Determining functional significance of subclavian artery stenosis using exercise thallium-201 stress imaging.

Subclavian artery stenosis (SAS) is a rare lesion accounting for nearly 2.5% of all extracranial arterial occlusions. Symptoms from SAS usually relate to subclavian steal, and include syncope, vertigo, ataxia, and, rarely, upper limb paralysis or hemipareses. Upper extremity ischemia may result in intermittent or constant arm pain. The majority of patients with SAS are asymptomatic. Upper extremity ischemia is particularly unusual. More commonly, patients with significant SAS have symptoms of cerebral ischemia, which are usually triggered by vigorous motion of the arm on the side of the severe proximal subclavian obstruction. Stress exercise radionuclide imaging appears to be a valuable modality in determining the functional significance of SAS. We describe a case in which radionuclide imaging with thallium-201 after stress of the upper extremities was used for risk stratification of subclavian stenosis, and to help decide treatment options.

How do HMG-CoA reductase inhibitors prevent stroke?

Stroke is a heterogeneous disorder with significantly high morbidity and mortality. The relationship between serum cholesterol level and the incidence of stroke remains controversial. Recent evidence from primary and secondary prevention trials suggests that treatment with hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors may reduce the incidence of stroke in patients with coronary artery disease (CAD). In this review, we attempt to outline and describe the potential mechanisms of HMG-CoA reductase inhibitors in the prevention of stroke. In addition to their lipid-lowering action HMG-CoA reductase inhibitors appear to exert their beneficial effects by various nonlipid-lowering mechanisms including anti-inflammatory effects, effect on endothelial function and coagulation cascade. Treatment with HMG-CoA reductase inhibitors is associated with decreased progression, plaque stablization and even regression of atheromatous plaque in the carotid arteries. HMG-CoA reductase inhibitors also inhibit the coagulation cascade at various levels such as activation of prothrombin, factor V, factor X and liberation of tissue factor in response to vascular injury. Inhibition of fibrinolysis occurs secondary to inhibition of plasmin generation. Pravastatin therapy is associated with a reduction in the size of aortic atheroma which is an independent risk factor for stroke. Lastly, left ventricular dysfunction after acute myocardial infarction is associated with an increased risk of stroke and HMG-CoA reductase inhibitors may indirectly decrease the incidence of stroke by reducing coronary events. Most of these effects are independent of the cholesterol-lowering effects of HMG-CoA reductase inhibitors. In conclusion, HMG-CoA reductase inhibitors may have a role in primary prevention of stroke in patients with CAD.