The relationship of altitude and cold to cardiovascular risk is complex. Cold is hard to separate from altitude. This review highlights the latest information on cardiovascular disease associated with high altitude and cold; both represent unique clinical situations.
Evolution and genetics are relevant to high altitude, with much new information available. Specific physiology explains some congenital heart disease at altitude. New reports of hematological changes associated with altitude and cold help clarify thrombosis, which is relevant to reports of very late in-stent thrombosis at altitude. Multiple cardiovascular risk factors are affected by altitude and cold, and an increased incidence of myocardial infarction occurs. There is new research on acute mountain sickness associated with inflammation with relevance for clinical study of pulmonary edema. Socioeconomics plays a part in altitude and cold effects on cardiovascular disease. In addition to acute disease, high altitude involves chronic mountain sickness with new knowledge of associated cardiovascular endothelial abnormalities.
High altitude and cold involve acute disease, chronic disease, and public health issues. Continued research is essential to enable the best clinical management in this era of rapid worldwide travel.
[Show abstract][Hide abstract] ABSTRACT: Platelet function was studied in 11 patients with Raynaud's syndrome and 11 healthy controls. Platelets obtained from patients with Raynaud's syndrome were significantly more responsive to adrenaline, produced more thromboxane A2, and were resistant to prostaglandin inhibitors (prostacyclin and prostaglandin E1) of platelet aggregation. Platelets from control subjects and patients with Raynaud's syndrome were more resistant to prostaglandin inhibitors when reactions were carried out at 27 degrees C rather than at 37 degrees C. Patients with Raynaud's syndrome also had significantly increased plasma concentrations of beta-thromboglobulin, fibrinogen, and circulating platelet aggregates. In an attempt to elicit local platelet responses, the forearms of control subjects and patients with Raynaud's syndrome were cooled in water tanks and platelet function tests performed before and after cooling. No significant difference in the results was observed. The potential role of platelets in the pathogenesis of Raynaud's syndrome is discussed.
[Show abstract][Hide abstract] ABSTRACT: Chronic mountain sickness (CMS) is a major public health problem characterized by exaggerated hypoxemia and erythrocytosis. In more advanced stages, patients with CMS often present with functional and structural changes of the pulmonary circulation, but there is little information on the systemic circulation. In patients with diseases associated with chronic hypoxemia at low altitude, systemic vascular function is altered. We hypothesized that patients with CMS have systemic vascular dysfunction that may predispose them to increased systemic cardiovascular morbidity.
To test this hypothesis, we assessed systemic endothelial function (by flow-mediated dilation [FMD]), arterial stiffness, and carotid intima-media thickness and arterial oxygen saturation (Sao(2)) in 23 patients with CMS without additional classic cardiovascular risk factors and 27 age-matched healthy mountain dwellers born and permanently living at 3,600 m. For some analyses, subjects were classified according to baseline Sao(2) quartiles; FMD of the highest quartile subgroup (Sao(2) ≥ 90%) was used as a reference value for post hoc comparisons.
Patients with CMS had marked systemic vascular dysfunction as evidenced by impaired FMD (CMS, 4.6% ± 1.2%; control subjects, 7.6% ± 1.9%; P < .0001), greater pulse wave velocity (10.6 ± 2.1 m/s vs 8.4 ± 1.0 m/s, P < .001), and greater carotid intima-media thickness (690 ± 120 μm vs 570 ± 110 μm, P = .001). A positive relationship existed between Sao(2) and FMD (r = 0.62, P < .0001). Oxygen inhalation improved (P < .001) but did not normalize FMD in patients with CMS, although it normalized FMD in hypoxemic control subjects (Sao(2) < 90%) and had no detectable effect in normoxemic control subjects (Sao(2) ≥ 90%).
Patients with CMS show marked systemic vascular dysfunction. Structural and functional alterations contribute to this problem that may predispose these patients to premature cardiovascular disease.
ClinicalTrials.gov; No.: NCT01182792; URL: www.clinicaltrials.gov.
[Show abstract][Hide abstract] ABSTRACT: We assessed the association between Gln27Glu and Trp64Arg genetic polymorphisms of the beta(2) (ADRB2) and beta(3) (ADRB3) adrenergic receptor genes with body mass index and other cardiovascular risk factors.
In a cross-sectional study, adult Aymara subjects (n = 152) living in the Andean regions of northern Chile were characterized with respect to their ADRB2 and ADRB3 genotypes, body mass index, plasma leptin and insulin levels, fasting glucose concentration, blood pressure, and plasma lipid profile.
The frequency of the Glu27 allele of the ADRB2 gene was estimated to be 0.04, and the allele frequency of the Arg64 variant of the ADRB3 gene was estimated as 0.13. No associations were found between the Trp64Arg polymorphism of the ADRB3 gene and body mass index or other cardiovascular risk factors. The small number of subjects with the allele encoding Glu27 in the ADRB2 gene seriously limited the analysis of the association between genotype and phenotype with the use of this polymorphism, although no clear associations were found.
We found insufficient evidence to support an association between polymorphisms Gln27Glu and Trp64Arg of the ADRB2 and ADRB3 genes, respectively, with body mass index and other cardiovascular risks in the rural Aymara population from Chile.
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