Lack Of Atherosclerosis Research Articles

Atherosclerosis as the Damocles' sword of human evolution: insights from nonhuman ape-like primates, ancient human remains, and isolated modern human populations.

Atherosclerosis is the leading cause of death worldwide, and the predominant risk factors are advanced age and high-circulating low-density lipoprotein cholesterol (LDL-C). However, the findings of atherosclerosis in relatively young mummified remains and a lack of atherosclerosis in chimpanzees despite high LDL-C call into question the role of traditional cardiovascular risk factors. The inflammatory theory of atherosclerosis may explain the discrepancies between traditional risk factors and observed phenomena in current literature. Following the divergence from chimpanzees several millennia ago, loss of function mutations in immune regulatory genes and changes in gene expression have resulted in an overactive human immune system. The ubiquity of atherosclerosis in the modern era may reflect a selective pressure that enhanced the innate immune response at the cost of atherogenesis and other chronic disease states. Evidence provided from the fields of genetics, evolutionary biology, and paleoanthropology demonstrates a sort of circular dependency between inflammation, immune system functioning, and evolution at both a species and cellular level. More recently, the role of proinflammatory stimuli, somatic mutations, and the gene-environment effect appear to be underappreciated elements in the development and progression of atherosclerosis. Neurobiological stress, metabolic syndrome, and traditional cardiovascular risk factors may instead function as intermediary links between inflammation and atherosclerosis. Therefore, considering evolution as a mechanistic process and atherosclerosis as part of the inertia of evolution, greater insight into future preventative and therapeutic interventions for atherosclerosis can be gained by examining the past.

Association of High Density Cholesterol With Hyperemic Epicardial Flow and Frame Count Reserve in Patients With Moderate Coronary Lesions and Slow Coronary Flow.

BackgroundPatients with microvascular angina and non-obstructive coronary atherosclerotic disease have an elevated risk of adverse events and all-cause mortality compared with individuals without ischaemic heart disease. The diagnosis coronary microvascular dysfunction in this setting relies on the detection of impaired coronary flow at rest or on calculation of coronary flow reserve. Previous studies demonstrate that the coronary flow reserve assessed by the corrected thrombolysis in myocardial infarction method - the frame count reserve is an objective quantitative alternative to other widely used invasive methods for microvascular status evaluation.PurposeWe assessed the significance of clinical, hemodynamic, angiographic variables and therapy with reference to FCR in a small group of patients with up to moderate atherosclerotic coronary lesions and slow coronary flow. Materials and methods: Frame count reserve was evaluated in 15 patients without flow-limiting (>50%) coronary stenoses admitted with unstable angina. Frame count reserve was calculated by dividing the baseline corrected thrombolysis in myocardial infarction frame count (cTFC) by the cTFC assessed after intracoronary infusion of 100 µg of the calcium channel blocker - verapamil.ResultsThe values of frame count reserve correlate positively with the levels of high density cholesterol (r= 0.900, p=0.001), inversely coronary flow after the application of verapamil - cTFCv (r= - 0.534, p=0.049). cTFCv was positively related with the levels of high density lipoproteins (r = - 0.645; p= 0.044) and was negatively influenced by the presence of atherosclerotic lesions at quantitative angiography (42.8±19.1 (n=8) vs 23±5.4 (n=7), p=0.029).The therapy with β-blocker and long-acting nitrate was associated with insignificantly higher frame count reserves after intracoronary verapamil compared to the continuous intake only of β-blocker or β-blocker and verapamil (2.1±0.78 vs 1.34±0.14 vs 1.70±0.70, p=NS).ConclusionsHigher high-density lipoproteins relate to higher frame count reserves evaluated using verapamil. The improved blood flow after this microvascular vasodilator is consistently positively related to high-density cholesterol and the lack of atherosclerosis at conventional coronary angiography. The combined intake of micro- and macrovascular vasodilator could be associated with higher frame count reserves compared to therapy with β-blocker and one vasodilating drug.

Binswanger disease may benefit from omental arteries.

Binswanger disease may benefit from omental arteries.

Segmental mediolytische Arteriopathie – Ursachenforschung bei unter 60-jährigen Patienten mit Aneurysmen und Dissektionen

Complications deriving from arterial aneurysm and dissection without signs of atherosclerosis are rare clinical entities. In recent literature case reports show a descriptive similarity of pathological findings summarized as segmental arterial mediolysis (SAM). The purpose of this study was to answer the question whether, among 16 patients suffering from SAM histological findings corresponded and assess causality. In a prospective prognostic trial sixteen patients were enrolled between 1st January 2008 and 31st October 2011. Inclusion criteria were a lack of atherosclerosis, age under 60 and clinical findings. Most of these sixteen patients were treated as emergency cases of life-threatening blood loss or organ system ischemia. Thirteen of the patients were male, 3 female and their average age was 44 (28-59) years. Localisation of the segmental aneurysm or dissection showed a broad variability from central to renovisceral and peripheral lesions. Imaging diagnostics (e.g., US and CT-A) were complemented by exclusion of positive family history, connective tissue diseases and autoimmune or inflammative disorders. In 8 patients with open vascular reconstructions, it was possible to obtain a biopsy from the target lesion to analyse morphological and immunochemical expression levels (e.g., MMP1-12, vWF, vSMC or CD 68). None of the patients died nor had described familiar associations. Even the examination of twins with sCAD showed no coincidence. Differential diagnostic findings were excluded. All patients agreed to undergo human genetic screening. The 8 biopsy tissues showed homogeneously mediolysis with focal and increasingly confluent lesions. Main findings were that the vessel wall layering was destroyed and that capillarisation was initiated from the adventitial layer. Furthermore, all patients suffered from hypertension associated to the SAM, or developed it during surveillance. SAM is a rare, life-threatening diagnosis and has to be taken into consideration in young patients with aneurysm and dissection of unusual locations. Rare vascular diseases should have a forum in future investigations which might highlight molecular genetic triggers and associated diseases, e.g., hypertension and aortic type B dissection.

Angina pectoris and sudden death in the absence of atherosclerosis following ergotamine therapy for migraine

In a woman with migraine headaches, angina-like symptoms developed and sudden death occurred following the administration of therapeutic doses of ergotamine. The lack of atherosclerosis at autopsy suggested coronary vasospasm as a possible mechanism for her death. The ergot alkaloids, which are widely used in the treatment of migraine, are potent vasoconstrictors. We report here the development of angina-like symptoms and sudden death in a woman given therapeutic doses of ergotamine for migraine. At autopsy, no coronary atherosclerosis was found.