No abstract

Patients on statin treatment produce less heat from the culprit coronary lesion than those not treated. Thus, statins seem to have a favourable effect on heat release from atherosclerotic plaques, and whether this effect has an impact on plaque stabilization needs to be investigated in future studies.

Experimental studies suggest that bone marrow-derived endothelial progenitor cells (EPCs) play an important role in the maintenance of endothelial integrity and hemostasis. The number of circulating EPC has been shown to be inversely correlated with cardiovascular risk factors and vascular function and to predict cardiovascular events independent of both traditional and non-traditional risk factors. Thus, EPCs provide a clinical advantage over the use of other biomarkers as their measurement is directly associated with endothelial function, and available evidence suggests that they are consistently and significantly associated with a spectrum of cardiovascular complications, such as acute coronary syndromes and coronary artery disease. However, many issues in the field of EPC isolation and identification, particularly in regards to the effective and unequivocal molecular characterization of these cells still remain unresolved. In addition, simple EPC counts do not adequately describe cardiovascular disease risk. This limitation is attributable to variation in the definition of EPCs, the number of existing cardiovascular risk factors in different patients as well as a difference in the interaction between EPCs and other hematopoietic progenitor, inflammatory cells or platelets.

The clinical relevance of nocturnal hypertension (NH) in comparison with non-dipping status has not been clarified yet, as regards subclinical target organ damage. We aimed to elucidate whether NH or dipping status reflects better organ damage. The study population included 319 newly diagnosed hypertensive patients. Subclinical organ damage was evaluated to all participants. On the basis of nocturnal blood pressure (BP) levels the population was divided into two groups: NH and nocturnal normotension. Also, individuals were defined as dippers and non-dippers according to systolic BP fall. Patients with NH were characterized by increased arterial pulse wave velocity (PWV; 9.1±1.7 vs 8.4±1.5 m s(-1), P=0.0001) and carotid intima-media thickness (0.77±0.18 vs 0.69±0.15 mm, P=0.016) compared with normotensive subjects. Notably, they also exhibited higher values of left ventricular mass index (88.1±22.9 vs 82.8±16.6 g m(-)(2) P=0.043). On the contrary, non-dipping status was associated only with differences in PWV (9.26±0.2 vs 8.64±0.2 m s(-1), P=0.031, 8) and in creatinine clearance (95±3 vs 106±4, P=0.025) in the group of NH. The presence of NH is accompanied by subclinical atherosclerosis, as well as structural abnormalities of the left ventricle. Therefore, NH rather than non-dipping status could be preferably integrated with the risk of organ damage.

Background. It has been suggested that recurring coronary artery spasm may lead to the development of fixed atherosclerotic coronary obstructions.Methods and Results. We studied 10 patients with typical Prinzmetal's variant angina in whom the disease remained active for years and in whom occlusive coronary spasm occurred reproducibly at the same arterial site during repeat coronary arteriography (25+12 months after initial angiography). At initial evaluation, four patients had significant (>50%N fixed coronary diameter reduction) one-vessel coronary artery disease, and six had nonsignificant disease. Spasm developed at stenotic sites (20-65% diameter reduction) in nine patients and at an angiographically normal site in one patient. Progression of coronary disease was assessed in 62 segments: 10 spastic (of which nine were stenotic) and 52 nonspastic (eight stenotic and 44 angiographically normal), using computerized arteriography. Mean diameters (millimeters) of spastic segments, nonspastic stenoses, and angiographically normal nonspastic segments were not significantly different at first and second arteriograms (1.52+±0.14 versus 1.43+±0.21, 1.32+0.17 versus 1.12±4-0.23, and 2.40±0.12 versus 2.42±0.12, respectively). Stenosis progression (from 65% diameter reduction to total occlusion) occurred in one patient at a spastic site and in two at nonspastic sites (from 34% to 65% and from 84% to 100%O). Complicated stenoses suggestive of plaque fissuring were not observed during the study.Conclusions. In patients with chronic Prinzmetal's variant angina without myocardial infarction, stenosis progression was not frequently observed at spastic sites despite the recurrence of focal coronary spasm over relatively long periods of time. (Circulation 1992;85:619-626)