Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In subjects with coronary artery diseases (obstructive and vasospastic angina pectoris (AP)) who have no diabetes, hypertension, obesity and physical inactivity, insulin sensitivity was significantly reduced with compensated hyperinsulinemia on OGTT. Insulin resistance significantly correlated with coronary atherosclerosis score. In vasospastic AP (VAP), those who fulfilled more than 3 risk factors out of 5 (hyperinsulinemia, obesity, glucose intolerance, hypertension, dyslipidemia) consist of 70 and 40% for smokers and nonsmokers respectively. Insulin resistance syndrome who fulfilled all the criteria was 9-10% for VAP. In atherothrombotic brain infarction (ATTI) with the same exclusion criteria, the similar insulin resistance and hyperinsulinemia have been observed, but not in embolic (cardiac origin) or lacunar infarction. In ATTI, high TG and apo B with low HDL-chol were noted in blood. In essential hypertension without diabetes and obesity, hyperinsulinemia was noted in 25-35% and insulin resistance in 56-88%. Reduction of blood pressure with alpha blocker (bunazosin), ACE inhibitor (cilazapril), long-acting Ca++ blocker (amlodipine) significantly improved lowered insulin sensitivity. Insulin resistance rather than hyperinsulinemia is more closely associated with blood pressure. Cardiovascular diseases (vasospastic and obstructive AP, brain cortical artery diseases) are prone to develop diabetes because of insulin resistance and also promote the generation of cumulative risk factors resulting in a vicious cycle. Efforts to alleviate insulin resistance is crucial for the primary and secondary prevention of cardiovascular diseases.
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PMID:Clinical impact of insulin resistance syndrome in cardiovascular diseases and its therapeutic approach. 924 Jul 71

Calcium antagonists are useful for treating hypertension, stable exertional and vasospastic angina, and supraventricular arrhythmias. Recent studies have proven their ability to decrease the rate of nonfatal strokes. Short-acting calcium antagonists should be avoided with hypertensive emergencies and urgencies, unstable angina, and acute myocardial infarction. The use of calcium antagonists in systolic heart failure should not be as the primary therapy. Care must be taken in using non-dihydropyridines because of multiple drug-drug interactions. Prospective trials are in progress through the next decade that will compare traditional drugs such as diuretics and beta-blockers to calcium antagonists, converting enzyme inhibitors, and angiotensin II receptor blockers.
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PMID:Calcium antagonists--clinical considerations. 959 57

There are only a few reports concerning coexistent hypertrophic cardiomyopathy (HCM) and vasospastic angina. Clinical characteristics in patients with both diseases have not been clarified yet. This study was designed to elucidate the relationship between chest pain and coronary vasospasm in HCM patients and to delineate clinical characteristics in patients with both HCM and coronary vasospasm. First, 36 patients with HCM underwent acetylcholine provocation test for coronary vasospasm and were divided into two groups on the basis of presence or absence of coronary vasospasm. Next, the following risk factors for coronary artery disease were compared between the two groups: hypertension, smoking, hyperlipidemia, diabetes mellitus, and hyperuricemia. Coronary vasospasm was induced in 10 (28%) of 36 patients with HCM. There were no significant differences in age and male gender between the two groups. Smoking was more prominent in HCM patients with than without coronary vasospasm (80% vs 35%, p<0.05), but there were no differences in the prevalence of other risk factors between the two groups. In conclusion, coronary vasospasm appears to play a significant role in the etiology of myocardial ischemia in Japanese patients with HCM, and smoking might be a major risk factor for coexistence of HCM and coronary vasospasm.
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PMID:Clinical characteristics in Japanese patients with coexistent hypertrophic cardiomyopathy and coronary vasospasm. 978 50

Nifedipine is a Ca-antagonist drug that reduces contractility of vascular smooth muscle, and is used in the treatment of arterial hypertension and of stable and vasospastic angina. Aim of this study is to evaluate long-term effect of nifedipine on distribution of body fluid compartment, assessed by BIA (Bio-Impedance Analysis), and on cardiac function, in hypertensive patients on dialysis. Two groups of hypertensive patients were compared: a) a first group of nine patients (5 Male, 4 Female; age 62.67 +/- 10.39) treated with nifedipine (30 mg/day) for one year; b) a control group of sixteen dialysis patients (9 Male, 7 Female; age 56.31 +/- 14.44), previously hypertensive, with normal blood pressure without anti-hypertensive drugs for three months or more. By BIA, extracellular water percentage (ECW%) is higher in nifedipine-treated patients (p < 0.001) in comparison with the control group before dialysis; no other difference is present. The intradialytical variations (before dialysis vs. the end of dialysis) of body fluid compartments are a significant decrease of total body water % (52.33 +/- 2.89 vs. 48.72 +/- 3.35, p < 0.001), ECW% (40.97 +/- 2.2 vs. 37.56 +/- 3.47, p < 0.005), Left Ventricular End-Diastolic Volume (81.1 +/- 14.6 vs. 63.4 +/- 21.66 ml/m2, p < 0.003), Cardiac Output (3.35 +/- 0.71 vs. 2.51 +/- 0.76 l/min/m2, p < 0.04) and Stroke Volume (45.76 +/- 10.21 vs. 34.34 +/- 9.98 ml/m2, p < 0.02) in nifedipine-treated patients. Our findings suggest that nifedipine induces intermittent and prolonged expansion of extra-cellular volume. This condition, in patients otherwise without clinical and echocardiographic signs of heart failure, can be potentially detrimental for cardiac function on long-term nifedipine treatment.
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PMID:Nifedipine and extracellular water in dialysis arterial hypertension. 979 73

The term X syndrome is used to indicate a group of patients who present anginous symptoms and ischemic-type electrocardiographic alterations which appear during exercise tolerance tests, dipiridamol tests or Holter's dynamic monitoring where coronary ultrasonography reveals no evident coronary lesions, vasospastic angina, arterial hypertension and/or diabetes mellitus, block of the left branch when resting or exercising, cardiomyopathy or valvulopathy. The highest incidence is in females with a mean age of around 50. A reduced reserve of coronary flow, highlighted both in response to vasodilatators or rapid stimulation and by positron emission tomography (PET), underlies this syndrome. It is thought to be caused by a dysfunction of the coronary microcirculation which consists in a deficit of the endothelium-dependent vasodilatory mechanisms, probably also owing to the accumulation of vasoconstrictive type substances, like endothelin-1. In addition to a dysfunction of the coronary microcirculation, one widely backed hypothesis concerns the existence of an altered perception of painful symptoms in patients with X syndrome: the anomalous constriction of prearteries might cause an increased release of adenosine, able to provoke angina despite the scarce signs of myocardial ischemia in terms of the metabolic or functional profile. From a therapeutic point of view, treatment of these patients is often ineffective: treatment should be based on the use of nitrates, calcium-antagonists or beta-blockers, if necessary moving on to other forms of therapy (aceinhibitors, xanthine methylate, estrogens, alphablockers, imipramine); the simultaneous use of tranquillizers may be useful in view of the anxious personality often characteristic of these patients.
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PMID:[Syndrome X and microvascular angina]. 988 62

Amlodipine is a calcium channel antagonist of the dihydropyridine group. It is effective for treating hypertension, chronic stable angina, and vasospastic angina. However, it is difficult clinically to pinpoint the maximum dosage for antihypertensive activity of the drug without having parallel data on the plasma drug concentrations. The methods for assaying amlodipine are either gas chromatography with electron capture detector or liquid chromatography coupled with tandem mass spectrometry (or with an electrochemical detector), which needs tedious derivatization, and is expensive and time consuming. Therefore, in this study we developed an enzyme immunoassay for determining amlodipine in plasma. Anti-amlodipine antibodies were produced following immunization of bovine serum albumin-amlodipine conjugate. These specific antibodies were used in a competitive biotin-avidin-based enzyme-linked immunosorbent assay to measure amlodipine in plasma. Biotin was linked to the antibodies in order to enhance the sensitivity of the assay. The assay was specific for the free form of amlodipine with a detection limit of 0.1 ng/ml and the intra- and interassay coefficient of variation ranged from 1.6-10.2%. This immunoassay provides a sensitive, reliable, rapid, and accurate method for determination of amlodipine in plasma, which can be used in therapeutic drug monitoring pharmacokinetic studies and pharmaceutical analysis.
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PMID:Enzyme linked immunosorbent assay for determination of amlodipine in plasma. 1117 Feb 35

Drugs classified as calcium channel blockers (CHBs) are now among the most frequently prescribed drugs for the treatment of cardiovascular disease. Although the currently available CCBs have major differences in their structural and cardiovascular effects, they share the common property of blocking the transmembrane flow calcium ions through voltage gated L-type channels. These drugs have been approved for the treatment of hypertensive heart disease: they reduce left ventricular hypertrophy and improve its sequelae, such as ventricular dysrhythmias, impaired filling and contractility, and myocardial ischemia. Long-acting CCBs have been shown to reduce mortality and morbidity in elderly patients with systolic hypertension, appear to be extremely useful in patients with cyclosporin-induced hypertension, and can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus, renal disease, Raynaud's phenomenon or migraine. Long-acting dihydropyridine have been shown to be effective and safe in the treatment classic angina pectoris and vasospastic angina, supraventricular arrhythmias, particularly reentrant AV-nodal tachycardia, others to be beneficial in patients with congestive heart failure, and all of them have potential for decreasing atherogenesis.
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PMID:[Calcium channel blockers in the treatment of cardiovascular disease]. 1157 40

Coronary artery calcification (CAC) was assessed by cinefluoroscopy and its extent was scored (CAC score) in 2,163 consecutive patients undergoing coronary angiography, based on the angiographic and clinical data, the patients were categorized into 8 types of coronary artery disease (CAD). The CAC score was lowest in angiographically normal subjects (0.12+/-0.60) and highest in patients with silent myocardial ischemia (14.31+/-8.61). Risk factors for CAC were advanced age, male sex (at age <80 years), hypertension, diabetes mellitus, and a high grade of organic coronary stenosis. The CAC score in patients with acute coronary syndrome (unstable angina+acute myocardial infarction; 5.48+/-7.42) was significantly lower than that in those with chronic CAD (silent ischemia+stable angina; 9.72+/-8.73; p<0.0001), but was still higher than that in normal subjects or those with vasospastic angina (0.92+/-2.88; p<0.0001). The results indicate that CAC is a manifestation of coronary atherosclerosis and its appearance depends on the pathological type of ischemic heart disease. Fixed stenosis with a slow and chronic process tends to be associated with CAC. The clinical implication of extensive CAC in acute coronary syndrome compared with normal subjects should be further investigated.
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PMID:Clinical significance of coronary calcification. 1203 Mar 43

The present study was conducted to evaluate the validity and reproducibility of noninvasive brachial-ankle pulse wave velocity (baPWV) measurements and to examine the alteration of baPWV in patients with coronary artery disease (CAD). Simultaneous recordings of baPWV by a simple, noninvasive method and aortic pulse wave velosity (PWV) using a catheter tip with pressure manometer were performed in 41 patients with CAD, vasospastic angina, or cardiomyopathy. In 32 subjects (15 controls and 17 patients with CAD), baPWV was recorded independently by two observers in a random manner. In 55 subjects (14 controls and 41 patients with CAD), baPWV was recorded twice by a single observer on different days. baPWV were compared among 172 patients with CAD (aged 62 +/- 8 years); 655 age-matched patients without CAD but with hypertension, diabetes mellitus, or dyslipidemia; and 595 age-matched healthy subjects without these risk factors. baPWV correlated well with aortic PWV (r=0.87, p<0.01). Pearson's correlation coefficients of interobserver and intraobserver reproducibility were r=0.98 and r=0.87, respectively. The corresponding coefficients of variation were 8.4% and 10.0%. baPWV were significantly higher in CAD patients than in non-CAD patients with risk factors, for both genders (p<0.01). In addition, baPWV were higher in non-CAD patients with risk factors than in healthy subjects without risk factors. Thus, the validity and reproducibility of baPWV measurements are considerably high, and this method seems to be an acceptable marker reflecting vascular damages. baPWV measured by this simple, noninvasive method is suitable for screening vascular damages in a large population.
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PMID:Validity, reproducibility, and clinical significance of noninvasive brachial-ankle pulse wave velocity measurement. 1989 68

The main peripheral sources of 5-hydroxytryptamine (5-HT) are as a neurotransmitter and local hormone in the gastrointestinal tract, and stored in circulating platelets and pulmonary neuroepithelial bodies. 5-HT has been shown to have many possible physiological and pathophysiological roles on the cardiovascular and renal systems. Thus, 5-HT may contribute to valvular heart disease, coronary artery disease, pulmonary hypertension, pulmonary embolism, pre-eclampsia, peripheral vascular disease and diabetic nephropathy. Consequently, modulators of the 5-HT system have diverse clinical potential. For instance, selective 5-HT subtype 3 receptor (5-HT(3)) antagonists may have potential in the treatment of the pain associated with myocardial infarction. MCI-9042 (sarpogrelate) or other 5-HT(2A) antagonists may have clinical potential for the treatment of vasospastic angina, ischaemic heart disease, reperfusion injury and hindlimb ischaemia. Several modulators of 5-HT (5-HT transporter inhibitors, 5-HT(1B) and (2B) antagonists) may have potential alone or in combination in the treatment of pulmonary hypertension. In hypertension, agonists at the 5-HT(7) and antagonists at the 5-HT(2B) may reduce blood pressure, and in diabetes, sarpogrelate may protect against nephropathy.
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PMID:The role of 5-HT on the cardiovascular and renal systems and the clinical potential of 5-HT modulation. 1272 Apr 92


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