Coronary Heart Disease in Smokers

Abstract

Background-Coronary endothelial function and vasomotion are impaired in smokers without coronary disease, and this is thought to be due to increased oxidative stress. Methods and Results-We used positron emission tomography to measure the coronary flow reserve, an integrated measure of coronary flow, through both the large epicardial coronary arteries and the microcirculation in 11 smokers and 8 control subjects before and after administration of the antioxidant vitamin C. At baseline, coronary flow reserve was reduced by 21% in smokers compared with control subjects (PϽ0.05) but was normalized after vitamin C, whereas the drug had no effect in control subjects. Conclusions-The present study is the first to demonstrate that the noxious prooxidant effects of smoking extend beyond the epicardial arteries to the coronary microcirculation and affect the regulation of myocardial blood flow. Vitamin C restores coronary microcirculatory responsiveness and impaired coronary flow reserve in smokers, which provides evidence that the damaging effect of smoking is at least in part accounted for by an increased oxidative stress.

Inflammation in the vascular bed: Importance of vitamin C

“…That ascorbate is beneficial to the endothelium in vivo is also supported by clinical studies of endothelium-dependent vasodilatation in patients with endothelial dysfunction due to atherosclerosis Heitzer et al, 2001;Tousoulis et al, 2005) and related conditions, including hypertension (Duffy et al, 1999;Duffy et al, 2001;Taddei et al, 1998), smoking (Heitzer et al, 1996;Kaufmann et al, 2000;Solzbach et al, 1997), and diabetes (Tousoulis et al, 2007). Many of the studies in atherosclerosis used high doses of intravenous ascorbate to acutely demonstrate this improvement in endothelial function in humans.…”

Protocol for measuring myocardial blood flow by PET/CT in cats

“…Partial volume and spillover (both accounting for the resolution distortion) were corrected as previously reported [11,13,22] using the method developed [23] and validated [24] by Hutchins et al MPR was calculated as the ratio of hyperaemic to resting MBF values [10,13,22]. Under normal conditions, myocardial oxygen consumption is linearly related to the heart rate-BP product (RPP), an index of external cardiac work, and both are related to coronary blood flow [9]. To allow meaningful interpretation of the quantitative data, it has been proposed that resting MBF be corrected for RPP.…”

“…In view of the median RPP value of 15,000 under anaesthesia at rest in the present study, it seemed appropriate to use this value for normalization. In addition, to account for the variability of coronary driving pressure, coronary resistance (mmHg×min×g×ml −1 ) was also calculated as the ratio of mean arterial pressure (MAP) to MBF [9].…”

“…An abnormal MPR can be due to narrowing of the epicardial coronary arteries [6] or, in the absence of angiographically demonstrable atherosclerotic disease, may reflect dysfunction of the coronary microcirculation [7][8][9][10][11]. In fact, PET is particularly helpful in circumstances where the MPR is diffusely blunted due to a widespread abnormality of the coronary microcirculation, such as in hypertrophic cardiomyopathy (HCM) [7,12,13].…”

Koronare Herzkrankheit: konservative statt invasive Therapie?

“…zu einer Normalisierung der vorher eingeschränkten Myokardperfusion führen kann [42]. Wasserlösliche Antioxidantien wie Vitamin C haben das Potential, bei Rauchern die Gefäss-und Myokardperfusion zu verbessern, was dafür spricht, dass eine Störung der oxidativen Balance mit einem Überwiegen von Sauerstoffradikalen («oxida-tiver Stress») innerhalb der Gefässwand an der Fehlregulation der Vasomotion bei Rauchern beteiligt ist [43] …”