Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased coronary disease rates, as well as increased all-cause mortality, in persons with high levels of hostility/anger and in persons suffering from panic disorder or phobic anxiety suggest that biological concomitants of these traits/conditions lead to major medical illnesses. Benzodiazepines have effects, e.g. blunting of stress hormone responses, that could prevent disease in persons so predisposed. It will be necessary to identify subgroups with sufficiently high absolute rates of disease risk to justify pharmacological interventions, and then to carry out controlled prevention trials to document the benefits, before such approaches can be recommended for the general population. This approach (use of drugs when other measures fail) is now standard for more traditional risk factors, such as hyperlipidemia and hypertension. In contrast to primary prevention, a stronger case can be made for the use of benzodiazepines in secondary prevention. Research has shown benzodiazepine treatment to improve control of angina and to reduce "silent ischemia", directly suggesting clinical benefits to be gained from the effects of benzodiazepines to reduce stress hormone responses. While benzodiazepines have long been prescribed for the postmyocardial infarction patient, there are no controlled clinical trials documenting such benefits. These are now clearly in order so that the use of benzodiazepines in coronary patients can be advised on a rational basis.
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PMID:Do benzodiazepines have a role in the prevention or treatment of coronary heart disease and other major medical disorders? 198 Jun 99

Regional sympathetic activity can be studied in humans using electrophysiological methods measuring sympathetic nerve firing rates and neurochemical techniques providing quantification of noradrenaline spillover to plasma from sympathetic nerves in individual organs. Essential hypertension: Such measurements in patients with essential hypertension disclose activation of the sympathetic outflows to skeletal muscle blood vessels, the heart and kidneys, particularly in younger patients. This sympathetic activation, in addition to underpinning the blood pressure elevation, most likely also contributes to left ventricular hypertrophy, and to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidaemia. Antihypertensive drugs, such as moxonidine, which act primarily by inhibiting the sympathetic nervous system, should have additional clinical benefits beyond those attributable to blood pressure reduction, in protecting against hypertensive complications. Obesity-related hypertension: Understanding the neural pathophysiology of hypertension in the obese has been difficult. In normotensive obesity, renal sympathetic tone is doubled, but cardiac noradrenaline spillover (a measure of sympathetic activity in the heart) is only 50% of normal. In obesity-related hypertension, there is a comparable elevation of renal noradrenaline spillover, but without suppression of cardiac sympathetics (cardiac sympathetic activity being more than double that of normotensive obese and 25% higher than in healthy volunteers). Increased renal sympathetic activity in obesity may be a 'necessary' cause for the development of hypertension (and predisposes to hypertension development), but apparently is not a 'sufficient' cause. The discriminating feature of the obese who develop hypertension is the absence of the adaptive suppression of cardiac sympathetic tone seen in the normotensive obese. Heart failure: In cardiac failure, the sympathetic nerves of the heart are preferentially stimulated. Noradrenaline release from the failing heart at rest in untreated patients is increased as much as 50-fold, similar to the level seen in the healthy heart during near-maximal exercise. Activation of the cardiac sympathetic outflow provides adrenergic support to the failing myocardium, but at a cost of arrhythmia development and progressive myocardial deterioration. Psychosomatic heart disease: No more than 50% of clinical coronary heart disease is explicable in terms of classical cardiac risk factors. There is gathering evidence that psychological abnormalities, particularly depressive illness, anxiety states, including panic disorder and mental stress, are involved here, 'triggering' clinical cardiovascular events, and possibly also contributing to atherosclerosis development. The mechanisms of increased cardiac risk attributable to mental stress and psychiatric illness are not entirely clear, but activation of the sympathetic nervous system seems to be of prime importance.
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PMID:Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease. 1134 14