The Role of Tobacco Cessation, Antiplatelet and Lipid-Lowering Therapies in the Treatment of Peripheral Arterial Disease

1997 ◽  
Vol 2 (3) ◽  
pp. 243-251 ◽  
Author(s):  
Alan T Hirsch ◽  
Diane Treat-Jacobson ◽  
Harry A Lando ◽  
Dorothy K Hatsukami

Despite the widely held belief that there are no effective medical therapies for peripheral arterial disease (PAD), current data suggest that medical therapies can effectively modify the natural history of atherosclerotic lower extremity arterial occlusive disease. The ideal medical therapy would improve claudication, forestall the onset of limb-threatening events, decrease rates of invasive interventional therapies and improve long-term patient survival. These ideal outcomes might be achieved through the use of smoking cessation interventions, including behavioral and pharmacological therapy, and the administration of antiplatelet and lipid-lowering medications in patients with PAD.

2017 ◽  
Vol 52 (2) ◽  
pp. 140
Author(s):  
Yudi Her Oktaviono

Peripheral arterial disease (PAD) is usually caused by multilevel atherosclerotic disease, typically in patients with a history of cigarette smoking, diabetes mellitus, or both. Intermittent claudication (IC), an early manifestation of PAD, commonly leads to reduced quality of life for patients who are limited in their ambulation. Percutaneous intervention for peripheral artery disease has evolved from balloon angioplasty for simple focal lesions to multimodality techniques that enable treatment of severe arterial insufficiency. Especially for high-grade stenoses or short arterial occlusions, percutaneous transluminal angioplasty (PTA) should be the method of first choice followed by the best surgical procedure later on. To achieve good long-term efficacy, a close follow-up including objective tests of both the arterial lesion and hemodynamic status, surveillance of secondary preventive measures and risk factor control is mandatory.


1996 ◽  
Vol 1 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Alan T Hirsch

Patients with peripheral arterial disease are often perceived to suffer from a disorder whose pathogenesis and symptoms are not amenable to drug therapies. This clinical misperception remains prevalent despite an abundance of data suggesting that diverse pharmacotherapies may modulate the natural history of this disease. Patients with chronic limb arterial occlusive disease suffer from a disease that is characterized by: (1) a prolonged asymptomatic state that can be identified by simple physical examination and confirmed by measurement of the ankle brachial index; (2) a multi-year period of symptomatic claudication; and (3) a variable rate of progression to critical limb ischemia or acute arterial occlusion. This stage-dependent disease progression is mediated via the dynamic, but as yet incompletely understood, interaction of factors that elicit endothelial dysfunction, atherogenesis, and thrombosis. Current data suggest that each of these contributory disease processes can be modulated by extant pharmacotherapies. Additionally, many novel pharmacotherapeutic agents that are currently under investigation may further improve the ability of clinicians to modulate these fundamental biologic processes. Pharmacologic therapies should be targeted to decrease the rate of limb arterial disease progression, to improve limiting symptoms, and to prolong life. Symptoms of claudication can be objectively assessed via both exercise testing and disease-specific questionnaires. The presence of lower extremity atherosclerotic disease is predictive of the presence of coronary heart disease and a foreshortened five-year survival. Current data suggest that clinical investigations should be able to effectively stratify this relative risk via use of both clinical variables (e.g., age, diabetes mellitus, tobacco use, etc.) or by measurement of the ankle brachial index (ABI). The role of the physician is to decrease suffering and to prolong life. Judicious administration of medical therapies can play a critical role in helping the vascular practitioner accomplish these goals.


2007 ◽  
Vol 45 (5) ◽  
pp. 936-943 ◽  
Author(s):  
Harm H.H. Feringa ◽  
Stefanos E. Karagiannis ◽  
Virginie H. van Waning ◽  
Eric Boersma ◽  
Olaf Schouten ◽  
...  

2015 ◽  
Vol 29 (5) ◽  
pp. 877
Author(s):  
Isabella Possagnolli ◽  
Christian Bianchi ◽  
Teruya Theodore ◽  
Chiriano Jason ◽  
Vicki Bishop ◽  
...  

2001 ◽  
Vol 85 (02) ◽  
pp. 234-239 ◽  
Author(s):  
M. L. Bots ◽  
F. Haverkate ◽  
P. Meijer ◽  
A. Hofman ◽  
C. Kluft ◽  
...  

SummaryTo determine the presence of a ‘hypercoagulable state’ as assessed by indices of thrombin and plasmin generation and of the amount of fibrin that is lysed, in patients with stable coronary, cerebral and peripheral arterial disease a population-based cross-sectional study was performed. From a population-based cohort comprising 7983 men and women aged 55 years and over, we randomly selected 127 subjects with a history of myocardial infarction, 124 with a history of stroke and/or transient ischemic attack, 131 patients with peripheral arterial disease and 263 control subjects in the same age group without arterial disease. Subjects using anticoagulant drugs were not selected. F1+2, TAT, and PAP were not associated with a history of cardiovascular events, nor with peripheral arterial disease. In contrast, positive associations were found for D-Dimer. Mean D-Dimer level was 40 μg/l (95% CI 35,44) in control subjects; 53 μg/l (47, 61) in those with a history of myocar-dial infarction and 51 μg/l (45, 58) in those with a history of stroke and or transient ischemic attack. D-Dimer increased gradually with increasing severity of peripheral atherosclerosis; a decrease in ankle/arm systolic blood pressure ratio of 0.1 was associated with an increase in D-Dimer of 3.9 μg/l (p<0.01). This was more pronounced in subjects with higher F1+2, TAT and PAP concentration. In conclusion, the markers of onset of coagulation F1+2, TAT and PAP are not associated with the presence of arterial disease, but increased levels of these markers are necessary for the positive association between D-Dimer and arterial disease.


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