Echocardiography based estimation of pulmonary vascular resistance in patients with pulmonary hypertension: a simultaneous Doppler echocardiography and cardiac catheterization study.

AIMS: Pulmonary vascular resistance (PVR) is an important measurement for the diagnosis of patients with pulmonary hypertension (PH) but needs accurate determination of mean pulmonary artery pressure (PAMP). We aimed to test the accuracy of a Doppler-derived measurement of PVR, using the conventional invasive equation in patients with PH. METHODS AND RESULTS: We investigated 30 patients undergoing right heart catheterization (RHC), mean age 62 ± 13 years, 21 females, with different diseases; idiopathic pulmonary arterial hypertension (PAH) (n = 5), associated PAH (n = 16), chronic thromboembolic PH (n = 6), interstitial lung disease (n = 2), and after closure of an atrial septal defect (n = 1). Patients with impaired left ventricular systolic function (EF < 50%) or elevated pulmonary capillary wedge pressure (PCWP >15 mmHg on RHC) were excluded. We used the formula: PAMP = PASP(echo) × 0.61 + 2 mmHg, where PASP(echo) is the peak tricuspid regurgitation pressure drop + 10 or 7 mmHg. Pulmonary vascular resistance was then calculated as PAMP(echo)- PCWP/cardiac output. Pulmonary capillary wedge pressure was estimated at 10 mmHg in all cases. The Doppler-derived estimation of PVR(echo) was achievable in 90% of patients, in whom accurate calculation of PAMP was obtainable. Pulmonary vascular resistance echo individual values strongly correlated with those from RHC (r = 0.85, P < 0.001 and r = 0.87, P < 0.001 for the two estimated values for right atrial pressure, respectively). The regression equation using this formula was PVR(rhc) = 0.95 × PVR(echo)- 0.29, and the regression line was close to identity. The Bland-Altman plot showed a good agreement between PVR(echo) and PVR(rhc) values, with a mean difference of -0.66 ± 2.1 Wood unit. CONCLUSION: The proposed Doppler-derived formula for estimating PVR based on the conventionally used invasive equation strongly correlates with invasive gold standard measures.

Diesel exhaust inhalation does not affect heart rhythm or heart rate variability.

OBJECTIVE: Exposure to air pollution is associated with increases in cardiovascular morbidity and mortality. This study was undertaken to determine the effect of diesel exhaust inhalation on heart rhythm and heart rate variability in healthy volunteers and patients with coronary heart disease. DESIGN AND SETTING: Double-blind randomised crossover studies in a university teaching hospital. PATIENTS: 32 healthy non-smoking volunteers and 20 patients with prior myocardial infarction. INTERVENTIONS: All 52 subjects were exposed for 1 h to dilute diesel exhaust (particle concentration 300 µg/m³) or filtered air. MAIN OUTCOME MEASURES: Heart rhythm and heart rate variability were monitored during and for 24 h after the exposure using continuous ambulatory electrocardiography and assessed using standard time and frequency domain analysis. RESULTS: No significant arrhythmias occurred during or following exposures. Patients with coronary heart disease had reduced autonomic function in comparison to healthy volunteers, with reduced standard deviations of the NN interval (SDNN, p < 0.001) and triangular index (p < 0.001). Diesel exhaust did not affect heart rate variability compared with filtered air (p > 0.05 for all) in healthy volunteers (SDNN 101 ± 6 vs 91 ± 6, triangular index 20 ± 1 vs 21 ± 1) or patients with coronary heart disease (SDNN 47 ± 5 vs 38 ± 4, triangular index 8 ± 1 vs 7 ± 1). CONCLUSIONS: Brief exposure to dilute diesel exhaust does not alter heart rhythm or heart rate variability in healthy volunteers or well-treated patients with stable coronary heart disease. Autonomic dysfunction does not appear to be a dominant mechanism that can explain the observed excess in cardiovascular events following exposure to combustion-derived air pollution.

Air pollution and atherothrombosis.

Observational studies have consistently demonstrated an association between exposure to air pollution and increased cardiovascular morbidity and mortality. This association is strongest for particulate matter (PM), of which combustion-derived particulate is an important component. Studies assessing the effects of PM exposure in vitro and in vivo have provided insight into the biological mechanisms underlying these observations. In this review we discuss the potential for inhaled particles to impact on the development and progression of atherosclerosis. Oxidative stress and inflammation are central to both the toxicology of PM and the pathogenesis of atherosclerosis. It is possible that nanoparticulates or soluble components of PM may translocate into the bloodstream, resulting in direct effects on atherosclerotic plaque stability, the vascular endothelium, platelet function, and thrombosis. We summarize the latest experimental research and relate this to current understanding of the role of inflammation and vascular dysfunction in the pathogenesis of atherothrombosis. Ongoing research in this area will continue to provide insight into the adverse vascular effects of PM, with the possibility of therapeutic interventions to reduce the impact of environmental air pollution on cardiovascular disease a realistic goal.

Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease.

BACKGROUND: Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function. METHODS: In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 mug per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions. RESULTS: During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (-22+/-4 vs. -8+/-6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve). CONCLUSIONS: Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138 [ClinicalTrials.gov].).