Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review describes the ability of certain diseases, such as essential hypertension, atherosclerosis, angina, and vasospasm, to reduce vascular nitric oxide (NO) formation or to increase its metabolism. In contrast, others, such as hypotension, sepsis, stroke, myocardial depression, and inflammatory responses, increase NO synthesis. The mechanism implicated in the changes in the formation and metabolism of NO are described. To prevent or treat these pathological processes, in which a deficiency in vascular NO formation plays a causative role, NO may be provided through methods such as direct NO administration or indirect NO supply through either NO donors or L-arginine, which facilitates NO formation.
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PMID:Role of vascular nitric oxide in physiological and pathological conditions. 942 1

The aim of this study was to estimate the incidence of silent myocardial ischaemia in patients with mild to moderate hypertension, white-coat hypertension (WCH) and those with normal blood pressure. Ambulatory electrocardiographic (ECG) monitoring was carried out in 272 cases with normal blood pressure, 164 cases with mild to moderate hypertension (diastolic blood pressure >95 and <114 mm Hg), and 106 cases with white-coat hypertension who were diagnosed with ambulatory blood pressure monitoring. The ages of the patients of all groups were between 42-61 years. There were no differences between the groups according to age, gender and other parameters. There were no anginal symptoms, and resting ECGs were in normal limits in all cases. The diagnosis of silent ischaemia was considered to be present if there was ST depression >2 mm/at least 120 sec in ambulatory ECG examination without angina or its equivalent cardiac symptoms. The incidence of silent ischaemia was 6.4%, 18.8%, and 26.2% in cases with normal blood pressure, WCH, and hypertension, respectively. The differences between groups were significant. It was concluded that WCH is not a benign condition, but shares some characteristics with essential hypertension.
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PMID:The prevalence of silent myocardial ischaemia in patients with white-coat hypertension. 965 56

Essential hypertension has a genetic basis. Accumulating evidence, including findings of elevation of arterial blood pressure in mice lacking the endothelial nitric oxide synthase (eNOS) gene, strongly suggests that alteration in NO metabolism is implicated in hypertension. There are, however, no reports indicating that polymorphism in the eNOS gene is associated with essential hypertension. We have identified a missense variant, Glu298Asp, in exon 7 of the eNOS gene and demonstrated that it is associated with both coronary spastic angina and myocardial infarction. To explore the genetic involvement of the eNOS gene in essential hypertension, we examined the possible association between essential hypertension and several polymorphisms including the Glu298Asp variant, variable number tandem repeats in intron 4 (eNOS4b/4a), and two polymorphisms in introns 18 and 23. We performed a large-scale study of genetic association using two independent populations from Kyoto (n=458; 240 normotensive versus 218 hypertensive subjects) and Kumamoto (n=421; 223 normotensive versus 187 hypertensive subjects), Japan. In both groups, a new coding variant, Glu298Asp, showed a strong association with essential hypertension (Kyoto: odds ratio, 2.3 [95% confidence interval, 1.4 to 3.9]; Kumamoto: odds ratio, 2.4 [95% confidence interval, 1.4 to 4.0]). The allele frequencies of 298Asp in hypertensive subjects were significantly higher than those in normotensive subjects in both groups (Kyoto: 0.103 versus 0.050, P<0.0017; Kumamoto: 0.120 versus 0.058, P<0.0013, respectively). No such disequilibrium between genotypes was significantly associated with any other polymorphisms we examined; the Glu298Asp variant was also not linked to any other polymorphisms. In conclusion, the Glu298Asp missense variant was significantly associated with essential hypertension, which suggests that it is a genetic susceptibility factor for essential hypertension.
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PMID:Endothelial nitric oxide synthase gene is positively associated with essential hypertension. 967 30

Among cardiovascular diseases, hypertension, angina pectoris, acute myocardial infarction and ischemic stroke present a circadian pattern with a greater incidence of unfavourable events between awakening and noon. Chronotherapy aims to use drugs that release their active principles at different times during the day, according to biological needs. In chronotherapy of cardiovascular diseases, a particular attention has been paid to slow-release drugs that assure a 24 hours therapeutic effect with once a day administration. In primary hypertension well controlled by monotherapy (dipper hypertensives), the morning administration of long-acting beta-blockers and calcium antagonists has shown to control blood pressure over 24 hours, whereas ACE-inhibitors have proved more effective when administered at evening. In secondary hypertension (non dipper hypertensives) the administration of calcium antagonists is more effective at evening. Patients with severe hypertension need polytherapy. In that case, at least one of the antihypertensive drugs should be given at evening to lower night blood pressure values, which are particularly elevated also during sleep, and so to prevent an excessive blood pressure rise on awakening. In chronic monotherapy of ischemic heart disease, long-acting beta-blockers and calcium antagonists have shown to be equally effective when they are administered at morning, whereas slow-release nitrates, which need a nitrate-free interval, are to be administered either at morning or at evening, according to the expected time of onset of anginal pain. ASA seems to reduce the morning incidence of acute myocardial infarction, while tissue-type plasminogen activator presents a circadian variation of its thrombolytic activity with a higher efficacy between noon and midnight.
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PMID:[Application of chronotherapy to cardiovascular diseases]. 979 79

Primary aldosteronism (PA) is widely believed to be a relatively benign form of hypertension associated with a low incidence of vascular complications. However, several recent studies showed that cardiovascular complications were not rare in PA. PA is known as one of the most typical forms of sodium-sensitive hypertension. Recently, we found that the sodium sensitivity of blood pressure was a marker for greater risk for cardiovascular complications, especially stroke, in patients with essential hypertension. Therefore, we investigated cardiovascular complications in 58 patients with PA confirmed to be Conn's adenoma. Cardiovascular complications were found in 34% of 58 patients. Coronary artery disease was found in only one patient (1.7%), as angina pectoris. Stroke was found in nine patients (15.5%), four patients (6.9%) with cerebral infarctions and five patients (8.6%) with cerebral hemorrhages. Proteinuria and renal insufficiency were found in 14 (24.1%) and 4 (6.9%) patients, respectively. The incidence of cerebral infarction and renal insufficiency was greater in men than women. The prevalence of proteinuria was greater in patients with than without stroke (P = 0.03) among those aged older than 40 years. These results indicated that cardiovascular complications, especially stroke and proteinuria, were common in patients with PA, and proteinuria might be an indicator for stroke as target-organ damage.
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PMID:Cardiovascular complications in patients with primary aldosteronism. 1002 36

Biological functions and processes, including cardiovascular ones, exhibit significant circadian (24-hour) and other period rhythms. Ambulatory blood pressure assessment reveals marked circadian rhythms in blood pressure both in normotensive persons and hypertensive patients, whereas Holter monitoring substantiates day-night patterns in electrocardiographic events of patients with ischemic heart disease. The concept of homeostasis, that is, constancy of the milieu interne, which has dominated the teaching, research, and practice of medicine during the 20th century,is now being challenged by emerging concepts from the field of chronobiology-the science of biological rhythms. Epidemiologic studies document the heightened morning-time risk of angina, myocardial infarction, and stroke. Circadian rhythms in coronary tone and reactivity, plasma volume, blood pressure, heart rate, myocardial oxygen demand, blood coagulation, and neuroendocrine function plus day-night patterns in the nature and strength of environmental triggers all contribute to this morning vulnerability. Homeostatically devised pharmacotherapies, that is, medications formulated to ensure a near-constant drug concentration, may not be optimal to adequately control diseases that vary in risk and severity during the 24 hours. Moreover, circadian rhythms in the physiology of the gastrointestinal tract, vital organs, and body tissues may give rise to administration-time differences in the pharmacokinetics and effects of therapies. Thus the same medication consumed in the same dose under identical conditions in the evening and morning may not exhibit comparable pharmacokinetics and dynamics. New technology makes possible chronotherapy, that is, increase of the efficiency and safety of medications by proportioning their concentrations during the 24 hours in synchrony with biological rhythm determinants of disease. The chronotherapy of peptic ulcer disease achieved by the evening dosing of H 2-receptor antagonists and of asthma by the evening dosing of special drug delivery forms of theophylline and morning methylprednisolone administration has proven to be beneficial. Controlled-onset extended-release verapamil constitutes the first chronotherapy of essential hypertension and ischemic heart disease; once-a-day bedtime dosing results in a high drug concentration in the morning and afternoon and a reduced one overnight. Studies demonstrate effective 24-hour control of blood pressure, including the attenuation of its rapid rise in the morning, without induction of nighttime hypotension. Moreover, this formulation effectively controls angina, especially in the morning when the risk of ischemia is greatest. Determination of the role of verapamil chronotherapy in the primary prevention of cardiovascular morbidity and mortality awaits the results of the CONVINCE trial now in progress.
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PMID:Chronopharmacology and chronotherapy of cardiovascular medications: relevance to prevention and treatment of coronary heart disease. 1009 42

Nifedipine, as most calcium-antagonist drugs, is widely used for the treatment of angina pectoris and primary hypertension. Among its side effects, edema of lower limbs may expose patients to traumatic ulcers which become chronic. A case with painful ulcers and remarkable swelling of the ankles is reported. In this case, misdiagnosed as chronic venous insufficiency, good results were obtained with topical treatment and discontinuation of nifedipine. Leg ulcers and edema resolved in four months after ten years of disease history.
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PMID:[Edema and skin ulcers of the lower limbs as a collateral effect of nifedipine. A clinical case report]. 1052 48

Four hundred and nineteen elderly and old patients with pulmonary tuberculosis were examined. One hundred and ninety six patients were found to have an active tuberculous process and contaminant diseases: essential hypertension in 20.7%, functional classes II-III angina pectoris in 55.6%, postinfarct cardiosclerosis in 23.7%. Hypertrophy of the right cardiac cavities was frequently accompanied with that of the left ones (38.1%). Respiratory diseases caused by comorbidity were prevalent among acid-alkali balance disorders. Metabolic disturbances were detected in 90 (21%) patients. Evaluation of pulmonary and cardiac functions by the analysis of acid-alkali balance, gases, blood, and ECG in geriatric patients allows pathogenetic therapy to be timely and soundly.
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PMID:[Pulmonary and cardiac functions in patients with pulmonary tuberculosis]. 1075 Apr 25

Long-acting calcium antagonists have been shown to be safe and effective in lowering blood pressure, both as first-line agents and in combination with other classes of antihypertensive drug. They have also been shown to reduce the incidence of cerebrovascular and cardiovascular events in elderly patients with predominantly systolic hypertension. It is clear that reduced morbidity and mortality in hypertension is related to the degree to which blood pressure is reduced, regardless of the therapy used. This is the single most important conclusion of all recent trials, especially in the sub-group of hypertensive patients with diabetes. The World Health Organization-International Society of Hypertension guidelines acknowledge this and do not make specific recommendations as to initial therapy in the absence of other medical factors. However the use of thiazide diuretics and beta-blockers has strong support from large placebo-controlled trials in patients with mild-moderate essential hypertension. The British Hypertension Society and JNC VI guidelines restrict their recommendations for the use of calcium antagonists to isolated systolic hypertension and angina, or when other agents have failed, are contraindicated or are not tolerated. However, their efficacy in lowering blood pressure, their tolerability and potentially beneficial secondary effect on proteinuria, especially in combination with an angiotensin-converting enzyme inhibitor, still make them attractive antihypertensive agents. The results of further long-term outcome trials that make direct comparisons between calcium antagonists and other classes of antihypertensive drug are still awaited. Unlike angiotensin-converting enzyme inhibitors, the antiproteinuric effect of calcium antagonists, even that of the non-dihydropyridine type, seems to depend on an adequate and stable reduction in blood pressure.
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PMID:Are calcium antagonists effective in preventing complications of hypertension and progression of renal disease? 1099 Mar 66

Accumulating evidence strongly suggests that an alteration in nitric oxide metabolism is involved in the pathogenesis of hypertension. We recently found 2 polymorphisms in the endothelial nitric oxide synthase (eNOS) gene, a Glu298Asp missense variant in exon 7 and a T-786-->C variant in the 5'-flanking region, which are not linked to each other. In our previous reports, we showed a positive association between the Glu298Asp variant and essential hypertension, myocardial infarction, and coronary spastic angina. We also revealed that the T-786-->C variant is strongly associated with coronary spastic angina and leads to the reduction of the eNOS gene promoter activity. To further investigate the genetic involvement of the eNOS gene in essential hypertension, we examined the frequency of T-786-->C variant in two independent populations of persons with essential hypertension in Kyoto (n=215) and Kumamoto (n=186) and compared the frequency with that in each age- and gender-matched control (233 controls in Kyoto and 223 controls in Kumamoto). In both groups, the frequency of T-786-->C variant was similar in patients with hypertension and normal controls. In conclusion, the T-786-->C variant was not positively associated with essential hypertension. Given the evidence of positive association of another polymorphism in the eNOS gene, the Glu298Asp polymorphism, with essential hypertension, special attention will be required to interpret the results of a case-control study for genetic risk factors.
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PMID:Lack of association between T-786-->C mutation in the 5'-flanking region of the endothelial nitric oxide synthase gene and essential hypertension. 1113 Dec 66


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