simultaneous left and right heart catheterisations. Of these, 684 patients (age 63+/-14 years) were classified according to presence of absence of left heart disease. Multilinear regression explored the relationship between mean PAP and PCWP, age, gender, systemic haemodynamics and left heart disease diagnosis. RESULTS: Increasing PCWP, age and heart rate and female gender were associated with higher PAP (p<0.0001, p=0.049, p<0.0001 and p=0.0015, respectively). Thus, in males: (mean PAP)=0.94+[1.15 x (mean PCWP)]+[0.03 x (age)]+[0.07 x (heart rate)] (for females add 1.38 mm Hg). This model accounted for 75% of variability in PAP, with PCWP alone accounting for 74%. CONCLUSIONS: A strong linear relationship exists between PAP and PCWP, which may help identify PAP 'out-of-proportion' to PCWP, facilitating the diagnosis of PVD in patients with pulmonary hypertension and left heart disease.


Subject(s)
Cardiomyopathies/complications , Heart Valve Diseases/complications , Hypertension, Pulmonary/diagnosis , Myocardial Ischemia/complications , Pulmonary Artery/physiopathology , Pulmonary Wedge Pressure , Cardiac Catheterization , Cardiomyopathies/diagnosis , Confidence Intervals , Female , Heart Valve Diseases/diagnosis , Hemodynamics , Humans , Hypertension, Pulmonary/physiopathology , Linear Models , Male , Middle Aged , Multivariate Analysis , Myocardial Ischemia/diagnosis , Prognosis , Retrospective Studies , Risk Factors
2.
Catheter Cardiovasc Interv ; 71(3): 327-32, 2008 Feb 15.
Article in English | MEDLINE | ID: mdl-18288727

ABSTRACT

OBJECTIVE: It has previously been observed that coronary diameter may increase following relief of flow-limiting obstruction. Flow mediated dilatation (FMD) is a fundamental adaptive mechanism for arteries, which is dependent on intact endothelial function. We thus aimed to characterize whether the degree of this flow-mediated dilatation was related to risk factors, which may impair endothelial function. DESIGN: We measured coronary diameter with quantitative angiography before and after relief of chronic total or subtotal (>or=99%) occlusion in 171 patients, in which TIMI-0 or TIMI-1 flow was rapidly restored to TIMI-3 (with attendant increase in flow hypothesized to result in FMD). PATIENTS: Of the 171 patients, 73% were male, 62% were current or ex-smokers, 47% were diabetic, 53% had hypertension, 64% had dyslipidemia (documented hypercholesterolemia or total cholesterol >5.0 mg/dL) and 65% were taking statin therapy. RESULTS: Mean vessel diameter was 2.8 +/- 0.7 mm and flow-mediated dilatation measured 15.1% +/- 20.1% in target vessel, compared with 1.6 +/- 3.1 in control vessels (P < 0.05). FMD was strongly and inversely related to baseline vessel diameter (r = -0.48, P < 0.001). The degree of vessel dilation correlated negatively with the presence of diabetes (r = -0.33, P < 0.001), smoking (r = -0.30, P < 0.001) and extent of coronary artery disease (CAD, r = -0.17, P = 0.01) and positively with the use of statins (r = 0.27, P = 0.001). These factors, apart from extent of CAD, remained significant predictors of FMD on multivariate analysis. CONCLUSIONS: FMD occurs in human coronary arteries following restoration of flow. The magnitude of FMD appears related to vascular risk factors and their treatment.


Subject(s)
Coronary Angiography/methods , Coronary Circulation/physiology , Coronary Stenosis/diagnostic imaging , Coronary Stenosis/therapy , Vascular Patency/physiology , Analysis of Variance , Angioplasty, Balloon, Coronary/methods , Blood Flow Velocity , Case-Control Studies , Cohort Studies , Coronary Stenosis/mortality , Endothelium, Vascular/physiopathology , Female , Follow-Up Studies , Humans , Male , Middle Aged , Multivariate Analysis , Probability , Reference Values , Severity of Illness Index , Survival Rate , Treatment Outcome , Vascular Resistance/physiology
3.
PLoS One ; 7(3): e33331, 2012.
Article in English | MEDLINE | ID: mdl-22479385

ABSTRACT

BACKGROUND: There is increasing recognition that pulmonary artery stiffness is an important determinant of right ventricular (RV) afterload in pulmonary arterial hypertension (PAH). We used intravascular ultrasound (IVUS) to evaluate the mechanical properties of the elastic pulmonary arteries (PA) in subjects with PAH, and assessed the effects of PAH-specific therapy on indices of arterial stiffness. METHOD: Using IVUS and simultaneous right heart catheterisation, 20 pulmonary segments in 8 PAH subjects and 12 pulmonary segments in 8 controls were studied to determine their compliance, distensibility, elastic modulus and stiffness index ß. PAH subjects underwent repeat IVUS examinations after 6-months of bosentan therapy. RESULTS: AT BASELINE, PAH SUBJECTS DEMONSTRATED GREATER STIFFNESS IN ALL MEASURED INDICES COMPARED TO CONTROLS: compliance (1.50±0.11×10(-2) mm(2/)mmHg vs 4.49±0.43×10(-2) mm(2/)mmHg, p<0.0001), distensibility (0.32±0.03%/mmHg vs 1.18±0.13%/mmHg, p<0.0001), elastic modulus (720±64 mmHg vs 198±19 mmHg, p<0.0001), and stiffness index ß (15.0±1.4 vs 11.0±0.7, p = 0.046). Strong inverse exponential associations existed between mean pulmonary artery pressure and compliance (r(2) = 0.82, p<0.0001), and also between mean PAP and distensibility (r(2) = 0.79, p = 0.002). Bosentan therapy, for 6-months, was not associated with any significant changes in all indices of PA stiffness. CONCLUSION: Increased stiffness occurs in the proximal elastic PA in patients with PAH and contributes to the pathogenesis RV failure. Bosentan therapy may not be effective at improving PA stiffness.


Subject(s)
Hypertension, Pulmonary/diagnostic imaging , Pulmonary Artery/diagnostic imaging , Ultrasonography, Interventional/methods , Vascular Stiffness/physiology , Aged , Antihypertensive Agents/therapeutic use , Bosentan , Familial Primary Pulmonary Hypertension , Female , Humans , Hypertension, Pulmonary/diagnosis , Hypertension, Pulmonary/physiopathology , Male , Middle Aged , Pulmonary Artery/pathology , Pulmonary Artery/physiopathology , Pulmonary Wedge Pressure/drug effects , Pulmonary Wedge Pressure/physiology , Reproducibility of Results , Sensitivity and Specificity , Sulfonamides/therapeutic use , Treatment Outcome , Vascular Stiffness/drug effects
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