Michael E. DeBakey Institute for Comparative Cardiovascular Science and Biomedical Devices, Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843, USA.
Coronary collateral vessels serve as a natural protective mechanism to provide coronary flow to ischemic myocardium secondary to critical coronary artery stenosis. The innate collateral circulation of the normal human heart is typically minimal and considerable variability occurs in extent of collateralization in coronary artery disease patients. A well-developed collateral circulation has been documented to exert protective effects upon myocardial perfusion, contractile function, infarct size, and electrocardiographic abnormalities. Thus therapeutic augmentation of collateral vessel development and/or functional adaptations in collateral and collateral-dependent arteries to reduce resistance into the ischemic myocardium represent a desirable goal in the management of coronary artery disease. Tremendous evidence has provided documentation for the therapeutic benefits of exercise training programs in patients with coronary artery disease (and collateralization); mechanisms that underlie these benefits are numerous and multifaceted, and currently under investigation in multiple laboratories worldwide. The role of enhanced collateralization as a major beneficial contributor has not been fully resolved. This topical review highlights literature that examines the effects of exercise training on collateralization in the diseased heart, as well as effects of exercise training on vascular endothelial and smooth muscle control of regional coronary tone in the collateralized heart. Future directions for research in this area involve further delineation of cellular/molecular mechanisms involved in effects of exercise training on collateralized myocardium, as well as development of novel therapies based on emerging concepts regarding exercise training and coronary artery disease.
"The mechanism of such an improvement was generally attributed to the enhanced endothelial synthesis of NO, which is stimulated by an increase in blood flow . Improvement in blood flow could be due to collateralization, which has been suggested in patients with coronary artery disease after exercise training . Confirmation of this thesis is justified by a significant improvement in ABI at the end of the program, which is closely associated with an increase in blood flow. "
[Show abstract][Hide abstract] ABSTRACT: In this prospective study we evaluated the effects of treadmill training on patients' walking ability, as well as endothelial function, high-sensitivity C-reactive protein (hs-CRP), and fibrinogen concentration.
A total of 67 patients with stable intermittent claudication were included in a 12-week supervised training program. An observational follow-up period then lasted a mean of 37 weeks. Forty patients completed follow-up. Changes in blood pressure, flow-mediated dilatation (FMD), and treadmill walking performance expressed as maximal walking time (MWT) were assessed before and after the training program and during the follow-up period. Moreover, ankle/brachial index (ABI), plasma levels of hs-CRP, fibrinogen, as well as a lipid profile were assessed before and after the training program.
Maximal walking time improved significantly after treadmill training by 90% (p<0.001) and after follow-up by 64% (p<0.001) in comparison to baseline. FMD values increased by 43% (p<0.001) after the training program, and by 29% (p=0.058) after follow-up, compared to baseline. We noticed a significant decrease in hs-CRP concentration (p=0.025) and an increase in ABI values (p=0.039) in response to the treadmill training program. No effect on lipid profile was observed.
The 12-week treadmill training program prolonged the asymptomatic walking distance. The improvement in FMD indicates a systemic effect of the treadmill program on endothelial function. The supervised treadmill training provides an effective and safe treatment option in patients with PAD. The effects of unsupervised exercise during follow-up period after treadmill programs remain tentative and underestimated.
Journal of Cardiology 01/2014; 64(2). DOI:10.1016/j.jjcc.2013.12.002 · 2.78 Impact Factor
"Also physical activity was most often limited by non-specific symptoms such as shortness of breath, fatigue, and weakness, and limitation by chest tightness or discomfort was less common. In clinical trials, exercise training reduces dyspnoea and fatigue, increases muscle strength, and improves angina.6,20,21 It is therefore possible that lack of fitness in part explains the association between symptoms and less physical activity. "
[Show abstract][Hide abstract] ABSTRACT: Despite the known benefits of regular exercise, the reasons why many coronary heart disease (CHD) patients engage in little physical activity are not well understood. This study identifies factors associated with low activity levels in individuals with chronic CHD participating in the STABILITY study, a global clinical outcomes trial evaluating the lipoprotein phospholipaseA2 inhibitor darapladib.
Prior to randomization, 15 486 (97.8%) participants from 39 countries completed a lifestyle questionnaire. Total physical activity was estimated from individual subject self-reports of hours spend each week on mild, moderate, and vigorous exercise, corresponding approximately to 2, 4, and 8 METS, respectively. Multivariate logistic regression evaluated clinical and demographic variables for the lowest compared with higher overall exercise levels, and for individuals who decreased rather than maintained or increased activity since diagnosis of CHD. The least active 5280 subjects (34%) reported exercise of ≤24MET.h/week. A total of 7191 subjects (46%) reported less exercise compared with before diagnosis of CHD. The majority of participants were either 'not limited' or 'limited a little' walking 100 m (84%), climbing one flight of stairs (82%), or walking 1 km/½ mile (68%), and <10% were limited 'a lot' by dyspnoea or angina. Variables independently associated with both low physical activity and decreasing exercise after diagnosis of CHD included more co-morbid conditions, poorer general health, fewer years of education, race, and country (P < 0.001 for all).
In this international study, low physical activity was only partly explained by cardiovascular symptoms. Potentially modifiable societal and health system factors are important determinants of physical inactivity in patients with chronic CHD.
European Heart Journal 09/2013; 34(42). DOI:10.1093/eurheartj/eht258 · 15.20 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: A combination of poor diet and physical inactivity was the second leading "actual cause of death" in 2000 in the United States, with cardiovascular disease and atherosclerosis, in particular, being the most significant contributor. It is widely recognized that the development of atherosclerosis and coronary heart disease (CHD) is blunted by a life style incorporating moderate levels of physical activity. Physical inactivity is an independent risk factor for CHD, however the mechanisms underlying the protective effect of a physically active lifestyle remain largely unknown. This Highlighted Topic series of mini-reviews will examine some of the most plausible mechanisms, and how the effect of activity may be modified by genetics and disease. The goal is to provide new information addressing these important questions and provide the impetus for future studies. We believe the field is on the verge of a major advance in understanding how exercise training programs work with lifestyle interventions to prevent and treat atherosclerosis and CHD.
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