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)

Serum creatine-kinase activity was above the upper normal limit in 40-80% of the 632 patients admitted to hospital for angina pectoris and deteriorating essential hypertension. The highest (4-6-fold) increase over the mean control values was associated with myocardial ischemia, paroxysmal tachycardia and hypertensive crises. Intramuscular injections were shown to be unrelated to increased incidence or magnitude of creatine-kinase activation in the examined patients. Creatine-kinase levels were particularly high in cases of cerebral stroke (a 7-fold increase above normal) and alcoholic cardiopathies (a 8-fold increase).
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PMID:[Blood serum creatine kinase in diseases of the cardiovascular system]. 406 63

Direct arterial pressure and electrocardiogram have been measured continuously over a period of 24 hours in 15 patients. Observations have been made on the behaviour of these variables during 30 separate episodes of motor car driving. The patients were divided into three groups: (1) five normotensive subjects, (2) five patients with essential hypertension who were not receiving therapy, and (3) five patients with angina pectoris who were either normotensive or hypertensive.In all but one subject, apart from variable changes in heart rate, no significant arrhythmias or S-T segment changes were observed in the electrocardiogram. The arterial pressure remained remarkably stable throughout the driving period in all three groups and there was no significant difference between the levels of blood pressure at the beginning and end of a journey. There were short periods of raised arterial pressure during driving related to such episodes as overtaking, but these quickly returned to baseline levels. Two patients experienced anginal pain during driving.It is concluded that motor car driving does not have such a pronounced effect on the blood pressure as might have been thought.
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PMID:Direct arterial pressure and electrocardiogram during motor car driving. 470 96

First, blood pressure and heart rate variability was studied in 89 normotensive and hypertensive ambulatory subjects with the use of an intra-arterial monitoring device. Short- and long-term variabilities were analyzed by computer. Absolute variabilities (standard deviations) were greatest in patients with hypertension, but relative variabilities (variation coefficients, i.e., standard deviations as percent of means) were slightly lower in the subjects with more severe hypertension. Second, the effect of nadolol on 24-hour blood pressure and heart rate values and on their variability was assessed in seven ambulatory patients with essential hypertension by means of the same intra-arterial device and computer analysis. Two recording sessions were performed (1) without treatment and (2) after 10 days' administration of nadolol once a day (dose range, 80 to 320 mg). Nadolol, given once a day, was shown to reduce blood pressure uniformly throughout the 24-hour period without loss of activity in the hours farthest from administration. The lack of alteration in relative blood pressure variability suggests that nadolol lowers blood pressure without interfering with the mechanisms involved in cardiovascular homeostasis. Reduction in heart rate variability after nadolol suggests less chance of tachycardia episodes in patients with angina and/or arrhythmias receiving nadolol.
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PMID:Twenty-four-hour blood pressure profile and blood pressure variability in untreated hypertension and during antihypertensive treatment by once-a-day nadolol. 614 66

This review summarizes the available medical literature about plasma norepinephrine, which as been used as an indicator of sympathetic neural activity in clinical cardiology. Plasma norepinephrine levels are elevated myocardial infarction and congestive heart failure, and the norepinephrine concentration varies with severity of disease. Patients with ischemic heart disease at rest show essentially normal plasma norepinephrine, but no studies have assessed norepinephrine levels during spontaneously occurring typical angina pectoris. Plasma norepinephrine also is increased during hypertension occurring after coronary bypass surgery or repair of aortic coarctation. Propranolol increases plasma norepinephrine, and acute withdrawal of propranolol does not. Sodium restriction increases plasma norepinephrine in healthy persons, but no information is available about its effect on patients with congestive heart failure. Insufficient data are available to make strong inferences about sympathetic activity in cardiomyopathy, essential hypertension or pulmonary hypertension, and little or no information is available about plasma norepinephrine in ventricular fibrillation without myocardial infarction, the mitral valve prolapse syndrome, digoxin effect, syndromes associated with prolonged electrocardiographic Q-T interval and the hyperkinetic heart syndrome.
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PMID:Plasma norepinephrine as an indicator of sympathetic neural activity in clinical cardiology. 617 Nov 57

We investigated the alteration of the ACE in different parts of the circulation in 21 patients with essential hypertension, who suffered from angina pectoris attacks. Blood samples were taken during diagnostic cardiac catheterisation. The ACE was fluorimetrically measured and compared to 48 normotensive patients. In 11 patients the Plasma Renin Activity (PRA) was additionally determined by means of bioassay. The ACE was significantly (p less than 0.001) elevated in all investigated regions but a different distribution was not observed. We found a positive correlation between the ACE from the left ventricle and the systolic, mean arterial and diastolic blood pressure. Furthermore, we observed a negative correlation between ACE and PRA. No relationship could be calculated between ACE and electrolytes, creatinine or haemodynamic parameters. Our results indicate that the ACE may contribute to the pathogenesis of so-called essential hypertension.
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PMID:Elevated angiotensin-I-converting enzyme (ACE) in patients with essential hypertension. 628 14

The pharmacokinetics, clinical efficacy, and adverse effects of three calcium-channel blocking agents--verapamil, nifedipine, and diltiazem--are reviewed. Verapamil, nifedipine, and diltiazem are absorbed well after oral dosing, but absolute bioavailability of each is reduced substantially by a first-pass effect. Each drug is metabolized extensively (verapamil and diltiazem to moderately active metabolites) by the liver. A substantial percentage of each drug is bound to plasma proteins, but the binding is of clinical importance only for nifedipine (92--98% protein bound). Intravenous verapamil has become the agent of first choice for treatment of acute paroxysmal supraventricular tachycardia (PSVT); use of chronic oral verapamil therapy for prophylaxis remains controversial. Verapamil and diltiazem have been evaluated with mixed results for atrial flutter and fibrillation. For treatment of myocardial ischemia, calcium-channel blockers may be of some value (possibly in combination with nitrates of B blockers). All three agents have been studied in patients with exertional angina with good results. Calcium-channel blockers appear to be equal with nitrates for treatment of variant angina. Patients with hypertropic cardiomyopathy have been treated with verapamil and nifedipine with promising results. Nifedipine has been effective for treatment of essential hypertension. Adverse effects of calcium-channel blockers have been relatively minor or infrequent. Diltiazem overall has the best side-effect profile, with adverse effects causing discontinuation of therapy in about 2--10% of patients; verapamil in intermediate (8--10%) and nifedipine the worst (17%) in this respect. The most common side effects generally are fatigue, headache, dizziness, skin rash, and peripheral edema. While they generally should be reserved for patients in whom more conventional therapy has failed (except those with PSVT), calcium-channel blockers appear to have a valid role as reserve agents for exertional and variant angina, cardiomyopathy, and hypertension.
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PMID:Update on calcium-channel blocking agents. 635 66

The present study was undertaken to quantify the circulating kinins in patients with various cardiovascular diseases using a newly developed radioimmunoassay technique and to evaluate this method in terms of its clinical application. For the determination of bradykinin (BK), this assay uses a rabbit anti-serum which has been injected with kallidin. This assay shows good specific activity, recovery and reproducibility. In order to avoid the formation of kinin as well as to block its inactivation, human blood samples were collected with a polypropylene syringe containing an inhibitor mixture (EDTA, trasylol, 1-10-phenanthroline, soybean trypsin inhibitor, polybrene). 1) The plasma BK concentration in normal human subjects, in patients with essential hypertension, effort angina and other cardiac diseases were 12.2, 9.2, 8.0 and 14.0 pg/ml, respectively. 2) Thirty min after captopril (12.5 mg, p.o.) administration, blood pressure and pulmonary wedge pressures decreased, and cardiac output increased accompanied with increases in plasma renin activity, plasma BK concentration and plasma norepinephrine concentration. 3) During the cold pressor test, both plasma BK concentration and blood pressure increased in the normal human subjects, whereas plasma BK levels decreased and blood pressure increased in the patients with hypertension. This radioimmunoassay for plasma BK determination makes it possible to measure plasma BK concentration in patients with various cardiac diseases.
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PMID:[Plasma bradykinin concentration in patients with cardiovascular diseases]. 636 31

Hemorheological considerations are beginning to alter routine clinical practice. A hemorheological defect may play a primary etiological role not only in classical diseases like polycythemia, but also in conditions such as essential hypertension and non-coronary angina. Hemorheological abnormalities may also play a part in arterial thrombosis through a number of mechanisms, and are a frequent accompaniment in many cases of atherosclerosis, where they carry a bad prognosis. Our new awareness of the dangers of a high hematocrit, even in the normal range, has had widespread consequences on the management of not only all kinds of ischemic disease, but also for instance on surgical practice in general. Finally, hemorheological treatment has much wider applications than simply in conditions where a hemorheological abnormality has been detected. Treatment aimed at improving the flow properties of blood, whether by drugs, hemodilution or plasmapheresis, may also be the most practical and effective therapy for ischemia due to insufficient blood flow down narrowed arteries.
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PMID:[The influence of hemorrheology on the practice of clinical medicine]. 636 97

In this overview of the achievements of the National Heart, Lung, and Blood Institute (NHLBI), the major developments in each major form of heart disease since the birth of the Institute 35 years ago are reviewed. In the case of congenital heart disease, it has become possible to establish an accurate diagnosis, often by noninvasive methods, and to correct by surgical treatment almost all congenital cardiac malformations. The major challenge now is to eliminate these disorders; this will require an understanding of the fundamental molecular basis of these lesions. Acquired valvular heart disease can also now be characterized by hemodynamic, angiographic, as well as noninvasive techniques, principally echocardiography. Surgical treatment is usually successful, but improvement in the durability of valves without thromboembolic potential remains an important challenge. While essential hypertension can now be managed pharmacologically in almost every patient and while such management reduces the excess mortality resulting from this condition, current research focuses on elucidating the underlying basis of this disorder. Atherosclerosis remains the most common cause of cardiac and vascular disease. Although its cause has not been defined, several abnormalities in lipid metabolism that play an etiologic role in many patients with atherosclerosis have been identified. The treatment of these disorders with cholesterol-binding resins, which increase the number of cellular receptors for low-density lipoprotein, and with inhibitors of the enzyme required for cholesterol biosynthesis holds considerable promise. Noninvasive techniques will be used increasingly for detection of atherosclerosis in asymptomatic persons and for determining the efficacy of therapy. The mortality resulting from acute myocardial infarction has been reduced in half by the development of coronary care units and the prompt treatment of potentially fatal ventricular tachyarrhythmias. Current research is focused on preventing pump failure by limiting infarct size; lysis of coronary thrombi now appears to be the most promising method of accomplishing this. Chronic angina pectoris can be relieved by the judicious use of three classes of drugs--organic nitrates, beta-adrenergic blockers, and calcium antagonists, and two mechanical approaches--percutaneous transluminal coronary angioplasty and coronary artery bypass grafting--are usually successful in relieving angina in patients who do not respond adequately to medical management. Whether or not any of these approaches prolong life is not yet settled.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Thirty-five years of progress in cardiovascular research. 638 25

In order to clarify the hemodynamic characteristics in essential hypertension (HT) with angina pectoris (AP), systolic time intervals (STIs) were measured in 13 normal subjects (N), 23 patients with AP, 43 HT (WHO stage I: 13, WHO stage II: 23, WHO stage III: 7) and 19 HT with AP (WHO I: 9, WHO II: 10). The ET/PEP ratio was 2.41 +/- 0.24 in N, 2.70 +/- 0.34 in AP (p less than 0.02, vs N), 2.25 +/- 0.29 in WHO I, 2.13 +/- 0.25 in WHO II (p less than 0.01, vs N), 1.54 +/- 0.37 in WHO III (p less than 0.001, vs N), 2.68 +/- 0.32 in WHO I with AP (p less than 0.05, vs N: p less than 0.005, vs HT) and 2.71 +/- 0.30 in WHO II with AP (p less than 0.02, vs N: p less than 0.001, vs HT). Ejection time index (ETI) was 385 +/- 15 msec in N, 399 +/- 16 in AP (p less than 0.05, vs N), 387 +/- 13 in WHO I, 385 +/- 15 in WHO II, 363 +/- 25 in WHO III (p less than 0.05, vs N), 393 +/- 16 in WHO I with AP and 402 +/- 15 in WHO II with AP (p less than 0.05, vs N: p less than 0.01, vs HT). Pre-ejection period index (PEPI) was 142 +/- 10 msec in N, 135 +/- 11 in AP, 148 +/- 12 in WHO I, 156 +/- 13 in WHO II (p less than 0.005, vs N), 192 +/- 24 in WHO III (p less than 0.001, vs N), 134 +/- 13 in WHO I with AP (p less than 0.05, vs HT) and 136 +/- 9 in WHO II with AP (p less than 0.001, vs HT). These results showed that the ET/PEP ratio in HT with AP was significantly higher than that in HT alone, and this increase in ET/PEP ratio was mainly due to the shortening of PEP interval in WHO stage I and the lengthening of ET in addition to it in WHO stage II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Noninvasive evaluation of left ventricular function by systolic time intervals in essential hypertension with angina pectoris. 651 40


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