Role of Endothelial Dysfunction and Insulin Resistance in Angina Pectoris and Normal Coronary Angiogram

Egami²,

et al. 2012

Int. Heart J.

SUMMARYCoronary microvascular hyperplasia is a cause of microvessel angina, although the underlying cellular mechanisms remain unclear. We examined how mononuclear cells expressing β-actin (β-MNCs), which were identified in coronary vessels, induce coronary microvascular hyperplasia.The presence of β-MNCs in coronary hyperplastic arterial (HAM) and venous microvessels (HVM) was examined by endomyocardial biopsy in 25 patients with suspected microvessel angina. β-MNCs were identified in 14 HAMs obtained from 11 patients. Basic fibroblast growth factor and heparin sulfate were injected into the infarcted myocardium to induce HAM and HVM in 28 beagles, and then we examined the role of β-MNCs in the onset of HAM and HVM. The following changes were observed after infarction induction in beagles: (a) migration of β-MNCs from the existing microvessels into the interstitial space at 1-2 weeks; (b) those traversing the adventitia into the media, but not intima, of microvessels; (c) their transformation to smooth muscle cells (SMCs) and/or connective tissues (collagen and elastin fibers); (d) and medial hyperplasia without intimal hyperplasia. Medial hyperplasia was classified into SMC-proliferative and both SMC-and connective tissue-proliferative types. β-MNCs expressed CD 34 but did not express other major vessel-related cell markers.β-MNCs are a vascular progenitor, and migrate out of the adventitia into media, and participate in the etiology of coronary microvascular medial hyperplasia. (Int Heart J 2012; 53: 43-53) Key words: β-MNC migration, Coronary microvessels, Medial hyperplasia, Microvessel angina C hest pain accompanied by ischemic electrocardiographic changes, but without demonstrable angiographic coronary changes, is called "microvessel angina". 1-4)Anatomical and functional abnormalities of coronary microvessels are considered the cause of this phenomenon, including microvascular spasm due to endothelial dysfunction, [5][6][7] coronary capillary swelling, 8) and microvascular luminal narrowing by swollen endothelium. 9)In addition to these endothelium-related changes, arteriolar and small arterial medial hyperplasia have been observed in endomyocardial biopsy specimens. 10,11) The exact cellular mechanisms of medial hyperplasia are, however, not known.In an earlier study, histological examination of coronary microvessels in patients with microvessel angina revealed mononuclear cells expressing β-actin (β-MNCs) in the media and adventitia of the hyperplastic coronary microvessels. We also found β-MNCs in animals. 12,13) In this study, we performed more detailed examinations of the role of β-MNCs in hyperplastic coronary microvessels in patients with microvessel angina and in animals treated with basic fibroblast growth factor (bFGF) and heparin sulfate after induction of myocardial infarction. 14,15) MethodsSubjects: A total of 25 consecutive patients with chest pain with depression of the ST segment on electrocardiography (during spontaneous angina or treadmill-induced), but without demonstrable angiogra...

Section: -4)mentioning

confidence: 99%

mentioning

confidence: 99%

β-Actin-Positive Mononuclear Cells Participate in Coronary Microvascular Medial Hyperplasia by Migrating Through Adventitia into Media, With Special Reference to Microvessel Angina

Egami²,

et al. 2012

Int. Heart J.

“…Such and other recently emerging reports have challenged the traditional view of the excellent prognosis of patients with cardiac syndrome X and the diagnostic criteria for this syndrome [44]. As both endothelium-dependent and endothelium-independent coronary blood flow can be found to be impaired in this heterogeneous group of patients, the role of classic endothelial dysfunction for the pathophysiology and presentation of cardiac syndrome X remains to be defined [45]. Endothelial dysfunction is also considered but not proven to contribute to the clinical presentation of variant angina, i.e., typical chest pain episodes with ST segment elevation and nonobstructed coronary arteries on angiography [46].…”

Section: The Clinical Presentation Of Endothelial Dysfunctionmentioning

confidence: 99%

The Endothelium – the Cardiovascular Health Barometer

Herrmann¹,

Lerman

2008

Herz

Once considered to fulfill no other purpose than that of a physical barrier between blood and tissue, the multifunctional nature of the endothelium was discovered in the later half of the 20th century. In cardiology, the dysfunctional nature of the endothelium has received even more attention, initially mainly within the research community but later also in the clinical community, serving as a prime example for the translation of bench research to patient care. In this review, the entity of endothelial dysfunction, its modes of diagnosis in clinical practice, its prognostic implications, and its treatment options will be defined. From past conceptual ideas to current practical applications to the road ahead, the endothelium is to be viewed as the cardiovascular health barometer.

“…6,7) Until recently, the coronary microcirculation has been evaluated by contrast echocardiography, 8) radionucleide imaging, 9) magnetic resonance imaging, 10) computed tomography, 11) electron beam computed tomography, 12) pressure wire, 13) Doppler guidewire, 14) coronary angiography 15) and left ventricular pressure. 16) These techniques can evaluate coronary microcirculation as a whole, but functional evaluation of the individual microvessels has been beyond the scope of these imaging modalities.…”

mentioning

confidence: 99%

Cardioscopic Observation of Subendocardial Microvessels in Patients With Coronary Artery Disease

et al. 2011

SummaryCoronary microvessels play a direct and critical role in determining the extent and severity of myocardial ischemia and cardiac function. However, because direct observation has never been performed in vivo, the functional properties of the individual microvesssels in patients with coronary artery disease remain unknown.Subendocardial coronary microvessels were observed by cardioscopy in 149 successive patients with coronary artery disease (81 with stable angina and 68 with old myocardial infarction).Twenty-four arterial microvessels (AMs) and 27 venous microvessels (VMs) were observed in the left ventricular subendocardium. All 12 AMs and 13 of 14 VMs that were located in normokinetic-to-hypokinetic left ventricular wall segments were filled with blood during diastole and were collapsed during systole. In contrast, 8 of 12 AMs and 9 of 13 VMs that were located in akinetic-to-dyskinetic wall segments were filled with blood during systole and were collapsed during diastole. There were no significant correlations between the timing of blood filling and the severity of coronary stenosis and collateral development.In patients with coronary artery disease, the timing of blood filling of AMs and VMs was dependent on the regional left ventricular contractile state; during diastole when contraction was preserved and during systole when it was not. It remains to be elucidated whether and how blood filling is disturbed in other categories of heart disease. (Int Heart J 2011; 52: 274-279)