cardiovascular-agents and Glucose-Intolerance

The obstructive sleep apnoea syndrome (OSAS) had become a major public health concern in modern society due to its high prevalence but, above all, to its associated morbidity, especially cardiovascular.. Untreated OSAS is associated with an increased incidence of fatal (myocardial infarction and stroke) (odds ratio: 2.87) and non-fatal cardiovascular events (myocardial infarction, stroke, coronary artery bypass surgery and coronary angiography) (odds ratio: 3.17). Moreover, the prevalence of hypertension in patients with OSAS is high, between 35 and 80%. The pathophysiological mechanisms leading to these complications are mainly due to intermittent hypoxia secondary to repeated episodes of apnoea/hypopnoea during sleep. These mechanisms include sympathetic hyperactivation, impairment of vasomotor reactivity, vascular inflammation, oxidative stress and metabolic disorders. In patients with OSAS, the impact of continuous positive pressure is proven in terms of prevention of cardiovascular events although blood pressure reduction is limited. Obviously these effects are proportional to observance.. OSAS does increase the cardiovascular risk, independently of other risk factors. Although the impact of treatment is relatively low in decreasing blood pressure, it seems essentially effective in preventing cardiovascular morbidity. Therefore, OSAS screening, and the association of specific treatments in cardio-metabolic patients and OSAS patients respectively, should be included in clinical strategies.

Topics: Cardiovascular Agents; Cardiovascular Diseases; Cerebrovascular Disorders; Comorbidity; Continuous Positive Airway Pressure; Endothelium, Vascular; Glucose Intolerance; Humans; Hypertension; Hypoxia; Metabolic Syndrome; Nitric Oxide; Obesity; Oxidative Stress; Prevalence; Sleep Apnea, Obstructive; Sympathetic Nervous System; Vasculitis

Certain cardiovascular drugs have adverse effects on glucose homeostasis, which may lead to important long-term implications for increased risks of adverse outcomes. Thiazide diuretics, niacin, and beta-adrenergic blockers impair glucose homeostasis. However, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have demonstrated beneficial metabolic effects. The newer vasodilating beta-blocking agents and calcium antagonists appear to be metabolically neutral. These considerations, in addition to meticulous attention to blood pressure control and lifestyle changes, have the potential to beneficially modify glycemia and long-term risks. These considerations have particular importance in younger patients who may also have pre-diabetes or the metabolic syndrome and who are likely to require therapy over the course of decades.

Topics: Adrenergic beta-Antagonists; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Blood Glucose; Cardiovascular Agents; Coronary Artery Disease; Glucose Intolerance; Homeostasis; Humans; Hyperglycemia; Hypoglycemic Agents; Insulin; Metabolic Syndrome; Niacin; Risk Reduction Behavior; Sodium Chloride Symporter Inhibitors

The metabolic syndrome of vascular risk is threatening large numbers of ever-younger people. To date, the syndrome has been chiefly viewed as a potential risk marker that confers a heightened probability of developing type 2 diabetes and occlusive atherothrombotic disease of large- and medium-sized arteries. Accumulating evidence suggests that the components of the metabolic syndrome may also adversely affect the microvasculature through several inter-related mechanisms. These include the following observations: classic risk factors for macrovascular disease such as high blood pressure and dyslipidaemia also accelerate microvascular complications of diabetes, lesser disturbances of glucose metabolism (i.e. impaired glucose tolerance) may be associated with some forms of microvascular dysfunction, non-glucose intermediary metabolites may promote renovascular hypertension thereby damaging the microvasculature, and insulin resistance appears to be directly associated with microvascular dysfunction. In turn, microvascular complications such as nephropathy and autonomic neuropathy may promote the development and progression of atherosclerosis. We argue that the vascular implications of the metabolic syndrome should be broadened to include the microvasculature. The hypothesis that vascular events can be prevented, or at least deferred, through earlier therapeutic intervention in pre-diabetic subjects with glucose intolerance is amenable to testing in clinical trials.

Topics: Anti-Obesity Agents; Antihypertensive Agents; Atherosclerosis; Cardiovascular Agents; Disease Progression; Glucose Intolerance; Humans; Hypoglycemic Agents; Hypolipidemic Agents; Insulin Resistance; Metabolic Syndrome; Microcirculation; Prediabetic State; Risk Assessment; Risk Factors; Signal Transduction; Vascular Diseases

To assess the role of percutaneous coronary intervention (PCI) for in-hospital and one-year prognosis of ST elevation (STE) myocardial infarction (MI) patients with impaired glucose tolerance (IGT) or type 2 diabetes mellitus (T2DM).. This registry study included 601 STEMI patients admitted to hospital within 24 hours after STEMI onset during one year. According to medical history, dynamics of glycemia and results of oral glucose tolerance test patients were divided into 3 groups: (1) without disturbances of carbohydrate metabolism (DCM), (2) with IGT and (3) with T2DM. Primary PCI was performed in 373 (62.06%) patients while 228 (37.94%) received pharmacological treatment only. The following events were registered during one year after PCI: recurrent MI, stroke, admission for decompensated chronic heart failure (CHF), repeat emergency PCI.. Patients with IGT and DM compared with those without DCM had similarly more severe course of the index MI and worse one-year prognosis. PCI significantly improved one-year prognosis in patients with and without DCM.. Use of urgent PCI in STEMI patients with both DM and IGT is prognostically more beneficial in terms of lowering rate of adverse events during one year after MI.

Topics: Carbohydrate Metabolism; Cardiovascular Agents; Diabetes Mellitus, Type 2; Electrocardiography; Female; Follow-Up Studies; Glucose Intolerance; Humans; Male; Middle Aged; Myocardial Infarction; Percutaneous Coronary Intervention; Postoperative Complications; Prognosis; Registries; Risk Factors; Russia; Severity of Illness Index; Treatment Outcome