Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Beta adrenoceptor blocking drugs are relatively well tolerated and adverse reactions to them are not common. The ones that do occur are reviewed in this paper under the following headings: Short term adverse reactions, drug interactions, long term adverse reactions, risks in pregnancy and hazards of abrupt withdrawal. Predictable short term effects may be caused either by the actions of these drugs on the beta 1- or beta 2-receptors. The beta 1 adverse effects are hypotension, bradycardia and cardiac failure; these are best avoided by not giving beta-adrenoceptor blocking drugs to susceptible patients with cardiac disease. The beta 2 adverse effects on the bronchi, the peripheral arteries and various metabolic functions may be reduced to some extent by using a relatively cardioselective drug. Unpredictable short term effects such as fatigue, sexual dysfunction and gastrointestinal symptoms may occur but are not common problems with this group of drugs. Similarly, serious drug interactions are infrequent. Under the heading of long term adverse effects the practolol problem and the risk of causing malignant disorders have been considered. There is no evidence that any of the currently available drugs will cause either a practolol syndrome or malignant disease in man. However, the need for careful appraisal by drug regulatory bodies and continued vigilance by all prescribers of beta-adrenoceptor blocking drugs remains. The possible adverse effects of treatment during pregnancy are also considered. It now appears that beta-adrenoceptor drugs can be used safely in pregnancy but since neonatal bradycardia and hypoglycemia may occur, care should be taken to look for these complications. A serious deterioration may occur when beta-adrenoceptor drugs, given to patients with significant ischemic heart disease, are suddenly stopped. This is a rare occurrence but prescribers should be aware of it.
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PMID:Beta-adrenoceptor blocking drugs: adverse reactions and drug interactions. 613 87

There is a well-documented association between depression, ischemic heart disease, and cardiovascular mortality. This association has a number of dimensions including: (1) depressed patients have a higher than expected rate of sudden cardiovascular death; (2) over the course of a lifetime, patients with depression develop symptomatic and fatal ischemic heart disease at a higher rate compared with a nondepressed group; and (3) depression after myocardial infarction (MI) is associated with increased cardiac mortality. Depression is also associated with sexual dysfunction, particularly erectile dysfunction. If depression is the primary illness, then erectile dysfunction can be considered a symptom of the depressive illness. However, if the erectile dysfunction is primary, men may develop a depressive syndrome in reaction to the loss of sexual function. Regardless of whether erectile dysfunction is a symptom of depression or depression is a consequence of erectile dysfunction, these conditions are frequently comorbid. Thus, the patient with ischemic heart disease who is depressed is more likely to have erectile difficulties. An attempt by this patient to engage in sexual activity is therefore more likely to be unsuccessful and, given the increase in cardiac mortality associated with depression, it may result in a serious cardiac event.
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PMID:Sexual activity and cardiac risk: is depression a contributing factor? 1089 77

Diabetic autonomic neuropathy (DAN) is a serious and common complication of diabetes. Despite its relationship to an increased risk of cardiovascular mortality and its association with multiple symptoms and impairments, the significance of DAN has not been fully appreciated. The reported prevalence of DAN varies widely depending on the cohort studied and the methods of assessment. In randomly selected cohorts of asymptomatic individuals with diabetes, approximately 20% had abnormal cardiovascular autonomic function. DAN frequently coexists with other peripheral neuropathies and other diabetic complications, but DAN may be isolated, frequently preceding the detection of other complications. Major clinical manifestations of DAN include resting tachycardia, exercise intolerance, orthostatic hypotension, constipation, gastroparesis, erectile dysfunction, sudomotor dysfunction, impaired neurovascular function, "brittle diabetes," and hypoglycemic autonomic failure. DAN may affect many organ systems throughout the body (e.g., gastrointestinal [GI], genitourinary, and cardiovascular). GI disturbances (e.g., esophageal enteropathy, gastroparesis, constipation, diarrhea, and fecal incontinence) are common, and any section of the GI tract may be affected. Gastroparesis should be suspected in individuals with erratic glucose control. Upper-GI symptoms should lead to consideration of all possible causes, including autonomic dysfunction. Whereas a radiographic gastric emptying study can definitively establish the diagnosis of gastroparesis, a reasonable approach is to exclude autonomic dysfunction and other known causes of these upper-GI symptoms. Constipation is the most common lower-GI symptom but can alternate with episodes of diarrhea. Diagnostic approaches should rule out autonomic dysfunction and the well-known causes such as neoplasia. Occasionally, anorectal manometry and other specialized tests typically performed by the gastroenterologist may be helpful. DAN is also associated with genitourinary tract disturbances including bladder and/or sexual dysfunction. Evaluation of bladder dysfunction should be performed for individuals with diabetes who have recurrent urinary tract infections, pyelonephritis, incontinence, or a palpable bladder. Specialized assessment of bladder dysfunction will typically be performed by a urologist. In men, DAN may cause loss of penile erection and/or retrograde ejaculation. A complete workup for erectile dysfunction in men should include history (medical and sexual); psychological evaluation; hormone levels; measurement of nocturnal penile tumescence; tests to assess penile, pelvic, and spinal nerve function; cardiovascular autonomic function tests; and measurement of penile and brachial blood pressure. Neurovascular dysfunction resulting from DAN contributes to a wide spectrum of clinical disorders including erectile dysfunction, loss of skin integrity, and abnormal vascular reflexes. Disruption of microvascular skin blood flow and sudomotor function may be among the earliest manifestations of DAN and lead to dry skin, loss of sweating, and the development of fissures and cracks that allow microorganisms to enter. These changes ultimately contribute to the development of ulcers, gangrene, and limb loss. Various aspects of neurovascular function can be evaluated with specialized tests, but generally these have not been well standardized and have limited clinical utility. Cardiovascular autonomic neuropathy (CAN) is the most studied and clinically important form of DAN. Meta-analyses of published data demonstrate that reduced cardiovascular autonomic function as measured by heart rate variability (HRV) is strongly (i.e., relative risk is doubled) associated with an increased risk of silent myocardial ischemia and mortality. The determination of the presence of CAN is usually based on a battery of autonomic function tests rather than just on one test. Proceedings from a consensus conference in 1992 recommended that three tests (R-R variation, Valsalva maneuver, and postural blood pressure testing)or longitudinal testing of the cardiovascular autonomic system. Other forms of autonomic neuropathy can be evaluated with specialized tests, but these are less standardized and less available than commonly used tests of cardiovascular autonomic function, which quantify loss of HRV. Interpretability of serial HRV testing requires accurate, precise, and reproducible procedures that use established physiological maneuvers. The battery of three recommended tests for assessing CAN is readily performed in the average clinic, hospital, or diagnostic center with the use of available technology. Measurement of HRV at the time of diagnosis of type 2 diabetes and within 5 years after diagnosis of type 1 diabetes (unless an individual has symptoms suggestive of autonomic dysfunction earlier) serves to establish a baseline, with which 1-year interval tests can be compared. Regular HRV testing provides early detection and thereby promotes timely diagnostic and therapeutic interventions. HRV testing may also facilitate differential diagnosis and the attribution of symptoms (e.g., erectile dysfunction, dyspepsia, and dizziness) to autonomic dysfunction. Finally, knowledge of early autonomic dysfunction can encourage patient and physician to improve metabolic control and to use therapies such as ACE inhibitors and beta-blockers, proven to be effective for patients with CAN.
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PMID:Diabetic autonomic neuropathy. 1271 21

There is ample evidence from many epidemiological studies that lower urinary tract symptoms (LUTS) and sexual dysfunction are strongly linked, independently of age and comorbidities such as hypertension, diabetes, dyslipidaemia and coronary heart disease. However, a causal link between both conditions is not yet established. Four pathophysiological mechanisms currently support the relationship between LUTS and erectile dysfunction (ED): (i) The nitric oxide synthase (NOS)/NO theory; there is a reduction in NOS-containing nerves in the prostate and bladder/urethra in patients with bladder outlet obstruction (BOO), and that lack of NO or loss of protein kinase G causes ED; (ii) The autonomic hyperactivity and metabolic syndrome hypothesis: benign prostatic hyperplasia (BPH) may be part of the metabolic syndrome, which includes cardiovascular diseases (e.g. hypertension, ischaemic heart disease) and diabetes mellitus, known risk factors for ED. Hypertension, obesity, and hyperinsulinaemia have all been claimed to be associated with an increased sympathetic activity. Increased sympathetic activity is involved in LUTS/BPH and may have a role in ED/sexual dysfunction, with noradrenaline and alpha1-adrenoceptors representing a common link; (iii) the Rho-kinase activation/endothelin pathway; there can be increased Rho-kinase activity, and consequently calcium sensitivity of the contractile machinery, in prostate smooth muscle in BPH, the detrusor in BOO, corpora cavernosa in ED, and in the resistance vessels in hypertension. The actions of several factors beside noradrenaline (e.g. endothelin-1, angiotensin II), possibly involved in the increased smooth muscle activity found in both LUTS/BPH and sexual dysfunction, are dependent on Rho-kinase activity. Thus increased Rho-kinase activity might represent a common link between LUTS and sexual dysfunction; (iv) Pelvic atherosclerosis; animal models mimicking pelvic ischaemia and hypercholesterolaemia show similar smooth muscle alterations of the detrusor and corpora. Pelvic ischaemia may induce the biological modifications described above and may thus represent as well a common link between LUTS and sexual dysfunction. Studies treating one condition (e.g. ED) and measuring the impact on the other (e.g. LUTS) should further contribute to support this common link.
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PMID:Lower urinary tract symptoms and sexual dysfunction: epidemiology and pathophysiology. 1650 50

Relieving the symptoms of angina and improving the quality of life and functional status are important objectives in the management of patients with chronic stable angina. A high heart rate induces or exacerbates myocardial ischemia and angina because it both increases oxygen demand and decreases myocardial perfusion. Beta-Blockers are effective at reducing anginal symptoms largely by decreasing heart rate. Physician use and patient compliance may be limited by the side effects of Beta-blockers which include fatigue, depression and sexual dysfunction. Heart rate reduction can also be obtained by the calcium antagonists verapamil and diltiazem and by the new selective heart-rate-reducing agent ivabradine. Ivabradine (Procoralan) is a selective and specific I(f) inhibitor that acts on one of the most important ionic currents for the regulation of the pacemaker activity of sinoatrial node cells. Ivabradine has demonstrated dosedependent anti-ischemic and antianginal effects in a placebo-controlled study. The INITIATIVE trial is a large multicenter trial in which 939 patients with stable angina were randomized to ivabradine or atenolol. The noninferiority of ivabradine was shown in the INITIATIVE trial at all doses and for all criteria including time to limiting angina. The number of angina attacks per week was decreased by two thirds with both ivabradine and atenolol. In another trial of 1,195 patients, time to 1mm ST segment depression was increased by 45 s with ivabradine 7.5 mg b.i.d. and by 40 s with amlodipine 10 mg daily. Unlike beta-blockers, ivabradine is devoid of intrinsic negative inotropic effects and does not affect coronary vasomotion. A whole range of patients with angina may benefit from exclusive heart rate reduction with ivabradine, including those with contraindications or intolerance to the use of beta-blockers and patients that are insufficiently controlled by beta-blockers or calcium channel blockers.
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PMID:Heart rate slowing versus other pharmacological antianginal strategies. 1693 73

Sexual dysfunction is currently considered a serious quality-of-life-related health problem, exerting a major impact on patients' and their sexual partners' life. Available data indicate that essential hypertension is a risk factor for sexual dysfunction, as male and female sexual dysfunction is more prevalent in hypertensive patients than normotensive individuals. Several mechanisms have been implicated in the pathogenesis of sexual dysfunction in hypertensive patients, and major determinants include severity and duration of hypertension, age, and antihypertensive therapy. Female sexual dysfunction, although more frequent than its male counterpart, remains largely under-recognized. Older antihypertensive drugs (diuretics, beta-blockers, centrally acting) exert negative results, whereas newer drugs have either neutral (calcium antagonists, angiotensin-converting enzyme inhibitors) or beneficial effects (angiotensin receptor blockers). Erectile dysfunction is related to ischemic heart disease and might be an 'early therapeutic window' of asymptomatic coronary artery disease. It seems of utmost importance for every physician treating hypertensive patients to become familiar with sexual dysfunction (through better education and specific seminars) for the proper management of these patients.
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PMID:Sexual dysfunction: the 'prima ballerina' of hypertension-related quality-of-life complications. 1885 43

Erectile dysfunction (ED) is a sensitive indicator of wider arterial insufficiency and an early correlate for the presence of ischemic heart disease. Among patients with coronary artery disease, prevalence reports of ED range from 42% to 75%. The US Food and Drug Administration has approved 3 phosphodiesterase-5 (PDE-5) inhibitors for treatment of male sexual dysfunction: sildenafil, tadalafil, and vardenafil. PDE-5 inhibitors also have cardiovascular effects. They inhibit PDE-5 enzymes in pulmonary vasculature, which causes vasodilation that decreases pulmonary vascular pressure. Sildenafil is approved for treatment of patients with pulmonary hypertension. PDE-5 inhibition with sildenafil improves cardiac output by balancing pulmonary and systemic vasodilation, and augments and prolongs the hemodynamic effects of inhaled nitric oxide in patients with chronic congestive heart failure and pulmonary hypertension. In vivo and in vitro studies are examining the possible beneficial effects of PDE-5 inhibitors in conditions such as myocardial infarction and endothelial dysfunction.
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PMID:The relationship between erectile dysfunction and cardiovascular disease. Part II: The role of PDE-5 inhibition in sexual dysfunction and cardiovascular disease. 1895 78

Medical comorbidities and complications are expected following stroke, traumatic brain injury, and spinal cord injury. The neurorehabilitation physician's role is to manage these comorbidities, prevent complications, and serve as a medical and neurologic resource for the patient, family, and neurorehabilitation team. The most common comorbidities are similar to those found in the general population, namely hypertension, dyslipidemia, diabetes mellitus, and ischemic heart disease. Frequent complications encountered in the neurorehabilitation unit relate to medication side effects, medical comorbidities, and the direct effect of the neurologic injury. They include orthostatic hypotension; syncope or presyncope; cardiac arrhythmia; bowel and bladder dysfunction; seizures; pressure sores; dysphagia-related pneumonia, dehydration, and malnutrition; venous thromboembolism; falls; and sexual dysfunction. This article discusses strategies for managing comorbidities and avoiding complications.
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PMID:Management of medical complications. 2281 Aug 65

Premature menopause affects 1% of women under the age of 40 years. The women are at risk of premature death, neurological diseases, psychosexual dysfunction, mood disorders, osteoporosis, ischemic heart disease and infertility. There is need to use simplified protocols and improved techniques in oocyte donation to achieve pregnancy and mother a baby in those women at risk. Review of the pertinent literature on premature menopause, selected references, internet services using the PubMed and Medline databases were included in this review. In the past, pregnancy in women with premature menopause was rare but with recent advancement in oocyte donation, women with premature menopause now have hoped to mother a child. Hormone replacement therapy is beneficial to adverse consequences of premature menopause. Women with premature menopause are at risk of premature death, neurological diseases, psychosexual dysfunction, mood disorders, osteoporosis, ischemic heart disease and infertility. Public enlightenment and education is important tool to save those at risk.
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PMID:Premature menopause. 2363 37

The obesity affects around 312 million people over the world. In The United States it causes more than 300 000 deaths per year. It leads to many complications, such as ischemic heart disease, hypertension, dyslipidemia, atherosclerosis and abnormal carbohydrate metabolism. It was proven recently that obesity is also an independent risk factor for erectile dysfunction in men. 79% of men presenting erectile disorders have BMI of 25 kg/m2 or greater. BMI in the range 25-30 kg/m2 is associated with 1,5 times, and in the range of over 30 kg/m2 with 3 times greater risk of sexual dysfunction. The occurrence of erectile dysfunction in patients with obesity is caused by a number of complications which are characteristic for an excessive amount of fat tissue, in example: cardiovascular diseases, diabetes or dyslipidemia. In the United States diabetes and obesity are responsible for 8 million cases of erectile dysfunction. Scientific evidence indicates that excessive body weight should be considered as an independent risk factor for erectile dysfunction. This risk increases with increasing BMI. Erectile disorders correlate with the occurrence of obesity at any time during the patient's life. Obesity leads to erectile dysfunction in a considerably greater extent than aging. Mechanisms responsible for the independent influence of obesity on the erectile dysfunction are: hormonal imbalance, endothelial dysfunction, insulin resistance, psychological factors and physical inactivity. The basis for erectile dysfunction treatment in obesity is body weight loss. Erectile disorders in obese men are significantly more frequent than in general population. Obesity is beyond any doubts an independent risk factor of erectile dysfunction.
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PMID:[Obesity--significant risk factor for erectile dysfunction in men]. 2472 Jan 14


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