Depressive symptoms and heart rate variability in postmenopausal women.

BACKGROUND: Depressive symptoms have been associated with increased cardiac morbidity and mortality rates, but the pathophysiologic mechanism linking depressive symptoms to cardiovascular outcome has yet to be fully understood. Lower heart rate variability has also been associated with increased risk of cardiac events in healthy individuals and in patients with coronary artery disease. Findings regarding a relationship between depressive symptoms and heart rate variability that could explain increased cardiovascular risk have been inconsistent across studies. METHODS: As an ancillary study to the Women's Health Initiative Observational Study, 3372 postmenopausal women aged 50 to 83 years were enrolled for further evaluation using 24-hour ambulatory electrocardiographic monitoring. A shortened version of the Center for Epidemiological Studies Depression Scale and the Diagnostic Interview Schedule were administered. Women with adequate electrocardiographic data and depressive symptom information and without coronary artery disease were analyzed (n = 2627). RESULTS: Two hundred sixty-nine women (10.2%) had depressive symptoms as measured using the 2 instruments. Women with depressive symptoms had a higher mean +/- SD heart rate (77.4 +/- 9.6 vs 75.5 +/- 8.5 beats/min) and lower heart rate variability than women without depressive symptoms. All differences remained significant after adjusting for age (P<.01). CONCLUSIONS: Women with depressive symptoms had significant reductions in heart rate variability and higher heart rates, suggestive of increased sympathetic tone. These findings may contribute to the increased cardiac morbidity and mortality rates associated with depression in other studies.

Pharmacological treatment of patients with peripheral arterial disease.

Atherosclerosis is a disease process that affects the coronary, cerebral and peripheral arterial circulation. While great emphasis has been placed on the aggressive pharmacological management of coronary artery disease, less attention has been paid to the pharmacological management of peripheral vascular disease, despite its significant morbidity and mortality. The purpose of medical management in peripheral arterial disease is to relieve symptoms of claudication and to prevent thrombotic vascular events. These goals are best achieved through aggressive risk factor modification and pharmacotherapy. Risk factor modification includes smoking cessation, adequate control of blood pressure and cholesterol, as well as aggressive glycaemic control in patients with diabetes mellitus. Antiplatelet therapy and relief of claudication is also achieved through pharmacotherapy. With aggressive risk factor modification and adequate pharmacotherapy, patients with peripheral arterial disease can have an improved quality of life as well as prolonged survival.

Detection and reproducibility of mental stress-induced myocardial ischemia with Tc-99m sestamibi SPECT in normal and coronary artery disease populations.

BACKGROUND: Mental stress-induced ischemia, as detected by radionuclide studies, has yielded reversible ischemia in only 30% to 60% of patients with exercise-induced ischemia. Little is known about the reproducibility of myocardial perfusion imaging in detecting mental stress-induced ischemia. The purpose of this study was to further evaluate the occurrence and reproducibility of mental stress-induced ischemia in patients with coronary artery disease (CAD) and in normal control subjects with a low likelihood of CAD by using sestamibi single photon emission computed tomography (SPECT) imaging. METHODS AND RESULTS: A total of 40 patients were enrolled in this study: 19 patients with CAD and typical angina or reversible ischemia (positive exercise treadmill study or positive adenosine thallium study) and 21 normal control subjects underwent mental stress testing as well as myocardial perfusion imaging. The subjects were given a speaking task, and SPECT imaging was subsequently performed. Two experienced readers compared mental stress imaging with a resting image using a 20-segment cardiac model. Hemodynamic changes in blood pressure and heart rate with mental stress were also measured in all subjects. Each patient with CAD also underwent repeat mental stress testing and myocardial imaging approximately 2 weeks later. Of the 19 patients with CAD and typical angina or with evidence of reversible ischemia, 16 (84%) demonstrated ischemia with mental stress, as detected by sestamibi SPECT imaging. The mean number of new or worsened perfusion defects attributable to mental stress was 3.5, with a mean severity of 1.7. These results were also reproducible. With repeated mental stress testing and myocardial imaging, 12 of the 16 CAD patients (75%) demonstrated evidence of myocardial ischemia. None of the 21 normal control subjects had evidence of mental stress-induced myocardial ischemia. Mental stress also induced reproducible and significant hemodynamic changes in CAD patients. CONCLUSIONS: In patients with known CAD with typical angina or with evidence of reversible ischemia despite taking medications, mental stress was very effective in inducing myocardial ischemia, as detected by sestamibi SPECT imaging. Mental stress was also found to elicit significant hemodynamic responses. Furthermore, these findings demonstrated good reproducibility.