In experiments on the closed-chest dogs it was shown that NOS inhibition resulted in the significant alterations of hemodynamic indices (coronary and peripheral vascular resistance, cardiac output and heart rate) under local myocardial ischemia/reperfusion in comparison with control experiments. At the first time it was shown that NOS inhibition activated the autophagic destruction of cardiomyocytes in the ischemic myocardium and could reduce an area of functionally active myocardium. L-arginine administration attenuated cardio- and hemodynamic disturbances, that substantially improved the course of ischemia/reperfusion, diminished the ultrastructural changes in myocardium and prevented development of autophagic programmed cell death.
In a cross-sectional autopsy study of 107 Inuit in Greenland, the extent of arterial surface involvement with atherosclerosis was evaluated in the presence of known or estimated environmental risk factors for coronary heart disease (CHD): age, gender, obesity, serum lipids, smoking, and hypertension. Mean, median, and range values for all of the risk factor variables and for the extent of atherosclerosis in the thoracic aorta, abdominal aorta, right coronary artery, and left anterior descending coronary artery are reported by age strata, along with the results of covariant analysis of the dependence of the extent of atherosclerosis upon the risk factors. No significant differences between females and males were found in either the risk factors or prevalence and extent of atherosclerosis in the aorta and in the coronary arteries. It appears that the extent of advanced atherosclerotic lesions in Greenlanders appears to be the same as that previously reported in a similar study in Alaska Natives.
Coronary artery calcium (CAC) and physical performance have been shown to be associated with mortality, but it is not clear whether one of them modifies the association. We investigated the association between the extent of CAC and physical performance among older individuals and explored these individual and combined effects on cardiovascular disease (CVD) mortality and non-CVD mortality.
We studied 4074 participants of the AGES-Reykjavik Study who were free from coronary heart disease, had a CAC score calculated from computed tomography scans and had data on mobility limitations and gait speed at baseline in 2002-2006 at a mean age of 76 years. Register-based mortality was available until 2009.
Odds for mobility limitation and slow gait increased according to the extent of CAC. Altogether 645 persons died during the follow-up. High CAC, mobility limitation and slow gait were independent predictors of CVD mortality and non-CVD mortality. The joint effect of CAC and gait speed on non-CVD mortality was synergistic, i.e. compared to having low CAC and normal gait, the joint effect of high CAC and slow gait exceeded the additive effect of these individual exposures on non-CVD mortality. For CVD mortality, the effect was additive i.e. the joint effect of high CAC and slow gait did not exceed the sum of the individual exposures.
The extent of CAC and decreased physical performance were independent predictors of mortality and the joint presence of these risk factors increased the risk of non-CVD mortality above and beyond the individual effects.
Cites: J Nutr Health Aging. 2009 Dec;13(10):881-919924348
Cites: Heart. 2010 Mar;96(5):380-419955091
Cites: Stroke. 2010 May;41(5):891-720360538
Cites: BMJ. 2010;341:c446720829298
Cites: JAMA. 2011 Jan 5;305(1):50-821205966
Cites: Int J Cardiol. 2012 Mar 22;155(3):474-522243934
Cites: Eur J Epidemiol. 2005;20(7):575-916119429
Cites: J Am Geriatr Soc. 2005 Oct;53(10):1675-8016181165
Cites: Stroke. 2005 Oct;36(10):2198-20216166578
Cites: Circulation. 2006 Oct 17;114(16):1761-9117015792
Cites: Circulation. 2007 Jan 23;115(3):402-2617220398
Cites: Am J Epidemiol. 2007 May 1;165(9):1076-8717351290
Cites: Am J Epidemiol. 2007 Sep 1;166(5):599-60517566063
Cites: N Engl J Med. 2008 Mar 27;358(13):1336-4518367736
OBJECTIVE: To examine the relationship of coronary estrogen receptor (ER) expression with atherosclerotic lesions and central fat accumulation in premenopausal women. SUBJECTS: A total of 52 female forensic autopsy cases aged between 18 and 49 y. METHODS: Height, body weight and waist and hip circumferences were measured and body mass index (BMI) and waist-to-hip ratio (WHR) were calculated. Intima thickness or maximal thickness of the plaque were measured from samples taken from the left anterior descending artery (LAD). Macrophage infiltration and smooth muscle cells were localized by immunostaining. ER was detected immunohistochemically and by Western blot analysis, and the ER immunopositive area in the intima was measured. RESULTS: ER immunoreactivity was observed in the intima in 60% of the samples, and it was most intense in the advanced plaques near the lipid core next to the maximal intensity of macrophage staining. The ER immunopositive area had a significant positive correlation with LAD intima thickness, which in turn was significantly correlated with waist circumference and WHR when adjusted for age and BMI. CONCLUSIONS: Premenopausal women with the central type of fat accumulation have advanced coronary plaques in which ER expression is localized near the lipid-rich and macrophage-rich zone. The higher expression of ER in the arterial plaques may represent a compensatory mechanism against atherosclerosis.
AIM: The myocardial uptake of substrates in children has only been investigated on a small scale. The purpose of this study was to define myocardial substrate uptake in relation to the arterial supply of substrates, age, growth and oxygen saturation. METHODS: Thirty patients with congenital heart disease, aged 3 months to 16 years, were studied during cardiac catheterization. Arterial and coronary sinus blood was analyzed for the major fuel metabolites and amino acids. RESULTS: The uptake of all major substrates correlated significantly with the arterial supply: free fatty acids (r = 0.52, p = 0.004), beta-hydroxybutyrate (r = 0.74, p
New data suggest that persistent chest pain, despite normal coronary angiography, is less benign than previously thought. It has long been recognized that cardiac syndrome X (CSX) is associated with significant suffering, disability, and health care costs, but the biggest shift in thinking comes in terms of long-term risk. It is now recognized that the prognosis is not benign and that a significant proportion of patients are at increased cardiovascular disease risk. Of major debate is the question of whether the mechanisms that explain this chest pain are cardiac vs noncardiac. The most current definition of CSX is the triad of angina, ischemia, and normal coronary arteries, which is associated with an increased cardiovascular risk. This paper provides a review of CSX, epidemiology of the problem, proposed explanatory mechanisms, and important next steps in research. Central to this review is the proposition that new insights into CSX will be fostered by both clinical and scientific collaboration between cardiovascular and pain scientists.