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1
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A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis.
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N Engl J Med
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4.93
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3
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Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis.
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4.71
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4
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Smoke-free legislation and hospitalizations for acute coronary syndrome.
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2.66
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Omega 3 fatty acids and cardiovascular disease--fishing for a natural treatment.
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2.47
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Endothelial function is associated with pulse pressure, pulse wave velocity, and augmentation index in healthy humans.
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2.29
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16
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The ROSE (risk stratification of syncope in the emergency department) study.
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2.22
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17
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2.21
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Randomized controlled trial of dual antiplatelet therapy in patients undergoing surgery for critical limb ischemia.
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2.06
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Reducing personal exposure to particulate air pollution improves cardiovascular health in patients with coronary heart disease.
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2.02
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2.01
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Diesel exhaust inhalation increases thrombus formation in man.
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1.96
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Vascular dysfunction in chronic obstructive pulmonary disease.
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1.84
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Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.
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1.79
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Previous coronary stent implantation and cardiac events in patients undergoing noncardiac surgery.
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1.75
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Do inhaled carbon nanoparticles translocate directly into the circulation in humans?
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Auto-titrating continuous positive airway pressure therapy in patients with chronic heart failure and obstructive sleep apnoea: a randomized placebo-controlled trial.
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Calcific aortic stenosis: a disease of the valve and the myocardium.
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1.52
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1.51
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Non-invasive measurement of cardiac output in patients with chronic heart failure.
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1.51
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Role of the endothelium in the vascular effects of the thrombin receptor (protease-activated receptor type 1) in humans.
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Reduced vascular complications and length of stay with transradial rescue angioplasty for acute myocardial infarction.
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1.46
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1.45
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Abdominal aortic aneurysm growth predicted by uptake of ultrasmall superparamagnetic particles of iron oxide: a pilot study.
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49
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Direct impairment of vascular function by diesel exhaust particulate through reduced bioavailability of endothelium-derived nitric oxide induced by superoxide free radicals.
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Increased platelet activation in patients with stable and acute exacerbation of COPD.
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