PURPOSE:The purpose of this investigation was to evaluate the efficacy of PoleStriding exercise (a form of walking that uses muscles of the upper and lower body in a continuous movement similar to cross-country skiing) and vitamin E (alpha-tocopherol) to improve walking ability and perceived quality of life (QOL) of patients with claudication pain secondary to peripheral arterial disease (PAD). METHODS:Fifty-two subjects were randomized into four groups: PoleStriding with vitamin E (N = 13), PoleStriding with placebo (N= 14), vitamin E without exercise (N= 13), and placebo without exercise (N = 12). The dose of vitamin E was 400 IU daily. Only the PoleStriding with vitamin E and PoleStriding with placebo groups received PoleStriding instruction and training. Assignment to vitamin E or placebo was double blind. Subjects trained three times weekly for 30-45 min (rest time excluded). Individuals in vitamin E and placebo groups came to the laboratory biweekly for ankle blood-pressure measurements. RESULTS:Results of this randomized clinical trial provide strong evidence that PoleStriding significantly (P< 0.001) improved exercise tolerance on the constant work-rate and incremental treadmill tests. Ratings of perceived claudication pain were significantly less after the PoleStriding training program (P= 0.02). In contrast, vitamin E did not have a statistically significant effect on the subjects' ratings of perceived leg pain (P= 0.35) or treadmill walking duration ( P= 0.36). Perceived distance and walking speed (Walking Impairment Questionnaire) and perceived physical function (Rand Short Form-36) improved in the PoleStriding trained group only (P< 0.001, 0.022 and 0.003, respectively). CONCLUSION:PoleStriding effectively improved the exercise tolerance and perceived QOL of patients with PAD. Little additional benefit to exercise capacity was realized from vitamin E supplementation.

The mechanisms for symptomatic improvement following lung volume reduction surgery for emphysema are poorly understood. We hypothesized that enhanced neuromechanical coupling of the diaphragm is an important factor in this improvement. We studied seven patients with diffuse emphysema before and 3 mo after surgery. Patients showed improvements in 6-min walking distance (p = 0.002) and dyspnea (p = 0.04). The pressure output of the respiratory muscles, quantified as pressure-time product per minute (PTP/min), decreased after surgery (p = 0.03), as did PaCO2 (p = 0.02). Maximal transdiaphragmatic pressures (Pdi(max)) increased from 80.3 +/- 9.5 (SE) to 110.8 +/- 9.3 cm H2O after surgery (p = 0.03), and the twitch transdiaphragmatic pressure response to phrenic nerve stimulation (Pdi(tw)) increased from 17.2 +/- 2.4 to 25.9 +/- 3.0 cm H2O (p = 0.02); these increases were greater than could be accounted for by a decrease in lung volume. The contribution of the diaphragm to tidal breathing, assessed by relative changes in gastric and transdiaphragmatic pressures, increased after surgery (p = 0.008). Net diaphragmatic neuromechanical coupling, quantified as the quotient of tidal volume (normalized to total lung capacity) to tidal change in Pdi (normalized to Pdi(max)), improved after surgery (p = 0.03) and was related to the increase in 6-min walking distance (r = 0.86, p = 0.03) and decrease in dyspnea (r = 0.76, p = 0.08). In conclusion, lung volume reduction surgery effects an improvement in diaphragmatic function, greater than can be accounted for by a decrease in operating lung volume, and enhances diaphragmatic neuromechanical coupling.

The purpose of this initial study was to evaluate a new wheelchair ergometer (WCE) and exercise test protocol for the detection of coronary artery disease in men with lower limb disabilities. Forty-nine patients (63 +/- 9 yr) completed WCE tests without complications. Peak heart rate was 84 +/- 15% (mean +/- SD) of age-predicted maximum and peak double product was 223 +/- 62 x 10(2). The specified target heart rate (> or = 80% age-predicted maximal) or a positive result was achieved in 76% of tests. Fourteen tests were rated positive, 21 as negative and 14 as nondiagnostic for exercise-induced ischemia. In 18 patients who underwent coronary angiography, the predictive value was 100% (10/10) for a positive, and 50% (2/4) for a negative WCE test result. These results suggest that WCE is a viable initial diagnostic option for some persons who cannot adequately perform treadmill or cycle ergometry exercise.

Unstable angina describes an acute, progressive ischemic syndrome. In its initial stages, it is indistinguishable from impending myocardial infarction. Variant angina includes a variety of clinical syndromes caused by coronary artery spasm. Both require approaches to pharmacologic therapy different from those used in the treatment of classic stable angina. Therapy for these syndromes must be aggressive and aimed not only at reducing or eliminating ischemia, but also at preventing progression to myocardial infarction. Pharmacologic agents used in the treatment of unstable angina include nitrates, antiplatelet agents and anticoagulants, beta-blockers, and combination therapies. At present, recommendations for the pharmacologic management of unstable angina include heparin (or aspirin) and IV nitroglycerin. The addition of a beta-blocker and/or calcium channel blocker should be further individualized to the particular patient. For variant angina, nitrates remain the mainstay of therapy. Calcium channel blockers have demonstrated clinical efficacy and may improve survival.

While coronary artery bypass graft surgery and percutaneous transluminal coronary artery angioplasty have been shown to be effective therapeutic interventions for stable angina, pharmacologic interventions have proven to be efficacious, as well. The pharmacologic management of stable angina syndromes involves the select utilization of agents designed to disrupt the ischemic process at various levels. Nitrates, beta-blockers, and calcium channel blockers all have demonstrated usefulness in alleviating ischemia and symptoms of stable angina. Various combinations of antianginal drugs have also been used successfully to treat angina. Research has shown that many of the medications currently in use not only acutely interrupt the ischemic process, but also confer protection against the development of cardiac sequelae in symptomatic patients.