Biomedical subjects

Laurie G Futterman

Publications and source records attributed to Laurie G Futterman.

23 records · Page 2Linked to original sources

PubMed2002

Focus: hypertension in the aged population.

The treatment of the elderly hypertensive patients has reduced the incidence of strokes, cardiovascular events, and cardiovascular morbidity. Regrettably, few hypertensive patients over 80 years of age are being treated, and those who are, are not being treated effectively. Hypertension, at any age, should be treated with a goal of BP <140/90 mmHg, as set by the Joint National Committee on Hypertension. This message should be spread throughout the medical community.

Aged↗

PubMed2002

Novel markers in the acute coronary syndrome: BNP, IL-6, PAPP-A.

Most patients (about 85%) seen in the ED to rule out an acute coronary event do not have acute coronary disease. In addition, the presenting ECG findings have been nondiagnostic in 50% of patients with acute MI. Our current knowledge of atherosclerosis as being a chronic low-grade inflammatory process triggered the search for reliable serum markers that have improved the diagnostic accuracy management and prognosis of this prevalent disease. Newer and potential inflammatory markers currently under investigation deserve watching in future reports. These among others include those markers produced by the arterial wall itself, that is, cell adhesion molecules (CAM), inter-cellular adhesion molecules (ICAM), and vascular adhesion molecules (VCAM). The expression of CAM is a marker of dysfunctional endothelial cells. It is likely that more cardiac markers will be reported in the future. Time will tell.

Acute Disease↗

PubMed2002

Peripheral arterial disease is only the tip of the atherosclerotic "iceberg".

The peripheral vascular system makes up the largest single "organ system" and holds many biological secrets that, when unlocked, can open doors for new treatments for all vascular beds, including those of the coronary and cerebral arteries. The coronary and noncoronary circulations are inseparable and interdependent. Cardiologists as well as primary care physicians should have a global view in the management of patients with PAD. The treatment of atherosclerosis in any of the arterial beds is a multifactorial problem. PAD is underrecognized. Antiplatelet and lipid-lowering therapy is underutilized in patients with PAD. Clopidogrel, an antiplatelet drug, has proven to prevent adverse cardiovascular events in patients with PAD. Therapeutic angiogenesis has been reported to improve severe claudication.

Arteries↗

PubMed2002

High-sensitivity C-reactive protein is the most effective prognostic measurement of acute coronary events.

Inflammation plays a major role in the pathogenesis of arterial atherosclerosis. The stages of atheroma development from early recruitment of leukocytes and fatty streaks to the unstable plaque and finally rupture are mediated by the inflammatory process. Several markers of vascular wall inflammation that can predict future risk of plaque rupture have been identified. However, these lack the specificity of CRP. Numerous large-scale prospective studies established hs-CRP as a strong biochemical marker for the prediction of future first or recurrent coronary events. A Food and Drug Administration-approved method for measuring hs-CRP is currently available.

Biomarkers↗

PubMed2002

Anger and acute coronary events.

A high level of anger has a powerful effect on the incidence of preventable cardiovascular death. Persuasive clinical evidence indicates that anger evokes physiological responses that are potentially life-threatening in the setting of CAD. Finally, emotional stress, anger, or worry have a dominant influence on the severity, frequency, and treatment of angina. The natural history of angina is characterized by episodic variations in the frequency and severity of symptoms coincident with periods of emotional stress. When angina is associated with periods of emotional stress or anger, the angina is not usually a result of progressive coronary disease, but rather is due to an increase in oxygen demand. Appreciation of this concept will help to rule out "true" unstable angina due to progressive coronary disease from recurrent angina that results from an increase in oxygen demand related to emotional stress. The former requires aggressive medical or surgical therapy; the latter, a demand-induced angina, responds to beta-adrenergic blockade and a tranquilizer.

Acute Disease↗